Modified Ashworth Scale and Spasm Frequency Score in Spinal Cord Injury
Total Page:16
File Type:pdf, Size:1020Kb
Load more
Recommended publications
-
Hereditary Spastic Paraparesis: a Review of New Developments
J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.69.2.150 on 1 August 2000. Downloaded from 150 J Neurol Neurosurg Psychiatry 2000;69:150–160 REVIEW Hereditary spastic paraparesis: a review of new developments CJ McDermott, K White, K Bushby, PJ Shaw Hereditary spastic paraparesis (HSP) or the reditary spastic paraparesis will no doubt Strümpell-Lorrain syndrome is the name given provide a more useful and relevant classifi- to a heterogeneous group of inherited disorders cation. in which the main clinical feature is progressive lower limb spasticity. Before the advent of Epidemiology molecular genetic studies into these disorders, The prevalence of HSP varies in diVerent several classifications had been proposed, studies. Such variation is probably due to a based on the mode of inheritance, the age of combination of diVering diagnostic criteria, onset of symptoms, and the presence or other- variable epidemiological methodology, and wise of additional clinical features. Families geographical factors. Some studies in which with autosomal dominant, autosomal recessive, similar criteria and methods were employed and X-linked inheritance have been described. found the prevalance of HSP/100 000 to be 2.7 in Molise Italy, 4.3 in Valle d’Aosta Italy, and 10–12 Historical aspects 2.0 in Portugal. These studies employed the In 1880 Strümpell published what is consid- diagnostic criteria suggested by Harding and ered to be the first clear description of HSP.He utilised all health institutions and various reported a family in which two brothers were health care professionals in ascertaining cases aVected by spastic paraplegia. The father was from the specific region. -
Effectiveness of Myofascial Release on Spasticity and Lower Extremity
hysical M f P ed l o ic a in n r e u & o R J International Journal of Kumar and Vaidya, Int J Phys Med Rehabil 2014, 3:1 l e a h n a DOI: 10.4172/2329-9096.1000253 o b i t i l a ISSN: 2329-9096i t a n r t i e o t n n I Physical Medicine & Rehabilitation Research Article Open Access Effectiveness of Myofascial Release on Spasticity and Lower Extremity Function in Diplegic Cerebral Palsy: Randomized Controlled Trial Chandan Kumar1* and Snehashri N Vaidya2 1Associate Professor, Smt Kashibai Navale College of Physiotherapy, Narhe, Pune, Maharashtra, India 2MGM’S School of Physiotherapy, Aurangabad, India Abstract Purpose: To find out the effectiveness of Myofascial Release in combination with conventional physiotherapy on spasticity of calf, hamstring and adductors of hip and on lower extremity function in spastic diplegic subjects. Methodology: 30 spastic diplegic subjects of age group 2-8 years were taken by random sampling method from MGM College and other private clinics in Aurangabad. 15 subjects were assigned in each group. Group A: Myofascial release and conventional PT treatment. Group B: conventional PT treatment. Both the groups received training for 4 weeks. Baseline and Post treatment measures of Modified Ashworth Scale (MAS), Modified Tardieu Scale (MTS) and Gross Motor Function Test (GMFM-88) were evaluated. Results: Mean difference of MAS and R2 value of MTS in group A was more than group B, for calf, hamstring and adductors, whereas GMFM showed nearly equal improvement in both groups. Conclusion: Overall, it can be concluded from our study that the MFR along with conventional treatment reduces spasticity in calf, hamstring and adductors of hip in spastic diplegic subjects. -
Cerebral Palsy
Cerebral Palsy Cerebral palsy encompasses a group of non-progressive and non-contagious motor conditions that cause physical disability in various facets of body movement. Cerebral palsy is one of the most common crippling conditions of childhood, dating to events and brain injury before, during or soon after birth. Cerebral palsy is a debilitating condition in which the developing brain is irreversibly damaged, resulting in loss of motor function and sometimes also cognitive function. Despite the large increase in medical intervention during pregnancy and childbirth, the incidence of cerebral palsy has remained relatively stable for the last 60 years. In Australia, a baby is born with cerebral palsy about every 15 hours, equivalent to 1 in 400 births. Presently, there is no cure for cerebral palsy. Classification Cerebral palsy is divided into four major classifications to describe different movement impairments. Movements can be uncontrolled or unpredictable, muscles can be stiff or tight and in some cases people have shaky movements or tremors. These classifications also reflect the areas of the brain that are damaged. The four major classifications are: spastic, ataxic, athetoid/dyskinetic and mixed. In most cases of cerebral palsy, the exact cause is unknown. Suggested possible causes include developmental abnormalities of the brain, brain injury to the fetus caused by low oxygen levels (asphyxia) or poor circulation, preterm birth, infection, and trauma. Spastic cerebral palsy leads to increased muscle tone and inability for muscles to relax (hypertonic). The brain injury usually stems from upper motor neuron in the brain. Spastic cerebral palsy is classified depending on the region of the body affected; these include: spastic hemiplegia; one side being affected, spastic monoplegia; a single limb being affected, spastic triplegia; three limbs being affected, spastic quadriplegia; all four limbs more or less equally affected. -
