THE SYNDROMES of the ARTERIES of the BRAIN and SPINAL CORD Part 1 by LESLIE G
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The Segmentation of the Posterior Cerebral Artery: a Microsurgical Anatomic Study
Neurosurgical Review (2019) 42:155–161 https://doi.org/10.1007/s10143-018-0972-y ORIGINAL ARTICLE The segmentation of the posterior cerebral artery: a microsurgical anatomic study Aysun Uz1,2 Received: 1 November 2017 /Revised: 3 February 2018 /Accepted: 22 March 2018 /Published online: 6 April 2018 # Springer-Verlag GmbH Germany, part of Springer Nature 2018 Abstract There are still different descriptions of the segmentation of the posterior cerebral artery, although there is a radiological and anatomical consensus on the segmentation of the anterior and the middle cerebral artery. This study aims to define the most appropriate localization for origin and end points of the segments through reviewing the segmentation of the posterior cerebral artery. The segments and the cortical branches originating from those segments of the 40 posterior cerebral arteries of 20 cadaver brains were examined under operating microscope. In this research, the P1,P2,P3,P4,andP5 classification of the segmentation of the posterior cerebral artery is redefined. This redefinition was made to overcome the complexities of previous definitions. The P1 segment in this research takes its origin from the basilar tip and ends at the junction with the posterior communicating artery. The average diameter of this segment at the origin was 2.21 mm (0.9–3.3), and the average length was 6.8 mm (3–12). The P2 segment extends from the junction with the posterior communicating artery to the origin of the lateral temporal trunk. This point usually situates on one level of posterior of the cerebral peduncle. The average diameter of this segment at the origin was 2.32 mm (1.3–3.1), and the average length was 20.1 mm (11–26). -
Primary Lateral Sclerosis, Upper Motor Neuron Dominant Amyotrophic Lateral Sclerosis, and Hereditary Spastic Paraplegia
brain sciences Review Upper Motor Neuron Disorders: Primary Lateral Sclerosis, Upper Motor Neuron Dominant Amyotrophic Lateral Sclerosis, and Hereditary Spastic Paraplegia Timothy Fullam and Jeffrey Statland * Department of Neurology, University of Kansas Medical Center, Kansas, KS 66160, USA; [email protected] * Correspondence: [email protected] Abstract: Following the exclusion of potentially reversible causes, the differential for those patients presenting with a predominant upper motor neuron syndrome includes primary lateral sclerosis (PLS), hereditary spastic paraplegia (HSP), or upper motor neuron dominant ALS (UMNdALS). Differentiation of these disorders in the early phases of disease remains challenging. While no single clinical or diagnostic tests is specific, there are several developing biomarkers and neuroimaging technologies which may help distinguish PLS from HSP and UMNdALS. Recent consensus diagnostic criteria and use of evolving technologies will allow more precise delineation of PLS from other upper motor neuron disorders and aid in the targeting of potentially disease-modifying therapeutics. Keywords: primary lateral sclerosis; amyotrophic lateral sclerosis; hereditary spastic paraplegia Citation: Fullam, T.; Statland, J. Upper Motor Neuron Disorders: Primary Lateral Sclerosis, Upper 1. Introduction Motor Neuron Dominant Jean-Martin Charcot (1825–1893) and Wilhelm Erb (1840–1921) are credited with first Amyotrophic Lateral Sclerosis, and describing a distinct clinical syndrome of upper motor neuron (UMN) tract degeneration in Hereditary Spastic Paraplegia. Brain isolation with symptoms including spasticity, hyperreflexia, and mild weakness [1,2]. Many Sci. 2021, 11, 611. https:// of the earliest described cases included cases of hereditary spastic paraplegia, amyotrophic doi.org/10.3390/brainsci11050611 lateral sclerosis, and underrecognized structural, infectious, or inflammatory etiologies for upper motor neuron dysfunction which have since become routinely diagnosed with the Academic Editors: P. -
