Second Congress International Society of Intraoperative Neurophysiology (ISIN) Dubrovnik, Croatia Dubrovnik, 2009 November 12-14
November, 2009
Dear Friends and Colleagues,
We would like to cordially welcome all participants to the Second Congress of the International Society of Intraoperative Neurophysiology.
The Congress has been designed to provide an innovative and comprehensive overview of the latest research developments in intraoperative monitoring during neurosurgical procedures.
As many of you may already know, two years ago we held our first ISIN congress in Lucerne, Switzerland and it was a resounding success. This year, in lieu of our past experience we are introducing lectures devoted to new developments in intraoperative neurophysiological testing of eloquent cortical areas. Our functional neurosurgery program will also cover both monitoring during functional neurosurgical procedures and modeling of the neural systems. The program will include topics on movement disorders, deep brain stimulation, cortical stimulation, epilepsy, and stimulation modeling. In addition to lectures by invited speakers and breakfast sessions, we are including a session on selected posters. Our attendees and speakers include neurosurgeons, neurophysiologists, neurologists, orthopedic surgeons, neuroradiologists, anesthesiologists, ENT surgeons, neuroscientists, movement disorder specialists, and technicians from around the world.
We hope that you will enjoy the Congress and that your interaction with your international colleagues will stimulate a creative exchange of ideas and be personally rewarding. Lastly, we hope and trust you will enjoy your visit to the very beautiful Croatia and city of Dubrovnik.
Yours sincerely,
Vedran Deletis, MD, PhD Congress Host
Organizing Committee Host Vedran Deletis, MD, PhD Director, Intraoperative Neurophysiology Institute for Neurology & Neurosurgery St. Lukes/Roosevelt Hospital Suite 2B-30 1000 Tenth Avenue New York, NY 10019 Tel 212 636 3280 Fax 212 636 3159
Organizing Committee Francesco Sala Jay Shils Karl Kothbauer David B MacDonald Jorge J. Gomez Ilaria Tonelli
Under the Auspices of International Society of Intraoperative Neurophysiology (ISIN)
Please visit our webpage to download this book: www.isincroatia2009.org Invited Speakers ISIN 2009
Vahe Amassian, MB Josep M Espadaler, MD, PhD Dept. of Physiology and Neurology, SUNY Director, Clinical Neurophysiology Department 450 Clarkson Av, Box 31 Hospital del Mar Brooklyn, NY 11203 Associate Professor, Medicine School Tel: 718 270 3900, Tel: 718. 270.3105 Universidad Autonoma de Barcelona F: 718.270.3840 F: 914.967.3682 Barcelona, Spain [email protected] Jeffery E. Arle, MD, PhD Department of Neurosurgery Professor Janet Eyre, BSc, MB ChB, D Phil, Lahey Clinic FRCP, FRCPCH 41 Mall Road Institute of Neuroscience, Newcastle University Burlington, MA 01805 Sir James Spence Institute, Royal Victoria Tel 781 744 8644 (5440), Fax 781 744 3160 Infirmary, Queen Victoria Infirmary, [email protected] Newcastle upon Tyne NE1 4LP Phone 0191 2821386; Fax 0191 2824725 Lorenzo Bello, MD [email protected] Associate Professor of Neurosurgery, Dept of Neurological Sciences, Isabel Fernandez-Conejero, MD Università degli studi di Milano Department of Intraoperative Neurophysiology Via Francesco Sforza 35 Hospital Universitari de Bellvitge Tel: 39 02 5503 5502, Fax 39 02 59902239 Feixa Llarga, s/n. 08907 L´Hospitalet de Llobregat. [email protected] Barcelona, Spain. Tel: 0034 933 357 011, Fax: 0034 932 607 887 Beatrice Cioni, MD [email protected] Assistant Professor Neurosurgery [email protected] Catholic University Lg. A. Gemelli 8 Ursula S. Hofstoetter, MSc Rome, Italy 00168 Institute of Analysis and Scientific Computing, Tel: +39 o6 30155468; Cell: +39 3394960037 Vienna University of Technology, Vienna, [email protected] Austria; and Center for Biomedical Engineering and Physics, Medical University of Vienna Paolo Costa, MD Wiedner Hauptstrasse 8-10/101, A-1040 Section of Clinical, Neurophysiology, Center for Biomedical Engineering and Physics, CTO Hosp, Medical University of Vienna, Vienna, Austria: Torino, Italy Waehringer Guertel 18-20/4L, A-1090 Phone/fax: +39 366 3658416 Vienna, Austria. [email protected] Tel: +43 1 40400 1988; Cell: +43 676 336 80 74 [email protected] Vedran Deletis, MD, PhD Director, Intraoperative Neurophysiology H. Louis Journee, MD, PhD St Luke's/Roosevelt Hospital Depts. of Neurosurgery UMC-Groningen and 1000 Tenth Avenue, Ste. 2B-30 Orthopedics Sint Maartenskliniek Nijmegen, New York, NY 10019 The Netherlands Tel: 212 636 3281, Fax: 212 636 3159 [email protected] [email protected] Prof. Dr. med. Spyros S. Kollias, Charles Dong, PhD Chief of MRI , Institute of Neuroradiology EEG Lab, Vancouver General Hospital University Hospital of Zurich 855 West 12th Avenue Frauenklinikstrasse 10 Vancouver, B.C. CH 8091, Switzerland Canada V5Z 1M9 Tel: + 044 2555644 (dir), + 044 2555600 (sec) Tel: 604-8754400; Fax: 604-8755669 Fax:+ 044 2554504 [email protected]. [email protected] www.neuroscience.ethz.ch/research/biomedical_tec hnology/kollias Karl F. Kothbauer, M. D. Robert J. Morecraft, PhD Chief, Division of Neurosurgery, Dept. of Surgery Professor, Laboratory of Neurological Sciences General and Pediatric Neurosurgery Director, Medical and Allied Health Gross Anatomy Luzerner Kantonsspital Sanford School of Medicine CH-6000 Luzern University of South Dakota Switzerland [email protected] Tel: 0041-41-2054504 Fax: 0041-41-2055740 Georg Neuloh, MD [email protected] Senior Neurosurgeon, www.ksl.ch Friedrich-Wilhelm University of Bonn Joachim K. Krauss, MD Germany Professor of Neurosurgery [email protected] Chairman and Director, Department of Neurosurgery Yasunari Niimi, M.D., Ph.D Medical School Hannover Center for Endovascular Surgery Carl-Neuberg-Str. 1 Institute for Neurology and Neurosurgery, 30625 Hannover, Germany Roosevelt Hospital, 10 G Tel: 0511-5326651 or 6652 New York, NY, USA Fax: 0511-5325864 1000 Tenth Avenue [email protected] New York, NY 10019 Tel: 212-636-3400 ; Fax: 212-636-3296 David B. MacDonald, MD, FRCP(C), ABCN [email protected] Head, Section of Neurophysiology Department of Neurosciences Dachling Pang, MD, FRCS (C), FRCS (Eng), King Faisal Specialist Hospital & Research Center FACS MBC 76, PO Box 3354 Professor of Pediatric Neurosurgery University of Riyadh, 11211 Saudi Arabia California, Davis Chief, Regional Centre for Tel: +966-1-464-7272 Ext. 32772 Pediatric Neurosurgery Fax: +966-1-442-4763 Kaiser Permanente Hospitals [email protected] Northern California Kaiser Permanente Medical Center Gayane Margaryan, M. Sc., PhD Department of Pediatric Neurosurgery Neurobiology Sector 280 W. MacArthur Blvd. International School for Advanced Studies Oakland, CA 94611 (SISSA/ISAS) Tel: (510) 752-1759; Fax: (510) 752-1758 Via Beirut 2-4, 34151, Trieste, Italy [email protected] Tel: +39 040 3756557, Lab: +39 040 3756553, Fax: +39 040 3756502 Zvezdan Pirtošek, MD [email protected] Department of Neurology University Medical Center Karen Minassian, PhD Zaloška 7, SI-1525 Ljubljana, Slovenia Institute of Analysis and Scientific Computing, Tel: (386) (01) 522 2864 Vienna University of Technology, Austria; [email protected] Center of Biomed, Engineering and Physics, Medical University of Vienna, Austria John Rothwell, PhD [email protected] Professor of Human Neurophysiology Sobell Dept, Box 146 Institute of Neurology Aage R. Møller, PhD, D. Med. Sci. Queen Sq, London WC1N 3BG Professor of Cognition and Neuroscience [email protected] MF Jonsson Endowed Chair School of Behavioral and Brain Sciences Francesco Sala, MD The University of Texas at Dallas Department of Neurological Sciences and Vision MP4.1 Section of Neurosurgery 800 W. Campbell Rd. University Hospital Richardson, TX 75080 Piazzale Stefani 1 [email protected] 37100 Verona, Italy Tel: 011-39-045-8072695 Fax: 011-39-045-916790 [email protected] Jay L. Shils, PhD, D.ABNM, FASNM Vernon L. Towle, PhD Director, Intraoperative Monitoring Professor of Neurology, Surgery Lahey Clinic Pediatrics and Psychiatry 41 Mall Rd. Department of Neurology, MC-2030 Burlington, MA 01805 The University of Chicago [email protected] 5841 S. Maryland Ave. Chicago, IL 60637 Tod Sloan, MD, MBA, PhD Tel: 773-702-3271 Associate Chair for Development [email protected] University of Colorado at Denver, http://towlelab.uchicago.edu School of Medicine Department of Anesthesiology, Sedat Ulkatan, MD Anschutz Office West (AO1), P.O. Box 6511 Attending, Intraoperative Neurophysiology 12631 E 17th Avenue, Aurora, Colorado 80045 St Luke's/Roosevelt Hospital Tel: 303-724-1751, Fax: 303-724-1761 1000 Tenth Avenue, Ste. 2B-30 [email protected] New York, NY 10019 Tel 212 636 3281, Fax 212 636 3159 Caspar Stephani, MD, PhD [email protected] Clinical Neurophysiology, University Hospitals Goettingen, Takamitsu Yamamoto MD, PhD Robert-Koch-Strasse 40, Department of Neurological Surgery 37075 Goettingen, Germany and Applied System Neuroscience, Case Western Reserve University, Nihon University School of Medicine Department of Neurology, Tokyo 173-8610, Japan 11100 Euclid Avenue, [email protected] Cleveland 44106, Ohio, U.S.A. [email protected]
PD Dr. med. Andrea Szelényi Department for Neurosurgery Johann Wolfgang Goethe University Hospital Schleusenweg 2 - 16 D 60528 Frankfurt Germany Tel (49) 69 6301 83452 Fax (49) 69 6301 7175 [email protected]
We would like to acknowledge and thank the following for their support in this year’s Congress
Inomed Medizintechnik GmbH Julia Thiemann Marketing Assistant Tullastrasse 5 a 79331 Teningen, Deutschland
Tel: +49 7641 9414-53 Fax: +49 7641 9414-94 http://www.inomed.com
Ad Tech Medical Instrument Corporation Angie Rico 1901 William Street Racine, WI 53404 [email protected];[email protected]
Care Fusion (Cardinal) Stephanie Schroeter 5225 Verona road Madison, WI 53711- 4495 USA [email protected]
Micromed Medizin-Elektronik GmbH Richard Brandmeier Bajuwarenstrasse 6 DE-86492 Egling an der Paar Deutschland / Germany Tel. +49-(0)8206 - 96 22 0 - 0 Fax +49-(0)8206 - 96 22 0 - 22 Email : [email protected] www.micromed-medizin.de
Cadwell Laboratories, INC Lori Kaufmann 909 N. Kellogg Street Kennewick, WA 99336 509-735-6481 [email protected]
ROLAND Instruments Carola Zaleska Friedrich-Franz TSrasse 19 Brandeburg an der Havel Stasche & Finger GmbH D-14770 Brandenburg [email protected]
ANT B.V. (Advanced Neuro Technology) Lamija Pašalić Eemagine GMBH, Berlin, Germany T: +31 (0)53 436 5175 F: +31 (0)53 430 3795 [email protected]
inomed started as a pioneer within the range of "intraoperative Neuromonitoring" (IONM). In a long history and in close cooperation to Neuro and ENT surgeons, inomed developed amplifiers, software, special needles and instruments for the cranial nerve monitoring and for the monitoring of the vocal cord nerve (recurrent laryngeal nerve) in thyroid surgery, where inomed has been the market leader since 1996.
Nowadays, inomed is the market leader in Europe in the Neurosurgical field of multimodal intraoperative Neuromonitoring including Micro Electrode Recording. With new intelligent solutions, inomed is further expanding its product range into other IOM fields as orthopaedic surgery, gynaecologic surgery and plexus surgery.
SECOND CONGRESS INTERNATIONAL SOCIETY OF INTRAOPERATIVE NEUROPHYSIOLOGY DUBROVNIK, CROATIA
Wednesday, November 11, 2009 17:30-19:30 Board Meeting ISIN
Day one: Thursday, November 12, 2009 Anatomical and Neurophysiological Aspect of the Corticospinal Tract Town Mayor 7:45-8:00 Opening Ceremony David B. MacDonald Vedran Deletis
8:00-8:45 The Corticospinal System in Health and Trauma Vahe Amassian
Some History of Monitoring Corticospinal Function Using Transcranial 8:45-9:30 John Rothwell Stimulation in Humans
9:30-10:10 Neurophysiology of the Corticospinal Tract Janet Eyre
Subcortical Organization of Motor Pathways to Brainstem Motor Nuclei 10:10-10:50 Robert J. Morecraft and the Spinal Cord
10:50-11:20 Coffee break
Recovery of Spinal Cord Functions and the Locomotor Central Pattern Generator from Experimental Research Model to Human (Clinical) Neurosciences Model New insights into the Pathophysiology of Acute Spinal Cord 11:20-11:50 Gayane Margaryan Injury in Vitro
Model of Spinal Cord Reflex Circuits in Humans: Stimulation Frequency- 11:50-12:05 Ursula S. Hofstoetter Dependence of Segmental Activities and their Interactions
12:05-12:20 Human Lumbar Cord model of the Locomotor Central Pattern Generator Karen Minassian
Neurophysiology of Acute Spinal Cord Injury (SCI) 12:20-12:40 Intraoperative Neurophysiology of the Spinal Cord Injured Patients Vedran Deletis
12:40-13:00 ION of Acute SCI Patients - Torino Experience Paolo Costa
13:00-13:20 Neuromonitoring of Acute Spinal Cord Injury: Verona experience Francesco Sala
13:20-13:40 How Safe and Accurate is Transcranial Electrical Stimulation? H. Louis Journee
13:40-15:10 Lunch break
Free Oral Papers 15:10-16:50
16:50-17:10 Coffee break
17:10-18:30 Free Oral Papers Continues
Day Two: Friday, November 13, 2009 Imaging of Spinal Cord 8:00-8:25 Imaging of Spinal Cord Function and Physiology Spyros S. Kollias
Endovascular Treatment of Vascular Malformations and Tumors of the 8:25-8:50 Yasunari Niimi Spine and Spinal Cord
Memorial Lecture - Fred Epstein The use of Electrophysiology Monitoring during Surgery for 8:50-9:30 Dachling Pang Spinal Dysraphism
9:30-9:55 Epilepsy Surgery: Functional Aspects Georg Neuloh
9:55-10:20 Coffee Break
10:20-11:00 Stimulation of the Insula Caspar Stephani
Mapping and Monitoring of the Eloquent Cortex Subcortical Mapping and DTI Fiber Tracking for Surgery in 11:00-11:25 Lorenzo Bello Language Areas
Navigated TMS Associated with DTI as a Tool for 11:25-11:50 Josep M. Espadaler Neurosurgical Planning.
11:50-12:15 Mapping Language and Memory Areas with ECoG Vernon L. Towle
A New Contribution to the Neurophysiologic Exploration of the 12:15-12:40 Vedran Deletis Broca Area
12:40-14:10 Lunch Break
ION Tumor and Vascular Surgery of the Brain Mary Menniti Memorial Lecture Functional Preservation in Surgery for Brain Tumors and Vascular 14:10-14:40 Georg Neuloh Malformations
14:40-15:10 Intraoperative Neurophysiology in Tumor and Vascular Neurosurgery Andrea Szelényi
15:10-15:40 ION for Brain Tumor Resection and Functional Neurosurgery Takamitsu Yamamoto
15:40-16:10 ION Tumor and Vascular Surgery of the Brain Aage R. Møller
16:10-16:30 Coffee Break
Anesthesia and ION Anesthetic Considerations During Intraoperative Neurological Monitoring 16:30-17:00 Tod Sloan Anesthesia Protocols for Surgery during Neuromonitoring
Poster Session 17:00-19:00
Dinner for Participants 20:00
Day Three, Saturday, November 14, 2009. Breakfast Session I 7:00-8:00 • Neurophysiological Mapping and Monitoring in Brain Surgery - Francesco Sala
• Interaction between the Neurophysiologist and Neurosurgeon during Functional Neurosurgical Procedures - Jay L. Shils and Jeffery E. Arle • Matching Stimulation and Recording Techniques to Different Functional
Requirements - Vahe Amassian • Guiding Surgeons in MVD of Hemifacial Spasm - Aage R. Møller • SEP/MEP Optimization - David B. MacDonald
Breakfast Session II 8:00-9:00 • ION in Aneurysm Surgery - Andrea Szelényi • Intraoperative Monitoring of CT, a Neurophysiological Point of View - Vedran Deletis • Intraoperative Monitoring of the Corticobulbar Tract - Isabel Fernandez-Conejero • Monitoring During Functional Neurosurgery other than DBS - Beatrice Cioni • Monitoring for Spinal Cord Tumor Resection - Karl F. Kothbauer
New IOM Methodologies Isabel Fernandez- 9:00-9:20 Corticobulbar Tract Monitoring - New York Experience Conejero
Corticobulbar Motor Evoked Potentials and their Application in Facial 9:20-9:40 Charles Dong Nerve Monitoring during Skull Base Surgery - Canada Experience
9:40-10:00 What's New in SEP Monitoring? David B. MacDonald
Isabel Fernandez- 10:00-10:20 Intraoperative Recording of Blink Reflex Conejero
Facial Nerve Monitoring and Mapping in Extracranial Surgery and 10:20:10:40 Sedat Ulkatan Sclerotherapy Procedures
10:40-11:00 Posterior Root-Muscle Reflex Karen Minassian
Persistently Electrified Pedicle Stimulation During Minimally Invasive 11:00-11:20 Jay L. Shils Lumbo-Sacral Fixation
11:20-11:50 Coffee Break
Stereotactic and Functional Neurosurgery 11:50-12:10 Neurophysiology of Movement Disorders Zvezdan Pirtošek
New Developments in Stereotactic and Deep Brain Stimulation 12:10-12:30 Joachim K. Krauss and Recording
12:30-12:50 Deep Brain Stimulation in Parkinson Disease and Dystonia Jay L. Shils
12:50-13:10 Motor Cortex Stimulation for Treatment in Parkinson's Disease Beatrice Cioni
13:10-13:30 Computational Models and Applications to Functional Neurosurgery Jeffery E. Arle
Round Table Discussion 13:30-14:30 Current Status and Future of ION
Farewell Lunch 14:30-16:30
SECOND CONGRESS INTERNATIONAL SOCIETY OF INTRAOPERATIVE NEUROPHYSIOLOGY DUBROVNIK, CROATIA
Page
Vahe Amassian The Corticospinal System in Health and Trauma 2
John Rothwell Some History of Monitoring Corticospinal Function Using Transcranial Stimulation in Humans 4
Janet Eyre Neurophysiology of the Corticospinal Tract 5
Robert J. Morecraft Subcortical Organization of Motor Pathways to Brainstem Motor Nuclei and the Spinal Cord 6
Gayane Margaryan New insights into the Pathophysiology of Acute Spinal Cord Injury in Vitro 7
Ursula S. Hofstoetter Model of Spinal Cord Reflex Circuits in Humans: Stimulation Frequency-Dependence of Segmental Activities and their Interactions 8
Karen Minassian Human Lumbar Cord model of the Locomotor Central Pattern Generator 11
Vedran Deletis Intraoperative Neurophysiology of the Spinal Cord Injured Patients 14
Paolo Costa ION of Acute SCI Patients - Torino Experience 15
Francesco Sala Neuromonitoring of Acute Spinal Cord Injury: Verona Experience 16
H. Louis Journee How Safe and Accurate is Transcranial Electrical Stimulation? 18
Spyros S. Kollias Imaging of Spinal Cord Function and Physiology 21
Yasunari Niimi Endovascular Treatment of Vascular Malformations and Tumors of the Spine and Spinal Cord 23
Dachling Pang The use of Electrophysiology Monitoring during Surgery for Spinal Dysraphism 29
Georg Neuloh Epilepsy Surgery: Functional Aspects 30
Caspar Stephani Stimulation of the Insula 31
Lorenzo Bello Subcortical Mapping and DTI Fiber Tracking for Surgery in Language Areas 33
Josep M. Espadaler Navigated TMS Associated with DTI as a Tool for Neurosurgical Planning. 34
Vernon L. Towle Mapping Language and Memory Areas with ECoG 36
Vedran Deletis A New Contribution to the Neurophysiologic Exploration of the Broca Area 42
Georg Neuloh Functional Preservation in Surgery for Brain Tumors and Vascular Malformations 44
Andrea Szelényi Intraoperative Neurophysiology in Tumor and Vascular Neurosurgery 45
Takamitsu Yamamoto ION for Brain Tumor Resection and Functional Neurosurgery 48
Aage R. Møller ION Tumor and Vascular Surgery of the Brain 49
Tod Sloan Anesthetic Considerations During Intraoperative Neurological Monitoring Anesthesia Protocols for Surgery during Neuromonitoring 51
Isabel Fernandez-Conejero Corticobulbar Tract Monitoring - New York Experience 62
Charles Dong Corticobulbar Motor Evoked Potentials and their Application in Facial Nerve Monitoring during Skull Base Surgery - Canada Experience 65
David B. MacDonald What's New in SEP Monitoring? 66
Isabel Fernandez-Conejero Intraoperative Recording of Blink Reflex 70
Sedat Ulkatan Facial Nerve Monitoring and Mapping in Extracranial Surgery and Sclerotherapy Procedures 71
Karen Minassian Posterior Root-Muscle Reflex 77
Jay L. Shils Persistently Electrified Pedicle Stimulation During Minimally Invasive Lumbo-Sacral Fixation 81
Zvezdan Pirtošek Neurophysiology of Movement Disorders 84
Joachim K. Krauss New Developments in Stereotactic and Deep Brain Stimulation and Recording 87
Jay L. Shils Deep Brain Stimulation in Parkinson Disease and Dystonia 88
Beatrice Cioni Motor Cortex Stimulation for Treatment in Parkinson's Disease 89
Jeffery E. Arle Computational Models and Applications to Functional Neurosurgery 94
Abstracts-Oral Presentations 96
Abstracts-Poster Presentations 128
Invited Speaker-Lectures
THE CORTICOSPINAL SYSTEM IN HEALTH AND TRAUMA
Vahe Amassian, MB Department of Physiology, SUNY, New York
Introduction It has been long known that a brief electrical stimulus delivered to the motor cortex of a mammal elicits an unrelayed, i.e. direct (D) discharge in corticospinal tract (CT) fibers followed by transynaptically generated i.e. indirect (I) discharges. The I discharge develops from a broad wave in rodents to a series of 3-4 waves with precise periodicity of 1.5-2.0 ms (~600 Hz) in primates, including humans. It must be emphasized that a true measure of the amplitude and duration of D and especially I waves can only be obtained with “killed” or “blocked” conduction at the semi microelectrode site in the medullary pyramid or lateral CT; in such recordings the fiber membrane near the microelectrode acts as a source, yielding monophasic positive potentials that add, without phase cancellation due to asynchronicity of conducted triphasic action potentials. In the monkey, attenuation of the I wave component is at least three times greater than that of the D wave in surface recordings.
The sequence of I waves in the monkey is generated by a vertically oriented interneuronal chain with superficial laminae (II and III) exciting the Betz cell layer (V). This was shown by the occurrence of late I waves when a stimulating microelectrode was superficially located and their selective loss with pial cooling.
In intraoperative monitoring, level of anesthesia may permit only recording the D wave to one or a train of stimuli. Under light anesthesia when I waves are present, the optimal interstimulus interval is influenced by (a) optimal facilitation at the I wave period, (b) CT fiber refractoriness and (c) decay of the alpha motoneuron EPSP after each stimulus.
Monitoring The D wave amplitude gives an approximate linear measure of the number of CT axons discharging. By contrast, monitoring the EMG response is inherently nonlinear because a finite CT induced EPSP summation is required to reach firing threshold of the alpha motoneuron. Furthermore, local factors, e.g. impaired blood supply may alter motoneuron excitability. The reverse relationship, persistence of an EMG response with reduced D wave amplitude would occur with desynchronization but continued CT fiber conduction because the duration of the motoneuron EPSP is of the order of one magnitude longer than the D wave.
Properties of Large Contrasted with Small CT Neurons and Their Projections To a remarkable extent, the effects of electrical or magnetic coil stimulation of motor cortex depend on the very small fraction, a subset of the 3.4% that are deemed “large” (Lassek). In the monkey, blocked end D and I waves are superimposable when conducted ~2 cm apart and the start of the D waves aligned. In humans, the D and I waves have similar configurations whether recorded at cervical or thoracic levels. Evidently, a rather homogeneous set of very fast CT fibers is activated in the D wave (or a mechanism exist for synchronizing, the traveling impulses).
Within the very fast CT group, does the Henneman Size principle shown first for hindleg alpha motoneurons apply to fast CT neurons and FDI motoneurons? The simplest synaptic test for CT neurons is provided by their monosynaptic excitation by sTMS of parietal lobe. With weak focal anodic stimulation, the CT axons excited at bends in white matter should be among the largest; shifted approximately 2ms later the FDI responses to monosynaptic I1 activation and D activation occlude one another, i.e. the fastest CT neurons are activated transynaptically when I1, is a small fraction of the CT pool. Interestingly, the peripheral conduction times of FDI motor units are among the fastest alpha motoneurons activated by weak parietal lobe TMS (Lalli). Apparently, the fast CT neurons innervate some alpha motoneurons with very rapidly conducting axons that lack the high multiple muscle fiber innervation and tension generation (Bigland-Ritchie). (Earlier investigators were misled into believing that the Size principle was obeyed).
Concerning small CT neurons, critical questions are incompletely answered, including: (a) Are the extracellular action potentials too small and dispersed in velocity to be readily recorded? (b) Are the excitation thresholds too high for conventional types of stimulation? High intensity stimulation through bipolar wires inserted in white matter elicits in the pyramid a typical D wave, but now followed by a smaller and much more dispersed wave uncontaminated by I activity. Sporadically, a small D wave with 4 ms latency is recorded in monkey pyramid when the electrical stimulus is applied anterior to classical motor cortex. More clearly, intracellular recording in cat motor cortex revealed that both slowly conducting. PT neurons and neurons that could not be invaded were also excited by nearby pial bipolar stimuli that also excited the fast PT neurons. Significantly, both types of small
2 motor cortical neuron were monosynaptically excited with latencies similar to those of the fast (D) group from Betz. Cells (Rosenthal et al.). The tentative conclusion is that small PT neurons are probably easily stimulated and certainly tonically active (Evarts), but poorly represented in tract recordings.
Least is known of the motor role of small CT neurons. The heavy projection from parietal lobe to dorsal horn neurons suggest an influence on processing of sensory information. Resting discharge of area of 4 small PT neurons in awake, but immobile monkeys (Evarts) could tonically contribute to stretch reflexes and fusimotor drive. TMS of motor cortex drives sudomotor activity and skin, but not muscle postganglionic C fibers (Rossini et al 1993; Nichaus etal.,1998; Silber etal.,2000). It would be of interest in intraoperative monitoring to determine if these small motor cortical projection pathways persist when the D wave is diminished and what role they play in recovery after severe CT damage.
Susceptibility of CT Fibers to Damage During spinal cord surgery, damage to the CT may occur from a number of causes, including (a) physical damage to the fibers and/ or (b) interference with blood supply. The remedies are varied, including (a) irrigation with Saline and (b) elevating the arterial pressure; both procedures would tend to change the extracellular environment of the CT fibers. Pressure on myelinated axons in peripheral nerve is known to block selectively the largest diameter axons first; by contrast, nerve ischemia blocks all classes of myelinated A fibers, but has delayed effects on C fibers.
A model for traumatic injury to spinal cord fibers is to use graded weight drops on exposed spinal cord of anesthetized cats and monkeys (rather than rats) because their large CT fibers have velocities comparable to those of humans. Within one second of the weight drop, CT and dorsal column conduction is abolished. Subsequently and clearly related to the height of the drop there occurs: (a) complete recovery within an hour; (b) near complete recovery followed by depression of conduction over a period of hours i.e. secondary depression; (c) no recovery. Significantly, with graded drops, individual CT neurons recorded in motor cortex show the greatest loss of antidromic invasion if their control latencies were the briefest in the population of the units recorded. Thus the impact of the physical trauma is greatest on the fastest CT axons i.e. those that contribute to the D wave.
The mechanism of weight drop block was elucidated as follows. Protection against irreversible block (c) was obtained by pretreating the exposed spinal cord with tetrodotoxin (TTX) a selective voltage gated Na+ channel blocker. After the (c) level weight drop, the TTX was washed out followed by recovery of conduction. It was concluded that trauma to the spinal cord opens Na+ voltage gated channels, allowing Na+ entry, which then permits intracellular K+ to exit into the extracellular space. Conduction of impulses fails through depolarization block. However, calculation of the entry of Na+ through nodes of axons, with corresponding exit of K+ could not account for the levels of K+ outside recorded by other investigators. A possibility is that voltage gated Na+ channels present in glia are the likely source of the raised extracellular K+. Significantly, weight drop to the cauda equina does not have the (a) and (b) pattern of block of spinal cord, possibly because of the absence of glia but the (c) type block. At the level of minimal trauma (a) when complete recovery would be soon expected, pretreatment of the spinal cord with a Na+, K+ ATPase inhibitor (Strophanidin) results in permanent block. Evidently restoring ionic gradients across membranes of nerve fibers (and possibly glia) is crucial in recovery of conduction.
Therapeutically, there would clearly be reluctance to use a Na+ channel blocker however briefly. Potentiation of Na+ K+ ATPase activity is of interest in treating ischemic strokes and would be potentially useful intraoperatively. Also of interest is the secondary delayed or permanent loss of conduction with grades (b) or (c) drops. Pretreatment of the spinal cord with Leupeptin, a tripeptide, which inhibits Ca activated cathepsins protects the spinal cord from category (c) weight drops. Possibly, prolonged depolarization by high extracellular K+ leads to increased intracellular Ca ++, but this could not be prevented by using Ca channel blocker.
Notes
3 SOME HISTORY OF MONITORING CORTICOSPINAL FUNCTION USING TRANSCRANIAL STIMULATION IN HUMANS
John Rothwell, PhD UCL Institute of Neurology, Queen Square, London WC1N 3BG, UK
The first recordings of corticospinal volleys from epidural electrodes in the spinal cord were reported by Boyd et al (1986) in a series of scoliosis patients from Great Ormond Street Children’s Hospital. They used transcranial electrical stimulation of the motor cortex and observed a short latency traveling wave of activity that descended the cord at about 60m/s. Although they did not comment in detail, the recordings also contain later potentials that follow the initial wave by 2-3ms, particularly after high intensity stimulation. These are presumably I-waves. Interestingly they also attempted to record evoked EMG activity form the external anal sphincter but were unsuccessful.
The method was then taken up in several centres, but the most prolific scientific work came from David Burke’s laboratory in Sydney. In a series of papers they showed that D waves evoked by transcranial electrical stimulation could be initiated at three preferential sites depending on the intensity of the stimulus: in the subcortical white matter, the cerebral peduncle and at the pyramidal decussation in the brainstem. They hypothesised that these preferred sites corresponded to points where there was a sudden change in direction of the corticospinal fibres which made them more sensitive to the applied current. They also observed clear I waves, although these were more sensitive to the depth of anaesthesia than the D waves.
There had also been a number of attempts to record descending volleys from the spinal cord of conscious patients with implanted epidural electrodes. Di Lazzaro et al finally proved that transcranial magnetic stimulation of the hand area preferentially activated I wave inputs, but that its selectivity depended on the orientation of the induced current in the brain. They also confirmed that transcranial electrical simulation preferentially evoked D waves, although in conscious humans they were not able to stimulate as strongly as Burke et al in anaesthetised patients and therefore did not observe spread of the stimulus to distal parts of the corticospinal axon. Voluntary contraction was found to increase the amplitude of the I waves, but only at rather high contraction levels (20% MVC). Finally, the I waves appeared to be differentially sensitive to a range of conditioning stimuli, suggesting very strongly that at least some of them (the I1 and I2/3 in particular) are produced by activity in separate neural pathways.
All of these studies employed TMS/TES of the primary motor cortex. However it is becoming clear that stimulation of other regions in the frontal lobes such as SMA, and areas anterior to the premotor cortex, can in some individuals give rise to evoked EMG activity (in preactivated muscles) without stimulation spreading to M1. Responses in a variety of muscles from intrinsic hand to trunk and back muscles can be activated. There are also reports that there are changes in the strength of these projections after stroke that correlate with recovery of trunk muscle control. I will illustrate some of these new features of descending pathway organisation in the talk.
Notes
4 NEUROPHYSIOLOGY OF THE CORTICOSPINAL TRACT
Janet Eyre, BSc, MB ChB, D Phil, FRCP, FRCPCH Institute of Neuroscience, Newcastle University Sir James Spence Institute, Royal Victoria Infirmary, Queen Victoria Infirmary, Newcastle
Abstract not available
Notes
5 SUBCORTICAL ORGANIZATION OF MOTOR PATHWAYS TO BRAINSTEM MOTOR NUCLEI AND THE SPINAL CORD
Morecraft RJ, Stilwell-Morecraft KS. Sanford School of Medicine, University of South Dakota, US
A detailed understanding of the course of descending motor pathways can assist in guiding intraoperative neuronavigation, interpreting the effects of deep brain stimulation to enhance the margin of safety between resection cavity and functional motor pathways, and designing neurosurgical approaches to manage movement disorders and psychiatric illness. Equally important is a precise understanding of corticofugal fiber organization for assessing the functional status of patients following subtotal brain injury and predicting their potential for motor recovery. First, we will review the subcortical organization of the corticospinal pathways through the corona radiata, internal capsule and midbrain cerebral peduncle originating from 5 separate arm representations in the frontal and cingulate motor cortices of the monkey brain (Morecraft et al., 2002, 2007). Specifically, we will review the organization of the descending pathway from the arm representation of the primary motor cortex (M1), dorsolateral premotor cortex (LPMCd), supplementary motor cortex (M2), rostral cingulate motor cortex (M3) and caudal cingulate motor cortex (M4). Second, we will present new findings on the subcortical organization of the corticobulbar pathways through the corona radiata, internal capsule and cerebral peduncle which originate from 5 separate face/head representations in the same motor cortices in the monkey brain (Morecraft et al., in preparation).
In all cases, the course of each subcortical pathway was defined by surgically exposing the cerebral cortex, localizing the head/face representation and the arm representation in motor cortex, then injecting a high resolution neural tract tracer into the respective somatotopic representation. The surgical field was then closed using standard neurosurgical techniques. Following an appropriate post-surgical time period to allow for axonal transport of the tract tracer, the brain was removed and the tissue was immunohistochemically processed for tract tracer visualization. Finally, the course of each pathway was plotted in the tissue sections in the anatomical region of the coronal radiata, internal capsule and cerebral peduncle using a microscopic based computer assisted data collection system.
The descending pathway of each face/head representation, as well as each arm representation followed highly organized trajectories throughout their descending course in the corona radiata and internal capsule. All pathways were characterized by a progressive and gradual shift in position throughout their descent. Simultaneous consideration of the trajectories of all 10 pathways (e.g., 5 face/head pathways and 5 arm pathways) show there is considerable overlap of face/head and arm representation in the internal capsule. When considering the position of the head/face representation versus the position of the arm representation from the same motor area (e.g. within M1), face/head representation assumed a position anterior to its arm representation in the internal capsule as classically defined, but was partially overlapping. In the midbrain cerebral peduncle, there was extensive overlap of face/head and arm representation when considering all pathways. From the same motor area, face/head fibers in the peduncle were generally located medial to arm fibers with substantial overlap. These observations suggest that a complex, but highly organized arrangement of subcortical motor fiber representation occurs in the primate brain. These observations may be useful for interpreting the effects of intraoperative subcortical stimulation, evaluating the descending pathways of motor tracts as determined with diffusion tensor imaging, and predicting/interpreting the clinical consequences of subcortical neurosurgical treatments designed to manage intractable movement disorders and psychiatric illness.
References 1. Morecraft RJ, Louie JL, Herrick JL and Stilwell-Morecraft, KS. Cortical Innervation of the Facial Nucleus in the Non-Human Primate: A New Interpretation of the Effects of Stroke and Related Subtotal Brain Trauma on the Muscles of Facial Expression. Brain, 124:176-208, 2001. 2. Morecraft RJ, Herrick J, Stilwell-Morecraft KS and Louie JL. Localization of Arm Representation in the Corona Radiata and Internal Capsule in the Non-Human Primate. Brain, 125:176-198, 2002. 3. Morecraft RJ, McNeal DW, Stilwell-Morecraft KS, Dvavajscak Z, Ge J and Schnieder P. Localization of Arm Representation in the Cerebral Peduncle of the Non-Human Primate, Journal of Comparative Neurology, 504:149-167, 2007. 4. Morecraft RJ, Stilwell-Morecraft KS and Ge J. Localization of Face Representation in the Corona Radiata and Internal Capsule in the Non-Human Primate, in preparation.
Notes
6 NEW INSIGHTS INTO THE PATHOPHYSIOLOGY OF ACUTE SPINAL CORD INJURY IN VITRO
Gayane Margaryan, M.Sc., PhD Neurobiology Sector, International School for Advanced Studies, Trieste, Italy
Spinal cord injury (SCI) represents a significant health problem associated with life-long disability and a broad range of secondary complications. Acute spinal cord injury evolves rapidly within hours and days after the initial trauma, producing secondary damage even to initially spared areas. The early pathophysiological mechanisms affecting spinal networks remain largely obscure despite widespread incidence of this condition and its social consequences. Regardless of their etiology, spinal lesions are believed to include combinatorial effects of excitotoxicity and severe metabolic perturbations. The present study used an in vitro spinal cord model from the neonatal rat to investigate the relative contribution by excitotoxicity and toxic metabolites to dysfunction of locomotor networks, spinal reflexes and intrinsic network rhythmicity. Preparations were treated (1 h) with either kainate or a pathological medium (containing free radicals and hypoxic/aglycemic conditions), or their combination. Damage was measured by taking as outcome locomotor network activity for up to 24 h after the primary insult. Kainate led to irreversible suppression of fictive locomotion, while intrinsic bursting induced by synaptic inhibition block persisted. This result was associated with significant neuronal loss around the central canal. The pathological medium slowed down fictive locomotion and intrinsic rhythmicity. This phenomenon was associated with polysynaptic reflex depression and preferential damage to glial cells, while neurons were comparatively spared. Combination of kainate with pathological medium evoked extensive, irreversible damage to the spinal cord. Thus, while suggesting distinct roles of excitotoxicity and metabolic dysfunction in the acute damage of locomotor networks, our model indicates that different strategies might be necessary to treat the various early components of acute spinal cord lesion.
Next, we investigated the role of extracellular Mg2+ in the lesion evoked by pathological medium, as the recent clinical trials to treat this condition with i.v. Mg2+ to stabilize its extracellular concentration provided disappointing results. Pathological medium in 1 mM Mg2+ solution (1 h) largely depressed spinal reflexes and suppressed fictive locomotion on the same and the day after. Conversely, pathological medium in either Mg2+- free or 5 mM Mg2+ solution evoked temporary network depression and enabled fictive locomotion the day after. While global cell death was similar regardless of extracellular Mg2+ solution, white matter was particularly affected. In ventral horn the number of surviving neurons was the highest in Mg2+ free solution and the lowest in 1 mM Mg2+, while motoneurons were unaffected. Although the excitotoxic damage elicited by kainate was insensitive to extracellular Mg2+, 1 mM Mg2+ potentiated the effect of combining pathological medium with kainate at low concentrations. These results indicate that preserving Mg2+ homeostasis rendered experimental spinal injury more severe.
Treatment to block the pathophysiological processes triggered by acute spinal injury remains unsatisfactory as the underlying mechanisms are incompletely understood. We further investigated the feasibility of neuroprotection of lumbar locomotor networks by the glutamate antagonists CNQX and APV against acute lesions induced by either pathological medium or excitotoxicity. Inhibition of fictive locomotion by pathological medium was contrasted by simultaneous and even delayed (1 h later) co-application of CNQX and APV. Delayed neuroprotection was accompanied by increased survival of ventral horn premotoneurons and lateral column white matter. Neither CNQX nor APV alone provided neuroprotection. Kainate-mediated excitotoxicity always led to loss of fictive locomotion. CNQX and APV co-applied with kainate functionally protected 1/3rd of preparations, although they failed when their application was delayed. Our data suggest that locomotor network neuroprotection was possible when introduced very early during the pathological process of spinal injury, but also showed how the borderline between presence or loss of locomotor activity was a very narrow one that depended on the survival of a certain number of neurons or white matter elements. The present report provides a model not only for preclinical testing of novel neuroprotective agents, but also for estimating the minimal network membership compatible with functional locomotor output.
Notes
7 MODEL OF SPINAL CORD REFLEX CIRCUITS IN HUMANS: STIMULATION FREQUENCY-DEPENDENCE OF SEGMENTAL ACTIVITIES AND THEIR INTERACTIONS
US Hofstoetter1, 2, K Minassian1, 2, F Rattay1, MR Dimitrijevic1, 3 1. Institute of Analysis and Scientific Computing, Vienna University of Technology, Austria; 2. Center of Biomed. Engineering and Physics, Medical University of Vienna, Austria; 3. Dept. of Physical Medicine and Rehab, Baylor College of Medicine, Houston, TX, USA.
Introduction Electrical stimulation delivered by electrodes close to the lower (lumbosacral) spinal cord of humans with complete spinal cord injury elicits muscle activities in the paralyzed lower limbs (Dimitrijevic et al., 1980; Murg et al., 2000). With low repetition rates of stimulation (2.1 Hz), twitches are elicited in multiple lower limb muscles that have been suggested to be the simplest spinal reflexes transmitted via single synapses (Jilge et al., 2004; Minassian et al., 2004). By contrast, the same stimulation applied at higher rates (frequency range of 25-50 Hz) produces automatic stepping-like movements in the supine individuals with long-standing paraplegia (Dimitrijevic et al., 1998; Minassian et al., 2004, 2007).
The aim of the present study was to further elaborate the ‘standard’ spinal reflexes in response to 2.1 Hz- stimulation by analyzing a large size of human electrophysiological data. Furthermore, a main focus was on the effect of increased stimulation frequencies on the modification of these simple reflexes due to the integration of interneuronal circuit activities. The elicitation of simple periodic patterns covering only two successive responses was thereby regarded as an indication for interneuronal activity. Such patterns with interactions between antagonistic muscle groups were readily evoked when the stimulation frequencies were between the ones eliciting twitches and those resulting in stepping-like lower limb movements.
The hypothesis that at higher frequencies the stimulation effect expands to lumbar circuits that influence the activity between muscles shall be tested by a biologically realistic mathematical model. In particular, circuits including interneurons specialized in adjusting excitability of motoneurons during spinal reflexes as well as locomotion (Ia interneurons and Renshaw cells) were tested for their efficacy in generating simple periodic outputs.
Methods Analysis of electrophysiological data and neuromathematical modeling were chosen as two independent methods. First, electromyographic (EMG) recordings of reflex activities derived from six individuals with chronic complete spinal cord injury were evaluated. The subjects had epidural spinal cord stimulation systems implanted at lumbar cord levels. A large number of compound muscle action potentials (CMAPs) associated with the responses to 2.1 Hz-stimulation (the lowest available stimulation frequency) were analyzed for their EMG characteristics, i.e., latencies, peak-to-peak amplitudes, and waveforms. Furthermore, the effect of increasing the stimulation frequency to 5, 11, 16, and 22 Hz on the EMG activities was explored. The elicitation of responses with simple periodic patterns was documented.
Second, the capacity of biologically realistic network models to re-produce the simple periodic patterns covering two successive responses was tested by means of computer simulation. For this purpose, a novel mathematical model was developed that extends the widely used Leaky Integrate-and-Fire model by detailed neurophysiological time courses of postsynaptic potentials gained from experimental studies. The present model was designed as a biologically realistic mathematical integrator of postsynaptic effects of specialized spinal cord neurons. Particularly, it considered monosynaptic excitatory and disynaptic inhibitory actions exerted by populations of Ia fibers, Ia interneurons as well as Renshaw cells on the motor pools. Thereby, the mathematical model based on a non-linear recursive algorithm simulating spatially and temporally distributed neuronal effects. In order to test the functional roles of the network elements on the generation of particular motor outputs, the complexity of the complete model was approached by successively adding interneuronal populations and connectivities.
Results The neurophysiological study produced three main findings. (i) Epidural stimulation of the human lumbosacral cord (deprived of brain influence by accidental lesion) at a low frequency of 2.1 Hz elicited monosynaptic, segmental reflexes in multiple lower limb muscles bilaterally. These responses had short and constant latencies and rather simple CMAP waveforms. There were no interactions between muscles during continuous stimulation.
8 (ii) By increasing the stimulation frequency to 11-22 Hz, the independence of successively elicited reflexes was replaced by periodic modulations with cycle periods covering two responses in 20.8% of all data sets (Figure 1). In the thigh muscle groups quadriceps and hamstrings, the pattern most frequently detected at 16 Hz-stimulation was characterized by anti-phase alternations of responses in the antagonistic motor pools (Fig. 1a). (iii) Independently from the effects induced by higher stimulation frequencies, a not yet described type of reflex was detected in the flexor muscle tibialis anterior. These responses to 2.1 Hz-stimulation had both features of simple monosynaptic reflexes as well as characteristics of more complex oligo-/polysynaptic reflexes.
Figure 1. Simple periodic patterns elicited by epidural spinal cord stimulation in complete spinal cord injured subjects. Displayed are responses recorded from quadriceps (Q) and hamstrings (Ham), arrows depict the times of stimulus application. a Reciprocal attenuation of Q and Ham responses. b Pattern characterized by attenuation of every second response recorded from Q and stable output in Ham. c In-phase- modulation of Q and Ham responses. Data derived from individual subjects, stimulation parameter settings a, electrode combination 0+3–, 5 V, 16 Hz; b, 0+3–, 5 V, 11 Hz; and c, 0-3+, 6V, 11 Hz.
The generation of simple periodic patterns could be re-produced by the assumed network models. In particular, it was rather the activity of Renshaw cells and their mutual interactions that accounted for stable response modulations. On the other hand, the Ia interneurons, responsible for reciprocal inhibition during various spinal network activities, had less impact on the generation of simple periodic patterns. The segmental circuits associated with a single motoneuron population could produce alternating motor outputs independent from the activity in the antagonistic circuit. However, the generation of anti-phase alternations of antagonistic motoneuron pool firings required the incorporation of interconnections between the two circuits. Such type of patterned output was most readily produced when assuming two network circuits with asymmetric parameter settings corresponding to ‘flexor’ and ‘extensor’ connectivities. In the complete model network considering Ia interneuron and Renshaw cell activity, the influence of the latter was largely reduced and the capacity of producing stable rhythmic patterns was lost.
Conclusions The reflexes elicited by 2.1 Hz-stimulation were due to the activation of large-diameter group Ia afferent fibers within the posterior roots and the concomitant strong monosynaptic excitatory drive of the spinal motor cells (Mendell & Hennemann, 1971; Willis & Coggeshall, 1978). The additional recruitment of some group II fibers accounted of the elicitation of the more complex polyphasic responses detected in tibialis anterior (Pierrot- Deseilligny & Burke, 2005). At stimulation frequencies of 11-22 Hz, the central state of excitability was increased, hence leading to the concomitant activation of spinal interneuronal circuits that led to a modification of the successive responses with simple periodic patterns.
The computer model revealed temporal summation of postsynaptic potentials elicited by stimulation pulses applied in close succession as leading mechanism elevating the central state of excitability. At the same time, the
9 independence of segmental reflexes at 2.1 Hz was due to the cessation of even the longest lasting interneuronal activities induced by one stimulation pulse before the next stimulus was applied. The present model thus provided strong evidence for the frequency-dependence of the effective incorporation and activation of segmental circuits in the sensory-motor transmission. The motor outputs produced by the mathematical model closely resembled those derived from the neurophysiological recordings and particularly, inter-segmental coordination of segmental activities was demonstrated for stimulation frequencies of 16 Hz.
The significance of the present work is manifold. Electrophysiologically, it scrutinizes the standard human lower limb muscle reflexes in response to 2.1 Hz-epidural stimulation of the lumbosacral spinal cord isolated from supraspinal influence. In the field of neurosciences, it contributes to the understanding of the role of signal frequency in the configuration of neuronal circuits. Furthermore, it elaborates the functional roles of specialized interneurons of the lumbar spinal cord machinery in generating rhythmic activities.
References 1. Dimitrijevic MR, Faganel J, Sharkey PC & Sherwood AM (1980). Study of sensation and muscle twitch responses to spinal cord stimulation. Int Rehabil Med 2, 76-81. 2. Mendell LM & Henneman E (1971). Terminals of single Ia fibers: location, density, and distribution within a pool of 300 homonymous motoneurons. J Neurophysiol 34, 171-187. 3. Minassian K, Jilge B, Rattay F, Pinter MM, Binder H, Gerstenbrand F & Dimitrijevic MR (2004). Stepping-like movements in humans with complete spinal cord injury induced by epidural stimulation of the lumbar cord: electromyographic study of compound muscle action potentials. Spinal Cord 42, 401-416. 4. Minassian K, Persy I, Rattay F, Pinter MM, Kern H & Dimitrijevic MR (2007b). Human lumbar cord circuitries can be activated by extrinsic tonic input to generate locomotor-like activity. Hum Mov Sci 26, 275-295. 5. Murg M, Binder H & Dimitrijevic MR (2000). Epidural electric stimulation of posterior structures of the human lumbar spinal cord: 1. muscle twitches - a functional method to define the site of stimulation. Spinal Cord 38, 394-402. 6. Pierrot-Deseilligny E & Burke D (2005). Group II pathways. In: The Circuitry of the Human Spinal Cord: Its role in motor control and movement disorders, 1st edn, ed. Pierrot-Deseilligny E & Burke D, pp. 288-336. Cambridge Univ. Press, New York, USA. 7. Willis WD & Coggeshall RE (1978). Peripheral Nerves, Sensory Receptors, and Spinal Roots. In: Sensory Mechanisms of the Spinal Cord, 1st edn, ed. Willis WD, Coggeshall RE, pp. 9- 52. New York: Plenum Press. 8. Jilge B, Minassian K, Rattay F, Pinter MM, Gerstenbrand F, Binder H & Dimitrijevic MR (2004). Initiating extension of the lower limbs in subjects with complete spinal cord injury by epidural lumbar cord stimulation. Exp Brain Res 154, 308-326. 9. Dimitrijevic MR, Gerasimenko Y & Pinter MM (1998). Evidence for a spinal central pattern generator in humans. Ann N Y Acad Sci 860, 360-376.
Support: We kindly acknowledge the support by the Austrian Science Fund (FWF), Vienna, Austria, Proj.Nr. L512-N13
Notes
10 HUMAN LUMBAR CORD MODEL OF THE LOCOMOTOR CENTRAL PATTERN GENERATOR
K Minassian,1, 2 US Hofstoetter,1, 2 F Rattay,1 MR Dimitrijevic1, 3 1, Institute of Analysis and Scientific Computing, Vienna University of Technology, Austria; 2, Center of Biomed. Engineering and Physics, Medical University of Vienna, Austria; 3, Dept. of Physical Medicine and Rehab, Baylor College of Medicine, Houston, TX, USA
Vertebrate locomotion is complex and characterized by rhythmic activity as well as utilization of multiple degrees of freedom, i.e., numerous joints and muscles. Locomotion control, however, seems to be simplified by an autonomous organization of neural networks at spinal cord level capable of generating the basic rhythmic patterns necessary for locomotion. These neural networks are called "central pattern generators" (CPGs) for locomotion (Grillner, 1985). Higher control centers interact with the CPGs for postural control and accurate limb movements. CPGs further interact with afferent feedback to adapt the locomotor pattern to external demands.
CPGs for locomotion have been found in a large number of species including invertebrates, primitive vertebrates, and mammals like cats as well as non-human primates (Fredirchuck et al., 1998). The autonomous operation of the CPGs can be demonstrated in animal experiments by the complete separation of the spinal cord networks from suprasegmental influences (spinalization or decerebration) and isolation from sensory input (deafferentation). They are then artificially activated by simple tonic, i.e., non-oscillating, electric or pharmacological stimulation. Coordinated patterns of rhythmic efferent output (fictive locomotion) can then be recorded as neurograms from motoneurons.
Evidence for the existence of a locomotor CPG in humans according to the definition originally established in animal preparations (capacity to produce rhythmic motor output in the complete absence of phasic, movement- related sensory input and of supraspinal input) can not be adduced. Peripheral segmental input cannot be completely removed like in the experimental animal model and even in clinically complete spinal cord injured persons there is a potential for some influence of residual supraspinal descending influence upon the lumbar spinal cord.
Still, indirect evidence for the existence of a spinal locomotor pattern generator was adduced in spinal cord injured individuals (Bussel et al., 1988; Calancie et al., 1994). The view that humans possess a functional spinal rhythm-generating network finds further support from rehabilitating gait abilities of individuals with spinal cord lesions by treadmill training (Dietz & Harkema, 2004).
Epidural spinal cord stimulation (SCS) as a clinical method for the control of spasticity of the lower limbs of spinal cord injured individuals (Dimitrijevic, 1998) requires continuous stimulation of the posterior structures of the upper lumbar cord segments (Pinter et al., 2000). These spinal levels correspond to the respective segments in the rat and cat spinal cord that are critical for hindlimb locomotion (Gerasimenko et al., 2008).
Dimitrijevic et al. (1998) found that the tonic signals delivered by epidural SCS at 25-60 Hz could produce locomotor-like movements of the paralyzed lower limbs in supine individuals with complete traumatic spinal cord injury. In addition to clinical examinations of the participants’ spinal cord functions, non-invasive techniques for the neurophysiological assessment of sub-clinical spinal cord functions were applied. The "brain motor control assessment" (BMCA) protocol was carried out for the examination of residual functional capabilities, i.e., of the degree to which brain influence is preserved below a spinal cord lesion (Sherwood et al., 1996). By using this method, the absence of trans-lesional brain influence over lumbar spinal motor activity could be documented in the studied subjects. During the generation of the rhythmic lower limb movements by tonic SCS, influence of afferent feedback could not be avoided. However, critical for the timing of the different phases in the locomotor cycle are proprioceptive inputs reflecting the load on extensors and the angle of hip extension (Hultborn & Nielsen, 2007). In the supine position of the studied subjects, essential contribution of load receptors cannot be expected, and hip extension was limited by the examination table. Thus, influence of sensory input in generation of the rhythm must have been insignificant.
We conclude that the model studied by Dimitirjevic et al. (1998) was the human lumbosacral spinal cord in complete (sub-clinical) isolation from supraspinal input. Externally controlled SCS provided a tonic input with defined constant frequency. It was thus demonstrated that the human lumbar cord circuitries could process simple tonic neural signals to generate coordinated oscillating motor outputs – a characteristic feature of a pattern generator (Pearson & Gordon, 2000).
11
Within the past years, our continuous studies of the locomotor capabilities of the human lumbar cord further advanced the findings of Dimitrijevic et al. (1998). We identified posterior root afferent fibers as the neural structures directly depolarized by spinal cord stimulation leading to the motor outputs (Rattay et al., 2000; Minassian et al., 2004). These pathways are mediating the activating input to the motor nuclei as well as to the locomotor circuits.
Each stimulus pulse of the applied trains gave rise to a posterior root-muscle reflex (PRM reflex) in the lower limb muscles associated with the stimulated roots. Each PRM reflex was recorded electromyographically (EMG) as a compound muscle action potential. The EMG signals of SCS-induced rhythmic activities consisted of series of PRM reflexes occurring with the stimulation frequency (Minassian et al., 2004; 2007). This specific EMG composition allowed us to explore the behavior of single compound muscle action potentials associated with the PRM reflexes within extension and flexion phases of rhythmic activity generated by SCS. We found that within the rhythmic activities, muscles responded with the alternation between two phases. Phases of successively elicited PRM reflexes with characteristically modulated amplitudes, forming the shape of an EMG burst, were followed by phases of PRM reflex suppression. The variations of PRM reflex amplitudes resulted in rhythmic EMG activities with periods of 0.8-1.9 s. The muscles displayed one major burst during a rhythmic cycle.
The motor patterns were thus produced by periodic amplitude modulations of successive PRM reflexes, in spite of constant stimulation conditions. Within the motor patterns, phase-dependent modifications of latency and CMAP morphology of the PRM reflexes were detected as well. We could identify two different types of PRM reflexes that built up the maximum amplitudes of the rhythmic bursts. The first type of PRM reflexes had short latencies similar to monosynaptic control responses, as well as similar CMAP waveforms. They occurred in the quadriceps (Q), hamstrings (Ham), and triceps surae (TS) muscle groups. The second type was identified in Q, tibialis anterior, and TS and demonstrated considerable delays of the onset latencies by 7.2-8.3 as well as modified CMAP waveforms.
