Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030567 (Parkinson's disease)
 63,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sixty cases of Parkinson's disease were treated with piribedil alone (dose : 274 mg/day, duration : 20,4 months). The overall clinical improvement, confirmed by recordings of tremor and EMG, was 34%, tremor being improved of 59%. Before treatment, an intravenous test does of piribedil with recording made it possible to predict the effectiveness of oral treatment. Side-effects (vasomotor, digestive, psychiatric) were moderate. Orthostatic hypotension, dyskinesia and fluctuations were exceptional. The basic indication for piribedil lies in forms of recent onset in which tremor predominates, patients in whom L-dopa is contraindicated and a certain number in whom the latter has failed (tremor, fluctuating action).
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PMID:[Piribedil, dopaminergic agonist. Prolonged clinical and electrophysiological study in 60 parkinsonian patients (author's transl)]. 2 44

Four patients with abnormal movements were treated with tiapridal. Very good results were obtained in a case of buccofacial dyskinesia associated with an extrapyramidal syndrome and dementia, and in another patient with middle-of-the-dose dyskinesias induced by L-dopa treatment for Parkinson's disease. No effect was observed, however in a case of beginning of the dose dyskinesias, and the extrapyramidal symptoms increased in severity. A dopadecarboxylase-inhibitor was associated with the L-dopa treatment in these three cases. In the fourth case, there was an increase in the spasms of the medial part of the face.
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PMID:[Cases of abnormal movements]. 3 19

Fluctuations in performance in patients with Parkinson's disease on chronic levodopa therapy (the "on-off" effect) are due to several factors. The increasing severity during treatment of early morning akinesia, "freezing" episodes, and end-of-dose deterioration are probably due to progression of the underlying disease. Peak-dose dyskinesia and peak-dose akinesia are due to levodopa over dosage. "Yo-yo-ing", which is the severest form of such fluctuation in mobility and dyskinesias, may represent the sum of these disorders.
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PMID:"On-off" effects in patients with Parkinson's disease on chronic levodopa therapy. 5 99

Plasmatic renin activity (PRA) was studied in patients receiving L-dopa, together with a decarboxylase inhibitor, at rest times and after periods of physical exertion. Although we can superimpose the results from unrelated Parkinson's disease patients on those of the control group, the results are inversed in stabilized patients (lowered PRA) and dyskinetic patients (increased PRA). There is a definite correlation between the increase in PRA and intensity of the dyskinesia. Dosage is the only other factor differentiating the two groups of Parkinsonians treated. The figures relative to arterial pressure are studied in the various groups.
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PMID:Plasmatic renin activity in patients treated with L-dopa and inhibitor of dopa decarboxylase (IDC). 10 37

Diphenylhydantoin (DPH) diminished the therapeutic effects of levodopa both in patients with parkinsonism and in patients with chronic manganese poisoning, as well as the levodopa-dependent dyskinesia for which the former were selected. In patients with Huntington chorea, it enhanced chorea and mental agitation and, thus, failed to conform with the postulated pharmacological reciprocity between Parkinson disease and Huntington chorea. These findings are in agreement with experiments done in animals in which DPH blocked a neuronal response to dopamine.
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PMID:Diphenylhydantoin. Blocking of levodopa effects. 12 56

The effect of sodium valproate 1200 mg daily on the disability of Parkinsonism and on levodopa-induced dyskinesia was assessed in a double-blind crossover trial with matched placebo in 12 patients with Parkinson's disease. No objective change in the severity of Parkinsonism or dyskinesias was noted. However, six out of nine patients who completed the trial noted a slight to moderate improvement in their dyskinesias with no change in their Parkinsonism. Excess salivation improved in four subjects on sodium valproate.
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PMID:Sodium valproate in the treatment of levodopa-induced dyskinesia. 35 1

Twenty-two patients entered a double-blind trial to test the efficacy of bromocriptine therapy in patients with Parkinson's disease who were already stabilized on conventional L-Dopa therapy. Of these, three patients who were receiving placebo withdrew when no improvement occurred and control became complicated. Another four patients taking active drug withdrew because of side effects, but only in one case was the symptom (nausea and vomiting) thought to be a true effect of the drug. Of the 15 patients who completed the trial, nine were taking active drug and six took placebo. Although more than half the patients in each group were subjectively improved, measurement scales of functional disability and physical examination revealed no significant change in either group. Side effects encountered included nausea, dyskinesia, and hallucinations. It was concluded that bromocriptine does not offer any additional benefit to patients with Parkinson's disease who are stabilized on L-Dopa therapy, but may have a place in those patients who encounter side effects due to fluctuations in serum and tissue levels of L-Dopa.
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PMID:A double-blind trial of bromocriptine in Parkinson's disease. 37 May 27

Because there is biochemical evidence of decreased GABAergic function in Parkinson's disease, sodium valproate, an inhibitor of GABA catabolism, was administered to eight Parkinsonian patients. Valproate treatment did not significantly alter any Parkinsonian feature, but tended to increase the dyskinesia in the "on-off" patients. The increased dyskinesias were not a result of altered peripheral metabolism of L-dopa. Despite obtaining high plasma levels of valproate, no consistent alteration of CSF GABA levels could be demonstrated. Thus, in these patients, an effect of valproate on GABA metabolism is unproven, and in turn, the role of GABA in Parkinsonism and dyskinesia uncertain.
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PMID:Treatment of Parkinson's disease with sodium valproate: clinical, pharmacological, and biochemical observations. 38 31

Levodopa has become established as the treatment of choice in Parkinson's disease. It is adsorbed by an active mechanism from the small bowel. Its pharmacological activity depends upon the formation of dopamine and possibly other metabolites. Its beneficial effect in Parkinson's disease probably depends upon temporarily restoring the ability of degenerating nigro-striatal cells to release dopamine. Its main side effect, that of dyskinesia, may reflect a direct action of dopamine on striatal receptors. Peripheral decarboxylase inhibitors reduce the incidence of levodopa-induced nausea, probably by lowering the concentration of dopamine in the area postrema. The introduction of levodopa in the treatment of Parkinson's disease is generally regarded as one of the uncommon examples in medicine where effective therapy has resulted from systematic research rather than seredipity. As our knowledge of the pharmacology of levodopa grows, we may be forced to admit that perhaps the right drug was chosen for the wrong reasons.
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PMID:A review of some aspects of the pharmacology of levodopa. 38 8

BRomocriptine (15-75 mg per day) alone or with L-dopa was studied during five to 29 months on 44 patients with Parkinson's disease. Used as sole therapeutic agent, it was found excellent in 12 patients who had never received regular L-dopa treatment either because it was never attempted or because of intolerance from the outset. Its anti-Parkinsonism activity was comparable with L-dopa. The gain was stable in the long term until this report. The side effects of L-dopa were not seen after bromocriptine. In cases where L-dopa had ceased to be active, bromocriptine produced a further improvement if mental deterioration was not associated. In very advanced forms of Parkinson's disease with associated dementia, bromocriptine did not produce durable results. Bromocriptine did not improve the "on-off" effects but reduced a number of the side effects of L-dopa, in particular cardiac, painful contractions, and dyskinesia without "on-off" effects.
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PMID:Long-term treatment of Parkinson's disease with bromocriptine. 42 61


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