Sacral Neuromodulation in Lower Urinary Tract Dysfunction
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Sacral Nerve Stimulation for Urinary Voiding Dysfunction and Fecal
Medical Coverage Policy Effective Date ............................................10/15/2020 Next Review Date ......................................10/15/2021 Coverage Policy Number .................................. 0404 Sacral Nerve and Tibial Nerve Stimulation for Urinary Voiding Dysfunction, Fecal Incontinence and Constipation Table of Contents Related Coverage Resources Overview .............................................................. 1 Biofeedback Coverage Policy ................................................... 1 Electrical Stimulation Therapy and Devices General Background ............................................ 3 Fecal Bacteriotherapy Medicare Coverage Determinations .................. 19 Injectable Bulking Agents for Urinary Conditions and Coding/Billing Information .................................. 19 Fecal Incontinence References ........................................................ 21 INSTRUCTIONS FOR USE The following Coverage Policy applies to health benefit plans administered by Cigna Companies. Certain Cigna Companies and/or lines of business only provide utilization review services to clients and do not make coverage determinations. References to standard benefit plan language and coverage determinations do not apply to those clients. Coverage Policies are intended to provide guidance in interpreting certain standard benefit plans administered by Cigna Companies. Please note, the terms of a customer’s particular benefit plan document [Group Service Agreement, Evidence of Coverage, Certificate of Coverage, -
Orienting Head Movements Resulting from Electrical Microstimulation of the Brainstem Tegmentum in the Barn Owl
The Journal of Neuroscience, January 1993, 13(l): 351370 Orienting Head Movements Resulting from Electrical Microstimulation of the Brainstem Tegmentum in the Barn Owl Tom Masino and Eric I. Knudsen Department of Neurobiology, Stanford University, Stanford, California 943055401 The size and direction of orienting movements are repre- movement latency, duration, velocity, and size each dem- sented systematically as a motor map in the optic tectum of onstrated dependencies on stimulus amplitude, frequency, the barn owl (du Lac and Knudsen, 1990). The optic tectum and duration. projects to several distinct regions in the medial brainstem The data demonstrate directly that at the level of the mid- tegmentum, which in turn project to the spinal cord (Masino brain tegmentum there exists a three-dimensional Cartesian and Knudsen, 1992). This study explores the hypothesis that representation of head-orienting movements such that hor- a fundamental transformation in the neural representation izontal, vertical, and roll components of movement are en- of orienting movements takes place in the brainstem teg- coded by anatomically distinct neural circuits. The data sug- mentum. Head movements evoked by electrical microstim- gest that in the projection from the optic tectum to these ulation in the brainstem tegmentum of the alert barn owl were medial tegmental regions, the topographic code for orienting cataloged and the sites of stimulation were reconstructed movement that originates in the tectum is transformed into histologically. Movements elicited from the brainstem teg- this Cartesian code. mentum were categorized into one of six different classes: [Key words: optic tectum, superior colliculus, saccadic saccadic head rotations, head translations, facial move- head movement, brainstem tegmentum, interstitial nucleus ments, vocalizations, limb movements, and twitches. -
Smedimnic INFORMATION for PRESCRIBERS Medtronic Interstimo Therapy
