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)

Dantrolen sodium is a muscle relaxant, which is used in the treatment of spasticity. Although it is given chronically, little is known about its pharmacokinetic behaviour. The relationship between the effect of a single oral dose of dantrolene sodium and its plasma concentration in healthy volunteers was studied by measuring the effect on the twitch tension, and in spastic patients on the decrease in muscle hypertonia. On the twitch tension dantrolene gave a depression of 49.1 +/- 9.4% (+/- DS) within 1.15 and 3.45 h after ingestion of 100 mg. The mean maximal plasma concentration was 1.24 +/- 0.32 microgram/ml (+/- SD). The effect and the plasma concentration were correlated. No relationship between the plasma concentration of dantrolene sodium and its effect could be established in patients, although definite activity in 6 out of 7 patients was observed after a single oral dose of 100 mg, and plasma concentration of dantrolene sodium greater than 0.3 microgram/ml were consistenly associated with better results than placebo treatment in 6 out of 7 patients.
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PMID:Relationship between plasma concentration and effect of dantrolene sodium in man. 49 21

In 4 patients, trauma to the lumbosacral area produced abnormalities similar to those seen after resection of the nervi erigentes. Mechanisms of the resulting constipation and fecal incontinence for liquid stools included a prolonged transit time through the entire colon, a low rectal pressure, spasticity of the anal canal, and abnormal anal reflexes. Previous trauma to the lower spine must be considered in the differential diagnosis of chronic constipation.
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PMID:Traumatic constipation. 49 13

Clinical assessment of equinus in children before and after operation was made over a twenty-year period (1958-1978), and three groups were defined. Forty-three muscles (Group I) had abnormal shortening without spasticity and the deformity progressed steadily despite immediate improvement after operation; this was considered to be the result of a lack of muscle growth during bone growth. Forty-one muscles (Group II) had both shortening and spasticity with an imbalance which might be unchanged after operation, or reversed or improved. Fourteen muscles (Group III) had spasticity only and progression was unpredictable and could not be defined. Improvement in gait was regularly observed in Group I in the early years after operation. In Groups II and III the results were variable. These results did not depend on surgical technique but on differences in pathophysiology.
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PMID:Variation in the long-term results of elongation of the tendo Achillis in children with cerebral palsy. 50 Jul 58

A trial of the antispastic drug baclofen was made in amyotrophic lateral sclerosis. Some patients noted reduction of tonus and spasticity; but others had no benefit, nor was the course of the disease altered by long-term administration of baclofen. No major side effects occurred.
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PMID:Trial of baclofen in amyotrophic lateral sclerosis. 50 32

Despite considerable speculation it remains unclear as to whether stretch reflexes perform a functional role in speech articulator muscles. Recent research, however, has shown that long loop stretch reflex mechanisms are brought into play during voluntary contraction of limb muscles and a functional role in oscillatory damping has been suggested. It was decided, therefore, to use a method and a technique of analysis similar to that used in limb muscles to search for tonic stretch reflex (TSR) responses in lip, tongue and jaw muscles during sustained voluntary contraction. The term 'action TSR' is used to differentiate stretch reflex responses measured from voluntary activity from those measured at rest. Simultaneous electromyogram (EMG) recordings were taken from the lip, tongue and jaw musculature in normal, stutterer and cerebral spastic subjects. Subjects were instructed to hold the appropriate articulator in a fixed position while the experiment applied an irregular, continuously changing, stretching force. The stretch and EMG signals were analyzed using a cross correlation and spectral analysis technique. This provided a sensitive means of detecting any EMG fluctuations which covaried with applied stretch and might therefore be classified as reflex. No suggestion of such action TSR responses could be found in lip or tongue muscles of any of the subjects tested, including the cerebral spastic subjects with dysarthric speech. It is therefore concluded that action TSR mechanisms are not operative in control of lip and tongue muscles in man. Furthermore, dysarthric speech in cerebral spasticity cannot be attributed to exaggerated tone of lip and tongue muscles resulting from hypersensitivity of TSR mechanisms. In contrast, clear action TSR responses were demonstrable in jaw closing muscles while in jaw opening muscles, small amplitude responses were detected but were not substantial in comparison with background activity. Since the action TSR is present in jaw and limb muscles, but absent in lip and tongue muscles, the suggestion of a functional role of this reflex in damping mechanical oscillations associated with inertial loads is further supported.
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PMID:Tonic stretch reflexes in lip, tongue and jaw muscles. 50 9

Passive cyclical electrical stimulation was applied during a four-week treatment program to the wrist and finger extensors of 16 hemiplegic patients with flexor spasticity. The study noted the effects of this treatment on the patients' sensation; spasticity; passive range of motion of the wrist, metacarpophalangeal, and proximal interphalangeal joints; and strength in the wrist extensor muscles. Patients were divided into chronic and subacute groups. Both groups received electrical stimulation for three half-hour periods a day, seven days a week, as a substitute for all other range-of-motion techniques. Flexion contractures were prevented in the subacute group of patients at the wrist, metacarpophalangeal, and proximal interphalangeal joints. A statistically and clinically significant increase in wrist extension range occurred in the chronic group that had wrist flexion contractures before the electrical stimulation. Increased extension was noted at the metacarpophalangeal and proximal interphalangeal joints of patients in the chronic group. Those patients with some voluntary wrist extension before the treatment began were able to increase their extension strength during stimulation. No changes in skin sensation were noted and only a general trend in decreasing spasticity was apparent.
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PMID:Electrical stimulation of wrist and fingers for hemiplegic patients. 51 86