Bursts of short-latency PRM reflexes characterized extension-like phases. During flexion-like phases of rhythmic activities, the short-latency PRM reflexes were replaced by PRM reflexes with increased latency that were otherwise not present. The delay in PRM reflex latency is not an attribute of the segmental spinal reflex pathway confined to a single flexor muscle. It is rather the manifestation of neural control by spinal locomotor circuits that can be present in all muscles recruited during the flexion phase. The activated locomotor circuits thus produce patterns of reflex pathway modifications in addition to the spatiotemporal patterns of motoneuron firing.
We can conclude that the generation of rhythmic lower limb muscle activity in humans does not require connectivity between the brain and spinal cord. Locomotor-like activity can be produced by repetitive, electrically induced inputs with distinct repetition (25-60 Hz) rates via multiple posterior roots. We suggest that the PRM reflexes evoked in series concomitantly produced the locomotor state of lumbar cord circuits via collaterals of the stimulated afferents. When set into action, the locomotor networks were in turn modifying the PRM reflex activity. On the basis of the exerted actions, these circuits can be recognized as locomotor rhythm- and pattern- generating networks. By integrating the influence of these networks, the reflex activity – the PRM reflexes – becomes part of locomotor activity. The network action is directly reflected in the periodic amplitude modulations of successive PRM reflexes and the delay of PRM reflexes during flexion phases of rhythmic activity.
References 1. Bussel B, Roby-Brami A, Azouvi P, Biraben A, YakovleV A, Held JP. Myoclonus in a patient with spinal cord transection. Possible involvement of the spinal stepping generator. Brain.1988; 111: 1235-1245. 2. Calancie B, Needham-Shropshire B, Jacobs P, Willer K, Zych G, Green BA. Involuntary stepping after chronic spinal cord injury. Evidence for a central rhythm generator for locomotion in man. Brain. 1994; 117: 1143-1159. 3. Dietz V, Harkema S J. Locomotor activity in spinal cord-injured persons. Journal of Applied Physiology. 2004; 96: 1954- 1960. 4. Dimitrijevic MR. Chronic spinal cord stimulation for spasticity. In: Gildenberg PL, Tasker RR, eds. Textbook for Stereotactic and Functional Neurosurgery. McGraw-Hill: New York, 1998: 1267-1273. 5. Dimitrijevic MR, Gerasimenko Y, Pinter MM. Evidence for a spinal central pattern generator in humans. Ann N Y Acad Sci. 1998; 860: 360-376. 6. Fedirchuk B, Nielsen J, Petersen N, Hultborn H. Pharmacologically evoked Wctive motor patterns in the acutely spinalized marmoset monkey (Callithrix jacchus). Experimental Brain Research. 1998; 122: 351-361. 7. Gerasimenko Y, Roy RR, Edgerton VR. Epidural stimulation: Comparison of the spinal circuits that generate and control locomotion in rats, cats and humans. Exp Neurol. 2008; 209:417-425. 8. Grillner S. Neurobiological bases of rhythmic motor acts in vertebrates. Science. 1985; 228: 143-149. 9. Hultborn H, Nielsen JB. Spinal control of locomotion - from cat to man. Acta Physiol (Oxf). 2007; 189: 111-121.
12 10. Minassian K, Jilge B, Rattay F, Pinter MM, Binder H, Gerstenbrand F, Dimitrijevic MR. Stepping-like movements in humans with complete spinal cord injury induced by epidural stimulation of the lumbar cord: electromyographic study of compound muscle action potentials. Spinal Cord. 2004; 42: 401-416. 11. Pearson KG, Gordon J. Locomotion. In: Kandel ER, Schwartz JH, Jessell TM, eds. Principles of Neural Science. 4th edition. McGraw-Hill: New York, 2000: 737-755. 12. Pinter MM, Gerstenbrand F, Dimitrijevic MR. Epidural electrical stimulation of posterior structures of the human lumbosacral cord: 3. Control Of spasticity. pinal Cord. 2000; 8: 24-31. 13. Rattay F, Minassian K, Dimitrijevic MR Epidural electrical stimulation of posterior structures of the human lumbosacral cord: 2. quantitative analysis by computer modeling. Spinal Cord. 2000; 38: 473-489. 14. Sherwood AM, McKay WB, Dimitrijevic MR. Motor control after spinal cord injury: assessment using surface EMG. Muscle Nerve. 1996; 19: 966-979.
Support: We kindly acknowledge the support by the Austrian Science Fund (FWF), Vienna, Austria, Proj.Nr. L512-N13
Notes
13 INTRAOPERATIVE NEUROPHYSIOLOGY OF THE SPINAL CORD INJURED PATIENTS
Vedran Deletis, MD, PhD Department for Neuroscience, School of Medicine, University of Split, Croatia and St. Luke's- Roosevelt Hospital, Institute for Neurology and Neurosurgery, New York, USA
The neuroimaging technique did not contribute significantly to the prognosis of the patients with SCI, while neurophysiologic testing still has not been done on the routine basis in order to make neurophysiologic profile of SCI patients. Furthermore, even not many neurophysiologic data has been published in acute SCI patients. There are many reason for that: (a) one of pragmatic reason is that intraoperative neurophysiologic team is not always available to perform testing, during spine stabilization in most cases occurred in non regular working hours, and (b) surgical team is not get used to work with neurophysiologic team in this category of patients.
On the basis of preliminary testing supported by “Science Program of Foundation for movement recovery”, Stiftelsen foundation, Oslo Norway, we will show a very promising results in creating neurophysiologic profile of SCI patients (see Costa P. et al., and Sala F., et al.) this issue. This preliminary data was collected on the basis of our work on the intraoperative neurophysiology (ION) of the spinal cord. In the field ION reliable methods to predict functional integrity of the long tracts during surgical intervention to the spinal cord, has been already developed and established. This is very much true for the (a) motor evoked potentials (MEPs) recorded from the spinal cord in the form of D and I waves and (b) MEPs recorded from the limb muscle.
The first method can semi quantitatively estimate number of the fast neurons of the corticospinal tract (CT), while other method give evidence of the integrity of the fast neurons plus supportive system of the spinal cord (1). The both system are essential for generating muscle MEPs. Complete disappearance of the D wave during intramedullary surgery correspond with severe and definitive plegia, while disappearance of muscle MEPs, with preservation more than 50% of baseline amplitude of the D wave results in a transient plegia (2,3). Therefore we consider presence of the D wave as a reliable prognostic sign for the motor recovery, because it can semi quantify number of the fast neurons of the CT, as one of the essential element for voluntary movement; The same rule we can apply, for the acute SCI patients. Therefore only patients having the D wave recovered after SCI, even not having initially presence of the muscle MEPs. These data created neurophysiologic profile of the SCI patients concerning conduction system of the spinal cord, as a background for the further expansion of neurophysiologic testing to the gray matter of the spinal cord (processing system) and further categorization, intervention, and rehabilitation strategies.
References: 1. Deletis V. Intraoperative neurophysiology of the corticospinal tract of the spinal cord. In: Functional Neuroscience: Evoked Potentials and Related Techniques. (Suppl. to Clinical Neurophysiology Vol 59) (Eds. C. Barber , S. Tsuji, S. Tobimatsu, T. Uozumi, N. Akamatsu, A. Eisen) 2006, pp.105-109. 2. Kothbauer K, Deletis V, Epstein FJ. Motor evoked potential monitoring for intramedullary spinal cord tumor surgery: correlation of clinical and neurophysiological data in a series of 100 consecutive procedures. Neurosurg Focus 4(5) pp 1- 9, 1998 http://www.aans.org/journals/online_j/may98/4-5-1). 3. Sala F, Palandri G, Lanteri P, Deletis V, Facioli F, Bricolo A. Motor evoked potential monitoring improves outcome after surgery for intramedullary spinal cord tumor :a historical control study. Neurosurgery, 58 1-13, 2006.
Notes
14 ION OF ACUTE SCI PATIENTS-TORINO EXPERIENCE
Paolo Costa, MD Section of Clinical Neurophysiology, CTO Hosp, Torino, Italy Co-Authors: Alessandro Borio, Marta Giacobbi, Sonia Marmolino, Gianluca Isoardo, Palma Ciaramitaro Section of Clinical Neurophysiology, CTO Hosp, Torino, Italy
Introduction The need to improve methods for assessing the degree of traumatic spinal cord injury (SCI) is gaining importance in order to test the efficacy of new, promising therapies potentially beneficial to damaged spinal cord. Various animal models of experimental SCI showed that motor evoked potentials (MEPs) and somatosensory evoked potentials (SEPs) are a sensitive measure of post-injury sensory and motor status. Only a few studies have been reported on use of SEPs in evaluation of acute spinal cord injured patients. On the other hand, SEPs and MEPs have shown to be reliable in the assessment of the spinal cord functional integrity during spine and spinal cord surgeries. In particular, the combined use of muscle MEPs (m-MEPs) and epidurally recorded D wave (e-MEPs) provide relevant information on motor outcome.
Methods Intraoperative recording of m-MEPs and e-MEPs along with cortical SEPs and e-SEPs was attempted in 34 patients (14 with a complete SCI, 8 incomplete -4 of them with central cord syndrome and 12 uncompromised) during posterior stabilization for spine and spinal cord trauma. In order to test any kind of conductivity across the lesion site, in a subgroup of 6 subjects, all of them with a clinically complete SCI, the spinal cord has been stimulated cranially and caudally to the site of injury by the epidural electrodes in order to record responses from the scalp and the nerve.
Results The typical “neurophysiologic profile” of the complete SCI was the absence of both m-MEPs and e-MEPs caudally to the lesion site associated with a lack of cortical and e-SEPs cranially to the lesion site. None of these patients recovered motor function in the follow up period up to one year. In one patient with central cord syndrome the presence of D wave recorded from the caudal epidural electrode correctly predicted motor recovery. In the subgroup of 6 patients the intraoperative spinal cord stimulation with catheter electrode positively add to the confirmation of the completeness of their lesion.
Conclusion Intraoperative neurophysiological evaluation of SCI patients can provide information about spinal cord function that is not retrievable by other clinical means and correctly predict the neurological outcome. Intraoperative testing during early stabilization of the spine of deeply paraparetic SCI patients provide additional information about neurological profile.
References • Kirshblum SC, O'Connor KC. Predicting Neurologic Recovery in Traumatic Cervical Spinal Cord Injury. Arch Phys Med Rehab 1998 ;79:1456-1466. • Halter JA, Haftek I, Sarzynska M, Dimitrijevic MR. Spinal cord evoked injury potentials in patients with acute spinal cord injury. J Neurotrauma 1989 Winter;6(4):231-45. • Deletis V, Sala F. Intraoperative neurophysiological monitoring of the spinal cord during spinal cord and spine surgery: a review focus on the corticospinal tracts. Clin Neurophysiol 2008; 119(2):248-64.
Notes
15 NEUROMONITORING OF ACUTE SPINAL CORD INJURY- VERONA EXPERIENCE*
Francesco Sala, Paolo Rizzo, Vincenzo Tramontano, Paolo Manganotti, Franco Faccioli, Massimo Gerosa Department of Neurosurgery and Intraoperative Neurophysiology Unit, University Hospital, Verona, Italy Section of Rehab. Neurology, Department of Neurological and Visual Sciences, University of Verona, Italy
Introduction Clinical neurophysiological studies are routinely performed in the subacute and chronic phase after spinal cord injury (SCI), while there are virtually no studies in the acute (0-72 h) phase. Yet, most of the transition from primary to secondary injury takes place within hours after trauma and therefore this is the critical time where the pathophysiology of the injured cord should be investigated.
In this pilot study, we explored the possibility to apply intraoperative neurophysiological monitoring (INM) to surgical procedures performed during the acute phase (0-72 h) after SCI, with the aim of defining the neurophysiological profile of the injured spinal cord. We focused specifically on the research of the so called killed-end potential (KEEP), also known as “injury potential”. This has proved to be a neurophysiological landmark of SCI in experimental studies, while clinical data are only anecdotal.
Methods From December 2006 to October 2008 we succeed in performing INM in 13 patients (11 males, 2 females) operated on within 72 hours after acute spinal cord injury. Posterior decompressive laminectomy and fixation were performed in 12 patients; an anterior decompression was done in one patient. The ASIA score was assessed on admission and then 12 hours, 7 days and 3, 6, 12 months after surgery. Transcranially elicited motor evoked potentials were recorded from limb muscles (mMEPs) after multipulse stimulation and from the epidural spinal space after single transcranial stimulus (D-wave). Somatosensory evoked potentials were elicited after median and tibial nerve stimulation and recorded from the spinal cord (spinal SEPs) and the scalp (cortical SEPs). Epidural electrodes were placed rostral and caudal to the level of the laminectomy to record D-waves and spinal SEPs both proximal and distal to the injury site. This epidural electrode was also moved across the injury site to attempt the recording of the KEEP. All patients received methylprednisolone prior to surgery according to the National Acute Spinal Cord Injury Study protocol.
Results (table 1) On admission, 7 patients were on ASIA A, 2 on ASIA C, 4 on ASIA D. Time between SCI and surgery was 7.5 hours (median; range 3.5-24 hours). After surgery, these patients were followed with a mean follow-up time of 11.3 months (range 4-22). At surgery, caudally to the level of the lesion mMEPs were absent in all but two ASIA D patients, and unmonitorable in one because of myorelaxation. D-wave caudal to the level of injury was absent in 6 patients (5 ASIA A, 1 ASIA D), present in 2 (one ASIA C, one ASIA D), unmonitorable in 4 patients (3 because of low spinal cord level, 1 because of anterior surgical approach), and questionable in one (ASIA A). Spinal SEPs cranially to the level of the lesion were absent in 7, present in 4 (1 ASIA C, 3 ASIA D) and unmonitorable in 2 patients. A D-wave and spinal SEP KEEP was recorded in 4 patients: these 4 patients were ASIA A on admission and remained ASIA A at the follow-up. The other 2 patients with absent D-wave caudally to the lesion (one ASIA A, one – with extradural hematoma- ASIA D), were unchanged at discharge from hospital, but one recovered to ASIA B at the follow-up. The patient with questionable D-wave on admission (ASIA A), recovered to ASIA B at discharge and ASIA D at the follow-up.
Conclusions This preliminary study suggests that the presence of a KEEP may represent a neurophysiological landmark indicating irreversible complete SCI. Conversely, whether or not – in the absence of a KEEP - the absence of D- wave on the acute phase after SCI necessarily indicates a complete and irreversible motor deficit does not emerge clearly from our results.
Further data should clarify whether the combination of D-wave and KEEP recordings will allow to establish reliable prognostic criteria, possibly differentiating transient block of conductivity from permanent corticospinal tract injury.
* This abstract has been previously presented at the Summer School for the Biological Treatment of Chronic Spinal Cord Injury, Vienna October 5-10, 2008
16 Table 1: Correlation between intraoperative neurophysiological data and ASIA scores
Pt. Tc-MEP D-wave Spinal SEPs D-wave Spinal SEPs ASIA ASIA ASIA from limb caudal rostral to the KEEP KEEP on at at muscles caudal to the level of level of injury admission discharge follow-up to the level of injury injury GF Absent Questionable Absent Questionable Questionable A B D (absent) (no) (no)
TM Unmonitorable Unmonitorable Unmonitorable Unmonitorable Unmonitorable C D D (anesthesia) (anesthesia) (cortical SEPs (L1) (L1) only)
SS Absent Absent Absent Yes Yes A A A
TC Absent Present Present No No C D E
SG Absent Absent Absent No No D D D
PMK Absent Unmonitorable Unmonitorable Unmonitorable Unmonitorable A A A (anterior (anterior (anterior (anterior approach) approach) approach) approach) CG Absent Absent Absent Yes Yes A A A
AM Present Unmonitorable Present Unmonitorable Unmonitorable D D D (L1) (L1) (L1)
DRG Absent Absent Absent Yes Yes A A A
SB Absent Present Present No No D D D
KA Absent Absent Absent Questionable Questionable A A B (no) (no)
TG Present Unmonitorable Present No No D D D
ZC Absent Absent Absent Yes Yes A A A
Notes
17 HOW SAFE AND ACCURATE IS TRANSCRANIAL ELECTRICAL STIMULATION?
H. L. Journee, MD, PhD Depts. of Neurosurgery UMC-Groningen and Orthopedics Sint Maartenskliniek Nijmegen, The Netherlands
In the last 15 years transcranial electrical stimulation (TES) has rapidly developed as a useful technique for monitoring the conduction of evoked motor responses directly on the corticospinal tract or as muscle evoked potentials. Despite high voltages required for direct extracranial stimulation no persistent neurological deficits or tissue damage related to the procedure have been reported. During TES, considerable less cases with epileptic activity has been noticed than in cortical stimulation. Mechanical damage due to bite injuries is more likely to occur when no bite blocks are used. TES evoked motor potentials depend on stimulus paradigms, choice of electrodes and their placement on the head. Consequently, the motor monitoring depends on the accuracy of stimulus parameters, electrode shape and size and their impedances and shape of the administered pulses.
A. Safety of TES Safety concerns in transcranial electrical stimulation can be categorized as 1) direct tissue damage, 2) kindling and seizures and 3) complications due to mechanical impact from muscle contraction and from electrode placement.
Direct tissue damage Tissue damage due to direct physical impact occurs most likely on places with the highest dissipation of electrical energy. These are the locations with the highest impedance of in series connected resistors of the TES electrodes. The local electrode impedances contribute mainly to the total TES electrode impedance (4). The dissipation will therefore occur at the electrodes that enclose the low net impedance of the head. Consequently, the dissipated energy is expected in small tissue volumes near the electrodes. In the worst case one might get small (<2mm2) superficial skin burns from surface electrodes that are not properly attached to the skin or dried out. Needle electrodes used for TES can be considered as safe. When skin burns have an electrical origin, monopolar cautery is a likely cause (6) and precautions are similar to those that apply to any intra-operatively used electrodes for physiological measurements in general.
According to Agnew and McCreery, in TES, the currents are sufficiently dispersed to attenuate the stimulus charge density at the brain surface to a safe level (less than 40 μC/cm2.phase) to be sure not to cause damage to neural tissue (1). However, this limit of 40 μC/cm2.phase value is a highly inaccurate estimate since it is based on a transformation from cortical to transcranial stimulation in which only the attenuation of the current density is considered. However, other factors are also important. These concern non-linearity, the role of complex tissue impedances, relation between electrical field strength, [which correlates to the electrical power dissipation in tissue volumes] and activation functions [these describe the stimulating force on corticospinal axons]. Moreover there is a marked difference in pulse paradigms: where TES is based on trains of high frequency pulses (ipi = 1 4 ms), the well conducted experiments of Agnew and McCreery use continuous pulse series of 20 or 50 Hz that last several hours, instead. According to our volume conduction models, skull defects will not introduce unsafe conditions as long as the electrodes are separated far enough from the brain surface, which is the case with subcutaneous placed TES electrodes, even in very young children.
Neural damage due to electrochemically produced toxic products (chloride oxidation, pH changes and oxidation of organics), which likely is the most aggressive cause of neural tissue damage in cortical stimulation, is avoided with extracranial electrodes.
The remaining causes for neural damage are toxic effects from neuronal hyperactivity. In all TES-MEP protocols for monitoring the maximum frequency of repeated stimuli is 1 Hz. This is far below the sustained 20-50 Hz stimulation frequencies used by the authors. One Hertz is below the physiological maximum frequency of voluntary repetitive voluntary muscular contractions. This makes neural hyperactivity, resulting in neural damage, unlikely, unless when epileptic activity is induced. To obtain realistic limits of charge per phase, charge density per phase and other TES parameters like number of pulses per train and intertrain intervals, there is a call for experiments that better approach the situation of transcranial stimulation and result in more accurate limits for safety.
Kindling and seizures Kindling has indiscriminative been considered as potential danger in transcranial stimulation. Kindling, which refers to the induction of self-perpetuating epileptic foci that has been induced by daily repeated electrical
18 stimulation of 50Hz for several seconds in an experimental primate model, has not been reported as a complication of TES. In contrast to bipolar cortical stimulation, TES with a short train of anodal high-frequency pulses has an extremely low risk of inducing seizures. There is no increased risk of the occurrence of TES associated seizures in patients with symptomatic epilepsy compared with those patients without seizures (9). In a review of more that 15.000 TES-MEP monitoring cases, McDonald reports only 5 non published seizures of which some were not related to TES(7). The relative insensitivity of TES for induced seizures could be due to the preferential stimulation of the vertical oriented corticospinal axons near the anode whereas the horizontal oriented axons of the cortex near the anode are hyperpolarized and hence will not expose a permissive influence on seizures.
Mechanical impact from muscle contraction There is a relative close distance between TES electrodes and the temporal and masseter muscles. TES causes extracranial current pathways that directly can stimulate closely located muscles like the temporal and masseter muscles via a current route through the scalp. With mechanical measurements during complete neuromuscular blockade we could demonstrate that the fields from normally used TES intensities are from axon mediated muscle stimulation. The muscular force increases progressively with the number of pulses in a TES train. The masseter muscle is one of the strongest muscles in man and can induce maximum bite forces between 50 and 80 kgf. When TES is performed at C3 and C4 electrodes, the masseter contractions were most pronounced when compared to stimulation at Cz’/Fz, C3/Cz or C4/Cz montages. The mechanism may involve both corticobulbar activation by pulse-trains and direct stimulation of the motor branches of the trigeminal nerve, because jaw clenching also occurs with single pulses. Thus, C3/C4 TES may produce stronger biting than C1/C2 TES because the electrodes are closer to the facial and trigeminal nerves (8). Moreover, TES induced muscle contractions of the facial innervated muscles and tongue may also contribute to the problem. Lip lacerations and tongue bites are likely to occur when precautions of bite blocks are not adequately used. Furthermore complications mentioned by the study of McDonald were 29 tongue or lip lacerations, 2 scalp burns, 5 cardiac arrhythmias and 1 mandible fracture(2). Bite injuries due to jaw muscle contractions during TES are the most common but still infrequent complications (7).
Although possible, no spinal epidural recording electrode complications or injuries resulting from TES-induced movement were reported, nor were adverse neuropsychological effects.
B. Accuracy of TES. The quality of monitoring of motor evoked potentials depends on the accuracy of stimulus parameters, electrode shape and size and their impedances and shape of the administered pulses. The amplitude of MEP signals usually is a function of any these parameters. So depends the MEP amplitude not only on TES-intensity, but also on other factors like the impedance of TES electrodes. This impedance may change in time. An example is the development of scalp edema. Scalp edema introduces a higher conducting scalp and therefore initiates an extra shunting current. Transcranial stimulation can be performed by, by choice, voltage or current stimulators.
Ideal voltage stimulators deliver voltages that are resistant to the impedance of TES electrodes. When the local electrode impedance is small compared to the head impedance, the current through the brain will theoretically be unaffected while the stimulator delivers the extra current for the shunting resistor of the extracranial component. Electrodes with large contact surfaces fulfill these conditions (3). However, not all commercial available voltage stimulators are resistant to changes in the load resistance. For example, Digitimers D185 multipulse stimulator has an internal resistor of 120 Ω, which is in the middle of the typical range of the head resistance of80 - 150 Ohm. This already predicts a 50%voltage drop whereas pulse waves become distorted at the low TES impedances (5). These problems can be reduced partly using TES electrodes with higher local impedances, but the administered voltage and also threshold alarm voltage levels, which are an accepted method for detection of significant events (2), remain dependent on impedance. In this context, current stimulators would be a better choice since the delivered current is independent of the load impedance and this make the choice of electrodes less critical.
Conclusions The methodology for monitoring of the functional integrity of motor pathways over the last decade has progressed into a reliable, fast and relatively simple tool that easily can be used intraoperatively. Almost all of these complications can be prevented by adequate measures like using bite blocks, restriction of TES induced movement and proper choice and placement of TES electrodes. One should take care of possible increased risk factors like epilepsy, raised intracranial pressure, cardiac disease, proconvulsant medication and cardiac pacemakers. When in expert hands, the benefits of TES MEP monitoring convincingly outweighs associated risks.
References
19 1. Agnew WF and McCreery DB. Considerations for safety in the use of extracranial stimulation for motor evoked potentials. Neurosurgery 20: 143-147, 1987. 2. Calancie B, Harris W, Brindle GF, Green BA and Landy HJ. Threshold-level repetitive transcranial electrical stimulation for intraoperative monitoring of central motor conduction. J Neurosurg 95: 161-168, 2001. 3. Journee H.L, Polak HE and deKleuver M. Influence of electrode impedance on threshold voltage for transcranial electrical stimulation in motor evoked potential monitoring. Med Biol Eng Comput 42: 2004. 4. Journee HL, Polak HE and de Kleuver M. Influence of electrode impedance on threshold voltage for transcranial electrical stimulation in motor evoked potential monitoring. Med Biol Eng Comput 42: 557-561, 2004. 5. Journee HL, Shils J, Bueno de Camargo A, Novak K, Deletis V. Failure of Digitimer's D-185 transcranial stimulator to deliver declared stimulus parameters. Clin Neurophysiol 114: 2497-2498, 2003. 6. Knickenbocker GG and Neufeld GR. Electrotrauma in the Operating Room: Shock, Electrocution and Burns. In: Complications in Anesthesiology, edited by Gravenstein N and Kirby NN. Lippincott-Raven Publishers, 1996, p. 79-91. 7. MacDonald DB. Safety of intraoperative transcranial electrical stimulation motor evoked potential monitoring. J Clin Neurophysiol 19: 416-429, 2002. 8. MacDonald DB. Intraoperative motor evoked potential monitoring: overview and update. J Clin Monit Comput 20: 347- 377, 2006. 9. Szelényi A, Joksimovic B and Seifert V. Intraoperative risk of seizures associated with transient direct cortical stimulation in patients with symptomatic epilepsy. J Clin Neurophysiol 24: 39-43, 2007.
Notes
20 IMAGING OF SPINAL CORD FUNCTION AND PHYSIOLOGY
Spyros S. Kollias, MD Institute of Neuroradiology, University Hospital of Zurich, Switzerland
The past ten years have witnessed a revolution in the diagnosis and management of spinal disorders. MR imaging has quickly emerged as the study of choice for virtually all disorders of the spine. With the inherent contrast sensitivity, the high spatial and temporal resolution, the multiplanar sampling of anatomy, the reliable differentiation between normal and pathologic tissue and the lack of irradiation hazards of MR, the morphology of the spinal cord, and nerve roots but also of the vertebrae, intervertebral disk, epidural space, can be visualized with striking clarity. The use of paramagnetic contrast agents became well established in a variety of disorders allowing definition of abnormal vessels, leptomeninges, and disrupted blood-cord barrier. State-of-the-art MR has increased the specificity of diagnosis of spinal disease, aided earlier diagnosis of spinal lesions and increased the anatomical precision of disease localization. It is now possible to diagnose processes that were previously only inferred from imaging studies. Diagnostic innovations have been followed by considerable therapeutic advances. But also therapeutic advancements particularly in the field of regeneration of the neural tissue in spinal cord injury are driving technological developments in imaging. Despite this progress, the modality remains in an evolution stage, with almost unlimited room for improvement. New imaging methodologies have been developed over the last years that are used to clarify not only morphological changes but also the physiology and pathophysiology of neural tissue.
High-resolution Magnetic Resonance (MR), diffusion-weighted (DWI) and diffusion-tensor (DTI) imaging, functional MR imaging (f-MRI) and MR spectroscopy (MRS) have evolved into important research tools for examining the structural and functional nature of neurological pathology, in both animal and human tissue. Applications in the brain have already gained widespread clinical acceptance however, imaging the spinal cord places additional demands on imaging, due to its fine structure and its elasticity, the requirement for high in-plane resolution and avoidance of artifacts arising from cord and CSF motion, respiratory motion, and swallowing. Optimization and application of these non-invasive MR techniques on studying the human spinal cord can potentially provide new morphological, physiological and functional information in vivo and eventually, important insight into a variety of disease processes affecting the spinal cord and its functional recovery after injury improving the specificity of conventional imaging approaches.
Presently, application of advanced imaging methodologies for in vivo imaging of the human spinal cord gain widespread acceptance for potential use in clinical studies. These include high resolution differentiation between spinal cord grey and white matter using high field (3-T) MR systems, evaluation of microstructural changes in the integrity of white matter using DTI, mapping functional activity of the spinal sensorimotor neurons using fMRI, as well as metabolical imaging of the spinal cord tissue using MR spectroscopy. First clinical applications in patients with demyelinating disease, (i.e., multiple sclerosis), spinal cord injury (SCI), neoplastic processes etc, indicate that these techniques provide better demonstration of the structural damage and understanding of its functional consequences and its evolution in the human spinal cord. Quantitative imaging parameters can be used as surrogate markers of disability for determining prognosis and for following up rehabilitation and pharmacologically induced recovery. With the progression of regeneration enhancing treatment for spinal cord injury form basic research to patient trials, these new diagnostic tools for the clinical assessment, including prognosis and post-treatment follow- up, become of utmost importance for assessing with increased specificity and sensitivity the structural, physiological and functional status of the human spinal cord in vivo and in the clinical setting.
It must be always remembered, however, that the body has a limited range of responses to an apparently infinite variety of insults from infectious, inflammatory, traumatic, and neoplastic entities. Images are often sensitive but not specific, and a logical pathologic differential diagnosis must be given. Further, many morphologic derangements can be demonstrated in asymptomatic individuals, which further complicates the concept of abnormality. In certain situation there may only be a moderate correlation between the imaging evidence of morphologic alteration and the presence of symptoms. These facts emphasize that we need to concentrate more effort on determining the significance of the morphological changes we can now so exquisitely demonstrate, and the central importance of both the clinical and electrophysiological evaluation in the work-up of patients with spine disorders. Imaging is an intermediate test that must be integrated into, rather than isolated from, the clinical and neurophysiological evaluation. The management of patients with spinal disorders must begin and end with a thorough clinical assessment and imaging findings must be correlated and validated with clinical and electrophysiological parameters.
21 Notes
22 ENDOVASCULAR TREATMENT OF VASCULAR MALFORMATIONS AND TUMORS OF THE SPINE AND SPINAL CORD
Yasunari Niimi, MD, PhD Center for Endovascular Surgery and Intraoperative Neurophysiology Institute for Neurology and Neurosurgery, Roosevelt Hospital, New York, NY, USA
1. Introduction All vascular lesions involving the spine, spinal cord and surrounding tissues are potential candidates for endovascular embolization. The indications include preoperative treatment to decrease vascularity and therefore intra-operative blood loss, palliation for incurable diseases and curative therapy by embolization alone. Various embolic agents are used depending on the purpose of the treatment and the nature of the disease. In order to avoid neurological complications, it is important to preserve the blood supply to the normal spinal cord during embolization. For this purpose, it is essential to superselectively catheterize the feeder to the lesion and carefully analyze the vascular anatomy. All spinal endovascular procedures are performed under general anesthesia and neurophysiologic monitoring in our institution. The role of neurophysiologic monitoring varies depending on the nature of the disease and procedures performed.
2. Vascular anatomy of the spine and spinal cord. The vascular supply to the spine and paraspinal musculature arises from the main trunk of the intercostal or lumbar artery as well as the dorsospinal artery. Vascular supply to the spinal dura and spinal cord is derived from the ventral division of the dorsospinal artery. There are rich longitudinal and transverse anastomoses between the adjacent segmental arteries. Nerve roots and the spinal dura are supplied by the radicular artery. If a radicular artery supplies the anterior spinal artery (ASA), it is called a radiculomedullary artery, and if it supplies the posterior spinal artery (PSA), it is called a radiculopial artery.
There are 4-8 radiculomedullary arteries and 10 to 20 radiculopial arteries. The ASA extends almost uninterrupted from the medulla to the filum terminale. Major contributions to the ASA arise from 3 sources, one from the two vertebral arteries near the vertebro-basilar junction, one at the level of the cervical enlargement from the vertebral, deep cervical or ascending cervical artery, and the other one from thoracolumbar territory, called “artery of Adamkiewicz”. This artery usually rises from the 9th to the 12th intercostal artery, on the left side in approximately 80% of the cases.
The paired posterior spinal arteries arise either from the vertebral artery or from the postero-inferior cerebellar artery at the cervical level. They are often ventral to dorsal nerve roots and called lateral spinal artery. Caudally, these paired posterior spinal axes are located on the posterolateral surface of the cord dorsal to the dorsal roots. Circumferential vessels from the ASA anastomose with the PSAs through a complex pial network, the so-called Vasa Corona.
Intrinsic blood supply to the spinal cord is from sulcal arteries ventrally and radial perforating arteries from the circumferential pial network or vasa corona. Each sulcal artery supplies one side (right or left) of the ventral portion of the spinal cord. They anastomose with adjacent caudal and rostral sulcal arteries within the ventral sulcus. They supply up to the 50% of the section at the level of the spinal cord enlargement but only 15-20% at the thoracic level. Because their supply includes the anterior column of the central gray matter, the anterior and lateral corticospinal tracts, and the anterior and lateral spinothalamic tracts, the ASA accounts for vascularization of the structures involved in the propagation of motor evoked potentials from their cortical generators to the a- motoneurons. In contrast, the PSAs supply the posterior horns of the central gray matter and the dorsal columns; although the debate is still open, these posterior columns are usually considered the main tracts for central propagation of somatosensory evoked potentials after peripheral stimulation. There are rich axial and longitudinal anastomoses among these intrinsic arteries. These anastomoses are richer in the thoracic level and more potent adjacent to the spinal cord arteriovenous malformation.
The venous drainage of the spinal cord is characterized by rich intra- and extra-medullary anastomoses. The extra- medullary veins include the pial venous network, the longitudinal collectors, and the radicular veins. The radicular veins can be along the ventral or dorsal nerve root and pierce the dura to drain into the epidural veins. They lack valves but typically narrow at the dural penetration to prevent retrograde venous flow. Epidural venous plexus is small dorsally and large ventrally. The ventral plexus drains the vertebral bodies and appears as hexagonal channels anastomosing across the midline and with the caudal and rostral systems, and continues from the sacrum
23 to the base of the skull. Flow in the epidural veins is affected by gravity, position, and changes in the abdominal and intrathoracic pressure, which in turn affects the venous drainage of the spinal cord below the heart level.
3. Spinal angiography Several vessels must be angiographically evaluated to delineate the vascular supply of the spine and spinal cord. At the cervical level, the ascending cervical artery, the vertebral artery and the deep cervical artery on both sides must be studied. Additionally, at the C1-C2 levels, the ascending pharyngeal and occipital arteries should also be studied. For the thoraco-lumbar levels, angiographic evaluation of the bilateral supreme intercostal, intercostal and lumbar arteries need to be studied. At the sacral level, bilateral lateral sacral and iliolumbar arteries arising from the internal iliac artery as well as median sacral artery may supply the sacral nerve roots, spinal cord, vertebrae, and parasacral musculature.
Angiographically, the radiculomedullary artery has a characteristic hairpin configuration which continues to the ASA. The ASA continues caudally to the filum terminale and forms basket-shape anastomoses with bilateral PSAs at the level of the conus. The PSA appears as a relatively small paramedian longitudinal straight vessel. The PSA axis is smaller and discontinuous compared to the ASA axis. The radiculopial artery also forms a hairpin configuration that has a more acute angle than the radiculomedullary artery because of its paramedian location.
Spinal angiography and subsequent endovascular treatment are best performed under general anesthesia. This not only provides the patients with comfort, but also allows for extended periods of apnea (up to 40 seconds) and thus provides the opportunity to obtain high-resolution images necessary to identify small spinal cord arteries and to evaluate slow flow lesions.
In general, pre-therapeutic spinal angiography should evaluate the vascular anatomy of both the pathology and normal surrounding spinal cord.
4. Neurophysiologic monitoring and pharmacological provocative testing Intraoperative neurophysiologic monitoring has been used to assess the functional integrity of neural pathways during endovascular procedures of spine and spinal cord vascular lesions under general anesthesia. We routinely use SEPs and MEPs monitoring for all spinal angiography procedures with intent to treat by embolization.
4.1. Neurophysiologic monitoring During angiographic assessment and embolization, the patients are maintained under general anesthesia using continuous infusion of propofol (100-150 μg / Kg / min) and fentanyl (1 μg / Kg / hr). Short acting muscle relaxant is used for intubation purpose only. After anesthesia induction, no inhalational anesthetics are used.
SEPs were elicited by stimulating the right and left posterior tibial nerves at the ankle and median nerves at the wrist with electric stimuli (40 mA, 0.2ms duration and 4.3 Hz repetition rate). Recordings are performed via corkscrew-like electrodes inserted subcutaneously in the scalp (CS electrodes Nicolet, Madison, WI) respectively at C3’/C4’-CZ’ (median nerve) and at CZ’- FZ (tibial nerve) according to the International 10/20 EEG System.
The MEPs are elicited with transcranial electrical stimulation of the motor cortex using CS electrodes. Short trains of 5-7 square-wave stimuli of 0.5 ms duration each and interstimulus intervals of 4 ms are applied at a repetition rate of 2 Hz and intensity up to 200 mA, through electrodes placed at C1 and C2 scalp sites, according to the International 10/20 EEG System. MEPs are then recorded via needle electrodes inserted into the bilateral abductor pollicis brevis (APB) for upper extremities and anterior tibial (TA) and abductor hallucis (AHB) muscles for the lower extremities. Recording from the upper extremity muscles were used as a control for embolization of thoracic or lumbar lesions.
Whenever the lesion involves the lumbosacral segments, we add the monitoring of the bulbocavernosus reflex (BCR). This oligosynaptic reflex allows the assessment of the functional integrity of both the afferent and efferent fibers of the pudendal nerves together with the reflex center located in the gray matter at S2-S4 spinal segments. For stimulation of the dorsal penile nerve (pudendal afferents), two silver/silver chloride disc electrodes are placed on the dorsal aspect of the penis with the cathode proximal. In female patients, the cathode is placed over the clitoris and the anode over the labia majora. Rectangular pulses of 0.2-0.5 ms duration are applied as a train of 5 stimuli (interstimulus intervals of 4 ms) at a repetition rate of 2.3 Hz. Stimulus intensities do not exceed 40 mA. Recordings are made from the anal sphincter muscles using two pairs of intramuscular teflon-coated hooked wire electrodes stripped 2mm at the tip inserted into the anal hemisphincters.
24 With regard to the feasibility of evoked potentials during endovascular procedures, our series demonstrate that these potentials are easily elicitable in the majority of the patients, unless severe neurological deficits have already compromised the functional integrity of neural pathways. Monitorable SEPs often cannot be obtained in patients who have lost proprioception. In over 110 endovascular procedures in 87 patients who were treated for spine and/or spinal cord vascular lesions, monitorability of evoked potentials was 80% for SEPs, 85% for the BCR and 92% for MEPs. Monitorability is defined as the presence of a reliable response after the induction of anesthesia. There were no significant differences in monitorability between males and females for MEPs and SEPs, while the BCR seemed more difficult to elicit in females, most likely because of technical difficulties in placing stimulating electrodes. Absent BCR is so far well correlated with symptoms of bladder, bowel or sexual dysfunction. Clinical usage of BCR monitoring for spine and spinal cord embolization is still under investigation.
4.2 Provocative testing In addition to the careful angiographic analysis, pharmacological provocative testing is a method used to identify the functional eloquence of the territory of a catheterized vessel.
Pharmacological provocative testing consists of intra-arterial injection of short acting barbiturates (e.g. sodium amytal) and lidocaine through a microcatheter. A low dose of a short-acting barbiturate (e.g. sodium amytal) predominantly suppresses neuronal activity as opposed to a low dose of lidocaine, which predominantly suppresses axonal conduction in the central nervous system. In our series, lidocaine caused more positive results than sodium amytal. The most likely reason for this observation is because lidocaine blocks the nerve transmission through the fibers traversing the anesthetized area, as opposed to sodium amytal which blocks transmission within neurons in the anesthetized area.
The motor pathway affected by injection of sodium amytal may not be detected because of limited number of muscles monitored with MEPs technique. We, therefore, have added monitoring of important muscles for specific cases, such as MEPs from diaphragm for high cervical cord lesions. For radicular feeders to a malformation, we also place additional electrodes to monitor MEPs from the muscles supplied by the nerve root at the level of the lesion.
Provocative testing has the most important role for embolization of intradural spinal cord AVMs among all spine and spinal cord vascular lesions, because they are supplied by the spinal cord arteries and embolization for these lesions carries the highest risk of causing spinal cord ischemia. This test can be performed for dural or extradural lesions, if the existence of a spinal cord artery distal to the tip of the microcatheter cannot be confidently excluded before embolization. In cases with previous interventions and an altered anatomy, we find these testing of great value.
It is important to obtain baseline recordings just before the provocative testing, because SEPs and MEPs are sensitive to the depth of anesthesia. Prior to provocative testing, superselective digital subtraction angiography is performed through the microcatheter placed as close as possible to the AVM, in order to study the normal and abnormal vascular anatomy at the location intended for embolization. Contrast material is then injected under road map fluoroscopy, in order to determine the optimal force for injection which will distribute the anesthetic distal enough without creating reflux proximal to the tip of the microcatheter. Provocative testing for neuronal function follows this by the intra-arterial (IA) injection of 25-50 mg of sodium amytal. If there are no changes in SEPs or MEPs, this is then followed by the IA injection of 20-40 mg of lidocaine. If there are still no changes in SEPs or MEPs, embolization is performed using a liquid embolic agent such as N-butyl cyanoacrylate (NBCA) from that catheter position. If over 50% decrease in the amplitude of SEPs and/or disappearance of MEPs occurred after injection of sodium amytal or lidocaine, the provocative test is considered positive and liquid embolization from that catheter position is not performed. If sodium amytal produced a positive result, the test is considered positive and lidocaine is not injected.
If a provocative test is positive, the best solution is to advance the microcatheter closer to the nidus and repeat provocative testing. Another solution is to protect the normal territory using a fiber or liquid coil. If neither of the above is possible, embolization may still be performed using particles, depending on the flow dynamics in the feeder. If none of these alternatives are possible, embolization from another feeder should be considered.
25 5. Clinical application of neurophysiologic monitoring 5.1. Vascular malformations Vascular malformations can be simply classified into dural/extradural and intradural lesions. This distinction is important because the risk of embolization and the role of neurophysiologic monitoring are significantly different between these two categories.
5.1.1. Intradural vascular malformations Intradural vascular malformations are supplied by spinal cords arteries and drained by spinal cord veins. They are further classified into spinal cord AVMs, AVFs, telangiectasias, and cavernous malformations. Endovascular embolization is indicated and is the first choice of treatment for spinal cord AVMs and AVFs. Embolization is usually curative for simple AVMs and AVFs, but palliative or rarely curative for complex AVMs. Palliative embolization is targeted to occlude dangerous structures such as aneurysms or high flow fistulas and is performed to decrease the risk of hemorrhage or to improve neurological symptoms. Endovascular treatment for this disease group is considered as a potentially high risk procedure because embolization is performed through the ASAs or PSAs. A liquid embolic agent, such as NBCA, is preferred for nidus AVMs and small fistulas due to its ability to penetrate distally and cause permanent occlusion. For large fistulas and associated aneurysms, coils are also effective. Particles are used mainly for small AVMs or AVFs for which distal catheterization through the feeder is difficult.
Angiographic identification of spinal cord vascular supply in the presence of a spinal cord AVM may be difficult due to their small sizes and overlapping normal and pathological vessels. In addition, supply to the normal spinal cord adjacent to the malformation can be modified and unpredictable due to the hemodynamic changes caused by the spinal cord AVM or previous treatment.
Neurophysiologic monitoring including provocative testing is most important in this disease category because of the high-risk nature of the treatment. The main purposes of the monitoring are early detection of spinal cord ischemia and prediction of the safety of embolization from a certain microcatheter position by performing provocative testing. Spinal cord ischemia due to compromised spinal cord vascular supply during the embolization procedure can occur not only by injection of embolic agents but also by catheterization of a feeder, either due to blockage of the flow by the catheter itself, or spasm or dissection created by catheter manipulation.
In a rare situation where vascular anatomy of the lesion is so complicated that it is difficult to differentiate a feeder to the malformation and a normal spinal cord artery, provocative testing can be used as an aid for analysis of the vascular anatomy. It should be emphasized, however, that availability of provocative testing does not decrease the importance of precise angiographic analysis of the vascular anatomy of the malformation and surrounding normal spinal cord. Worsening of MEPs and SEPs after embolization usually correlates with clinical deterioration. Improvement of MEPs or SEPs after embolization, however, does not necessarily correlate with clinical improvement for intradural AVFs and AVMs. Further accumulation of experience is needed to assess the role of neurophysiologic monitoring for prediction of clinical outcome.
In our experience of provocative testing, each positive test resulted in either unilateral or bilateral loss of MEPs or SEPs. After positive provocative testing, MEPs and / or SEPs recovered to the baseline within 15 minutes for the initial testing in most patients. Recovery of MEPs or SEPs tended to be delayed up to one hour after the second or third injection of sodium amytal or lidocaine in the same patient.
Our observation suggests that the motor pathway can be affected by superselective injection of anesthetics through the PSA. This may be due to the rich anastomosis between the ASA and the PSA branches, especially in the existence of an AVM. There may also be hemodynamic shift of the watershed zone between the ASA and the PSA territories, either due to existence of the AVM or a previous embolization procedure. Our data suggest that both SEPs and MEPs should be monitored regardless the provocative test is performed either in the ASA or PSA.
The numbers of true positive and false positive are unknown, because we generally do not embolize the malformation with a liquid embolic agent from that catheter position, if a provocative test is positive. Therefore, sensitivity, specificity, accuracy and positive predictive value cannot be calculated. Theoretically, false positive results can occur because of the different distribution pattern of the liquid embolic material from the anesthetics due to different viscosity and different injection force as well as progressively polymerizing nature of the embolic material as opposed to persistently liquid nature of anesthetics. False negative results can also happen for the same reasons, but it is very rare in our experience. This may be due to the relatively large doses of sodium amytal and lidocaine to anesthetize a small territory distal to the tip of the microcatheter, as well as the tendency of the embolic agent to penetrate less than sodium amytal or lidocaine because of its higher viscosity and progressively
26 polymerizing nature. Therefore, we think that this method of provocative testing tends to overestimate the risk of embolization, resulting in the high negative predictive value.
5.1.2. Dural or extradural lesions Dural or extradural lesions include spinal dural arteriovenous fistulas (SDAVFs), epidural or paraspinal arteriovenous malformations (AVMs) or fistulas (AVFs), and spine AVMs or AVFs. We prefer to use liquid adhesives, such as NBCA, as the embolic agent for these lesions because of its ability to penetrate into small vessels and its permanent occlusive effect. For the permanent cure of an AVF, the liquid embolic material should penetrate into the proximal portion of the draining vein through the fistula site. Insufficient penetration of the embolic material frequently results in recanalization of the lesion due to rich collateral vessels. Coils may be used as an adjunct agent in NBCA embolization to protect normal territory or a primary agent for high flow AVFs. Particles are not used because their occlusive effect tends to be temporary resulting in a high recanalization rate.
Angiogram of the bilateral segmental arteries should be obtained at the level of the feeders as well as at least 2 levels above and below the level of the malformation. If there is intradural venous drainage to the perimedullary veins, it is essential to evaluate the circulation time of the ASA. If it is prolonged with no opacification of the spinal cord venous drainage, this indicates existence of spinal cord venous hypertension and explains the most likely etiology of the patient’s neurological deficits.
The primary role of neurophysiologic monitoring for this disease group is to detect a masked spinal cord artery originating from the same pedicle as the feeder to the malformation. If there is an ASA or a PSA originating from the same pedicle as the feeder, endovascular embolization is contraindicated. Provocative testing should be performed if there is any suspicion for existence of an unidentified spinal cord artery from the feeding vessel to the malformation. The necessity of provocative testing in dural or extradural vascular malformations, however, is exceptional because, compared to tumor cases, identification of a spinal cord artery is easier due to less distortion of the spine and spinal cord and less overlapping abnormal vascularity or metallic devices. Careful analysis of the vascular anatomy of the lesion and the normal spinal cord is far more important than provocative testing. Another role of neurophysiologic monitoring is early detection of possible spinal cord ischemia. If significant changes in SEPs or MEPs are detected during embolization, the procedure should be suspended until full recovery of SEPs and MEPs or terminated to minimize the permanent damage to the spinal cord.
For certain diseases in this category, neurophysiologic monitoring has another promising but not yet proven role; that is, the prediction of functional recovery after embolization. Significant improvement of SEPs or MEPs after embolization is frequently observed for the diseases symptomatic due to spinal cord venous hypertension, including SDAVFs and spinal epidural fistulas with intradural venous drainage. Reduction of spinal cord venous hypertension after embolization is sometimes associated with improvement of SEPs and MEPs and correlated with immediate improvement of neurological symptoms. However, improvement of SEPs or MEPs after embolization is not always associated with clinical improvement. The patient needs intensive rehabilitation after the treatment to maximize functional recovery. Clinical improvement typically occurs first in motor function, followed by sensory functions. Improvement of bladder, bowel, and sexual dysfunctions tends to be delayed and less satisfactory, if at all. It should be noted that improvement of MEPs or SEPs immediately after embolization does not guarantee complete cure of the disease or long lasting remission of the symptoms. Therefore, correlation of neurophysiologic improvement (SEPs and MEPs) with angiographic cure of the lesion is important to predict permanent clinical improvement.
5.2. Tumors Vascular tumors are classified as benign and malignant. Malignant tumors can be further classified as primary and metastatic. For the purpose of endovascular embolization, it is also useful to differentiate between intramedullary and extramedullary tumors. Intramedullary tumors are supplied by the spinal cord arteries and their embolization carries higher risk than extramedullary tumors which are not supplied by the spinal cord arteries. Hemangioblastoma is practically the only intramedullary tumor that is a candidate for embolization. This tumor is benign but usually hypervascular and is embolized primarily as a preoperative procedure to decrease the intraoperative blood loss. Indication for embolization is determined based on the angiographic assessment of the feeders (ASA or PSA), their sizes, and vascularity of the tumor. Angiographic assessment and endovascular treatment are performed in a similar manner to that utilized for intradural spinal cord vascular malformations.
Intradural extramedullary tumors such as meningiomas and neurinomas are not usually very vascular and embolization is not indicated. In contrast, vascular tumors located in the extradural or paraspinal compartments are frequently amenable to embolization as a preoperative or palliative measure. These tumors include benign and malignant lesions. Common benign tumors include hemangiomas, giant cell tumors, and aneurysmal bone cysts.
27 Malignant tumors include primary sarcomas, plasmacytomas, hemangiopericytomas, and metastatic carcinomas such as those from the breast, thyroid, kidney, and stomach.
We usually use particles as the primary embolic agent. Coils are used to protect normal territory from inadvertent embolization. Liquid adhesive, such as n-butyl cyanoacrylate (NBCA), is not routinely used for tumors because of its higher potential risk of penetration into the spinal cord artery. It may, however, be used in highly vascular tumors to obtain a better occlusive effect. For palliative embolization of malignant tumors, ethanol may also be used as an embolic agent, resulting in a long lasting effect due to its cytotoxicity.
Pre-therapeutic angiographic study is important to evaluate the vascularity of the lesion including feeding arteries, draining veins, existence of arteriovenous shunting and associated aneurysms as well as the extension of the lesion. It is also important to determine if there is ASA or PSA contribution at or near the level of the lesion. For this purpose, angiographic evaluation should include not only the assessment of bilateral segmental arteries at the level of the lesion, but also at least two levels above and below the lesion. In the case of distortion of the spine or the spinal cord from the previous treatment, the disease itself, or the existence of overlapping metallic stabilization instruments or hypervascularity of the tumor, oblique and lateral views may be necessary to identify spinal cord arteries.
The main purpose of neurophysiologic monitoring for spinal or paraspinal tumor embolization is to detect masked and unrecognized spinal cord arteries. If existence of a spinal cord artery is suspected but uncertain on the superselective angiography from the feeder to the lesion before or during embolization, provocative testing may be performed. Also, if a significant change in SEPs or MEPs occurs during an embolization procedure, spinal cord ischemia should be suspected and the procedure should be terminated to minimize the risk of permanent damage and maximize the possibility of recovery. Improvement of SEPs or MEPs after tumor embolization is sometimes observed in association with clinical improvement. This phenomenon most often occurs in a tumor with epidural extension and spinal cord compression and is probably due to decreased mass effect secondary to tumor devascularization and shrinkage. This improvement is an indicator of effective embolization either as a preoperative or palliative treatment.
4. Conclusions Neurophysiologic monitoring is feasible and useful in the great majority of patients undergoing endovascular treatment for spine or spinal cord lesions. Neurophysiologic monitoring and pharmacological provocative testing during endovascular procedures also offers a unique opportunity to investigate the spinal cord hemodynamics and to integrate functional and vascular anatomy.
Notes
28 THE USE OF ELECTROPHYSIOLOGY MONITORING DURING SURGERY FOR SPINAL DYSRAPHISM
Dachling Pang, MD, FRCS (C), FRCS (Eng), FACS Professor of Pediatric Neurosurgery University of California, Davis Chief, Regional Centre for Pediatric Neurosurgery, Kaiser Permanente Hospitals, Northern California, US
The main aim of this presentation is to show how we use intraoperative electrophysiology monitoring (IOM) for complex spinal dysraphism surgery. We routinely utilize lower extremity and anal spincter EMG, somatosensory and pudendal sensory evoked potentials, bulbocavernosus reflex, and transcranial evoked motor potentials. The stimulator is a micro-concentric bipolar probe.
The most important aspect of IOM in spinal dysraphic surgery is motor root mapping for functional nerve roots especially the anal roots, and in cord mapping to distinguish between functional from non-functional vestigial neural tissues. Examples are given to highlight IOM’s role in total resection of complex transitional spinal cord lipomas, in determining the terminal detaching site in confusing chaotic spinal cord lipomas, in dealing with some split cord malformations, in Currarino triads, in resecting retained medullary (secondary) neural cords, and in sorting out other exotic and baffling caudal spinal cord malformations.
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29 EPILEPSY SURGERY: FUNCTIONAL ASPECTS
Georg Neuloh, MD Friedrich-Wilhelm, University of Bonn, Germany
Abstract not available
Notes
30 STIMULATION OF THE INSULA
Stephani C1, 3, Fernandez Baca-Vaca G1, Koubeissi M1, Maciunas R2, Lüders HO1 The Neurological Institute, Departments of 1Neurology and 2Neurosurgery, 11100 Euclid Avenue, Cleveland 44106, Ohio, U.S.A.; Department for 3Clinical Neurophysiology, University Hospitals Goettingen, Robert-Koch-Strasse 40, 37075 Goettingen, Germany
Introduction The human insula is found under the frontal, parietal and temporal opercula. The circuminsular sulcus represents the structure which separates the insula from its adjacent cortical regions. The white matter underneath the insular cortex is named the extreme capsule. Histological studies in non-human primates have suggested the existence of three different types of cortex within the insula namely agranular cortex in the anteroventral insula, a transitional dysgranular cortex and granular cortex in the posterodorsal insula [1]. Due to its hidden position the characterization of the human insula and of surrounding structures has been difficult. While its first known anatomical description reaches back to the late 18th century many aspects of the function of the insula are still matter of debate. Studies of intra-operative or extra-operative stimulation of the insula in patients with refractory epilepsy have repeatedly located somatosensory and viscerosensory representation in the insula lobe [2, 3]. Nonetheless, there are only few of such studies and their comparability is limited. We present new results of electrocortical stimulation of the insula.
Methods 5 patients (5 female, mean age = 40.2 yrs) with medically refractory epilepsy underwent invasive Video-EEG- Monitoring that included placement of depth electrodes in the insula. MRI was basically normal in 4 of the 5 patients and showed an area of encephalomalacia in the right inferior frontal and right anterior insula lobe in 1 patient. Electrodes with 10 or 12 platinum contacts (Integra Neuroscience®) were inserted in a rostro-caudal direction along the dorso-ventral axis of the insula (Figure 1). Three of these electrodes were implanted in each insular lobe with one electrode in the anterior part, one in the middle and one in the posterior part of the insula. Using this technique each insular lobe was covered with 18 to 22 (mean = 20.5) electrode contacts. There were 123 electrode contacts in 6 insular lobes of 5 patients. Location of the electrodes was established with superimposition of presurgical cranial MRI and postsurgical cranial CT (iplan-stereotaxy 2.6®, Brainlab). While being used for delineation of the epileptogenic zone we were also able to stimulate the insular electrode contacts in all of these patients. For stimulation we used alternating current with a frequency of 50 Hertz and a pulse width of 0.5 milliseconds. Intensity varied due to clinical responses between 1.5 and 14 milliAmpere as well as duration of stimulation that lasted for 3 to 5 seconds.
Results Out of 123 electrode contacts within the insula there were 61 in right insular lobes and 62 in left insular lobes. 26 electrode contacts were within the anterior insula, 49 in the middle part of the insula and 48 in the posterior insula. Stimulation of 64 of the 123 contacts (54%) did elicit clinically detectable responses without subsequent afterdischarges. 59 of these responses could be confirmed at least once. We separated responses into four major groups: Somatosensory responses (19), sensation of warmth/pain (6), viscerosensory responses (13), gustation (9). Additionally, there were responses that could not be definitely assigned to only one of these qualities. 5 responses had gustatory as well as viscerosensory elements, a combination of the feeling of warmth and general somatosensation was evoked at 4 electrode contacts and a combination of somatosensation and viscerosensation was found after stimulation of one electrode contact.
Somatosensory responses were found to be in the most posterior part of the insula. The subgroup of sensations of warmth or painful sensations respectively was induced by stimulation of electrodes in the dorsal part of the posterior insula. Viscerosensory responses were regularly induced more anteriorly close to gustatory phenomena that occurred after stimulation of the middle part of the insula. A distinct type of response was found after stimulation of the most anterior and dorsal part of the insula and its adjacent cortex in two patients and consisted in a perception of speech and the perception of “thinking out loud”. Stimulation of other electrodes in the anterior insula did not produce any responses.
