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

In rats the application of 10 mg/kg 6-amino-nicotinamide (6-AN) leads to an accumulation of 6-phosphogluconate, by inhibition of 6-phosphogluconate dehydrogenase in the pentose phosphate pathway, in the cells of the spinal cord. The accumulation reaches its maximum after 18-24 h. It seems that there exists a relationship between the accumulation of 6-phosphogluconate and the lesion of the neuroglia, which is found in electron microscopic studies. Symptoms of a spastic paresis only develop later when the spinal interneurones are destroyed as a consequence of the lesion of the neuroglia. The accumulation of 6-phosphogluconate almost exceeds the 400 fold of the norm. No considerable differences are found between the effects of a dose of 35 mg 6-AN/kg and one of 10 mg 6-AN/kg. Free gluconate is identified enzymically in the cells of the spinal cords of the rats treated with 6-AN. The compound is very probably formed by dephosphorylation and diffuses into the blood. 6-Phosphogluconate is an inhibitor of the phosphoglucose isomerase. Its accumulation shifts the equilibrium towards glucose 6-phosphate. The lactate concentration decreases as compared with the untreated controls. Muscular action potentials are recorded extracellularly with a concentric needle electrode from the musculus gastrocnemius of rats treated with 6-AN. First activations of the electromyograms are found 48 h after the application of 10 mg 6-AN/kg. The electrical activities increase during the time in which a progressive destruction of the interneurones occurs. The electromyogram displays a permanent state of excitation with high amplitudes and an increased frequency. The continuity and intensity of the increased activity recorded by the electromyograph is the most important pathological finding. p-Chlorophenyl-GABA and, still more so, chlorpromazine cause temporary reduction of the excitation processes and an electromyogram nearly at rest. Under the same conditions, haloperidol is only slightly effective. The symptoms developed by the chemical destruction of the interneurones of the spinal cord, with rigidity and spasticity of the hind limbs, are suitable for testing antispastic drugs.
 ...
PMID:Spastic paresis after 6-aminonicotinamide: metabolic disorders in the spinal cord and electromyographically recorded changes in the hind limbs of rats. 13 91

The effects of dantrolene sodium, an anti-spasticity drug with a site of action within the muscle fibres, were studied in 19 patients with spastic paresis. Oral doses were successively increased from 100 mg/day to a maximal tolerated level or up to 800 mg/day. Trial periods were 8-13 weeks. The responses of stretch reflexes to local cooling over the spastic muscles were used to differentiate alpha and gamma spasticity. In the knee extensor and flexor muscle groups, cryo-negative alpha-spasticity was seen in 25 and cryo-positive gamma-spasticity in 4 muscle groups. Ankle clonus was cryo-positive in 14 of 15 cases. Resistance to passive knee joint movements, ankle clonus and isometric or isokinetic muscle strength was determined quantitatively. The gait was recorded by intermittent-light photography and the muscle activation patterns in gait were studied in recordings of the average EMG from limb muscles. Functional disability and spasms were assessed from clinical examinations and interviews. Passive resistance at slow (6%/sec) and fast (30 degrees/sec) knee joint movements decreased by 32% in the extensor muscles (p = 0.005 resp. 0.001) and by 23-26% in the flexor muscles (not significant). Reduced passive resistance was observed in 16 of the muscles with alpha-spasticity and in all 4 of the muscle groups with gamma-spasticity. Clonus was diminished or abolished in 14 of 15 patients with this sign. Maximal isometric or isokinetic muscle strength was unaltered in the majority of the patients. In a few the strength was increased, in some it was decreased. The averaged EMG activity during walking as studied in 10 patients were increased in 35 of the 57 muscle groups examined. In some muscle groups, exaggerated activity attributable to spastic reflexes was reduced. Motor disability was decreased significantly in 10 patients. It was not significantly changed in 5 and deteriorated in 4 patients. Drowsiness and subjective muscle weakness were the most frequent side-effects. SGOT and SGPT were increased in 3 cases.
 ...
PMID:Action of dantrolene sodium in spasticity with low dependence on fusimotor drive. 13 20