Following spinal cord transection there occurred decreases in Km and Vmax of glutamate decarboxylase (GAD) both above and below the lesion, and an initial decrease in the concentration of GABA. Concomitantly, there was a gradual decrease in presynaptic inhibition. Eight to 12 weeks after spinal cord transection, Km and Vmax for GAD returned to control values, but the GABA content of the spinal cord below the lesion increased significantly and presynaptic inhibition became maximally depressed. These results suggested that during the chronic phase of spinal cord injury there is a decrease in release of GABA, the interneuronal inhibitory neurotransmitter which mediates presynaptic inhibition. Diazepam, a GABA enhancer, increased presynaptic inhibition in acute and chronic spinal cats, this being accompanied by a reduction in somatic muscular spasticity. The degree of this enhancement by diazepam, however, is attenuated with gradual loss of presynaptic inhibition. In the acute cat, a conditioning volley applied to cutaneous afferents blocked the inhibition of the monosynaptic response to extensor motoneurones. In contrast, in chronic spinal cats (eight to 12 weeks), the duration of complete blockade was markedly reduced and was followed by a prolonged period which cutaneous nerve stimulation potentiated the monosynaptic discharge. Similar to GABA, there also occurred an increase of substance P below the level of the lesion. Other neurotransmitters (e.g., norepinephrine, serotonin) accumulated above and disappeared below the transection level. Although somatic msucular spasticity appears to be, to some extent, due to GABA dysfunction in the spinal cord, alterations in "normal" functioning of other neurotransmitters and the loss of supraspinal control also contribute to this state.
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PMID:Correlation of changes in the GABA-ergic system with the development of spasticity in paraplegic cats. 51 79

Telemetered gait electromyography was used to investigate gait patterns and the phasic behavior of the quadriceps femoris and medial hamstring muscles in 26 normal children and 32 children with spastic cerebral palsy. The average child with spastic cerebral palsy was found to have a shorter stance phase than the normal, but the cadence, while more variable, was nearly the same as normal. The spastic muscles typically exhibited prolonged phasic activity or a dysphasic pattern. Most of the patients with spastic hamstrings also had spastic quadriceps, suggesting that over-weakening the hamstrings may produce an unwanted genu recurvatum or hyperextended knee gait. Care must be taken to balance hamstring spasticity with quadriceps spasticity. A final result with slight knee flexion is preferable to hyperextension.
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PMID:Gait electromyography in normal and spastic children, with special reference to quadriceps femoris and hamstring muscles. 52 Jul 11

A review was made of 88 adult institutionalized patients with spastic cerebral palsy and contractural deformity of the hips. 21 were untreated for dislocated hip, and 11 of these suffered from hip pain. The degree of pain was directly related to neurological maturity and to the coexistence of athetosis and spasticity. Decubitus ulcers and perineal care problems were more associated with contractures than with dislocation alone. It is concluded that dislocation and subluxation should be prevented by surgical means, but that surgical treatment of the already dislocated hip should be reserved for the neurologically mature and athetoid patient.
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PMID:Natural history of the dislocated hip in spastic cerebral palsy. 52 Jul 12

The patient, H.Chr.B., was among the first reported with hyperuricemia and central nervous system symptoms. He has been found to have a variant of hypoxanthine guanine phosphoribosyl transferase (HPRT; E.C.2.4.2.8) distinct from the enzyme present in patients with the Lesch-Nyhan syndrome. The patient had chroeoathetosis, spasticity, dysarthric speech, and hyperuricemia. However, his intelligence was normal and he had no evidence of self-mutilation. There was no activity of HPRT in the lysates of erythrocytes and cultured fibroblasts when analyzed in the usual manner. Using a newly developed method for the study of purine metabolism in intact cultured cells, this patient was found to metabolize some 9% of 8-14C-hypoxanthine, and 90% of the isotope utilized was converted to adenine and guanine nucleotides. In contrast, cells from patients with the Lesch-Nyhan syndrome were virtually completely unable to convert hypoxanthine to nucleotides. The patient's fibroblasts were even more efficient in the metabolism of 8-14C-guanine, which was utilized to the extent of 27%, over 80% of which was converted to guanine and adenine nucleotides. The growth of the cultured fibroblasts of this patient was intermediate in media containing hypoxanthine aminopterin thymidine (HAT), whereas the growth of Lesch-Nyhan cells was inhibited and normal cells grew normally. Similarly in 8-azaguanine, 6-thioguanine, and 8-azahypoxanthine, the growth of the patient's cells was intermediate between normal and Lesch-Nyhan cells. These observations provide further evidence for genetic heterogeneity among patients with disorders in purine metabolism involving the HPRT gene. They document that this famous patient did not have the Lesch-Nyhan syndrome.
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PMID:Utilization of purines by an HPRT variant in an intelligent, nonmutilative patient with features of the Lesch-Nyhan syndrome. 52 96


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