These findings were solid among subjects. The distribution of the different qualities is displayed in figure 1. None of the 5 patients were found to have primary insular epilepsy.
31
Figure 1: Example of depth electrodes in the insular lobe inserted in a dorso-ventral direction. AI = anterior insula, MI = middle insula, PI = posterior insula. Numbers indicate functionally different cortical areas due to results of stimulation. 1 = general somatosensation 2 = thermosensation/nociception 3 = gustation 4 = viscerosensation 5 = perception of speech
Discussion This study adds topographic precision to the existing data on the functional neuroanatomy of the insula. Using the technique of extra-operative electrocortical stimulation we found evidence for the existence of at least four distinct qualities represented in the insular cortex. Responses of general somatosensation and thermosensation/nociception were found in the most posterior part of the insula. Viscerosensory and gustatory phenomena were elicited after stimulation of more central parts of the insula. These qualities had been assigned to insular cortex in previous studies and are consistent with neuroanatomic and histologic data [4]. We postulate distinct topographic areas for these functions primarily in the posterior half of the insula.
Stimulation of the anterior insula did not result in any clinically noticeable change with the exception of an area in the transition zone of the most anterior insula to the frontal operculum which evoked sensation of speech after stimulation. This may relate to the proximity to the Broca’s speech region and related neuronal networks.
Literature 1. Mesulam M-M and Mufson EJ (1982): Insula of the old world monkey. I: Architectonics in the insulo-orbito- temporal component of the paralimbic brain. J Comp Neurol 212:1-22. 2. Penfield W and Faulk ME (1955): The insula – further observations on its function. Brain 78:445-470. 3. Isnard J, Guénot M, Sindou M, Mauguiére F (2004): Clinical manifestations of insular lobe seizures – a stereo- electroencephalography study. Epilepsia 45:1079-1090. 4. Augustine JR (1996): Circuitry and functional aspects of the insular lobe in primates including humans. Brain Res Rev 22:229-244.
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32 SUBCORTICAL MAPPING AND DTI FIBER TRACKING FOR SURGERY IN LANGUAGE AREAS
Lorenzo Bello (1), Enrica Fava (1), Giuseppe Casaceli (1), Antonella Castellano (3), Costanza Papagno (2), Andrea Falini (3) 1. Neurosurgery, Dept of Neurological Sciences, Università degli Studi di Milano, Milano 2. Psychology, Università Milano Bicocca, Milano 3. Neuroradiology, istituto Scientifico San Raffaele, Università Vita e Salute, Milano
Surgical resection of lesions involving language areas or pathways requires the intraoperative identification of functional cortical and subcortical sites to effectively and safely guide resection. Diffusion Tensor Imaging (DTI) and Fiber Tractography (FT) are MR techniques based on the concept of anisotropic water diffusion in myelinated fibers, which enable three-dimensional reconstruction and visualization of white matter tracts, and provide information about the relationship of these tracts with the tumor mass. We have routinely used DTI-FT to reconstruct various tracts involved in the language system in a series of 250 patients with low or high grade gliomas involving the language areas or pathways. DTI-FT informations were loaded into the neuronavigational system and combined intraoperatively with those obtained with direct electrical stimulation applied at subcortical level. In this work we report the results of such experience, describing the DTI FT and intraoperative findings for each tract and discussing technical aspects of the combined use, as well as the pitfalls. Results will be initially analyzed according to those are considered as essential tracts for the preservation of language (Inferior fronto occipitalis – IFO, for the semantic system, superior longitudinalis- SLF for the phonologic system, and premotor face fibers, for the articulatory system). Furthermore, data on additional language tracts, such as Inferior Longitudinalis – ILF, Subcallosum, Uncinatus will be also presented. The clinical impact on the availability of DTI FT images on both surgical planning, pre operative evaluation of extent of resection, and on language bilateral representation will be also discussed.
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33 NAVIGATED TMS ASSOCIATED WITH DTI AS A TOOL FOR NEUROSURGICAL PLANNING
Josep M Espadaler Clinical Neurophysiology Dept., Hospital del Mar, Barcelona, Spain
The need of functional localization, previous or during, brain tumors surgery is usually achieved by the use of different techniques, as fMRI, Direct Cortical Stimulation (DCS) or PET. f MRI provides functional information, but only at a cortical level, without giving information of the subcortical region, where are the fibers that connect the cortical areas activated in a specific task, and also, where are mainly located the brain tumors. DCS stills being the gold standard in cortical localization, however it requires time during the operation, has the risks of post- stimulation seizures, and there is also, an associated stress compound for the patient if awake surgery is used.
Navigation TMS systems allows us to elaborate cortical functional maps, after locating the cortical point were the TMS is delivered, and also, provides functional information when muscle response after cortical stimulation are recorded.
Diffusion Tensor Imaging is software than lets us have a representation of fibers tracts in the MRI. ROI volumes show the fibers tracts contained inside it. Placing this ROI in the cortical points previously located by the Navigated TMS maps, fibers tracts of stimulated neurons by TMS are shown by DTI.
In 12 patients with hemispheric brain tumors of different types and location, we perform cortical map of primary motor area. In 5 of these patients we also study pre-motor area and Supplementary Motor Area (SMA) in four. In 5 patients we study speech area in Broca’s Region.
1. Mapping Primary Motor Area In 12 patients, Navigated TMS maps and DCS maps of the Primary Moor Area, were made and compared.
1. Anatomic Comparison: Navigated TMS maps were compared with DCS in order to evaluate anatomic accuracy and correlation in between them. This correlation was made in two ways, a visual analysis by superposition of a grid and, on second method by introducing the cortical points identified by DCS into the OR Navigation System, and comparing with the points in the TMS navigation system. The anatomical comparison shows excellent accuracy in both methods of comparison.
2. Physiological Correlation: All positive response points to TMS stimulation, had positive response to DCS, and at reversal, all negative points to DCS were also negative to TMS, in this Primary Motor Area. Once Navigated TMS maps are obtained we export the response points by means of a DICOM export software and introduced into Dextrospe to perform DTI studies. Each ROI was adjusted at 10 mm size and placed on each TMS point to study fibers underlying it. This combination brings us an anatomical map of the cortical motor primary area, but also, the map of the Pyramidal tract at subcortical levels. As the TMS points can be categorized according the amplitude of muscle responses, additional information of functional value of the point stimulated can be added to the fiber tract of that point shown by DTI. With this method we obtain a cortical but also subcortical anatomical map, and moreover, a combination of both anatomical and physiological and functional information.
2. Mapping Complex Task Areas of the Brain Topographic accuracy of the previous Primary Motor Area maps is based in the volume of the magnetic field and the calculated area of the cortex surface with enough intensity to reach a slightly supra-threshold intensity of the motor neurons at rest. During complex task of the brain, voluntary activation of neurons involved on it, will probably be accompanied of threshold reduction of this neurons, in consequence the area of the cortex surface that receive and intensity field enough to reach a supra-threshold is bigger and certainly difficult to define. Moreover, to inhibit this complex task repetitive TMS stimulation is needed, adding a more complex paradigm in terms of the topographic characteristics of the magnetic field and the neurons involved in the stimulation.
A) Supplementary Motor and Premotor Areas SMA was stimulated by means of rTMS at 10 Hz during to 2 second with a total or 20 stimuli at the intensities of 120% increased until the 140% until expected response is obtained: the interruption of a voluntary, bilateral movement of the hands. This is essentially, the movement of a non consecutive movement of counting with the fingers. This interference of the voluntary movement was achieved in 5 patients. The EMG recording shows an
34 interruption of the movement of counting fingers. Expanding the EMG recording, a muscle response after each stimuli of short latency is recorded. This let us into the discussion of if it is a real interference in the SMA or it is only a repetitive cortical silent period. However, light movements of the coil in the midline do not produces the task interference and, in this case, the expanded EMG does not show any muscle response of short latency. DTI studies of this SMA showed two directions fiber tracts, one going two the midbrain, in parallel to the Pyramidal Tract, and a second one, crossing the midline through the Corpus Callosum, and going up to contra lateral cortex.
Pre -motor Area is easy to obtain in both hemispheres with the same bilateral movement task. However in PMA, inhibition of the movement is clearly marked only in the contra lateral hand.
B) Mapping of the Broca’s Region The study of Broca´s Region by means of TMS using a magnetic coil has several side effects due to extra-cranial structures stimulated that has to be considered. Stimulation of facial nerve may difficult the interpretation of real speech disorders induced by cortical stimulation, and also, temporo-masseterine muscles stimulation can be painful, and create also interruption of the speaking that can let to a mistake in the interpretation of a false speech arrest. Localization of motor efferents from Broca’s area is clearly obtained, but inferior temporal areas a really difficult to study due to this side effects of the stimulation.
However, we localize several points of speech areas in 5 patients. In those points, DTI showed two different directions of tract fibers. One is going probably to the SMA while the other is going to primary motor area. This suggests that the points located have essentially a motor function of the speech.
The double cricotiroideous muscle response post-electrical stimulation of Broca´s area recorded by Deletis et all. are very suggestive when this double fibers tracts of the DTI are seen.
We also studied cricotiroideous muscle response after TMS. Single short latency response is recorded when single TMS is delivered at the inferior and anterior part of M1 area. During rTMS at Broca’s area, when speech arrest is produced, we only see and EMG pauses without any response. Of course stimulation paradigm of the TMS is different from DCS or TES used by Deletis et al. so, differences in stimulation conditions must be considered.
Although this studies in Broca’s region are promising, we are far to build a complete functional map of temporal lobe, as can be easily made in primary motor area or, premotor or, supplementary motor area.
While neurons involved in speaking movement are probably well located by Navigated TMS, lateral inferior temporal lobe areas are difficult to study without extracranial muscle stimulation, making very uncertain language perturbation evaluation. Special language paradigm must be designed, for example, in comprehensive linguistic studies, an alternative press-button system can be used, using hand muscles instead of oro-laringeal muscles.
Finally, normal process of progress in Neuroscience knowledge is based on anatomic studies, the injury localization, and the association with functional troubles associated to the injury. With this method, this process of knowledge has been turned 180 degrees, going from stimuli and response to functional evaluation and, then going to the anatomy.
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35 MAPPING LANGUAGE AND MEMORY AREAS WITH ECoG
Vernon L. Towle, PhD The University of Chicago, Chicago, Illinois, USA
The preservation of language and memory function becomes an important issue for surgical planning if surgical resections involve temporal lobe structures or lateral frontal or parietal cortex. Identification of the cortical and subcortical areas that mediate these higher cortical functions is more difficult than mapping primary sensory and motor areas, for which sensory evoked potentials and direct electrical stimulation are useful. This article will discuss recently developed techniques for identifying cortical areas associated with expressive and receptive language and verbal memory storage and recall. It focuses mostly on the clinical goal of identifying crucial areas which must be preserved to prevent postoperative deficits, and the scientific goal of obtaining a better understanding the cortical networks involved in such tasks. Medically intractable epilepsy patients with chronically implanted subdural grids provide an ideal venue for the investigation of the electrophysiologic correlates of higher cognitive function.
Epilepsy Compromises Verbal Memory and Language Epilepsy, a common neurologic disorder characterized by chronic seizures, affects about 3 million people in North America and more than 1% of the world population (Hauser, 1997; Theodore et al. 2006). In addition to seizures, many patients suffer cognitive deficits, including speech and memory problems (Marques et al. 2007). Decline in word-finding ability is one of the most common post-operative complaints, even after "successful" epilepsy surgery (Helmstaedter, 2004; Langfitt et al. 2007). Occasionally, when resections are close to language areas, expressive or receptive language function is severely compromised, limiting employment and reducing the quality of life for these patients. The presence of post-operative language deficits is as high as 60% when resections are near language areas (Haglund et al. 1994), associated with a 50% rate of verbal memory deficits (Gleissner et al. 2002). For these reasons, clinicians are interested in ways to identify memory and language areas to reduce post- operative morbidity of these important skills. There is currently no clinically accepted way to map or protect cortical areas related to memory function beyond the lateralization obtained from the Wada test.
Locating Language Areas Using Direct Electrical Stimulation The primary cortical areas that serve as the necessary substrate for language were first identified almost 150 years ago, with the clinicopathological studies of Broca (1865) and Wernicke (1874) who found left frontal and perisylvian lesions in patients with expressive and receptive speech disorders, respectively. Identifying the cortical substrates of language was of particular importance to neurosurgeons, who came to refer to this area as the "forbidden territory" (Penfield & Roberts, 1959). These initial observations have been replicated and expanded in a large body of studies of stroke patients with language defects (Caplan et al. 1995). It was not until Wilder Penfield popularized Forester's cortical stimulation technique that cortical areas necessary for expressive speech could be identified (Penfield & Boldrey, 1937; Penfield & Roberts, 1959). There were a few studies of single-unit activity recorded during speaking and listening (Creutzfeldt et al. 1989), which described both excitation and inhibition of cells in the superior and middle temporal gyrus. Extensive cortical stimulation mapping studies of surgical patients have indicated that language areas are organized in a mosaic pattern, the location of which cannot be predicted before surgery (Ojemann et al. 1989). The technique has been refined by others over the years (Lesser et al. 1994; Boatman et al. 1995) and is the gold standard for identifying language areas in the surgical setting. However, direct electrical stimulation of cortex has limitations: proper application is time-consuming, it is difficult to perform on children, direct stimulation may cause seizures, and it is difficult to map areas related to higher cognitive function, such as receptive speech and the many forms of memory. Historically, it does not guarantee that there will not be post-operative speech or memory deficits.
Functional MRI Studies of Language and Verbal Memory Since its initial description about 15 years ago (Belliveau et al. 1991), there has been an explosion of functional MRI studies that have mapped language-related areas (reviewed by Price, 2000; Bookheimer, 2002). In addition to identifying the classical perisylvian language areas, several new areas have been described, especially executive language areas in the dorsal and ventral lateral frontal cortex. Even though hemodynamic techniques (PET, fMRI) have been used to locate cortical and subcortical language-related areas (Peterson et al. 1998; Mummery et al. 1999; Belin et al. 2000; Binder et al. 2000; Cooke et al. 2006; Karunanayaka et al. 2007), several problems have precluded its clinical utilization (Detre, 2006). These hemodynamic techniques largely remain a very promising research tool for patients that can perform in scanners, but are not routinely relied upon in the surgical suite. The lack of clear indexes of reliability and validity, difficulty testing children, discordance with other neurophysiological findings (Bookheimer et al. 1997; Sinai et al. 2005), and issues regarding accurate
36 registration of the functional findings to the operative setting remain problematic. An additional difficult issue is determining how crucial or necessary the functional MRI-defined language areas are for adequate language functioning: Which areas can be resected without clinically significant loss of function? The classic studies of memory involve complete loss of episodic memory due to bilateral medial temporal lobe lesions (reviewed by Squire & Zola-Morgan, 1991; Butters & Delis, 1995; McGaugh, 2000). Many functional MRI studies have confirmed the role of medial temporal lobe structures in long term memory (Gabrieli et al. 1997; VarghaKhadem et al. 1997; Wagner et al. 1998; Stark & Squire, 2000). All of these functions depend on immediate working memory (Fiebach et al. 2005; Aboitiz et al. 2006), which holds both phonological (Baddeley, 1966) and visuospatial information available for deeper processing (Baddeley, 2003).
Gamma Activation During Verbal Memory Tasks Changes in the spectral composition of the electroencephalogram (EEG) as a function of cognition were noted in the initial description of EEG (Berger, 1929), with its potential use for functional mapping of cortex suggested only three years later (Kornmüller, 1932). For half a century high frequency activity was invisible to researchers because of the mechanical inertia of EEG pens, which could not vibrate fast enough to track it. Interest in higher frequency oscillations originated with Freeman's observation that olfactory events were associated with localized gamma activity in the rabbit olfactory bulb (Freeman, 1975). Task-related gamma band dynamics (reviewed by Jensen et al. 2007) have been studied in both ECoG (Murthy & Fetz, 1992; Edwards et al. 2005; Miller et al. 2007) and scalp EEG recordings (Pfurtscheller & Aranibar, 1977), although scalp EEG in higher frequencies has been shown to Figure 1. Electrodes revealing increases be contaminated by EMG (Whitham et. al., 2007). Gamma (large dots) or decreases (small dots) activation appears to be closely related to the rhythmic firing of during a verbal LTM retrieval task. fast-spiking pyramidal cells in primates (Gray & McCormick, 1996; Naya et al. 2001; Sakurai & Takahashi, 2006; Cardin et al. 2009) and humans (Cameron et al. 2001; Creutzfeldt et al. 1989a, b) and has been associated with the coordination and temporal integration of visual, auditory, and sensorimotor signals (Fries et. al. 2007). The degree to which high-frequency activity is associated with language processes has only begun to be explored using subdural electrode recordings (Crone et al. 1998, 2001a, 2001b; Aoki et al. 1999; Trautner et al. 2006). Theorists have employed the concept of Dm, the index of differential neural phenomena observed during memory encoding that predict successful recall (Paller & Wagner, 2002). For example, Cameron et al. (2001) found that neurons firing in the hippocampus during encoding of word pair associations differentially predicted subsequent recall (Dm). Another recent report of Dm is the finding that gamma activation recorded from subdural electrodes is associated with correct encoding and retrieval of words (Sederberg et al. 2007). Correct verbal recall was associated with activation of the hippocampus, areas within the temporal lobe, and inferior frontal gyrus. Fell et al. (2001) reported that rhinal and hippocampal gamma activity becomes briefly coupled during memory formation. Associative memory, by its very nature, requires communication and integration across different modalities, perhaps at subcortical levels (Schroeder & Foxe, 2005). Our own studies of ECoG during language and memory tasks have revealed a widely distributed language system (Towle et al. 2008) as identified by extended increases in gamma activity during different task events. Memory activation also appears to be widespread and distributed, with participation of the anterior medial and lateral temporal areas, mostly inferior to the language system (Figure 1).
Modeling Memory and Language Networks with Functional MRI To understand how language and memory function in the human brain, one must do more than identify individual anatomical structures or "functional spots"; one must study the complex flow of information between distributed neural assemblies at many levels. Friston (1994) described two ways at characterizing the hemodynamic coupling between independent groups of voxels: functional connectivity, an index of the observed correlations between areas, and effective connectivity, an index of the causation of activations between regions. Such analyses were first performed on functional MRI data sets by Mcintosh and Gonzales (1994) using structural equation modeling (SEM). SEM has recently been used to test models of functional connectivity during language development (Kim et al. 2007; Karunanayaka et al. 2007). Effective connectivity between brain regions has been described using dynamic causal models (DCMs) (Friston, 2003; Penny et al. 2004). DCMs employ various modeling techniques (Stephan et al. 2007) but have the disadvantage of requiring a defined sensory input when applied to functional MRI data sets. Unfortunately, for some memory and language tasks, no such obvious input may exist (Schlosser et al., 2006). Even the most elaborate models based on hemodynamic activity have been severely hampered
37 because of their poor temporal resolution, which limits their ability to infer the rapid changes and bidirectional information flow characteristic of cognitive tasks (Korzeniewska et al. 2007). Unfortunately, SEM models with many hypothesized bidirectional information flow parameters between brain regions tend to be unstable (Schlosser et al., 2006). In fact, all effective connectivity techniques require substantial a priori knowledge of the underlying anatomical connections to formulate the structure of the model. Such theoretical models are often hypothesized by generalizing from knowledge of primate brain connectivity, which may be adequate for modeling basic sensory and motor systems, but are likely inappropriate for studies of human language and memory. It is often suggested that some of the aspects of structural models, especially the direction of the connectivity, might be gained from electrophysiologic studies, because of their superior time resolution. Many investigators have suggested that electrophysiologic and hemodynamic studies be combined to benefit from the different advantages of each technique (Nunez & Silberstein, 2000; Penny et al. 2004; Riera et al. 2005; Sinai et al. 2005; Marrelec et al. 2006; Schlosser et al. 2006).
Modeling Memory and Language Networks with ECoG Although there have been many investigations of the electrophysiologic correlates of cognitive and motor tasks, surprisingly few have resulted in formal quantitative models of distributed information processing such as seen in functional MRI studies (Sinai et al. 2005; Astolfi et al. 2005; Marrelec et al. 2006; Oya et al. 2007; Korzeniewska et al. 2008). This is surprising, because like hemodynamic coupling, for electrophysiologic measures there are two possible ways in which inter-regional functional connectivity can be assessed: One approach has been to study "temporal binding," where the cross-correlation between spike trains or coherence between graded local field potentials are calculated (Gray et al. 1989; Rolfsema et al. 1997; Weiss & Mueller, 2003; Baruchi et al. 2007; Fries et al. 2007). Alternatively, one can study the task-related causal dynamics of highly processed EEG/ECoG, such as the event-related variations in local gamma activation (Sinai et al. 2005; Astolfi et al. 2005; Miller et al. 2007).
Studies of coherence and correlation do not allow conclusions about direction of connectivity or causality (Hesse et al. 2003; Towle et al. 1999; 2007). Structural equation modeling shares this limitation (Blinowska et al. 2004; Astolfi et al. 2005, 2007). On the other hand, electrophysiologic signals, with their high temporal resolution and sequential nature, naturally lend themselves to such analyses by Granger causality, which allows the source and direction of information flow to be determined (Hesse et al. 2003; Samelin & Kujala, 2006; Oya et al. 2007). A variant of Granger causality was utilized by Crone, which they called event-related causality (Gourevitch et al. 2006; Korzeniewska et al. in press), and was used to infer the organizational network underlying speech perception. Based on several information processing models of language presented in the literature (Rauschecker, 1998; Kaas & Hackett, 2000; Price, 2000 and many others), it should be possible to apply the directional information obtained from electrophysiologic studies to structural equation models of functional MRI data from the same patients. Combining the information obtained from invasive electrophysiological recordings with noninvasive hemodynamic studies should lead to a better understanding of the spatio-temporal organization of the information processes underlying verbal memory and expressive and receptive speech in the human brain.
Acknowledgements This study was supported in part by NIH 5 R01 NS40514, The Brain Research Foundation and the Susman and Asher Foundation.
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Notes
41 A NEW CONTRIBUTION TO THE NEUROPHYSIOLOGIC EXPLORATION OF THE BROCA AREA
Vedran Deletis, MD, PhD Department for Neuroscience, School of Medicine, University of Split, Croatia and St. Luke's- Roosevelt Hospital, Institute for Neurology and Neurosurgery, New York, USA
The final common organ for the speech is larynx and its muscles. Phylogeneticaly, in the speech development laryngeal muscles are more specialized than other oropharyngeal muscles. Therefore, in our study we used them as a target organ from which we have recorded neurophysiologic marker generated by electrical stimulation of motor speech related cortical areas (MSRCA).
For the purpose of recording neurophysiologic marker we have developed two methodologies:
Transcranial magnetic stimulation (TMS), transcranial electric stimulation (TES), and direct cortical stimulation (DCS) of the MRSCA with recordings from: a) Vocal muscles (primarily in intubated patients under general anaesthesia) b) Cricothyroid muscles (primarily in awake patients/subjects but can be used in the patients under general anaesthesia)
Most of our experience is coming from recording from vocal muscles, because recording from cricothyroid muscle has been recently introduced (Fig. 1)
We gave evidence that: (1) Stimulation of primary motor cortex (M1) for laryngeal muscles by using a short train of high frequency stimuli, generates a short latency response (SLR) in vocal and cricothyroid muscles via corticobulbar pathway for vagal motor nuclei and recurrent and superior laryngeal nerve, respectively. (2) Stimulation of phonological part of Broca’s area (pars opercularis, Brodmann’s area 44) by using short train of high frequency stimuli, generates a long latency response (LLR) in vocal and cricothyroid muscles. (3) Stimulation with the 50-60 Hz of the both regions (M1 and phonological part of Broca’s area) generates tonic activity in the laryngeal muscles.
Figure 1. Direct cortical stimulation. Schematics of the brain surface with three original responses obtained from vocalis muscle after direct cortical stimulation of the motor speech areas , (LLR, long latency response), primary motor cortex (SLR, short latency response) abductor pollicis brevis (APB) muscles after electrical stimulation of the primary motor corteex for small hand muscles. 1. Stimulation of the Broca area 2. Stimulation of primary motor cortex 3. Stimulation of primary motor cortex for laryngeal muscles
42 References • Deletis, V., Ulkatan, S., Cioni, B., Meglio, M., Colicchio, G., Amassian, V., Shrivastava, R. (2008). Responses elicited in the vocalis muscles after electrical stimulation of motor speech areas. Rivista Medica. 14:159-165. • Deletis,V., Fernandez-Conejero, I., Ulkatan, S., Costantino, P. (2009). Methodology for intraoperatively eliciting motor evoked potentials in the vocal muscles by electrical stimulation of the corticobulbar tract. Clinical Neurophysiology. 120:336-341.
Notes
43 FUNCTIONAL PRESERVATION IN SURGERY FOR BRAIN TUMORS AND VASCULAR MALFORMATIONS
Georg Neuloh, MD Friedrich-Wilhelm, University of Bonn, Germany
Abstract not available
Notes
44 INTRAOPERATIVE NEUROPHYSIOLOGY IN TUMOR AND VASCULAR NEUROSURGERY
Andrea Szelényi, MD, PhD Department of Neurosurgey, Johan Wolfgang Goethe University Hospital, Frankfurt, Germany
Introduction Intraoperative neurophysiology in tumor and vascular neurosurgery should be tailored to the surgical needs and thus the cortical and subcortical areas at potential risk should be monitored.
This lecture provides an overview with special remark to motor evoked potentials and their correlation with postoperative clinical and neuroradiological outcome.
Methodological aspects The armentarium of intraoperative neurophysiological methods consists of auditory (AEP), motor (MEP) and somatosensory evoked potentials (SEP) as well as of methods of direct cortical and subcortical stimulation.
Whereas the technique of SEP is well established and is performed according to diagnostic neurophysiological standards (9), the intraoperative application of MEPs – either elicited transcranially or with direct cortical stimulation – and its optimization were focus of research during recent years. Being established in spine surgery its use in intracranial surgery advances slowly.
Technical aspects of MEPs elicited by transcranial electric stimulation (TES) TES can be performed using either a constant current or a constant voltage stimulator. The advantage of a constant current stimulator is its relative independence of the stimulating electrodes’ impedance. To elicit MEPs recorded from muscles a train of five stimuli consists ideally of rectangular pulses with an interstimulus interval of 2 to 4 ms. Trains can be applied with repetition rates up to 2 Hz. The individual pulse width of constant voltage stimulators is usually set at 0.05 ms (e. g. D185 Digitimer Co, Uk). Commercially available constant current stimulators allow for a variation of pulse widths. A duration of 0.4 or 0.5 ms is mostly applied.
For stimulating, corkscrew-like electrodes are recommended as dislocation is very unlikely. Predominantly right hemispheric stimulation is achieved with C2(+)/C1(-) or C4(+)/Cz(-) and predominantly left hemispheric stimulation with C1(+)/C2(-) or C3(+)/Cz(-). With C4(+)/Cz(-) resp. C3(+)/Cz(-), muscle MEPs in the contralateral hand and arm muscle could be elicited most focally, and with Cz(+)/+6cm(-) anterior to Cz in the muscles of the lower extremities. Especially in supratentorial tumor surgery, where the motor cortex is not exposed or subdurally placement of strip resp. grid electrodes is not possible, TES is an essential adjunct. In motorwise unaffected patients, with the stimulating electrodes montage at C1(+)/C2(-)resp. C2(+)/C1(-)an average intensity of 69 mA was needed to elicit muscle MEPs for the contralateral abd. pollicis brevis muscles and 95 mA for the tibialis anterior muscles (13). In 90 % of the patients, muscle MEPs in the abd. pollicis brevis muscle could be elicited with less than 100 mA and in the tibialis anterior muscles with less than 127 mA. It has been described that in patients with motor deficits higher stimulation intensities for eliciting muscle MEPs are needed (4).
Technical aspects of MEPs elicited by direct cortical electric stimulation (DCS): Direct cortical stimulation subsumes two techniques. First, the 60-Hz-technique was introduced to the neurosurgical community by Penfield in 1937 (10). The technique is commonly performed for mapping of cortical areas representing motor and language function in awake surgery. Second, the train-of-five-stimuli technique, a technical modification being described by Taniguchi in 1993, can be applied for mapping and continuous monitoring of cortical and subcortical motor pathways (16). Just recently the application for language testing was described (1). Comparing both methods the train-of-five-stimulation is more seizurogenic compared to the 60-Hz- technique (12) and thus the latter one is limited for mapping. For DCS according to Taniguchi, the stimulation parameters are the same as for TES except the limitation of the maximum stimulation intensity to 25 mA (for safety considerations see also H. L. Journee’s lecture). For continuous stimulation, a strip electrode containing 4 to 8 disc electrodes with a diameter of 5 to 10 mm is used. The disc electrodes serve as anode, the cathode (a needle electrode) is placed at Fz or Fpz. The technique of phase reversal is performed for determining the central sulcus (2). Thereafter, optimally, this strip electrode would be placed parallel over the precentral gyrus with the medially located leads reaching the leg area and the laterally located leads the arm and hand areas (15). Electrodes not being used for stimulation might be used for electrocorticography or SEP. Alternatively the exposed motor
45 cortex is mapped first with a stimulating probe, and to follow the strip electrode is being placed parallel over the precentral gyrus. The optimal position should cover the area at most risk.
Intraoperative assessment and postoperative outcome Studies have demonstrated the strong correlation between intraoperative MEP alteration and postoperative motor outcome (3, 4, 6-8, 14, 15). In intracranial surgery, permanent MEP losses are followed by long-term motor deficits. In comparison to cortical SEPs, which are generated in the grey matter, intraoperative MEPs are elicited within the white matter. Thus, in vascular surgery or in tumor dissection along major artery branches, MEPs are indicative for impending lesion affecting the corticospinal tract (7). Whereas in spine surgery the all-or nothing principle in judging intraoperative MEP amplitude is commonly accepted, this has to be refined in supratentorial surgery (5). Even amplitude deterioration and prolonged transient losses might be correlated by postoperative motor deficit. This empirical experience has led to 50 % amplitude decrement criteria also being used in SEPs. For further understanding between the relation of MEP alteration with postoperative neuroradiological findings were studied in a distinct group of 29 patients suffering only MEP alteration during the course of tumor resection (5, 11). MEP alteration resulted in a corresponding new motor deficit in all 5 patients (100 %) with irreversible MEP loss, in 7/10 patients (70 %) with irreversible MEP deterioration, in 1/6 patients (17 %) with reversible MEP loss and in none of the 8 patients (0 %) with reversible MEP deterioration. Thus, irreversible MEP alteration was significantly more often correlated with postoperative motor deficit compared to reversible MEP alteration (p < 0.0001). Postoperative MRI was available in 27 patients. In 20 patients, 22 new signal alterations affecting 29 various locations (precentral gyrus (5), corticospinal tract (19)) were observed. Irreversible MEP alteration was more often associated with postoperative new signal alteration in MRI compared to reversible MEP alteration (12/14 patients vs. 5/13 patients, p =0.018). MEP loss was significantly more often associated with subcortically located new signal alteration (16/19 vs. 3/10; p = 0.006). On the contrary, MEP deterioration was significantly more often followed by new signal alterations located in the precentral gyrus (4/10 vs 1/19; p = 0.036).
Summary MEPs elicited by TES or DCS can be safely used in intracranial surgeries. Their use in combination with SEPs is essential for real-time monitoring of motor and somatosensory pathways. The stimulation electrode location according to the homunculus allows for most focal excitation of the cortex limiting excitation of the corticospinal tract deep within the white matter. Further, this minimizes interfering patients’ movements with microsurgery. MEP loss bears a higher risk than MEP deterioration to postoperative motor deficit resulting from subcortical postoperative MR signal alteration of the corticospinal tract. In contrast, MEP deterioration points to motor cortex lesion and thus even MEP deterioration should be considered as a warning sign if surgery close to the motor cortex is performed.
References 1. Axelson HW, Hesselager G, Flink R: Successful localization of the Broca area with short-train pulses instead of 'Penfield' stimulation. Seizure 18:374-375, 2009. 2. Cedzich C, Taniguchi M, Schafer S, Schramm J: Somatosensory evoked potential phase reversal and direct motor cortex stimulation during surgery in and around the central region. Neurosurgery 38:962-970, 1996. 3. Fujiki M, Furukawa Y, Kamida T, Anan M, Inoue R, Abe T, Kobayashi H: Intraoperative corticomuscular motor evoked potentials for evaluation of motor function: a comparison with corticospinal D and I waves. J Neurosurg 104:85-92, 2006. 4. Kombos T, Suess O, Ciklatekerlio O, Brock M: Monitoring of intraoperative motor evoked potentials to increase the safety of surgery in and around the motor cortex. J Neurosurg 95:608-614, 2001. 5. MacDonald DB: Intraoperative motor evoked potential monitoring: overview and update. J Clin Monit Comput 20:347-377, 2006. 6. Neuloh G, Pechstein U, Cedzich C, Schramm J: Motor evoked potential monitoring in supratentorial surgery. Neurosurgery 54:1061-1072, 2004. 7. Neuloh G, Pechstein U, Schramm J: Motor tract monitoring during insular glioma surgery. J Neurosurg 106:582-592, 2007. 8. Neuloh G, Schramm J: Monitoring of motor evoked potentials compared with somatosensory evoked potentials and microvascular Doppler ultrasonography in cerebral aneurysm surgery. J Neurosurg 100:389-399, 2004. 9. Nuwer MR, Aminoff M, Desmedt J, Eisen AA, Goodin D, Matsuoka S, Mauguiere F, Shibasaki H, Sutherling W, Vibert JF: IFCN recommended standards for short latency somatosensory evoked potentials. Report of an IFCN committee. International Federation of Clinical Neurophysiology. [see comments]. Electroencephalogr Clin Neurophysiol 91:6-11, 1994. 10. Penfield W, Boldrey E: Somatic motor and sensory representation in the cerebral cortex of man as studied by electric stimulation. Brain 60:389-443, 1937. 11. Szelenyi A, Hattingen E, Weidauer S, Seifert V, Ziemann U. Intraoperative MEP alteration in intracranial tumor surgery and its relation to signal alteration in postoperative MRI. Neurosurgery(in press) 12. Szelenyi A, Joksimovic B, Seifert V: Intraoperative risk of seizures associated with transient direct cortical stimulation in patients with symptomatic epilepsy. J Clin Neurophysiol 24:39-43, 2007.
46 13. Szelenyi A, Kothbauer KF, Deletis V: Transcranial electric stimulation for intraoperative motor evoked potential monitoring: Stimulation parameters and electrode montages. Clin Neurophysiol 118:1586-1595, 2007. 14. Szelenyi A, Langer D, Beck J, Raabe A, Flamm ES, Seifert V, Deletis V: Transcranial and direct cortical stimulation for motor evoked potential monitoring in intracerebral aneurysm surgery. Neurophysiol Clin 37:391-398, 2007. 15. Szelenyi A, Langer D, Kothbauer K, Camargo AB, Flamm ES, Deletis V: Motor Evoked Potentials Monitoring during cerebral aneurysm surgery: Intraoperative changes and postoperative outcome. J Neurosurg 105:675-681, 2006. 16. Taniguchi M, Cedzich C, Schramm J: Modification of cortical stimulation for motor evoked potentials under general anesthesia: technical description. Neurosurgery 32:219-226, 1993.
Notes
47 ION FOR BRAIN TUMOR RESECTION AND FUNCTIONAL NEUROSURGERY
Takamitsu Yamamoto, Hideki Oshima, Chikashi Fukaya, Yoichi Katayama Dept. Neurological Surgery and Applied System Neuroscience, Nihon University School of Medicine, Tokyo, Japan
It has been reported that motor disturbance caused by tumor resection in the supplementary motor cortex or injury of the premotor cortex can undergo complete recovery within several weeks, and that the corticospinal motor evoked potential (corticospinal MEP) is recorded only when the primary motor cortex is stimulated. We employed the corticospinal MEP (D-wave) as a monitoring index of motor function to perform maximal resection of brain tumors located around the motor cortex.
For monitoring of the D-wave, operations were performed under general anesthesia with muscle relaxant and completely controlled ventilation. No special arrangements for anesthesia were required. Direct cortical stimulation revealed that if one electrode was placed on the posterior half of the precentral gyrus, the D-wave could be recorded even with 10 mm-distant bipolar cortical stimulation, and the amplitude was larger with anode rather than cathode stimulation. Monitoring of the D-wave enabled the function of the corticospinal tract to be evaluated selectively. A less than 30% decrease could be a clinical index to guarantee a postoperatively preserved motor function which included a period of transient motor disturbance with subsequent complete recovery.
Intraoperative monitoring of the D-wave is suitable for open cranial surgery with general anesthesia. It is useful for detection of the primary motor cortex and for achieving maximal resection of brain tumors located around the motor cortex.
We reported more than decade ago that motor cortex stimulation (MCS) is sometimes useful in controlling post- stroke pain. During MCS for such purpose, we noticed that some patients also show obvious improvement in their motor function. This effect was not dependent on post-stroke pain control. In 6 patients with motor weakness, Fugl-Meyer score of the upper extremity recovered in 3 of the 6 patients. These effects resulted in significant improvement in their motor performance. These results indicate that MCS could be a new therapeutic approach to improve motor performance after stroke.
Based on these results, I will talk about the intra-operative monitoring of cortico-spinal motor evoked potential for brain tumor resection, control of post-stroke pain, and recovery of motor function.
Notes
48 ION TUMOR AND VASCULAR SURGERY OF THE BRAIN
Aage R. Møller, PhD, D. Med., Sci School of Behavioral and Brain Sciences, The University of Texas and Dallas, Richardson, Texas, US
About 40 years ago electrophysiologic techniques were introduced in operations on the spine, especially operations for sclerosis where ION made a major difference in dramatically lowering the risk of permanent deficit including paraplegia. In neurosurgery beginning about 30 years ago ION provided perhaps the most dramatic improvements in operations for acoustic tumors (now known as vestibular schwannoma) in that it made it possible to preserve facial function even after resection of large tumors. Before that, it was regarded impossible to preserve the facial nerve in patients with large tumors, not even worth trying. Slightly later, similar techniques were applied to operations of large skull base tumors where monitoring of many of the cranial nerves reduced the risk of disabling deficits. Monitoring of the function of the auditory nerve reduced the risk of hearing loss and tinnitus from microvascular decompression operations for face pain and hemifacial spasm, and later for disabling positional vertigo and tinnitus.
Monitoring of cranial nerves can effectively reduce the risk of sensory and motor deficits in many kinds of operations on the brain. In operations of vestibular schwannoma, first and foremost monitoring of the facial nerve is important. Before any resection is done, the tumor should be probed by a handheld monopolar stimulating electrode, with the stimulator set to deliver constant voltage impulses. Regions of the tumor that do not include any parts of the facial nerve are identified and resected. The facial nerve is often split up in several parts. Probing the operative field while observing a display of the recorded EMG potentials is used for identification of the anatomical location of anyone of the different parts of the facial nerve. If the amplitude of the EMG increases when the electrode is moved from one location of the tumor to another away it is a sign that it was moved towards the location of the facial nerve; if the amplitude decreases, the electrode was moved away from the part of the facial nerve in question. Using this simple technique makes it possible to find the different parts of the facial nerve in a short time.
Listening to the EMG potentials made audible provides much useful information about how the facial nerve is affected by surgical manipulations. The use of tones triggered by the EMG potentials as used in some commercial equipments leave out much important information.
Similar techniques as used for monitoring the facial nerve can be used for monitoring other cranial motor nerves that may become at risk in operations for large skull base tumors, such as the nerves that controls the extraocular muscles (CNIII, IV, VI) and lower cranial nerves (CNIX, X, XI and XII).
Recording from sensory cranial nerves mainly regards the auditory nerve, which is at risk of being injured in operations in the cerebella pontine angle such as for vestibular schwannoma and microvascular decompression of CNV, VII, VIII and IX. Either recording of ABR or recordings directly from the intracranial portion of the auditory nerve, or from the surface of the cochlear nucleus can provide useful monitoring of the function of the auditory nerve. When ABR is used, it is important to be able to obtain an interpretable record in as short a time as possible. When it is possible, recordings should be made from the cochlear nucleus by placing a recording electrode in the lateral recess of the fourth ventricle (though the foramen of Luschka), providing almost real time monitoring of the auditory nerve). For that, optimal stimulus and recording parameters should be used: High repetition rate (40-50pps), high sound level (65-70dBHL), optimal filtering (zero-phase finite impulse response digital filters have many advantages over conventional electronic filters or spectral filters implemented by computer programs). Optimal electrode placement is important (for recording in two channels: earlobe-earlobe, for peak I-III, and vertex-neck for peak V). It is also important to reduce electrical and magnetic interference as much as possible. Clicks with alternating polarity should not be used because condensation and rarefactions clicks often give different responses.
In all monitoring of auditory evoked potentials it should be taken into account that patients with pre-existing hearing loss that the waveform of the recorded potentials are likely to be different from those recorded in individuals with normal hearing (which are usually shown in textbooks).
In operations of large skull base tumors it is valuable to use monitoring of ABR for other purposes than preservation of the function of the auditory nerve. Knowledge about the neural generators of the different components of the ABR often can make it possible to detect excessive manipulations of specific parts of the
49 brainstem. ABR monitoring makes it possible to detect compressions such as from bleeding and swelling in various regions of the brainstem.
ABR monitoring is also useful for monitoring the general condition of the brainstem. It has been shown that changes in the ABR (Peak V) occur earlier than changes in heart rate and blood pressure in most situations of brainstem manipulations. ABR is therefore an important complement to monitoring cardiovascular parameters in operations where the brainstem may be manipulated.
(For details regarding monitoring techniques in connection with operations of brain tumors, see Møller AR "Intraoperative Neurophysiologic Monitoring", 2nd Edition. 2006, Totowa, New Jersey: Humana Press Inc.(2006))
Notes
50 ANESTHETIC CONSIDERATIONS DURING INTRAOPERATIVE NEUROLOGICAL MONITORING
Tod Sloan, MD, MBA, PhD University of Colorado at Denver, School of Medicine, Department of Anesthesiology, Aurora, CO, US
Although the exact mechanism of anesthesia is not known, the major target of anesthetic action appears to be alteration in synaptic function that results in neural system changes which result in loss of consciousness, amnesia, loss of reaction to noxious stimuli (surgery) and also results in immobility (lack of movement in response to painful stimuli) via suppression of spinal cord reflex activity. Since electrophysiological recordings that depend on these structures will be most susceptible to depressant agents, the changes from anesthetic agents can usually be predicted by examining the anatomy of the neural pathways involved and the specific target receptors of the drugs involved. The net effect of anesthetic agents is due to at least 4 synaptic mediated effects as well as changes in physiology (e.g. BP). Since the electroencephalogram (EEG) is also generated by synaptic activity the effect of anesthetic agents on evoked responses parallels the effect on the EEG.
The first anesthetic action is the general depression of synaptic function. This effect can be generally predicted by knowing the location of synapses within the neural pathway involved and the specific synaptic receptors and peak generators being affected by the drugs. Since synaptic effects will, like the effects on the EEG, result in prominent anesthetic effects on the cortically generated responses, it is not surprising that anesthetic effects on evoked responses parallel anesthetic effects on the EEG (which is also cortically and synaptically derived). In 1967 Winters [1] proposed a schema for anesthesia effects on cortical auditory evoked potential (AEP) that mimics a similar schema for anesthetic effects on the EEG [2].
Each anesthetic agent has a different neural “fingerprint” based on their actions on the different synapses for different neurotransmitters. Further, each synapse is made up from different subunit varieties with these subunits being distributed in the spinal cord, brainstem and cortex differently. Hence different anesthetic agents have differing effects on the various anesthetic components of amnesia, unconsciousness and immobility. This also means that they differ in their impact on evoked responses. This is seen in the two basic EEG patterns; some cause simple depression of the EEG (and cortical evoked responses) until an electrical silence while others initially activate the EEG (and cortical evoked responses) leading to seizures or switch to depression and electrical silence after the initial activation. This makes each agent somewhat unique with some similarities but also some unique differences which can make certain anesthetic agents valuable for some monitoring challenges (especially motor evoked potentials).
The second type of anesthetic effect is the alteration in synaptic function of ancillary neural pathways that interact on the pathway that mediate the response being measured. These effects could cause additional depression, could release the current state of depression, or could result in enhancement of the responses. This effect may account for some of the effects of anesthetics which increase responses at low doses and result in depression at higher doses such as etomidate which appears to cause depression of neurons which depress neural pathways such that the pathway has less depression and enhancement occurs. At higher doses the state of depression extends to other neurons which result in a net depression of the pathway so that the response is depressed. This effect may also be mediated via synapses or by anesthetic effects on parallel pathways (such as non-cortico-spinal motor pathways that change anterior horn cell excitability).
The third mechanism is the more global cortical effect of anesthetic agents on neural networks that results in the state of unresponsiveness (“hypnosis”) referred to as “general anesthesia.”[3] The receptors involved are primarily gamma-amino-butyric-acid (GABAa), central alpha2, with some contributions from n-methyl-D-aspartic acid (NMDA) and neuronal acetylcholine (nACH). One model of anesthesia action on networks suggests that drug effects at the brainstem result in ascending neural influences that result in the blockage of sensory information to the brain at the thalamus and also blockage of cortical cognitive and memory processing. This “thalamic gating” may explain why cortical sensory responses are substantially blocked at anesthetic doses associated with anesthesia and unconsciousness. Also worth mentioning is that the anesthetic effects on consciousness is a threshold type response with an “on-off” type of change in consciousness. Other cortical effects include those on memory formation which result in amnesia with general anesthesia (similar receptors as unconsciousness with the exception of the central alpha2).
51 This thalamic gating is also a mechanism for blocking noxious sensory information which also occurs in other locations, including the spinal cord. This sensory blocking is mediated through the NMDA, nACH and opioid channels with some contribution from the central alpha2.
The fourth mechanism is the “immobilizing” effect of anesthetic agents that results in the lack of movement to painful skin incision used to characterize volatile inhalational agents and referred to as “MAC” (minimal alveolar concentration of an inhaled volatile agent where 50% of patients do not move to skin incision). The location of action is an anesthetic effect on the reflex pathways in the spinal cord and involves primarily the glycine channel with some contribution from GABAa and opioid mu. This effect alters the spinal reflex activity evoked by noxious stimuli and may block descending signals from cortical stimulation (MEP) or from peripheral stimulation (such as a painful surgical incision). This effect can block MEP, F and H-reflex, and may contribute to why some neurogenic spinal stimulated responses are primarily sensory in nature. When the drug effect on the H-reflex is overlaid with the traditional measure of movement the two are similar. This suggests that this blockade happens on 50% of people at 1 MAC and virtually all at 1.3 MAC, however, different agents have differing profiles on the immobility component of general anesthesia.
Volatile Inhalational agents The most prominent anesthetic effects on evoked responses during clinical anesthesia are those of the potent inhalational agents (isoflurane, sevoflurane, desflurane). These drugs have a broad action on multiple types of synapse in multiple neural structures including the GABAa receptor in the synapses, the NMDA channel, and the Na+/K+ ATP’ase channel and neuronal nicotinic acetylcholine receptor. These are “complete” anesthetics with a broad range of anesthetic effects. They are particularly effective hypnotics, immobilizers, and amnestics. A variety of studies have been done with these agents and an understanding of their effects serves as a good reference for comparison of the other agents.
The somatosensory evoked response from peripheral nerve stimulation demonstrates the effects of anesthetic agents on synapses. As such, the lack of synapses between stimulation of the peripheral nerve and the cervico- medullary junction is associated with minimal changes in the responses recorded in the peripheral nerve and spinal responses. Studies of recordings at Erb’s point (brachial plexus from upper extremity stimulation) and over the cervical spine (from lower extremity stimulation) show minimal changes (0-9%), that are not dose related. This also demonstrates that the anesthetic effects are primarily at synapses and not on neural conduction (hence amplitude is effected with minimal changes in latency. Major changes are seen above the thalamus and from the cerebral cortex. Consistent with the network effects that result in “thalamic gating”, the responses above the thalamus are disproportionately affected. Of note, the effect on the cortical responses is a non-linear reduction consistent with the “on-off” switch of consciousness seen in the model of anesthetic action on consciousness.
Higher concentrations of these agents also affect the spinal cord. Changes in the H reflex confirm the effect at the spinal level. Depth electrode studies in the spinal cord suggest that halothane and nitrous oxide may have effects in lamina I-VI and thereby account for the changes seen in epidural recordings and cervical spinal recordings from posterior tibial nerve stimulation.
The anesthetic effect of inhalational agents is also seen with the auditory response (Waves I-V in the ABR) which shows a progressive increase in effect as the number of synapses increases along the auditory pathway, with a substantial increase in the effect at the cortical level in the mid-latency auditory response consistent with a reduction in cortically transmitted sensory information. The effect on the cortical visual evoked response is among the most dramatic, perhaps also due to the multiple synapses involved.
Synaptic anesthetic effects help explain the anesthetic effect in the motor pathways. Motor evoked potentials are susceptible to anesthetic agents at three sites. The first is in the motor cortex. Stimulation of the motor cortex pyramidal cells is either by direct stimulation of the pyramidal cells (leading to the production of ‘D waves’) or indirect stimulation via internuncial neurons (leading to production of ‘I waves’). The ‘D waves’ are relatively unaffected by anesthetics since no synapses are involved in their production. I waves (generated through synaptic activity) are substantially affected by anesthetics. This means the recording of D waves epidurally is rather resistant to anesthetic agents.
The second site of anesthetic action in the motor pathway is in the anterior horn cell (the same effect mentioned above and referred to as “immobilizing”). At this location the ‘D’ and ‘I’ waves summate temporally to produce a peripheral nerve action potential. Up to 95% of the corticospinal tract may reach the anterior horn cell via interneurons (especially the medial system) meaning several synapses become targets for anesthetic depression. Partial synaptic blockade here, induced by anesthetics, make it more difficult to reach threshold for a peripheral
52 nerve and muscle response. Hence the combined effect of anesthetics to block ‘I waves’ from the cortex, and synapses at the spinal cord reduce the probability of generating a compound muscle action potential (CMAP). At higher anesthetic doses, an even more profound synaptic block at the anterior horn cell may prohibit synaptic transmission regardless of the composition of the descending spinal cord volley of activity. In addition, the excitability of the anterior horn cell is regulated by influences of the parallel motor pathways (tectospinal, rubrospinal, propriospinal, reticulspinal tracts) and anesthesia influences here could depress the formation of a muscle MEP response.
Since this is a location for the anesthetic induced effect associated with lack of movement in response to pain (MAC), it also explains the non-linear decrease in muscle responses associated with the induction of anesthesia. As such CMAP responses from transcranial motor stimulation are among the most difficult to obtain with volatile anesthetics. Because of the resistance of the D wave, the anesthetic effect at the a-motoneuron cell can be partially overcome at low concentrations by multiple pulse transcranial stimulation [4,5]. As a consequence, low concentrations of inhalational agents appear acceptable when high frequency transcranial stimulation is used in some patients with robust responses [6-8].
The inhalational agents have differing profiles of effect on synaptic subtypes. Hence they are not identical in their effects. Studies suggest a relative potency of the volatile agents is isoflurane (most potent) = sevoflurane = desflurane > enflurane > halothane which parallels their depression of the EEG.
Nitrous Oxide Nitrous Oxide differs from the potent volatile agents in the synaptic receptor subtypes where it has its action. It is believed to have actions of antagonizing the NMDA receptor, inhibiting the neuronal nicotinic acetylcholine receptor, and exhibiting opioid-like effects on the opioid receptors. As such it is a potent analgesic with less hypnotic and immobilizer activity. Clinically it is considered a weak anesthetic compared to the potent inhalational agents, however its electrophysiologic effects may be more potent on a relative anesthetic effect scale (e.g. MAC). Some of its action may be mediated through alpha2 adrenoreceptors, especially in the locus ceruleus which has efferent neural connections to the thalamus and cerebral cortex.
The effects of nitrous oxide vary with the other anesthetic agents being employed with it. When used alone, nitrous oxide tends to produce graded amplitude SSEP changes in a dose dependent manner, with minor or no changes in subcortical responses. However, when combined with other agents the effect may be synergistic and may vary with the specific agents used (i.e. context sensitive) depending on the specific synaptic receptors being affected.
Intravenous Analgesic Agents Because the inhalational anesthetic agents have marked depressant effects on cortical evoked potentials and motor evoked potentials, anesthesiologists frequently choose intravenous analgesics (opioids or ketamine) supplemented with intravenous sedative agents (e.g. propofol) when monitoring is required. The goal of a complete anesthetic is to use a mixture of agents to reduce noxious stimuli, hypnosis (sedation), amnesia, immobilization (lack of movement) and muscle relaxation (in some circumstances).
Opioid agents Opioids (e.g. fentanyl, alfentanil, sufentanil, remifentanil) provide excellent reduction of noxious sensory input. The effect of the opioid analgesics on evoked responses is generally mild although transient effects are seen with bolus doses. The difference between the opioid agents and the inhalational agents likely is the result of opioid action on the opioid receptor pathways rather than the GABA and NMDA pathways.
Ketamine An alternative to opioids and the inhalational agents for reducing noxious sensory stimuli is ketamine. Ketamine acts by decreasing NMDA receptor activity, inhibition of the neuronal nicotinic acetylcholine receptors, decreasing the presynaptic release of glutamate and through opioid like actions on the opioid receptors. It provides excellent reduction in noxious sensory stimuli and hypnosis, but increases in intracranial pressure in patients with cortical abnormalities limit is usefulness with cortical pathology. One of the actions appears to be a reduction in the sensory “filtering” such that more information is sent to the sensory cortex (referred to as a dissociative state). Hallucinations in adults that results requires other sedatives (e.g. propofol or benzodiazepines) to minimize this effect. Perhaps to this effect, ketamine has been reported to increase cortical somatosensory evoked potential (SSEP) amplitude [9,10] and increase the amplitude of muscle and spinal recorded responses following spinal stimulation. Ketamine has minimal effects been on auditory brainstem response (ABR), cortical auditory evoked potential (AEP), visual evoked potentials (VEP), and in myogenic MEP. Ketamine also increases the H-reflex
53 suggesting a change in alpha motor neuron excitability may contribute to the MEP enhancement [11,12]. Its greatest contributions to anesthesia are likely the addition of a potent analgesic in patients tolerant of opioids and to add hypnosis such that the dose and effect of propofol could be reduced (see below).
Dexmeditomidine Another agent which produces analgesia and sedation is dexmeditomidine. As a central, selective alpha2 adrenoreceptor agonist drug, it blocks noxious sensory information at the spinal cord, anxiolysis, hypnosis and sedation. The side effects of hypotension and bradycardia relating to its sympatholytic properties (reduced nor epinephrine release) limit the drug to a role as a supplement to other anesthetic agents. Dexmeditomidine was studied as a supplement to isoflurane and it caused no additional depression to the cortical mid-latency auditory response and the cortical SSEP [13]. It has also been used as a supplement to propofol-fentanyl-nitrous oxide anesthetic where the later cortical peaks (P25-N35) of the SSEP were affected but the early cortical peak (N15- P20) was unaffected [14]. It also appears to be compatible with MEP, however higher doses or mixing with other depressant agents may prevent MEP recording. This is an area that is still evolving but it appears Dexmeditomidine is compatible with MEP if the dose is kept small and additional drugs are kept to a minimum.
Sedative-Hypnotic Drugs In some patients, excellent anesthesia for cortical evoked response recording can be provided with opioids or ketamine, supplemented with nitrous oxide or low dose inhalational agents. When inhalational agents must be avoided, the anesthesiologist may choose to substitute with intravenous sedative agents in a total intravenous anesthetic (TIVA). The currently pure hypnotics are thought to act on synapses via the GABAA receptor and extrasynaptic GABAA receptors. They are excellent hypnotics and amnestics with minimal analgesia and immobilizer activity.
Propofol Propofol is currently the most commonly used hypnotic/amnestic in TIVA. The drug is very rapidly metabolized such that the drug effect can usually be titrated down to levels compatible with adequate TIVA and MEP recording. Propofol does not generally appear to enhance cortical responses. When the SSEP is recorded in the epidural space, propofol has no significant effect. The latencies of the ABR were increased without significant amplitude decreases but the cortical response is markedly altered. This is consistent with a postulated site of anesthetic action of propofol on the cerebral cortex [7,15-19].
Studies with transcranial electric or magnetic elicited motor evoked potentials have demonstrated a depressant effect on the F wave and compound muscle action potentials (CMAP) response amplitude, also consistent with a cortical effect as well as some effect at the spinal cord. Propofol has been used in tcEMEP when the recordings are epidural. As a component of TIVA, induction of anesthesia can include propofol and infusions of propofol have been combined with opioids. However, as a component of TIVA, infusions of propofol have been combined with opioids and produced acceptable conditions for myogenic tcEMEP monitoring, especially when a multipulse stimulation technique is used. Higher doses of propofol can depress sensory and motor responses and prevent monitoring. In these circumstances some individuals have utilized ketamine to allow reduction of the propofol dose and depression.
Note that a propofol syndrome of fatal lactic acidosis can occur, especially in children or long term infusions. At present this may be the result of abnormal metabolism in the mitochondria and more information is needed to better understand the circumstances where it should be replaced with other hypnotic/amnestics. In addition it is prepared in a soy emulsion with egg lecithin such that patients allergic to these may not be able to receive propofol. A new preparation (fospropofol) is water soluble so these will not be needed. This drug is a “prodrug” and is metabolized to propofol in the liver so it has a slower onset and longer duration of action.