InterStim lBowelenlcvm W141/08 1:40pm Medtronic Confidential US Mlar1elRelease er 4.5 aS6nches (114 mma 152Mm) NuoFO SMedimnic INFORMATION FOR PRESCRIBERS Medtronic InterStimO Therapy Rx only M925905AW3 Rev X Inter~fir Sowan c.ahtm W/l4/0 1:40 M Medtronic Confidential US Mautt Release 4,5x 6inchesa(114 mm x 152 mm) NeurolPO m Medironic * and InlerStim' are registered trademarks and SoftStartStop ' is a trademark of Meduronic, Inc. Additional Information available for the InterStin, Therapy system Documents packaged with this product: * For therapy-specific information, refer to the Indications Insert. * For Information regarding device compatibility, refer to the System Overview and Compatibility Insert - For information on the clinical study resuita for InterStinm Therapy and for a complete summary of adverse events, refer to the Clinical Summary. * For warranty Information, refer to the Limited Warranty and Special Notice Insert Documents packaged with the clinician programmer software application card: *For neurostimulator selection, battery longevity calculations, and specific neurostimulator specifications, refer to the System Eligibility Battery Longevity, Specifications Reference Manuoal. M925905AC03 Rev X InterSdm_ oeIenTOCm B11408 1:40pm Medtronlc Confidential USMat Release 4.5 x inches (114 mm a I5 ramm) NeurolFPROO Contraindications 5 Warnings 5 Electromagnetic interference (EMI) 5 Case Carnage 7 Effects on other implanted devices 7 Precautions 7 Clinician programming 7 Clinician training 9 Patient activities 9 Patient programming -
Optogenetic Activation of Cholinergic Neurons in the PPT Or LDT Induces REM Sleep
Optogenetic activation of cholinergic neurons in the PPT or LDT induces REM sleep Christa J. Van Dorta,b,c,1, Daniel P. Zachsa,b,c, Jonathan D. Kennya,b,c, Shu Zhengb, Rebecca R. Goldblumb,c,d, Noah A. Gelwana,b,c, Daniel M. Ramosb,c, Michael A. Nolanb,c,d, Karen Wangb,c, Feng-Ju Wengb,e, Yingxi Linb,e, Matthew A. Wilsonb,c, and Emery N. Browna,b,d,f,1 aDepartment of Anesthesia, Critical Care, and Pain Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114; and bDepartment of Brain and Cognitive Sciences, cPicower Institute for Learning and Memory, eMcGovern Institute for Brain Research, fHarvard-MIT Division of Health Sciences and Technology, and dInstitute for Medical Engineering and Science, Massachusetts Institute of Technology, Cambridge, MA 02139 Contributed by Emery N. Brown, December 3, 2014 (sent for review September 19, 2014; reviewed by Helen A. Baghdoyan and H. Craig Heller) Rapid eye movement (REM) sleep is an important component of REM sleep regulation, a method that can modulate specific cell the natural sleep/wake cycle, yet the mechanisms that regulate types in the behaving animal is needed. Optogenetics now pro- REM sleep remain incompletely understood. Cholinergic neurons vides this ability to target specific subpopulations of neurons in the mesopontine tegmentum have been implicated in REM sleep and control them with millisecond temporal resolution (30). regulation, but lesions of this area have had varying effects on REM Therefore, we aimed to determine the role of cholinergic sleep. Therefore, this study aimed to clarify the role of cholinergic neurons in the PPT and LDT in REM sleep regulation using neurons in the pedunculopontine tegmentum (PPT) and laterodor- optogenetics. -
Medical Policy
Medical Policy Joint Medical Policies are a source for BCBSM and BCN medical policy information only. These documents are not to be used to determine benefits or reimbursement. Please reference the appropriate certificate or contract for benefit information. This policy may be updated and is therefore subject to change. *Current Policy Effective Date: 5/1/21 (See policy history boxes for previous effective dates) Title: Sacral Nerve Neuromodulation/Stimulation Description/Background Sacral nerve neuromodulation (SNM), also known as sacral nerve stimulation (SNS), is defined as the implantation of a permanent device that modulates the neural pathways controlling bladder or rectal function. This policy addresses use of SNM in the treatment of urinary or fecal incontinence, urinary or fecal nonobstructive retention and chronic pelvic pain in patients with intact neural innervation of the bladder and/or rectum. Urinary and Fecal Incontinence Urgency-frequency is an uncontrollable urge to urinate, resulting in very frequent, small volumes and is a prominent symptom of interstitial cystitis (also called bladder pain syndrome). Urinary retention is the inability to completely empty the bladder of urine. Fecal incontinence can arise from a variety of mechanisms, including rectal wall compliance, efferent and afferent neural pathways, central and peripheral nervous systems, and voluntary and involuntary muscles. Fecal incontinence is more common in women, due mainly to muscular and neural damage that may occur during vaginal delivery. Treatment Treatment using SNM, also known as indirect SNS, is one of several alternative modalities for patients with fecal or urinary incontinence (urge incontinence, significant symptoms of urgency- frequency, or nonobstructive urinary retention) who have failed behavioral (e.g., prompted voiding) and/or pharmacologic therapies. -
