Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026838 (spasticity)
6,471 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

I examined the isokinetic knee extension torque (KET) produced by the paretic and nonparetic lower limbs of 27 stroke patients, with hemiparesis, at knee extension velocities (KEVs) of 30 degrees, 60 degrees, 120 degrees, and 180 degrees/sec. The purpose of this study was to determine whether the relative decreases in KET at velocities greater than 30 degrees/sec were different on the two sides. To further investigate this relative decrease, the relationship between the torque at 30 degrees/sec and those at higher speeds also was examined on each side. Relative decreases in KET differed between speeds, but not between sides. Torques at speeds greater than 30 degrees/sec were correlated significantly with the torque at 30 degrees/sec. These findings suggest that patients with hemiparesis and minimal muscle spasticity may have difficulty moving forcefully at higher speeds because they are weak. Therapeutic interventions, therefore, might be most beneficial when they are directed toward helping patients with hemiparesis activate their weak muscles.
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PMID:Relative decreases in knee extension torque with increased knee extension velocities in stroke patients with hemiparesis. 361 90

The centrally active, alpha-2 adrenergic receptor agonist clonidine was given to 12 spinal cord injury patients with problematic spasticity not adequately controlled by recognized spasmolytic drug therapy. Five patients had an excellent reduction and 2 patients had some reduction in clinical spasticity (average dose 0.39 mg daily). Four of the 7 responders discontinued clonidine because of adverse reactions after an average of ten weeks of therapy. Three responders have continued to tolerate the drug well with excellent control of spasticity for 18 to 34 months. Five patients had no change in clinical spasticity (average dose of 0.24 mg daily). Three of the non-responders discontinued clonidine because of adverse reactions after an average of three weeks of therapy. Significant associated adverse reactions included syncopal seizures (3), cerebrovascular accident (1), deep vein thrombosis (1), autonomic hyperreflexia (3), lethargy/drowsiness (3), and nausea/vomiting (1). Possible mechanisms of action for clonidine to affect spasticity and the unstable cardiovascular system of quadriplegics is discussed. While spinal cord injured patients with severe spasticity may benefit from clonidine, great caution is recommended during its use until further study establishes safe parameters of administration and efficacy is confirmed on controlled studies.
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PMID:Early clinical experience with clonidine in spinal spasticity. 374 98

Shoulder pain is probably the most frequent complication of hemiplegia. In this study 219 hemiplegia patients were regularly followed up after their cerebrovascular accident (CVA) for one year (166 men, 53 women, with a mean age of 47 years). Criteria and parameters for evaluation of these shoulders were established at the outset. Distinction was made between flaccid and spastic hemiplegia. Other influencing factors were subluxation reflex sympathetic dystrophy syndrome (RSD), isolated tendon lesion cuff rotator tear or association of some of these. Roentgen examinations were done for each patient. In our series of patients, 72% had shoulder pain at least once during the course of their recovery. This problem occurred more often in patients having spasticity (85%) than in those with flaccidity (18%). An evolution towards spasticity was noted in 80% of the patients in this series, whereas 20% remained hypotonic. Among the other possible causes of shoulder pain, anteroinferior subluxation was incontrovertibly the most frequently cited. The RSD syndrome was present in only 23% of all cases but was seen more often in spastic patients, that is 27% compared to 7% among flaccid patients. Whatever the cause, the subluxation with flaccid paralysis should be corrected and spasticity should be combatted as early and as vigorously as possible.
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PMID:Painful shoulder in hemiplegia. 394 79

Acute appearance of hemiparesis or hemiplegia with initial marked spasticity was observed in 8 stroke patients. All had intracerebral hematomas and in 7 it was located in the region of the basal ganglia. By contrast, none of 121 hemiplegic patients with hemispheric ischemic stroke hospitalized during the same period had increased muscle tone in the involved limbs at stroke onset. Study indicates that association of hemiplegia with immediate spasticity at stroke onset is a clinical clue to a possible deeply located intracerebral hematoma.
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PMID:Immediate spasticity with acute hemiplegia is a sign of basal ganglia hemorrhage. 398 83

Muscle strength for knee extension, both isokinetic and isometric, and walking capacity, maximum velocity and walking rate, were examined in 11 post-stroke hemiparetic patients. The degree of spasticity of the affected lower extremity was not related to the isokinetic and isometric torques, or to the walking capacity. Although both the isokinetic and isometric torques decreased on the affected side compared to the non-affected side, the rate of decrease was remarkable in isokinetic torque at fast velocities. The walking capacity was well correlated with isokinetic torque of the affected side at fast velocities but not isometric torques. These results suggest that reduction of muscle strength at rapid movements is an essential feature of spastic paresis and is primary cause of motor disabilities such as impaired locomotor function.
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PMID:Relationship of muscle strength for knee extension to walking capacity in patients with spastic hemiparesis. 400 20