Other sedative agents - Etomidate A variety of other agents can be used to supplement opioids for TIVA. Of particular note is etomidate. It is also thought to mediate its synaptic effects via the synaptic GABAA receptors. Etomidate can enhance synaptic activity at low doses, probably by its action of inhibition of neurons that inhibit the cortical sensory pathway (hence releasing inhibition). At low doses etomidate may produce seizures in patients with epilepsy [20]. This effect has been used to enhance amplitude in both sensory and motor evoked responses. This amplitude increase appears coincident with the myoclonus seen with the drug, suggesting a heightened cortical excitability. A sustained increase with constant drug infusion has been used to enhance cortical SSEP recordings that were otherwise not monitorable [21]. Higher doses of etomidate are depressant on the EEG, SSEP and MEP.
54 Studies with transcranial elicited motor evoked potentials have suggested that etomidate is an excellent agent for induction and monitoring of this modality. This effect has also been used to enhance amplitude in motor evoked responses [21,22]. Etomidate is also unusual in that it depresses the production of cortisol. This may not be an issue with many surgeries in which steroid agents are given routinely. However, when not given as a part of the surgery, it is unclear if supplemental steroids should be given when etomidate is used [21]. Studies to date demonstrate increased mortality in intensive care patients with sepsis and multisystem organ failure raising concern for its use in some patients.
Muscle Relaxants Since muscle relaxants have their major site of action at the neuromuscular junction they have little effect on electrophysiologic recordings that do not derive from muscle activity. Suppression of muscle activity may be helpful in recording transcranial motor evoked potentials epidurally where paraspinal muscle activity can obscure recording and when recording neurogenic responses from spinal stimulation. For recording of epidural or neurogenic responses, complete or near complete neuromuscular blockade is highly desirable.
Certainly, complete neuromuscular blockade will prevent recording of muscle responses (CMAP) during MEP. Partial neuromuscular blockade has been used when recording muscle activity from stimulation. Although recording of myogenic responses is possible with partial neuromuscular blockade, the amplitude of the CMAP will be reduced by the blockade. As a consequence, the ability to record with partial neuromuscular blockade will be dependent on the neurological pathology in the pathway monitored that may reduce the baseline CMAP response. This reduction can impact on pedicle screw testing or activity from mechanically elicited responses. As such, the use of neuromuscular blockade is controversial during monitoring of muscle responses from mechanical stimulation of nerves and partial paralysis may reduce the ability to record these responses (e.g. facial nerve monitoring or monitoring for pedicle screw placement). Techniques with titanic stimulation of the lower motor neuron prior to the MEP may amplify the CMAP in a patient with partial neuromuscular blockade and may offer help with monitoring during this situation.
Conclusion In general, the effect of anesthetic agents on the evoked responses parallels the effects on the EEG. By understanding the synaptic effects of the medications the appropriate combinations of drugs can be chosen for monitoring using specific modalities. In most patients an anesthetic suitable for monitoring sensory and motor potentials can be found, when the anesthesiologist is familiar with the monitoring methods, the underlying physiology and the different effects of anesthetic agents. When appropriate responses are not recorded, different anesthetic agents may be needed, such as changing from inhalational agents to TIVA.
References 1. Winters WD, Mori K, Spooner CE, Bauer RO: The neurophysiology of anesthesia. Anesthesiology 1967;28:65-80. 2. Winters WD: Effects of drugs on the electrical activity of the brain: anesthetics. Annual Review of Pharmacology & Toxicology 1976;16:413-426. 3. John ER, Prichep LS: The anesthetic cascade: a theory of how anesthesia suppresses consciousness. Anesthesiology 2005;102:447-471. 4. Taylor BA, Fennelly ME, Taylor A, Farrell J: Temporal summation—the key to motor evoked potential spinal cord monitoring in humans. Journal of Neurology, Neurosurgery & Psychiatry 1993;56:104-106. 5. Machida K, Shinomiya K, Komori H, Furuya K: A new method of multisegment motor pathway monitoring using muscle potentials after train spinal stimulation. Spine 1995;20:2240-2246. 6. Kawaguchi M, Sakamoto T, Ohnishi H, Shimizu K, Karasawa J, Furuya H: Intraoperative myogenic motor evoked potentials induced by direct electrical stimulation of the exposed motor cortex under isoflurane and sevoflurane. Anesthesia & Analgesia 1996;82:593-599. 7. Pechstein U, Nadstawek J, Zentner J, Schramm J: Isoflurane plus nitrous oxide versus propofol for recording of motor evoked potentials after high frequency repetitive electrical stimulation. Electroencephalography & Clinical Neurophysiology 1998;108:175-181. 8. Ubags LH, Kalkman CJ, Been HD: Influence of isoflurane on myogenic motor evoked potentials to single and multiple transcranial stimuli during nitrous oxide/opioid anesthesia. Neurosurgery 1998;43:90-94; discussion 94-95. 9. Schubert A, Licina MG, Lineberry PJ: The effect of ketamine on human somatosensory evoked potentials and its modification by nitrous oxide.[erratum appears in Anesthesiology 1990 Jun;72(6):1104]. Anesthesiology 1990;72:33-39. 10. Schwender D, Klasing S, Madler C, Poppel E, Peter K: Mid-latency auditory evoked potentials during ketamine anaesthesia in humans. British Journal of Anaesthesia 1993;71:629-632. 11. Kano T, Shimoji K: The effects of ketamine and neuroleptanalgesia on the evoked electrospinogram and electromyogram in man. Anesthesiology 1974;40:241-246. 12. Shimoji K, Kano T: Evoked electrospinogram: interpretation of origin and effects of anesthetics. in Phillips MI (ed): Brain Unit Activity During Behavior. Springfield: Charles C. Thomas, 1973, 171-190.
55 13. Thornton C, Lucas MA, Newton DE, Dore CJ, Jones RM: Effects of dexmedetomidine on isoflurane requirements in healthy volunteers. 2: Auditory and somatosensory evoked responses. British Journal of Anaesthesia 1999;83:381-386. 14. Bloom M, Beric A, Bekker A: Dexmedetomidine infusion and somatosensory evoked potentials. . J Neurosurg Anesthesiol 2001;13:320-322. 15. Angel A, LeBeau F: A comparison of the effects of propofol with other anaesthetic agents on the centripetal transmission of sensory information. General Pharmacology 1992;23:945-963. 16. Kalkman CJ, Drummond JC, Ribberink AA, Patel PM, Sano T, Bickford RG: Effects of propofol, etomidate, midazolam, and fentanyl on motor evoked responses to transcranial electrical or magnetic stimulation in humans. Anesthesiology 1992;76:502-509. 17. Taniguchi M, Nadstawek J, Langenbach U, Bremer F, Schramm J: Effects of four intravenous anesthetic agents on motor evoked potentials elicited by magnetic transcranial stimulation. Neurosurgery 1993;33:407-415; discussion 415. 18. Jellinek D, Jewkes D, Symon L: Noninvasive intraoperative monitoring of motor evoked potentials under propofol anesthesia: effects of spinal surgery on the amplitude and latency of motor evoked potentials. Neurosurgery 1991;29:551- 557. 19. Keller BP, Haghighi SS, Oro JJ, Eggers GW, Jr.: The effects of propofol anesthesia on transcortical electric evoked potentials in the rat. Neurosurgery 1992;30:557-560. 20. Rampil IJ: Electroencephalogram. in Albin MA (ed): Textbook of Neuroanesthesia with Neurosurgical and Neuroscience Perspectives. New York: McGraw-Hill, 1997, 193-220. 21. Sloan TB, Ronai AK, Toleikis JR, Koht A: Improvement of intraoperative somatosensory evoked potentials by etomidate. Anesthesia & Analgesia 1988;67:582-585. 22. Kochs E, Treede RD, Schulte am Esch J: [Increase in somatosensory evoked potentials during anesthesia induction with etomidate]. Anaesthesist 1986;35:359-364
Notes
56 ANESTHESIA PROTOCOLS FOR SURGERY DURING NEUROMONITORING
Tod Sloan, MD, MBA, PhD University of Colorado at Denver, School of Medicine, Department of Anesthesiology, Aurora, CO, US
A variety of anesthesia methods can be used during surgery where intraoperative neurophysiological monitoring is used. Clearly the anesthesia must be titrated to each patient to adjust for the various comorbidities, including the degree of neural compromise that may impact monitoring, as well as searching to find an anesthetic that allows an adequate monitoring signal while keeping the patient adequately anesthetized. In general, with respect to monitoring, the choice of anesthesia depends on the particular monitoring modalities being used. The major limitations are when techniques are sensitive to inhalational agents (IH) and when they are sensitive to neuromuscular blocking agents (NMB). Some modalities are insensitive to both (e.g. ABR), others are sensitive to muscle relaxants only (e.g. EMG), or inhalational agents only (e.g. cortical SSEP), and some are sensitive to both inhalational agents and muscle relaxants (e.g. transcranial motor evoked potentials (MEP)). The most restrictive techniques among the techniques used for a specific surgery define the overall anesthetic approach and the protocols below are the protocols which I usually start with for various types of monitoring. I have also mentioned some alternatives to the approach I use. These protocols are for adults; children may require different doses or approaches.
Monitoring During Posterior Fossa Surgery When surgery in the posterior fossa involves only the Auditory Brainstem Response (ABR), there are no anesthetic considerations since this is neither sensitive to inhalational agents or muscle relaxants; any anesthetic technique is fine with respect to monitoring and should be guided to the patient and surgery. In the unlikely event that the Eustachian tube is blocked then Nitrous Oxide could cause a middle ear tension that would make its use a problem.
Anesthesia for ABR (techniques insensitive to IH or NMB) Induction as usual Maintenance as usual (IH and NMB as desired)
The most common addition to ABR is monitoring using EMG of various cranial nerves, especially the facial nerve. As such the monitoring then becomes sensitive to muscle relaxants. For some EMG techniques where the nervous system is stimulated (e.g. MEP, Pedicle screws), partial muscle relaxation is often acceptable (see below), but when monitoring is designed to be sensitive to mechanical stimulation of the nerves (as is usually the case with cranial nerves) muscle relaxants reduce the EMG amplitude and make the monitoring less sensitive to impending neural injury. For this reason I try to avoid muscle relaxation during the case. In surgeries where ABR is combined with EMG, since there is no inhalational agent restriction, I usually use a balanced anesthetic (e.g. some opioids and inhalational agents) and allow the muscle relaxants that were used with intubation to wear off. Since higher doses of inhalational agents can be used, this anesthetic works fine. The situation gets a bit more complex when the SSEP is used as in cortical surgery.
Anesthesia for ABR with EMG (insensitive to IH sensitive to NMB) Induction as usual Maintenance as usual (IH as desired) Let NMB wear off after induction
Monitoring the Cerebral Cortex A variety of procedures involve monitoring for potential neural compromise to the cerebral cortex. A good example is Carotid Endarterectomy. If the only monitoring modality is EEG, the anesthesia is made rather easy since it is insensitive to muscle relaxants and only sensitive to high doses of inhalational agents. Hence the choice of anesthesia is usually designed to produce a rhythmic EEG in the alpha range (8-12 Hz) that is associated with light to moderate anesthesia with inhalational agents. Higher doses will produce burst suppression or electrical silence which impairs monitoring so inhalational doses in the 1 MAC or lower range is usually fine and can be titrated to the EEG. This usually produces excellent anesthesia provided that additional opioids are used to supplement the analgesia (with the inhalational agents producing amnesia and sedation). A processed EEG monitor may be used to help insure adequate sedation in most patients if the IH dose is low (less than ½ MAC). The opioids have the additional advantage of slowing the heart rate and blunting hypertensive episodes which are important in reducing the cardiac risk in these patients. This technique also allows maintenance of the blood pressure in the patient’s usual range and is excellent for TCD monitoring. For this reason I usually load these
57 patients with 1 µg/kg or more of fentanyl (or a similar dose of another opioid) with induction and run a balanced anesthetic with inhalational agents.
Anesthesia for EEG (moderately sensitive to IH insensitive to NMB) Induction as usual Balanced Maintenance (6% Des ~ 1 MAC) Opioids and NMB as needed
Anesthesia comes a bit more difficult if SSEP is used with the EEG for cortical monitoring as would be done in intracranial aneurysm surgery. Here the inhalational agent must be kept low enough to keep the cortical SSEP responses monitorable. In general, cortical SSEP amplitudes will be acceptable with inhalational agent concentrations between ½ and 1 MAC, however the effect is non-linear; there is usually a concentration “threshold” in that range above which the cortical SSEP response is markedly reduced in amplitude. The problem is that each patient may have a different threshold so the inhalational agent must be titrated to effect. My approach is to plan a balanced anesthetic with some opioid, muscle relaxants as needed, and adjust the inhalational agent, observing the response. I use Desflurane or Sevoflurane when possible because their insolubility allows rapid increase and decrease of effect. For young, healthy patients with minimal neurological debility I usually start at 1 MAC and titrate down, and for older and neurologically compromised patients I start at ½ MAC and titrate up. Recall that inhalational doses in excess of 1 MAC may produce brain swelling from increased cerebrovascular arterial volume (as well as amplitude depression of the SSEP) so I don’t go above 1 MAC with intracranial cases. If the dose of inhalational agents must be kept low to allow monitoring, I often will add a propofol infusion to insure adequate sedation and opioids as needed. A processed EEG monitor is often helpful with this, provided the electrode contacts with the brain are not altered by the craniotomy and the brain does not move away from the frontal bone. For intracranial surgery this additional infusion of propofol to prevent awareness and sedation is often not necessary (it something about operating on the brain), but there is a high possibility of this in spinal surgery where SSEP is used since awareness appears to be more common.
Anesthesia for Cortical Surgery with SSEP (sensitive to IH insensitive to NMB) Induction as usual, preferably Propofol Balanced Maintenance (3-6% Des ½-1 MAC) Opioids and NMB as needed Propofol infusion if needed by EEG
Monitoring during Spinal Surgery using the SSEP When I am providing anesthesia for spinal surgery where only the SSEP is used (such as spinal corrective surgery below L2), I approach the choice as above – a balanced anesthetic using opioids and muscle relaxation as needed and ½ to 1 MAC inhalational agent (Des) as acceptable to acquire a cortical response (titrating as described above). As opposed to intracranial surgery, I find I usually need a supplemental infusion of propofol and usually use an infusion of opioid. The propofol usually runs at 60-120 µg/kg/min (often titrated with the help of a processed EEG). For the opioid I usually use sufentanil (unless it’s an elderly frail patient where I bolus fentanyl to effect). Sufentanil infusions usually run 0.15-0.3 µg/kg/hr, but can be higher depending on the patient’s tolerance from preoperative analgesic use. Note the sufentanil infusion needs to be turned off about 30 minutes before ending. Note that fentanyl (infusion 4-5 µg/kg/hr) can be used as can remifentanil (0.2-0.5 ug/kg/min). Fortunately the inhalational agents help a lot with the anesthetic.
Anesthesia for Spinal Surgery with SSEP (sensitive to IH insensitive to NMB) Induction as usual (preferable Propofol) Balanced Maintenance (3-6% Des ½-1 MAC) Opioids – sufentanil bolus as needed than 0.15-0.3 ug/kg/hr turn off 30 minutes before end Propofol infusion guided by EEG (60-120 ug/kg/min) NMB as needed if EMG not monitored
An alternative approach here is to use dexmeditomidine instead of, or supplementary to the propofol. Some individuals use Dex infusions of 0.2-0.5 ug/kg/hr. I usually don’t load the Dex (which cuts the cost) if it’s started at the beginning of the case. The infusion of Propofol will be a lower dose due to the sedation from the Dex. Because the mechanism of action is not opioid like (it’s a central alpha2 stimulant), it appears to be helpful in opioid tolerant patients.
Alternate anesthesia for Spinal Surgery with SSEP (sensitive to IH insensitive to NMB) Induction as usual (preferable Propofol)
58 Balanced Maintenance (3-6% Des ½-1 MAC) Opioids – sufentanil bolus as needed than 0.15-0.3 ug/kg/hr turn off 30 minutes before end Dexmeditomidine (0.2-0.5 ug/kg/hr) Propofol infusion (60-100 ug/kg/min) NMB as needed if no EMG
If EMG is also monitored with the SSEP (which is usually the case with our surgeries), the muscle relaxants must be restricted. I prefer to let the muscle relaxants wear off after the beginning of surgery. After the baseline recordings are done, sometimes we will use some relaxation for the opening of a large spinal surgery to reduce the muscle activity or assist in the exposure of an anterior abdominal case. Although I prefer to use no relaxation during the monitoring portion of the procedure, acceptable EMG monitoring can be done with 2 twitches in a train of four, optimally using a titrated infusion of an intermediate acting drug such as rocuronium (5-10 ug/kg/min) or vecuronium (0.5-0.8 ug/kg/min). Data suggests that a deeper block (only 1 twitch), may artificially increase the pedicle screw threshold which could reduce the ability to signal the need for repositioning of the screws. In addition, the detection of nerve root compromise from mechanical means might be reduced similar to facial nerve monitoring above, such that no relaxation is desirable. In general, since the sensitivity of muscle groups to muscle relaxants varies, where the TOF is monitored is important. Since distal muscles are most sensitive (and frequently where monitoring is done), if we monitor the TOF using the ulnar nerve and hand response is probably best since more proximal muscles (such as on the face) may underestimate the effect in the periphery. The best neuromuscular monitoring of TOF will be done by the monitoring team in the muscles they are monitoring (note they need to use the same technique as anesthesia with a TOF at 2 Hz).
Anesthesia for Spinal Surgery with SSEP & EMG (sensitive to IH & NMB) Induction as usual (preferable Propofol) Balanced Maintenance (3-6% Des ½-1 MAC) Opioids – sufentanil bolus as needed than 0.15-0.3 µg/kg/hr turn off 30 minutes before end Propofol infusion guided by EEG (50-150 µg/kg/min) NMB as needed for induction, possibly for muscle dissection then none (acceptable 2+/4 twitches in TOF in muscles monitored for monitoring nerve stimulation)
Monitoring the SSEP when a Reduction or Elimination of the Inhalational Agents is Needed In general, the ability to use inhalational agents and partial muscle relaxation is very helpful in anesthetizing the spine surgery patients (particularly if they are opioid tolerant). The situation becomes much more difficult when the responses are so poor that the inhalational agent must be reduced or eliminated. In this case the anesthesia becomes a total intravenous anesthetic (TIVA) with the sedation being provided by propofol (75-150 µg/kg/min, usually titrated to processed EEG) with an opioid infusion (e.g. sufentanil 0.3-0.5 µg/kg/hr). If the SSEP remains too small for monitoring, an infusion of etomidate (0.6 mg/kg/hr) can be used instead of the propofol (as etomidate enhances the cortical SSEP at low doses). Alternatively a ketamine infusion (1-2 mg/kg/hr) can be used with the opioid infusion (see below for our approach to ketamine) since ketamine also increases the cortical SSEP response. Since our spine surgeries most often use transcranial motor evoked responses when we need to eliminate the inhalational agents, we take the TIVA approach described below when low dose of inhalational agents are not acceptable for MEP.
Monitoring when Motor evoked Potentials are used The most challenging anesthetic is required during monitoring of surgery when motor evoked potentials are being used because both the inhalational agents and neuromuscular blocking agents must be severely restricted or not used. With these cases SSEP and EMG are also usually being monitored, but the MEP defines the major restrictions. For a medically healthy patient who is without marked neurological problems (i.e. usually presents with severe pain that prompts surgery), I usually start with a TIVA technique supplemented with ½ MAC of inhalational agent (e.g. 3% Des). Some folks start with pure TIVA, but frequently a small amount of Des or Sevo is acceptable and I believe it is helpful, especially with patients who are opioid tolerant. Hence, after a standard induction with propofol and a short or intermediate acting muscle relaxant (which I let wear off), I will use 3% Des, a sufentanil infusion (0.3-0.5 µg/kg/hr) and a propofol infusion (75-150 µg/kg/min titrated to processed EEG). Note that some individuals would prefer to use 50-60% nitrous oxide instead of the Des (but not both IH and N2O together at the same time since they are synergistic and the effect is usually too much). This works similarly but I prefer to not have my FiO2 restricted by nitrous oxide and that when turning the nitrous off in a time of concern may cause an abrupt change in anesthesia and monitoring.
This technique usually works well, but occasionally the MEP responses are too small which necessitates turning off the Des and adjusting the Propofol and sufentanil infusions as needed. It’s important to note that moderate
59 doses of benzodiazepines and barbiturates have been reported to reduce the MEP response and that this may last a long time (much longer than the drug duration of action). It is not clear how this pertains to the modern multipulse technique; however, small doses of midazolam appear quite acceptable such as those that are customarily used for preinduction or occasionally during the case.
Anesthesia for Spinal Surgery with MEP & EMG (very sensitive to IH & NMB) Induction as usual (preferable Propofol) Low dose IH (3% Des) Opioids – sufentanil bolus as needed than 0.15-0.3 µg/kg/hr turn off 30 minutes before end Propofol infusion guided by EEG (75-150 µg/kg/min) NMB as needed for induction, possibly for muscle dissection then none (acceptable 2+/4 twitches in TOF in muscles monitored for monitoring nerve stimulation)
Monitoring MEP with Opioid Tolerant Patients or Who have Significant Neurological Disability In patients who are not young and healthy or have moderate neural disability or where turning off the Des is required in the above technique, I usually use pure TIVA using propofol and sufentanil.
Anesthesia for Spinal Surgery with MEP & EMG (very sensitive to IH & NMB) Induction as usual (preferable Propofol) Pure TIVA – no IH Opioids – sufentanil bolus as needed than 0.15-0.3 µg/kg/hr turn off 30 minutes before end Propofol infusion guided by EEG (75-175 µg/kg/min) NMB as needed for induction, possibly for muscle dissection then none (acceptable 2+/4 twitches in TOF in muscles monitored for monitoring nerve stimulation)
If this isn’t sufficient to allow monitoring, or in patients who are very opioid tolerant or who have significant neurological debility where the responses are likely to be poor I use TIVA enhanced with ketamine. In this case I use ketamine to supplement the analgesia (recall it has NMDA action that the opioids do not). It also supplements the sedation which allows a reduction in the propofol infusion rate (and a reduction in the depressant effect of the propofol). The notable thing about ketamine is that it is metabolized slower than propofol so that the infusion must be turned down earlier than the propofol. One approach is to run a separate infusion of ketamine (1-2 mg/kg/hr), but since we currently titrate the sedation to the processed EEG, it’s more convenient to mix the ketamine with the propofol. As such, we mix ketamine in the propofol for an initial infusion that has 2 mg of ketamine in each cc of propofol (e.g. 100 mg ketamine in a 50 cc syringe of propofol). This infusion is titrated to the EEG (since ketamine can increase the numeric value of the processed EEG, I titrate to the high end of the acceptable processed EEG range). This concentration of ketamine is reduced with each subsequent 50 cc syringe of propofol. For a shorter case I usually go 2, then 1.5, then 1, then 0.5 mg of ketamine per cc and use no ketamine in the final syringes. For a much longer case I taper more slowly. Note that the ketamine will increase the SSEP amplitude so you may see a slow decline in SSEP amplitude over the case (often to 50%) and this is expected and must be differentiated from a pathologic change.
Anesthesia for Spinal Surgery with MEP & EMG (very sensitive to IH & NMB) Induction as usual (preferable Propofol) Pure TIVA – no IH Opioids – sufentanil bolus as needed than 0.3-0.5 µg/kg/hr turn off 30 minutes before end Propofol infusion guided by EEG (75-175 µg/kg/min) Ketamine mixed in the Propofol (initial 2 mg/cc) and tapered to off NMB as needed for induction, possibly for muscle dissection then none (acceptable 2+/4 twitches in TOF in muscles monitored for monitoring nerve stimulation)
The major alternative to this is to use dexmeditomidine as described above. Hence some individuals use <0.5 µg/kg/hr Dexmeditomidine instead of the propofol (or with a small dose of Propofol 50-60 µg/kg/min). However, I must note that many individuals report that MEP are difficult to obtain with Dex. As such the use of Dex is evolving.
Anesthesia for Spinal Surgery with MEP & EMG (very sensitive to IH & NMB) Induction as usual (preferable Propofol) Pure TIVA – no IH Opioids – sufentanil bolus as needed than 0.3-0.5 µg/kg/hr turn off 30 minutes before end Propofol infusion guided by EEG (60-100 µg/kg/min)
60 Dexmeditomidine (0.3-0.5 µg/kg/hr) NMB as needed for induction, possibly for muscle dissection then none (acceptable 2+/4 twitches in TOF in muscles monitored for monitoring nerve stimulation)
Dexmeditomidine would also be an acceptable alternative in patients where propofol is contraindicated (such as allergy to soy or eggs or a history of propofol infusion syndrome). Similarly, etomidate could be used. Low dose IH or nitrous oxide might also be acceptable as long as the depressant effect was not excessive.
It is also worth mentioning that in patients where an intravenous line is not available for induction a mask induction with sevoflurane with or without nitrous oxide works fine. Usually these can be eliminated after transition to intravenous techniques in time for the need for intraoperative monitoring.
Conclusion In general, I pick the initial anesthetic technique based on the patient comorbidities (choice of anesthesia drugs independent to monitoring), patient tolerance to analgesics used preoperatively, the degree of patient neural disabilities, the actual surgery to be performed, and the specific monitoring modalities to be used. As such the doses above are only approximate and should be verified as appropriate and adjusted for each individual patient. My goal is to get the maintenance anesthetic on board and see how the monitoring responses are doing, making required changes in the technique as rapidly as possible so that I can have a steady state anesthetic effect during the period of the surgery when monitoring needs to focus on changes that might be the result of surgical or physiological changes (hence infusions are extremely valuable).
I uniformly use the processed EEG to titrate/insure sedation (BIS, Sedline, SNAP, etc.), relying on blood pressure and heart rate to guide adequate analgesia. Although I recognize that these devices will not always insure adequate sedation or anmesia, especially when ketamine is present since it increases the processed indices. However, if recall was to occur, I can say in good faith that I did what might be helpful. I most often use sufentanil with bolus doses around induction and then by infusion. Fentanyl and remifentanil work fine when used in a similar fashion. I favor Desflurane because its insolubility allows rapid changes, however Isoflurane, Sevoflurane and Nitrous Oxide will also work. If a mask induction is used then Sevoflurane is preferable. I also prefer propofol for induction so that the patient is loaded for an infusion (ketamine and dexmeditomidine are described as needing loading doses, but do not appear to need them when used as above). Obviously substitutions may be necessary for individual drug sensitivities and some individuals express concern with propofol in children (propofol infusion syndrome). I also favor no muscle relaxation when the technique is sensitive (especially spontaneous EMG). I recognize that there is ample literature showing partial relaxation is acceptable, however, I am concerned about regulating the degree of relaxation leading to an iatrogenic loss of response.
Usually these protocols work quite well, although I occasionally have a patient a couple times a year who I just can’t keep down. My approach is usually to add inhalational agents so that we maintain the SSEP and EMG monitoring, sacrificing the MEP rather than using NMB and losing the EMG and MEP.
Notes
61 CORTICOBULBAR TRACT MONITORING: NEW YORK EXPERIENCE
Isabel Fernandez-Conejero, MD Department of Intraoperative Neurophysiology, Hospital Universitari de Bellvitge, Barcelona, Spain
Introduction Historically, the first intraoperative neurophysiologic methodology for the study of cranial motor nerves (CMN) was intraoperative identification of these nerves by electrical stimulation with a hand held probe (mapping). This method was first applied for mapping the facial nerve because of the high incidence of loss of facial function in operations for acoustic neurinoma. These techniques came into general use in operations in the cerebellopontine angle during 1980’s. Subsequently methods for intraoperative monitoring of several other CMN were introduced.
Despite advantages in preventing injury by intraoperative mapping the CMN, this methodology can only be used if the nerves are exposed, or if surgery is performed around the nerves’ anatomical location. Furthermore, mapping can be performed intermittently and cannot be used for continuous monitoring.
In order to overcome the mapping technique shortcomings in CMN, a methodology has been developed to continuously monitor the functional integrity of the CMN by eliciting corticobulbar motor evoked potentials (CoMEPs) in the cranial motor nerves innervated muscles. Dong et al. were the first to describe a methodology for continuously monitor the corticobulbar tract (CBT) for the facial nerve by eliciting facial motor evoked potentials with transcranial stimulation during skull base surgery (Dong et al., 2005). Deletis et al., 2009 described methodology for continuous monitoring of CBT for vagal nerves. The method for intraoperative monitoring CBT for other CMN has not been yet described.
In its anatomical definition, the CBT is formed by axons that are homologous to corticospinal fibers, but terminate in the motor nuclei of the cranial nerves in the brain stem (e.g., nuclei V, VII, IX, X, XI and XII. Thus, they are the axons of the upper motor neurons that synapse on the lower motor neurons of the cranial nerves. The corticobulbar fibers accompany the corticospinal axons through the internal capsule and cerebral peduncle and then gradually leave the corticospinal tract to enter the tegmentum of the pons and medulla to terminate in the different CMN nuclei.
Methodology Previous experience with transcranial electrical stimulation (TES) in anesthetized patients has shown that temporal summation of multiple descending volleys is necessary to activate lower motor neurons (Taniguchi et al. 1993). Therefore it is necessary to use a short train of electrical stimuli to activate CBT and to record CoMEPs from the innervated muscles by each CMN.
Stimulation Parameters It was used transcranial electrical stimulation consisting of a short train consisting of 3 to 5 stimuli with 0.5 ms duration each. These stimuli are separated by 2 ms interstimulus interval, with a train repetition rate of 2 Hz and an intensity of up to 120 mA. The montage is C3 (+) vs. Cz (-) for left hemispheric stimulation and C4 (+) vs. Cz (-) for right hemispheric stimulation. Ninety milliseconds after the train we delivered a single stimulus over the same stimulating montage. The rational for this kind of stimulation is the fact that in most patients under general anesthesia only a short train of stimuli can elicit “central” responses generated by the motor cortex or subcortical part of CBT. If a single stimulus elicits a response, this should be considered a “peripheral” response which activates the CN directly (Dong et al., 2005; Ulkatan et al., 2007).
Electrical stimuli are delivered through subcutaneously placed corkscrew electrodes over the scalp (CS electrode, Viasys Healthcare WI, MA, USA). The intensity of TES is determined when CoMEPs that appear in the muscles are equal to or 10 to 20 mA higher than the set threshold for eliciting MEPs in the contralateral abductor pollicis brevis muscle.
Recording Parameters To record CoMEPs from the different muscles we use two hook wire electrodes and each consisted of a teflon coated wire 76 μm in diameter passing through 27 gauge needles (hook wire electrode, specially modified, Viasys Healthcare WI, MA). The recording wires have stripped 2 mm from Teflon isolation at the tip and are curved to form the hook to anchor them in the muscle after the needle is withdrawn. The impedance of electrodes was below 20 Kohl. When the patient is intubated, two electrodes are inserted in each muscle. After inserting the wire electrodes in the muscles, wires are twisted and needles are withdrawn and covered in order to protect the patient from a possible accidental injury. The
62 intensity of TES was adjusted at the level of maximal amplitude of CoMEPs (suprathreshold intensity). Depend of specific surgeries, recordings are performed from the following muscles: • V CN (Trigeminal): Masseter muscle. • VII CN (Facial): Frontalis, Orbicularis Oculi, Nasalis, Orbicularis Oris, Mentalis muscles. • IX CN (Glossopharyngeal): Posterior wall of oropharynx. • X CN (Vagal): Vocalis muscles.
• XI CN (Accesori spinal): Trapezius muscle. • XII CN (Hypoglossal): Lateral side of the tongue.
2 mV
20 ms
Figure 1. Example of normal parameters of the CoMEPs for the facial nerve. The responses were obtained after the train of stimuli but not after single stimuli from each muscle innervated by different brunches of the facial nerve.
Clinical Utility Corticobulbar Tract Monitoring The methodology for eliciting and recording CoMEPs allows for continuous monitoring of the functional integrity of the corticobulbar tract from the motor cortex to the neuromuscular junction. Furthermore recording from the different muscles innervated by the CMN can be used in the different types of surgeries where, either the upper motor neuron (CBT) or the lower motor neuron, including the motor cranial nerve nuclei, the cranial nerves and the muscles innervated by them, could be damaged during the procedure.
It is therefore that CoMEPs monitoring can be used in supratentorial surgery, skull base, brain stem, face and neck surgeries. In our ongoing study the monitorability rate is 100%. In 100 patients that underwent different type of posterior fossa surgeries we monitored CoMEPs for facial nerve. Eight of them (8%) presented a postoperative facial paresis/paralysis and all of them showed significant changes in the CoMEPs (Table 1). (Fernandez-Conejero et al., 2009, in progress).
It was a difficult task to establish criteria for predicting the clinical outcome for these patients. In our experience we have observed that if CoMEPs are preserved through the surgery till the end, no motor deficit will exist, while if CoMEPs decrease in amplitude more than 50% or increase threshold for eliciting CoMEPs more than 20-40 mA compared with the baseline recordings the patient could have slight motor deficit, in most of the cases transient. When CoMEPs are lost at the end of the surgery the outcome is a severe or complete motor deficit for the particular cranial nerve. In few occasions after an intense surgical manipulation of the cranial nerves the CoMEPs might temporarily disappeared. We have observed that many times parameters of the responses come back to normal before the surgery ended. This phenomenon might be explained by a temporary axonal block after the nerve manipulation and this is the reason why CoMEPs monitoring should be done until the end of surgery, in order to avoid false positive results.
To conclude, the corticobulbar tract monitoring offers on line information about the functional integrity of the upper and lower motor neuron for cranial nerves and can predict their outcome with sufficient accuracy.
63
Patient Pathology HB preop HB postop CoMEPs changes 1 Acoustic neurinoma 1 4 LOST
2 Acoustic neurinoma 1 6 LOST
3 Acoustic neurinoma 1 2 TI (120/180 mA) 4 Acoustic neurinoma 1 3 LOST
5 Acoustic neurinoma 1 4 TI (100/220 mA) 6 Acoustic neurinoma 1 6 LOST
7 Acoustic neurinoma 1 3 TI (80/140 mA)
8 Acoustic neurinoma 1 3 TI ( 70/160 mA)
Table 1. Patients from our study that presented facial paresis/paralysis after surgery and changes in CoMEPs at the end of the procedure. HB: House Brackman score to grade the degree of facial nerve damage preoperatively (preop) and postoperatively (postop). TI: Threshold increment, the first value in the brackets shows the threshold at the beginning of surgery (opening baselines) and the second one shows the threshold at the end of surgery (closing baselines).
References 1. Dong C, MacDonald D, Akagami R, WesterbergB, AlKhani A, Kanaan I, Hassounah M. Intraoperative facial motor evoked potential monitoring with transcranial stimulation during skull base surgery. Clin Neurophysiol 2005;116:588-596. 2. Fernandez-Conejero et al., 2009 (in progress). 3. Taniguchi, M., Cedzich C, Schramm, J. Modification of cortical stimulation for motor evoked potentials under general anesthesia: technical description. Neurosurgery 1993; 32(2): 219-226. 4. Ulkatan S, Deletis V, Fernandez-Conejero I. Central or peripheral activations of the facial nerve? J Neurosurg 2007; 106(3):519-520. 5. Deletis V, Fernandez-Conejero I, Ulkatan S, Costantino P. Methodology for intraoperatively eliciting motor evoked potentials in the vocal muscles by electrical stimulation of the corticobulbar tract. Clin Neurophysiol, 2009,120, 336-341.
Notes
64 CORTICOBULBAR MOTOR EVOKED POTENTIALS AND THEIR APPLICATION IN FACIAL NERVE MONITORING DURING SKULL BASE SURGERY-CANADA EXPERIENCE
Charles Dong, PhD EEG Lab, Vancouver General Hospital, Vancouver BC, Canada
The facial nerve is at risk of iatrogenic injury during cerebellopontine angle (CPA) and other skull base surgeries with dreaded clinical sequelae. Standard electromyography (EMG) monitoring techniques have been shown to improve postoperative facial outcome, but they have some inherent limitations. The presence or absence of spontaneous discharges in free-running EMG does not correlate well with postoperative facial function. Stimulus- triggered compound muscle action potentials (CMAPs), albeit better in assessing the function, are unavailable before the proximal facial nerve is exposed especially with large tumors, and testing is necessarily intermittent. Thus, these EMG techniques cannot provide ongoing assessment of facial nerve function during surgery.
Corticospinal motor evoked potentials (MEPs) elicited with transcranial electrical stimulation (TcES) have been successfully used for monitoring spinal cord function during spine and descending aortic aneurysm procedures and helped reduce postoperative neurological deficits. It is partially because corticospinal MEPs can be recorded from the peripheral muscles throughout the procedure, providing continuous assessment and timely feedback of spinal cord motor function. Anatomically, both the corticobulbar and corticospinal tracts are a part of the pyramidal tract and share many similarities. By extending the TcES corticospinal MEP methodology to corticobulbar pathway monitoring, we developed a novel method of facial nerve monitoring to overcome the limitations of EMG monitoring techniques and help improve postoperative facial outcome.
Localized contralateral pulse train TcES (i.e. C3 or C4 as the anode contralateral to the operative side and Cz as the cathode) was used to elicit facial MEPs. Responses were recorded from the ipsilateral orbicularis oris muscle with those from ipsilateral hand muscles as a control. Direct distal or extracranial facial nerve activation was excluded by demonstration of the absence of responses to single pulse stimulation and by the onset latency consistent to a central origin.
Analyses of our results including 286 patients undergoing CPA (n=237) and other skull base (n=49) surgeries revealed that valid facial MEPs could be recorded in 98% of patients throughout the procedure. In 30% of these patients, stimulus triggered CMAPs were unable to be obtained from proximal facial nerve stimulation until late in the procedure. Using a 50% baseline facial MEP amplitude criterion, significant facial deficits were predicted with a sensitivity of 0.91 and specificity 0.96.
Our results have demonstrated that facial MEP monitoring can circumvent difficulties of standard EMG monitoring techniques, provide ongoing surgeon-independent evaluation of facial nerve function and predict facial outcome with sufficiently useful accuracy. This method has a potential to be used for monitoring other motor cranial nerves and their nuclei during brainstem surgeries.
References • Dong CC, Macdonald DB, Akagami R, et al. (2005) Intraoperative facial motor evoked potential monitoring with transcranial electrical stimulation during skull base surgery. Clin Neurophysiol. 116(3):588-96 • Deletis V, Fernandez-Conejero I, Ulkatan S, Costantino P. (2009) Methodology for intraoperatively eliciting motor evoked potentials in the vocal muscles by electrical stimulation of the corticobulbar tract. Clin Neurophysiol. 120(2):336-41.
Notes
65 WHAT’S NEW IN SEP MONITORING?
David B. MacDonald, MD, FRCP(C), ABCN Head, Section of Neurophysiology, Dept. of Neurosciences King Faisal Specialist Hospital & Research Center, Riyadh, Saudi Arabia
Introduction Non-invasive somatosensory evoked potential (SEP) monitoring is a mature technique with decades of clinical experience, proven efficacy and established guidelines. Nevertheless, recent studies indicate that traditional laboratory-based methods are suboptimal for OR use and that SEP monitoring can instead be optimized to fastest surgical feedback [1-6].
Fundamental concepts Signal The SEP signal is a time-locked electrical response of the nervous system to peripheral nerve stimulation. It has a principle peak and an after-following peak of opposite polarity. Signal magnitude is the most important intraoperative consideration and varies with recording derivation and anesthetic management. The simplest measurement is the peak-to-peak amplitude in µV that is normally monitored. More detailed analysis uses the root mean square (RMS) amplitude in µV measured from just before the principle peak to just beyond the after- following peak [6]. The square of RMS signal amplitude gives signal power in µV2, which is the preferred engineering measure of signal magnitude [6].
Noise The noise in an SEP sweep consists of extraneous interference and biologic sources unrelated to the stimulus [4, 6]. Its magnitude varies with technique, recording derivation and anesthetic management. Extraneous noise includes lines interference, electrosurgery, amplifier noise and other sources. Biologic noise consists of EMG, ECG and EEG. One can determine noise magnitude by the RMS amplitude in µV measured when stimulation is off. Noise power in µV2 is given by the square of RMS noise.
Averaging Because SEPs are generally smaller than noise, they are usually resolved by averaging a number of sweeps. Noise tends to average toward zero because it is random, while the time-locked signal present in each sweep remains in the averaged waveform. Jitter does gradually reduce estimated signal amplitude by about 3% for each doubling of sweep number. Because RMS noise decreases by the square root of the number of averaged sweeps, the noise reduction efficacy of averaging progressively declines as the number of averaged sweeps increases. Most noise reduction occurs in the first 100-200 sweeps, so that one hopes to resolve the signal within 200 sweeps or less.
Reproducibility One must realize that each averaged SEP is an estimate distorted by residual noise and jitter [4, 6]. The fundamental requirement for valid interpretation is that the signal estimate be sufficiently reproducible. For intraoperative monitoring, this means less than 20-30% trial-to-trial random amplitude variation and ‘nearly exact’ superimposition of sequential waveforms [4, 6]. It is possible to precisely quantify amplitude and waveform variation [6], but in daily practice, reproducibility is visually judged, which introduces a degree of subjectivity.
Signal-to-noise ratio (SNR) SNR is defined as signal power / noise power and is equivalent to (RMS signal amplitude)2 / (RMS noise amplitude)2 [6]. It is usually expressed in decibels (dB), or 10logSNR. It is the main determinant of the amount of averaging needed to reproducibly resolve an SEP from background noise. Signals with SNRs above about 10 dB do not require averaging and those with SNRs between about 10 to -12 dB require little averaging (usually less than 200 sweeps), while those with SNRs below about -12 dB require a lot of averaging (often 200 to 1000 or more sweeps), or may not be practically reproducible [6].
Surgical feedback The faster the surgical feedback, the better. Rapid feedback makes the likely cause of an iatrogenic signal decrement more obvious by providing a close correlation to surgical events and because it gives one more time to react [4, 5, 6]. These properties improve the design and efficacy of intervention to restore potentials and avert or minimize neurologic injury. Thus, minimizing SEP averaging time while maintaining reproducibility becomes critical and can be accomplished by maximizing SNR [4, 6].
66 The problem with traditional techniques Traditional SEP monitoring derivations have basically been exported from the laboratory to the operating room. They have not been based on SNR because SNR is not a critical consideration in the laboratory. In fact, many traditionally recommended recording derivations have suboptimal intraoperative SNRs, including those commonly used for scalp cortical SEPs, subcortical SEPs and Erb’s Point [1, 3, 4, 6]. Using these derivations can unnecessarily delay surgical feedback if averaging is carried through to reproducibility, or degrade interpretability if averaging is truncated short of reproducibility in an effort to speed feedback. The problem may be compounded by traditional inhalational anesthesia that produces marked dose-dependent suppression of cortical responses.
Optimizing SEP monitoring Intraoperative SEP optimization involves maximizing signal power and minimizing noise power to maximize SNR and is accomplished by general measures, anesthetic management and derivation selection.
General measures One can minimize extraneous electrical noise by ensuring low balanced recording electrode impedance (e.g. < 2 kOhms), tight braiding of recording leads, and favoring short inter-electrode distance derivations. It may be necessary to turn off or unplug the operating room table, blood warmer, or other medical electrical devices that are found to be generating problematic interference.
Restricted filtering to a 30-300 Hz bandwidth is helpful. Filtering can be opened to 5-1500 Hz for peripheral knee and elbow SEPs; occasionally a low frequency filter setting of 0.2 Hz can diminish stimulus artifact baseline shift sometimes encountered in these recordings. Individual tuning of filter settings may sometimes be helpful.
Anesthetic management Total intravenous anesthesia (TIVA) improves signal power through less cortical SEP suppression. Propofol, benzodiazepines, ketamine, etomidate and opioids are some favorable agents. Low dose (<0.5 MAC) halogenated gases with opioid infusion while omitting nitrous oxide may also be favorable.
Neuromuscular blockade (NMB) may eliminate EMG noise, but nowadays is almost always contraindicated by the need to monitor muscle potentials. Adequate depth of anesthesia usually eliminates EMG is scalp bipolar and peripheral SEP derivations at the knee and elbow. If some EMG appears in these derivations, additional anesthesia or analgesia usually eliminates it, presumably by further blocking pain reflexes. Warming the patient can eliminate shivering reflexes.
Derivation selection SNR-based derivation selection can substantially hasten surgical feedback. Based on a series of articles defining optimal SEP derivations [1-6], the following conclusions can be made: • One should include a peripheral limb control and a bipolar scalp cortical SEP monitor. • The fastest reproducing (highest SNR) derivation should be used at each site. • The cubital fossa (CF) is superior to Erb’s point for upper limb control due to very high SNR (Fig. 1). • The popliteal fossa (PF) is generally a good lower limb control. • Since rare patients (especially with scoliosis) have non-decussation, one should test decussation by making a recording from at least CP3 and CP4 to unilateral stimulation [2]. With normal decussation, the upper limb N20 is contralateral to the stimulated nerve and the lower limb P37 is ipsilateral, usually with a contralateral N37. Non-decussation reverses these potentials’ lateralization. • Once the patient’s decussation status is known, the appropriate scalp bipolar derivations can be compared for each side and the highest SNR (fastest reproducing) one used for monitoring. • The largest-signal derivation may not be optimal if it contains more noise than another derivation having a smaller signal but much less noise and therefore higher SNR. • Centro-parietal derivations are generally better than frontal reference derivations because they have less anesthetic fast EEG noise. An exception is CPc-Fz that is sometimes optimal for the upper limb SEP. • Because of individual variation no single scalp SEP derivation is always optimal. • With normal decussation the optimal upper limb derivation may be CPc-CPz, CPc-Fz or CPc-CPi. One can initially compare the three and select the best. However, since CPc-CPz is optimal for 75% of limbs, one could use it routinely and try the others if it seems overly small and possibly suboptimal. With non-decussation, the candidate derivations are CPi-CPz, CPi-Fz and CPi-CPc instead. • Lower limb SEPs show much greater variation between individuals and sides. With normal decussation, the optimal lower limb scalp SEP derivation may be CPz-CPc, Cz-CPc, Pz-CPc, iCPi-CPc, CPi-CPc, or Cz-Pz. One can initially compare these and select the best one for monitoring. Fig. 2 illustrates one way to do this while
67 simultaneously assessing decussation. While CPz-CPc is the most frequently optimal derivation, this is true for less than half of lower limbs. Consequently, initial comparison is recommended. With non-decussation, the derivation candidates are CPz-CPi, Cz-CPi, Pz-CPi, iCPc-CPi, CPc-CPi, Cz-Pz instead. Programs wanting to limit scalp electrodes to CP3, CPz, CP4 and FPz will have fewer derivations to compare, but will miss opportunities for optimal results. • Programs insisting on fixed routine derivations should use CPc-CPz and CPz-CPc for the upper and lower limbs (CPi-CPz and CPz-CPi in the case of non-decussation), but should not expect consistently optimal results. • The optimal upper limb Erb’s point and cervical derivations are EPi-Ms and C5S-Ms, where Ms is the mastoid. Since there is already a control and monitor, they are optional. • Subcortical SEP derivations should normally be excluded because they exhibit slow or non-reproducibility due to very low SNRs (around -20 dB). They might be fallback potentials in the case of overly depressed cortical SEPs from inappropriate anesthesia or antecedent cerebral pathology.
To summarize: Upper Limb Control: CF Monitor (decussation): Best of CPc-CPz, CPc-Fz, CPc-CPi Monitor (non-decussation): Best of CPi-CPz, CPi-Fz, CPi-CPc Optional: EPi-Ms, C5S-Ms Fallback subcortical (normally omitted): CPi-Ms (CPc-Ms for non-decussation)
Lower Limb Control: PF Monitor (decussation): Best of CPz-CPc, Cz-CPc, Pz-CPc, iCPi-CPc, CPi-CPc, Cz-Pz Monitor (non-decussation): Best of CPz-CPi, Cz-CPi, Pz-CPi, iCPc-CPi, CPc-CPi, Cz-Pz Fallback subcortical (normally omitted): FPz-C5S or FPz-Ms
Best = Fastest reproducing (highest SNR); Bold = most frequently optimal; CPi and CPc = CP3 or CP4, ipsilateral and contralateral to the stimulated limb; iCPi and iCPc = CP1 or CP2 intermediate centro-parietal sites ipsilateral and contralateral; Ms = mastoid
Conclusion Recent evidence demonstrates that traditional laboratory-based SEP monitoring techniques are suboptimal for OR use due to low intraoperative SNRs. Instead, highest-SNR derivation selection can optimize the rapidity and quality of surgical feedback to improve SEP monitoring.
Figures
Fig. 1. Cubital fossa recording. After light abrasive skin preparation, two standard disposable ECG recording electrodes are placed over the course of the median nerve medial to the biceps tendon, one just above the elbow crease and the other 3 cm proximal. They are connected to the headbox with pre-braided reusable snap-on leads. Note single-sweep reproducibility in the inset recording showing four superimposed single sweeps.
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Fig. 2. Tibial cortical SEP optimization. M, mastoid; PF, popliteal fossa. Referential recording showed P37 maxima at Cz for each nerve and confirmed sensory decussation by showing ipsilateral P37 fields and contralateral N37 potentials. Bipolar recording confirmed Cz-CP4 and Cz-CP3 optimal derivations. Note greater noise in -FPz derivations evident by lesser trace reproducibility.
References (1) MacDonald DB. Individually optimizing posterior tibial somatosensory evoked potential P37 scalp derivations for intraoperative monitoring. J Clin Neurophysiol 2001;18(4):364-71. (2) MacDonald DB, Streletz L, Al-Zayed Z, Abdool S, Stigsby B. Intraoperative neurophysiologic discovery of uncrossed sensory and motor pathways in a patient with horizontal gaze palsy and scoliosis. Clin Neurophysiol 2004;115(3);576- 82. (3) MacDonald DB, Stigsby B, Al-Zayed Z. A comparison between derivation optimization and Cz'-FPz for posterior tibial P37 somatosensory evoked potential intraoperative monitoring. Clin Neurophysiol 2004;115:1925-30. (4) MacDonald DB, Al Zayed Z, Stigsby B. Tibial somatosensory evoked potential intraoperative monitoring: Recommendations based on signal to noise ratio analysis of popliteal fossa, optimized P37, standard P37 and P31 potentials. Clin Neurophysiol 2005;116(8):1858-69. (5) MacDonald DB, Al Zayed Z, Al Saddigi A. Four-limb muscle motor evoked potential and optimized somatosensory evoked potential monitoring with decussation assessment: Results in 206 thoracolumbar spine surgeries. Eur Spine J. 2007;16 Suppl 2:S171-87. (6) Macdonald DB, Al-Zayed Z, Stigsby B, Al-Homoud I. Median somatosensory evoked potential intraoperative monitoring: Recommendations based on signal-to-noise ratio analysis. Clin Neurophysiol 2009;120(2):315-28.
Notes
69 INTRAOPERATIVE RECORDING OF BLINK REFLEX
Isabel Fernandez-Conejero, MD Department of Intraoperative Neurophysiology, Hospital Universitari de Bellvitge, Barcelona, Spain
In 1952 Kugelberg was the first to report the presence of two electrically induced blink reflex (BR) components, R1 and R2. The R1 response corresponds to the oligosynaptic reflex arc, which includes trigeminal afferents, brainstem connections between the sensory part of the trigeminal nucleus, the motor nucleus of the facial nerve, the facial nerve proper, and the orbicularis oculi muscle. The R2 component is more complex in its central, polysynaptic connections within the brainstem, but it has the same afferent and efferent pathways as the R1.
The BR has become an important tool in neurophysiology.
Until now, there have been no reports on eliciting the BR during anesthesia at a depth compatible with surgery.
We introduce a novel method for eliciting the R1 component of the BR under inhalation or total intravenous anesthesia by using a short train of four to seven stimuli applied over the supraorbital nerve. (Figure 1). Recording is done from the ipsilateral orbicularis oculi muscle. We set out to record the BR in 27 patients (age 1-78 years) without clinical involvement of the facial nerve, trigeminal nerve, or brainstem. The BR could not be recorded in only 4 patients (recordability: 86,2 %). All patients received at least one bolus of propofol while in surgery. Using this method, the BR was recorded on 4 awake healthy subjects. Boluses of propofol and muscle relaxants should be avoided in order to successfully record the responses. BR recording is feasible in patients under general anesthesia by using this novel technique.
Figure 1. Recordings of the R1 component of the BR from a patient. In this patient a train of four stimuli elicited the responses, whereas trains of one, two, and three stimuli did not. Each trace represents the average of two responses
Notes
70 FACIAL NERVE MONITORING AND MAPPING IN EXTRACRANIAL SURGERY AND SCLEROTHERAPY PROCEDURES
Sedat Ulkatan, MD Institute for Neurology and Neurosurgery, Roosevelt Hospital, New York, NY, USA
Facial vascular malformation (FVM) surgeries require reliable facial nerve monitoring (FNM). Unfortunately the existing methods (NIM®) are insufficient in many aspects. Understanding of facial nerve anatomy is the key to success for the FNM. Facial nerve (FN) completes its full structural (myelination) and functional development approximately at age 4. The anatomical feature of FN that affects the FNM the most is the depth of FN trunk from the skin surface. In newborns and children up to 2 years of age, facial nerve at this level is just deep to the subcutaneous tissue underlying the skin. After 2 years of age, mastoid tip and tympanic ring develop and facial nerve takes a deeper position. In adults the depth of the facial nerve is up to 5cm (figure 1). Another factor which affects the FNM is a superficial location of marginal mandibular branch above the mandibular edge in early ages, while it is 2 cm below the mandible in adults.
The methodology presented here, has been developed to comply an accurate monitoring of extra cranial part of FN in surgery and interventional radiological treatment of facial vascular malformations.
.
Newborn External acoustic meatus Adult
Facial Nerve
Figure 1: Anatomical relationship of the facial nerve in early years to temporal bone development1
Monitoring and mapping of extracranial part of the facial nerve in surgery has three imperative steps. 1- Mapping of the facial nerve preoperatively 2- Monitoring of the facial nerve intraoperatively 3- Mapping of the facial nerve intraoperatively
Mapping of the Facial nerve (Preoperatively) Utilization Mapping of the facial nerve is essential procedure for orientation and planning surgery. 1. Exploration of depth of the various branches of the facial nerve (according to the stimulation threshold changes) (Figure 2) a- Is it anatomical position of nerve under or in the lesion? b- Is it anatomical position of nerve over the lesion? 2. Distortion of route of branches due to the mass effect of lesion. (Figure 3) 3. Mapped and non mapped branches. (Figure 3)
71
Figure 2: Mapping of the facial nerve in a patient with congenital hemangioma. Stimulation threshold over the lesion is higher than at the non affected part of the face. This can be a good example for understanding mapping of other complex lesions of the face. (arrow heads depicts the muscle twitch points)
R L
Figure 3: In this young patient with a bilateral vascular malformation of the face, the lower buccal branch was not possible to map on left side.
Methodology Stimulation: Using a hand held stimulator with a stimulating probe (cathode) and a stick pad electrode (anode) is a necessary technique for successful mapping (Figure 4). Stimulation parameters: single stimulus (the range between 2 to 40 mA intensity, 0.2 ms duration and repetition rate of 2 Hz). Mapping of the facial nerve is also important for the optimal placement and recording CMAP with recording needle electrodes in to each muscle. Observed muscle twitch points can be seen in Figure 2 as dots at the end of the lines.
Figure 4: Technique of preoperative mapping of the facial nerve
72 Monitoring of the facial nerve (intraoperatively) Our current methodology was modified from a previously published methodology by Camargo et al.2
Stimulation Different lengths of monopolar EMG needle electrodes (MNE) can be used for comply the FN depth. MNE should be the cathode, (Figure 5). A surface stick pad electrode (Disposable disk electrodes, Viasys Healthcare, Madison, WI) should be placed over the mastoid process as the anode. The appropriate insertion depth of the stimulating needle electrode is established at the moment when the stimulating current elicits twitches in the muscles innervated by all four branches of the facial nerve (or by recording CMAPs in all muscles). Stimulation parameters: Single stimulus of up to 20 mA intensity, 0.2 ms duration and repetition rate of 1-2 Hz. In most cases current up to 10 mA was sufficient to elicit responses. (Figure 6)
A
C
Figure 5: The setting steps for facial nerve stimulation before monitoring starts. B
Recordings Twisted pair subdermal needle electrodes are suitable/ for recording of CMAPs. Electrodes should be inserted into the orbicularis oculi, nasalis, orbicularis oris and mentalis muscles (Figure 6)
Figure 6: Placement of subdermal needle electrodes
73 Interpretation of facial nerve monitoring results Facial nerve injury criteria:
1. 5 mA or more changes in the monitoring stimulation threshold.2 2. Muscle-twitch decrement or complete disappearance. 3. CMAP amplitude decrement (50% or more)
Important factors affecting facial nerve monitoring After induction of anesthesia without using any muscle relaxant, facial nerve mapping can proceed very quickly without delaying surgery. However, due to the FVMs extensive involvement in the face, mouth and neck, special anesthesia and muscle relaxants can be required. Mapping should be done after using “Train of Four” technique to check the muscle relaxant wearing off. The most accurate mapping can be achieved after TOF is 100% recovered from muscle relaxant agent.
During surgery, neurophysiologist should observe muscle twitches (if possible) and CMAP constantly and make correlations with surgical maneuvers. This will prevent misinterpretation and unnecessary delay of surgery. Most of the time, surgical maneuvers such as stretching tissues or compressing over the branches make reversible changes of the CMAP amplitude.