Brainstem Dental 2012.Doc
Dental Neuroanatomy January 12 and 19, 10-12, 2012 Suzanne S. Stensaas, Ph.D. Dear Students: Please print these notes and bring them with you. My style is to use a Tablet PC and I draw on either a Word or pdf copy with colors. Be prepared to draw. Have at least 5 colors. Please try to look at the notes AHEAD OF TIME for each lecture in this course. This way you can see the direction and organization of the lecture and be more familiar with the terms. There will be a quiz (that does not count) at the beginning to cover topics in the two gross anatomy lectures by Dr. Morton in Phase 1. They are G 17B and GL 18 Waxman, S Clinical Neuroanatomy, 26th ed.2010. THE OLD EDITION IS FINE TOO. Review Ch 5 on the spinal cord organization, but not the tracts in the middle or lesions at the end of the chapter. Also review the basic concept of a reflex. Review or skim Ch 12 on the vascular supply of the brain. Just look at pictures and legends for the clinical part at the end. NEW material: Chapter 7 Waxman, Brainstem, but not the cerebellum part. NEW material: Chapter 8 Waxman, Cranial nerves, all of it including autonomic. BEWARE THE CRANIAL NERVES ARE KILLERS! There are about 50 copies of the following bright yellow paperback book, which can be checked out from the Eccles Health Sciences Library and kept for the duration of the course. They are on reserve as: Cranial nerves: anatomy and clinical comments Linda Wilson-Pauwels, 1988 Toronto; Philadelphia: B.C. -
Sacral Nerve Stimulation for Urinary Indications
Sacral nerve stimulation for urinary indications November 2008 MSAC application 1115 Assessment report © Commonwealth of Australia 2008 ISBN 1-74186-790-8 ISBN 1-74186-791-6 ISSN 1443-7120 ISSN 1443-7139 First printed Paper-based publications © Commonwealth of Australia 2008 This work is copyright. Apart from any use as permitted under the Copyright Act 1968, no part may be reproduced by any process without prior written permission from the Commonwealth. Requests and inquiries concerning reproduction and rights should be addressed to the Commonwealth Copyright Administration, Attorney General’s Department, Robert Garran Offices, National Circuit, Barton ACT 2600 or posted at http://www.ag.gov.au/cca Internet sites © Commonwealth of Australia 2008 This work is copyright. You may download, display, print and reproduce this material in unaltered form only (retaining this notice) for your personal, non-commercial use or use within your organisation. Apart from any use as permitted under the Copyright Act 1968, all other rights are reserved. Requests and inquiries concerning reproduction and rights should be addressed to Commonwealth Copyright Administration, Attorney General’s Department, Robert Garran Offices, National Circuit, Barton ACT 2600 or posted at http://www.ag.gov.au/cca Electronic copies of the report can be obtained from the Medical Service Advisory Committee’s Internet site at http://www.msac.gov.au/ Printed copies of the report can be obtained from: The Secretary Medical Services Advisory Committee Department of Health and Ageing Mail Drop 106 GPO Box 9848 Canberra ACT 2601 Enquiries about the content of the report should be directed to the above address. -
Isolated Necrosis of Central Tegmental Tracts Due to Neonatal Hypoxic-Ischemic Encephalopathy: MRI Findings
Journal of Neurology & Stroke Case Report Open Access Isolated necrosis of central tegmental tracts due to neonatal hypoxic-ischemic encephalopathy: MRI findings Abstract Volume 11 Issue 1 - 2021 Perinatal hypoxia is an old entity that still prevails today and may lead to neurological Tomás de Andrade Lourenção Freddi, Luiz sequelae that can go unnoticed until a certain age, generating many costs for public health. In this case report, we demonstrate on magnetic resonance imaging an unusual pattern of Fellipe Curvêlo Ciraulo Santos, Nelson Paes perinatal hypoxia in a preterm 5-month-old infant, involving the central tegmental tracts Fortes Diniz Ferreira, Felipe Diego