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Myelopathy—Paresis and Paralysis in Cats
Myelopathy—Paresis and Paralysis in Cats (Disorder of the Spinal Cord Leading to Weakness and Paralysis in Cats) Basics OVERVIEW • “Myelopathy”—any disorder or disease affecting the spinal cord; a myelopathy can cause weakness or partial paralysis (known as “paresis”) or complete loss of voluntary movements (known as “paralysis”) • Paresis or paralysis may affect all four limbs (known as “tetraparesis” or “tetraplegia,” respectively), may affect only the rear legs (known as “paraparesis” or “paraplegia,” respectively), the front and rear leg on the same side (known as “hemiparesis” or “hemiplegia,” respectively) or only one limb (known as “monoparesis” or “monoplegia,” respectively) • Paresis and paralysis also can be caused by disorders of the nerves and/or muscles to the legs (known as “peripheral neuromuscular disorders”) • The spine is composed of multiple bones with disks (intervertebral disks) located in between adjacent bones (vertebrae); the disks act as shock absorbers and allow movement of the spine; the vertebrae are named according to their location—cervical vertebrae are located in the neck and are numbered as cervical vertebrae one through seven or C1–C7; thoracic vertebrae are located from the area of the shoulders to the end of the ribs and are numbered as thoracic vertebrae one through thirteen or T1–T13; lumbar vertebrae start at the end of the ribs and continue to the pelvis and are numbered as lumbar vertebrae one through seven or L1–L7; the remaining vertebrae are the sacral and coccygeal (tail) vertebrae • The brain -
Clinical Decision Making in Neurology
CLINICAL DECISION MAKING IN NEUROLOGY The Neurological Examination The goals of the neurological examination are to detect the presence of a neurologic disease and to determine the location of the lesion within the nervous system. The neurologic examination should be performed in a systematic manner in order to assure that the animal's neurologic status is completely evaluated. The parts of a customary neurologic examination include evaluation of the head (mentation and cranial nerves), gait, limbs (postural reactions and spinal reflexes) and pain/nociception (normal and abnormal pain responses). Gait Evaluation I find gait evaluation the most useful and important part of the neurologic exam. Clinical evaluation of gait usually involves observation of the animal's movements while walking. This is best accomplished by having a handler walk the animal over a flat, non-slippery area. I typically evaluate gait by having a handler walk the animal approximately 100 feet, away and back, as well as circling clockwise and counterclockwise. I have the animal short on the leash and under good control and have the dog typically walk slowly. I may have them walk on and off the curb. Overall, evaluation is made by watching for paresis, ataxia, stride length, lameness, stiffness, spasticity, dysmetria and shuffling or scuffing of limbs or digits. I also note position of head and tail during gait evaluation. Gait analysis is broken down between the axial and appendicular skeleton. The axial vertebral column is made up of many joints and is divided into anatomical segments. The axial portion includes the head, neck, thoracic, lumbar, lumbar/pelvic and tail. -
Neurological Principles and Rehabilitation of Action Disorders
Neurorehabilitation and Neural Repair Neurological Principles and Rehabilitation Supplement to 25(5) 21 S-32S ©TheAuthor(s) 2011 Reprints and permission: http://www. of Action Disorders: Common sagepub.com/journalsPermissions.nav 001: 10.1177/1545968311410941 Clinical Deficits http://nnr.sagepub.com ~SAGE I 3 K. Sathian, MO, PhO , Laurel J. Buxbaum, Psy02, Leonardo G. Cohen, M0 , 4 6 John W. Krakauer, M0 , Catherine E. Lang, PhO\ Maurizio Corbetta, M0 , 6 and Susan M. Fitzpatrick, Ph0 ,7 In this chapter, the authors use the computation, anatomy, and physiology (CAP) principles to consider the impact of common clinical problems on action They focus on 3 major syndromes: paresis, apraxia, and ataxiaThey also review mechanisms that could account for spontaneous recovery, using what is known about the best-studied clinical dysfunction-paresis-and also ataxia. Together, this and the previous chapter lay the groundwork for the third chapter in this series, which reviews the relevant rehabilitative interventions. Paresis may tilt as it is raised or a key may fall from the fingers. Once Phenomenology the object is in hand, a person with paresis has difficulty mov ing it to some locations. Lifting the cup to the mouth, where The most common motor disorder experienced by individuals the ann movement is close to and directly in front of the body, after central nervous system damage is paresis. In the strictest is usually much easier than lifting the cup to a shoulder-height sense, paresis is the reduced ability to voluntarily activate the shelf on the opposite side of the body. Reaching movements spinal motor neurons. -
The Clinical Approach to Movement Disorders Wilson F