A B
Fig 7: A) Patient with a large lymphatic cyst just over the retroaricular fossa. A stimulating needle in this patient cannot be placed. B) Patient had an extremely fragile and pulsatile lesion. Any attempt to place a needle electrode can cause serious bleeding and the stability of stimulation electrodes are the main obstacle for monitoring
Possible causes of facial nerve injury during surgery and direct puncture sclerotheraphy (DPS) DPS 1. Edema secondary to injection of sclerotic material 2. Pharmaceutical agent’s direct effect (ethanol, sodium morruahate, doxycycline etc).
Surgical excision 1. Electro-coagulation (bipolar or monopolar coagulators) 2. Cutting 3. Stretching or compressing over the nerve branches
Intraoperative mapping of the facial nerve A facial nerve exploration after the skin dissection in FVM surgeries needs intraoperative mapping. Sterile monopolar or bipolar probes are common tools for this procedure.
Stimulation parameters Single stimulus of up to 10 mA intensity, 0.2 ms duration and repetition rate of 2 Hz.
At the beginning of surgery, maximum CMAP amplitude values should be obtained (baseline maximum amplitude). When intraoperative mapping is requested, CMAP amplitude of the mapped branch should be compared with baseline maximum value.
74
X% = (IOM mapping amplitude /Baseline maximum amplitude) x100
If ratio less than 30% or less, that branch is considered as a minor branch.
Pitfall During Intraoperative mapping, some very close muscles innervated by different braches of the facial nerve ( such as mentalis or platysma), can cause confusion and lead to misinterpretation, because needle electrode can pickup far field potentials from near by muscles.
The results of Facial Nerve Monitoring during surgeries and sclerotherapy for Facial Vascular Malformations (New York Experience) Surgery As a preliminary presentation, we reviewed 20 patients with different FVM diagnosis (AVM, VVM, LVM, HMG) which underwent surgery in 2008. Monitorability rate of facial nerve was 100%. All 4 major branches of the facial nerve were mapped before surgery for guiding surgeons during excision.
During surgery, facial nerve CMAP changes were noticed in 11 out of 20 patients, only one of these patients had a postoperative minimal reversible facial nerve deficit. During surgery in this patient when facial CMAP changes occurred, surgeons were immediately informed and the ongoing dissection was stopped and further damage of the nerve was prevented. None of the patients in this group showed postoperative permanent facial nerve deficits.
Endovascular and Direct Puncture Sclerotherapy Procedures In this group of 54 patients we discovered facial nerve neuropathy in FVM. Patients’ ages ranged from 4 to 58 years and it included 34 males and 20 females. The diagnoses were 10 patients with AVM, 38 with VVM, 5 with LM and 1 patient with hemangioma.
Only 19% of patients in this group of 54 did not have facial neuropathy
Distribution of neuropathy in different branches:
One branch 22%, Two branches 26%, Three branches 24%. All four branches 9%
The anatomical location of lesion corresponds to the involvement (neuropathy) of the particular facial nerve branches.
During this study, we performed search using various literature search engines (Pubmed®, Ovid online®) and electrophysiology textbooks. We couldn’t find any complete normative value data from 5 main branches of facial nerve. Therefore we established our own laboratory normative values by collecting data from 8 healthy subjects and healthy side of the face from 7 patients. Total 23 facial nerves were studied.
Normative values for facial nerve branches Frontalis muscle: 4.1±0.48 ms Orbicularis oculi muscle: 3.3±0.43 ms Nasalis muscle: 3.6±0.36 ms Orbicularis oris muscle: 3.4±0.45 ms Mentalis muscle: 3.8±0.50 ms.
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Figure 9: Neurophysiological evidence of marginal mandibular branch neuropathy
References 1. Anatomy of the Clinician. Mark May, and Barry Shatkin The Facial Nerve May’s second edition. Thieme New York pp46, 2000 2. Bueno de Camargo A. Szelényi, A, Novak K,. Niimi Y, Berenstein A., Deletis V. Neurophysiological Assessment Of Facial Nerve During Percutaneous Angio-embolization Of Vascular Malformations Of The Face, 2003.
Notes
76 POSTERIOR ROOT-MUSCLE REFLEX
K Minassian, 1, 2 US Hofstoetter,1,2 J Ladenbauer,1 F Rattay,1 W Mayr,2 MR Dimitrijevic,1,3 1. Institute of Analysis and Scientific Computing, Vienna University of Technology, Austria; 2. Center of Biomed. Engineering and Physics, Medical University of Vienna, Austria; 3. Dept. of Physical Medicine and Rehab., Baylor College of Medicine, Houston, TX, USA.
Introduction Spinal cord stimulation (SCS) with electrodes placed in the dorsal epidural space can activate lumbar spinal locomotor circuits in complete spinal cord injured people (Dimitrijevic et al., 1998; Minassian et al., 2007a). By applying continuous epidural SCS to the upper lumbar cord segments at 25-50 Hz and 1.2-3.3 times the motor threshold, locomotor-like lower limb movements can be produced in the absence of translesional brain influence.
The identification of the neural structures directly depolarized by SCS resulting in the motor outputs became a central question of our studies. These pathways are mediating the activating input to the locomotor circuits (Rattay et al., 2000; Minassian et al., 2004). We found that the muscle responses were elicited by stimulation of large-diameter afferents within several lumbar posterior roots. Each stimulus pulse of the applied trains gave rise to a posterior root-muscle reflex (PRM reflex) in the lower limb muscles associated with the stimulated roots. Each PRM reflex was recorded electromyographically as a compound muscle action potential. PRM reflexes evoked in series at 25-50 Hz co-activated lumbar spinal circuits that in turn modified the PRM reflex activity with a locomotor-like pattern. When the repetition rate was decreased to 2 Hz, however, PRM reflexes were ‘simple’ monosynaptic reflexes.
One specific low-threshold site for external stimulation of posterior root fibers was determined by the lumbar cord and roots anatomy (Rattay et al., 2000). First, by entering the spinal cord, posterior root fibers pass the interface of the well-conducting cerebrospinal fluid and the spinal white matter. Secondly, the longitudinal lumbar posterior roots bathed in the cerebrospinal fluid change their orientation with respect to the stimulating field to a transversal direction, with the afferent projections being part of spinal segmental circuits. Both facts together result in a sudden voltage drop of the external electric field along the posterior root fibers at the dorsal root entry zone and leads to low stimulation thresholds.
Following the theoretical findings we hypothesized that these effects could also result in low-thresholds for posterior roots even if stimulation is delivered with a transcutaneous technique that produces a more widespread electric field within the spinal canal. In fact, we have recently demonstrated that single pulses with moderate stimulus intensities delivered through surface electrodes attached over the lumbar paraspinal muscles and abdomen can elicit PRM reflexes in several lower limb muscles simultaneously (Minassian et al., 2007b). In the following, we will describe the method of transcutaneous elicitation of PRM reflexes, report on the biophysical effects of the stimulationn and give details on the electrophysiological characteristics of PRM reflexes in healthy individuals with intact nervous system.
Methods Transcutaneous posterior root stimulation. The stimulation method utilizes equipment available in electrodiagniostic laboratories and in physical rehabilitation departments. Stimulation was performed using commercially available self-adhesive transcutaneous electrical neural stimulation electrodes. Stimulation electrodes were a pair of electrodes (∅ = 5 cm) placed over the paravertebral skin on each side of the spine (Fig. 1). Stimulation over the lumbosacral cord was studied with the paravertebral electrodes positioned at the T11–T12 interspinous space. Cauda equina stimulation was tested by more caudal locations of the electrodes up to a position at the L4–L5 interspinous space. Reference electrodes were a pair of rectangular electrodes (8 cm x 13 cm) placed over the abdomen, one on either side of the umbilicus. The two electrodes of each pair were connected to function as a single electrode.
Symmetric, biphasic rectangular pulses with pulse widths of 2 ms were delivered by a constant-voltage stimulator. The electrodes were connected to the stimulator such that the paravertebral electrodes acted as the anode during the first phase of the stimulus pulse. Neural elements were stimulated at the transition from the first to second phase of the biphasic stimulus, when the function of the paravertebral electrodes changed from anode to cathode.
77
Figure 1. A. Electrode placement for transcutaneous lumbar posterior root stimulation. B. Sketch of stimulating electrodes with respect to spine and spinal cord. C. Sketch of the stimulated posterior roots.
The reference abdominal electrodes had a surface area more than 5 times larger than the stimulating paravertebral electrodes. This resulted in a correspondingly smaller current density and less voltage drop near the abdominal electrodes. A larger portion of the total stimulation voltage was therefore available under the paravertebral electrodes, hence a stronger stimulating effect of the electrode set-up near the vertebral columns.
Alternative electrode set-ups with both stimulating and reference electrodes placed over the back were similarly effective to elicit PRM reflexes. Electrodes with diameters of less than 3 cm were not used to avoid discomfort at the stimulation site due to high current densities.
Results Our computer simulations (Ladenbauer, 2008) suggested that the current penetrates the vertebral canal through the better conducting anatomical structures between the bony structures of the spine. Posteriorly, the ligaments in- between the spinal processes and laminae of adjacent vertebrae have a significantly higher electrical conductivity than the bony structures. Anteriorly, the intervertebral discs, mostly constituted of water, have a higher conductivity than the vertebral bodies. Within the spinal canal, most of the current flows through the cerebrospinal fluid, that has a 30 times higher conductivity than the epidural fat and a 19 times higher conductivity than the white matter in transverse direction. We calculated that as much as 9% of the total current produced by the surface electrodes penetrates that relatively small region of the thecal sac that contains the roots bathed in the cerebrospinal fluid, where the current reaches high densities.
The calculations confirmed the dorsal root entry zones as low-threshold sites of posterior root fiber stimulation (cf. Introduction) also for the transcutaneous technique. Moreover, when stimulating electrodes are placed over the cauda equina, additional “hot spots” for transcutaneous posterior root stimulation are located at the exits of the fibers from the spinal canal. In those regions again the change of electrical conductivity (cerebrospinal fluid-dura mater-epidural fat) and curvatures of the fiber trajectories result in low thresholds for the external stimulation.
Electrophysiologically, a single pulse applied at the T11-T12 interspinous space elicited short-latency PRM reflexes in all recorded lower limb muscles in the supine subjects (Minassian et al., 2007b). Figure 2 shows representative CMAPs in the left and right quadriceps (Q), hamstrings (Ham), tibialis anterior (TA), and triceps surae (TS) elicited by a single pulse. A mean intensity of 28.6 V in a group of 8 subjects elicited simultaneous, bilateral PRM reflexes in the thigh and leg muscles by depolarization of lumbosacral posterior root fibers (impedance within a range of 700-900Ω; Ladenbauer, 2008). Mean latencies of PRM reflexes amounted to: Q, 10.3 ± 1.1 ms; Ham, 11.2 ± 0.4 ms; TA, 19.1 ± 0.9 ms; and TS, 19.7 ± 1.1 ms.
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Figure 2. Electromyography of PRM reflexes simultaneously recorded from left (solid lines) and right lower limb muscles. Stimulation site: T11–T12 interspinous space; stimulus intensity: 30 V.
PRM reflexes were attenuated when a prior stimulus was given at intervals of 50 ms, as well as during tendon vibration (Minassian et al., 2007b). Moreover the triceps surae PRM reflex was suppressed during voluntary activity of the antagonistic tibialis anterior. Regarding these characteristics, PRM reflexes are electrophysiologically similar to the monosynaptic H reflex.
Investigating the time course of excitability changes of test PRM reflexes elicited at progressively increasing intervals after conditioning PRM reflexes revealed differences between the lower limb muscles (Minassian et al., 2009). Preliminary results suggest that these excitability curves have a faster recovery and earlier initial peaks of recovery for the thigh as compared to the lower leg muscles.
Transcutaneous stimulation applied over the cauda equina elicitated PRM reflexes as well as direct M waves in the same muscle. Applying graded stimulation through paravertebral electrodes placed over the L4–L5 interspinous space resulted in a complex but characteristic sequence of indirect and direct responses in the lower limb muscles. The average muscle recruitment order was elicitation of PRM reflexes in TS first, TA second, and Ham third. These responses had latencies longer by 1.6-2.1 ms than the latencies of PRM reflexes to lumbar cord stimulation. With yet stronger stimulation, M waves could be elicited in the same muscles, as well as in Q. Their latencies could be as short as approx. 8 ms in the thigh and 16 ms in the lower leg muscles. The recruitment of PRM reflexes and M waves in Ham, TA, and TS responses to cauda equina stimulation resembled the H-reflex and M-wave recruitment known from mixed peripheral nerve stimulation.
Conclusions The transcutaneous technique of posterior root stimulation is non-invasive, involves simple electrode placement and moderate stimulus intensities, and delivers stimulation at a fixed site. The method may have an important impact in numerous fields.
The electrically stimulated structures are similar to the ones directly depolarized by epidural SCS, i.e., large diameter afferents of multiple cord segments. Hence “transcutaneous SCS” can open new avenues as a neuromodulation technique.
Electrophysiological similarities between the PRM reflex and the H reflex can enable novel neurophysiological studies testing the excitability of motoneuron pools under different conditioning influences. In fact, PRM reflexes allow extending H-reflex studies of a single muscle to the assessment of synaptic transmission of two-neuron reflex arcs at multiple segmental levels simultaneously (Hofstoetter et al., 2008).
As an intraoperative monitoring technique, elicitation of PRM reflexes could emerge as an electrophysiological method to assess the functional integrity of the lumbosacral cord and the associated roots, and of the cauda equina. Elicitation of single PRM reflexes can provide a reliable measure of conduction within the spinal canal, paired elicitation of PRM reflexes assesses the excitability states of myotatic reflex arcs of several muscles.
79 References 1. Dimitrijevic MR, Gerasimenko Y, Pinter MM. Evidence for a spinal central pattern generator in humans. Ann N Y Acad Sci. 1998; 860: 360-376. 2. Hofstoetter US, Minassian K, Hofer C, Mayr W, Rattay F, Dimitrijevic MR. Modification of reflex responses to lumbar posterior root stimulation by motor tasks in healthy subjects. Artif Organs. 2008; 32: 644-648. 3. Ladenbauer J. Simulation of the excitation of human lower spinal cord structures with surface electrodes: 3d finite element analysis and nerve fiber modeling. M.S. thesis, Inst. Analysis and Scientific Computing, Vienna Univ. of Technology, Austria, 2008. Available: http://www.ub.tuwien.ac.at/dipl/2008/AC05039071.pdf 4. Minassian K, Jilge B, Rattay F, Pinter MM, Binder H, Gerstenbrand F, Dimitrijevic MR. Stepping-like movements in humans with complete spinal cord injury induced by epidural stimulation of the lumbar cord: electromyographic study of compound muscle action potentials. Spinal Cord. 2004; 42: 401-416. 5. Minassian K, Persy I, Rattay F, Pinter MM, Kern H, Dimitrijevic MR. Human lumbar cord circuitries can be activated by extrinsic tonic input to generate locomotor-like activity. Hum Mov Sci. 2007a; 26: 275-295. 6. Minassian K, Persy I, Rattay F, Dimitrijevic MR, Hofer C, Kern H. Posterior root-muscle reflexes elicited by transcutaneous stimulation of the human lumbosacral cord. Muscle Nerve. 2007b; 35: 327-336. 7. Minassian K, Hofstoetter US, Rattay F, Mayr W, Dimitrijevic MR. Posterior root-muscle reflexes and the H reflex in humans: Electrophysiological comparison. Program No. 658.12. Neuroscience Meeting Planner. Chicago, IL: Society for Neuroscience, 2009. Online 8. Rattay F, Minassian K, Dimitrijevic MR. Epidural electrical stimulation of posterior structures of the human lumbosacral cord: 2. quantitative analysis by computer modeling. Spinal Cord. 2000; 38: 473-489.
Support: We kindly acknowledge the support by the Austrian Science Fund (FWF), Vienna, Austria, Proj.Nr. L512-N13
Notes
80 PERSISTENTLY ELECTRIFIED PEDICLE STIMULATION DURING MINIMALLY INVASIVE LUMBO - SACRAL FIXATION
Feltz CR2, Magge SN1, Arle JE1, Kim S1, Martin CJ1, Moul M2, Shils JL1 1. The Lahey Clinic, Dept of Neurosurgery, Burlington, MA 2. Impulse Monitoring Inc., Columbia, MD
The use of screws for spinal fixation surgery dates back to 1944 when King placed screws across the facet joints to facilitate spinal stabilizationr {15}. Later, Boucher began placing screws into the vertebral pedicles providing the rigidity necessary for fixation and fusion of vertebral segments {3}. This system’s superiority to the hook and rod method is proven in its provision of multi-dimensional fixation, allowing the surgeon greater flexibility to accommodate a patient’s individual anatomy, rather than the instrumentation itself {12}. Due to significant variation in pedicle anatomy the placement of pedicle screws has a relatively high rate of neurologic injury, ranging from 1% to over 11% {4, 7, 8}. Construct failures and visceral injuries can increase the overall complication rate to as much as 40% {32}. In an attempt to minimize the errors associated with pedicle screw placement, intra-operative fluoroscopy has become a standard during this procedure. Even with sagittal and AP fluoroscopy images, the lack of an axial image still means that breaches of the pedicle and/or vertebral body can still occur undetected. Intra-operative image guidance is a technique that is presently starting to gain acceptance in the field, but still has some associated errors as demonstrated in Nottimeier et. al. who describe a 9% unintentional breach rate {33}. Moreover, fluoroscopy can be misleading in some cases and has been demonstrated to have a high false positive rate {9, 17, 19, 22}. Using fluoroscopy in conjunction with stimulation of the pedicle screw, after it has been placed, includes another major shortcoming: the surgeon can only be informed of a possible pedicle breach after it has occurred, and thus has already placed a large hole in the pedicle, harming the integrity of the bone.
In 1992, Calancie, et al. {4} described a new method for guiding and evaluating pedicle screw placement using electrically stimulated pedicle screw driven triggered electromyography (tEMG) in a pig model. Two years later, they evaluated the technique in 18 patients, testing 102 pedicle screws {5} where they utilized a continuously delivered 200 μSec constant current square wave pulse through the surgical instruments used for creating the hole (called an awl) and placing the screw. During the initial pilot hole creation, a constant 7mA current was applied through the awl. This was referred to as the “searching intensity”. If the pedicle wall was breached medially, the current most likely activated adjacent nerve roots, thus resulting in an tEMG response in one of the end organ muscles. If the pedicle wall is not breached, then the high resistance of the intact bone would necessitate a much greater current for activation of the nerve roots, and thus not show any tEMG activity. The diameter of the pedicle screw is slightly larger than either the awl or the tap, and the possibility exists that the screw could crack or perforate the pedicle wall even though the other instruments did not. In order to test for this condition, the pedicle screw itself was stimulated after placement utilizing a safety criteria of 10mA. If tEMG activity was noted at this level or lower, a recommendation for screw repositioning was made. The study concluded that the “searching intensity” technique was safe and reliable for the detection of perforations during pedicle screw placement {5}.
Minimally invasive (MI) methods for placing pedicle screws {34} allow for the placement of cages and screws though very small incisions, thus minimizing the damage to the lumbar musculature and reducing the post- operative hospitalization and recovery time for the patient. Lack of direct visualization of anatomic landmarks during pilot hole creation and pedicle screw placement makes x-ray imaging and tEMG testing more critical for proper placement. The method of intraoperative monitoring using persistently electrified instrumentation is the core concept in ensuring proper pedicle screw placement during minimally invasive lumbosacral procedures and is the basis of the current study. Presently, the standard tEMG analysis for pedicle screw evaluation is to deliver the stimulus to the screws themselves. However, in MI procedures the screws cannot be tested due lack of insulated tools for screw placement and alignment; in such cases, other segments of the pedicle application procedure need to be studied for testing pedicle integrity.
As the minimally invasive technique for lumbosacral spinal fixation becomes more common, the use of a multi- modal intraoperative testing paradigm consisting of both active and passive tools becomes increasingly important. Intraoperative tEMG offers the surgeon a non-invasive active functional tool to help ensure proper pedicle screw placement. Fluoroscopy and/or free run electromyography (EMG, a passive functional tool) with pedicle hole, tap, and/or screw stimulation are typically used to determine proper placement of pedicle screws. Persistent stimulation of the pedicle access (PAC) needle, however, helps guide the direction of the initial pilot hole. This allows the surgeon to re-direct the hole at the earliest breach encounter, thus potentially minimizing the breach,
81 decreasing the chance of mechanical instability of the bone due to large screw holes, and bypassing screw-related iatrogenic nerve root injury.
While the MI posterior lumbar interbody fusion (PLIF) procedure allows for less muscle dissection resulting in shorter hospital and rehabilitation time {10, 14}, the procedure has certain disadvantages. Since screw placement is often done percutaneously, the surgeon is unable to visualize the pedicle or inspect the screws and surrounding structures after they are placed. Also, the screw itself cannot be stimulated because the screw and guiding extensions cannot be properly insulated from surrounding soft tissue. Consequently, the surgeon must rely on stimulation of the final position of the tap, an instrument used to make the thread pattern in the bone, to determine the proper placement of the screw. Finally, the surgeon is unable to stimulate the nerve root directly, which is a technique used by surgeons to evaluate a nerve root’s stimulation threshold. These issues represent the potential shortcomings of the procedure from a monitoring standpoint to be described in this paper.
The incidence of misplaced screws and in conjunction with the usefulness of spontaneous and triggered EMG, direct screw stimulation and the criteria for safe screw thresholds are all well documented {1, 4, 6-8, 11, 16, 21}. However, there is little information regarding persistent pilot hole stimulation, especially during minimally invasive procedures {4, 16}. The goal of the present study is twofold: the first goal is to investigate the “safe” threshold parameters of the PAC needle as the initial pilot hole is being made. Since current density differences exist between the tip of the insulated PAC needle and the entire shaft of the tap, the safe criteria threshold for each will differ significantly. The second goal is to compare tap and screw thresholds during open procedures to compare to the data described in existing literature. The tap and screw are made of differing materials, and this variation can change the thresholds reached during stimulation. MI procedures rely on the tap for accurate stimulation thresholds as compared to the screw. In comparing the two stimulation thresholds, we aim to shed new light on the current literature. The ultimate goal in comparing the two parts of this one study is the development of a monitoring technique that will provide the surgeon with instant and reliable feedback while performing MI procedures requiring pedicle fixation.
References 1. Balzer, JR, Rose, RD, Welch, WC, Sclabassi, RJ: (1998) Simultaneous Somatosensory Evoked Potential and Electromyographic Recordings During Lumbosacral Decompression and Instrumentation. Neurosurgery, 42: 1318-1324. 2. Bindal, RK, Ghosh, S: (2007) Intraoperative Electromyography Monitoring in Minimally Invasive Transforaminal Lumbar Interbody Fusion. J. Neurosurg Spine, 6: 126-132. 3. Boucher, H: (1959) A Method of Spinal Fusion. Journal of Bone and Joint Surgery, 41: 248-259. 4. Calancie B, Lebwohl N, Madsen P, Klose KJ: (1992) Intraoperative Evoked EMG Monitoring in an Animal Model. A New Technique for Evaluating Pedicle Screw Placement. Spine, 17: 1229-35 5. Calancie B, Madsen P, Lebwohl N: (1994) Stimulus Evoked EMG Monitoring During Transpedicular Lumbosacral Spine Instrumentation. Spine, 19: 2780-86 6. Castro WH, Halm H, Jerosch J, Malms J, Steinbeck J, Blasius S: (1996) Accuracy of Pedicle Screw Placement in Lumbar Vertebrae. Spine, 21: 1320-24 7. Clements DH, Morledge DE, Martin WH, Betz RR: (1996) Evoked and Spontaneous Electromyography to Evaluate Lumbosacral Pedicle Screw Placement. Spine, 21: 600-604. 8. Darden BV, Wood KE, Hatley MK, Owen JH, Kostuik J: (1996) Evaluation of Pedicle Screw Insertion Monitored by Intraoperatiove Evoked Electromyography. J. of Spinal Disorders, 9: 8-16. 9. Farber GL, Place HM, Mazur RA, Jones DEC, Damiano TR: (1995) Accuracy of Pedicle Screw Placement in Lumbar Fusions by Plain Radiographs and Computed Tomography. Spine, 20: 1494-99. 10. Foley KT, Holly HT, Schwender JD: (2003) Minimally Invasive Lumbar Fusion. Spine, 28: (15 suppl), S26-S35. 11. Holland NR, Lukaczyk, TQ, Riley LH, Kostuik JP: (1998) High Electrical Stimulus Intensities are Required to Activate Chronically Compressed Nerve Roots. Spine, 23: 224-227. 12. Isley MR, Pearlman RC, Wadsworth JS: (1997) Recent Advances in Intraoperative Neuromonitoriing of Spinal Cord Function: Pedicle Screw Stimulation Techniques. Am. J. END Technol., 37: 93-126. 13. Jellinek D, Jewkes D, Symon L: (1991) Noninvasive Intraoperative Monitoring of Motor Evoked Potentials Under Propfol Anesthesia: Effects of Spinal Surgery on Amplitude and Latency of Motor Evoked Potentials. Neurosurgery, 29: 551-557. 14. Khoo LT, Palmer S, Laich DT, Fessler RG: (2002) Minimally Invasive Percutaneous Posterior Lumbar Interbody Fusion. Neurosurgery, 51: (5 suppl) S166-S181. 15. Maguire J, Wallace S, Madiga R, Leppanen R, Draper V: (1995) Evaluation of Intrapedicular Screw Position using Intraoperative Evoked Electromyography. Spine, 20: 1068-74. 16. King, D: (1944) Internal Fixation for Lumbo-Sacral Fusion. American Journal of Surgery, 66: 357. 17. Roberts, RM, Bernhardt M: (1992) Accuracy of Fluoroscopic Guided Pedicle Screw Placement in the Lumbosacral Spine. Scoliosis Research Society Abstract. 18. Rose RD, Welch WC, Balzer JRJacobs GB: (1997) Persistently Electrified Pedicle Stimulation Instruments in Spinal Instrumentation. Spine, 22: 334-343. 19. Skelly JP, Toleikis JR, Carlvin AO: (1999) Pedicle Screw Stimulation in a Fluid Environment. Proceedings of the 10th annual meeting of the American Society of Neurophysiological Monitoring, Denver, CO.
82 20. Steinman JC, Herkowitz HN, El-Kommos H, Wesolowski P: (1993) Spinal Pedicle Fixation: Confirmation of an Image Based Technique for Screw Placement. Spine, 18: 1856-61. 21. Toleikis JR, Skelly JP, Carlvin AO, Toleikis SC, Bernard TN, Burkus JK, Burr ME, Dorchak JD, Goldman MS, Walsh TR: (2000) The Usefulness of Electrical Stimulation for Assessing Pedicle Screw Placements. J. Spin. Disord. 13: 283- 289. 22. Weinstein JN, Spratt KF, Spengler D, Brick C, Reid S: (1988) Spinal Pedicle Fixation: Reliability and Validity of Roetgenoram Based assessment and Surgical Factors on Successful Screw Placement. Spine, 13: 1012-18. 23. Reidy DP, Houlden D, Nolan PC, Kim M, Finkelstein JA: (2001) Evaluation of electromyographic monitoring during insertion of thoracic pedicle screws. The Journal of Bone & Joint Surgery (Br), 83-B:1009-1014. 24. Cotton, M.A., Jenkins, J.A., Ehle, A., Schafer, M. (1997). The efficacy of evoked EMG from direct stimulation of pedicle screws. Proceedings of the 8th annual meeting of the American Society of Neurophysiological Monitoring, Chicago. 25. Owen, J.H., and Toleikis, J.R. (1997). Nerve root monitoring. In “The textbook of spinal surgery,” 2nd ed. (K.H. Bridwell, and R.L. DeWald, eds.), pp. 61–75. Lippincott-Raven, Philadelphia. 26. Szkiladz, E., Calder, H.B., and Easton, R.W. (1995). Intraoperative lumbo-sacral nerve root threshold measurement. Proceedings of the sixth annual meeting of the American Society of Neurophysiological Monitoring, San Francisco. 27. Darden, B.V., Owen, J.H., Hatley, M.K., Kostuik, J., and Tooke, S.M. (1998). A comparison of impedance and electromyogram measurements in detecting the presence of pedicle wall breakthrough. Spine, 23, 256–262. 28. Glassman, S.D., Dimar, J.R., Puno, R.M., Johnson, J.R., Shields C.B., and Linden, R.D. (1995). A prospective analysis of intraoperative electromyographic monitoring of pedicle screw placements with computed tomographic scan confirmation. Spine, 20, 1375–1379. 29. Lenke, L.G., Padberg, A.M., Russo, M.H., Bridwell, K.H., and Gelb, D.E. (1995). Triggered electromyographic threshold for accuracy of pedicle screw placement: An animal model and clinical correlation. Spine, 20, 1585–1591. 30. Rose, R.D. (1997). Spinal cord monitoring. Curr. Opin. Orthop., 8(2), 49–57 31. Young WF, Morledge DE, Martin W, Park KB. (1995). Intraoperative stimulation of pedicle screws: A new method for verification of screw placement. Surgical Neuology, 44, 544-547. 32. Ozgur BM, Berta S, Khiatani V, and Taylor WR. (2006). Automated Intraoperative EMG Testing During Percutaneous Pedicle Screw Placement. The Spine Journal, 6, 708-713. 33. Nottmeier EW, Seemer W, and Young PM. (2009). Placement of thoracolumbar pedicle screws using three-dimensional image guidance: experience in a large patient cohort. Journal of Neurosurgery Spine, 10(1), 33-39. 34. Ringel F, Stoffel M, Stuer C, and Meyer B. (2008). Minimally invasive transmuscular pedicle screw fixation of the thoracic and lumbar spine. Neurosurgery, 59(4), 361- 367. 35. Donohue ML, Murtagh-Schaffer C, Basta J, Moqurin RR, Bashir A, and Calancie B. (2008). Pulse-train stimulation for detecting medial malpositioned thoracic pedicle screws. Spine, 33(12), E378-85. 36. Raynor BL, Lenke LG, Bridwell KH, Taylor BA, and Padberg AM. (2007). Correltaion between low triggered electromyographic thresholds and limbar pedicle screw malpositions: analysis of 4857 screws. Spine, 33(24), 2673-2678.
Notes
83 NEUROPHYSIOLOGY OF MOVEMENT DISORDERS
Zvezdan Pirtošek, MD Department of Neurology, University Medical Center, Ljubljana, Slovenia
The complex diagnosis of movement disorders is essentially one of phenomenology first, neurologic examination and history second, and any supportive laboratory testing, such as neurophysiology, last. Movement disorders are broadly classified as either hyperkinetic--too much movement--and hypokinetic--too little movement.
Hyperkinetic movements include: • Dystonia. Sustained muscle contractions, often causing twisting or repetitive movements and abnormal postures. Dystonia may be limited to one area (focal) or may affect the whole body (general). Focal dystonias may affect the neck (cervical dystonia or torticollis), the face (one-sided or hemifacial spasm, contraction of the eyelid or blepharospasm, contraction of the mouth and jaw or oromandibular dystonia, simultaneous spasm of the chin and eyelid or Meige syndrome), the vocal cords (laryngeal dystonia), or the arms and legs (writer's cramp, occupational cramps). Dystonia may be painful as well as incapacitating. • Tremor. Tremors are defined as rhythmic involuntary oscillatory movements of a body part. Tremor may occur only when muscles are relaxed or it may occur only during an action or holding an active posture. • Tics. Involuntary, rapid, nonrhythmic movement or sound. Tics can be controlled briefly. • Myoclonus. A sudden, shock-like muscle contraction. Myoclonic jerks may occur singly or repetitively. Unlike tics, myoclonus cannot be controlled even briefly. • Chorea. Rapid, nonrhythmic, usually jerky movements, most often in the arms and legs. • Ballism. Like chorea, but the movements are much larger, more explosive and involve more primal parts of the arm or leg. The condition can occur on both sides of the body or on one side only (hemiballismus). • Akathisia. Restlessness and a desire to move to relieve uncomfortable sensations. Sensations may include a feeling of crawling, itching, stretching, or creeping, usually in the legs. • Athetosis. Slow, writhing, continuous, uncontrollable movement of the arms and legs.
Hypokinetic movements include: • Bradykinesia. Slowness of movement. • Akinesia: inability to move • Freezing. Inability to begin a movement or involuntary stopping of a movement before it is completed.
Hypokinetic movements are often accompanied by • Rigidity. An increase in muscle tension when an arm or leg is moved by an outside force. • Postural instability. Loss of ability to maintain upright posture caused by slow or absent righting reflexes.
Morphologically, movement disorders reflect abnormal activity of the basal ganglia and their connections with the upper brainstem, thalamus and the cortex. Functional anatomy of the basal ganglia can be presented on four functional organizational levels: (i) macroscopic anatomy, (ii) (ii) connectivity (complex loops processing motor, cognitive and emotional informations), (iii) neuronal morphology and (iv) (iv) dopaminergic innervation (as a dual system with antagonistic effects).
Basal ganglia form a major centre in the complex extrapyramidal motor system, as opposed to the pyramidal motor system (corticobulbar and corticospinal pathways). Basal ganglia are involved in many neuronal pathways having emotional, motivational, associative and cognitive functions as well. They receive inputs from all cortical areas and, throughout the thalamus, project in a circuit-like manner to frontal lobe areas (prefrontal, premotor and supplementary motor areas) which are concerned with planning and execution. There are several circuits which: (i) have an important regulatory influence on cortex, providing information for both automatic and voluntary motor responses to the pyramidal system; (ii) play a role in predicting future events, reinforcing wanted behaviour and suppressing unwanted behaviour, and (iii) are involved in shifting attentional sets and in both high-order processes of movement initiation and spatial working memory.
84 The best known is the motor loop which acts to scale movement or/and focuses motor activity. It maintains somatotopic organisation of movement-related neurons throughout the circuit. Disruption in this circuit will therefore lead to errors in scaling and focusing of movement, resulting in either hypokinetic (Parkinson's disease) or hyperkinetic (tremor, dystonia) movement disorders.
Current models for movement disorders take into account not only changes in neuronal activity in the basal ganglia, but also metabolic and excitability changes in the cerebral cortex and the loss of inhibition to spinal and brainstem reflexes.
Clinical neurophysiology has greatly contributed to the diagnosis of movement disorders and, lately, it is used also as a therapeutic tool
According to Shibasaki (2002), movement disorders are physiologically studied based on three principles; 1. relation between movements and brain activities, 2. excitability and inhibitory mechanisms of motor cortices, and 3. sensorimotor integration.
The way the movement is related to the brain activity can be studied by neuroimaging techniques such as PET, SPECT and fMRI, and by neurophysiological techniques: of simultaneous recording of EEG or MEG with EMG - jerk-locked averaging of electroencephalogram or magnetoencephalogram in case of involuntary movements; - recording of electric or magnetic fields associated with the movement Readiness potential (for self-initiated movements) Contingent negative variation (for cued movements) - analysis of change of cortical rhythmic oscillations related to the movement (event-related desynchronization or synchronization) - coherence analysis between EEG or MEG and EMG - electromyography: three EMG patterns may underlie involuntary movements o reflex (EMG burst 10 – 30 ms, activity in antagonists synchronous) o ballistic (triphasic – agonist, antagonist, agonist, each burst lasting 50 – 100 ms ) o tonic (continuous 200 – 1000 ms, activity either solely in the agonists or co-contraction)
Excitability and inhibitory mechanisms of motor cortices can be studied by applying transcranial magnetic stimulation. Studies have been done in patients with positive and negative myoclonus of cortical origin (related to abnormal hyperexcitability of the positive and negative components, respectively, of the primary motor cortex) and in focal dystonia (associated with impairment of inhibitory mechanisms in primary motor cortex).
Studies of sensorimotor integration used parameters such as contingent negative variation, choice reaction times, somatosensory evoked potentials (abnormalities are described in cortical reflex myoclonus and in task-specific focal dystonia. Effect of movement on somatosensory processing (gating) is abnormal immediately before the movement onset in focal dystonia in a task-specific way.
Some examples of the diagnostic role of neurophysiology in movement disorders: - claryfing various phenomenology: Is it tic? Myoclonus? Psychogenic? Studies of the surface EMG and correlative EEG or the presence/absence of Readiness Potential or a study of the latency of a muscle jerk after the stimulus & its comparison to reaction time can give a decisive support to the diagnosis. - Clarifying within a single phenomenological entity, e.g. tremor (accelerometry with wieghting of the limb)
Although the most important role of neurophysiology in movement disorders is diagnostic, there is an emerging field of therapeutic neurophysiology, e.g. EMG guided delivery of botulinum toxin, the use of magnetic transcranial stimulation and deep brain stimulation in some movement disorders.
However, it is important to stress that recent research emphasizes co-existance of the motor and sensory and cognitive and affective and autonomic impairment in what is increasingly erroneously labeled as movement disorders. Neurophysiology of sensory processing, of cognition, of emotion, of autonomic nervous system, of sleep is entering the field clarifying the basic pathophysiology of movement disorders. As an example, our studies demonstrated abnormalities of the P300, visual and auditory selective attention, and reaction times in Gilles de la Tourette and various parkinsonisms, as well as the role of these neurophysiological parameters in the differential diagnosis of akineto-rigid syndromes (Pirtosek et al 2001).
85 References • Pirtosek Z, Jahanshahi M, Barrett G, Lees A (2001). Attention and cognition in bradykinetic-rigid syndromes: an event- related potential study. Ann Neurol., 50: 567-573. • Shibasaki H (2002) Clinical neurophysiology of movement disorders. Clinical Neurology, 42;11:1095-1097
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86 NEW DEVELOPMENTS IN STEREOTACTIC AND DEEP BRAIN STIMULATION AND RECORDING
Joachim K. Krauss, MD Department of Neurosurgery, Medical School Hannover, Hannover, Germany
Abstract not available
Notes
87 DEEP BRAIN STIMULATION IN PARKINSON DISEASE AND DYSTONIA
Jay L. Shils, PhD, D.ABNM, FASNM Intraoperative Monitoring, Lahey Clinic, Burlington, MA, US
Surgical treatment for movement disorders in the basal ganglia dates back to the 1930’s when Meyers first described campotomy. In the 1940’s Spiegel and Wycis described the first human use of stereotactic surgery for treatment of psychiatric illnesses. From the 1930’s through the 1960’s neurophysiology played a small role in these procedures, but it was the work of Dr. Albe-Fessard in the 1960’s that opend the door for intra-operative micro-electrode recording that has become a critical tool for functional localization during movement disorders surgery and most centers. Specifically this type of monitoring falls into a category termed interventional neurophysiology by Dr. Marc Sindou.
The neurophysiologists id not longer the reporter of previous events, the information gained, interpreted, and analyzed by the neurophysiologist is used by the surgeon to plan the course of the procedure. In order for the neurophysiologist to perform these actions they need to not only have a detailed knowledge of the anatomy, basic physiology, and equipment, they also need to be familiar with the affects of the disease on the physiology, and the affects of the particular operative technique on the physiology. At present there are three primary targets for movement disorders surgery that the neurophysiologists needs to be familiar with and they are the Ventral Intermediate nucleus of the thalamus (VIM), the Internal Globus Pallidum (GPi) and the Sub-thalamic Nucleus (STN). This lecture will describe the role of the neurophysiologist in the operating room, the methodology that is used by the neurophysiologist to locate the appropriate targets, and physiological characteristics of the targets.
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88 MOTOR CORTEX STIMULATION FOR PARKINSON’S DISEASE
B Cioni, M D’Ercole, C De Simone, C Nucci, M Meglio Neurochirurgia Funzionale e Spinale – Università Cattolica – Roma – Italy
Introduction A total of 100 patients with Parkinson’s disease have been treated by MCS (1-6, 8, 9, 11, 15, 18-20)), according to an analysis of the Literature.
Only open-label studies in small cohort of patients are reported; no control, no randomization, no double blind, no long term results are described. Patients population was not homogeneous, as well as parameters of stimulation. MCS appears to induce some improvement but only class IV evidence (evidence from uncontrolled studies, case reports or experts opinion) is present in the Literature.
We present here the long term clinical results obtained in a series of PD patients, homogeneous as regard as clinical features, site and parameters of stimulation.
Personal experience In 2003, we started a prospective study to evaluate the safety and efficacy of MCS in patients with advanced Parkinson’s disease with clear inclusion (idiopathic Parkinson disease; at least 5 years disease’s length; disease in the advanced state: UPDRS in off >/= 40/180, Hoehn and Yahrs>/= 3, motor complications; positive response to L-Dopa; DBS not accepted by the patient or contraindicated; patient ability to give informed consent to the study) and exclusion criteria (history of epilepsy or EEG epileptic activity; alcohol or drug abuse; mental deterioration; psychiatric symptoms; previous basal ganglia surgery; other major illness).
10 patients met the above mentioned criteria: 3 were submitted to the implant of an epidural plate electrode over the motor cortex controlateral to the worst clinical side, and 7 to a bilateral implant (Fig 1). During the first year the stimulation was through the electrode controlateral to the worst clinical side in all the cases; parameters were: 120microsec, 80Hz, 3-6V (subthreshold for movements, and motor or sensory feelings), delivered continuously through contacts 0 (anode) and 3 (cathode). After 12 months, in cases of bilateral implant, stimulation became bilateral (same parameters for the side ipsilateral to the worst clinical side). The clinical assessment before implant and at 1, 3, 6, 12, 18, 24, 36, and 48 months included: - UPDRS ( Unified Parkinson Disease Rating Scale); - PDQL (Parkinson Disease Quality of Life Scale); - neuropsychological evaluation including MMSE (Mini Mental State Evaluation), behavioral assessment of mood and anxiety, tests for verbal short term memory, spatial short term memory, episodic verbal memory, non-verbal abstract reasoning, frontal executive functions and verbal fluency; - EEG: - oral medications and adverse events. The clinical motor evaluation was performed both in the off and in the on medication state and the motor assessment was videotaped. The “OFF” condition was achieved by withdrawing antiparkinsonian medications as follows: Levodopa for at least 12 hours, pergolide, pramipexole, ropinirole for at least 48 hours, cabergoline for at least 168 hours, apomorphine for at least 3 hours. The “ON” condition was achieved 60 minutes after administering a supra-threshold dose of standard levodopa, according to daily schedule.
Cognitive and behavioural assessment were performed preoperatively and at 6, 12 and 18 months, in the on med status.
A statistical (Wilcoxon’s test) significant improvement was present after 12, 24, 36, and 48 months of MCS, regarding total UPDRS off-med, UPDRS II, UPDRS III off-med, subscore for axial symptoms (UPDRS III: items 27-31), UPDRS IV, PDQL.
The effect of unilateral MCS was bilateral, with no significant difference between the two sides. It was evident after 1-2 weeks of stimulation, and in a case of accidental switching off of the stimulator, the patient became aware of something going wrong after 2-3 weeks.
Notably, in all the patients, the UPDRS III off med at 24, 36, and 48 months was always lower than UPDRS III off med at preoperative evaluation.
Cognitive assessment in the overall group of patients showed a significant postoperative improvement on the MMSE and no significant postoperative decline was observed on any cognitive task, including those of
89 phonological and semantic verbal fluency (22); on the contrary in DBS patients a significant decline on verbal fluency has been consistently reported (12).
We studied the functionality of the presynaptic dopaminergic system with single-photon emission computed tomography (SPECT) with 123-Ioflupane (DAT-scan) in order to evaluate binding to the dopamine transporters before and after 6 and 12 months of unilateral MCS.
This preliminary study showed that clinical improvement in patients with advanced PD undergoing unilateral MCS was paralleled by stable DAT availability in the putamen, especially on the side ipsilateral to the implant. On the contrary, the loss of DATs measured with [123I]FP-CIT SPECT continued to progress in the caudate, particularly on the side contralateral to the implant (13).
MCS may act as a “protective” mechanism against further neuronal degeneration in putamen. Further longitudinal studies on larger series are necessary to investigate effects of EMCS on dopaminergic function. In particular, the potential influence of long-term treatment with antiparkinsonian drugs on DAT binding needs to be evaluated.
We are now performing a controlled randomized study on the clinical usefulness of MCS in Parkinson’s disease. The protocol has been published on www.ClinicalTrials.gov (Identifier # NCT00637260) 20 patients will be enrolled. Inclusion criteria are: - Idiopathic PD, - response to Levodopa, - disease duration > 5 years, - UPDRS motor score in off condition ≥ 40/108, - Hoehn & Yahr stage ≥ 3, - DBS not indicated or refused, - signed informed consent.
After implantation of bilateral epidural strip electrodes over the motor cortex, and of a Kinetra neurostimulator, Medtronic, the patient will be randomly assigned to group A (Motor cortex stimulation on) or to group B (sham stimulation) for 6 months. At the 6 months visit, a cross-over is scheduled: group A will receive sham stimulation and group B will receive stimulation of the motor cortex for the next 6 months. Both the patients and the evaluating neurologists will be blind. At 12 months, all the patients will be programmed as stimulation on and followed up for further 18 months.
The primary endpoint will be the UPDRS III at 12 months (end of the cross over). Secondary outcome measures will be: UPDRS, Finger tapping, Walking time, PDQL (Parkinson’s Disease Quality of Life scale), neuropsychological evaluation.
Surgery A multicontact electrode (Resume lead, model 3587A, Medtronic, Minneapolis,Mn, USA) is usually placed through one or two burr holes or through a small craniotomy in the epidural space over the motor cortex unilaterally or bilaterally, parallel to the motor knob for the hand (2, 3, 7, 10). The electrode lead(s) is (are) then tunneled to a subclavicular site and connected to a neurostimulator placed in a subcutaneous pocket (Kinetra, model 7428, Medtronic).
The key point of surgery is the accurate placement of the electrode over the motor cortex the identification of which is the result of the integration of anatomical, neuroradiological, functional and neurophysiologic data, taking into account the huge population variability. Sophisticated tools, (fMRI, magnetoencephalography, diffusion tensor imaging) may be of help but a precise neurophysiologic location is mandatory.
We use craniometer landmarks (10-20 EEG System: CZ, C3 and C4 points) to draw the central sulcus over the scalp; the anatomical location of the motor strip is confirmed by MRI and neuronavigation. Under TIVA (total intravenous anesthesia) a burr hole is drilled in front of the central sulcus, medially to the presumed hand motor area, and then the electrode paddle is slipped epidurally, parallel to the motor strip at the hand knob. Then the position of the electrode is verified neurophysiologically.
We use the phase reversal technique to identify the central sulcus. We stimulate the controlateral median nerve at the wrist (0.5ms, 4.7Hz, 20mA) and record from each contact of the strip electrode; a cortical N20 potential is recorded over the sensory cortex, a cortical P20 potential is recorded over the motor cortex; the central sulcus is between the two contacts showing the phase reversal. Motor mapping is obtained by motor cortex focal anodal stimulation through each contact of the same strip electrode (reference Fz) with a short train of stimuli (5 stimuli, 0.5ms, ISI 4ms, 10-30mA). Muscle responses are recorded from muscle bellies of the controlateral hemi body, with needle electrodes. The morphological and neurophysiologic positions are then integrated in an anatomic- functional location. This mapping technique allows the use of general anesthesia (a total intravenous anesthesia using Propofol and Remifentanyl, avoiding muscle relaxants after intubation) and has a very low rate of induced
90 epileptic seizures (less than 4%) compared to the classical so called “Penfield’s technique” for motor cortex mapping.
Mechanisms of action As regard as the possible mechanisms of action, the motor cortex is part of the cortico-basal ganglia loop and modulation at one of the stations, will interfere with all the others.
MCS is sub threshold for any movement, so we can rule out the pyramidal cells and axons as point of action. MCS is probably interfering with small inhibitory axons in the cortex itself and/or with the axons of afferents and efferents running parallel to the stimulating electrodes as postulated by a computer modeling study (16. 17). So MCS may orthodromically and/or antidromically activate fibres connecting the motor cortex to the basal ganglia or it may act at local level decreasing cortical excitability or disrupting oscillatory rhythms and abnormal patterns of activity. The clinical course of some MCS effects suggests the possibility of time consuming processes such as synaptic plasticity, long term potentiation or depression, expression of secondary messengers, polarization of brain tissue.
Fibers recruitment is more likely to occur than cells activation, and it will depend on the modality of stimulation. The distance between the electrodes and the neural elements is important; a modeling study stresses the importance of CSF thickness: every 1 mm of CSF we need 6.6V to obtain the same effect on the neural tissue (16). Probably this problem was overestimated; in the clinical practice the straight paddle implanted over the convex surface of the dura at the hand knob, will squeeze the CSF underlying the paddle. The bipolar stimulation between two contacts of the electrode paddle corresponds to a bifocal monopolar stimulation, due to the wide distance between contacts. The anode excites the fibers that run perpendicular to the electrode surface, while the cathode excites the fibers running horizontally under the paddle (16, 17, 21).
The intensity of stimulation is intuitively very important for the fibers recruitment as well as the pulse width. Frequency of stimulation is another crucial variable: with frequency up to 130Hz, the fibers are more likely to be depolarized and excited. However if the stimulation is maintained for long periods of time, some synapses may not follow the stimulus train and be blocked, with consequent inhibition. Specific frequencies may be necessary to impose specific patterns of activity, or to suppress abnormal rhythms, or in time consuming processes. In 2008, our group published (14) the case of a 72 year old PD patient who underwent bilateral MCS. Before the operation in off-med condition the patient was unable to raise from a chair and to stand without assistance. MCS at 3 and 60Hz failed to provide any improvement; whereas stimulation at 130Hz induced a consistent improvement in axial akinesia and walking. Unfortunately, the benefit of MCS gradually disappeared after five months.
Discussion Our personal data and the reports present in Literature so far, suggest that MCS can modulate some symptoms of Parkinson disease, as well as other motor symptoms in movement disorders. Axial symptoms, gait, akinesia and freezing are improved.
The clinical effect of MCS cannot be compared with that of STNDBS due to the different inclusion criteria. DBS is usually contraindicated in the patients submitted to MCS, because of age or because of the presence of MRI anatomical abnormalities (cerebral atrophy, vascular lesions, ..). However, STNDBS appears to be more effective on motor symptoms, but MCS seems to be more effective on axial symptoms subscore; complication rate and adverse events rate is lower for MCS; particularly, verbal fluency is not impaired by MCS; finally, our data from DAT-Scan suggest that MCS may have a protective effect on putaminal degeneration at least at short follow up.
The clinical effect of MCS seems to decrease with time. This may be due to a placebo effect, and/or to the progressive nature of the disease; or it may reflect a true loss of effectiveness of the stimulation; changing the parameters of MCS may be of help in resuming the clinical effect. Changing the frequency or the intensity of stimulation according to the impedances (some fibrosis may develop between electrode surface and dura layer) may be useful. Neurostimulators delivering impulses in current may overcome this problem. Usually the stimulation is delivered continuously. The slight decline in the clinical benefit may be due to a sort of habituation of the cortex. To change type of stimulation may restore the effect. If this is true, alternate stimulation (right side or left side) may be a solution. The clinical effect is long lasting, therefore a cyclic stimulation (only during daytime or 30min on and 2-3 hours off) may be proposed
Not all the patients respond to MCS: this may be due to the rather large inclusion criteria, or to the different electrode position and different stimulation parameters. The effect of rTMS may be predictive of the clinical outcome following MCS. However, the frequency and the duration of rTMS certainly differs from that used for
91 MCS. As regards as electrode position and stimulation parameters the number of patients treated with MCS is still to low to allow statistical correlation analysis to identify prognostic factors
Different surgical techniques may be used to place the epidural cortical electrode: general vs. local anaesthesia, burr hole vs. craniotomy, craniometer landmarks vs. neuronavigation with MRI or with fMRI. No matter the technique used, we believe that a neurophysiologic precise location is mandatory if we want to exactly know where is our electrode. Our methodology allows motor mapping under general anaesthesia with a very low incidence of epileptic seizures (4-5% compared to 20-25% of the so called Penfield’s technique).
The need for a bilateral implant has still to be demonstrated. In our experience unilateral MCS improves motor performances bilaterally, but bilateral stimulation seems to increase such an improvement.
According to the data reported so far, we suggest the use of MCS in PD patients with prominent axial symptoms, gait disturbances and therapy complications.
References 1. Arle JE, Apetauerova D, Zani J, Deletis V, Penny D, Hoit D, Gould C, Shils JL (2008) Motor cortex stimulation for Parkinson disease: 12 months follow up in 4 patients. J Neurosurg, 109: 133-139 2. Arle JE, Shils J (2008) Motor cortex stimulation for pain and movement disorders. Neurotherapeutics 5:37-49 3. Bentivoglio AR, Cavallo MA, Cioni B, Contarino F, Eleopra R, Lavano A, Mazzone P, Meglio M, Signorelli CD, Sturiale C, Valzania F, Zeme S, Zenga F, Pagni CA (2005) Motor cortex stimulation for movement disorders In: Meglio (Eds) Proceedings of the 14th Meeting of the Worls Society for Stereotactic and Functional Neurosurgery. Medimond, Bologna, pp89-97 4. Benvenuti E, Cecchi F, Colombini A, Gori G (2006) Extradural motor cortex stimulation as a method to treat advanced Parkinson’s disease:new perspectives in geriatric medicine. Aging Clin Exp Res 18:347-348 5. Canavero S, Paolotti R (2000) Extradural motor cortex stimulation for advanced Parkinson’s disease. Mov Disord 15:169-171 6. Canavero S, Paolotti R, Bonincalzi V, Castellano G, Greco-Crasto S, Rizzo L, Davini O, Zenga F, Ragazzi P (2002) Extradural motor cortex stimulation for advanced Parkinson’s disease: report of two cases. J Neurosurg 97:1208-1211 7. Canavero S, Bonincalzi V (2007) Extradural cortical stimulation for movement disorders. In: D Sakas, B Simpson, E Krames, eds. Operative Neuromodulation. Springer-Verlag; Acta Neurochir Suppl 97/2:223-232 8. Cilia R, Landi A, Vergari F, Sganzerla E, Pezzotti G, Antonini A (2007) Extradural motor cortex stimulation in Parkinson’s disease Mov Disord 22:111-114 9. Cioni B. (2007) Motor cortex stimulation for Parkinson’s disease. In: D Sakas, B Simpson, E Krames, eds. Operative Neuromodulation. Springer-Verlag; Acta Neurochir Suppl 97/2:233-238 10. Cioni B, Meglio M, Perotti V, DeBonis P, Montano N (2007) Neurophysiological aspects of chronic motor cortex stimulation. Neurophysiologie Clinique/Clinical Neurophysiology 37:441-447 11. Cioni B, Bentivoglio A.R., Daniele A, De Simone C, Fasano A, Piano C, Zinno M, Meglio M. Acta Neurochir (Wien) 2008 Sept 150(9):936 12. Daniele A, Albanese A, Contarino MF, Zinzi P, Barbier A, Gasparini F, Romito A, Bentivoglio AR, Scerrati M (2003) Cognitive and behavioural effects of chronic stimulation of the subthalamic nucleus in patients with Parkinson’s disease J Neurol Neurosurg Psychiatry 74:175-182 13. Di Giuda D, Calcagni M L, Totaro M, Cioni B, Bentivoglio A, Bruno I, Mattioli D, Meglio M and Giordano A. Motor cortex stimulation in advanced Parkinson’s disease and dopamine transporter imaging: a follow-up study. Acta Neurochir (Wien) 2008 Sept 150(9) 936-937 14. Fasano A, Piano C, De Simone C, Cioni B, Meglio M, Bentivoglio AR (2008) High frequency extradural motor cortex stimulation dramatically improves axial symptoms in a patient with Parkinson’s disease Mov Disord 23(13):1916-9 15. Lavano A, Cioni B, Sturiale C, Landi A, Romanelli M, Dario A, Cavallo M, De Rose M, Meglio M, Zeme S Pagni CA (2008) Extradural motor cortex stimulation in advanced Parkinson’s disease: results of the study group of the Italian Society of Neurosurgery. Acta Neurochir (Wien) 2008 Sept 150(9) 936 P 16. Manola L, Roelofsen BH, Holsheimer J, Marani E, Geelen J (2005) Modelling motor cortex stimulation for chronic pain control: electrical potential field, activating functions and responses of simple nerve fibre models Med Biol Eng Comput 43:335-343 17. Manola L,Holsheimer J, Veltink P, Buitenweg JR (2007) Anodal vs cathodal stimulation of motor cortex: a modeling study Clin Neurophysiol 118:464-474 18. Pagni CA, Altibrandi MG, Bentivoglio AR, Caruso G, Cioni B, Contarino F, Insola A, Lavano A, Maina R, Mazzone P, Signorelli CD, Sturiale C, Valzania F, Zeme S, Zenga F (2005) Extradural motor cortex stimulation for Parkinson’s disease: History and first results by the study group of the Italian Neurosurgical Society. Acta Neurochir (Suppl) 93:113- 119 19. Pagni CA, Zeme S, Zenga F, Maina R (2005) Extradural motor cortex stimulation in advanced Parkinson’s disease: the Turin experience. Neurosurg 57 (ONS Suppl 3): ONS-402 20. Pagni CA, Zeme S, Zenga F, Maina R,, Mastropietro A, Papurello D (2003) Further experience with extradural motor cortex stimulation for treatment of advanced Parkinson’s diseases. Report of 3 new cases J Neurosurg Sci 47:189-193
92 21. Patton HD, Amassian VE (1954) Single and multiple unit analysis of cortical stage of pyramidal tract activation. J Neurophysiol 17:345-363 22. Zinno M, Cioni B, Bentivoglio AR, De Simone C, Fasano A, Piano C, Meglio M, Daniele A. Cognitive effects of extradural motor cortex stimulation. Acta Neurochir (Wien) 2008 Sept 150(9) 937.