Management of Neurogenic Dysphagia
694 Postgrad Med J 2001;77:694–699 Postgrad Med J: first published as 10.1136/pmj.77.913.694 on 1 November 2001. Downloaded from Management of neurogenic dysphagia A M O Bakheit Dysphagia is common in patients with neuro- of the cerebral cortex, basal ganglia, brain logical disorders. It may result from lesions in stem, cerebellum, and lower cranial nerves may the central or peripheral nervous system as well result in dysphagia. Degeneration of the as from diseases of muscle and disorders of the myenteric ganglion cells in the oesophagus, neuromuscular junction. Drugs that are com- muscle diseases and disorders of neuromusc- monly used in the management of neurological ular transmission, for example myasthenia conditions may also precipitate or aggravate gravis and Eaton-Lambers syndrome, are other swallowing diYculties in some patients. Neuro- less common causes. genic dysphagia often results in serious compli- cations, including pulmonary aspiration, dehy- CEREBRAL CORTEX dration, and malnutrition. These The commonest condition associated with complications are usually preventable if the dysphagia resulting from cortical lesions is stroke. Acute stroke is complicated by dys- dysphagia is recognised early and managed 1 appropriately. phagia in about 25%–42% of all cases. Dysphagia in these patients is usually associ- Physiological mechanisms of neurogenic ated with hemiplegia due to lesions of the brain stem or the involvement of one or both dysphagia The act of swallowing may be viewed as three hemispheres. However, on rare occasions, dys- discrete but inter-related physiological stages: phagia may be the sole manifestation of a cer- the oral, pharyngeal, and oesophageal phases. -
Cerebellar Ataxia
CEREBELLAR ATAXIA Dr. Waqar Saeed Ziauddin Medical University, Karachi, Pakistan What is Ataxia? ■ Derived from a Greek word, ‘A’ : not, ‘Taxis’ : orderly Ataxia is defined as an inability to maintain normal posture and smoothness of movement. Types of Ataxia ■ Cerebellar Ataxia ■ Sensory Ataxia ■ Vestibular Ataxia Cerebellar Ataxia Cerebrocerebellum Spinocerebellum Vestibulocerebellum Vermis Planning and Equilibrium balance Posture, limb and initiating and posture eye movements movements Limb position, touch and pressure sensation Limb ataxia, Eye movement dysdiadochokinesia, disorders, Truncal and gait Dysmetria dysarthria nystagmus, VOR, ataxia hypotonia postural and gait. Gait ataxia Types of Cerebellar Ataxia • Vascular Acute Ataxia • Medications and toxins • Infectious etiologies • Atypical Infectious agents • Autoimmune disorders • Primary or metastatic tumors Subacute Ataxia • Paraneoplastic cerebellar degeneration • Alcohol abuse and Vitamin deficiencies • Systemic disorders • Autosomal Dominant Chronic • Autosomal recessive Progressive • X linked ataxias • Mitochondrial • Sporadic neurodegenerative diseases Vascular Ataxia ▪ Benedikt Syndrome It is a rare form of posterior circulation stroke of the brain. A lesion within the tegmentum of the midbrain can produce Benedikt Syndrome. Disease is characterized by ipsilateral third nerve palsy with contralateral hemitremor. Superior cerebellar peduncle and/or red nucleus damage in Benedikt Syndrome can further lead in to contralateral cerebellar hemiataxia. ▪ Wallenberg Syndrome In -