REVIEWS The clinical approach to movement disorders Wilson F. Abdo, Bart P. C. van de Warrenburg, David J. Burn, Niall P. Quinn and Bastiaan R. Bloem Abstract | Movement disorders are commonly encountered in the clinic. In this Review, aimed at trainees and general neurologists, we provide a practical step-by-step approach to help clinicians in their ‘pattern recognition’ of movement disorders, as part of a process that ultimately leads to the diagnosis. The key to success is establishing the phenomenology of the clinical syndrome, which is determined from the specific combination of the dominant movement disorder, other abnormal movements in patients presenting with a mixed movement disorder, and a set of associated neurological and non-neurological abnormalities. Definition of the clinical syndrome in this manner should, in turn, result in a differential diagnosis. Sometimes, simple pattern recognition will suffice and lead directly to the diagnosis, but often ancillary investigations, guided by the dominant movement disorder, are required. We illustrate this diagnostic process for the most common types of movement disorder, namely, akinetic –rigid syndromes and the various types of hyperkinetic disorders (myoclonus, chorea, tics, dystonia and tremor). Abdo, W. F. et al. Nat. Rev. Neurol. 6, 29–37 (2010); doi:10.1038/nrneurol.2009.196 1 Continuing Medical Education online 85 years. The prevalence of essential tremor—the most common form of tremor—is 4% in people aged over This activity has been planned and implemented in accordance 40 years, increasing to 14% in people over 65 years of with the Essential Areas and policies of the Accreditation Council age.2,3 The prevalence of tics in school-age children and for Continuing Medical Education through the joint sponsorship of 4 MedscapeCME and Nature Publishing Group. -
Progressive Supranuclear Palsy: Clinicopathological Concepts and Diagnostic Challenges
Review Progressive supranuclear palsy: clinicopathological concepts and diagnostic challenges David R Williams, Andrew J Lees Lancet Neurol 2009; 8: 270–79 Progressive supranuclear palsy (PSP) is a clinical syndrome comprising supranuclear palsy, postural instability, and Faculty of Medicine mild dementia. Neuropathologically, PSP is defi ned by the accumulation of neurofi brillary tangles. Since the fi rst (Neurosciences), Monash description of PSP in 1963, several distinct clinical syndromes have been described that are associated with PSP; this University, Melbourne, discovery challenges the traditional clinicopathological defi nition and complicates diagnosis in the absence of a reliable, Australia (D R Williams FRACP); Reta Lila Weston Institute of disease-specifi c biomarker. We review the emerging nosology in this fi eld and contrast the clinical and pathological Neurological Studies, characteristics of the diff erent disease subgroups. These new insights emphasise that the pathological events and University College London, processes that lead to the accumulation of phosphorylated tau protein in the brain are best considered as dynamic London, UK (A J Lees FRCP, processes that can develop at diff erent rates, leading to diff erent clinical phenomena. Moreover, for patients for whom D R Williams); and Queen Square Brain Bank for the diagnosis is unclear, clinicians must continue to describe accurately the clinical picture of each individual, rather Neurological Disorders, than label them with inaccurate diagnostic categories, such as atypical parkinsonism or PSP mimics. In this way, the University College London, development of the clinical features can be informative in assigning less common nosological categories that give clues London, UK (A J Lees) to the underlying pathology and an understanding of the expected clinical course. -
GAIT DISORDERS, FALLS, IMMOBILITY Mov7 (1)
GAIT DISORDERS, FALLS, IMMOBILITY Mov7 (1) Gait Disorders, Falls, Immobility Last updated: April 17, 2019 GAIT DISORDERS ..................................................................................................................................... 1 CLINICAL FEATURES .............................................................................................................................. 1 CLINICO-ANATOMICAL SYNDROMES .............................................................................................. 1 CLINICO-PHYSIOLOGICAL SYNDROMES ......................................................................................... 1 Dyssynergy Syndromes .................................................................................................................... 1 Frontal gait ............................................................................................................................ 2 Sensory Gait Syndromes .................................................................................................................. 2 Sensory ataxia ........................................................................................................................ 2 Vestibular ataxia .................................................................................................................... 2 Visual ataxia .......................................................................................................................... 2 Multisensory disequilibrium ................................................................................................. -
