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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Clinical trial. The effects of protirelin tartrate (TRH-T) administration on chronic post-stroke spasticity were studied in a multicentre trial (study on the treatment of chronic post-stroke spasticity--11 centres involved). Patient evaluation included the quantification of muscular strength examined in proximal and distal areas, muscular tone according to the Ashworth scale, reflex intensities (using a 5 graded scale); daily autonomy was also considered according to the Parkside Behaviour Rating Scale (PBRS). Patients were administered 2 mg of TRH-T twice daily by intramuscular route. The most interesting finding emerging from the trial was that TRH-T administration elicited, at the same time, a reduction of spasticity, hypertonia and hyperreflexia together with an increase in muscular strength and improvement of daily activities. The therapeutic profile of TRH-T therefore seems to be based on its unusual capacity of acting simultaneously on deficiency symptoms (hyposthenia, loss of dexterity) and positive symptoms (hypertonia, hyperreflexia), both of which are present in cases of post-stroke spasticity. Electrophysiological findings. By means of coded electrophysiological tests it is possible to explore specific compartments of the motorial and spinal network and consequently obtain activity profiles for each single substance capable of modifying its reactivity. The H/M ratio, reciprocal Ia inhibition and the activities of the Renshaw circuit were not changed following TRH-T administration. Opposite findings were recorded with regard to the F wave according to whether the flector or extensor nucleus was explored; the consequent hypothesis of TRH-T activity at the interneuron level was supported by the inhibition of the short head biceps reflex following administration of the drug.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Use of TRH-T for the symptomatic treatment of the pathology of the upper motoneurons and electrophysiologic evaluation of its efficacy]. 212 88

The F response represents the recurrent discharge of a small percentage of the motoneuron pool activated antidromically by any single impulse delivered to the nerve. We studied F waves from median nerve stimulation in 22 controls, in 30 patients with spasticity after cerebrovascular accident (CVA), and in 4 patients with familial spastic paraplegia (FSP). The following parameters were analyzed: median nerve conduction velocity, median nerve M response amplitude (M), average amplitude of 16 F responses (F16); persistence of F response (Fp) defined as the percentage of measurable responses to 16 stimuli, average amplitude of F response expressed as percentage of maximal M amplitude: (F16/M%). Results showed that Fp, F16 and F16/M% values were significantly increased on the spastic side of CVA patients and in FSP. Our findings indicate that after upper motor neuron lesions (whatever etiology and course) a change in the frequency of recurrent discharge and/or in the total number of lower motor neurons capable of backfiring occurs. Therefore, F response reflects the hyperexcitability state of the lower motor neurons in spasticity.
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PMID:F response in vascular and degenerative upper motor neuron lesions. 229 Apr 10

The purpose of this investigation was to determine in 17 stroke patients the correlation between two independent variables (knee extensor muscle torque [KET] and spasticity on the paretic side) and one dependent variable (gait speed). The patients had a mean age of 59 years; time since onset of first stroke was 51 days. Each variable was measured twice on each of two consecutive days. Both KET and spasticity were measured on a Cybex II dynamometer. Peak torque was measured during five-second maximal voluntary isometric knee extension efforts. Spasticity was defined by the relative angle of reversal (RAR) of the Cybex electrogoniometer curve obtained during pendulum tests. Gait speed was measured as patients walked 8.0 meters at their most comfortable speed while using their usual devices. The average of each day's KETs, RARs, and gait speeds was used in the calculation of Pearson product moment correlations. The correlations between KET and gait speed were significant (p less than .05) and were .574 (day 1) and .571 (day 2). The correlations between the RAR and gait speed were not significant (-.204 day 1 and -.262 day 2). All measurements had intraday and/or interday reliability coefficients (ICC 3,1) exceeding .930. The results of this study confirm that gait performance is correlated with measures of KET but not spasticity in stroke patients. Thus, at the knee, extensor muscle torque, unlike spasticity, appears to be justified as a practical and objective clinical measure.
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PMID:Correlation of knee extensor muscle torque and spasticity with gait speed in patients with stroke. 232 87

Shoulder pain is a frequent and debilitating problem in hemiplegic patients, and its etiology remains poorly understood. The role played by hemineglect in the appearance of shoulder pain was studied. During two years, 94 hemiplegic subjects were involved in a rehabilitation program after cerebrovascular accidents. Their average age was 68 years; 45 (47.9%) subjects had shoulder pain, and 24 subjects (22.5%) had hemineglect. The subjects with shoulder pain were compared to those without pain (the control group) with respect to gender, age, diabetes, heart failure, cardiac ischemia, scapulohumeral arthritis, and calcified tendinitis of the rotator cuff. We were unable to demonstrate a relationship between hemineglect and shoulder pain in the hemiplegic (X2 (1) = 2.03, p = .15), although pain was significantly more frequent in subjects with right hemispheric cerebrovascular accident (X2 (1) = 5.0, p less than .025). The subjects with shoulder pain had significantly more spasticity of the affected limb (X2 (1) = 26.3, p less than .01), less sensitivity to pinprick of the upper paralyzed extremity (X2 (1) = 10.8, p less than .01), and a more severe subluxation of the affected shoulder (t(51) = 14.0, p less than .01).
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PMID:Painful shoulder in the hemiplegic and unilateral neglect. 237 73

