Cerebral and Brainsten1 Diseases of Cattle: Diagnosis and Review of Causes
Total Page:16
File Type:pdf, Size:1020Kb
Load more
Recommended publications
-
Cp-Research-News-2014-06-23
Monday 23 June 2014 Cerebral Palsy Alliance is delighted to bring you this free weekly bulletin of the latest published research into cerebral palsy. Our organisation is committed to supporting cerebral palsy research worldwide - through information, education, collaboration and funding. Find out more at www.cpresearch.org.au Professor Nadia Badawi Macquarie Group Foundation Chair of Cerebral Palsy PO Box 560, Darlinghurst, New South Wales 2010 Australia Subscribe at www.cpresearch.org/subscribe/researchnews Unsubscribe at www.cpresearch.org/unsubscribe Interventions and Management 1. Iran J Child Neurol. 2014 Spring;8(2):45-52. Associations between Manual Abilities, Gross Motor Function, Epilepsy, and Mental Capacity in Children with Cerebral Palsy. Gajewska E, Sobieska M, Samborski W. OBJECTIVE: This study aimed to evaluate gross motor function and hand function in children with cerebral palsy to explore their association with epilepsy and mental capacity. MATERIAL & METHODS: The research investigating the association between gross and fine motor function and the presence of epilepsy and/or mental impairment was conducted on a group of 83 children (45 girls, 38 boys). Among them, 41 were diagnosed with quadriplegia, 14 hemiplegia, 18 diplegia, 7 mixed form, and 3 athetosis. A neurologist assessed each child in terms of possible epilepsy and confirmed diagnosis in 35 children. A psychologist assessed the mental level (according to Wechsler) and found 13 children within intellectual norm, 3 children with mild mental impairment, 18 with moderate, 27 with severe, and 22 with profound. Children were then classified based on Gross Motor Function Classification System and Manual Ability Classification Scale. RESULTS: The gross motor function and manual performance were analysed in relation to mental impairment and the presence of epilepsy. -
Dystonia and Chorea in Acquired Systemic Disorders
J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.65.4.436 on 1 October 1998. Downloaded from 436 J Neurol Neurosurg Psychiatry 1998;65:436–445 NEUROLOGY AND MEDICINE Dystonia and chorea in acquired systemic disorders Jina L Janavs, Michael J AminoV Dystonia and chorea are uncommon abnormal Associated neurotransmitter abnormalities in- movements which can be seen in a wide array clude deficient striatal GABA-ergic function of disorders. One quarter of dystonias and and striatal cholinergic interneuron activity, essentially all choreas are symptomatic or and dopaminergic hyperactivity in the nigros- secondary, the underlying cause being an iden- triatal pathway. Dystonia has been correlated tifiable neurodegenerative disorder, hereditary with lesions of the contralateral putamen, metabolic defect, or acquired systemic medical external globus pallidus, posterior and poste- disorder. Dystonia and chorea associated with rior lateral thalamus, red nucleus, or subtha- neurodegenerative or heritable metabolic dis- lamic nucleus, or a combination of these struc- orders have been reviewed frequently.1 Here we tures. The result is decreased activity in the review the underlying pathogenesis of chorea pathways from the medial pallidus to the and dystonia in acquired general medical ventral anterior and ventrolateral thalamus, disorders (table 1), and discuss diagnostic and and from the substantia nigra reticulata to the therapeutic approaches. The most common brainstem, culminating in cortical disinhibi- aetiologies are hypoxia-ischaemia and tion. Altered sensory input from the periphery 2–4 may also produce cortical motor overactivity medications. Infections and autoimmune 8 and metabolic disorders are less frequent and dystonia in some cases. To date, the causes. Not uncommonly, a given systemic dis- changes found in striatal neurotransmitter order may induce more than one type of dyski- concentrations in dystonia include an increase nesia by more than one mechanism. -
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 -
PPCO Twist System