An unusual neurovisceral lipid storage disorder in two unrelated juvenile patients manifested itself by dystonia and involuntary movements, with facial grimacing, dysarthria, gait difficulty, and impaired manual dexterity. Supranuclear paresis of vertical gaze and splenomegaly were present. Absent were seizures, major intellectual deterioration, spasticity, or blindness. Histiocytes showed lysosomal storage of various phospholipids, cholesterol, neutral lipids, and autofluorescent material. Appendiceal neurons showed only an increse of phospholipids by histochemistry. Neuronal deposits differed ultrastructurally from these in histiocytes. Leukocyte sphingomyelinase activity was normal. The nosology of this disease and its relationship to so-called juvenile types of Niemann-Pick disease is discussed. The primary metabolic defect in these patients remains unknown.
 ...
PMID:Juvenile dystonic lipidosis: an unusual form of neurovisceral storage disease. 18 51

Reciprocal reflex connections were studied in capsular hemiplegia and spastic paresis with spinal cord lesions, using Lloyd's technique. Effects of conditioning stimulation of the tibial or peroneal nerve on the H reflex in the antagonists were examined. Stimulus intensity was controlled with reference to the threshold of the M wave. Weaker stimulation than this threshold was regarded as stimulation of group I afferents. It aroused no subjection sensation in intact subjects. Early and strong inhibition, comparable to Ia inhibition in the cat (Lloyd 1946), was observed from weak stimulation of the tibial nerve on the pre-tibial (flexor) H reflex, but not from the peroneal nerve on the triceps surae (extensor) H reflex in capsular hemiplegia. Alcohol block of extensor motor points resulted in reduction of spasticity without further paralysis in the blocked muscle and a remarkable increase in strength of the antagonist pre-tibial muscles. These results suggest that an extensor spasticity withe flexor weakness, which is common in capsular hemiplegia, may be due to an imbalance of reflex activities via Ia muscle afferents, and that a part of flexor weakness can be restored by "disinhibition' by reduction of Ia inflow from extensor muscles. Ia inhibition was also observed in one third of cases with spinal cord lesions at rest. It returned to normal after recovery from spastic paresis by radical therapy in some cases.
 ...
PMID:Reciprocal Ia inhibition in spastic paralysis in man. 28 52

Report on the immediate and late results obtained in the period from January 1973 to December 1976 in a series of 44 patients suffering from a spastic syndrome who were operated on by selective partial lumbar radiculotomy. The intervention which mainly consisted of a partial separation of the individual radiculae of the posterior lumbar and first sacral roots was followed by a distinct improvement of the clinical picture in 30 patients without observing aneurlogical, especially sensitive deficit or immediate or later complications. The indication for this intervention is established together with the other specialists concerned with the care and the rehabilitation of the patient. Only such patients are selected in whom the spasticity is not useful and who still can carry their body-weight. No operation is in particular carried out in the presence of considerable paresis of the extensors and in patients who have for a long time been able to walk and stand. Favourable results can be expected in para-tetraspasticity and in patients who, when standing with support, show equinism, hyperadduction or crossing of the legs, hyperextension and internal rotation.
 ...
PMID:[Selective partial posterior radiculotomy in the therapy of spasticity]. 55 Jun 49

Outcomes in self-care following rehabilitation in 226 patients were correlated with 11 stroke syndromes, reflecting several pathophysiologic disturbances subsequent to either infarction or hemorrhage in cerebral or vertebro-basilar vessels. Self-care was scored on a 20-point scale for bed movements, transfers, feeding, dressing, personal hygiene, and bathing. Interjudge error among therapists did not exceed 2.5%. Mean score in left cerebral infarction without aphasia was used as a referent value. Scores in left cerebral infarction with aphasia and right parietal lobe syndrome with and without spatial agnosia were similar to the referent. Brain stem dysfunction with spasticity and right cerebral infarction with paresis and spatial agnosia fell below the referent value (Pless than 0.05). Higher levels were achieved in the syndromes of left and right anterior cerebral artery territories, brain stem dysfunction with ataxia, and left parietal lobe syndrome with comprehension aphasia, although t-values were not significant. Length of stay among the 11 groups was fairly uniform except for the group with brain stem dysfunction with spasticity and the group with left hemiplegia with spatial agnosia. These groups indicated rather severe disabilities. Aside from neurologic dysfunction the range of scores was influenced by associated cardiopulmonary involvement.
 ...
PMID:Neurophysiologic syndromes in stroke as predictors of outcome. 68 54