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93 COMPUTATIONAL MODELS AND APPLICATIONS TO FUNCTIONAL NEUROSURGERY
JE Arle, MD, PhD Department of Neurosurgery, Lahey Clinic, Burlington, MA, US
The Computational Approach is characterized by several important points: it requires knowledge across multiple regimes (biophysics, electrical engineering, applied mathematics, neuroscience, neurosurgery), it allows access to hypotheses impossible with other techniques, and with solid validation, can generate new hypotheses about mechanism/function. It has been applied in many areas of neurosciences. We have used it to investigate mechanisms of deep brain stimulation in tremor and Parkinsons Disease, as well as in a general sense involving the interface of the DBS electrode with cell bodies and transiting axons, as well as in exploring potential mechanisms of cortical stimulation for treating chronic pain problems.
We have used our own software called UNCuS (Universal Neural Circuitry Simulator) which allows us to simulate a single neuron, or millions, on a level of ionic conductance able to capture combinations of channel dynamics that lead to non-linear current-voltage relationships in the cells if necessary. These neurons also have a form of dendritic processing that involves using an electrotonic compartmentalization of passive current spread with up to 10 distances from the axon hillock for every synapse. Cells may make as few or as many synaptic connections on as many target cells as is desired, and every synaptic event is accounted for on a time scale of 0.25ms. Active calcium spikes in the dendrites can also be added, and axonal delays are also in place that can be adjusted in half-millisecond increments. The DBS electrode model is an accurate rendering of the actual Medtronic electrode used clinically and it’s field characteristics have been mathematically computed for homogeneous media (Arle et al, 2008) accounting for frequency, pulse width, and mono- or bi-polar configurations of the 4 contacts. The MCS electrode itself is explicitly modeled, using charge density to solve for the voltage gradient in homogeneous tissue. It is essentially the same field as the DBS electrode but affecting only one half of the adjacent volume, since usually paddle-type leads are placed over the dura of the M1 cortex.
The basal ganglia were modeled using UNCuS with 7000 cells in 8 discrete groups, interconnected based on data from anatomical and physiological literature sources to include the SNc, SNr, Striatum, GPe, GPi, thalamus, Cortex, and STN described well in Shils et al. (2008). The cortical models for MCS were set up with an UNCuS model of the M1 and S1 regions of 6-layer cortex, fully implemented with interconnections and connections to a thalamic model based on anatomical literature, described by Arle and Shils (2008). Total cells in this model were similar (7000) with over 50 million individual synapses. Scaling in the MCS model was approximately 1:2000 with the real system in humans.
Findings in modeling for PD and Tremor showed that even with this fairly simple, yet biologically informed, model of the circuitry and electrode, significant firing rate changes and regularity changes were found when the electrode was ‘on’ that correspond well to what is found to benefit patients clinically. For example, significant changes in interspike interval variance in the STN, with STN stimulation, occurs only above stimulation of 100Hz. Tremor power also decreases notably in the tremor-like cells of the thalamic part of the model at stimulation amplitude levels exactly in the same range as used clinically. Very little if anything was configured in the model setup to create such findings or bias the model toward having such findings.
In the MCS model, a putative ‘pain’ stimulus was created in a region of the sensory thalamus part of the model (topographically oriented). Dynamically, it was appreciated that changes in S1 coding for this signal were blunted to a baseline level during M1 stimulation. Again, only anatomical and physiological relationships between the cells in the model based on literature were put into the model circuitry.
Conclusions from taking a computational approach in examining important aspects of basal ganglia modeling and use of the DBS electrode include:
• DBS electrode and circuitry of Basal Ganglia can be rendered in a reasonably biologically-based manner. • Examination of the circuitry dynamics could not be obtained currently in other ways. • Salient features of DBS are reproduced and therapeutic aspects (including the beneficial frequency and underlying mechanism of tremor control) can be better elucidated. • New Hypotheses can be generated and tested such as the unlikely need for regularity in managing tremor, or the quantitative contributions of axons of transit where DBS is used.
94 Conclusions from computational studies of MCS for pain were:
• M1 stimulation similar to that used with MCS and accounting only for the known anatomical intrinsic and connecting circuitry between M1, S1, and thalamus can give rise to at least short-term inhibition of a pulsed ‘pain’ signal from sensory thalamus • Likely, this mechanism would consist of an overdriving of inhibitory reciprocal connections from M1 to S1 on layer 4p, where sensory thalamic inputs synapse primarily • Such changes are consistent with findings suggestive of both excitation and inhibition from MCS since some inhibitory cells are excited, but some local cells will then be over-inhibited by this activity.
Overall, Computational Approaches can serve as an important adjunct in examining hypotheses in functional neurosurgery that would be difficult to study by more traditional means.
References 1. Arle JE, Mei LZ, and Shils JL, Modeling Parkinsonian Circuitry and the DBS Electrode: Biophysical Background and Software, Stereotact Funct Neurosurg, 86:1-15, 2008. 2. Shils JL, Mei LZ, and Arle JE, Modeling Parkinsonian Circuitry and the DBS Electrode: Evaluation of a Computer Simulation Model of the Basal Ganglia with and without Subthalamic Nucleus Stimulation, Stereotact Funct Neurosurg, 86:16-29, 2008. 3. Arle JE and Shils JL, Motor Cortex Stimulation for Pain and Movement Disorders, Neurotherapeutics, 5:37-49, 2008.
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95
Oral Presentations
96
PREDICTORS OF SUCCESSFUL FEASABILITY OF MULTIMODAL NON INVASIVE NEUROPHYSIOLOGIC MONITORING DURING SCOLIOSIS SURGERY
First Author-Presenter: Eric AZABOU (1), MD, MSc. Co-Authors: V. Manel(1), N. André-Obadia(2),C. Fischer(2),V. Cunin(3),C. Garin(3),R. Kohler(3),J. Bérard(3). Institution : Hospices Civils de Lyon (University hospitals of Lyon). 59 Boulevard Pinel, 69003 Lyon, France. 1) Department of Epilepsy, Sleep, and Paediatric Neurophysiology (HFME). 2) Department of Functional Neurology and Epileptology (Neurological Hospital). 3) Department of Paediatric Orthopaedic Surgery (HFME). Email: [email protected]. Phone: +33-613706785.
Introduction Combining multi pulse transcranial electrical stimulation motor (TES-mMEPs) and somatosensory evoked potentials (SEPs) is widely proven to be reliable for scoliosis surgery monitoring. However, its feasibility is sometime a big challenge despite advances in anesthesia. Predictors of successful feasibility of this method are needed. Here we investigated the feasibility rate of this method when mMEPs and SEPs are preoperatively recordable.
Methods The non invasive intraoperative monitoring (ni-IOM) method used in this study was described by MacDonald DB et al. 2003. We recruited 103 children undergoing posterior spinal fusion for scoliosis in our hospital between November 2005 and March 2009. Eligibility for the ni-IOM was established according to preoperative TMS- mMEPs and SEPs assessment. For neuromuscular scoliosis, maximum efforts were made to search and select the nerve which elicited the best SEPs response and the muscle providing the best TMS-mMEPs response. When no reliable preoperative TMS-mMEPs and SEPs could be recorded, a patient was considered non monitorable using ni-IOM, and excluded from this study. Feasibility, sensibility and specificity of the ni-IOM protocol were evaluated postoperatively.
Results Seventy six out of 103 children recruited (15 idiopathic scoliosis, 35 cerebral palsies, 28 myopathies, and 25 other neuromuscular scoliosis ) were eligible. Excluded children were mainly holders of severe neurological disabilities and those under 5 years old. Reliable TES-mMEPs and SEPs were successfully elicited intraoperatively in all the 76 selected subjects (feasibility 100 %). Intraoperative transient instrumentation related signal loss occurred in six cases. Rapid riposte actions permitted signal recovery within few minutes in all six cases. No post operative neurological deficit occurred. Both sensibility and specificity were 100%.
Conclusion Preoperative SEPs and mMEPs recordability strongly predicts successful feasibility of ni-IOM during scoliosis surgery. Therefore, preoperative assessment is useful in identifying scoliosis patients monitorable by intraoperative combined TES-mMEP and SEPs.
References 1. MacDonald DB, Al Zayed Z, Khoudeir I, Stigsby B. Monitoring scoliosis surgery with combined multiple pulse transcranial electric motor and cortical somatosensory-evoked potentials from the lower and upper extremities.Spine. 2003 Jan 15;28(2):194-203. 2. DiCindio S, Theroux M, Shah S, Miller F, Dabney K, Brislin RP, Schwartz D. Multimodality monitoring of transcranial electric motor and somatosensory-evoked potentials during surgical correction of spinal deformity in patients with cerebral palsy and other neuromuscular disorders. Spine. 2003 Aug 15;28(16):1851-5; discussion 1855-6. 3. Deletis V. Basic methodological principles of multimodal intraoperative monitoring during spine surgeries. Eur Spine J. 2007 Nov;16 Suppl 2:S147-52. Epub 2007 Jul 11. 4. Deletis V, Sala F. Intraoperative neurophysiological monitoring of the spinal cord during spinal cord and spine surgery: a review focus on the corticospinal tracts. Clin Neurophysiol. 2008 Feb;119(2):248-64. Epub 2007 Nov 28. Review. 5. Schwartz DM, Auerbach JD, Dormans JP, Flynn J, Drummond DS, Bowe JA, Laufer S, Shah SA, Bowen JR, Pizzutillo PD, Jones KJ, Drummond DS. Neurophysiological detection of impending spinal cord injury during scoliosis surgery. J Bone Joint Surg Am. 2007 Nov;89 (11):2440-9.
97 MOTOR MAPPING & MONITORING USING HIGH-FREQUENCY ELECTRICAL STIMULATION & EMG PICKUP
First Author-Presenter: Terrance M. Darcey, PhD, D.ABNM Dept of Neurology & Section of Neurosurgery, Dartmouth-Hitchcock Med Ctr, Lebanon NH, USA Phone/fax: 603.650.8402, 603.650.0458 Email: [email protected] Co-Authors: *BC Jobst, *VM Thadani, *GL Holmes, **RP Morse, ***DW Roberts, ***AC Duhaime Institution: *Dept of Neurology, **Dept of Pediatrics, ***Section of Neurosurgery Dartmouth-Hitchcock Medical Center, Lebanon NH, USA
Introduction In this paper, we describe a motor cortex mapping and a monitoring method that can be applied in the operating room under local or general anesthesia. The method is able to distinguish primary motor cortex (M1) from supplementary motor area (SMA) and internal capsule (IC) elements based on the nature of EMG responses.
Methods Stimulation is applied via a handheld probe and subdural electrodes. Stimuli are brief trains of constant-current, monophasic pulses repeated until motor responses are elicited or the maximum safe current reached. Local anesthesia is used when language functions are also at risk, whereas general anesthesia (TIVA no paralytic) is employed in cases with only motor risk. EMG from up to 16 muscles on the contralateral face, arm and leg are used, along with ipsilateral muscles when M1 and SMA need to be distinguished.
Results After craniotomy, the surgeons stimulate the cortical surface, locating M1and exploring the area overlying the area of planned resection. We then continuously monitor M1 responses stimulated via subdural electrodes, and the surgeons use the handheld stimulator to test the resection margins frequently as the operation proceeds. In 39 cases considered to have significant risk of motor function disruption due to location, resections were limited when cortical MEP signal loss was observed and by the detection of low threshold MEPs in the resection margins. This led to maximal resections with minimal residual tumor. In 4 cases with MEP signal loss at closing, 2 recovered fully, 1 partially and 1 had permanent deficit. In 2 cases with no MEP signal loss at closing, but IC elements detected in the tumor bed, there were transient deficits with full recovery.
Conclusion The described method appears to be an effective approach for motor system mapping and monitoring in awake and anesthetized patients.
References: None
98 POSTERIOR ROOT-MUSCLE REFLEXES: METHODOLOGICAL ASPECTS AND PRELIMINARY RESULTS IN HEALTHY SUBJECTS
Pérez-Fajardo G., Lladó-Carbó E., Araus-Galdós E., Climent-Perin A., Ulkatan S., Deletis V. Intraoperative Neurophysiology Monitoring Department. St. Luke's-Roosevelt Hospital. New York. NY
Introduction Posterior root-muscle reflexes (PRMR) are equivalent to the monosynaptic Hoffmann (H)-reflex but can be evoked in several muscles simultaneously. Evidence has been provided that monosynaptic PRMR are equivalent to the H-reflex. It has been shown that the PRMR and H-reflex of triceps surae (TS) are both elicited in the same afferents, but at different sites of the afferent reflex arc; proximal part of cauda equina and peripheral nerve respectively. The aim of this study is to obtain PRMR in healthy subjects in order to apply this method in the OR for spinal surgeries.
Material and Methods Subjects: 5 males and 5 females, aged between 20 to 39 years (mean 31.3) with a mean height of 170.9 cm Study protocol: Two square electrodes (5 by 5 cm) were placed in midline over interspinous space at L1 (cathode) and L3 (anode) vertebral spinal level.
Stimulation: Paired stimuli of identical parameters were used with an interstimulus interval of 50 ms, and duration of 0.5 ms. Stimulus intensity were increased until a steady PRMR responses had been elicited (mean intensity = 87 mA).
Recording: pair of disk (stick pad) recording electrodes were used for recording the CMAP from bilateral quadriceps (Q), hamstring (H), tibialis anterior (TA) and gastrocnemius (G) muscles.
Results: Mean intensity thresholds (mA) for PRMR were: RQ, 84.9; LQ, 87.9: RH, 79.4; LH, 83.5; RT, 81.9; LT, 85.7; RG, 84.4; LG 86.9. Mean latencies (ms): RQ, 12.7± 1.9; LQ 11.4 ± 0.8; RH, 13.2 ± 2.9; LH, 11.6 ± 1.1; RT 16.8 ± 3.0; LT 16.3 ± 2.8; RG, 17.1 ± 1.7; LG, 16.9 ± 1.5. Mean amplitudes (µV): RQ, 91.0 ± 80.4; LQ, 154.1 ± 148.4; RH, 404.1 ± 454.6; LH, 578.6 ± 504.9; RT 288.7 ± 250.6; LT 264.5 ± 218.7; RG 904.7 ± 421.4; LG 630.9 ± 392.4. In one healthy subject the PRMR in the LtH muscle was not elicited, whereas bilateral PRMR were elicited in the other muscles. The intensity required for eliciting and amplitude of recorded PRMR responses have great interindividual variability, while the latencies were more homogenous. (Table 1, Figure 1).
Muscle Quadriceps (Q) Hamstring (H) Tibialis Gastrocnemius (G) Anterior(TA) Mean R L R L R L R L Intensity 84.9 87.9 79.4 83.5 81.9 85.7 84.4 86.9 (mA) Latency 12.7± 1.9 11.4 ± 0.8 13.2 ± 2.9 11.6 ± 1.1 16.8 ± 3.0 16.3 ± 2.8 17.1 ± 1.7 16.9 ± 1.5 (ms) Amplitude 91.0 ± 154.1 ± 404.1 ± 578.6 ± 288.7 ± 264.5 ± 904.7 ± 630.9 ± (µV) 80.4 148.4 454.6 504.9 250.6 218.7 421.4 392.4
Table 1.
99
Figure 1. PRMR from the right and left quadriceps (Q), hamstring (H), tibialis anterior (TA) and gastrocnemius (G) muscles.
Conclusion: PRMR methodology has a great potential of use as a diagnostic tool in the pathology of cauda equina as well as a monitoring method during surgery on conus cauda as well as LS spinal cord. PRMR has potential to give more specific information of integrity of cauda equina than MEP and SEP.
References: Posterior root muscle reflexes elicited by transcutaneous stimulation of the human lumbosacral cord. Minassian K, Persy I, Rattay F, Dimitrijevic MR, Hofer C, Kern H. Muscle & Nerve. March 2007, pp327-336.
100 INTRAOPERATIVE NEUROPHYSIOLOGICAL MONITORING DURING SURGERY OF A GIANT THORACIC MENINGOCELE (GTM): CASE REPORT
Martínez – Martínez M. 1.; Martínez Agueros J. A. 2 ; Valduvieco Juaristi I. 2; Naranjo Gozalo S. 3; Maldonado Vega S.4, Gutierrez Gutierrez A.5 Ortiz Portal F.6 Clinical Neurophysiology Department 1 ; Spinal Cord Unit 2 ; Thoracic Surgery Department 3 ; Anesthesia Department 4 Radiology Department 5 Pneumology Department 6 Marqués de Valdecilla University Hospital, Santander. Spain
Introduction Intrathoracic meningocele is a rare pathology associated with neurofibromatosis type I in 60%-85% of cases. Surgery is indicated when large or symptomatic cysts are present. We describe the intraoperative neurophysiological monitoring (INM) results obtained during the surgery of a GTM.
Patient and Method A 39-year-old woman with family history of neurofibromatosis type I was referred for dyspnea on moderate exertion. Helical CT and MRI showed a small (4 cm) left-sided cyst, a giant (13x6.5 cm) right-sided thoracic meningocele with compressive effect over the upper lung lobe, and a severe kiphoescoliosis. Videothoracoscopy and costotransversectomy in the region of the giant meningocele were carried out. We performed continuous monitoring of motor evoked potentials (MEP) and somatosensory evoked potentials (SSEP) according to standard methods during the surgical procedure.
Results During the lesion excision, when the stalk was partially incised, a CSF leakage occurred. At that moment, we detected transitory loss of the left leg MEPs, probably due to a sudden displacement and trauma to the spinal cord. After the increase of the blood pressure and application of corticoids, we observed a partial recovery of left leg MEPs responses. Unfortunately, 15 minutes later, the progressive CSF leakage led to the complete loss of MEPs in both legs. Subsequently, both posterior tibial SSEP responses were also absent. The patient woke up with complete paraplegia. Postoperative MRI revealed a spinal cord infarct at the cervicodorsal junction.
Conclusion Surgeries for GTM are challenging. Despite the poor outcome in our patient, our results suggest that the application of INM techniques in this kind of surgeries: 1° provides valuable information about possible mechanisms of neural damage. 2°may be useful to prevent and predict neurologic deficits in some cases. To our knowledge, this is the first report with a focus on INM during GTM surgical procedure.
References: 1. de Andrade GC, Braga OP, Hisatugo MK, de Paiva Neto MA, Succi E,Braga FM. Giant intrathoracic meningoceles associated with cutaneous neurofibromatosis type I: case report. Arq Neuropsiquiatr 2003 Sep; 61 ( 3A): 677 – 681. 2. Dolynchuk KN, Teskey J, West M. Intrathoracic meningocele associated with neurofibromatosis: case report. Neurosurgery 1990 Sep; 27(3): 485-7.
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102 REDUCING RISK OF BITE INJURIES IN TRANSCRANIAL ELECTRICAL STIMULATION (TES) BY OPTIMIZING STIMULATION PARAMETERS
Hoebink Eric A MD1 ; van Hal Chantal MD2; de Kleuver Marinus MD PhD2; Racz Ilona2, Polak Bert2, Journée Louis H MD PhD2,3 From the Departments of 1 Orthopedics, Amphia Hospital Breda, 2 Orthopedics Sint Maartenskliniek Nijmegen and 3 Department of Neurosurgery, University Medical Center Groningen, the Netherlands. First Author Presenter: Eric A. Hoebink Institution: St. Maartenskliniek Nijmegen, The Netherlands Phone/fax: +31 6 15632898 Email: [email protected]
Introduction Transcranial electrical stimulated motor evoked potential monitoring (TES-MEP) during spinal surgery is a safe neuromonitoring technique. However TES induced movements can cause bite injuries in tongue and endotracheal tubes (MacDonald 2002). When TES movements are evoked by other than monitored muscles, one may expect that adjustments in stimulation paradigms and TES electrode montages may minimize movement while preserving quality of TES-MEP’s for monitoring. In this pilot study, TES evoked seismic evoked responses (SER) are studied at different stimulation settings to minimize jaw movements.
Methods In 7 patients, (3 m/ 4f), aged 22.9 (mean) ± 13.4 (SD) years undergoing corrective spine surgery, intra-operative TES-MEP was derived from 6 muscle groups while accelero transducers (Temec®) recorded SER at the lower jaw and three other locations on the body. TES parameters used in this study: n=1 and 5 pulses/train and electrode montages: Cz’-Fz, C3-C4 and C3-Cz. Measurement data were taken at intensities that were used for clinical monitoring. In an experimental model of bite injuries a proportional relationship between SER of the jaw and bite force is assumed by considering a spring constant of the bite block (figure 1).
Results Maximum acceleration was found at the jaw. At single pulse TES, the mean jaw SER remained about unaltered while at other locations the SER was reduced 3-16% from the jaw SER. Maximum SER amplitudes were at C3- C4 (148%) and C3-Cz (193%) montages.
Conclusion SER at the jaw was dominant and about independent on number of TES-pulses. An extracranial stimulation route, bypassing the cortico bulbar pathway, is most likely the main cause. Maximum values were found at C3/C4 electrodes montages. These are most closely located near the masseter and temporal muscles and therefore support the possibility of a dominant extracranial stimulation route to these muscles that generate bite force. The least jaw movement is at Cz – Fz TES.
References • MacDonald DB Safety of intraoperative transcranial electrical stimulation motor evoked potential monitoring. J Clin Neurophysiol. 2002 Oct;19(5):416-29.
Figure 1.
103 SUCCESSFUL LOCALIZATION OF THE BROCA AREA WITH SHORT-TRAIN PULSES INSTEAD OF ‘PENFIELD’ STIMULATION
First Author-Presenter: Hans Axelson Institution: Neuroscience, Clinical Neurophysiology, Uppsala University Hospital Phone/fax: +46 18 6113955 Email: [email protected] Co-Authors-Institution: Göran Hesselager and Roland Flink , Uppsala University Hospital
Introduction Direct electrical stimulation of functional cortical areas is a standard procedure in epilepsy and glioma surgery. Previous studies support that stimulation of the motor cortex with short train pulses is a less epileptogenic alternative to the 50-60 Hz ‘Penfield’ technique. While there seems to be a trend towards the use of short train stimulation (STS) instead of 50–60 Hz stimulation during motor mapping, there is little information on whether this technique is also useful for mapping out eloquent areas. In this case report, however, we present a patient with oligodendroglioma near the Broca area who had speech arrest from STS.
Methods Extraoperative electrical cortical stimulation via a subdural grid electrode was primarily performed to locate the Broca area. The cortex was stimulated with 1-3 second 50 Hz monopolar pulses. In addition, 1-2 Hz STS (anodal monopolar stimulation, 5 pulses, 0.5 pulse duration and 3 ms interpulse interval) was tested in those electrode locations that produced speech disturbance in the patient.
Results The patient had speech arrest from both types of stimulation techniques at three electrode positions (at the anatomical Broca area) during a naming task. The timing between the short (14.5 ms) train stimulation and the presentation of the naming objects seemed to be critical.
Conclusion This case report provides some evidence that direct electrical stimulation with short trains produces speech arrest in similar way as 50 Hz stimulation and may serve as a less epileptogenic technique for mapping eloquent areas.
References: 1. Penfield W, Boldrey E (1937) Somatic motor and sensory representation in the cerebral cortex of man as studied by electrical stimulation. Brain 1937;60:389–443. 2. Szelényi A, Joksimovic B, Seifert V. Intraoperative risk of seizures associated with transient direct cortical stimulation in patients with symptomatic epilepsy. J Clin Neurophysiol 2007;24(1):39-43. 3. Taniguchi M, Cedzich C, Schramm J. Modification of cortical stimulation for motor evoked potentials under general anesthesia: technical description. Neurosurgery 1993;32:219–226. 4. Tharin S, Golby A. Functional brain mapping and its applications to neurosurgery. Neurosurgery 2007;60(4) Suppl 2:185-202.
104 PRE-OPERATIVE NEUROLOGICAL STATUS AND D WAVE MONITORABILITY IN SURGERY FOR SPINAL CORD TUMORS
First Author-presenter: Alba Leon Jorba Institution: Department of Neurology, Hospital de Viladecans. Barcelona. Spain Phone: 660335046 Email: [email protected] Co-Authors-Institution: Vincenzo Tramontano, Giovanna Squintani, Paolo Manganotti, Francesco Sala- Intraoperative Neurophysiology Unit, Department of Neurosurgery, University Hospital. Verona. Italy.
Introduction D-wave monitoring is considered the most reliable neurophysiological technique to assess the functional integrity of the corticospinal tract during surgery for intramedullary spinal cord tumors (ISCTs). However, in about one third of patients with ISCTs rostral to the conus, D-wave is not recordable at the beginning of the surgery. This is usually explained as a desynchronization of the D-wave in patients with previous surgery, spinal cord irradiation or extensive ISCTs and cysts. Anecdotal reports suggest that D-wave monitorability decreases also with more severe neurological deficits, but the correlation between pre-operative neurological status and D-wave monitorability has not been further investigated.
Our goal was to correlate D-wave monitorability and pre-surgical functional status in patients with ISCTs.
Methods The pre-operative neurological status was graded I (best) to IV (worse) using the McCormick Scale. D wave was retrospectively analyzed in 166 patients operated on for ISCTs. It was obtained after single-pulse TES (0.5ms duration, intensity up to 200mA) and recorded with an epidural electrode inserted distally to the tumor.
Results In 28 patients, D wave was not monitored due to technical problems or tumor level caudal to T10-T11. 69% of the remaining 138 patients had a monitorable D wave before myelotomy. The monitorability rate was 81,1 % for patients in Mc Cormick grade I; 75,7% for those in grade II; 38,9% for those in grade III, and 25,2% for those in grade IV. This difference was statistically significant (Chi-square p<0.05).
Conclusion Besides desynchronization phenomena, D-wave monitorability is significantly limited by the preoperative motor status. In patients arriving to surgery with only mild motor deficits D wave is monitorable in about 80% of the cases. Given the critical value of D-wave monitoring in ISCT surgery, this is one more argument to encourage early diagnosis and surgery.
105 THE PREVENTION OF NEURAL COMPLICATIONS IN THE SURGICAL TREATMENT OF SCOLIOSIS: FROM WAKE UP TEST TO NEUROPHYSIOLOGICAL INTRAOPERATIVE MONITORING (IOM)
Pastorelli F. MD1,2, Di Silvestre M. MD3, Fini N. MD2, Pelosi M1, Greggi T. MD3, Bonarelli S. MD 4, Michelucci R. MD2, Toccaceli L. 4, Plasmati R. MD1,2 (1) Servizio di Neurofisiopatologia, Istituti Ortopedici Rizzoli, Bologna; (2) UOC Neurologia, Ospedale Bellaria, Bologna (3) Rep. Chirurgia del rachide, Istituti Ortopedici Rizzoli, Bologna; (4) Servizio di Anestesia e Terapia intensiva, Istituti Ortopedici Rizzoli, Bologna First Autor: Francesca Pastorelli UOC Neurologia, Ospedale Bellaria, Bologna, Italy +390516225348 [email protected] The study received no financial support. All authors have read and agreed with the content of this abstract submitted for the Second Congress of the International Society of Intraoperative Neurophysiology
Introduction Iatrogenic spinal cord injury is the most feared complication in scoliosis surgery. The importance of combined Somatosensory Evoked Potentials (SSEP) and Motor Evoked Potentials (MEP) monitoring during spine surgery is well known. We retrospectively evaluated the results of IOM in a large population of patients who underwent surgical treatment of the spine deformity.
Materials and Methods 172 patients underwent intraoperative monitoring of SSEPs and transcranial electrical stimulation MEPs (tce MEP) during surgical treatment of idiopathic (129), congenital (13) or syndromic (30) scoliosis. 106 patients (group 1) underwent only SSEP monitoring under Sevoflurane anaesthesia (end tidal concentration 0.8–1.6%). 66 patients (group 2) underwent combined SSEP and tce MEP monitoring under TIVA with Propofol infusion (6- 10mg/kg/h). Cortical SSEPs were recorded after stimulation of the median and posterior tibial nerves. TceMEPs were recorded from the abductor pollicis brevis (ABP) and from the tibialis anterior (TA) muscles. A relevant neurophysiological change (an alert) was defined as a reduction in amplitude (unilateral or bilateral) of at least 50% for SSEPs and/or for tceMEPs compared with baseline.
Results Group 1 The criteria for an alert were met during 14/106 (13,2%) procedures. Three patients demonstrated signal amplitude changes attributed to surgical manoeuvres (true-positive). One patient showed transient reduction of lower limb cortical SSEPs related to hypotension and awoke with paraparesis due to anterior spinal cord ischemia (false-negative). In 10 cases the alert was apparently unrelated to surgical manoeuvres or to pharmacological interventions and no postoperative neurologic deficits were noted (false-positive). Group 2 7/66 (10,6%) patients showed an alert related to hypotension in 2 cases and to surgical manoeuvres in 4 (true- positive). One patient with preoperative pathologic motor responses due to myelopathy showed the complete loss of MEPs during intervention with no neurologic sequelae (false-positive). The overall prevalence of postoperative neurologic deficit was 2,9% (5/172). Motor impairment resolved completely within three months after surgery in 4 patients. One patient developed irreversible paraparesis due to pedicle screw malpositioning. When combined SSEP and tce MEP monitoring was performed, the sensibility and specificity of IOM for sensorimotor impairment was 98% and 100% respectively.
Conclusions Combined SSEP and tce MEP monitoring must be regarded as the neurophysiological standard for intraoperative detection of emerging spinal cord injury during corrective spine surgery. Early detection provides the surgical team an opportunity to perform rapid intervention to prevent injury progression or possibly to reverse impending neurologic sequelae.
106 INTER- AND INTRA-PATIENT VARIABILITY OF FACIAL NERVE RESPONSE AREAS IN THE FLOOR OF THE 4th VENTRICLE
First Author – Presenter: Johannes Sarnthein Institution: UniversitätsSpital Zürich, Switzerland Phone: 0041 44 255 5672 Email: [email protected] Co-Author-Institution: Nadir Tissira - UniversitätsSpital Zürich Co-Author-Institution: Helmut Bertalanffy - UniversitätsSpital Zürich
Introduction The brainstem has a complex and dense anatomy and therefore the surgery of brainstem lesions requires precise localization of the surrounding healthy tissue. It is well known that the fibers of the facial nerve (CN VII) reach the surface of the rhomboid fossa at the level of the facial colliculus. However, the shape and size of the area where the facial nerve can be stimulated has not yet been systematically assessed.
Methods Over a period of 18 months, 20 patients were operated on for various brainstem and/or cerebellar lesions via the telovelar approach that gave wide access to the rhomboid fossa. Both facial colliculi were stimulated with the lowest current intensity that yielded a compound muscle action potential (CMAP). The sites of CMAP yield were marked in a coordinate frame referenced to the obex and the median sulcus. In this way a detailed functional map of the rhomboid fossa was constructed for each patient.
Results Lesions resected were 14 gliomas, 5 cavernomas, and 1 epidermoid cyst. In 19 of 40 colliculi, the CN VII response area reached the median sulcus. Over all patients, the distance from the obex to the caudal border of the response area ranged 8-27mm (median 16mm). The rostrocaudal length of the response area ranged 2-15mm (median 5mm). In individual patients, the rostrocaudal lengths of left and right response areas showed ratios between 1:1 and 3:1 (median 1.4:1).
Conclusions The CN VII response area showed an unexpectedly large variability in size and position even in cases with larger distance between the facial colliculus and the lesion. Lesions located close to the facial colliculus markedly distorted the response area. This documentation of the variability in CN VII response area facilitates the assessment of safe entry zones to the brainstem and enhances the safety in neurosurgical interventions.
107 THE BROCA'S CONTRIBUTION TO OUR KNOWLEDGE OF LOCALIZATION OF SPEECH PRODUCTION
Mario Tudor MD, MSc Department of Neurosurgery, Clinical Hospital Split, 21000 Split, Spinčićeva 1, Croatia Phone/fax: ++385 (021) 556 112; GSM 098 321783 Email: [email protected] Co-Authors-Institution: Vedran Deletis, MD, PhD, School of Medicine, Šoltanska 2, 21000 Split, Croatia
In current times of successful monitoring of newly discovered neurophysiological cortico-cortical connections between the Broca's area and orofaryngeal motor cortex (Greenlee et al.) and Broca's area and the Wernicke's auditory field (Matsumoto et al.) in the dominant hemisphere or vice versa, it is interesting to look back and remind ourselves how Broca’s discovery, became the cornerstone of our contemporary knowledge in cerebral localization beginning with the speech centre.
On the basis of Galvani’s experiments, Volta discovered the electrical pile in 1800 and a decade later, Rolando wrote about the electrical nature of the complex nerve-muscle. Broca, in the 2nd half of the 19th century, was of course, not familiar with the scientific (electrophysiological) methodology of our age as hemispheres back then were divided into cerebral lobes (Gratiolet). But Broca happened to live in an opportune time when a very controversial, but fruitful, discussion was developing among scientists, who were beginning to ask themselves on the location of the speech centre. Surprisingly enough, the unconventional chief of the Hôpital de la Charité in Paris, Bouillaud, offered 500 francs to whoever could demonstrate that speech disorders were not related to the frontal lobe. Bouillaud and Aubertin, his son in law, were named Gall’s “blind followers”, the founder of pseudoscience phrenology. Flourens, Bonaparte’s secretary of science and education, concluded, after investigating Gall’s theories, that the brain functioned as a whole– a holistic view as there ‘were no circumscribed functionally specialized cortical centers”. Such ‘erroneous’ conclusion, presented by the greatest authority of that time, became the scientific doctrine, which lasted for half a century until it was disapproved by Broca’s discovery.
Broca was appointed surgeon in Bicêtre Hospital in January the 1st 1861. He was 37 years of age then. Three months later, on the 4th of April 1861, in front of the Anthropological Society of Paris, Auburtin described an articulatory organ and a cerebral centre that he believed resided in the left frontal lobe. Auburtin’s claim was based entirely on clinical (Galls and Bouillaud’s) observations. Broca obviously heard Auburtin’s claims and was intrigued by the topic. Shortly thereafter, Broca published his paper in the Bulletin de la Société Anthropologique in which he related the destruction of the left frontal lobe to aphasia. Leborgne, also know as ‘Tan’, the patient who made Broca famous, was admitted to the hospital in 1840 when he was 30 years old. Tan died on April 17th 1861 (21 years after admission!) because of the widespread gangrene in the hip region. The following day, Broca presented the autopsy findings (macroscopic and without brain cuts!?) before the society and suggested that a softening of Tan’s brain in the third left frontal convolution was responsible for his speech disturbance. The next aphasic patient was M. Lelong. In Broca’s words, “The integrity of the third frontal convolution seems indispensable to the exercise of the faculty of articulate language.” Broca himself, although not fully aware of the historical importance, made the first step towards cerebral localization in spite of strong opposition (Flourens, Marie etc) by the establishment.
Thereafter in 1870 Fritsch and Hitzig referred on the electrical irritability of the nervous tissue in animals, and Bartholow in man. In 1874, Wernicke published his book Der aphasische Symptomencomplex“, describing sensory aphasia. Ferrier, together with Jalo (neurosurgeon), drew up the localization map in the monkey. Lichtheim described the importance of conductive fibers and came up with the connection theory between hearing and speaking. Dejerine pointed out in 1891/92 the importance of the pathways connecting visual cortex with Wernicke's area (alexia, dyslexia) – the problem of seeing and reading words. Foerster, and later his pupil Penfield, together with Jasper, Rasmussen and Boldrey, performed electrical cortical stimulation in awaken patients during numerous neurosurgical procedures, came up with the cortical map with motor and sensory homunculus in the central region. Geschwind (language theory) and other investigators (Amounts) eventually made numerous contributions to the field (citoarhitectonic, genetic, connections etc.)
In the modern light of the mirror neurons’ theory (Rizolatti-Arbib) and useful imitation in language development (“within our grasp”) (Jacoboni), and the idea that the Broca’s area, or its small part, represents a kind of “supramodal hierarchical processor” (not existing in other species) that controls the motor and premotor cortex for
108 speech production, one can just admire Broca’s determination when proclaiming “nous parlons avec le hemisphere gauche.” occurred prior to Fritsch and Hitzig, Bartholow, Wernicke, Dejerine, Ferrier, Penfield- Rasmussen’s works on cerebral localization and, above all, before the idea of handedness/hemispheric dominance.
It is astonishing for a researcher as Broca, who was not equipped with modern electrophysiological armamentarium, to realize such a discovery with a simple clinico-pathological correlation.
References 1. Apuzzo MLJ, Liu C, Sullivan D, Faccio R: Surgery of the Human Cerebrum. A Collective Modernity. Clinical Neurosurgery, Volume 49, Chapter 4; Lippincott Williams and Wilkins, 2002. 2. Broca P. Remarques sur le siège de la faculté du langage articulé, suivies d'une observation d'aphémie. Bulletin de la Société Anatomique, 1861c, tome XXXVI: 330-357. 3. Broca P. Sur le principe des localisations cérébrales. Bulletin de la Société d"Anthropologie. 1861a, tome II:190-204. 4. Broca P: Perte de la parole, ramollissement chronique et destruction partielle du lobe antérieur gauche. [Sur le siège de la faculté du langage.]. Bulletin de la Société d"Anthropologie. 1861b:(9)235-238. 5. Critchley M. The Citadel of the Senses, Raven Press, New York 1986. 6. Ferrier. D.: The Functions of the Brain. London: Smith, Elder. 1876. 7. Fritsch G, Hitzig E. Über die elektrische Erregbarkeit des Grosshirns. Archiv für Anatomie, Physiologie, und wissenschaftliche Medicin, 300–32. 1870. 8. Geschwind N. The Organization of the Language and the Brain. Science 1970;170:940-944. 9. Greenlee JDW, Oya H, Kawasaki H, Volkov IO, Kaufman OP, Kovach C, Howard MA, Brugge JF. A functional connection between inferior frontal gyrus and orofacial motor cortex in human. J Neurophysiol 2004;92:1153-1164. 10. Jackson JH. A study of convulsions. Transactions of the St. Andrews medical graduate's association, 1870. vol III. Reprinted in Taylor J (ed): Selected writings of John Hughlings Jackson. New York, Basic Books, Inc., 1958. 11. Matsumoto R, Nair DR, LaPresto E, Najm I, Bingaman W, Shibasaki H, Luders HO. Functional connectivity in the human language system: a cortico-cortical evoked potential study. Brain. 2004 Oct;127(Pt 10):2316-30. 12. Penfield W, Rasmussen Th. The Cerebral Cortex of Man. Macmillan, New York 1957. 13. Rolando L. Saggio sopra la vera struttura del cervello dell’uomo e degl’animali e sopra le funzioni del sistema nervoso. Sassari, Nella stamperia da S.S.R.M. Privi-legiata, 1809. reprinted as Rolando L. Saggio sopra la vera struttura del cervello dell’uomo e degl’animali e sopra le funzioni del sistema nervoso. Bologna, Arnaldo Forni Editore, 1974. 14. Schiller F. Paul Broca, Explorer of the Brain, Oxford University Press, New York 1992. 15. Wernicke C: Der aphasische Symptomenkomplex; Eine psychologische Studie auf anatomischer Basis. Max Kohn und Weigart, Wroclaw 1874. 16. Geschwind, N. Language and the Brain. Scientific American 1972;226 (4):76-83.
109 MOTOR MAPPING FINDINGS AND CORRELATION WITH DTI DATA DURING SURGICAL REMOVAL OF LESIONS INVOLVING MOTOR AREA OR PATHWAYS
Enrica Fava, Giuseppe Casaceli, Francesco Portaluri, Antonella Castellano, Andrea Falini, Lorenzo Bello First Author Presenter: Enrica Fava Institution: Neurosurgery, Università degli Studi di Milano, Milano, Italy Phone/fax: 390255035502; 390259902239 ; Email: [email protected] Co-Authors-Institution: Giuseppe Casaceli, Francesco Portaluri, Lorenzo Bello – Neurosurgery, Università degli Studi di Milano Co-Authors-Institution: Antonella Castellano, Andrea Falini- Neuroradiology, Ospedale San Raffaele, Milano
Introduction Surgery of lesions involving M1 or the corticospinal tract (CST) requires their intraoperative identification to guide resection and preserve functional integrity. The brain mapping technique allows performing such identifications. DTI-FT reconstructs tracts, including CST. This work reports the correlation of neurophysiological findings obtained during removal of lesions located in or within M1 or CST, and DTI data.
Methods the correlation was performed on 230 patients with gliomas. The neurophysiology includes mapping with Direct Electrical Stimulation (DES, bipolar and monopolar) and monitoring (EEG, ECoG, MEP) procedures. Motor responses were evaluated by multichannel-EMG. DTI-CST (3T DTI maps) was avalaible in all patients, and in 30 also with different FA thresholds. DTI-CST was loaded onto the neuronavigation system and available intraoperatively for correlation with DES data.
Results Motor responses were registered in all patients. They appeared as focal when CST was stimulated close to the surface, or affecting multiple muscles with deep stimulation. The near-cortical stimulation induced overt movements, deep subcortical stimulation induced muscle activations detected by EMG. In more than 95% of patients a good correlation was observed between DTI FT data and DES findings. When CST was highly infiltrated, DTI FT failed to show fibers in the upper part of CST, where DES induced responses. In such cases, bipolar stimulation didn’t evoke responses, which in turn were induced by monopolar stimulation. Monopolar stimulation evoked responses in a large cortical and subcortical area, even faraway from CST: indeed, bipolar stimulation allowed a more precise localization of CST, well correlated with DTI-CST. FA varied among the same area of the tumor and in its deep portion, accordingly with the degree of infiltration of tract.
Conclusion DTI-CST data showed a good correlation with DES findings. DES techniques, bipolar and monopolar, evoked motor responses in all patients. The combined used of DES and DTI-FT allowed to effectively and safely trace the tract.
110 SUPPLEMENTARY MOTOR AREA CONNECTIVITY REVEALED BY SUBCORTICAL MAPPING AND DTI FT FINDINGS
Giuseppe Casaceli, Enrica Fava, Giulio Bertani, Antonella Castellano, Andrea Falini, Lorenzo Bello First Author: Presenter: Giuseppe Casaceli Institution: Neurosurgery, Università degli Studi di Milano, Milano, Italy; Phone/fax: 390255035502; 390259902239 Email: [email protected] Co-Authors-Institution: Enrica Fava, Giulio Bertani, Lorenzo Bello – Neurosurgery, Università degli Studi di Milano Co-Authors-Institution: Antonella Castellano, Andrea Falini- Neuroradiology, Ospedale San Raffaele, Milano
Introduction This work studies the connectivity of the SMA and its clinical significance.
Methods 52 patients with gliomas (42 low, 10 high grade) had awake surgery with the aid of subcortical mapping. DTI-FT (CST, SMA, SLF, IFO) was available during surgery. Subcortical mapping was performed with multichannel- EMG, ECoG, MEP recordings. The type, number, and location of each subcortical response was registered into the neuronavigation system. These findings were retrospectively processed to reconstruct the course of subcortical tracts in DTI-FT maps. Onset and duration of SMA syndrome, extent of SMA resection were correlated with subcortical and DTI data. Reconstruction was performed by using deterministic and probabilistic approaches.
Results Motor responses (mainly contralateral, less ipsi or bilateral) were shown in all patients, sensory (numbness or paresthesias, subjective experience of movement without overt motor activity) in 40%, visceral (inspiration/expiration swallowing, tachycardia) in 45%, motor negative responses in 5%, and speech related disorders (vocalization, semantic or phonemic paraphasias) in 60%. Motor and sensory responses showed an anterior to posterior somatotopic distribution (from eye to leg). Visceral responses were evoked by stimulation of the more anterior portion of the SMA, close to the preSMA where also negative motor responses were induced. Ipsilateral motor responses were located more laterally to the fibers inducing contralateral responses. Correlation with DTI FT post processing data showed that SMA contributed to CST, was connected with ipsilateral M1, contralateral SMA, but not to contralateral M1. SMA was connected with ipsilateral S1, and with the thalamic VL and VPL nuclei. Ipsilateral motor or sensory fibers could be resected without sequelae. Postoperative SMA syndrome correlated with the resection of contralateral fibers. Permanent motor deficit correlated with resection of leg contralateral fibers that were mixed with those from M1. Resection of contralateral sensory fibers occasionally resulted in transient postoperative sensory deficits.
Conclusions SMA has complex motor and sensory connections. Intraoperative identification of such connections guide surgical removal and predicts the onset of postoperative deficits
111 CLINICAL AND NEUROPHYSIOLOGIC PHENOMENA DURING SPEECH ARREST
Rogić M.1, Fernández-Conejero I. 2, Ulkatan S.3, Szelenyi A.4, Deletis V.1,3 1 Department for Neuroscience, School of Medicine, University of Split, Croatia 2 Department of Intraoperative Neurophysiology, University Hospital Bellvitge, Barcelona, Spain 3 St. Luke's-Roosevelt Hospital, Institute for Neurology and Neurosurgery, New York, USA 4 Department of Neurosurgery, Johann Wolfgang Goethe University, Frankfurt, Germany
The electrical stimulation of eloquent cortical areas produces either an activation of neuronal circuitry or interference with ongoing function. One of the examples of interference with ongoing function is speech arrest induced by electrical stimulation of motor speech related cortical areas.
Speech arrest can be induced by stimulation of motor speech related cortical areas in: (a) patients with implanted grid electrodes for presurgical evaluation of epileptic foci, (b) patients during awake craniotomy, (c) healthy subjects or patients by transcranial rapid-rate magnetic stimulation.
The prerequisite for inducing speech arrest is an awake patient or healthy subject actively participating in a speech task (i.e. counting task). The usual stimulating rate for inducing speech arrest is 50-60 Hz (Penfield and Boldrey, 1937; Rasmussen and Milner, 1975). Recently, speech arrest was obtained by applying a short-train of high frequency stimuli (Axelson et al., 2009; Fernandez-Conejero, 2009).
Speech arrest during a counting task can be induced by the stimulation of three distinctive motor speech related cortical areas (Figure 1): (1) Broca area posterior part of inferior frontal gyrus (Rasmussen and Milner, 1975; Penfield and Roberts, 1959; Ojemann and Whitaker, 1978; Ojemann, 1979; Ojemann and Mateer, 1979; Lesser et al., 1984; Quiñones-Hinojosa et al., 2003; Bello et al., 2007; Sanai et al., 2008), (2) Negative motor areas (Lüders et al., 1995; Mikuni et al., 2006): (a) supplementary negative motor area (SNMA); (b) primary negative motor area (PNMA), located immediately in front of the primary motor face area, (3) Primary motor cortex (M1) for oro-pharyngeal-laryngeal muscles (Rasmussen and Milner, 1957).
Speech arrest during a counting task induced in different motor speech areas has the following clinical features: (1) Broca area; Speech arrest without simultaneous motor responses in oro- pharyngeal-laryngeal muscle group. During speech arrest the subject is able to execute voluntary tongue movement (i.e. wiggling from side to side). (2) Negative motor areas; Speech arrest without simultaneous motor responses in oro- pharyngeal-laryngeal muscle group. During speech arrest the subject is not able to execute voluntary tongue movement (i.e. wiggling from side to side). (3) Primary motor cortex (M1) for oro-pharyngeal-laryngeal muscles; Speech arrest with simultaneous motor response in oro-pharyngeal-laryngeal muscle group. During speech arrest the subject is not able to execute voluntary tongue movement (i.e. wiggling from side to side).
Speech arrest during a counting task of different motor speech areas has the following neurophysiologic features: (1) Broca area; Speech arrest with presence of long latency response in laryngeal muscles (Deletis et al., 2008), (2) Negative motor areas; Speech arrest with electrical silence in laryngeal muscles, (3) Primary motor cortex (M1) for oro-pharyngeal-laryngeal muscles; Speech arrest with a short latency response in laryngeal muscles (Amassian et al., 1987; Ertekin et al., 2001; Rödel et. al., 2004; Deletis et al., 2009).
Speech arrest during a counting task, produced by stimulation of motor speech related areas, is not easy to distinguish only on the basis of their clinical features. A new achievement in the neurophysiologic markers of these three areas: Broca’s area, negative motor areas and primary motor cortex, could significantly contribute to their intraoperative anatomical and functional separation. Furthermore, neurophysiologic markers can give us new insight into speech and language physiology.
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Figure 1. Anatomical localization of motor speech related areas of the frontal cortices of the left hemisphere. Electrical stimulation of those areas produces speech arrest during counting task. 1= Supplementary negative motor area (SNMA); 2 = Primary negative motor area (PNMA); 3 = Broca’s area; 4 = Primary motor cortex
References ■ Amassian, V.E., Anziska, B.J., Cracco, J.B., Cracco, R.Q., Maccabee, P.J. (1987). Focal magnetic excitation of frontal cortex activates laryngeal muscles in man. Physiological Society 41P. ■ Axelson, H., W., Hesselarger, G., Flink, R. (2009). Successful localization of the Broca area with short-train pulses instead of ‘Penfield’ stimulation. Seizure. 374-375. ■ Bello, L., Gallucci, M., Fava, M., Carrabba, G., Giussani, C., Acerbi, F., Baratta, P., Songa, V., Conte, V., Branca, V., Stocchetti, N., Papagno, C., Gaini, S.M. (2007). Intraoperative subcortical language tract mapping guides surgical removal of gliomas involving speech areas. Neurosurgery.60:67-82. ■ Deletis, V., Ulkatan, S., Cioni, B., Meglio, M., Colicchio, G., Amassian, V., Shrivastava, R. (2008). Responses elicited in the vocalis muscles after electrical stimulation of motor speech areas. Rivista Medica. 14:159-165. ■ Deletis,V., Fernandez-Conejero, I., Ulkatan, S., Costantino, P. (2009). Methodology for intraoperatively eliciting motor evoked potentials in the vocal muscles by electrical stimulation of the corticobulbar tract. Clinical Neurophysiology. 120:336- 341. ■ Ertekin, C., Turman, B., Tarlaci, S., Celik, M., Aydogdu, I., Secil, Y., Kiylioglu, N. (2001). Cricopharyngeal sphincter muscle responses to transcranial magnetic stimulation in normal subjects and in patients with dysphagia. Clinical Neurophysiology. 112:86-94. ■ Fernandez-Conejero, I., 2009, personal communication. ■ Lesser, R.P., Lϋders, Dinner, D.S., Hahn, J., Cohen, L. (1984). The location of speech and writing functions in the frontal language area. Brain. 107:275-291 ■ Lϋders, H.O., Dinner, D.S., Morris, H.H., Wyllie, E., Comair, Y.G. (1995). Cortical electrical stimulation in humans, the negative motor areas. Ed : Fahn, S., Hallett, M., Lϋders, H.O., Marsden, C.D. Negative motor phenomena. Advances in Neurology, 67. Lippincott-Raven Publishers, Philadelphia. ■ Mikuni, N., Ohara, S., Ikeda, A., Hayashi, N., Nisheda, N., Taki, J., Enatsu, R., Matsumoto, R., Shibasaki, H., Hashimoto, N. (2006). Evidence for wide distribution of negative motor areas in the periorolandic cortex. Clinical Neurophysiology. 117:33-40. ■ Ojemann, G., Whitaker, H.A. (1978). Language localization and variability. Brain and language. 6:239-260. ■ Ojemann, G., Mateer, C. (1979). Human language cortex: localization of memory, syntax, and sequential motor-phoneme identification systems. Science. 205:1401-1403. ■ Ojemann, G. (1979). Individual variability in cortical localization of language. Journal of Neurosurgery. 50:164-169. ■ Penfield, W., Boldrey, E. (1937). Somatic motor and sensory representation in the cerebral cortex of man as studied by electrical stimulation. Journal of Neurology. 60:389-443. ■ Penfield, W., Rasmussen, T. (1957). The cerebral cortex of man. A clinical study of localization of functions. The Macmillan Company. New York. ■ Penfield, W., Roberts, L. (1959). Speech and Brain Mechanisms. Princeton Univ. Press, Princeton. ■ Quiñones-Hinojosa, A., Ojemann, S.G. Sanai, N., Dillon, W.P., Berger, M.S. (2003). Preoperative correlation of intraoperative cortical mapping with magnetic imaging landmarks to predict localization of Broca area. Journal of Neurosurgery.99:311-318. ■ Rasmussen, T., Milner, B. (1975). Clinical and surgical studies of the cerebral speech areas in man. Ed: Zülch, K.J., Creutzfeldt, O., Galbraith, G.C. Cerebral localization. An Otfrid Foerster Symposium. Springer-Verlag. Berlin. 238-257. ■ Rödel, R.M.V., Olthoff, A., Tergau, F., Simonyan, K., Kraemer, D., Markus, H., Kruse, E. (2004). Human cortical motor representation of larynx as assessed by transcranial magnetic stimulation (TMS). The Laryngoscope. 114:918-922. ■ Sanai, N., Mirzadeh, Z., Berger, M.S. (2008). Functional outcome after language mapping for glioma resection. The New England Journal of Medicine. 358:18-26.
113 UTILITY OF SOMATOSENSORY AND MOTOR EVOKED POTENTIALS DURING CAROTID ENDARTERECTOMY
Lladó-Carbó E., Pérez-Fajardo G., Araus-Galdós E., Ulkatan S., Deletis V., Lantis J.*, Todd G.*, Benvensity A.* Intraoperative Neurophysiology Monitoring Department, St. Luke's-Roosevelt Hospital. New York, NY * Vascular Surgery Service. St.Luke’s-Roosevelt Hospital. New York, NY
Introduction Intraoperative neurophysiologic monitoring (IOM) during carotid endarterectomy under general anesthesia with Electroencephalography (EEG) and Cortical Somatosensory Evoked Potentials (CSEP) is gaining widespread use. Their sensitivity for predicting brain ischemia during carotid cross-clamp is estimated to be around 90%. The sensitivity of CSEP and Motor Evoked Potentials (MEP) use in combination during carotid endarterectomy has not been studied, yet.
Objective To analyze intraoperative changes in parameters of CSEP and MEP during carotid endarterectomy and to correlate with postoperative neurologic outcome
Material and methods Intraoperative data from 138 patients (100 male and 38 female), collected from 2005 to 2009, have been retrospectively analyzed. Age range is 48-92 years (mean age 71.2 SD +/-10). Surgery has been performed by a team of 3 vascular surgeons using the same operative technique (femoral vein graft, no shunting, unless indicated by IOM). CSEP (ipsilateral median / contralateral median and ulnar nerve) and (Rt / Lt posterior tibial nerve), as well as MEP (ipsilateral APB / contralateral APB and extensor digitorum) under T.I.VA., were collected.
Results Eleven patients (7.9%) showed intraoperative changes in the parameters of monitored modalities. CSEP and MEP changes were observed in 4/11 patients, pure MEP changes in 1 patient and CSEP changes in 10/11 patients. In all of them changes occurred after the clamp placement. All CSEP changes (> 50% amplitude decrement) in the contralateral median/ulnar nerve were detected within 40 seconds and 5 minutes after the clamp placement. Shunt was placed in 3.6% of all the patients (45% of those with intraoperative changes). All shunted patients had carotid stenosis at non-operated side. From all shunted patients 80% of them had changes in MEP parameters following clamp placement. After shunt application all changes in the parameters of MEP and/or CSEP returned to the baselines values and the patients didn’t show motor or sensory postoperative deficit, except one that showed pure transient motor hemiplegia.
Conclusion A combination of CSEP and MEP during carotid endarterectomy allows for one additional modality in IOM that can prevent motor deficits and diminishes morbidity during the procedure. We suggest that CSEP and MEP should be combined during carotid endarterectomy. A relative ischemia in the irrigation field of perforators for corticospinal tract in capsula interna could be a possible explanation for post operative “pure transient motor hemiplegia”, which occurred in one patient with changes in MEPs only.
Possible explanation for only changes in MEPs parameters, without changes in CSEP parameters, occurred in one patient, and resulting in transient hemiplegia, might be derived from a relative ischemia in the irrigation field of perforators for corticospinal tract in capsula interna resulting in postoperative “pure transient motor hemiplegia”.
114 NEUROMODULATION EFFECT AFTER CHRONIC ELECTRICAL STIMULATION OF SENSORIMOTOR CORTEX IN RATS
First Author-Presenter: Katsunori Shijo Institution: Division of Neurosurgery, Department of Neurological Surgery, and Division of Applied System Neruoscience, Department of Advanced Medical Science, Nihon University School of Medicine –Tokyo Phone :(+81)-3-3972-8111(ext.2231) FAX:(+81)-3-3554-0425 Email: [email protected] Co-Authors-Institution: Kazutaka Kobayashi, Akiko Yamashita, Hideki Oshima, Chikashi Fukaya , Takamitsu Yamamoto, Yoichi Katayama- Division of Neurosurgery, Department of Neurological Surgery, and Division of Applied System Neruoscience, Department of Advanced Medical Science, Nihon University School of Medicine
Introduction Motor cortex stimulation (MCS) has been used as a treatment for intractable pain and its clinical benefits have been confirmed. However, the mechanisms underlying the effects remain unclear. It has been speculated that electrical stimulation of the cerebral cortices could induce a functional reorganization and change in the neurocircuitry. In the present study, neuroplasticity induced by chronic sensorimotor cortex stimulation was investigated experimentally based on c-fos expression.
Methods The experimental animals employed were 20 adult male Wistar rats. A quadripolar stimulation electrode (2 mm wide, 5 mm long) was positioned over the sensorimotor cortex. We examined the functional activation of the cerebral cortex and related nuclei in response to chronic sensorimotor cortex stimulation for 2 months using c-fos immunopositivity as a marker for neural activation.
Results The following important findings of this were obtained. (1) c-fos was significantly expressed immediately after the stimulation as compared to the control. (2) Such c-fos expression underwent a time-dependent change. It generally became extensive over the cerebral cortices and deep brain structures in association with the duration of stimulation. (3) c-fos was expressed not only on the stimulation side, but also within the contralateral cerebral hemisphere. After 2 months, a higher density of c-fos-immunopositive cells was noted on the contralateral side to the stimulation as compared to the stimulation side.
