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

The prevalence of various manifestations of spasticity from questionnaire responses and from clinical examination of chronic spinal cord injured patients is reported. Extensor spasms, flexor withdrawal spasms, and clonus were reported by most subjects. Those with incomplete lesions reported more interference with activities, more pain, and less functional usefulness, than did those with complete lesions. Extensor spasms were reported to interfere more with transfers, whereas flexor withdrawal spasms were reported to be more frequent at night and to interfere more with sleep. Increased muscle tone was observed more often in extensor than in flexor muscles. Those with incomplete lesions had more hypertonus and more limited passive joint movements than did those with complete lesions. Flexor withdrawal reactions and extensor spasms were also more pronounced in those with incomplete lesions, particularly those with Frankel grade C lesions.
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PMID:Lower extremity manifestations of spasticity in chronic spinal cord injury. 291 56

Disruption of the upper motor neuron inhibitory pathways by stroke, brain trauma, or spinal cord injury leads to muscle spasticity. Spasticity is characterized by increased muscle tone, hyperactive reflexes, and possible clonus or rigidity. The increased muscle tone may result in loss of joint motion, leading to contractures. Treatment of established contractures is difficult. Prevention of contractures by joint mobilization is emphasized as a goal in the management of patients with spasticity.
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PMID:Spasticity and contracture. Physiologic aspects of formation. 304 37

The functional impairment due to spasticity must be carefully assessed before any treatment is considered. Therapeutic intervention is best individualized to a particular patient. Basic principles of treatment to ameliorate spastic hypertonia are: 1) avoid noxious stimuli and 2) provide frequent range of motion. Therapeutic exercise, cold or topical anesthesia may decrease reflex activity for short periods of time in order to facilitate minimal motor function. Casting and splinting techniques are extremely valuable to extend joint range diminished by hypertonicity. Baclofen, diazepam and dantrolene remain the three most commonly used pharmacologic agents in the treatment of spastic hypertonia. Baclofen is generally the drug of choice for spinal cord types of spasticity, while sodium dantrolene is the only agent which acts directly on muscle tissue. Phenytoin with chlorpromazine may be potentially useful if sedation does not limit their use. Tizanidine and ketazolam, not yet available in the United States, may be significant additions to the pharmacologic armamentarium. Intrathecal administration of antispastic medications allows high concentrations of drug near the site of action, which limits side effects. This form of treatment is the most exciting recent development in the treatment of spastic hypertonia. Peripheral electrical stimulation may have limited use in diminishing tone and facilitating paretic muscles. Dorsal column stimulation via electrodes within the spinal column was initially hailed as a therapeutic advance, but has subsequently been shown to be minimally effective. Phenol injections provide a valuable transition between short-term and long-term treatments and offer remediation of hypertonia in selected muscle groups. Tenotomies and tendon transfers offer significant benefit in carefully chosen patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Management of spasticity. 328 46

We report on 2 patients, less than age 5 years, and one adult patient with partial duplication 8p, due to interstitial duplication of bands 8p21.1-22. The phenotype in young and adult patients with this chromosomal unbalance syndrome is further documented. In young patients the craniofacial manifestations are very similar to trisomy 8 mosaicism. However, mental retardation is much more pronounced in 8p21-22 duplication than in trisomy 8 mosaicism. The phenotypic changes observed in adult patients are probably secondary and they are due to the great neurologic deficit with generalized spasticity and hypertonia.
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PMID:Partial duplication 8p due to interstitial duplication: inv dup(8)(p21.1----p22). Further delineation of the phenotype from birth to adulthood. 349 29

Twenty-five children with hemiplegic cerebral palsy between the ages of five and 15 years were examined in more detail, using a torque generator motor. A significant reduction in distal power, fatiguability and speed of movement was found on the hemiplegic side. Proximal power was relatively well preserved. Muscle tone, as would be expected, was significantly increased on the affected side and this was demonstrated by a significant rise in measured resonant frequency. Phasic spasticity in response to stretch was found on EMG to be much more common than phasic and tonic combined. Hand function correlated well with the loss of distal power and speed of movement. There was wide individual variation in the relationship between increased muscle tone and hand function. Thixotropy was normal in spastic muscles. Use of the unaffected hand had a marked effect on muscle tone and EMG of the affected side.
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PMID:A neurological study of hand function of hemiplegic children. 359 65

