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)

The previously described anti-spastic effect of oxcarbazepine and 10,11-dihydro-10-hydroxycarbamazepine was found accidentally in 2 patients undergoing a double-blind comparative study for evaluation of antiepileptic effect. In this study oxcarbazepine was given orally in doses of 300-2700 mg daily to one patient with transverse myelitis and to two patients with multiple sclerosis, all of whom had clinically disabling spasticity in the form of difficulty in walking, lower limb rigidity, spastic contractions of the lower limbs and ankle clonus. Anti-spastic effect was observed at doses between 600-1200 mg daily and consisted in a substantial decrease in the above symptoms of spasticity. The anti-spastic effect appears at a dose immediately below that which produces nausea, dizziness and somnolence.
Arq Neuropsiquiatr 1988 Dec
PMID:Oxcarbazepine and spasticity: further observations. 307 37

One of the most frequent neurological sequelae seen by the specialist in rehabilitation is the spastic foot. Spasticity in the foot may be responsible for abnormal posture and painful or trophic disturbances impairing standing and walking. This disability can be corrected by a simple neurosurgical procedure, the selective tibial neurotomy. In this procedure, one sections the tibial nerve branches to the muscles sustaining spasticity, i.e., the soleus and/or the gastrocnemius nerves for equinus and ankle clonus or the posterior tibialis branch for varus and the flexor fascicles for tonic flexion of the toes. After microsurgical dissection of each tibial nerve branch at the lower part of the popliteal region and their identification with bipolar electrostimulation, the selected branches are partially sectioned under the operating microscope. The present series consists of 62 operations performed in 53 patients, 9 bilaterally and 44 unilaterally. Operation obtained complete suppression of the disabling spasticity that had been present for 2 to 17 years (4 on average), total pain relief, and consequently improvement of the residual voluntary movements (by achieving a better balance between agonist and antagonist muscles) in 51 of the 62 spastic feet (i.e., 82% of the cases). For all of these patients, the beneficial effects were long-lasting over the 1- to 10-year follow-up (3 years on average). Selective neurotomy of the tibial nerve should be considered only after failure of intensive prolonged kinestherapy and of all available medical treatment. It must take place, however, before the onset of irreversible articular disturbances and musculotendinous retractions, which require complementary orthopedic corrections.
Neurosurgery 1988 Dec
PMID:Selective neurotomy of the tibial nerve for treatment of the spastic foot. 321 72

The inhibitory effect of IB interneurons on motoneurons was tested in both legs of six hemiplegic adults. On the normal side, an inhibition of 10 ms, (14.6%) was observed in all cases and was similar to that described previously. On the spastic side, the same technique results in a facilitation of same duration reaching a maximum of 15%. Hence the IB inhibitory effect is, at least functionally, absent in spasticity. Disappearance of IB inhibition is an additional mechanism to be considered in interpreting spasticity.
J Neurol Neurosurg Psychiatry 1988 Dec
PMID:Short-latency autogenic inhibition (IB inhibition) in human spasticity. 322 Dec 21

Progabide (PGB) is a gamma-aminobutyric acid (GABA)-agonist drug undergoing clinical evaluation for the treatment of spasticity, movement disorders, and epilepsy. Drug interactions were studied during a randomized, double-blind, crossover trial of the efficacy and toxicity of PGB in patients with partial seizures taking phenytoin (PHT) and carbamazepine (CBZ). In twenty-two of 32 patients (69%) receiving PGB, PHT dosage was reduced, while only four patients (12%) had their dosage reduced during placebo treatment (p less than 0.001). Carbamazepine dosage was decreased in five of 32 patients (16%) during the active treatment, while two patients (6%) had a dosage reduction when receiving placebo (p greater than 0.75). The mean PHT concentrations at the end of baseline, PGB, and placebo treatments were significantly different: 17.5, 20.4, and 16.8 mg/L, respectively (p less than 0.05). Nevertheless, careful adjustment of PHT dosage maintained serum concentration within +/- 25% of target values in both the PGB and placebo periods. Among patients who first received PGB and then placebo, PHT concentrations remained elevated relative to dose suggesting that PGB exerts a prolonged effect on PHT disposition. The addition of PGB to regimens including PHT results in a significant increase in serum PHT concentrations. This drug interaction most likely occurs as a result of PGB mediated inhibition of hepatic microsomal enzymes.
Clin Neuropharmacol 1987 Dec
PMID:Effect of progabide on serum phenytoin and carbamazepine concentrations. 342 61

Septo-optic dysplasia (De Morsier's syndrome) is a common cause of congenital optic nerve hypoplasia. Associated abnormalities such as hypothalamic/pituitary dysfunction, hypotonia or spasticity, may result in affected children presenting for surgical procedures under general anaesthesia. A 3.5-year-old boy with the undiagnosed condition had his Achilles tendons elongated under an uncomplicated general anaesthetic. The postoperative period was complicated by coma and a major convulsive seizure which responded to glucose and steroids. The importance of awareness of this condition in short children with poor visual acuity who require general anaesthesia is stressed, and the presenting features of seven other cases are demonstrated.
Anaesthesia 1987 Dec
PMID:Anaesthesia and septo-optic dysplasia. Implications of missed diagnosis in the peri-operative period. 343 62

