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Query: UMLS:C0026838 (spasticity)
 6,471 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Static and dynamic stiffnesses of voluntarily activated elbow muscles were compared in spastic and contralateral arms of 15 subjects with spastic hemiparesis. Stiffnesses were estimated from the positional deflections induced by applying load perturbations to each forearm. In 11/15 subjects (73%), stiffness were comparable on the two sides. In the remaining 4/15 subjects (27%), stiffness were consistently greater on the spastic side, however, EMG recordings from these spastic muscles were of much smaller amplitude than those of the contralateral muscles, indicating that this increase was probably caused by changes in the mechanical properties of elbow muscles, rather than by stretch reflex enhancement. We conclude that for voluntarily activated muscles of spastic hemiparetic subjects, reflex stiffness (and presumably stretch reflex gain), of spastic and contralateral limbs is not significantly different. These findings impose important constraints upon theories attempting to explain spastic hypertonia, and they also provide guidelines for clinical quantification of spasticity.
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PMID:Absence of stretch reflex gain enhancement in voluntarily activated spastic muscle. 366 81

In 4 patients with spastic hemiparesis the electromyograms (EMG) of leg muscles were recorded during walking and the gastrocnemius medialis on both sides was investigated by histochemistry and morphometry. During walking a reciprocal mode of muscle activation was preserved on the spastic side, but the EMG amplitude was reduced. In one patient the discharge behaviour of single motor units was investigated during stance. The mean discharge rate on both the spastic and the unaffected side amounted to about 5.5 Hz. Modification of this rate over a wider range by manoeuvres of the trunk was only observed on the unaffected side. Histochemistry and morphometry of the spastic muscle revealed: Increased levels of muscle fibre atrophy (especially type II); A predominance of type I fibres during later stages, when spasticity was established; Structural changes, such as the appearance of target fibres, mainly in type I fibres. These results suggest that the low level of tonic activation in spastic muscle develops tension enough during the stance phase of gait to support the body. The histopathological profile of the spastic gastrocnemius muscle is considered to be indicative of denervation, due to the combined effects of an impaired supraspinal control of the lower motoneurone and a concurrent transsynaptic muscle membrane dysfunction, muscle cell atrophy and fibre type transformation.
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PMID:Motor unit involvement in spastic paresis. Relationship between leg muscle activation and histochemistry. 374 41

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

In 15 patients with spastic hemiparesis the development of tension of calf muscles in relation to their electrical activation and their stretching period was studied on both sides during locomotion. Only in the spastic leg did isolated small biphasic potentials appear in the gastrocnemius E.M.G. with monosynaptic latency at the beginning of the stance phase, while the remaining gastrocnemius activation was reduced compared to the unaffected side. Perturbations of gait were followed in the spastic leg by a large monosynaptic response, while the polysynaptic reflex response was reduced. In the unaffected leg only a strong polysynaptic response appeared, which suggests a reciprocal modulation of monosynaptic and polysynaptic reflex responses. Tension development paralleled the gastrocnemius E.M.G. in the unaffected leg, while in the spastic leg tension was more closely correlated to muscle stretch. It is concluded that in spasticity the exaggerated monosynaptic reflexes represent only a small part of leg extensor activation during gait and that the tension development does not depend on these reflexes.
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PMID:Tension development and muscle activation in the leg during gait in spastic hemiparesis: independence of muscle hypertonia and exaggerated stretch reflexes. 609 May 90

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

H-reflex amplitudes were recorded after stimulation of the tibial nerve and different electrical stimuli in 18 normal persons and 26 patients showing pyramidal spasticity (8 spastic spinal paralysis, 6 spastic hemiparesis, 12 spinal lesions). A just subthreshold stimulus of the tibial nerve facilitated the H-reflex in spastic patients slightly after about 300 ms (up to 113%), following an early strong facilitation (10 ms) and a longer lasting depression (20-200ms). Similar postinhibitory facilitation was obtained in spastic patients after ipsilateral stimulation of the plantar surface and after direct stimulation of the dorsal columns. Conditioning by contralateral stimuli of the posterior tibial nerve caused a slight late facilitation in both normal and spastic patients. This late facilitation did not correlate significantly with the severity of spasticity, but it was more pronounced in cerebral pyramidal lesions than in spinal ones. It is assumed that this postinhibitory facilitation is probably generated as a spinal rhythm, similar to the clonus, and that it is modulated from supraspinal structures.
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PMID:The late facilitation in H-reflex recovery cycles in different pyramidal lesions. 625 75