PEER REVIEWED The NEUROLOGICNEUROLOGIC EXAMINATIONEXAMINATION in Companion Animals In the January/February issue of Part 2: Interpreting Today’s Veterinary Practice, Part 1 of this article discussed performing Abnormal Findings a neurologic examination; Part 2 will address interpretation of Helena Rylander, DVM, Diplomate ACVIM (Neurology) abnormal findings. complete neurologic examination should be THE BRAIN done in all animals presenting with suspected Lesions in the brain can be localized to the: Aneurologic disease. Abnormalities found during t Cerebrum and thalamus (ie, prosencephalon) the neurologic examination can reflect the location of t Brainstem the lesion, but not the cause, requiring further tests, t Cerebellum. such as blood analysis, electrodiagnostic tests, and In order to localize the lesion to a specific part of advanced imaging, to determine a diagnosis. the brain, an understanding of the anatomy and func- The neurologic examination evaluates different parts tion of the brain is necessary (see Brain Anatomy & of the nervous system; the findings from the examina- Related Functions). tion help localize the lesion to the: t Brain Ataxia t Spinal cord A patient with ataxia may have a lesion in the proprio- t Peripheral nervous system ceptive pathways (peripheral nerves, spinal cord, or t Cauda equina. cerebrum), vestibular system, or cerebellum. Ataxia A fundic examination is recommended, especially in can be described as an uncoordinated gait, with cross- patients with brain disorders. Repeat neurologic exami- ing of the limbs and, sometimes, listing or falling to 1 nations are helpful to discover subtle abnormalities and or both sides. Ataxia can be further characterized as: assess progression of disease. -
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. -
The Rostrocaudal Gradient for Somatosensory Perception in The
692 J Neurol Neurosurg Psychiatry 2000;69:692–709 J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.69.5.692 on 1 November 2000. Downloaded from A 49 year old right handed man suddenly shape, and texture weighing 50, 60, 70, 80, developed dysaesthesia in the right hand. 90, and 100 g. For texture perception, we LETTERS TO This recovered gradually, but 1 month later prepared six wooden plates of an identical he still had an impaired tactile recognition for size and shape, on which one of six diVerent THE EDITOR objects. His voluntary movements were skill- textures (sandpaper, felt, wood, wool, fine ful. Deep tendon reflex was slightly exagger- grain, synthetic rubber) were mounted. The ated in his right arm. Babinski’s sign was patient palpated one texture by either hand absent. His language was normal. Brain MRI with his eyes closed. Then he was asked to on the 35th day after the onset showed a select tactually a correct one among the six The rostrocaudal gradient for laminar necrosis on the caudal edge of the textures. For shape perception (three somatosensory perception in the human lateral portion of the left postcentral gyrus dimensional figures) the patient palpated one postcentral gyrus (figure). of the five wooden objects (cylinder, cube, Somaesthetic assessment was done during sphere, prism, and cone) with his eyes closed. Anatomical organisation of the primate post- the 21–28th days of the illness. Then he was asked to explain the shape ver- central gyrus has been described in terms of Elementary somatosensory functions were bally. -
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 -
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. -
Athlete Info
Name: DOB: HT: WT: M/F: Classification: Handler: Misc: BACKGROUND: Please provide us with the following information regarding your impairment in order for us to be better prepared to meet your needs and create a better learning experience. Q1. Using the attached Graphical Representation and Profiles List, please describe your impairment using a Profile number and marking the appropriate graphical representation (from ITU Paratriathlon Classification Rules and Regulations 2012 Edition). Please do your best and any questions we can answer at the camp. If you feel you fall under more than one profile, please include all that apply. Profile: ______ Q2. How long have you had this impairment: Birth: ______ Age: _______ / Reason: ___________ Additional comments: ________________________________________________________________ Q3. Type of prosthesis using for racing and/or training; please check which apply: a) Upper Limb (above elbow/below elbow): Cosmetic _____ Body-powered (cable controlled):_____: Externally powered (myoelectric, switch-controlled prostheses):_____ Hybrid : Cable to elbow or terminal device and battery powered: ___________ Excursion to elbow and battery-powered terminal device: __________ CONFIDENTIA Excursion to terminal device and battery-powered elbow: __________ Additional comments: _________________________________________________ b) Lower Limb (There are many types available, please specify): 1 Type of AK prosthesis: Type of BK prosthesis: Type of Foot: CONFIDENTIA 2 Q4. Training experience: - Do you use a heart rate -