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ONLINE FIRST This is a provisional PDF only. Copyedited and fully formatted version will be made available soon. ISSN: 0015-5659 e-ISSN: 1644-3284 Two cases of combined anatomical variations: maxillofacial trunk, vertebral, posterior communicating and anterior cerebral atresia, linguofacial and labiomental trunks Authors: M. C. Rusu, A. M. Jianu, M. D. Monea, A. C. Ilie DOI: 10.5603/FM.a2021.0007 Article type: Case report Submitted: 2020-11-28 Accepted: 2021-01-08 Published online: 2021-01-29 This article has been peer reviewed and published immediately upon acceptance. It is an open access article, which means that it can be downloaded, printed, and distributed freely, provided the work is properly cited. Articles in "Folia Morphologica" are listed in PubMed. Powered by TCPDF (www.tcpdf.org) Two cases of combined anatomical variations: maxillofacial trunk, vertebral, posterior communicating and anterior cerebral atresia, linguofacial and labiomental trunks M.C. Rusu et al., The maxillofacial trunk M.C. Rusu1, A.M. Jianu2, M.D. Monea2, A.C. Ilie3 1Division of Anatomy, Faculty of Dental Medicine, “Carol Davila” University of Medicine and Pharmacy, Bucharest, Romania 2Department of Anatomy, Faculty of Medicine, “Victor Babeş” University of Medicine and Pharmacy, Timişoara, Romania 3Department of Functional Sciences, Discipline of Public Health, Faculty of Medicine, “Victor Babes” University of Medicine and Pharmacy, Timisoara, Romania Address for correspondence: M.C. Rusu, MD, PhD (Med.), PhD (Biol.), Dr. Hab., Prof., Division of Anatomy, Faculty of Dental Medicine, “Carol Davila” University of Medicine and Pharmacy, 8 Eroilor Sanitari Blvd., RO-76241, Bucharest, Romania, , tel: +40722363705 e-mail: [email protected] ABSTRACT Background: Commonly, arterial anatomic variants are reported as single entities. -
Supranuclear and Internuclear Ocular Motility Disorders
CHAPTER 19 Supranuclear and Internuclear Ocular Motility Disorders David S. Zee and David Newman-Toker OCULAR MOTOR SYNDROMES CAUSED BY LESIONS IN OCULAR MOTOR SYNDROMES CAUSED BY LESIONS OF THE MEDULLA THE SUPERIOR COLLICULUS Wallenberg’s Syndrome (Lateral Medullary Infarction) OCULAR MOTOR SYNDROMES CAUSED BY LESIONS OF Syndrome of the Anterior Inferior Cerebellar Artery THE THALAMUS Skew Deviation and the Ocular Tilt Reaction OCULAR MOTOR ABNORMALITIES AND DISEASES OF THE OCULAR MOTOR SYNDROMES CAUSED BY LESIONS IN BASAL GANGLIA THE CEREBELLUM Parkinson’s Disease Location of Lesions and Their Manifestations Huntington’s Disease Etiologies Other Diseases of Basal Ganglia OCULAR MOTOR SYNDROMES CAUSED BY LESIONS IN OCULAR MOTOR SYNDROMES CAUSED BY LESIONS IN THE PONS THE CEREBRAL HEMISPHERES Lesions of the Internuclear System: Internuclear Acute Lesions Ophthalmoplegia Persistent Deficits Caused by Large Unilateral Lesions Lesions of the Abducens Nucleus Focal Lesions Lesions of the Paramedian Pontine Reticular Formation Ocular Motor Apraxia Combined Unilateral Conjugate Gaze Palsy and Internuclear Abnormal Eye Movements and Dementia Ophthalmoplegia (One-and-a-Half Syndrome) Ocular Motor Manifestations of Seizures Slow Saccades from Pontine Lesions Eye Movements in Stupor and Coma Saccadic Oscillations from Pontine Lesions OCULAR MOTOR DYSFUNCTION AND MULTIPLE OCULAR MOTOR SYNDROMES CAUSED BY LESIONS IN SCLEROSIS THE MESENCEPHALON OCULAR MOTOR MANIFESTATIONS OF SOME METABOLIC Sites and Manifestations of Lesions DISORDERS Neurologic Disorders that Primarily Affect the Mesencephalon EFFECTS OF DRUGS ON EYE MOVEMENTS In this chapter, we survey clinicopathologic correlations proach, although we also discuss certain metabolic, infec- for supranuclear ocular motor disorders. The presentation tious, degenerative, and inflammatory diseases in which su- follows the schema of the 1999 text by Leigh and Zee (1), pranuclear and internuclear disorders of eye movements are and the material in this chapter is intended to complement prominent. -