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

Clinical Neurophysiology brings about 2 major contributions in the study of Parkinson's disease: on the one hand, it makes it possible to measure the motor troubles; on the other, it enables their pathophysiological analysis. The 3 classical signs must be studied separately. Tremor can easily be recorded by electromyography. Moreover, its parkinsonian nature can be specified by studying the resetting of EMG bursts following electrical stimulation of the motor nerve. A pace maker has been demonstrated in the thalamus from where rhythmic messages are first sent to motor cortex and thereafter reverberated to spinal motoneurons. Rigidity can be assessed by sophisticated but not generalized methods. It is easier to evaluate it by long-loop responses evoked by proprioceptive or exteroceptive stimulations. These responses reflect activity in pathways relaying in supraspinal structures. Contrary to spasticity, rigidity is not basically due to dysfunctions in segmentary spinal circuits. It is more likely that it depends on hyperactive and hyperexcitable long loop pathways. This hypothesis is in agreement with well established facts showing that parkinsonian hypertonia vanishes after dorsal root section. Akinesia is complex semeiologically. It is made of various components some of which can be measured. Reaction times and movement times provide interesting data which however are not strictly correlated with the motor handicap. Motor programmes are assembled in normal delays but they are not "called upon" correctly, reflecting a disturbance in the motor planning. A lack of "energetization" of the motor cortex and the pyramidal tract is likely. A functional disconnection between the motor program/plan side and the execution side can be hypothesized to explain the 3 major signs; on the one hand, neural messages are not correctly transferred to the pyramidal system, on the other, spinoencephalospinal loops on the execution side become more active as they escape from the control normally exerted by the plan/program side where basal ganglia play a prominent role.
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PMID:[Clinical neurophysiology in the evaluation and physiopathology of Parkinson's disease]. 383 95

Spasticity is a known sequelae of spinal cord injury and head injury. We sought to examine whether there were any significant differences in the characteristics or underlying mechanisms of spasticity in these two groups in the chronic period which may be related to the level of injury of the neuraxis. The response to vibration applied to the muscle, or the tonic vibratory reflex, has been shown to be related to the degree of spasticity, and was therefore studied along with phasic reflexes and passive movements. These studies were carried out on cooperative, stabilized patients who were otherwise healthy, 5 with head injuries, and 5 with spinal cord injuries. The patients were examined in a supine position while surface EMG recordings were made of quadriceps and triceps surae muscles bilaterally. Tendon jerk responses, passive and volitional movements, and responses to a powerful vibratory stimulator were measured. In both head injury and spinal cord injury patient groups, a large EMG response was elicited by passive maneuvers, and tendon jerks were exaggerated. The tonic vibratory response, previously shown to be dependent upon brain influence, was present in both groups. These observations suggest that similar suprasegmental mechanisms may be responsible for hypertonia in both head-injured and spinal cord-injured patients.
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PMID:Characteristics of the tonic stretch reflex in spastic spinal cord and head-injured patients. 383 47

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 a double-blind cross-over trial of two 2-week periods, the clinical effect of progabide was compared to placebo. 16 patients with spasticity in a stationary phase completed the trial. 14 had multiple sclerosis, 2 hereditary spastic paraplegia. 5 were female and 11 male. The median age was 45.5 years (range 30-62 years). The median daily dosage of progabide was 24.3 mg/kg (range 14.3-32.7 mg/kg). During progabide treatment, there was a reduction in spastic hypertonia (P less than 0.01), a suppression of tendon reflexes (patellar) (P less than 0.01), and a reduction in the frequency of flexor spasms (P less than 0.05). No significant changes in voluntary power were registered. The global clinical impression revealed a therapeutic effect in 87% of the patients (95% confidence limits 61-98%). The improvement was judged as medium or important in 50% of the patients (95% confidence limits 23-77%). No side-effects or laboratory abnormalities were seen.
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PMID:The clinical effect of the GABA-agonist, progabide, on spasticity. 637 2


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