Botulinum Neurotoxin Injections in Childhood Opisthotonus
toxins Article Botulinum Neurotoxin Injections in Childhood Opisthotonus Mariam Hull 1,2,* , Mered Parnes 1,2 and Joseph Jankovic 2 1 Section of Pediatric Neurology and Developmental Neuroscience, Texas Children’s Hospital and Baylor College of Medicine, Houston, TX 77030, USA; [email protected] 2 Parkinson’s Disease Center and Movement Disorders Clinic, Department of Neurology, Baylor College of Medicine, Houston, TX 77030, USA; [email protected] * Correspondence: [email protected] Abstract: Opisthotonus refers to abnormal axial extension and arching of the trunk produced by excessive contractions of the paraspinal muscles. In childhood, the abnormal posture is most often related to dystonia in the setting of hypoxic injury or a number of other acquired and genetic etiologies. The condition is often painful, interferes with ambulation and quality of life, and is challenging to treat. Therapeutic options include oral benzodiazepines, oral and intrathecal baclofen, botulinum neurotoxin injections, and deep brain stimulation. Management of opisthotonus within the pediatric population has not been systematically reviewed. Here, we describe a series of seven children who presented to our institution with opisthotonus in whom symptom relief was achieved following administration of botulinum neurotoxin injections. Keywords: opisthotonus; opisthotonos; axial dystonia; botulinum toxin Key Contribution: This is the first series of pediatric patients with opisthotonus treated with bo- tulinum neurotoxin injections. Botulinum neurotoxin injections should be added to the armamentar- ium of treatment options in children with axial dystonia, including opisthotonos. Citation: Hull, M.; Parnes, M.; 1. Introduction Jankovic, J. Botulinum Neurotoxin Injections in Childhood Opisthotonus. Opisthotonus, derived from the Greek “opistho” meaning behind and “tonos” mean- Toxins 2021, 13, 137. -
Neurological Emergencies Natasha Olby Vetmb, Phd, MRCVS, DACVIM (Neurology) College of Veterinary Medicine, NCSU, Raleigh, NC In
Neurological Emergencies Natasha Olby VetMB, PhD, MRCVS, DACVIM (Neurology) College of Veterinary Medicine, NCSU, Raleigh, NC Introduction Neurological emergencies are common and require a cool head, careful patient assessment and prompt action! While there are many instances when an owner perceives their patient to be in a crisis when in fact they are not, any rapidly changing neurological dysfunction should be considered an emergency and the patient evaluated immediately. This presentation will give an overview of alterations in mentation, seizures and paralysis using case examples. An important general point is that you should have emergency protocols available as they improve outcomes in any emergency situation. Altered Mentation: Stupor and Coma Terms used to describe mental status include terms that describe level of consciousness (e.g. stupor, coma) and terms that describe behavior (e.g. dementia, hysteria). Level of consciousness is controlled by the ascending reticular activating system (ARAS). This mass of neurons extends through the brainstem to project to the thalamus and from there to the cortex. The ability to interact appropriately with the surrounding environment depends on the ability to process and integrate sensory information and to combine this information with learned information. The forebrain, and in particular the cerebrum and limbic system, is vital for normal behavior. Stupor is defined as decreased consciousness, but responsive to strong stimuli: these patients tend to be in sternal or lateral recumbency and are difficult to rouse. Coma is defined as unresponsive to stimuli. Stupor and coma are considered to be emergencies. Causes of changes in mental status There are numerous different causes of changes in mental status.