A minor tranquilizer, ketazolam, was tested in a double-blind, randomized, crossover study of 50 patients for its effects in neurologic spasticity. The drug was compared with diazepam (widely accepted as an effective antispasticity agent) and a placebo. The patients with spasticity were almost all cases of multiple sclerosis (24) or stroke (24). Thirty-nine patients completed the study. There was not statistically significant superiority of either diazepam or ketazolam, but both relieved symptoms significantly better than the placebo, as measured clinically and by electromyographic recording of deep tendon reflexes. Ketazolam is a relatively safe and clinically effective antispasticity agent (especially for patients with multiple sclerosis). The well-known "big 3"--dantrolene sodium, baclofen, and diazepam--produce large and small problems in many individual cases; hence, ketazolam now offers a safe and clinically useful alternative.
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PMID:Ketazolam treatment for spasticity: double-blind study of a new drug. 614 38

EMG denervation activity was studied in patients without peripheral neuron disorder but with upper motor neuron lesions. The time course of such central denervation activity, the local distribution and the quantitative relationship between denervation activity and the degree of paresis and spasticity were also studied. A total of 101 patients, who had developed hemiplegia or hemiparesis as a result of a cerebral vascular accident, underwent needle electromyographic examination at regular intervals in proximal and distal muscle groups. The maximum observation time was 1 year. Denervation activity in cases of central paresis first occurred 2-3 weeks after stroke. This could be observed most frequently in the distal arm and hand muscles. In the course of weeks and months the frequency of the denervation activity decreased in parallel with the development of spasticity and the increasing voluntary innervation. The occurrence and the dynamic properties of the denervation activity in cases of central paresis support the assumption of a trans-synaptic degeneration of alpha-motoneurons and of a compensating segmental "sprouting" of afferents.
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PMID:Denervation activity in the EMG of patients with upper motor neuron lesions: time course, local distribution and pathogenetic aspects. 619 9

Spasticity is a common neurologic condition in patients with multiple sclerosis, stroke, cerebral palsy or an injured spinal cord. Animal studies suggest that THC has an inhibitory effect on polysynaptic reflexes. Some spastic patients claim improvement after inhaling cannabis. We tested muscle tone, reflexes, strength and performed EMGs before and after double-blinded oral administration of either 10 or 5 mg THC or placebo. The blinded examiner correctly identified the trials in which the patients received THC in seven of nine cases. For the group, 10 mg THC significantly reduced spasticity by clinical measurement (P less than 0.01). Quadriceps EMG interference pattern was reduced in those four patients with primarily extensor spasticity. THC was administered to eight other patients with spasticity and other CNS lesions. Responses varied, but benefit was seen in three of three patients with "tonic spasms." No benefit was noted in patients with cerebellar disease.
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PMID:Treatment of human spasticity with delta 9-tetrahydrocannabinol. 627 39

Moyamoya disease was originally defined as a characteristic syndrome of recurrent headaches, occlusion of the distal internal carotid arteries and the foggy (moyamoya) clusters of collateral vessels at the base of the brain as demonstrated by cerebral angiography. The etiology is unknown and pathobiology is poorly understood. We examined the intracranial arteries in 3 patients to demonstrate characteristic changes and to obtain a better understanding of the basis mechanisms of the disease. Controls were obtained from 3 normotensive patients who died as a result of cancer. Occluded internal carotid arteries were characterized by severe thickening of the intima with a dense luminal array of smooth muscle cells, a deeper less cellular zone, pronounced tortuosity of the internal elastica and thinning of the media. Collateral vessels were arterial in structure and were affected by similar proliferative changes in the intima, thinning of the media, and contorted internal elastica. Stainable lipids were not part of the typical components. Severe contortion of the internal elastica, medial damage and intimal proliferation may result from recurrent and sustained spasticity of the cerebral arteries. The distal lenticulostriate arteries showed severe medial damage similar to what is termed as a moth-eaten change in hypertensive patients dying of massive cerebral hemorrhage.
Stroke
PMID:Ultrastructural studies of cerebral arteries and collateral vessels in moyamoya disease. 646 67

A study was carried out to determine the efficacy and long-term safety of dantrolene in treating stroke patients with spasticity limiting rehabilitation. Fifteen of the 18 patients studied experienced reduction in spasticity and clinical improvement after treatment with dantrolene sodium for 6 weeks. Fourteen of these patients participated in a 6-week, double-blind, placebo-controlled study. The 5 patients who continued to receive dantrolene did not experience clinical deterioration. However, the 9 patients given placebo noted increased deficits. Seven asked that the blind be broken and chose to resume dantrolene therapy. After 6 weeks, 13 of the 14 patients elected to continue on dantrolene (average dose 165.4 mg/day). All continued to improve. Side-effects were generally mild and transient. Although these patients took other drugs concomitantly, no drug interactions were reported.
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PMID:Long-term treatment with dantrolene sodium of stroke patients with spasticity limiting the return of function. 649 10


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