Homolateral Ataxia and Crural Paresis: a Vascular Syndrome1
J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.28.1.48 on 1 February 1965. Downloaded from J. Neurol. Neurosutrg. Psychiat., 1965, 28, 48 Homolateral ataxia and crural paresis: A vascular syndrome1 C. M. FISHER AND MONROE COLE From the Neurology Service ofthe Massachusetts General Hospital and the Department of Neurology, Harvard Medical School, U.S.A. In the past few years, at the Massachusetts General The general examination was not remarkable except for Hospital, we have observed 14 patients having moderate obesity and mild hypertension (138/104 mm. suffered strokes with an unusual neurological deficit Hg). On neurological examination the patient was alert and intelligent with no speech disorder. Visual acuity was in which the arm and leg on the same side showed a normal and the visual fields were full. The optic fundi combination of severe cerebellar-like ataxia and were not remarkable. The pupils were equal and reacted pyramidal signs. The cases so strongly resembled normally. The extraocular movements were full. Hori- one another that the clinical picture may be regarded zontal nystagmus with the quick component to the left as a cerebrovascular syndrome. was present on left lateral gaze. Facial sensation and In a typical case weakness of the lower limb, movements were normal. Hearing was not impaired on especially the ankle and toes, and a Babinski sign careful testing. There was neither dysarthria nor dys- were associated with a striking dysmetria of the arm phagia and the tongue protruded in the midline. Opto-Protected by copyright. and leg on the same side. The neurological examina- kinetic nystagmus was diminished with targets moving the was The only avail- to left. -
Diseases of the Bovine Central Nervous System
Diseases of the Bovine Central Nervous System Karl Kersting DVM, MS Food Animal Hospital, College of Veterinary Medicine, Iowa State University Ames, IA 50011 I. Diseases of the Spinal Cord - LMN signs to hind limbs, tail, bladder, A. Lower Motor Neuron (LMN) Disease anal sphincter 1. Clinical Signs 2. Diseases - Paralysis -Trauma - Areflexia/hyporeflexia - Breeding/riding injuries - Decreased muscle tone - Forced fetal extraction ( cow or calf) - Early and severe muscle atrophy - Head gate injuries - Anesthesia to specific myotomes - Parasitic 2. Diseases - Death of cattle grubs in the spinal cord - Botulism - Spinal abscesses - Organophosphate toxicity - Spondylitis (bulls) - Tick paralysis - Lymphosarcoma -Trauma - Rabies - Injection sites - Compartmental syndrome II. Diseases of the Brainstem B. Upper Motor Neuron (UMN) Disease A. Clinical signs 1. Clinical Signs 1. Cranial nerve deficits - Nuclei of Cranial nerves - Paresis - Paralysis (loss of voluntary III - XII are in the brain stem. Frequently mul 0 "'O movements) tiple cranial nerves involved with clinical deficit (D ~ - Normal/hyperreflexia on same side as lesion. ~ ('.") - Normal - increased muscle tone 2. Ataxia and paresis (D 00 - Late muscle atrophy 3. Depression - damage to reticular activating sys 00 - Decreased superficial and deep pain tem 0........ 00 ,-+- - Decreased proprioception '"i 2. Diseases B. Diseases ~ ~...... -Tetanus 1. Listeriosis 0 - Spastic Paresis 2. Thromboembolic Meningoencephalitis p - Spastic Syndrome (TEME) - Nervous Ergotism 3. Sporadic Bovine Encephalamyelitis - Dallis/Bermuda Grass Staggers (SBE) 4. Middle Ear Infections C. Mixed Spinal Cord Disease 5. Homer's Syndrome 1. Clinical Signs 6. Rabies a. Lesion of Cl - CS - UMN signs to all limbs III. Diseases of the Cerebellum - Tetra or hemiparesis - Rear limbs usually more affected than fore- A. -
A PRACTICAL APPROACH to GAIT PROBLEMS Gualtiero Gandini
ORTHOPAEDIC OR NEUROLOGIC? A PRACTICAL APPROACH TO GAIT PROBLEMS Gualtiero Gandini, DVM, Dipl. ECVN; Dipartimento di Scienze Mediche Veterinarie - Università di Bologna Via Tolara di Sopra, 50 – 40064 – Ozzano Emilia (BO) Email: [email protected] Gait examination is of crucial importance and is a relevant part of the neurological examination. The correct evaluation of gait requires experience and, especially during the first steps of the veterinary profession, may be necessary to observe carefully and for long time the gait of a patient in order to “decode” adequately what is appreciated during the examination. Re-evaluation of video recording and the use of slow motion video can be very helpful. During gait evaluation, the first aim should be the pure description of what was noticed. The interpretation of the observed signs should be done only in a second time, matching them with the categories of gait abnormalities. FUNCTIONAL ANATOMY: the normal gait –Normal gait in the dog and cat depends on the functional integrity of the cerebral cortex, the brainstem, cerebellum, spinal cord (including ascending and descending pathways), peripheral nerves (sensory and motor), neuromuscular junctions and muscles. A voluntary movement is initiated by nerve impulses generated in the cerebral cortex or brainstem. The cerebellum coordinates these voluntary movements and the vestibular system maintains balance during the performance of the movement. The nerve impulses from the brain to the peripheral nerves and, subsequently, to the muscles, travel along the descending tracts of the spinal cord. Information on the position of the limbs during movements reach the cerebellum and the forebrain from the periphery through the ascending tracts of the spinal cord and brainstem. -