Intramuscular injections of botulinum toxin (Botox) are followed by a dose-dependent focal paresis which can be used to treat several focal movement disorders. Botox injections are recommended as effective for the treatment of blepharospasm, hemifacial spasm, and cervical dystonia (torticollis). Focal dystonias elsewhere (for example, writer's cramp) can often be treated with similar success. Others, such as oromandibular dystonia, are more difficult to treat. In the case of more generalized dystonias, some focal muscle spasms can be treated with success by local intramuscular injections. New indications are still being investigated, for example in focal tremors and spasticity. Side effects are in general slight and disappear at the end of toxin effect. In general, it is necessary to repeat the injections after a couple of months, due to a cessation of effect after regrowth of nerve terminals. New injections have similar effects even over years of treatment.
 ...
PMID:[Treatment of movement disorders using botulinum toxin]. 141 87

A mechanomyographic response of the hind foot to passive straightening and bending, as well as an electromyographic activity of the gastrocnemius and tibialis anterior muscles were recorded in old (35-44-month-old) and young female rats. In old rats, spontaneous, tonic electromyographic activity patterns were concurrently observed in both antagonistic muscles; they were low-amplitude, dense tonic activity and continuous, high-amplitude, sparse electromyographic activity. The tonic electromyographic activity was correlated with a decline in the strength and mass of muscles, as well as with motor disturbances, including paresis of the rigidly straightened backward hind legs, dragged behind by an animal. In muscles of old rats, morphological features of a chronic denervation atrophy were found. Baclofen (10 and 15 mg/kg, i.p.) diminished the spontaneous tonic electromyographic activity and potently decreased the whole body muscle tone, whereas Madopar (50 mg/kg of L-DOPA+12.5 mg/kg of benerazide) was ineffective. It is suggested that old rats in which the above-described pathologic alterations are observed might be a useful animal model in the search for basic etiopathological mechanisms of spasticity and similar disturbances found in humans.
 ...
PMID:Muscle stiffness and continuous electromyographic activity in old rats; an animal model for spasticity? 146 80

Spasticity develops after supraspinal or spinal lesions of descending motor systems, with obligate involvement of the corticospinal tract. Spasticity is characterized by an increase in muscle tone, which, in contrast to many other types of enhanced muscle tone, shows a marked velocity-dependent increase when the muscle is passively stretched. The pathophysiological mechanisms underlying this spastic muscle tone remain obscure. Three major causes are currently considered possible: (1) changes in the excitability of spinal interneurones; (2) receptor hypersensitivity; (3) formation of new synapses by sprouting. The latter mechanism could account for the long time course over which spastic muscle tone develops in hemiplegic or paraplegic patients, but there is no experimental evidence for this hypothesis. The electromyographic (EMG) gait analysis of patients with spasticity has thrown doubt on the common belief that the velocity-dependent increase in spastic muscle tone is evoked by stretch reflex activity and has led to the idea that spastic muscle tone resides in the muscle fibres themselves. While such a mechanism may contribute to the slowness of active movements in spastic patients, recent experiments on patients with spastic arm paresis have confirmed the classical view that the spastic muscle tone is related to the EMG activity evoked in the passively stretched muscle. This pathological EMG activity is seen during the entire range of the dynamic phase of the stretch, during which a normal muscle exhibits only an early, phasic burst at the highest stretch velocities employed. For the pharmacological treatment of spasticity, substances with different central or peripheral actions are available. Their assumed receptor actions are described, together with their main indications and side-effects.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Trends in the pathophysiology and pharmacotherapy of spasticity. 186 88

The effects of cyproheptadine, a serotonergic antagonist, were studied in seven patients with spastic paresis of spinal origin. Six patients were included in a double blind crossover trial (maximal dose 24 mg/day). The patients were evaluated on both their spasticity and locomotor function. Four of the patients also participated in an open trial in which cyproheptadine was administered for a minimum of six months at optimal dose. Patients walked on a treadmill at full weight bearing when possible, or with 40% of their body weight externally supported, as required, by an overhead harness system. Cyproheptadine considerably decreased the sustained ankle clonus and episodes of spontaneous spasms observed in all the patients who previously presented these manifestations of spasticity. Two patients who required body weight support (BWS) during locomotion could walk at full weight bearing during cyproheptadine therapy. A more normal timing of EMG patterns in these patients during cyproheptadine therapy was associated with temporal distance changes and marked improvement of joint angular displacement. In contrast, the other patients showed marginal changes in the EMG and the kinematic pattern but eventually managed to walk at a higher speed. These preliminary results suggest that cyproheptadine can reduce spasticity and enhance locomotor function in spinal cord injured patients.
 ...
PMID:The effects of cyproheptadine on locomotion and on spasticity in patients with spinal cord injuries. 224 57


1 2 3 4 5 6 7 8 9 10 Next >>