ICD9 & ICD10 Neuromuscular Codes
ICD-9-CM and ICD-10-CM NEUROMUSCULAR DIAGNOSIS CODES ICD-9-CM ICD-10-CM Focal Neuropathy Mononeuropathy G56.00 Carpal tunnel syndrome, unspecified Carpal tunnel syndrome 354.00 G56.00 upper limb Other lesions of median nerve, Other median nerve lesion 354.10 G56.10 unspecified upper limb Lesion of ulnar nerve, unspecified Lesion of ulnar nerve 354.20 G56.20 upper limb Lesion of radial nerve, unspecified Lesion of radial nerve 354.30 G56.30 upper limb Lesion of sciatic nerve, unspecified Sciatic nerve lesion (Piriformis syndrome) 355.00 G57.00 lower limb Meralgia paresthetica, unspecified Meralgia paresthetica 355.10 G57.10 lower limb Lesion of lateral popiteal nerve, Peroneal nerve (lesion of lateral popiteal nerve) 355.30 G57.30 unspecified lower limb Tarsal tunnel syndrome, unspecified Tarsal tunnel syndrome 355.50 G57.50 lower limb Plexus Brachial plexus lesion 353.00 Brachial plexus disorders G54.0 Brachial neuralgia (or radiculitis NOS) 723.40 Radiculopathy, cervical region M54.12 Radiculopathy, cervicothoracic region M54.13 Thoracic outlet syndrome (Thoracic root Thoracic root disorders, not elsewhere 353.00 G54.3 lesions, not elsewhere classified) classified Lumbosacral plexus lesion 353.10 Lumbosacral plexus disorders G54.1 Neuralgic amyotrophy 353.50 Neuralgic amyotrophy G54.5 Root Cervical radiculopathy (Intervertebral disc Cervical disc disorder with myelopathy, 722.71 M50.00 disorder with myelopathy, cervical region) unspecified cervical region Lumbosacral root lesions (Degeneration of Other intervertebral disc degeneration, -
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Blepharospasm 40 Years Later Giovanni Defazio, University of Bari Mark Hallett, National Institutes of Health Hyder A Jinnah, Emory University Antonella Conte, Sapienza University Rome Alfredo Berardelli, Sapienza University Rome Journal Title: Movement Disorders Volume: Volume 32, Number 4 Publisher: Wiley | 2017-04-01, Pages 498-509 Type of Work: Article | Post-print: After Peer Review Publisher DOI: 10.1002/mds.26934 Permanent URL: https://pid.emory.edu/ark:/25593/s9pw2 Final published version: http://dx.doi.org/10.1002/mds.26934 Copyright information: © 2017 International Parkinson and Movement Disorder Society. Accessed September 28, 2021 7:17 PM EDT HHS Public Access Author manuscript Author ManuscriptAuthor Manuscript Author Mov Disord Manuscript Author . Author manuscript; Manuscript Author available in PMC 2018 May 09. Published in final edited form as: Mov Disord. 2017 April ; 32(4): 498–509. doi:10.1002/mds.26934. Blepharospasm 40 Years Later Giovanni Defazio, MD, PhD1, Mark Hallett, MD2, Hyder A. Jinnah, MD, PhD3, Antonella Conte, MD, PhD4,5, and Alfredo Berardelli, MD4,5,* 1Department of Basic Medical Sciences, Neurosciences and Sensory Organs, “Aldo Moro”, University of Bari, Bari, Italy 2Human Motor Control Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, USA 3Departments of Neurology, Human Genetics and Pediatrics, Emory University, Atlanta, Georgia, USA 4Department of Neurology and Psychiatry, Sapienza, University of Rome, Rome, Italy 5Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS) Neuromed, Pozzilli, IS, Italy Abstract Forty years ago, C.D. Marsden proposed that blepharospasm should be considered a form of adult- onset focal dystonia. In the present paper, we provide a comprehensive overview of the findings regarding blepharospasm reported in the past 40 years. -