Activation of leg musculature on both sides following a unilateral displacement was studied during stance on separate see-saws, or on stable force-measuring platforms, in patients with spastic hemiparesis and paraparesis. During balancing the movements on the spastic side were damped and the degree of muscle activation reduced. Whereas in healthy subjects the tibialis anterior muscles of both sides were activated, following a unilateral displacement, with the same strength and latency (see-saws 55 ms, platforms 85 ms), in hemispastic patients the EMG responses were delayed (by about 20 to 30 ms) and of reduced strength on the spastic leg, irrespective of whether the unaffected or the spastic side was displaced. In addition, the compensatory movements on the spastic side were damped in both conditions, although the amplitude of displacement was the same bilaterally. Although there was no correlation between the delay and the reduction in EMG response, the latter was correlated with the severity of paresis. In patients with spastic paraparesis quite similar results were obtained with delayed and reduced EMG responses on both sides. It is concluded that in spasticity the impaired regulation of quick compensatory movements is due to a dysfunction of a spinal interneuronal system by which the early EMG responses are mediated. This could be explained by loss of supraspinal control. In addition to the impaired neural activation of leg muscles, changes in the mechanical properties of muscle can be assumed to contribute to the damped movements on the spastic side.
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PMID:Interlimb coordination of posture in patients with spastic paresis. Impaired function of spinal reflexes. 647 85

This study investigated rationales underlying splinting decisions involving patients with hemiplegia. The survey incorporated a limited-choice, multiple-option questionnaire based on the case study of a man with a left hemiparesis at three hypothetical stages of recovery. Ninety-three occupational therapists who answered indicated whether they would or would not recommend a splint at each stage, and selected one or more reasons for their decisions. The respondents fell into three major categories: those who would 1. never splint, 2. always splint, and 3. splint only in the presence of moderate to severe spasticity. Those with longer clinical experience reflected more tendency to splint. The results indicated conflicting practices in splinting and showed the need for further clinical research in this area.
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PMID:A survey of rationales for and against hand splinting in hemiplegia. 722 29

Topical anesthesia was applied to the skin of the leg and thigh of a hemiparesis patient resulting from embolic infarction in the middle cerebral artery. After application of the anesthesia, the angular displacement of the ankle and knee joints measured during a full gait cycle showed a substantial shift towards normal. This response indicated a reduction in muscle spasticity which was confirmed by clinical tests. Neurophysiologic studies performed on the patient suggested that the reduction in muscular hypertonicity was mediated by reduced cutaneous inputs on the alpha - gamma motoneuron interaction. This conjecture is supported by studies of other investigators performed on animals as well as humans.
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PMID:Topical anesthesia: a possible treatment method for spasticity. 724 57

The effects of various cerebral cortical lesions on motor function and in particular on muscle tone have been studied quantitatively in the squirrel monkey (Saimiri sciureus) in an attempt to define the cause of muscular hypertonia and to develop a reliable model for human cerebral spasticity. Unilateral ablation of the primary motor area (MI), either alone or together with the supplementary motor area (MII), produced a contralateral hemiparesis especially marked for fine motor tasks, but did not cause hypertonia. Bilateral ablation of the supplementary motor area alone produced no impairment of motor function or change in muscle tone. Bilateral lesions of the primary motor area, either alone or together with the supplementary motor area, caused a disabling quandriparesis with striking hypertonia affecting chiefly the upper limb flexors and lower limb extensors. Quantitative electromyography revealed augmented stretch responses proportional to the rate of muscle lengthening. This velocity-dependent exaggerated stretch reflex, with a predominantly dynamic component reflecting hyperactivity of the Ia spindle afferents, is similar to that seen in human hemiplegic spasticity. Out results indicate that decorticate hypertonia depends upon the bilateral interruption of fiber tracts originating in motor cortex and distributed both ipsilaterally and contralaterally. Bilateral decortication in the primate seems to be a suitable laboratory model for the objective evaluation of measures proposed for the relief of spasticity in humans.
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PMID:Quantitative assessment of muscular hypertonia resulting from cortical lesions in primates. 727 72


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