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Freely available online Reviews Early Controversies Over Athetosis: II. Treatment 1* Douglas J. Lanska 1 Veterans Affairs Medical Center, 500 E. Veterans St., Tomah, Wisconsin, United States of America Abstract Background: Athetosis has been controversial since it was first described by William Hammond in 1871; many aspects of Hammond’s career were equally controversial. Methods: Primary sources have been used to review treatment controversies in the 50-year period following the initial description of athetosis. Results: The treatments used most commonly employed available pharmaceutical agents and modalities (e.g., galvanism). Initial anecdotal reports of success were seldom confirmed with subsequent experience. Several novel invasive therapies were also developed and promoted, all of which damaged or destroyed either upper or lower motor neuron pathways, and were also often associated with high mortality rates. In general, these therapies substituted paresis for abnormal spontaneous movements. These included peripheral nerve stretching, excision of a portion of the precentral gyrus, rhizotomy, nerve ‘‘transplantation’’ (i.e., neurotomy and nerve-to-nerve anastomoses), and ‘‘muscle group isolation’’ (i.e., alcohol neurolysis). There was no agreement on the appropriateness of such high-risk procedures, particularly given the intentional generation of further neurological morbidity. Discussion: Pharmaceutical agents and modalities initially employed for athetosis had little a priori evidence-based justification and no biologically plausible -
FUNCTIONAL SYMPTOMS and SIGNS in NEUROLOGY: I2 ASSESSMENT and DIAGNOSIS Jstone,Acarson,Msharpe
Downloaded from jnnp.bmj.com on March 13, 2014 - Published by group.bmj.com FUNCTIONAL SYMPTOMS AND SIGNS IN NEUROLOGY: i2 ASSESSMENT AND DIAGNOSIS JStone,ACarson,MSharpe J Neurol Neurosurg Psychiatry 2005;76(Suppl I):i2–i12. doi: 10.1136/jnnp.2004.061655 t’s a Tuesday morning at 11.30 am. You are already 45 minutes behind. A 35 year old woman is referred to your neurology clinic with a nine month history of fatigue, dizziness, back pain, left Isided weakness, and reduced mobility. Her general practitioner documents a hysterectomy at the age of 25, subsequent division of adhesions for abdominal pain, irritable bowel syndrome, and asthma. She is no longer able to work as a care assistant and rarely leaves the house. Her GP has found some asymmetrical weakness in her legs and wonders if she may have developed multiple sclerosis. She looks unhappy but becomes angry when you ask her whether she is depressed. On examination you note intermittency of effort and clear inconsistency between her ability to walk and examination on the bed. She has already had extensive normal investigations. The patient and her husband want you to ‘‘do something’’. As you start explaining that there’s no evidence of anything serious and that you think it’s a psychological problem, the consultation goes from bad to worse…. In this article we summarise an approach to the assessment and diagnosis of functional symptoms in neurology, paying attention to those symptoms that are particularly ‘‘neurological’’, such as paralysis and epileptic-like attacks. In the second of the two articles we describe our approach to the management of functional symptoms bearing in mind the time constraints experienced by a typical neurologist. -
Ipsilateral Hemiparesis: the Forgotten History of This Paradoxical Neurological Sign
NEUROSURGICAL FOCUS Neurosurg Focus 47 (3):E7, 2019 Ipsilateral hemiparesis: the forgotten history of this paradoxical neurological sign Rodrigo Carrasco-Moro, MD,1 Ines Castro-Dufourny, MD, PhD,2 Juan S. Martínez-San Millán, MD, PhD,3 Lidia Cabañes-Martínez, MD,4 and José M. Pascual, MD, PhD5 1Department of Neurosurgery, Ramón y Cajal University Hospital; 2Department of Endocrinology, Sureste University Hospital, Francisco de Vitoria University; Departments of 3Neuroradiology and 4Clinical Neurophysiology, Ramón y Cajal University Hospital; and 5Department of Neurosurgery, La Princesa University Hospital, Madrid, Spain OBJECTIVE Establishing the neurological localization doctrine for the contralateral hemispheric control of motor func- tions in the second half of the 19th century, researchers faced the challenge of recognizing false localizing signs, in par- ticular paradoxical or ipsilateral hemiparesis (IH). Despite tremendous progress in current methods of neuroradiological and electrophysiological exploration, a complete understanding of this phenomenon has yet to be attained. METHODS The authors researched the well-described cases of hemiparesis/hemiplegia ipsilateral to an intracranial lesion published in the scientific literature in the pre-MRI era (before 1980). A comprehensive review of the physiopatho- logical mechanisms proposed for paradoxical hemiparesis throughout this period, as well as the pathological evidence substantiating them, is provided. RESULTS A collection of 75 patients with hemiparesis/hemiplegia ipsilateral