Neurologic Outcomes in Friedreich Ataxia: Study of a Single-Site Cohort E415
Volume 6, Number 3, June 2020 Neurology.org/NG A peer-reviewed clinical and translational neurology open access journal ARTICLE Neurologic outcomes in Friedreich ataxia: Study of a single-site cohort e415 ARTICLE Prevalence of RFC1-mediated spinocerebellar ataxia in a North American ataxia cohort e440 ARTICLE Mutations in the m-AAA proteases AFG3L2 and SPG7 are causing isolated dominant optic atrophy e428 ARTICLE Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy revisited: Genotype-phenotype correlations of all published cases e434 Academy Officers Neurology® is a registered trademark of the American Academy of Neurology (registration valid in the United States). James C. Stevens, MD, FAAN, President Neurology® Genetics (eISSN 2376-7839) is an open access journal published Orly Avitzur, MD, MBA, FAAN, President Elect online for the American Academy of Neurology, 201 Chicago Avenue, Ann H. Tilton, MD, FAAN, Vice President Minneapolis, MN 55415, by Wolters Kluwer Health, Inc. at 14700 Citicorp Drive, Bldg. 3, Hagerstown, MD 21742. Business offices are located at Two Carlayne E. Jackson, MD, FAAN, Secretary Commerce Square, 2001 Market Street, Philadelphia, PA 19103. Production offices are located at 351 West Camden Street, Baltimore, MD 21201-2436. Janis M. Miyasaki, MD, MEd, FRCPC, FAAN, Treasurer © 2020 American Academy of Neurology. Ralph L. Sacco, MD, MS, FAAN, Past President Neurology® Genetics is an official journal of the American Academy of Neurology. Journal website: Neurology.org/ng, AAN website: AAN.com CEO, American Academy of Neurology Copyright and Permission Information: Please go to the journal website (www.neurology.org/ng) and click the Permissions tab for the relevant Mary E. -
Abadie's Sign Abadie's Sign Is the Absence Or Diminution of Pain Sensation When Exerting Deep Pressure on the Achilles Tendo
A.qxd 9/29/05 04:02 PM Page 1 A Abadie’s Sign Abadie’s sign is the absence or diminution of pain sensation when exerting deep pressure on the Achilles tendon by squeezing. This is a frequent finding in the tabes dorsalis variant of neurosyphilis (i.e., with dorsal column disease). Cross References Argyll Robertson pupil Abdominal Paradox - see PARADOXICAL BREATHING Abdominal Reflexes Both superficial and deep abdominal reflexes are described, of which the superficial (cutaneous) reflexes are the more commonly tested in clinical practice. A wooden stick or pin is used to scratch the abdomi- nal wall, from the flank to the midline, parallel to the line of the der- matomal strips, in upper (supraumbilical), middle (umbilical), and lower (infraumbilical) areas. The maneuver is best performed at the end of expiration when the abdominal muscles are relaxed, since the reflexes may be lost with muscle tensing; to avoid this, patients should lie supine with their arms by their sides. Superficial abdominal reflexes are lost in a number of circum- stances: normal old age obesity after abdominal surgery after multiple pregnancies in acute abdominal disorders (Rosenbach’s sign). However, absence of all superficial abdominal reflexes may be of localizing value for corticospinal pathway damage (upper motor neu- rone lesions) above T6. Lesions at or below T10 lead to selective loss of the lower reflexes with the upper and middle reflexes intact, in which case Beevor’s sign may also be present. All abdominal reflexes are preserved with lesions below T12. Abdominal reflexes are said to be lost early in multiple sclerosis, but late in motor neurone disease, an observation of possible clinical use, particularly when differentiating the primary lateral sclerosis vari- ant of motor neurone disease from multiple sclerosis. -