Treatment of Spastic Foot Deformities
TREATMENT OF SPASTIC FOOT DEFORMITIES penn neuro-orthopaedics service Table of Contents OVERVIEW Severe loss of movement is often the result of neurological disorders, Overview .............................................................. 1 such as stroke or brain injury. As a result, ordinary daily activities Treatment ............................................................. 2 such as walking, eating and dressing can be difficult and sometimes impossible to accomplish. Procedures ........................................................... 4 The Penn Neuro-Orthopaedics Service assists patients with Achilles Tendon Lengthening .........................................4 orthopaedic problems caused by certain neurologic disorders. Our Toe Flexor Releases .....................................................5 team successfully treats a wide range of problems affecting the limbs including foot deformities and walking problems due to abnormal Toe Flexor Transfer .......................................................6 postures of the foot. Split Anterior Tibialis Tendon Transfer (SPLATT) ...............7 This booklet focuses on the treatment of spastic foot deformities The Extensor Tendon of the Big Toe (EHL) .......................8 under the supervision of Keith Baldwin, MD, MSPT, MPH. Lengthening the Tibialis Posterior Tendon .......................9 Care After Surgery .................................................10 Notes ..................................................................12 Pre-operative right foot. Post-operative -
Motor Neuron Disease (Amyotrophic Lateral Sclerosis) Arising from Longstanding Primary Lateral Sclerosis
74274ournal ofNeurology, Neurosurgery, and Psychiatry 1995;58:742-744 SHORT REPORT J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.58.6.742 on 1 June 1995. Downloaded from Motor neuron disease (amyotrophic lateral sclerosis) arising from longstanding primary lateral sclerosis R P M Bruyn, J H T M Koelman, D Troost,J M B V de Jong Abstract family history was negative and consanguinity Three men were initially diagnosed as was excluded. Examination disclosed slight having primary lateral sclerosis (PLS), weakness of the left thigh muscles, mild spas- but eventually developed amyotrophic ticity of the legs, knee and ankle cloni, and lateral sclerosis (ALS) after 7-5, 9, and at extensor plantars. Blood chemistry, CSF, and least 27 years. Non-familial ALS and EMG were unremarkable. Magnetic reso- PLS might be different manifestations of nance imaging of the cervical spine was nor- a single disease or constitute completely mal and PLS was diagnosed. Micturition distinct entities. The clinical diagnosis of urgency began in 1987. Examination in 1988 PLS predicts a median survival that is showed definite spastic paraparesis and mild four to five times longer than in ALS. proximal weakness of the legs. Sural and tib- ial nerve somatosensory evoked potentials (J Neurol Neurosurg Psychiatry 1995;58:742-744) (SSEPs) were bilaterally absent and delayed respectively. Visual and brainstem auditory evoked potentials (VEPs, BAEPs), and brain Keywords: amyotrophic lateral sclerosis; primary MRI were normal. By 1990, walking had lateral sclerosis become troublesome and dysarthria was pre- sent; the calves showed fasciculation and Primary lateral sclerosis (PLS), defined as some atrophy. -
Hereditary Spastic Paraplegias
Hereditary Spastic Paraplegias Authors: Doctors Enza Maria Valente1 and Marco Seri2 Creation date: January 2003 Update: April 2004 Scientific Editor: Doctor Franco Taroni 1Neurogenetics Istituto CSS Mendel, Viale Regina Margherita 261, 00198 Roma, Italy. e.valente@css- mendel.it 2Dipartimento di Medicina Interna, Cardioangiologia ed Epatologia, Università degli studi di Bologna, Laboratorio di Genetica Medica, Policlinico S.Orsola-Malpighi, Via Massarenti 9, 40138 Bologna, Italy.mailto:[email protected] Abstract Keywords Disease name and synonyms Definition Classification Differential diagnosis Prevalence Clinical description Management including treatment Diagnostic methods Etiology Genetic counseling Antenatal diagnosis References Abstract Hereditary spastic paraplegias (HSP) comprise a genetically and clinically heterogeneous group of neurodegenerative disorders