A family with adrenoleukodystrophy and clinical manifestations of spinocerebellar degeneration was studied. Two adult male first cousins showed progressive limb and truncal ataxia, slurred speech and spasticity of the extremities. Brain CT scans demonstrated atrophy of the pons and cerebellum, in both cases. Very long chain fatty acids in plasma and erythrocyte membranes were elevated in the affected patients and intermediately increased in an aunt and the mother of one patient, thereby indicating homozygotes and carriers of adrenoleukodystrophy, respectively. This unusual type of adrenoleukodystrophy seems to be transmitted as an X-linked recessive trait.
J Neurol Neurosurg Psychiatry 1986 Dec
PMID:Familial spinocerebellar degeneration as an expression of adrenoleukodystrophy. 346 5

Baclofen is an analog of the inhibitory neurotransmitter, GABA, which is used clinically to control spasticity. Recent evidence has accumulated showing this compound to have profound inhibitory effects upon hippocampal neural activity at both the cellular and circuit levels, and to attenuate epileptiform bursting in the hippocampal slice. However, it does not appear as an anticonvulsant on most traditional drug screens. Baclofen can produce inhibition by increasing potassium conductance, and therefore may fail to appear efficacious in typical anticonvulsant screens due to techniques that cause rapid and massive increases in interstitial potassium. We tested the hypothesis that baclofen is less effective at attenuating epileptiform bursting in the hippocampal slice under conditions of elevated extracellular potassium. Male Sprague-Dawley rats were decapitated and hippocampal slices were prepared. Epileptiform bursting was induced by bathing the slices in an artificial cerebrospinal fluid solution which contained either 7.0 mM K+ or 30 microM bicuculline methiodide, or by stimulus train-induced bursting. In each of these media, baclofen was applied in a random presentation of concentration format. Baclofen attenuated epileptiform bursting in both bicuculline and elevated K+, although considerably higher concentrations were necessary to attenuate bursting in high K+ than in bicuculline or after stimulus train-induced bursting. These results further support the antiepileptic actions of baclofen and provide evidence that this drug may be of value for attenuating epileptiform activity when there is not a tonic elevation of interstitial brain potassium.
Exp Neurol 1986 Dec
PMID:Attenuation of epileptiform bursting by baclofen: reduced potency in elevated potassium. 378 Sep 17

Muscle tone, if defined as the resistance felt during passive movement of an extremity, is generally explained by the appearance of stretch reflexes. Consequently, hypotonia would be caused by a decrease or disappearance of these reflexes. This notion has never been challenged by experiments that reproduce the clinical situation. In this study two clinical tests, passive extension and flexion movements at the knee joint and a free fall of the lower leg with gravity, were applied to 72 control legs and 35 'hypotonic' legs. EMG activity was measured in the quadriceps muscle. Despite special care to obtain relaxation in the subjects, the majority of control legs showed voluntary EMG activity on passive movement. During free fall, long-latency reflexes were present in a minority of normal subjects, but the velocity of falling in these legs was within the range obtained in the legs without any EMG spikes. If the fall time was prolonged beyond the upper limit of relaxed legs, this was the result of voluntary activity, confirmed by EMG measurements. Therefore, long-latency stretch reflexes play no role in the clinical assessment of 'normal tone'. This conclusion was further supported by the observation that 'hypotonic' legs did not fall faster than relaxed control legs. If patient's legs feel flaccid this is the result of weakness preventing voluntary activity. Passive movements during the clinical examination are of great value, but only to detect spasticity or rigidity.
Brain 1986 Dec
PMID:Hypotonia: an erroneous clinical concept? 379 Sep 72

The formation of tolerance to the hypothermic effect of ethanol was inhibited in rats after intraperitoneal injection of the neurotoxin DSP-4 50 mg/kg. The neurotoxin also significantly suppressed the ethanol withdrawal syndrome; hyperlocomotion, audiogenic seizures and spasticity. These behavioural changes were accompanied by a 52% decrease of the brain norepinephrine (NE) content, with no alterations in the dopamine or serotonin levels. The results indicate that intact NE neurons are necessary for the development of tolerance to ethanol-induced hypothermia and are involved in the expression of the ethanol withdrawal syndrome.
Drug Alcohol Depend 1986 Dec
PMID:Suppression of ethanol tolerance and dependence in rats treated with DSP-4, a noradrenergic neurotoxin. 381 31

Video recordings during radiodynamic studies of miction (ERDM) in 50 patients with spinal cord injuries produced images markedly superior in quality to permictional films in cases of dysuria. Correlation with cystosphincterometry (CSM) findings were good for normal cases. Dynamic studies were more effective than CSM for the neck, but less reliable for the detrusor and striated muscle on the condition than an electromyogram had been performed. In patients with complete spasticity the type of miction cannot be predicted from the level of the lesion.
J Radiol 1985 Dec
PMID:[Dynamic study of miction in patients with spinal cord injuries. Comparison with cystomanometry in 50 cases]. 383 56


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