Topical Diagnosis in Neurology
V Preface In 2005 we publishedacomplete revision of Duus’ Although the book will be useful to advanced textbook of topical diagnosis in neurology,the first students, also physicians or neurobiologists inter- newedition since the death of its original author, estedinenriching their knowledge of neu- Professor PeterDuus, in 1994.Feedbackfromread- roanatomywith basic information in neurology,oR ers wasextremelypositive and the book wastrans- for revision of the basics of neuroanatomywill lated intonumerous languages, proving that the benefit even morefromit. conceptofthis book wasasuccessful one: combin- This book does notpretend to be atextbook of ing an integrated presentation of basic neu- clinical neurology.That would go beyond the scope roanatomywith the subject of neurological syn- of the book and also contradict the basic concept dromes, including modern imaging techniques. In described above.Firstand foremostwewant to de- this regard we thank our neuroradiology col- monstratehow,onthe basis of theoretical ana- leagues, and especiallyDr. Kueker,for providing us tomical knowledge and agood neurological exami- with images of very high quality. nation, it is possible to localize alesion in the In this fifthedition of “Duus,” we have preserved nervous system and come to adecision on further the remarkablyeffective didactic conceptofthe diagnostic steps. The cause of alesion is initially book,whichparticularly meets the needs of medi- irrelevant for the primarytopical diagnosis, and cal students. Modern medical curricula requirein- elucidation of the etiology takes place in asecond tegrative knowledge,and medical studentsshould stage. Our book contains acursoryoverviewofthe be taught howtoapplytheoretical knowledge in a major neurologicaldisorders, and it is notintended clinical settingand, on the other hand, to recognize to replace the systematic and comprehensive clinical symptoms by delving intotheir basic coverage offeredbystandardneurological text- knowledge of neuroanatomyand neurophysiology. -
History-Of-Movement-Disorders.Pdf
Comp. by: NJayamalathiProof0000876237 Date:20/11/08 Time:10:08:14 Stage:First Proof File Path://spiina1001z/Womat/Production/PRODENV/0000000001/0000011393/0000000016/ 0000876237.3D Proof by: QC by: ProjectAcronym:BS:FINGER Volume:02133 Handbook of Clinical Neurology, Vol. 95 (3rd series) History of Neurology S. Finger, F. Boller, K.L. Tyler, Editors # 2009 Elsevier B.V. All rights reserved Chapter 33 The history of movement disorders DOUGLAS J. LANSKA* Veterans Affairs Medical Center, Tomah, WI, USA, and University of Wisconsin School of Medicine and Public Health, Madison, WI, USA THE BASAL GANGLIA AND DISORDERS Eduard Hitzig (1838–1907) on the cerebral cortex of dogs OF MOVEMENT (Fritsch and Hitzig, 1870/1960), British physiologist Distinction between cortex, white matter, David Ferrier’s (1843–1928) stimulation and ablation and subcortical nuclei experiments on rabbits, cats, dogs and primates begun in 1873 (Ferrier, 1876), and Jackson’s careful clinical The distinction between cortex, white matter, and sub- and clinical-pathologic studies in people (late 1860s cortical nuclei was appreciated by Andreas Vesalius and early 1870s) that the role of the motor cortex was (1514–1564) and Francisco Piccolomini (1520–1604) in appreciated, so that by 1876 Jackson could consider the the 16th century (Vesalius, 1542; Piccolomini, 1630; “motor centers in Hitzig and Ferrier’s region ...higher Goetz et al., 2001a), and a century later British physician in degree of evolution that the corpus striatum” Thomas Willis (1621–1675) implicated the corpus