Conclusions Changes in c-fos expression induced by long-term sensorimotor cortex stimulation indicate the existence of a time-dependent neural plasticity in various regions of the brain. It has been speculated that the construction of an abnormal network in the upper part of a deafferentation site may be associated with the cause of deafferentation pain. Chronic MCS could exert effects to modulate such an abnormal neural network.
115 TRANSCORTICAL SENSORY APHASIA CAUSED BY SUBCORTICAL LESION OF MIDDLE FRONTAL GYRUS: ISSUES ON CORTICAL MAPPING AND AWAKE SURGERY
First Author-presenter: Chikashi Fukaya Institution: Department of Neurological Surgery and Division of Applied system Neuroscience, Nihon University School of Medicine, Tokyo, Japan Phone / fax: 81-3-3972-8111 (ext 8224) / 81-3-3554-0425 Email: [email protected] Co-Authors-Institution: Koichiro Sumi, Otaka Toshiharu, Shijo Katsunori, Nagaoka Takafumi, Kazutaka Kobayashi, Oshima Hideki, Takao Watanabe, Takamitsu Yamamoto, Yoichi Katayama - Department of Neurological Surgery and Division of Applied system Neuroscience, Nihon University School of Medicine, Tokyo, Japan
Introduction It has been reported that transcortical sensory aphasia (TCSA) is caused not only by lesions of the temporal lobe but also those of the frontal lobe. Recently, some researchers have reported that TCSA is associated with the dysfunction of the working memory localized in the middle frontal gyrus. The precise cortical region associated with TCSA and the mechanism underlying this disorder are, however, still unclear. In this report, we discuss the associated cortical region and the mechanism underlying TCSA and the strategy of physiological mapping during the surgery of a tumor located close to such an area on the basis of our experience.
Subjects and Methods Our subjects were 49 patients who underwent removal of a tumor located in the frontal lobe by awake craniotomy and/or grid electrode implantation. None of the patients had severe disturbance of language function preoperatively. We performed extraoperative cortical mapping using a subdural grid electrode in 21 patients and intraoperative cortical mapping during awake surgery in 32 patients. Only four patients adapted to both of the cortical mapping procedures.
Results and Discussion Evident disturbance of language as evaluated by the Japan standard aphasia examination was noted in six patients postoperatively. Two of the six patients showed TCSA manifesting a high-degree disturbance of language understanding with preservation of repetition. The removed tumor was mainly located in the middle frontal gyrus in those two patients. We restricted cortical evacuation only to the area that did not show any response induced by cortical mapping. In one of the patients, we found the subcortical lesion causing the symptom during the awake craniotomy. Postoperative delayed response task was injured in both of the patients and disturbance of working memory was suspected. The tumor location in both patients appears to be close to area 46. We considered that TCSA was caused by the injury of subcortical fibers from area 46. Neither awake craniotomy with the naming task nor the cortical mapping with subdual grid electrode implantation seemed to prevent the occurrence of such a type of aphasia.
116 THE IMPACT OF INTRAOPERATIVE NEUROPHYSIOLOGICAL MONITORING IN SPINAL CORD ASTROCYTOMA-SURGERY
Grossauer S., Tramontano V., Sqintani G., Faccioli F., Bricolo A., Sala F. Intraoperative Neurophysiology Unit, Dept. of Neurosurgery, Universitiy Hospital, Verona, Italy
Objective While the literature supports the role of intraoperative neurophysiological monitoring (INM) in intramedullary spinal cord tumor (ISCT) surgery, it remains unclear whether different histotypes of ISCT benefit of INM to a different extend. We therefore retrospectively analyzed the functional and neurooncological outcome in a series of spinal cord astrocytomas operated on under INM assistance.
Methods Between 2001 and 2008 32 patients underwent 34 surgeries for SCA. The extend of surgical resection was judged by the surgeon`s intraoperative impression and by postoperative magnetic resonance imaging (MRI). Multimodal INM included Somatosensory Evoked Potentials (SEPs) and transcranially elicited spinal (D-wave) and muscle (mMEPs) motor evoked potentials. Functional status was assessed preoperatively, postoperatively and at follow- up using the McCormick scale.
Results Six patients are lost to follow up. At a mean follow-up of 61 months (9-109 months) 14 patients are alive and all but one are progression free after gross total (n=3), subtotal (n=6) and partial (n=4) tumor removal. One patient was operated twice for symptomatic tumor recurrence.
Twelve patients that harboured high grade astrocytomas (WHO grade III and IV) deceased during the follow-up period with a mean postoperative survival of 13.3 months (7-25 months).
Monitorability in 34 surgeries was 94% for mMEPs, 91% for SEPs and 59% for D-wave.
In 6 patients neurophysiological data (MEP deterioration) either alone or in combination with intraoperative findings (hard tumor texture, neurovegetative disorders, abcense of a clear cleavage plane) prompted to stop surgery.
At the follow-up 79% of the patients showed either unchanged or improved McCormick grade compared to preoperatively.
Conclusions In SCA, the neurooncological outcome mainly depends on tumor grade. Long term progression free survival can be obtained in the vast majority of patients with low-grade astrocytomas even after subtotal tumor removal. Long term functional outcome depends mainly on the preoperative neurological status, emphasizing the need of an early diagnosis and therapy. When surgery is tailored according to INM data preoperative neurological functions can be preserved in most patients.
117 HOW RELIABLE IS INTRAOPERATIVE IMAGING OF CORTICOSPINAL TRACT IMAGING ON MR?
First Author-Presenter: Svatopluk Ostrý Institution: Dept. of Neurosurgery, Charles University in Prague – Prague, Czech Republic Phone/fax: +420-973202963 Email: [email protected] Co-Authors-Institution: David Netuka- Dept. of Neurosurgery, Charles University in Prague Daniel Hořínek- Dept. of Neurosurgery, Charles University in Prague
Introduction Identification of both motor strip and corticospinal tract (CST) by cortical and subcortical stimulation respectively are well established intraoperative monitoring techiques. Intraoperative corticospinal tractography in MRI is a new imaging technique. Goal of this study is to determine intraoperative CST imaging accuracy confirmed by cortical and subcortical stimulation.
Material and Methods 11 patients (2 males, 9 females, 34-68 years old) with no motor deficit were operated on for tumour in rolandic region or in the CST vicinity in white matter. Histology: 1x low grade glioma, 3x high grade glioma, 1x cavernoma, 6x meningeoma.
MRI navigation and CST tractography images were performed both preoperatively and intraoperatively (iMRI). The corresponding imagings were fused. Identification of both the motor strip and CST was performed using a bipolar navigated hand-held electrode on the cortex and in the resection cavity respectively. Stimulus was short train of 4 monophasic pulses (frequency 500Hz, pulse width 400us). Threshold intensity for MEP was set at every stimulation point and matched with CST course. The shortest distance between tumour border and CST on preoperative MRI, cavity wall and CST on iMRI and threshold intenstity for eliciting MEP were recorded and evaluated. When threshold intensity was ≤ 5 mA, further resection was stopped.
Results Preoperatively the shortest distance between tumour border and CST was < 5 mm in five, 5-10 mm in one and > 10 mm in five cases. Intraoperatively cavity wall and CST distance was 5-10 mm in 6 and > 10 mm in 5 cases. CST shift was recorded on iMRI i 3 patients in > 5 mm toward to resection cavity. No new motor deficit developed after surgery.
Conclusion CST well corresponded with MEPs elicited by subcortical stimulation. Threshold intensity 5-10 mA seems to represent approximately 5-10 mm distance between the wall of the resection cavity and CST.
118 THE PREDICTIVE VALUE OF INTRAOPERATIVE MONOTORING OF MEP ACCORDING TO THE NUMBER OF MUSCLES MONITORED
First Author-Presenter: Eun Mi Lee Institution: Asan Medical Center-Seoul Phone/fax: 82-2-3010-3440/82-2-474-4691 Email: [email protected] Co-Authors-Institution: Joong Koo Kang-Asan Medical Center
Introduction TES-MEP has proven to be a successful and reliable neuromonitoring technique during spine and spinal cord surgery. The aim of our study was to compare its usefulness according to the type of spinal surgery and determine whether number of muscles in MEP change provides proper neurophysiological alarm.
Methods Recordings of TES-MEP were obtained from 197 patients during spine and spinal cord surgery under propofol/remifentanil/nitrous oxide. TES-MEP were recorded from 6 muscles (bilateral abductor pollicis brevis, tibialis anterior, abductor hallucis brevis). We used amplitude criterion; persistent drop of more than 75% of baseline values. MEP changes were classified according to number of muscle as ‘single’ (1 muscle), ‘couple’ (2 muscles) or ‘multiple’ (≥3 muscles).
Results Successful MEPs (at least one of the target muscle) were obtained in 95.4% (188 of 197) of the procedures and, remained 4.57% was inadequate MEP monitoring (flat MEP). In corrective spinal surgery (n=71), there were no newly developed neurological motor deficit and MEP change. Post operative neurological deficits occured in 8 of 65 (12.3%) patients after initradural tumor surgeries with highest preoperative neurological deficit (54 patients, 83.1%) followed by 3 (5%) in decompressive surgery (n=60) which had second highest preoperative neurological deficit (30 patients, 50%). Sensitivity and specificity of MEP alarm criteria was 63.6% and 91.1%. In 7 cases of ‘true positives’, MEP change was observed as ‘multiple’ in 4 (57%) and ‘single’ in 3 (43%). The specificity of ‘multiple’ was 100% to predict the newly developed neurological deficits. However, in 14 cases of ‘false positives’, MEP change was ‘single’ in 11 (78.5%) and ‘couple’ in 3 (22.5%).
Conclusion ‘Multiple’ MEP change is of higher value in predicting newly developed postoperative neurological deficits. Careful interpretation is needed in cases of ‘single’ MEP change whether it indicates true or is merely a false alarm.
119 OPTIMUM INTERPULSE INTERVAL TIMES FOR THE TIBIALIS ANTERIOR MUSCLE AND THE ABDUCTOR POLLICIS BREVIS IN TES-MEP FOR CORRECTIVE SPINE SURGERY
First author-presenter: C. van Hal¹ MD E-mail: [email protected] Phone: 0031-643817886 Co-authors: E. Hoebink¹ MD, I Racz², B. Polak², M. de Kleuver¹ MD PhD, H.L. Journee¹ MD PhD. Depts of ¹Orthopedic Surgery and ²Anesthesiology, Sint Maartenskliniek Nijmegen, The Netherlands
Introduction Multi-pulse trains in transcranial electrical stimulation (TES) have made monitoring of muscular motor evoked potentials (mMEP) successful. Widely used settings are 4-5 pulses/train (ppt) with an interpulse interval (ipi) of 2ms at voltage TES and an ipi of 4ms at current TES. Recent literature1 reports optimum ipi’s (OIPI) of 1ms for the abductor pollicis brevis (APB). Furthermore, we experienced markedly improved MEP amplitudes when changing the ipi from 2 ms to 0.8-1.5ms or well above 2 ms in a few patients. Goal was to study the influence of the ipi on MEP’s of the tibialis anterior (TA) and APB representing the lower and upper extremities.
Methods For 26 TES-MEP monitored patients undergoing corrective spine surgery, mean age 33.9 years, ipi curves were measured during the set-up procedure. TES was performed by voltage stimulation using 4-7 ppt, pulse width 0.1 ms, TES intensity 1.3-3.7 motor threshold. Total intravenous anesthesia was used in all patients (remifentanyl, diprivan). IPI curves were obtained for ipi 0.5–5.0 ms. Furthermore the mean reduction of MEP amplitudes between the two oipi’s and between the oipi’s and ipi 2 msec is determined.
Results The mean oipiAPB is 1.82 ms and the mean oipiTA is 2.30 ms with a significant difference for p< 0.05 (Student T-test). The oipi histogram of the APB shows a bimodal distribution (fig 1). The mean mutual reduction in MEP amplitudes and amplitude reduction for the 2 ms ipi are summarized in table 1.
N=26 MEP reduction oipi to ipi2 (%) MEP reduction at mutual oipi (%) TA APB TA APB Mean 46.0 53.9 33.2 32.7 SD 28.4 25.7 27.7 27.2
N70% 7 (27%) 7 (27%) 4 (15%) 3 (12%)
Table 1: Mean and Sd for ipi 2 ms and mutual ipi reductions. N70% is number of patients with a MEP reduction more than 70%. Figure 1: histogram APB
Conclusion The large inter-individual variation and bimodal distribution of the oipi with for both extremities optimal ipi settings at 0.8-1.4 ms and 2.5-3.5 ms resulting in milder MEP reduction at mutual oipi’s are reasons to propose to change the start value of the ipi in a TES set up procedure from 2 ms to 0.8-1.3 ms.
Reference Scheufler KM, Reinacher PC, Blumrich W, Zentner J, Priebe HJ. Anesth.Analg. 2005;100:440-7.
120 USEFULNESS OF COMBINED INTRAOPERATIVE MEP AND SEP MONITORING IN SPINAL CORD AND SPINE SURGERY TO PREDICT POSTOPERATIVE MINOR MOTOR DEFICITS
First Author-Presenter: Joong Koo Kang Institution: Department of Neurology, College of Medicine University of Ulsan, Asan Medical Center, Seoul, Korea Phone: 82-2-3010-3448, Fax: 82-2-474-4691 E-mail: [email protected] Co-author: Eun Mi Lee Institution: Department of Neurology, College of Medicine University of Ulsan, Asan Medical Center, Seoul, Korea Phone: 82-2-3010-3440, Fax: 82-2-474-4691 E-mail: [email protected]
Introduction The use of transcranial electrical intraoperative motor-evoked potentials (MEP) and somatosensory-evoked potentials (SEP) in spinal cord and spine surgery have been useful to prevent the devastating postoperative neurological deficits, but limited data exist about how much such techniques can predict newly developed postoperative minor motor deficits. The aim of this study was to evaluate the usefulness of conventional warning criteria of intraoperative SEP and MEP in spinal cord or spinal surgery in predicting the risk of post operative motor deficits.
Methods We analyzed a consecutive series of patients who underwent spinal cord or spine surgery during a 2-year period at a university-based hospital. We applied combined intraoperative MEPs and SEPs in the majority of the 215 spinal cord or spine surgery. Six muscles (bilateral abductor pollicis brevis, tibialis anterior, abductor hallucis brevis) were monitored during MEP. We used the warning criteria for MEP as ‘more than 75% amplitude decrease compared to that of baseline and SEP as ‘more than 50% decrease of amplitude or more than 10% increased latency. We correlated it with postoperative minor motor deficits.
Results Eleven patients had newly developed postoperative minor motor deterioration (one or two grade motor power deterioration in MRC scale for motor strength) compared to preoperative state. No patients had newly developed postoperative major motor deficits after surgery. Intraoperative MEP showed 54% of sensitivity (6 of 11 cases) and 91.1% of specificity (174 of 191 cases) and intraoperative SEP showed 12.5% of sensitivity and 96.9% of specificity. Combined analysis with MEP and SEP monitoring also showed 54% of sensitivity (6 of 11 cases), did not increase the sensitivity to predict newly developed postoperative minor motor deficits.
Conclusion Conventional warning criteria for intraoperative MEP and SEP are not adequate to predict newly developed postoperative minor motor deficits. More useful criteria to predict postoperative minor motor deficit may be needed.
121 TRANSCRANIAL ELECTRICAL STIMULATION VOLTAGE THRESHOLDS ARE ELEVATED IN VERY YOUNG CHILDREN
C.M.C Oude Ophuis, E. Haitsma, E.W Hoving, H.L. Journée Dept of Neurosurgery UMCG Groningen, The Netherlands Key words: transcranial electrical stimulation, TES, motor evoked potentials, young children, myelination, threshold
Introduction In young children muscular motor evoked potentials (mMEP) from transcranial electrical stimulation (TES) are sometimes difficult to obtain and not useful for monitoring. One cause could relate to relatively small diameters of corticospinal axons and immature myelin which might predict increased stimulation threshold voltages. The relationship between TES threshold and age is explored in this study.
Subjects Retrospective study in 77 patients diagnosed, most diagnosed with a tethered cord due to spinal dysraphism; 4 myelomeningoceles, 13 lipomeningoceles, 17 tight filum terminale, 1 split cord malformations. Several patients showed a combination of these different types of dysraphism. The patients underwent surgery in the conus-cauda region undergoing dethetering of the filum terminale and resection of various kind of tumors (like lipoma, teratoma) and dermoid cysts by a single surgeon during a nine years period (1999-2008). Ages 22,9y ± 23.2 y (mean±SD). Subdivision: groups I. 0-4yrs, n=22; II: 4-10y, n=12 and III >10 y, n=43. 71 had TIVA with propofol combined with an opiate, and 6 (all younger than 6y) halogenated agents.
Methods Prior to the monitoring, TES parameters were optimized starting by single train (ST) 4 or 5 p/train and pulse width: PW=100μs, increase of the number of pulses per train (up to 10), application of double train stimulation (DTS), interpulse interval (IPI) in the range of 0.6 – 4 ms and occasionally increase of pulse width up to 0.5 ms. These optimizing steps were intended to optimize neurophysiological conditions for transmission of motor responses via the lower motor neurons to minimize segmental influences on motor thresholds. This would bring the absolute axonal threshold of the cortico spinal tract better in focus. The reference 95% confidence interval (CI) for Vthfor was obtained from group III and used for comparison of Vthfor in group A <10y.
Results TES-MEP responses could be obtained in all patients, except for 5 of 6 patients that were sedated by halogenated agents. Fig 1 shows significant increased thresholds Vth for ages below 2.5 years.
Fig 1: Function of the tibial TES voltage threshold of left tibial MEP’s as a function of age. Below 2.5 y age 7 of 10 voltage threshold are outside the 95% confidence interval as computed for the older age group above 10 years.
All muscle groups in the leg at both sides in group I (<4 yrs) had mean Vth’s in a range of 129 – 151 V; SD: =57- 63 which were significant different (p<0.0001) from the means of reference group III. When applying 95% confidence intervals of group III for all muscle groups, Vth’s were found outside for ages below 3.5 y. This supports the hypothesis of this study where increased thresholds were expected in immature myelinated axons of
122 the cortico-spinal tract. Moreover, different anatomy of the head and electrical conductivities of the skull and subcortical white matter, which conductivity is increased due to lacking myelin, may also play a role.
Conclusion Immature motor pathways in children below 3.5 y of age show significant elevated stimulation thresholds even after optimal conditioning of motor neurons resulting in opening of gates that relay cortico-spinal conducted motor potentials to peripheral muscles. The elevated voltage threshold for TES may reflect a functional condition of immature intracranial nerve fiber tissue in combination with different anatomy of the head and conductivities of the skull and white matter. Furthermore, TIVA is recommended.
Implications This study provides TES-MEP paradigms for very young children.
123 INTRAOPERATIVE NEUROPHYSIOLOGICAL MONITORING OF FACIAL NERVE FUNCTION IN PATIENTS WITH TUMOURS OF THE CEREBELLOPONTINE ANGLE
Klaus Novak Medical University of Vienna, Dept. of Neurosurgery Währinger Gürtel 18-20 A-1090 Wien Phone: +43-1-40400-4560 Fax +43-1-40400-4566 Email: [email protected] Co-Authors: Georg Widhalm, Vesna Malinova, Stefan Reitbauer, Christian Matula, Engelbert Knosp
Introduction Reliable estimation of the prognosis of postoperative facial nerve function has become available with the method of corticobulbar motor evoked potentials (MEPs)1. Continuous analysis of the intraoperative functional status of the facial nerve and the real-time correlation with surgical manoeuvres are the key points, which turn facial nerve MEPs into a novel neuroprotective tool in skull base surgery.
Methods In 2003 multimodality neurophysiological monitoring for skull base surgery was introduced at the Department of Neurosurgery at the Medical University of Vienna. Since then transcranial electrical stimulation was used to elicit electromyographical responses from the facial muscles in 96 patients with tumours of the cerebellopontine angle. After short trains of stimuli ranging from 4 to 6 stimuli at stimulus rates of 250 or 500 Hz, corticobulbar MEPs were recorded from intramuscular steel needle electrodes or from of hook wire electrodes placed in the facial muscles.
Results MEP monitoring was feasible in all 96 patients. Intraoperative changes of MEP monitoring influenced the surgical strategy of tumour removal. Irreversible changes closely correlated with postoperative outcome.
Conclusion Our preliminary experience indicates that corticobulbar MEP monitoring provides instant and reliable information correlating to the clinical function of the facial nerve without interfering with the surgical procedure. Immediate detection of innervation failure can lead to appropriate surgical action and measures to avoid severe or permanent facial nerve dysfunction. Temporary changes can support the reversibility of surgically induced impairment of nerve function. Thus, corticobulbar MEP monitoring is a feasible neuroprotective method in the neurosurgical operating room.
Reference 1) Dong CC et al. Intraoperative facial motor evoked potential monitoring with transcranial electrical stimulation during skull base surgery. Clin Neurophysiol. 2005 Mar;116(3):588-96
124 PRE-OPERATIVE MRI FEATURES AND D WAVE MONITORABILITY IN SURGERY FOR SPINAL CORD TUMORS
First Author-presenter: Vincenzo Tramontano Institution: Department of Neurosurgery, University Hospital. Verona. Italy Email: [email protected] – [email protected], Co-Authors-Institution:, Alba Leon Jorba, Giovanna Squintani, Paolo Manganotti, Franco Faccioli, Albino Bricolo, Massimo Gerosa, Francesco Sala Intraoperative Neurophysiology Unit, Department of Neurosurgery, University Hospital, Verona, Italy
Introduction Baseline D wave is not recordable caudal to the tumor in about one third of patients with intramedullary spinal cord tumors (ISCTs) rostral to the conus. Various clinical and radiological variables have been reported as possible explanations for the lack of monitorability: Pre-surgical spinal cord irradiation, extensive tumor compression, presence of syrinx and tumoral cysts, pre-operative neurological status. Yet no study has investigated in details the correlation between pre-operative MRI features and D-wave monitorability, and this was our goal.
Methods Between 2000 and 2009 we performed 165 procedures for ISCT. D-wave monitoring was not attempted in 29 patients for either technical problems (n=13) or tumor location in the conus (n=16). For the remaining 136 patients, we analyzed correlations between D-wave monitorability and the following neuroradiological variables: presence of syrinx or tumor cysts in the pre-op magnetic resonance and tumor extension.
Results D-wave was monitorable in 94 (69%) (group M) and unmonitorable in 42 (31%) (group U). The presence of tumoral cysts did not correlate with D-wave monitorability (p-value>0.05). Conversely, the incidence of syringomyelia was significantly higher (p-value=0.032) in group U (55%) than in group M (35%). Furthermore, tumor extension was significantly larger (p-value=0.007) in group U (4.6 spinal levels) as compared to group M (3.6 spinal levels).
Conclusion This study suggests that pre-operative MRI may provide insights on the D-wave monitorability for patients who will undergo surgery with intraoperative neurophysiological monitoring for ISCTs. The presence of syringomyelia and tumors extending for more than 3-4 spinal levels correlate with poor D-weave monitorability, most likely for desynchronization of the descending volleys traveling on the corticospinal tract.
125 CPA SURGERY AND INTRAOPERATIVE MONITORING
W. Bini, A.. Samii, M. Samii INI - International Neuroscience Institute Hannover, Germany
Microsurgical technique has definitely revolutionized the management and results when dealing with lesions of or located at the skull base. Advancements in neuroanesthesia (ie. TIVA), neuroimaging (ie. intraoperative image guidance ie. 3-D volumetric image rendering technology), positioning (ie. modified semi-sitting position), but also the routine use of sophisticated intraoperative neuro-monitoring, have contributed substancially to the state of the art and constitute nowadays a must for neurosurgical or multidisciplinary combined procedures when tackling tumours of this crossroad region.
Based on an experience of well over 1.500 skull base and CPA surgeries we present our overall diagnostic, surgical and "standard" intraoperative monitoring algorythm (focused on hearing preservation). Precisely regarding the outcome, such as hearing function, in CPA or acoustic neurinoma surgery we have used a multimodality monitoring protocol of the auditory pathway with the intention to increase the safety and speed of the recordings (Samii, Matthies). With this, the useful feedback to the surgeon can be improved by allowing during the operation possible modifications of the microsurgical procedure, in time.
Besides conventional ear to vertex recording of AEP by averaging 250 sweeps, two further recording modalities are usually applied. a.) a non-invasive electrocochleography is performed by placing a ball electrode in the EAC onto the tympanon and b.) a Nearfield brainstem recording is performed by using a neurosurgical retractor with smal tubes in the sides of its blade. Through these tubes, small ball electrodes are inserted with cables and pushed through up to the retractor tip. With the retraction of the brain, the elctrode becomes placed on the brainstem and thus in the vecinity of the cranial nerves and nuclei. We have observed that the sensitivity of EAC_Ecoch and of Nearfield AEP was superior to conventional AEP with regards to demonstrating relevant changes as well as to obtain responses of reduced number of active neurons. Recording time is reduced to 2-5 sec. in view of the large amplitude of EAC_Ecoch and Nearfield AEP. The recording in the vecinity of potential generators, for example the cochlear nucleus, provide large potentials and allows for reliable monitoring information in very short periods.
Also as further attempt to improve proximal control and microsurgical handling, ongoing trials are trying to adjust motor evoked potential techniques combining them with conventional EMG monitoring. Patients during surgery are being ivestigated ( Matthies ) by multipulse ( 3-4 pulses ) transcranial electrical activation elicited either by constant voltage ( 250-400V ) or constant current ( 60-190mA ) stimulators in an anodal mode ( M3_M4 versus Mz ). Recording is done by conventional EMG electrodes of motor cranial muscles ( specifically for the facial nerve at the orbicularis oculi and oris muscles of the tumour side and as individual control, at the orbicularis oris on the healthy side ). Single pulse stimulation is applied before the start of surgery in order to identify and exclude any direct peripheral nerve stimulation.The technique of cranial MEP needs considerable refinement and "fine tuning" compared to the extremities, but MEP are characterized by three advantages: 1. preserved MEP are reliable sign of functional nerve continuity, 2. stimulation conditions are stable throughout surgery and by far better for comparison than muscle action potentials and 3. preserved MEP is a favourable sign of early useful post-op function.
We have furthermore, in our ongoing attempts to improve the intraoperative recording options, observed the same as has been described by Tatagiba and col. with regards to the trigeminocardiac reflex (TCR). The hemodynamic alterations due to the appearance of the TCR are followed by BAEP changes. These changes may predict post-op hearing function. The TCR seems to have a negative prognostic impact on the quality of the post-op auditory function.
Even though we have our standard protocol as described above, numerous options or combination of techniques may be required to still improve the results of surgery by guiding and practically "online" warn us of possible functional repercussions. Technical developments will condition the availability of an optimal "single tool" perhaps.
126 MOTOR CORTEX STIMULATION FOR PAIN RELIEF: INTRAOPERATIVE NEUROPHYSIOLOGICAL IDENTIFICATION OF OPTIMAL ELECTRODE POSITION
B Cioni, M Meglio, C De Simone Neurochirurgia Funzionale e Spinale – Università Cattolica – Roma – Italy
Introduction The optimal contact position in order to obtain the best pain relief by motor cortex stimulation (MCS), is still matter of debate. In 2007 Yamamoto et al (2) found a significant direct correlation between D-wave amplitude and VAS reduction. Holsheimer et al (1) found that the anode providing the largest muscle response in the area of pain gave the best pain relief. But the muscle response shows a very high variability from trial to trial, and D wave, very stable, does not give somatotopic information.
We combined the two techniques to overcome these disadvantages, but the placement of an epidural spinal cervical electrode is an invasive, sometimes time-consuming procedure. We developed a novel methodology for the intraoperative identification of the best spot to be chronically stimulated.
Method After a small craniotomy, under TIVA, we identify the central sulcus by the SEP phase reversal. We epidurally stimulate the motor cortex by a monopolar handheld probe using the high frequency short train technique with increasing current and we record the muscle response in order to select the area somatotopically corresponding to the body region of pain with the lowest motor threshold. . Here we place the electrode paddle perpendicular to the central sulcus with at least one contact over the sensory cortex. We stimulate the spot with the lowest motor threshold as a cathode, while the contact over the sensory cortex is used as an anode.
Conclusion This methodology is simple and safe, comfortable for the patient because under general anesthesia and seems to improve the efficacy of MCS for pain.
References 1. Holsheimer J, Lefaucheur JP, Buitenweg JR, Guij0n C, Nineb A, Ngujen JP The role of intraoperative motor evoked potentials in the optimization of chronic cortical stimulation for the treatment of neuropathic pain Clin Neurophysiol 118(10):2287-96, 2007 2. Yamamoto T, Katayama Y, Obuki T, Kano T, Kobayashi K, Oshima H, Fukaya C, Kakigi R Recording of cortico-spinal evoked potential for optimum placement of motor cortex stimulation electrodes in the treatment of post-strke pain Neurol Med Chir 47:409-414,2007
127
Poster Presentations
128
OPTICAL STIMULATION OF NEURAL TISSUE IN RATS AND ITS POTENTIAL APPLICATION IN IOM
C. Chris Kao Vanderbilt University and Sentient Medical Systems-Nashville, TN 615-275-8896 [email protected] Jonathon Wells, Jonathon Cayce, Duco Jansen, Anita Mahadevan-Jansen, Peter Konrad, Vanderbilt University
Introduction For over a century, the traditional method of stimulating neural tissue has been based on electrical methods, which remain to be the gold standard. Here, we report a technological breakthrough in neural stimulation that uses low intensity, pulsed infrared laser light to elicit action potentials in peripheral nerve and central nervous system (CNS) neurons.
Methods Compound action potentials in rat sciatic nerve and whole cell patch clamp single neuronal action potentials in rat thalamocortical slice were recorded upon optical and electrical stimulation. Laser parameters: Lasers (wavelength): Free Electron Laser (FEL 2.1 – 3.5µm) and portable Holmium: YAG laser (2.12µm) 2-30 Hz, Radiant exposure: 0.3 – 1.0 J/cm2, Spot size: 200-600 µm, Pulse duration: 350 µsec (Ho: YAG) and 5 µsec macro (FEL).
Results Using a 2.1µm laser for stimulation, we evoked compound nerve and muscle potentials in sciatic nerve, as well as, muscle movements. Compared with electrical stimulation, optical stimulation evoked responses had much higher spacial resolution as individual digit movements could be elicited. In contrast, only whole hind limb movements were evoked with electrical stimulation. In the CNS tissue, a 3.3 µm laser optimally provided stimulation to evoke action potentials in both cortical and thalamic neurons. Evoked single neuronal action potentials had high following frequency (30 Hz).
Conclusion A novel approach to neural stimulation in both peripheral and CNS tissue is demonstrated using pulsed infrared laser light at radiant exposures well below tissue damage threshold. This contact-free, damage-free, artifact-free, spatially specific stimulation modality has the potential to change the future of neurophysiology in laboratory studies as well as in the introperative mapping for rhizotomy cases.
129 RECORDINGS OF LONG-LATENCY TRIGEMINAL SOMATOSENSORY EVOKED POTENTIALS IN PATIENTS UNDER GENERAL ANESTHESIA
First Author-Presenter: Michael Jörg Malcharek, MD Institution: Division of Neuroanesthesia and Intraoperative Neuromonitoring, Department of Anesthesiology, Intensive Care and Pain Therapy, St. Georg’s Hospital, Delitzscher Str. 141, 04129 Leipzig, Germany Phone/fax: 0049 341 9094009/0049 341 9092568 Email: [email protected] Co-Authors-institution: Janett Landgraf, MD - Department of Anesthesiology, Intensive Care and Pain Therapy, St. Georg’s Hospital Oliver Sorge, MD - Department of Neurosurgery, St. Georg’s Hospital Juliane Aschermann, MD - Department of Neurology, St. Georg’s Hospital Armin Sablotzki, MD, PhD - Department of Anesthesiology, Intensive Care and Pain Therapy, St. Georg’s Hospital
Introduction The reliability of intraoperative recordings of trigeminal induced scalp somatosensory evoked potentials (T-SSEP) is controversial. This investigation aimed to provide evidence that T-SSEP recordings are stable with standard neurophysiological methodology in combination with a standardized anesthesiological regime. Therefore we describe a) methodology of recording long-latency trigeminal SSEP’s during carotid surgery and compare b) amplitudes and latencies of measured T-SSEP’s in patients under general anesthesia to data from literature obtained in awake patients.
Methods We investigated 100 patients undergoing carotid endarterectomy under total intravenous anesthesia with an infusion of propofol and remifentanil. Long-latency T-SSEP responses were recorded from the scalp after simultaneously stimulating the 2nd and 3rd branches of the trigeminal nerve. The analysis included visual assessments of traces and measurements of latencies and amplitudes of the N13 and P19 sections of T-SSEP waveforms from the beginning of surgery until the moment of carotid cross clamping. Furthermore, the mean variation of latencie and amplitudes were calculated per patient and over all patients.
Results We reproducibly recorded the cortical responses to T-SSEPs in 99 patients. The mean latency was 12.4 ms (MAD = 0.93) and the mean amplitude was 5.7 mV (MAD = 4.7). The variations in amplitudes (N13/P19) and latencies of N13 and P19 were fairly constant over time. As far as possible amplitudes and latencies of T-SSEP’s in anesthetized patients were comparable to data from literature in awake patients.
Conclusion We demonstrated the reliability of recording stable intraoperative T-SSEP responses with standardized electrophysiological and anesthesiological regimes.
References Bennett MH, Janetta PJ. Trigeminal evoked potentials in humans. Electroencephalogr Clin Neurophysiol 1980;48:517-526.; Hashimoto I. Trigeminal evoked potentials following brief air puff: enhanced signal-to-noise ratio. Ann Neurol 1988;23:332- 338.; Stechison MT, Kralick FJ. The trigeminal evoked potential: Part I. long-latency responses in awake or anesthesized subjects. J Neurosurg 1993a;33:33-638.; Stöhr M, Petruch F. Somatosensory evoked potentials following stimulation of the trigeminal nerve in man. J Neurol 1979;220:95-98.
130 RECORDINGS OF LONG-LATENCY TRIGEMINAL SOMATOSENSORY EVOKED POTENTIALS DURING INDUCTION OF GENERAL ANESTHESIA A PILOT INVESTIGATION
First Author-Presenter: Janett Landgraf, MD Institution: Division of Neuroanesthesia and Intraoperative Neuromonitoring, Department of Anesthesiology, Intensive Care and Pain Therapy, St. Georg’s Hospital, Delitzscher Str. 141, 04129 Leipzig, Germany Phone/fax: 0049 341 9094009/0049 341 9092568 Email: [email protected] Co-Authors-institution: Michael J. Malcharek, MD: Dept. of Anesthesiology, Intensive Care and Pain Therapy, St. Georg’s Hospital Oliver Sorge, MD - Department of Neurosurgery, St. Georg’s Hospital Juliane Aschermann, MD - Department of Neurology, St. Georg’s Hospital Armin Sablotzki, MD, PhD – Dept. of Anesthesiology, Intensive Care and Pain Therapy, St. Georg’s Hospital
Introduction There appears to be some controversy in the literature regarding the source of responses of T-SSEP. It is not clear whether they represent muscle artifacts, trigeminal reflexes, or real subcortical/cortical responses. We hypothesized, that in case of a cortical source, better quality (high signal-to-noise) T-SSEP recordings may be possible under general anesthesia, particularly with total intravenous anesthesia in the presence of muscle relaxants. Thus, the goal of this research project was to answer following questions: a) Is it possible to record long-latency trigeminal SSEP’s during induction of general anesthesia? b) Are there any changes in amplitudes and latencies of T-SSEP responses according to different steps of induction?
Methods We investigated 4 patients, that where scheduled to have carotid endarterectomy under total intravenous anesthesia (propofol/remifentanil-infusion). After determination of sensory threshold and baseline in awake patients we recorded T-SSEP responses during 1) induction of unconsciousness (etomidate/remifentanil), 2) muscle relaxation (rocuronium, monitored by TOF) and 3) after intubation (propofol/remifentanil-infusion). T- SSEP responses where analyzed with regard to changes in waveforms, latencies (N13 and NP19) and amplitudes (N13//P19).
Results In all cases, the responses were stable during the stepwise administration of remifentanil, etomidate, propofol and rocuronium. The mean amplitudes increased to 17% above baseline within about 6 minutes of giving etomidate and rocuronium and decreased 3% after intubation. The mean latencies of N13 and P19 slightly increased (2%) after etomidate and increased by about 11% after the initiation of the continuous infusion of propofol. The increase in latencies persisted after intubation. Visual assessments indicated that the quality of the waveforms improved during induction of anesthesia; the signal-to-noise ratio was enhanced, particularly after muscle relaxation.
Conclusion We demonstrated the nonmuscular source of T-SSEP responses by eliciting T-SSEPs in four patients, recording from the awake state to the completely unconscious state (including muscle relaxation). Our results suggested that the T-SSEP responses were from a neuronal origin, because the administration of muscle relaxants blocked all muscle activity.
References Buettner UW, Petruch F, Schleglmann K, Stöhr M. Diagnostic significance of cortical somatosensory evoked potentials following trigeminal stimulation. In: Courjon J, Mauuiere F, Revol M, editors. Clinical applications of evoked potentials in neurology. New York: Raven Pr, 1982:359-365.; McCarthy G, Allison T, Spencer D. Localization of the face area of human sensorimotor cortex by cranial recording of somatosensory evoked potentials. J Neurosurg 1993;79:874-884.; Hashimoto I. Contamination of trigeminal evoked potentials by muscle artifacts. Ann Neurol 1989;25:527-528. Letter (Reply).; Leandri M, Parodi CI, Favale E. Contamination of trigeminal evoked potentials by muscular artifacts. Ann Neurol 1989;25:527-528. Letter.; Sloan TB, Jäntti V. Anesthetic effects on evoked potentials. In: Nuwer MR, editor. Intraoperative Monitoring of Neuronal Function. Handbook of Clinical Neurophysiology, Amsterdam: Elsevier, 2008:Vol.8;877-893.; Stechison MT, Kralick FJ. The trigeminal evoked potential: Part I. long-latency responses in awake or anesthesized subjects. J Neurosurg 1993a;33:33-638.;
131 PARTIAL NEUROMUSCULAR BLOCKADE FOR FACIAL NERVE MONITORING DURING EXCISION OF VESTIBULAR SCHWANNOMA
First Author-Presenter: Matthew TV Chan, FANZCA Institution: Department of Anaesthesia and Intensive Care. The Chinese University of Hong Kong, Prince of Wales Hospital, Hong Kong SAR Phone/fax: +852 2632 2736 Email: [email protected] Co-Authors-Institution: Quanmeng Liu: The Chinese University of Hong Kong Joseph Lam: Division of Neurosurgery, Department of Surgery, The Chinese University of Hong Kong Michael Tong: Department of Otorhinolaryngology, Head and Neck Surgery, The Chinese University of Hong Kong
Background Intraoperative facial nerve monitoring provides early detection of nerve injury during excision of vestibular schwannoma. Traditionally, neuromusclar blocking agents are avoided to prevent interference with monitoring. However, recent studies suggested that partial neuromuscular blockade could be used without compromising facial nerve monitoring while avoiding large doses of anesthetics. In this study, we compared the perioperative anesthetic and facial nerve outcomes between patients receiving low doses of neuromuscular blockade with those treated with no neuromuscular blocking agent during excision of vestibular schwannoma.
Methods The study was approved by the clinical ethics committee. Written informed consent was obtained from 150 patients. Anesthesia was maintained with target-controlled infusions of propofol and remifentanil. Anesthesia was titrated so that the bispectral index was kept between 40 and 60. Following a bolus dose of rocuronium and tracheal intubation, patients were randomly allocated to receive either no further neuromuscular blocking agent or an infusion of rocuronium to maintain 50% first twitch suppression. Facial nerve monitoring was accomplished by placement of subdermal electrodes in the orbicularis oris and orbicularis occuli muscles. Intraoperative feasibility of monitoring, anatomical preservation of the facial nerve, anesthetic doses administered and hemodynamic parameters were recorded. Postoperative facial nerve function was rated using the 6-point House and Brackmann (H-B) scale (1=normal function, 6=total paralysis) at discharge and 6 months after surgery. Data were compared using Fisher exact test or unpaired t test as appropriate. Logistic regression was used to identify factors that may affect facial nerve outcome. P value < 0.05 was significant.
Results Patient characteristics were similar between groups. The mean (± standard deviation) target plasma concentration of propofol in the rocuronium group, 3.3 ± 0.4 µg/ml, was similar to that of the non-relaxant group, 3.2 ± 0.3 µg/ml. Facial nerve was identified and preserved in 91% of patients receiving rocuronium infusion compared with 97% in the non-relaxant group (P = 0.09). The median (range) H-B scores in the rocuronium group, 3 (1-6) at discharge and 2 (1-6) at 6 months, were worse compared with the non-relaxant group, 2 (1-5) and 1 (1–5), P = 0.04, respectively. Logistic regression showed that rocuronium infusion increased the risk of facial nerve injury by 2.7 (95%CI, 1.1-7.1).
Conclusions Partial neuromuscular block impaired the integrity of facial nerve monitoring. Repeated injury may be missed during monitoring with partial neuromuscular block. This may contribute to worsen facial nerve function after excision of vestibular schwannoma.
Study Supported by: Departmental resources
132 PREOPERATIVE TRANSCRANIAL MAGNETIC STIMULATION (TMS) AND SOMATOSENSORY EVOKED POTENTIALS (SSEP) IN ASSESSMENT OF FUNCTIONAL STATE OF SPINAL CORD IN DECISION MAKING FOR SURGICAL APPROACH IN PATIENT WITH CERVICAL SPONDILOTIC MYELOPATHY
Maria A. Hit’, MD, Artem O. Gushcha, MD, PhD, Georgy A. Shekutiev, MD, PhD, Burdenko Neurosurgical Institute, Russian Academy of Medical Sciences, Moscow, Russia
Introduction Cervical spondylotic myelopathy (CSM) is the most serious and disabling consequence of cervical spondylosis. Although MRI can reveal spinal cord compression, additional information regarding the functional status of the corticospinal tract (CST) and posterior columns is also desirable for surgical planning. The aim of the study was to establish the role of preoperative TMS and SSEP in the surgical management of CSM.
Material and methods We prospectively studied 27 consecutive patients (mean age 39-76 yr) who were subjected to presurgical TMS and SSEP (median nerve) for evaluation of the functional state of the spinal cord.
Results According to neurophysiological data patients were divided in three groups. In the first group (n=4) anterior and posterior approaches to the cervical spine were performed since a disturbed conduction in both motor and sensory tracts including marked prolongation of central motor conduction time (CMCT), reduction and polyphasic motor- evoked potentials and somatic afferent disorder on SSEP had been revealed. In the second group (n=18) prolongation CMCT to palm and foot muscles but without conduction block and without posterior column disorder was found so that the anterior decompression was done. In the third group of patients (n=5) only posterior column dysfunction on SSEP was revealed and posterior decompression was performed. Neurophysiological findings were matched with MRI images. There were signs of compression of both anterior and posterior cervical spine cord on the MRI in all patients, however, preoperative TMS+SSEP revealed a dysfunction of both anterior and posterior tracts only in 19% of cases, CST and posterior column were affected solely in 66% in 15% of patients respectively. These neurophysiological data were used for selection of surgical approach.
Conclusion Preoperative TMS+SSEP provide important information about the functional status of the spinal cord and may be essential in planning of surgical treatments.
133 FALSE NEGATIVE MOTOR THRESHOLD DURING INTRAOPERATIVE MONITORING OF ROOT DECOMPRESSION
Chaparro-Hernández, P (*), Daza-Delgado, G (*), Cortes Moreno, A (**), Almazan, A(**) y Ortiz, R (***) Hospital Infanta Luisa. SEVILLA (Spain) (*) Neurofisiología Clínica, (** ) Cirugía de columna, (***) Anestesia
Intoduction Electrical stimulation of the screw during pedicle screw placement is useful method to indicate a presence of a contact between the screw and the nerve root, but may show false negative results in some patients.
Methods We performed an electrical stimulation of the pedicle screw using square wave electrical stimuli of 0.2 milliseconds duration and intensity above 5 milliamps.
Results We present a case in which pedicle screw placement showed positive results when stimullated with a current above 15 mA. Root was seen with a compression zone and ischemic , so we proceeded with the direct stimulation of the root above and below the compressed area, noting that the threshold above the compression was 10 mA and below 1 mA.
Conclusion In certain cases of nerve root compression there is a possibility that the pedicle screw is in contact with the nerve root making it ischemic. In this situation the threshold for the electrical stimulation could be very high giving false negative results, simulating pedicle screw being far away from the nerve root, but pedicle screw and root are in a close contact causing root ischemia. Therefore, in this situation it is advisible to sitmulate root above and below ischemic zone.
References: • Toleikis, J.R., Skelly, JP The usefulness of electrical stimulation for assessing pedicle screw placements. J.Spine Disord, 2000, 13:283-289 • Toleikis, JR Neurophysiological monitoring during pedicle screw placement in Neurophysiology in Neurosurgery, pp 231- 264. Ed. Deletis, V and Shils, J. Academic Press, Elesevier Science. NY, 2002 • Cortes, V Monitorización Intraoperatoria de las raíces nerviosas en la cirugía de la columna, Rev Neurol, 2004: 13(1):75- 78 • Sutter MA, Eggspuehler A, Grob D, Porchet F, Jeszenszky D, Dvorak J. Multimodal intraoperative monitoring (MIOM) during 409 lumbosacral surgical procedures in 409 patients Eur Spine J. 2007 Nov;16 Suppl 2:S221-8. • Alemo S, Sayadipour A. Role of intraoperative neurophysiologic monitoring in lumbosacral spine fusion and instrumentation: a retrospective study. Surg Neurol. 2009 Aug 6. [Epub ahead of print]
134 INTRAOPERATIVE ANTIDROMIC STIMULATION OF THE CORTICO-SPINAL TRACT
First Author-Presenter: Paolo Costa Institution: Section of Clinical Neurophysiology, CTO Hosp, Torino, Italy Phone/fax: +39 366 3658416 Email: [email protected] Co-Authors: Alessandro Borio, Marta Giacobbi, Sonia Marmolino, Angela Palmitessa, Gianluca Isoardo. Institution: Section of Clinical Neurophysiology, CTO Hosp, Torino, Italy
Introduction Intraoperative stimulation of the spinal cord has been used in order to record high amplitude cortical somatosensory evoked potentials (ScEPs: spinal cord evoked potentials) from the scalp; however, by using this method, a fast potential, clearly separated from cortical somatosensory potentials can also be recorded. It has been postulated that this potential could be generated by the antidromic stimulation of the cortico-spinal tract (ACSP: Antidromic Cortico Spinal tract Potential).
Methods Tibial nerve somatosensory evoked potentials (SEPs), trancranially elicited muscle motor evoked potentials (m- MEPs), epidural motor evoked potentials (D-wave), neurogenic mixed evoked potentials (NMEPs) as well as cortical spinal cord evoked potentials (ScEPs) and ACSP were recorded intraoperatively in 27 subjects (4 during scoliosis surgery, 12 during removal of spinal cord tumor and 11 during stabilization for complete spinal cord injury). ScEPs and ACSP were evoked by epidural stimulation of the spinal cord above and below the site of surgery and recorded on the scalp midline.
Results The ACSP was recordable in all the neurologically intact patients and was clearly separated from the ScEPs that showed longer latency; the ACSP was limited to anterior midline, its amplitude was only slightly reduced by increasing the stimulus rate or by cutting the low frequencies and its latency was slightly longer than D wave latency. In the spinal cord injured subjects the ACSP was absent by stimulating the spinal cord caudally to the site of injury. In compromised patients the ACSP and D wave had a similar behaviour, both of them were present in normal, or moderately compromised subjects and absent in the presence of complete quadri/paraplegia. In a patient with paraplegia due to T8 meningioma and in a subject in whom the cauda/conus was stimulated the ACSP and D wave, but not the cortical ScEPs were absent below the site of surgery.
Conclusion On the basis of latency, distribution and response to filtering and stimulus rate the ACSP seems to be originated in the rostral part of cortico-spinal tract.
References 1. Partanen J, Merikanto J, Kokki H, Kilpelainen R, Koistinen A. Antidromic corticospinal tract potential of the brain. Clin Neurophysiol. 2000; 111(3): 489-95. 2. Porter, R. (1955). Antidromic conduction of volleys in pyramidal tract. J. Neurophysiol. 18, 138-150.
135 EFFECTS OF SEVOFLURANE VERSUS PROPOFOL ANAESTHESIA ON UPPER LIMB AND LOWER LIMB SOMATOSENSORY EVOKED POTENTIAL MONITORING OF THE SPINAL CORD DURING SCOLIOSIS SURGERY
Pastorelli F. MD1,2, Bonarelli S. MD3, Di Silvestre M. MD4, Fini N. MD2, Pelosi M.1, Greggi T. MD4, Michelucci R. MD2, Toccaceli L. 4, Plasmati R. MD1,2 (1) Servizio di Neurofisiopatologia, Istituti Ortopedici Rizzoli, Bologna; (2) UOC Neurologia, Ospedale Bellaria, Bologna; (3) Servizio di Anestesia e Terapia intensiva, Istituti Ortopedici Rizzoli, Bologna; (4) Rep. Chirurgia del rachide, Istituti Ortopedici Rizzoli, Bologna First Autor: Francesca Pastorelli UOC Neurologia, Ospedale Bellaria, Bologna, Italy +390516225348 [email protected] The study received no financial support. All authors have read and agreed with the content of this abstract submitted for the Second Congress of the International Society of Intraoperative Neurophysiology
Introduction Somatosensory evoked potential (SSEP) monitoring is an important tool in spinal surgery. Anaesthesia has a significant influence on SSEP monitoring and false positive results are possible, exspecially when a sevoflurane/remifentanil regimen is adopted. We compared the effects of volatile and total intravenous anaesthesia on SSEPs during scoliosis corrective surgery
Materials and Methods We retrospectively analyzed the data of intraoperative SSEP monitoring in 100 patients who underwent surgical treatment of scoliosis. Group 1: 50 patients (25pts with adolescent idiopathic scoliosis and 25pts with adult scoliosis) underwent SSEP monitoring under Sevoflurane anaesthesia (end tidal concentration 0.8–1.6%). Group 2: 50 patients (25pts with adolescent idiopathic scoliosis and 25pts with adult scoliosis) underwent SSEP monitoring under TIVA with Propofol infusion (6-10mg/kg/h). Cortical SSEPs were recorded after stimulation of the median and posterior tibial nerves. The latency and amplitude of N20 and P40 components for the upper and lower limb respectively were analyzed and the variability of SSEP responses was compared to the variation of systemic parameters such as body temperature, median blood pressure, heart rate in each step of the surgical procedure. A relevant neurophysiological change (an alert) was defined as a reduction in amplitude (unilateral or bilateral) of at least 50% for N20 and/or P40 SSEP compared with baseline.
Results A high rate of false positive (7/50, 14%) and false negative (1/50, 2%) results were recorded only in group 1, but not in group 2. Changes of systemic parameters produced little effect on the SSEP latency in both groups. The variability of P40 amplitude was significantly higher in group 1 compared with P40 amplitude in group 2, while no statistical difference was noted in the variability of N20 amplitude in both groups.
Conclusions Our study is peculiar because it analyzes the behaviour of cortical responses recorded at all four limbs and not just at lower limbs, during SSEP intraoperative monitoring. The variability of the cortical responses in relation to the type of anaesthesia is much greater at lower limbs, while the upper limb components are much more stable. In particular, it is highlighted a significant sensitivity of cortical lower limb responses to changes in the systemic parameters such as blood pressure and body temperature, while included within the range normally considered acceptable.
This could account for the known possibility of false positive results when the intraoperative recording of SSEPs is performed during halogenate anaesthesia and which are unlikely to occur when TIVA is used.
136 MOTOR EVOKED POTENTIAL (MEP) IN SPINAL SURGICAL PROCEDURES: CASE PRESENTATION
Clinical Neurophysiology Department, Neuroscience, Riyadh Military Hospital, Riyadh, Saudi Arabia Presenter: Dr. Mohammad M.U.Kabiraj, MD Riyadh Armed Forces Hospital Neuroscience Dept: Riyadh 11159, Saudi Arabia Phone: 966-1-4568925 Fax: 966-1-4568925 [email protected] Email
Introduction Trans-cranial elicited MEP is essential method to provide a real time feedback information of the functional integrity of the anterior-lateral motor pathway and thereby, prevents iatrogenic injury to the spinal cord during surgery/
Objectives To demonstrate a preventive role of MEP in cortico-spinal tract injuries during surgery and to evaluate the effect of other non-surgical factor(s) influencing MEPs
Materials and Methods This is a prospective study of 46 patients, age range 2 to 52 years (mean = 23.30 years) with male-female ratio of 1:1.50 The surgical procedures were: scoliosis correction (n=43), one severe Kypho-scoliosis, one intra- medullary tumor resection case and one tumor mass in lower Medulla to C6 . Electrophysiological test modalities were SSEP and MEP. MEPs in the limb muscles are elicited by transcranial multi-pulse stimulation technique.
Results and Discussion The SSEP and MEP results were: in scoliosis group: 1 true positive result without intervention, 8 true positive results with intervention,1 False- Negative result , and 33 true-negative results .
One 16 yr old Saudi Girl with severe Kyphoscolisis lost her MEPs during the fixation of the peducular screw and the surgeons were informed. The screws were released and the surgery was stopped. Both MEPs and SEPs came back. The Intra-medullary Tumor case was a 52-year-old Saudi lady with low back pain. MRI of the spinal cord showed an intra-medullary mass extended from D2 to L2 with a swollen spinal cord. There was no motor deficit in the lower limbs. The SSEP to the left tibial stimulation was lost immediately following a dorsal myelotomy. However, MEPs were normal throughout the surgical removal of the mass. After few days she went home walking. The case with Crevico-medullary mass had absent lower limb SEP and MEP from the beginning. However, upper limb SEP and MEP remained unchanged during the tumor resection procedure. Lower limb SEPs start appearing. Among the non –surgical causes, hypoxia/ischemia and anesthetic agents like xylocaine were to blame.
Conclusions Our observations further support an opinion that an abnormal MEP is a sensitive indicator for cortico-spinal tract dysfunction and thereby offers insight towards immediate intervention.
137 PERCUTANEOUS PLACEMENT OF RECORDING ELECTRODE FOR D-WAVE MONITORING DURING TRANSORAL CERVICAL DECOMPRESSION APPROACH
First Author-Presenter: Enrico Bosco Institution: Treviso Hospital, Italy Phone/fax: 039422322518 Email: [email protected] Co-Authors-Institution:ZanattaP, SorbaraC, -Anesthesia and Critical Care, Bendini M°,C. -Neuroradiology° Sammartino F*,Longatti P*- Neurosurgery*
Introduction The aim of this study is to present the findings and early results of percutaneous placement of recording electrode for D-wave monitoring in 2 patients during transoral cervical decompression. A successful surgery achieving a stable decompression at the transoral cervico-medullary junction is an expertise demanding procedure. It requires an accurate preoperative evaluation and an appropriate neurophysiological assessment
Methods 2 consecutive patients with progressive neurological deterioration secondary to cervico-medullary junction disease underwent transoral surgery. D-waves were recorded via a catheter electrode inserted epidurally through a Touhy- needle below the site of potential injury . The position of catheter electrode was confirmed by a radiograph after the procedure. Muscle MEPs (Motor Evoked Potentials) were also recorded. Muscle MEPs/D wave were elicited by short trains/single transcranial electrical stimuli. SEPs (Somatosensory Evoked Potentials) were monitored continuously during the procedure.
Results Studied lesions were: atlanto-exial sublussation with pannus formation and cervical stenosis at C1-C2 level and an intradural/extramedullary tumor C1-C2. Mean age was 75 years. Both patients presented varying degrees of quadriparesis. All underwent synchronous anterior decompression and posterior occipito-cervical fixation. D- wave decreased by 12% and 20% of it baseline value during the critical steps. Intermittent muscle MEPs recording changed about 50% in one patient, in the other patient no motor responses were recorded both in upper and lower extremities. Postoperative sensory-motor status was stable. SEPs responses were stable during all the procedure. Both patients with severe preoperative neurological deficits improved.
Conclusions In our experience, the recording electrode can be easily and safely placed percutaneously. The percutaneous recording electrode for D-wave is useful for achieving continuous monitoring during the most critical steps of the procedure. Intermittent MEPs recording were affected by the degree of preoperative motor deficit and the functional type of the cord lesion. An appropriate choice of neurophysiological monitoring technique could help to minimize morbidity and mortality.
138 IMPROVED SPINAL CORD MONITORING WITH MOTOR EVOKED POTENTIALS BY OPTIMAL PLACEMENT OF THE RECORDING REFERENCE ELECTRODE
M. Garrett, A. Eriksson, H. Axelson Clinical Neurophysiology, Uppsala University Hospital, Sweden First Author: Malin Garrett Presenter: Annika Eriksson Institution: Uppsala University Hospital, Uppsala, Sweden Phone/fax: +46186113449 Email: [email protected]
Introduction It is well known that the position of the reference electrode may have a considerable effect on the motor amplitude in nerve conduction studies. Typically, the recording electrodes are placed in a muscle belly-tendon fashion for optimal recordings. In contrast, when recording muscle evoked potentials (MEPs), derived from transcranial electrical stimulation in surgery, it seems that less attention is paid to the placement of the recording electrodes.
Objective In view of the increasing request for sometimes challenging intraoperative spinal MEP monitoring in patients with neuromuscular disorders, we examined if the standard belly-tendon placement of the reference electrode results in increased MEP amplitudes and more successful monitoring.