Gomes and briefly discuss its possible pathophysiology. Dantas Department of Radiology, Hospital do Coração, Brazil Keywords: magnetic resonance imaging, asphyxia, hypoxic-ischemic encephalopathy, tegmentum, neonates, brainstem Correspondence: Tomás de Andrade Lourenção Freddi, Hospital do Coração, 147 Desembargador Eliseu Guilherme Street, São Paulo, SP, 04004-030, Brazil, Tel +5511976059280, Email Received: May 25, 2020 | Published: Febrauary 15, 2021 Abbreviations: MRI, magnetic resonance imaging; HII, that connect the red nucleus and the inferior olivary nucleus, being hypoxic-ischemic injury; FLAIR, fluid-attenuated inversion recovery; part of the dentato-rubro-olivary system, called Guillain–Mollaret CTT, central tegmental tract; VGB, vigabatrin triangle.3–5 Introduction Hypoxic-ischemic injury (HII) is one of the most important causes of encephalopathy in neonates, irrespective of gestational age, and may occur in the uterus or during delivery by different intrapartum conditions. In preterm or very low birth weight infants, brain magnetic resonance imaging (MRI) can demonstrate multiple different findings, which a detailed description is beyond the scope of this article, although being periventricular leukomalacia the most frequent (seen in at least 50% of cases). -
Chapter 128: Basic Mechanisms of Sleep: New Evidence On
128 BASIC MECHANISMS OF SLEEP: NEW EVIDENCE ON THE NEUROANATOMY AND NEUROMODULATION OF THE NREM-REM CYCLE EDWARD F. PACE-SCHOTT J. ALLAN HOBSON The 1990s brought a wealth of new detail to our knowledge NREM sleep (noradrenergic, serotonergic, and cholinergic of the brain structures involved in the control of sleep and systems damped), and REM sleep (noradrenergic and sero- waking and in the cellular level mechanisms that orchestrate tonergic systems off, cholinergic system undamped) (1–4). the sleep cycle through neuromodulation. This chapter pre- sents these new findings in the context of the general history Original Reciprocal Interaction Model: An of research on the brainstem neuromodulatory systems and Aminergic-Cholinergic Interplay the more specific organization of those systems in the con- trol of the alternation of wake, non–rapid eye movement The model of reciprocal interaction (5) provided a theoretic (NREM), and REM sleep. framework for experimental interventions at the cellular and Although the main focus of the chapter is on the our molecular level that has vindicated the notion that waking own model of reciprocal aminergic-cholinergic interaction, and REM sleep are at opposite ends of an aminergically we review new data suggesting the involvement of many dominant to cholinergically dominant neuromodulatory more chemically specific neuronal groups than can be ac- continuum, with NREM sleep holding an intermediate po- commodated by that model. We also extend our purview to sition (Fig. 128.1). The reciprocal interaction hypothesis the way in which the brainstem interacts with the forebrain. (5) provided a description of the aminergic-cholinergic in- These considerations inform not only sleep-cycle control terplay at the synaptic level and a mathematic analysis of per se, but also the way that circadian and ultradian rhythms the dynamics of the neurobiological control system. -
Urinary Incontinence Treatment
Urinary Incontinence Treatment Date of Origin: 07/2002 Last Review Date: 03/24/2021 Effective Date: 04/01/2021 Dates Reviewed: 01/2004, 02/2005, 01/2006, 02/2007, 03/2008, 03/2009, 02/2011, 02/2012, 02/2013, 02/2014, 10/2015, 03/2016, 06/2017, 08/2018, 03/2019, 03/2020, 03/2021 Developed By: Medical Necessity Criteria Committee I. Description A number of procedures have been investigated for the treatment of urinary incontinence, including pelvic floor muscle exercises, behavioral therapy, sacral nerve stimulation, pelvic floor stimulation, surgery, and radiofrequency energy. InterStim Continence Control Therapy is sacral nerve stimulation that involves the implantation, into the lower back, of electrical leads that are in contact with the sacral nerve root. The wire leads extend through an incision in the abdomen and are connected to an inserted pulse generator to deliver controlled electrical impulses. The physician programs the pulse generator and the individual is able to switch the pulse generator on and off. Percutaneous tibial nerve stimulation with Urgent® PC by Uroplasty involves the placement of a fine needle electrode into the lower, inner aspect of the leg, near the tibial nerve. The needle electrode is connected to pulse generator that delivers an electrical pulse to the tibial nerve that travels to the sacral plexus. The sacral plexus is responsible for regulating bladder and pelvic floor function. The treatment protocol is for 12 treatments, once a week. An artificial urinary sphincter is a device that involves an inflatable cuff that fits around the urethra. A balloon regulates the pressure of the cuff and a bulb controls inflation and deflation of the cuff. -