characterized by progressive spasticity and hyperreflexia of the lower limbs. Clinically, HSPs can be divided into two main groups: pure and complex forms. Pure HSPs are characterized by slowly progressive lower extremity spasticity and weakness, often associated with hypertonic urinary disturbances, mild reduction of lower extremity vibration sense, and, occasionally, of joint position sensation. Complex HSP forms are characterized by the presence of additional neurological or non-neurological features. Pure HSP is estimated to affect 9.6 individuals in 100.000. HSP may be inherited as an autosomal dominant, autosomal recessive or X-linked recessive trait, and multiple recessive and dominant forms exist. The majority of reported families (70-80%) displays autosomal dominant inheritance, while the remaining cases follow a recessive mode of transmission. To date, 24 different loci responsible for pure and complex HSP have been mapped. Despite the large and increasing number of HSP loci mapped, only 9 autosomal and 2 X-linked genes have been so far identified, and a clear genetic basis for most forms of HSP remains to be elucidated. -
Cerebral Palsy
Cerebral Palsy What is Cerebral Palsy? Doctors use the term cerebral palsy to refer to any one of a number of neurological disorders that appear in infancy or early childhood and permanently affect body movement and muscle coordination but are not progressive, in other words, they do not get worse over time. • Cerebral refers to the motor area of the brain’s outer layer (called the cerebral cortex), the part of the brain that directs muscle movement. • Palsy refers to the loss or impairment of motor function. Even though cerebral palsy affects muscle movement, it is not caused by problems in the muscles or nerves. It is caused by abnormalities inside the brain that disrupt the brain’s ability to control movement and posture. In some cases of cerebral palsy, the cerebral motor cortex has not developed normally during fetal growth. In others, the damage is a result of injury to the brain either before, during, or after birth. In either case, the damage is not repairable and the disabilities that result are permanent. Patients with cerebral palsy exhibit a wide variety of symptoms, including: • Lack of muscle coordination when performing voluntary movements (ataxia); • Stiff or tight muscles and exaggerated reflexes (spasticity); • Walking with one foot or leg dragging; • Walking on the toes, a crouched gait, or a “scissored” gait; • Variations in muscle tone, either too stiff or too floppy; • Excessive drooling or difficulties swallowing or speaking; • Shaking (tremor) or random involuntary movements; and • Difficulty with precise motions, such as writing or buttoning a shirt. The symptoms of cerebral palsy differ in type and severity from one person to the next, and may even change in an individual over time. -
The Effects of Botulinum Toxin Injections on Spasticity and Motor Performance in Chronic Stroke with Spastic Hemiplegia
toxins Article The Effects of Botulinum Toxin Injections on Spasticity and Motor Performance in Chronic Stroke with Spastic Hemiplegia 1,2,3, 4, 4 1,2 Yen-Ting Chen y, Chuan Zhang y, Yang Liu , Elaine Magat , Monica Verduzco-Gutierrez 1,2,5, Gerard E. Francisco 1,2, Ping Zhou 6, Yingchun Zhang 4 and Sheng Li 1,2,* 1 Department of Physical Medicine and Rehabilitation, University of Texas Health Science Center at Houston, Houston, TX 77030, USA; [email protected] (Y.-T.C.); [email protected] (E.M.); [email protected] (M.V.-G.); [email protected] (G.E.F.) 2 TIRR Memorial Hermann Hospital, Houston, TX 77030, USA 3 Department of Health and Kinesiology, Northeastern State University, Broken Arrow, OK 74014, USA 4 Department of Biomedical Engineering, University of Houston, Houston, TX 77204, USA; [email protected] (C.Z.); [email protected] (Y.L.); [email protected] (Y.Z.) 5 Department of Rehabilitation Medicine, University of Texas Health Science Center at San Antonio, San Antonio, TX 78229, USA 6 Guangdong Provincial Work Injury Rehabilitation Center, Guangzhou 510000, China; [email protected] * Correspondence: [email protected]; Tel.: +1-713-797-7125 Both authors contributed equally. y Received: 15 June 2020; Accepted: 27 July 2020; Published: 31 July 2020 Abstract: Spastic muscles are weak muscles. It is known that muscle weakness is linked to poor motor performance. Botulinum neurotoxin (BoNT) injections are considered as the first-line treatment for focal spasticity. The purpose of this study was to quantitatively investigate the effects of BoNT injections on force control of spastic biceps brachii muscles in stroke survivors. -
The Serotonin Syndrome