Methods 26 patients monitored during scoliosis surgery were included in the study. Two different electrode montages were studied. The active electrode was placed subdermally at the muscle motor point and the reference electrode placed either 1.5 cm more distally in the muscle (muscle-muscle montage) or at a more remote location over a joint (muscle-tendon montage). Three muscles were studied: abductor digiti minimi (ADM), tibialis anterior (TA) and abductor hallucis (AH).
Results The mean MEP amplitudes monitored from ADM, TA and AH were significantly (p<0.05) increased in the muscle-tendon montage compared to the pure muscle montage. There was a 320% increase in the TA muscle whereas there was only a slight effect in AH and ADM (124% and 125 % increase, respectively). In three out of seven patients with neuromuscular scoliosis there were MEPs in the TA muscle-tendon montage that, at numerous occasions, were not clearly detectable in the muscle-muscle montage.
Conclusion Changing the placement of the recording electrodes may substantially improve the quality of MEP monitoring of patients with neuromuscular disorders. Further, it may be worthwhile to perform preoperative neurographic mapping for the highest compound motor action potential in order to improve the recording of MEPs.
139 NEUROPHYSIOLOGIC MONITORING DURING D1-D3 INTRAMEDULLARY LIPOMA REMOVAL
First Author-Presenter: Giancarlo D’Andrea Institution: S Andrea Hospital, Neurosurgery; Rome, Italy Tel. +390633775298 Email [email protected] Co-Authors-Institution: Albina Angelini-S Andrea hospital, Ilaria Vetrone-S Andrea hospital, Giovanni Sessa-S Andrea hospital, Luigi Ferrante-S Andrea hospital
Introduction Dorsal intramedullary lipoma represents a rare case relating to the adult age of our patients and to the localization. Spinal cord lipma are more common in childhood and at level of cauda equine. We believe that transcranial motor evoked potentials and SEP from bilateral stimulation of tibial muscle during intramedullary lipoma removal are fundamental for a safe surgical approach to the lesion.
Methods: we operated on an adult female patient affected by thoracic intramedullary neoplasm (D1-D3). During surgery we used neurophysiologic monitoring with SEP, MEP, free run EMG and EEG.
Results: neurophysiologic monitoring warned the surgeon when detected a modification of the right transcranial motor potential amplitude, a lengthening of the P40 latency and a lengthening of the right SEP latency followed by bilateral lengthening of the P40 latency.
Conclusion Transcranial motor evoked potentials during during surgery allowed us to perform a safer surgery warnig the surgeon to perform a partial removal of the lesion as large extensive as possible. As widely described in literature such lesion allows a partial removal but neurophysiologic monitoring gives the neurosurgeon the warning data about the limit of his surgery. Neurophysiologic monitoring allowed us the maximum removal and the maximum respect of the motors pathways so that our patient had a uneventful postoperative course.
140 INTERVENTIONS DURING ACOUSTIC NEURINOMA RESSECTION INDICATED BY CHANGES AT THE BRAIN AUDITORY EVOKED POTENTIALS: A CASE REPORT
Lladó-Carbó E., Pérez- Fajardo G., Ulkatan S., Deletis V., Sen C. * Intraoperative Neurophysiology Monitoring Department, St. Luke's-Roosevelt Hospital. New York, NY * Cranial Base Surgery. Neurosurgery Department. St. Luke's-Roosevelt Hospital. New York, NY
Introduction Acoustic neurinoma ressection involves preservation of VIII nerve functional integrity. The Intraoperative Monitoring (IOM) with Brain Auditory Evoked Potentials (BAER) from both ipsi and contralateral VIII nerve during the surgery alerts the surgeon when the nerve functional integrity is at risk.
Material and methods 47 y.o. female diagnosed with a right acoustic neuroma (vestibular schwannoma), with bilateral preserved auditory function, scheduled for tumor ressection. The IOM includes Rt (ipsilateral) and Lt (contralateral) BAER, Cortical Somatosensory Evoked Potentials (CSEP) from upper extremities (R/L Med), Motor Evoked Potentials (MEP) from upper extremities (R/L Abductor pollicis brevis, and Lt extensor digitorum) and the Blink Reflex.
Results Bilateral BAER responses were considered as within the normal values and waveform (V wave latency for Rt BAER was 6.1 ms.During tumor excision , Rt BAER V wave latency started to fluctuate and increased up to 7.0 ms (considered as significantly delayed and correlated with postoperative hearing impairment). Two minutes later I-V complex of RtBAER disappeared. Surgeon and anaesthesiology team were informed, blood pressure increment as well as local papaverine application were requested by monitoring team and surgeon stopped the procedure for a while. Twenty-five minutes later, I-V complex started to reappear slowly with previous configuration, being almost normal at the end of the surgery (V wave latency 6.6 ms). No postoperative deficits after the clinical examination were observed and hearing function was preserved.
Conclusion BAER intraoperative monitoring during acoustic neurinoma surgery should be a standardized methodology in order to prevent VIII nerve functional injury and avoid intra and postoperative auditory deficits in patients with preserved hearing function. Cooperation between anesthesiologists, neurosurgeons and neurophysiologists is the key in order to take action and diminish neurological morbidity in this type of surgery.
141 REORGANIZATION OF THALAMIC SENSORY RELAY NUCLEUS IN PATIENTS WITH PHANTOM LIMB PAIN
First Author-Presenter: Hideki Oshima Institution: Department of Functional Morphology and Neurological Surgery, Nihon University School of Medicine Tokyo Phone/fax: +81.3.3972.8111/+81.3.3554.0425 Email: [email protected] Co-Authors-Institution: Koichiro Sumi, Toshiki Obuchi, Toshiharu Otaka, Katusnori Sijyo, Toshikazu Kano, Kazutaka Kobayashi, Chikashi Fukaya, Takamitsu Yamamoto, Yoichi Katayama - Division of Applied System Neuroscience, Department of Advanced Medical Science and Neurological Surgery, Nihon University School of Medicine,
The primary somatosensory cortex undergoes reorganization of receptive field representation in patients with phantom limb pain; the phantom limb area is taken over by the adjacent somatotopic area. The extent of cortical reorganization and the degree of phantom limb pain have been reported to be correlated. Similar reorganization of receptive field representation has been shown within the thalamic sensory relay nucleus (nuclei ventrocaudales: VC). The deafferented area of the thalamus is invaded by adjacent areas in receptive field representation, as evaluated by microelectrode recording, while projected field representation, as determined by sensation induced by microstimulation, remains unchanged. The invasion of receptive field representation is also demonstrated in the cortex, which is highly correlated with the presence of phantom limb pain.
We found that thalamic and cortical stimulation can reverse the invasion when pain is successfully controlled, while stimulation rarely alters phantom limb sensation itself in the same patients. The effects of stimulation on pain have been accounted for by inhibition of pathways mediating noxious information through activation of pathways mediating innocuous information. However, restoration of the original receptive field representation may better explain the therapeutic effects of stimulation.
142 EFFECT OF LESIONAL MASS ON fMRI AND N20 SOURCE LOCATION: A PRE-SURGICAL STUDY
G. Pauletto, R. Budai, L. Weiss, G. Valiante, M. Mondani, P. Bergonzi and M. Skrap First Author-Presenter: Giada Pauletto Institution: Neurology, Department of Neurosciences, Azienda Ospedaliero-Universitaria, S. Maria della Misericordia, Udine, Italy Tel: +39 0432 552569 e-mail: [email protected] Co-Authors-Institution: Riccardo Budai, Gabriele Valiante, Paolo Bergonzi - Neurology, Department of Neurosciences, Azienda Ospedaliero-Universitaria, S. Maria della Misericordia, Udine, Italy; Luca Weiss, Massimo Mondani, Miran Skrap - Neurosurgery, Department of Neurosciences, Azienda Ospedaliero-Universitaria, S. Maria della Misericordia, Udine, Italy.
Purpose Functional studies, such as fMRI and N20 source localization, are useful tools to study eloquent areas pre- surgically. The aim of the present study is to assess the localizing value of N20 source comparing with fMRI data and to evaluate how lesional mass affects motor and sensory function on both the healthy and the affected side.
Methods We evaluated 18 subjects affected by brain tumours, located before (10) and behind (8) the central sulcus, all with unremarkable neurological assessment. They underwent fMRI with finger tapping tasks and N20/N30 source localization (N20/N30 dipole and current source density N20/N30) as pre-surgical studies. Concordance between neurophysiological measures and fMRI results was calculated according to Kendall index. Asymmetry index was used to assess the relationship between lesion localization and functional cortical reshaping.
Results Concordance value was > 0.72, revealing a good match of the results obtained by the two different methods we considered. Calculating asymmetry index, we observed an inverse relationship between tumours localization with respect to central sulcus and functional reshaping of motor and sensitive areas. This result was comparable both in neurophysiological signals and haemodynamical parameters.
Conclusions The absence of neurological motor and sensory impairment does not exclude a functional cortical reshaping. The combination of data acquired by neurophysiological methods and fMRI permits to evaluate a possible reshaping of eloquent areas and provides useful information to plan the most suitable surgical approach and intraoperative monitoring.
143 MOTOR EVOKED POTENTIALS BY DIRECT STIMULATION OF MOTOR CORTEX: IS THERE A PLACE FOR THE SECOND MOTONEURON?
G. Pauletto, R. Budai, M. Mondani, P. Bergonzi and M. Skrap First Author-Presenter: Giada Pauletto Institution: Neurology, Department of Neurosciences, Azienda Ospedaliero-Universitaria, S. Maria della Misericordia, Udine, Italy Tel: +39 0432 552569 e-mail: [email protected] Co-Authors-Institution: Riccardo Budai, Paolo Bergonzi - Neurology, Department of Neurosciences, Azienda Ospedaliero-Universitaria, S. Maria della Misericordia, Udine, Italy; Massimo Mondani, Miran Skrap - Neurosurgery, Department of Neurosciences, Azienda Ospedaliero-Universitaria, S. Maria della Misericordia, Udine, Italy.
Purpose Motor evoked potentials (MEPs), obtained by direct electrical stimulation of motor cortex, are widely used in intraoperative monitoring. They present a degree of variability in amplitude of resulting composed motor action potentials (cMAPs). In the present study, we focus our attention on cMAP amplitude variability, with respect to the possible role played by spinal motoneuron in modulating amplitude values.
Methods We evaluated all patients who underwent intra-operative monitoring of internal capsule, in the period between July 2007 and April 2009. MEPs were obtained with cortical stimulation, according to the so-called technique of “train-of-five” (3-5 stimuli, inter-stimulus interval of 2 msec and duration of 300 μsec). Muscular response was recorded by superficial EMG of 4 upper limb muscles. In some cases, electrical stimulation was carried out also subcortically, with a deep electrode. Peripheral facilitation was elicited by performing a passive movement of the hand.
Results We collected data on 126 patients, mainly affected by primary brain tumours (87%); 89 of them underwent surgery under general anaesthesia, while 37 patients underwent “awake craniotomy”. The majority of patients presented with lesions localized in temporal and frontal lobe (48 and 29 respectively). In 90% of cases, we recorded fluctuations in cMAP amplitude, without any harms for the integrity of motor pathway. Facilitation always determined an increase in cMAPs amplitude, ranging from 30 to 50% of the base-line value.
Conclusions Fluctuations in cMAP amplitude are common both in general anaesthesia and awake craniotomy; they do not represent a risk for post-operative motor deficits. The mechanism underlying the variability of cMAP amplitude recognizes both cortical and peripheral influences.
144 TRANSCRANIAL ELECTRICAL STIMULATION IN PATIENTS WITH VENTRICULOPERITONEAL SHUNTS
First author-Presenter: Jonas K E Persson Institution: Department of Clinical Neurophysiology, Karolinska University Hospital, Solna, Sweden Phone/fax: +46 8 517 726 56 / +46 8 517 724 02 E-mail: [email protected] Co-authors-Institution: Gudrun Måbäck, Catharina Skote and Eeva Öhman Department of Clinical Neurophysiology,Karolinska University Hospital, Solna, Sweden
Introduction Transcranial electrical stimulation (TES) has emerged as an effective and practical way to monitor spinal motor function during surgery (MacDonald 2006, Deletis and Sala 2008). There are, however, a number of relative contraindications for TES, including the presence of ventriculoperitoneal shunts (MacDonald 2002). In our opinion there is a need for TES motor evoked potential (MEP) monitoring in these patients. The aim of this study was to summarize our experience of TES MEP monitoring in this patient group.
Methods All TES MEP monitoring procedures performed during 18 consecutive months at Karolinska University Hospital in patients having a ventriculoperitoneal shunt were included (n=9). The patients were between 35 months and 33 years of age, none had epilepsia.
Four different types of shunt systems were represented in these patients, two of which were adjustable. These adjustable systems were subjected to TES in six occasions. One of the adjustable systems could easily be checked with an extern magnet which was done pre-operative in three out of five possible cases and post-operative in all five, the other adjustable system (one single case) needed an x-ray which was not done. In the two occasions at which pre-operative magnetic checks were not performed, the original values were received from the patient files. Three of the four different shunt systems had metal components in the shunt mechanism.
Results The intra- or post-operative medical complications were limited to only one single patient which had a temporary post-operative complain of headace, yet without any obvious shunt malfunction. Four out of five post-operative magnetic checks showed no change in the shunt setting; in one, however, there was a need of post-operative adjustment.
Conclusion Patients with ventriculoperitoneal shunts is a small but significant group upon which surgery, which potentially could impair central nervous function, is performed. The need of TES MEP monitoring in this patient group is obvious; however, it is not known whether shunts increase TES hazards (MacDonald 2006). In our limited material, unselected with regard to patient age, type of procedure or shunt device, medical or technical complications were finite and reversible.
References: Deletis V, Sala F. Clin Neurophysiol 2008; 119: 248-64. MacDonald DB. J Clin. Monit Comput 2006: 20: 347-77. MacDonald.DB. J Clin Neurophysiol 2002; 19: 416-29.
145 OCD SYMPTOMS TREATED WITH NUCLEUS ACCUMBENS DEEP BRAIN STIMULATION: INTRAOPERATIVE OBSERVATIONS IN TWO CASES
First author-Presenter: Roberto Cordella R Institution: Fondazione IRCCS Neurologico “Carlo Besta”, Milan, Italy Phone\Fax:00390222932411\00390270635017 Email: [email protected] Co-author institution: Angelo Franzini, Carlo Marras, Giuseppe Messina, Giovanni Broggi- Dept of Neurosurgery, Fondazione IRCSS Neurologico “C. Besta”, Milan, Italy Riccardo Muffati: Dept Of Psychiatry, San Paolo Hospital, Milan, Italy
Introduction Obsessive Compulsive Disorder (OCD) is a relatively common disorder, characterized by the presence of intrusive thoughts and compulsive behaviors and rituals, and consequential in a poor quality of life1. Nucleus accumbens (NA) has been recognized to play an important role in reward, pleasure and addiction. Several neuroimaging studies of patients affected by OCD have pointed to basal ganglia and orbitofrontal cortex being relevant to the pathophysiology of this disorder2. As a central relay structure between amygdala, basal ganglia, mesolimbic dopaminergic areas, mediodorsal thalamus and prefrontal cortex, NA has been proposed as a target for deep brain stimulation (DBS) in OCD3. Due to the lack of data about to the firing rate and pattern of humans NA neurons, this study aimed to describe the microrecordings findings in patients who undergone to NA deep brain stimulation (DBS) leads to improve OCD symptoms.
Methods During the surgery subcortical exploration employing microelectrodes (250µm tip), was carried out to explore the anatomical structure of the nuclei. Continuous recording began as soon as the microelectrode extruded into the brain, usually 10mm above the target. Single unit activity was sampled in 2 OCD patients. Both were under general anesthesia during the surgery. Post-3D trajectory‘s reconstruction has allowed us to identify with a convinced accuracy the location of the sampled neurons. In addition spontaneous firing rate and firing discharge were studied. To assess the periodicity of the firing discharge autocorrelograms and power spectra were plotted to perform respectively, a time-domain and a frequency-domain analyses.
Results At the beginning of the each microelectrode trajectory, usually 10mm above the target, no activity was recorded for 3-5mm. From the 3D reconstruction this was recorded in the internal capsule. Lack of activity followed by some neurons firing tonically at very low frequencies (5Hz ca), and a few firing at higher rate (15Hz ca). From the trajectory reconstruction these activities were recorded in the NA. The discharge pattern was non periodic, although in this latter group a very small number of cases displayed periodicity. At the bottom of each trajectory it was sampled neuronal activity from the subgenual cortex. These neurons fired tonically at very high rate (>30Hz), and were easily distinguished from NA activity.
Conclusions Microrecordings were helpful to investigate the anatomical structures of the nuclei. In addition the firing discharge encountered has showed some similarity with previously published animal studies. Due to the small number of studied neurons, these data should be evaluated with caution, but they represent a beginning in understanding the NA neural organization in OCD.
References 1. Koran LM, Thienemann ML, Davenport R (1996): Quality of life for patients with obsessive-compulsive disorder. Am J Psychiatry 153:783–788. 2. Saxena S, Rauch SL: Functional neuroimaging and the neuroanatomy of obsessive-compulsive disorder. Psychiatr Clin North Am 2000 23:563–586. 3. Sturm V, Lenartz D, Koulousakis A, Treuer H, Herholz K, Klein JC, Klosterkötter J. The nucleus accumbens: a target for deep brain stimulation in obsessive-compulsive- and anxiety-disorders. J Chem Neuroanat. 2003 Dec;26(4):293-9.
146 CLINICAL OUTCOME IN CHILDREN WITH TETHERED CORD SYNDROME EARLY RELEASED UNDER INTRAOPERATIVE NEUROPHYSIOLOGICAL MONITORING
First Author Presenter: Conill, J. Institution: Hospital Universitari Vall d’Hebron. Clinical Neurophysiology Department 08035.-BARCELONA. SPAIN Phone: +34 93 489 3187 E-mail: [email protected] Co-Authors: ALONSO, I. Clinical Neurophysiology, GARCIA, G.; GUILLEN, A.; COSTA, JM. Neurosurgery SOLA, E. Anaesthesiology Institution: Hospital Universitari Sant Joan de Deu 08950.-Esplugues. BARCELONA. SPAIN
Introduction Tethered spinal cord secondary to lipoma of the conus can be responsible for progressive neurological impairment in children. It is suggested that early surgery in this congenital defect can help to prevent further deterioration of neurological functions, but there is no agreement. Moreover, surgery carries a risk of injuring normal nervous tissue. Thus, intraoperative neurophysiological monitoring (IOM) is advised. We performed a retrospective review of patients younger that one and half years of age and analyzed their clinical outcome for four years after surgery.
Material and Methods A total of 13 patients operated from March 2001 to November 2004 were identified. Mean age at surgery: 11, 2 months (4-18m). We excluded 2 cases without follow-up in our institution. Mean follow-up in 11 patients: 6years 5months (4-8y). All the patients were asymptomatic preoperatively. IOM was done under stable anaesthesia (Propofol and Fentanyl without neuromuscular blockade) conditions with cortical somatosensory evoked potentials by sciatic nerve stimulation, free-EMG from muscles of both lower limbs and anal sphincter, and mapping using a low intensity electrical stimulation of the cauda equina through the surgical field.
Results We found normal outcome in 8 of 11 patients. There were 2 cases of worsening in the immediately postoperative time. A patient presented weakness in his right leg and other one urinary tract infections. Only 1 case showed late deterioration with progressive signs of neurogenic bladder, without motor deficit.
Discussion In both cases, false negatives in IOM can be explained with the fact we did not use monitoring of motor evoked potential introaperatively. Moreover, the anal sphincter electrode could not differentiate left and right anal hemi sphincter activity. Other reported series found late deterioration in almost 50% of cases in which elderly patients were operated, in spite of the fact they were preoperatively asymptomatic. We advise for early surgical intervention with IOM in order to improve the clinical outcome. We will find more conclusive data as patients get older.
147 SUBCORTICAL MAPPING OF THE CORTICOSPINAL TRACT: CORRELATION WITH DTI TRACTOGRAPHY AND REAL-TIME INTRAOPERATIVE ULTRASOUND BASED NAVIGATION
First Author: Akiva Korn Institution: Department of Neurosurgery, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel Phone / Fax: 972-544623126 / 972-29920818 Email: [email protected] Co-Authors: Erez Nossek, Department of Neurosurgery, Tel Aviv Sourasky Medical Center Maya Weinstein, Advanced Brain Imaging Center, Tel Aviv University and Medical Center Odeya Marmor, Department of Neurosurgery, Tel Aviv Sourasky Medical Center Andrew Kanner, Department of Neurosurgery, Tel Aviv Sourasky Medical Center Shlomi Constantini, Department of Pediatric Neurosurgery, Tel Aviv Sourasky Medical Center Talma Hendler, Advanced Brain Imaging Center, Tel Aviv University and Medical Center Zvi Ram, Department of Neurosurgery, Tel Aviv Sourasky Medical Center
Introduction Subcortical mapping of the corticospinal-tract (CST) using motor evoked potentials (MEP) in supratentorial surgery is of current interest. While rough distance to CST/ MEP threshold associations have been described, most reported data remains empirical. A quantitative study correlating multiple distances from CST with respective MEP stimulus thresholds is necessary.
Methods 42 patients harboring deep-seated supratentorial tumors approaching the CST, who underwent preoperative diffusion tensor imaging (DTI) tractography were included. Intraoperatively, DTI tractography was registered into the navigation system and brainshift was corrected with integrated real-time ultrasound (IOUS) to determine accurate proximity to the CST. Intraoperative MEPs were collected from 10 channels of contralateral musculature. Points of cathodal subcortical stimulation (≤ 20mA) were evaluated at multiple resection depths. Collected variables were: threshold for MEP, MEP distribution, and corrected CST proximity. Exclusion criteria for data points included (1) maximum inherent navigational inaccuracies, (2) stimulation proximity to the primary motor cortex, and (3) low translational quality of IOUS/ MRI-DTI. Stimulation points were plotted in a distance/threshold curve and evaluated for best-fit R2 value. Postoperative clinical outcomes were correlated to lowest threshold values for respective patients.
Results Successful image registration and subcortical stimulation with positive MEP recordings was established in 33 patients (76%). A total of 65 subcortical stimulation points were assessed. 43 yielded positive MEP recordings. A distance /threshold curve showed a linear relationship of 0.97 mA/mm ±0.3 S.D. with a 0.69 R2 value. 22 points of negative MEP responses corresponded to distances beyond 25mm. There was a trend of generalized distribution of MEP responses correlating with deeper stimulus locations. There was a high association of immediate postoperative motor deficit rate associated with thresholds of ≤6.8mA.
Conclusion Our quantitative data support a linear relationship between distances to CST and MEP stimulation thresholds in the context of surgery for deep seated supratentorial tumors.
148 SHORTENING OF CORTICAL TIBIAL SEP-LATENCIES IMMEDIATELY AFTER COMPLETED SURGICAL CORRECTION OF SCOLIOSIS
Erik Nordh, Kristina Edvardsson, Anna Birkegård & Håkan Jonsson*/ Dep of Clinical Neurosciences, Div of Clinical Neurophysiology and Dep of Surgery and Perioperative Sciences; Div of Orthopaedic Surgery; Umeå University Hospital; Umeå, Sweden Phone: (+46) 90 785 3560 Email: [email protected]
Introduction Intra-operative monitoring of spinal cord integrity is done by recording responses in selected muscles to motor cortex stimulation, or the evoked somatosensory cortical responses (SEP) to tibial nerve stimulation. If total intravenous sedation is used, a loss of muscle responses is an early indicator of spinal cord injury. SEP is fairly unaffected by inhalation sedation, but is more time consuming to perform, and may also be notably unaffected until late in spinal cord injury (cf. [1]). SEP has also been used to enlighten trauma-related spinal pathop- hysiology. Recently, Wu et al [2], reported reversible increases in SEP latencies following occlusion of the segmental vessels during anterior spinal surgery, indicating that SEP may be sensitive to changes in circulation. The purpose of the present work was to study whether SEP performed immediately prior to and after corrective scoliosis surgery show any systematic change in latencies.
Methods Intraoperative SEP was recorded under complete intravenous anaesthesia in 25 patients with scoliosis (15 females/10 males, mean age 17.5 years). Spinal cord integrity was monitored with transcranially evoked responses bilaterally in the Tibialis anterior muscles [3]. Tibial SEPs were registered at Fz, Cz´and C3 (international 10-20 EEG montage) immediately before the start, and after the end of the corrective surgery. Latencies to the P40-vawe were determined off-line. Statistical tests were done with non-parametric methods.
Results The main finding was that all patients bilaterally showed significantly shorter SEP latencies direct after surgery compared to before, with a decrease in average latency from 39 to 37.5 msec (≈ 4% ; p<0.001, Mann-Whitney matched-pairs). The only increased latency (+0.1 msec) was found in a patient where introperative monitoring showed loss of muscle responses, and a postoperative neurological exam a temporary limb sensory deficit.
Conclusion Significantly shortened SEP latencies immediately after scoliosis surgery indicate that the correction not only improve the mechanical spinal conditions, but also improve the spinal signal transmission.
References 1. Chiappa, K.A. “Evoked Potentials in Clinical Medicine”; 2:nd ed. (1983); New York, Raven Press. 2. Wu, L., Qiu, Y., Ling, W. Shen, Q. Changed pattern of somatosensory-evoked potentials after occlusion of segmental vessels; possible indicator for spinal cord ischaemia, Eur. Spine J. 15 (2006), 335-340. 3. Andersson G., Ohlin A. Spatial facilitation of motor evoked responses in monitoring during spinal surgery, Clinical Neurophysiology 110 (1999) 720-724
149 MOTOR EVOKED POTENTIAL MONITORING IN THORACIC DISCECTOMY
First author-presenter: Vivianne van Kranen-Mastenbroek Institution: Maastricht University Medical Centre, Maastricht, the Netherlands Phone/fax: 0031433877272 / 0031433875265 Email: [email protected] Co-authors: Erwin Cornips, Ariane Bour, Paul Bergs, Werner Mess Co-authors institution: Maastricht University Medical Centre, Maastricht, the Netherlands
Introduction In recent years, discectomy using the anterior approach, either thoracoscopic or minitransthoracic, has become the treatment of choice for herniated thoracic discs, especially when they are large, central, and/or calcified. Nevertheless, some large and giant hernias present an enormous challenge to the surgeon. In order to prevent neurological complications intraoperative motor evoked potential (MEP) monitoring may be of advantage. The results of MEP monitoring in 46 thoracic discectomies are presented.
Methods Between 2002 and 2009 approximately 250 thoracic hernias were operated in our centre. The thoracoscopic or minitransthoracic procedure was performed during single lung ventilation. MEP monitoring was used in 46 selected patients with large to giant thoracic disc herniations and important clinical and/or radiological myelopathy. MEPs were achieved by transcranial electrical stimulation (TES) with recording of muscle MEPs from both arms and legs. Whenever reproducible MEP changes were noted, the neurosurgeon was informed and operation strategy was adjusted if possible.
Results MEP monitoring was successfully achieved in 40 out of 46 procedures (87%). In 27 of 40 procedures (67.5%) MEPs were stable and all patients remained neurologically unchanged. Significant MEP changes were noted in 13 patients (32.5%): temporary deterioration or disappearance of MEPs was seen in 8 patients. Permanent deterioration of MEP amplitudes was seen in 2 patients. None of these patients showed new neurological deficits.
In 2 patients both arm and leg MEPs disappeared during a hypotensive period. In one of them the already very low amplitude leg MEPs did not recover before the end of the procedure. Both patients remained neurologically unchanged. Permanent disappearance of leg MEPs with preservation of arm MEPs was seen in 1 patient. This patient postoperatively suffered from a complete and permanent paraplegia.
Conclusion In our large experience, after a learning curve of the operation team (including surgeon, neurophysiologist and anaesthetist), intraoperative MEP monitoring definitely improves safety during discectomy of large to giant thoracic hernias. It provides important feedback to the neurosurgeon working around the spinal cord. Adjustment of operation strategy to MEP changes, including correction of hypotension, can help to prevent permanent damage to the corticospinal tract. Complete loss of MEPs during manipulation around the spinal cord in normotensive conditions, predicts (transient or permanent) motor deficit.
150 INTRAOPERATIVE NEUROPHYSIOLOGICAL MONITORING IN SURGICAL TREATMENT OF SPINAL GANGLIOGLIOMA: A CASE REPORT
Chiara Minardi, Neurology Unit, Neuroscience Department Bufalini Hospital, Cesena, Italy 00390547352643 [email protected] Roberto Donati*, Armando Mastrilli*, Serenella Cerasoli**, Anna Maria Mauro, Massimo Frattarelli* *Neurosurgery Unit, **Patological Anatomy Unit
Ganglioglioma is a rare benign tumor. About 130 cases have been reported (Loftinia 2009, Jallo 2004). A total resection represents the first choice in surgery strategy and, if the diagnosis is made early, the patient could have no neurological deficit.
We report a case of a twelve year old boy presenting a dorsal back pain without any neurological deficit. A D9 level spinal cord lesion was detected at MRI. A total surgical removal was performed with neurophysiological monitoring. Transcranial electric motor evoked potential (MEP) were recorded from upper and lower limbs and a D wave was recorded with an epidural electrode under the lesion (Deletis 2002, Deletis and Sala 2008).
Somatosensory evoked potential were recording with stimulation of four limbs. During the surgery a decrement and a disappearance of MEP at the right lower limb was detected with a stable D wave. A transient weakness 4/5 MRC was present at right lower limb with a complete recovery and no permanent neurological deficit. Histological studies showed a ganglioglioma I grade according to OMS. In this case neurophysiological monitoring performed with motor evoked potential, D wave and somatosensory evoked potentials has permitted a radical resection with no permanent neurological deficit. The neurophysiological monitoring is adopted in child spinal cord neurosurgery (Kothbauer 2007) and is useful in order to improve the clinical outcome.
References 1. Deletis V. “Intraoperative neurophysiology and methodologies used to monitor the functional integrity of the motor system” cap 2, p25-49 in Neurophysiology in Neurosurgery Ed. Deletis V and Shils JL Academic Press Elsevier NY 2002 2. Deletis V and Sala F. Corticospinal tract monitoring with D and I waves from the spinal cord and muscle MEPs from limb muscle. Vol 8. Cap 16. p235-251 in Handbook of clinical Neurophysiology Ed. Nuwer Elsevier Amsterdam 2008 3. Jallo GI, Freed D and Epstein F. Spinal cord gangliogliomas: a review of 56 patients Journal of Neuro-Oncology 68: 71- 77, 2004. 4. Kothbauer KF. Neurosurgical management of intramedullary spinal cord tumors in children. Pediatric Neurosurgery 2007; 43: 222-235. 5. Lotfinia I and Vahedi P. Intramedullary cervical spinal cord ganglioglioma, review of the literature and therapeutic controversies. Spinal Cord 2009; 47, 87-90
151 POSTERIOR ROOT MUSCLE REFLEX: ELICITING H-REFLEX BY PERCUTANEOUS STIMULATION OF CAUDA EQUINA
Arapović D.¹, Rogić M.², Deletis V.³ ¹Shool of Medicine, University of Mostar, Bosnia and Herzegovina ² Department for Neuroscience, School of Medicine, University of Split, Croatia ³ St. Luke’s/Roosevelt Hospital, New York, USA Correspondence to: Arapović Dalibor. Phone: 00387 36 472784 E-mail: [email protected]
Aim To elicit H-reflex by percutaneous electric stimulation of lumbar region and determine H-wave parameters
Introduction This study is based on H-reflex, a deep tendon reflex elicited by electric stimulation of a peripheral nerve. It is analogous to tendon jerk reflex (1-3). It is reliably elicited only in triceps surae muscle with involvement of the S1 segment of the spinal cord, while other segments of the spinal cord are not involved (4). Posterior root muscle reflex (PRMR) is a new concept of eliciting H-reflex. Aferent nerve fibers are stimulated proximally and in various lumbo-sacral segments simultaneously (5,6).
Methods We tested ten healthy adult volunteers. Stimulation: constant current stimuli of 0.5 ms duration, manually triggered, every a couple of seconds. Percutaneous stimulating electrodes were placed over the skin of the projection of the first (cathode) and third lumbar (anode) spinous process, respectively. Recording electrodes were placed over the muscle belly of: Hamstring (H), Quadriceps (Q), Anterior tibial (TA) and Triceps surae (TS) muscles. Stimulation was performed by double stimuli with 50 ms interstimulus interval (Fig. 1)
Results PRMR in at least two muscle groups could be elicited in nine of ten subjects. In one subject PRMR was not obtained. In three subjects PRMR could not be recorded from quadriceps muscle. PRMR parameters are: Mean intensity threshold (ms): RQ, 80,71±25,12; LQ, 97,15±17,5; RH, 86,33±28,49; LH, 88,46±28,39; RTA, 85,77±28,85; LTA, 89,56±27,52; RTS, 87,16±30,54; LTS, 88,56±30,61. Mean latency time (ms): RQ, 11±0,8; LQ, 10,5±0,5; RH, 12,56±2,12; LH, 12,57±2,12; RTA, 17,74±2,4; LTA, 17,54±2,38; RTS, 17,66±1,52; LTS, 17,63±1,33. Mean H-wave amplitude (µV): RQ, 95±17,5; LQ 136,1±34,8; RH, 371,64±341,4; LH, 489,45±470,32; RTA, 401,43±270,95; LTA, 505,85±323,48; RTS, 1007,2±507,75; LTS, 955,55±848,91 (Table 1).
Conclusion H-reflex is elicitable in several lumbar spinal cord segments by percutaneous electrical stimulation of the lumbar region. Long latency response and lack of the response after the second stimulus lead us to conclusion that the response is of reflex nature, not due to the anterior root stimulation.
References 1. Lloyd DPC. Reflex action in relation to pattern and peripheral source of afferent stimulation. J Neurophysiol 1943;6:111–119. 2. Cooper R, Binnie C, Billings R. Techniques in clinical neurophysiology: A practical manual. Amsterdam: Elsevier Ltd: 2003. Chapter 4, Measurement of nerve conduction; p. 67-72. 3. Tucker JK, Tuncer M, Turker SK. A review of the H-refex and M-wave in the human triceps surae. Human Movement Science 2005;24:667-688. 4. Leppanen RE. Intraoperative applications of the H-reflex and Fresponse: a tutorial. J Clin Monit Comput 2006; 20: 267–304 5. Minassian K, Dimitrijevic RM. Posterior root–muscle reflexes elicited by transcutaneous stimulation of the human lumbosacral. Muscle Nerve 2007;35: 327–336. 6. Hofstoetter SU, Minassian K, Hofer C, Mayr W, Rattay F and Dimitrijevic RM. Modification of Reflex Responses to Lumbar Posterior Root Stimulation by Motor Tasks in Healthy Subjects. Artificial Organs 2008;32:644–648.
152
Fig. 1: PRMR amplitudes. A double stimuli with 50 ms interstimulus interval (arrows). After first stimulus H-wave occurs (big circle), while after second it is missing (small circle). Two PRMR trials have been superimposed.
Table 1. PRMR average values
INTENSITY (mA) LATENCY (ms) AMPLITUDE (µV)
QUADRICEPS R 80,71±25,12 11±0,8 95±17,5 (Q) L 97,15±17,5 10,5±0,5 136,1±34,8
HAMSTRING R 86,33±28,49 12,56±2,12 371,64±341,4 (H) L 88,46±28,39 12,57±2,12 489,45±470
TIBIALIS R 85,77±28,85 17,74±2,4 401,43±270,95 ANTERIOR (TA) L 89,56±27,52 17,54±2,38 505,85±323,48
TRICEPS R 87,16±30,54 17,66±1,52 1007,2±507,75 SURAE (TS) L 88,56±30,61 17,63±1,33 955,55±848,91
153 SUBDURAL AIR LIMITS THE SOMATOSENSORY AND MOTOR EVOKED POTENTIALS MONITORING DURING SURGERY IN THE SITTING POSITION
Pedro Perez, J*; Fernandez-Conejero*, I; Conesa Beltran, G**; Acebes Martin, JJ*** First Author Presenter: Pedro Perez, Jordi Institution: Hospital Universitari de Bellvitge, Barcelona, Spain Phone/fax: +34 932607711 Email: [email protected] CoAuthors-Institution: * Department of Neurology and ***Department of Neurosurgery, “Hospital Universitari de Bellvitge”, **Department of Neurosurgery, “Hospital del Mar”
Introduction In 1985 Mc Pherson et al. and in 1986 Schubert et al., reported for the first time the effect of intraoperative subdural air collection on the sensory evoked potentials (SEPs) during posterior fossa surgeries in the sitting position. They showed a decrement in amplitude of SEPs immediately after the dura was opened due to CSF leakage and the consecutive entrance of air in the subdural space. We show the importance of on time recognizing subdural air collection and its distribution and the effects on the SEPs and MEPs during skull base surgery in the sitting position.
Patient and Methods We present a 28 years old patient with brain stem cavernoma and gait ataxia, left side body paresthesias and slight weakness on right side of face. We performed SEPs by stimulation of both median nerves. The recording electrodes were corkscrew type placed subcutaneously at C3' and C4' vs. reference electrode placed at FPz. The MEPs were elicited by transcranial electrical stimulation (TES) using corkscrew electrodes with montage C1 vs. C2. The stimulation parameters were short train of 5 stimuli with 0.5 ms duration each, 4 ms ISI. The recording electrodes were two subdermal needle electrodes inserted in abductor pollicis brevis, extensor digitorum longus and anterior tibialis.
Results SEPs for upper extremities and MEPs from the all four extremities were recorded immediately after positioning the patient in the sitting position. Opening dura and arachnoidea were followed by progressive loss of upper extremities MEPs, and progressive amplitude decrement of right median SEP without changes of its latency, and complete loss of left median SEP. The increment of stimulation intensity of TES did not improve the amplitude of upper extremities MEPs. No changes in the lower extremities MEPs were observed. Immediately after surgery a brain CT was done, showing a significant collection of subdural and intraventricular air, mostly over the right hemisphere without presence of air in the midline.
Conclusion 1. Intraoperative neuromonitoring of long pathways in the sitting position can be limited by entrance of subdural air with its insulating effect to electrical current. 2. Neuromonitoring needs to be done with multimodality (SEPs and MEPs) and for all four extremities in order to distinguish between surgical and non-surgical related changes. 3. Intraoperative skull X ray should confirm/exclude subdural air collection and contribute to the differentiation between surgically and non-surgically induced changes of evoked potentials. 4. The sitting position can limit value of intraoperative monitoring.
References 1. McPherson, R.W., Toung, TJ.IL, Jolmsoh, R.M., Rosenbanm, A.E. Wang, H. Intracranial subdural gas: a cause of false- positive change of intraoperative somatosensory evoked potential. Anesthesiology, 1985, 62: 816-819. 2. Schubert A, Zornow MH, Drummond JC, Luerssen, T.G. Loss of cortical evoked responses due to intracranial gas during posterior fossa craniotomy in the seated position. Anesth Analg, 1986, 65: 203-206. 3. Eiju Watanabe, Johannes Schramm and Wolfgang Schneider, Effect of a subdural air collection on the sensory evoked potential during surgery in the sitting position. Electroencephalography and clinical Neurophysiology, 1989, 74:194-201 4. TH Kombos; O Suess; T Pietila; M Brock, Subdural air limits the elicitation of compound muscle action potentials by high frequency electric transcranial electrical stimulation British Journal of Neurosurgery; Jun 2000; 14(3), 240-243
154 PERIPHERAL NERVE GRAFTS IN A BIODEGRADABLE MULTI CHANNEL PROSTHESIS RESULT IN AXONAL REGENERATION AND POSITIVE MOTOR EVOKED POTENTIALS AFTER SPINAL CORD RESECTION
First author-Presenter: Jonas K E Persson Institution: Department of Clinical Neuroscience Karolinska Institute; Stockholm, Sweden Phone/fax: +46 8 517 726 56 / +46 8 517 724 02 E-mail: [email protected] Co-authors-Institution: Jonathan Nordblom, Mikael Svensson and Per Mattsson Department of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden; Olof Eriksson and Jonas Åberg Materials in Medicine, Uppsala University Uppsala, Sweden
Introduction The regeneration promoting capacity of peripheral nerves has previously been successfully tried to bridge the injury gap after spinal cord injury. Based on the knowledge of white matter regeneration inhibiting factors, directing outgrowing axons to permissive grey matter has been shown to improve functional outcome if combined with local application of acidic Fibroblast growth factor. The current work uses the strategy of guiding outgrowing axons from white to grey matter.
Methods We developed a spinal cord prosthesis to replace an injury gap after spinal cord resection in rat. The prosthesis contained 12 channels, each carrying a peripheral nerve graft. The positions of the channel entrances and exits were set in accordance with neuroanatomical maps to let the grafts guide descending motor tracts from the cranial spinal cord to the motor neuronal pools in the grey matter of the caudal cord and ascending sensory tracts from the caudal cord to sensory neuronal pools in the grey matter of the cranial cord. Adult rats were subjected to a 3 mm spinal cord resection at the level of T11, and the spinal cord was replaced by the nerve graft containing the prosthesis described above. The prosthesis contained vehicle, low or high concentration of acidic Fibroblast growth factor. The rats were sacrificed up to 20 weeks post lesion. Before sacrifice, the rats were tested for motor evoked potentials in the hind limbs after stimulation of the motor cortex of the brain.
Results The spinal cord prosthesis was completely degraded at 20 weeks post lesion. Electrophysiology showed positive motor evoked potentials (MEP) in all repair groups, but not in injured control animals. The tissue was analyzed by immunohistochemistry and semi-thin sections. From 4 weeks post lesion both descending and ascending tracts in the white matter had extensively grown into the nerve grafts. At 20 weeks post lesion axons had reached into the other side of the spinal cord. The nerve grafts in the prosthesis had neovascularized and the new axons within were of mature myelinated character.
Conclusion We conclude that a biodegradable prosthesis to guide outgrowing axons from white to grey matter after a spinal cord resection maintains the projections of the peripheral nerve grafts and results in central regeneration and consistent MEP. Local release of aFGF did not alter the MEP results in the current setting.
There were three groups of rats in this study, eight rats in each group. One group have been treated with a spinal cord prosthesis soaked in saline as a vehicle, one group treated with a spinal cord prosthesis soaked in a low concentration of acidic Fibroblast growth factor and one group treated with a spinal cord prosthesis soaked in a high concentration of acidic Fibroblast growth factor. We had positive MEPs in all three repair groups, but to a significant higher extent in FGF-soaked cases compared to the vehicle-soaked group. Furthermore, all positive MEPs were abolished following re-lesion of the spinal cord.
The injured control animals mentioned in the abstract were collected and presented in a previous, recently published study (Nordblom, Persson, Svensson and Mattsson. Restorative Neurology and Neuroscience 2009; 27: 285-95) and was done in five animals as a spinal cord transection and resection of 3 mm.
155 INTRAOPERATIVE NEUROPHYSIOLOGICAL IDENTIFICATION OF CONTRALATERAL STROKE DURING SURGERY OF ANTERIOR CEREBRAL ARTERY ANEURYSM
First Author-Presenter: E. Araus-Galdós Institution: St. Lukes/Roosevelt Hospital – New York Phone: 0034618100020 Email: [email protected] Co-Authors-Institution:I. Fernández-conejero-St. Lukes/Roosevelt Hospital; E. Lladó-Carbó St. Lukes/Roosevelt Hospital; J. Urriza St. Lukes/Roosevelt Hospital; S. Ulkatan St. Lukes/Roosevelt Hospital; V. Deletis St. Lukes/Roosevelt Hospital
Introduction Intracranial aneurysm can be surgicaly treated by permanent clipping of the aneurysm’s neck. Although this treatment can prevent an anurysm rapture, occlusion of blood flow from the feeding vessels to critical neural tissue can occur during the procedure.
In patients with anterior cerebral artery (ACA) or anterior communicant artery (AComA) aneurysm the standard methodology for intraoperatively monitoring includes bilateral somatosensory evoked potentials (SEPs) and bilateral motor evoked potentials (MEPs) from upper and lower extremities. ACA and AcomA supply lower extremities area of sensorimotor cortex, therefore, during clipping time intraoperative neurophysiological monitoring (IONM) is focused on lower extremities SEPs and MEPs.
Patients and Methods We present two patients with intracranial aneurysms and no neurological deficit before surgery. Patient #1 was 43 years old and had right AcomA aneurysm. Patient #2 was 54 years old and had Left ACA aneurysm. Both patients underwent craniotomy and aneurysm clipping. The methodology for IONM included: SEPs from upper and lower extremities were performed by stimulation of bilateral median nerve and bilateral posterior tibial nerve and MEPs after transcranial electrical stimulation (TES) in distal muscles of the all four limbs as well as direct cortical stimulation (DCS).
Results Patient #1 (Right Acom aneurysm) had decrement in the amplitude of the right lower extremity SEPs (>50%) compared with baseline after a permanent clip was placed and persisted low after repositioning of the clip. Post operative CT scan showed subarachnoid hemorrhage in the left frontal lobe. MEPs showed no changes.
Patient #2 (Left ACA aneurysm) had decrement in amplitude of the left lower extremity SEPs (>50%) compared with baseline during a temporary clip placement and. SEPs did not return to baseline after the temporary clip was removed. MEPs were elicited with very high threshold at a baseline, and were maintained till the end of surgery. Post operative CT scan showed right ACA infarct. Postoperatively patient had left crural monoplegia.
Conclusion: During surgery of intracranial aneurysms located at the anterior circulation, monitoring of lower extremities SEPs should be performed bilaterally in order to identify a potential contralateral stroke from the operated side and if it is possible to avoid it by repositioning the temporary or permanent clip.
We consider that TES elicited MEPs at this anerysm localization is not very reliable because it can bypass ischemic site by distal stimulation. Anterior circulation does not give perforator arteries in almost any patient, therefore IONM with SEPs can be sufficient methodology to detect cerebral ischemia.
156 INTRAOPERATIVE DIRECT CORTICAL VISUAL EVOKED POTENTIALS
First autor-Presenter: Victoria Fernández Institution: Clinical Neurophysiology Service. Hospital Regional Universitario Carlos Haya, Málaga, Spain Phone/fax: +34619020992 Email: [email protected] Co-Authors-Insititution: MªJose Postigoa, Miguel Angel Arraezb, Enrique Bauzanoa- Clinical aNeurophysiology Service. b Neurosurgery Service. Hospital Regional Universitario Carlos Haya , Málaga, Spain
Introduction Surgical approaches that give access to the hiatus tentorialis produce prolonged retraction of both occipital lobes of the brain, with the subsequent risk of ischemia because of compression and possible vascular flow reduction. These problems if persist could generate a cortical blindness. Our objective was to detect intraoperatively possible lesions of the occipital cortex in neurosurgeries that implies maintained occipital lobe retraction.
Methods We present an intraopertive technique that register visual evoked potentials directly from the occipital cortex. The stimulators are red diodes mounted in goggles and the response from the occipital cortex is registered by means of a subdural electrode of 4 contacts fixed to the surgical instrumental used in lobe retraction.
Results We have used this technique in 5 patients. The responses were reproducible and monitorable. The technique was safe with no complication due to the positioning or use of the electrode. Lost of intraoperative registered responses was followed by immediate release of retraction and repositioning of surgical instrumental. Rapid recuperation of the responses after these manoeuvres was a good predictor of an outcome without complications. None of our patients developed any postoperative visual deficit.
Conclusion The use of intraoperative direct cortical visual evoked potentials in neurosurgery interventions that imply maintained occipital lobe retraction is safe and of great usefulness to avoid possible serious complications as cortical blindness.
157 METHODOLOGY FOR INTRAOPERATIVE MULTIMODAL MONITORING IN SPINAL CORD TUMORS: FOUR PATIENTS REPORT
Climent A., St. Lukes/Roosevelt Hospital- New York Phone/fax: 212.222.4356 Email: [email protected] Perez-Fajardo G., Ulkatan S., Arranz B., Deletis V.- St. Lukes/Roosevelt Hospital- New York
Introduction The advances of neurophisiological methodologies changed significantly the intraoperative monitoring of the spinal cord surgeries. We present four patients with spinal cord tumors using the latest multimodal intraoperative techniques.
Material and Methods Three patients with intradural/extramedullary tumors and one patient with intramedullary tumor are presented. The extramedullary tumors were: C4- C6 neurofibroma, T8-T11 meningioma and conus dermoid tumor. Patient with intramedullary tumor had a C1-C3 ependimoma. The patients were two males and two females, age range 28 - 74 years.
Monitoring was performed using following methodologies: somatosensory evoked potential (SEP), recorded from the epidural space of the spinal cord (sSEP) and scalp (cSEP) after stimulation of median and tibial nerves. Motor evoked potential (MEP) was elicited by transcranial electrical stimulation (TES) and recorded from epidural space of the spinal cord (D wave) using catheter electrode as well from upper and lower extremities limb muscles (muscle MEP).
In addition to previously described methodologies, we used different specific techniques according to the patient tumor level. Those techniques were: lower cranial nerve corticobulbar MEP (CoMEP) in the cervicomedullary junction tumor, bulbocavernosus reflex (BCR), anal sphinter MEPs, for lumbosacral tumors.
In the patient with the intramedullary tumor we used a dorsal column mapping technique prior to myelotomy to determine the functional midline, in order to avoid myelotomy induced lesion to the dorsal columns, and according to its results, the surgeon performed myelotomy.
Results We successfully applied all these techniques and detected significant changes in some parameters of evoked potentials in three of four patients which correlated with the postoperative neurological exam.
Conclusion In small sample of patients we show utility of multimodal IOM correlated with neurological exam.
References Deletis V., Sala F. Intraoperative neurophysiological monitoring of the espinal cord during spinal cord and spine surgery: A review focus on the corticospinals tracts. Clinical Neurophysiology 119(2008) 248-264
158 ENHANCEMENT OF FLASH ELICITED VISUAL EVOKED POTENTIALS (VEP) BY DOUBLE PULSE STIMULATION IN HEALTHY SUBJECTS
Lladó-Carbó E., Ulkatan S., Pérez-Fajardo G., Araus-Galdós E., Fernández-Conejero I., Stecker M *., Shils J**., Deletis V. Department of Intraoperative Neurophysiology, St.Luke’s-Roosevelt Hospital. New York City. New York. USA. * Department of Neurology, Marshall University, Huntington, WV, USA **Department of Neurosurgery, The Lahey Clinic, Burlington, MA, USA
Introduction: There is a continuous interest in monitoring functional integrity of the visual system during surgery of lesions around the visual pathways. Unfortunately results reported in the literature on the usefulness of visual evoked potentials (VEP) for intraoperative monitoring are conflicting. Different methodologies such as flash-evoked VEPs by using light-emitting diodes and pattern VEPs have been tried with non-conclusive and reproducible results. Our studies introduce recently available ultra bright diodes to induce flash elicited VEPs in a group of healthy subjects.
Objective The objective is to enhance flash-elicited VEP eliciting by double pulse stimuli using ultra bright diodes in awake healthy subjects.
Material and Methods 10 healthy subjects (age range between 29 and 63 y), without ocular and/or vision pathology. They underwent VEPs testing after 10’ of accommodation to dark. Stimulation: An ultra bright array of 6 diodes mounted in the swimming goggles. (Fig. 2). The duration of entire test was about 60 min. Recordings: Cup electrodes are placed over the scalp at CZ/OZ according to the 10/20 International EEG system, and a corneal electrode referenced to FZ for recording electroretinogram (ERG) is placed on the eye in order to study ERG contribution to VEP. Specially designed goggles are used, consisting of embedded 6 diodes as a light source connected to the to external controller (Fig.1) for controlling light intensity, number and duration of stimuli (100 to 5000 µs). A 5 volts trigger signal initiates the flash and stimuli. The following protocol was applied:
- 1 to 2 stimuli with ISI of 10, 25, 40 and 50 ms and train repetition rate of 0.5, 1.0, 2.0, and 3.0 Hz). - The hardware filter (1.5-284 Hz) and digital filters 20-284 Hz, with 100 averaged a single sweeps, and epoch duration of 300 ms.
Fig. 1 Home made system for triggering and power supply to the goggles
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Fig 2. Swimming goggles with embedded array of 6 ultra bright goggles
Fig. 3. VEPs elicited by 1 and 2, stimuli 25 and 50 ms apart.
Preliminary Results 1. The highest amplitude of P-100 was recorded using 2 stimuli 50 ms apart, duration of individual stimuli of 5000 µs, intensity of 8000 mA and stimulating rate of 2-3 Hz. This ISI, resulted in a more reliable and reproducible response in comparison with single stimulus (Fig. 3). The mean amplitude of P-100 was 15-25 µV and mean latency of 115 ms. 2. The longest ISI which enhances amplitude of P-100 was 128 ms. 3. No contribution of ERG as a far-field potential is observed.
Conclusion Recently available ultra bright diodes embedded in the goggles enhanced flash elicited VEP P-100 amplitude in a group of healthy subjects if 2 stimuli 50 ms apart were used. Possible application of this new methodology in the operating room may be way to introduce a new VEP intraoperative monitoring methodology.
160 COMPARISON OF TWO METHODS OF ELECTRICAL STIMULATION DURING SUBCORTICAL GLIOMA RESECTION
Szelényi, A., Jardan M., Franz K., Senft C., Vatter H., Seifert V.. Department of Neurosurgery, Johann Wolfgang Goethe University Hospital, Frankfurt a. M., Germany
Introduction In glioma surgery, subcortical electrical stimulation (“mapping“) is used for activation of the corticospinal tract and thus to determine resection boundaries. Two techniques have evolved: a) bipolar 50 Hz stimulation introduced by Penfield (1930) and b) monopolar high frequency multipulse train introduced by Taniguchi (1995).
The stimulation frequency and polarity with regard to the motor threshold and reliability for eliciting MEPs were studied.
Patients and methods 21 patients (50 ± 17 years; 10 female) undergoing tumor resection (4 precentral, 9 postcentral, 7 temporal, 1 supracerebellar location) under general anesthesia participated. 50 Hz stimulation (monophasic cathodal pulses each of 0.5 ms pulse width, 1 s train duration) and a multipulse stimulation (5 monophasic cathodal pulses of 0.5 ms duration each, interstimulus interval of 4 ms, 0.5 Hz repetition rate) were applied with a bipolar probe (1.5 mm ball tip, 8 mm interelectrodes distance) and a monopolar probe (1.5 mm diameter tip). MEPs were recorded contralaterally to the stimulated hemisphere from abd. pollicis brevis, extensor digit. comm., biceps brachii and tibialis ant. muscles. Stimulation intensities for eliciting MEPs were determined in mA (constant current stimulation, max. 25 mA). Comparative stimulation was performed at the subcortical location, where the monopolar multipulse stimulation elicited MEPs with the lowest stimulation intensity.
Results Monopolar multipulse stimulation elicited MEPs with intensity of 8.2 ± 3.9 mA in all 21 patients; monopolar 50 Hz stimulation with intensity of 12 ± 5.4 mA in 18 patients; bipolar 50 Hz stimulation with intensity of 15.1 ± 6.3 mA in 11 patients and bipolar multipulse stimulation with intensity of 13.7 ± 8.1 mA in 12 patients. In 11 patients MEPs were elicited with monopolar technique was 5.4 ± 2.1 mA compared to 15.1 ± 6.1 mA with the bipolar technique (paired t-test p < 0.0001).
Conclusion Stimulation intensities for eliciting MEPs are significantly higher for bipolar compared to monopolar stimulation regardless of the stimulation frequency (p < 0.01). This resulted in eliciting MEPs in a higher number of tested patients (Fisher's p < 0.0001). Thus, subcortical stimulation with the monopolar probe is more reliable for the purpose of identifying the corticospinal tract. This is explained by the more radiant electric field properties of the monopolar probe compared to the bipolar probe.
161 LOSS OF MOTOR EVOKE POTENTIALS DURING LUMBAR SPINAL FUSION WITH INSTRUMENTATION: CASE REPORT
Authors: Baoqing Wang, Alice Kamp, Tracey Lacey, Lawrence Wierzbowski, Yutong Zhang Institution: Neurological Monitoring Services, The Reading Hospital and Medical Center, West Reading, Pennsylvania, USA Phone/Fax: 610.373.8900 / 610.373.9700 Email: [email protected]
Introduction The authors report a rare case of complete motor evoked potentials (MEP) loss in a female adult during a lumbar fusion and instrumentation, with significant post-operative neurological deficits. The possibilities of cauda equina or spinal nerve roots injury during such surgeries, and intraoperative neurophysiological monitoring strategy and techniques are discussed.
Case Presentation The patient was a 48-years-old female with a history of previous lumbosacral spinal surgeries with L3-S1 instrumentation. She presented with lower back pain and severe right leg pain, and underwent a minimally invasive decompressive hemilaminectomy L2-3 and revision instrumentation. When distraction was applied at L2-3 in preparation for insertion of the interbody cage, motor evoked potential by transcranial electrical stimulation recorded from bilateral lower extremities were lost, together with posterior tibial nerve somatosensory evoked potentials (SSEP). Brief spontaneous neurotonic EMG activity from tibialis anterior and gastrocnemis muscles were also recorded. Distraction was released, steroids protocol was administrated, and blood pressure was maintained. Tibial nerve SSEP returned with much reduced amplitudes and prolonged latencies; however the MEP remained absent for the rest of the surgical procedure. The surgeon elected not to implant the interbody cage. Post-operatively the patient presented with diffuse weakness and altered sensation in her legs, as well as neurogenic bladder and bowel. MRI studies did not show significant neural structural impingement. She received rehabilitation treatment and had gradual recovery of the lower extremity function.
Conclusion Lumbar spinal surgeries with instrumentation may have possible complications of either single or multiple spinal nerve roots injury, resulting in changes in neurophysiological signals such as motor evoked potentials. Intraoperative neurophysiological monitoring with multiple modalities is recommended, so that timely warning of altered neural function may enable the surgeon to initiate intervention to minimize post-operative impairment.
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