The primate middle cerebral artery (MCA) preparation has been studied as an animal model of human spasticity resulting from stroke. MCA occlusion in 3 squirrel monkeys was accomplished through a transorbital approach and animals were evaluated by 'clinical' examinations and studies of EMG responses to torque motor imposed joint displacement. Animals were transiently hemiparetic but not spastic postoperatively, although all were found to have a large infarct in MCA territory on post-mortem examination. The electromyographic (EMG) response of biceps in normal animals to torque motor imposed elbow extension consisted of both early (M1) and late (M2) components (Tatton et al. 1975). These components were unchanged following MCA occlusion. The EMG response to metacarpophalangeal joint extension in finger flexors or normal animals consisted solely of a long-latency (M2) component (Lenz et al. 1983a). Following MCA occlusion the M2 component in this muscle was decreased or absent, but a short-latency (M1) component appeared.
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PMID:Long-latency reflex activity in squirrel monkeys with occlusion of the middle cerebral artery. 244 58

Botulinum toxin, a product of Clostridium botulinum, produces presynaptic neuromuscular block by preventing release of acetylcholine from nerve endings. The toxin was injected directly into the skeletal muscles of six patients with severe spasticity due to stroke-related hemiplegia. It produced both subjective and objective improvement. The toxin injections were well tolerated and no significant side effect was reported.
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PMID:Effect of treatment with botulinum toxin on spasticity. 259 95

The value of locally injected botulinum toxin is emphasised. The toxin was injected directly into the skeletal muscles of eight patients with severe spasticity due to stroke-related hemiplegia. It produced both subjective and objective improvement. The toxin injections were well tolerated and no significant side effects were noted.
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PMID:Botulinum toxin in treating spasticity. 261 Oct 94

Clinical and experimental results are reviewed concerning muscle weakness in patients with hemiparesis after a stroke. The discussion includes the important role that alterations in the physiology of motor units, notably changes in firing rates and muscle fiber atrophy, play in the manifestation of muscle weakness. This role is compared with the lesser role that spasticity (defined as hyperactive stretch reflexes) of the antagonist muscle group appears to play in determining the weakness of agonist muscles. The contribution of other factors that result in mechanical restraint of the agonist by the antagonist (e.g., passive mechanical properties and inappropriate cocontraction) is discussed relative to muscle weakness in patients with hemiparesis.
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PMID:Weakness in patients with hemiparesis. 265 57

Selected surgical procedures to correct specific deformities of the upper extremity in the stroke patient related to muscle imbalance, spasticity, contracture, and joint instability as seen in spastic hemiplegia are described. The postoperative rehabilitation is also discussed with regard to functional and anatomic disabilities, considering first the patient, then the extremity, and finally, the hand.
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PMID:Evaluation and treatment of the upper extremity in the stroke patient. 265 27

CVA comprises a large number of clinical entities, depending on the site of infarction in the brain. Accurate evaluation of deficits in the patient's sensory and/or motor systems and the patient's intellectual status are paramount in establishing realistic rehabilitation goals. With respect to the motor system, two types of voluntary movement may occur. These include synergistic or pattern movement and selective movement. Spasticity in the affected lower extremity may result in a variety of lower-extremity deformities and contractures. Those most commonly encountered include hip flexion and adduction contracture, inadequate knee flexion and knee flexion contracture, and ankle equinus, varus, and equinovarus. Correct evaluation of deformities may be aided by the use of poly-EMG analysis and evaluation after nerve block or motor point blocks. In hemiplegic gait dysfunction, the basic requirements for functional ambulation include (1) ability to maintain standing balance; (2) voluntary hip flexion; (3) leg stability; and (4) ability to follow instructions and adequate motivation. Often a hemiplegic patient can be trained to ambulate if an adequate extensor synergy pattern develops, since mass extension can provide stability of the leg for weight bearing. Medical rehabilitative management of the CVA patient includes early mobilization, restorative exercises (including neuromuscular facilitation techniques), measures to prevent or correct contractures, the use of AFOs, and occasionally functional electrical stimulation. Orthopedic management of deformities in CVA is indicated where conservative measures fail. Surgical procedures seek to alter the forces causing shortening of the muscles and tendons. Hence, the most commonly performed surgical procedures include (1) tendon lengthening or release; (2) soft-tissue release; and (3) tendon transfer. Surgery for hip contractures is not common; however, occasional release of hip flexors is indicated when hip flexion contracture impedes ambulation or prone lying. Inadequate knee flexion, caused by dysphasic quadriceps contraction, can be corrected by release of the vastus medialis and rectus femoris muscles. Distal hamstring tendon release with or without knee joint capsule release is the surgical procedure of choice for severe knee flexion contractures. Surgical correction of an equinus deformity is by TAL, with or without neurectomy of tibial nerve branches to the gastrocsoleus muscles. Severe ankle varus may require a SPLATT procedure. Surgery for equinovarus includes the combined surgery for both equinus and varus (that is, TAL and SPLATT procedures). Toe curling is corrected by toe flexor releases.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Cerebrovascular accidents. 268 40


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