The new england journal of medicine review article current concepts The Serotonin Syndrome Edward W. Boyer, M.D., Ph.D., and Michael Shannon, M.D., M.P.H. From the Division of Medical Toxicology, he serotonin syndrome is a potentially life-threatening ad- Department of Emergency Medicine, verse drug reaction that results from therapeutic drug use, intentional self-poi- University of Massachusetts, Worcester t (E.W.B.); and the Program in Medical Tox- soning, or inadvertent interactions between drugs. Three features of the sero- icology, Division of Emergency Medicine, tonin syndrome are critical to an understanding of the disorder. First, the serotonin Children’s Hospital, Boston (E.W.B., M.S.). syndrome is not an idiopathic drug reaction; it is a predictable consequence of excess Address reprint requests to Dr. Boyer at IC Smith Bldg., Children’s Hospital, 300 serotonergic agonism of central nervous system (CNS) receptors and peripheral sero- 1,2 Longwood Ave., Boston, MA 02115, or at tonergic receptors. Second, excess serotonin produces a spectrum of clinical find- [email protected]. edu. ings.3 Third, clinical manifestations of the serotonin syndrome range from barely per- This article (10.1056/NEJMra041867) was ceptible to lethal. The death of an 18-year-old patient named Libby Zion in New York updated on October 21, 2009 at NEJM.org. City more than 20 years ago, which resulted from coadminstration of meperidine and phenelzine, remains the most widely recognized and dramatic example of this prevent- N Engl J Med 2005;352:1112-20. 4 Copyright © 2005 Massachusetts Medical Society. able condition. -
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. -
The Effects of Reflex Path Length on Clonus Frequency in Spastic Muscles
J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.47.10.1122 on 1 October 1984. Downloaded from Journal ofNeurology, Neurosurgery, and Psychiatry 1984;47:1122-1124 Short report The effects of reflex path length on clonus frequency in spastic muscles ROBERT IANSEK From the Department ofNeurology, Prince Henry's Hospital, Melbourne, Australia SUMMARY Clinical evaluation of clonus in spastic muscles was performed by comparing reflex path length with clonus frequency for different muscles in the same patient. It was found that clonus frequency varied inversely with reflex path length (r = 0-84, p < 0-001). The findings confirm that clonus is generated by a peripheral mechanism of self re-excitation rather than a central spinal pacemaker. Clonus is a well recognised clinical sign, usually Methods guest. Protected by copyright. occurring in spasticity. A normal, nonspastic limb may manifest clonus, but only under certain condi- Twenty-one unselected patients who were seen on the tions.' The repetitive self perpetuating movement is neurology service were used as subjects. Attempts were induced by brisk stretch of the involved muscle made to study patients with clonus in more than one mus- group, although cutaneous sensory inputs can initi- cle. No restriction was placed on the underlying pathologi- cal basis for the spasticity. Neurological examination and ate clonic movements in a susceptible limb.2 The routine nerve conduction studies were performed to underlying mechanism of clonus is poorly under- exclude an underlying neuropathy. Clonus frequency was stood and controversial. Some investigators34 have measured by use of surface electrodes and the raw EMG evidence to support the theory of a self re-excitation was recorded on photosensitive paper. -
What Polio Is Or What It Affects Or Causes: by Marny Eulberg, M.D., Director, Post Polio Clinic at What Polio Is Or What It St
VOLUME 23 NUMBER 3 SUMMER 2008 IN THIS ISSUE What polio is or what it affects or causes: By Marny Eulberg, M.D., director, Post Polio Clinic at What Polio Is or What It St. Anthonys Hospital, Denver Affects or Causes . p. 1 9 Polio kills or damages the anterior horn cell(s) in the In My Opinion . p. 2 spinal cord and thus results in no information being Comorbidities & sent to the muscle fibers of any voluntary (striated) Secondary Disabilities . muscle i.e. any muscle that can be controlled by p. 4 thought such as I think Ill point at that object with my index finger; this includes the muscles of the Book Review: Living hand, arm, shoulder, neck, trunk, back, abdominal wall, With Polio by Daniel J. entire leg and foot, face including muscles used in Wilson . p. 5 chewing, and muscles used for breathing and for the initiation of swallowing (the latter are known as Martha Logan: Mother, bulbar muscles). It does not affect the cardiac Teacher, Homemaker . (heart) muscle or smooth muscle which is in the p. 7 walls of the GI tract (esophagus, stomach, The Colorado Post-Polio intestines) or the walls of the urinary bladder. Educational Conference . 9 Atrophy (wasting) of a muscle(s) or the skinny arm p. 10 or leg is a result of the muscle not getting any And By the Way . p. 12 messages from the nerve that it needs to work. Talking About Physical 9 Polio leg (the cold to the touch) happens because of Rehabilitation . p. 13 blood pooling in the weakened extremity, radiant heat loss, and some lack of blood vessel constriction that A special thanks to Oran normally happens when exposed to cold temperatures.