A Confocal Microscopic Study of Gene Transfer Into the Mesencephalic Tegmentum of Juvenile Chum Salmon, Oncorhynchus Keta, Using Mouse Adeno-Associated Viral Vectors
International Journal of Molecular Sciences Article A Confocal Microscopic Study of Gene Transfer into the Mesencephalic Tegmentum of Juvenile Chum Salmon, Oncorhynchus keta, Using Mouse Adeno-Associated Viral Vectors Evgeniya V. Pushchina * , Ilya A. Kapustyanov, Ekaterina V. Shamshurina and Anatoly A. Varaksin A.V. Zhirmunsky National Scientific Center of Marine Biology, Far East Branch, Russian Academy of Sciences, 690041 Vladivostok, Russia; [email protected] (I.A.K.); [email protected] (E.V.S.); [email protected] (A.A.V.) * Correspondence: [email protected] Abstract: To date, data on the presence of adenoviral receptors in fish are very limited. In the present work, we used mouse recombinant adeno-associated viral vectors (rAAV) with a calcium indicator of the latest generation GCaMP6m that are usually applied for the dorsal hippocampus of mice but were not previously used for gene delivery into fish brain. The aim of our work was to study the feasibility of transduction of rAAV in the mouse hippocampus into brain cells of juvenile chum salmon and subsequent determination of the phenotype of rAAV-labeled cells by confocal laser scanning microscopy (CLSM). Delivery of the gene in vivo was carried out by intracranial injection of a GCaMP6m-GFP-containing vector directly into the mesencephalic tegmentum region of Citation: Pushchina, E.V.; Kapustyanov, I.A.; Shamshurina, E.V.; juvenile (one-year-old) chum salmon, Oncorhynchus keta. AAV incorporation into brain cells of the Varaksin, A.A. A Confocal juvenile chum salmon was assessed at 1 week after a single injection of the vector. AAV expression in Microscopic Study of Gene Transfer various areas of the thalamus, pretectum, posterior-tuberal region, postcommissural region, medial into the Mesencephalic Tegmentum and lateral regions of the tegmentum, and mesencephalic reticular formation of juvenile O. -
Midbrain Tegmental Lesions Affecting Or Sparing the Pupillary Fibres
J7ournal ofNeurology, Neurosurgery, and Psychiatry 1996;61:401-402 401 J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.61.4.401 on 1 October 1996. Downloaded from SHORT REPORT Midbrain tegmental lesions affecting or sparing the pupillary fibres Naokatsu Saeki, Naohisa Murai, Kenro Sunami Abstract lesion in the upper midbrain and close to the Two patients with oculomotor palsy third ventricle (fig 1). caused by midbrain infarction are Three months later the oculomotor palsy reported. In the first, pupillary reaction improved. The patient returned to his previ- was affected and in the second this reac- ous work after a further three months. tion was spared. Because the lesions in the anterior part of the tegmentum were CASE 2 in the upper midbrain in the first patient A 68 year old woman with hypertension for and in the lower midbrain in the second, eight years suddenly developed vertigo and it is suggested that the pupillary compo- nents of the oculomotor nerve are located in the upper midbrain. (7 Neurol Neurosurg Psychiatry 1996;61:401-402) Keywords: midbrain; oculomotor nerve; pupil sparing We report the details of two patients with a small midbrain infarction, the first with impairment of pupillary reaction to light and the second in which this reaction was pre- served. The aim of this study was to elucidate the topography of oculomotor pupillary fibres in the midbrain tegmentum based on findings using MRI. http://jnnp.bmj.com/ Case studies CASE 1 A 67 year old man with a 10 year history of hypertension presented with difficulty in open- ing his left eye on waking up in the morning.