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)

Apomorphine in combination with a peripheral dopamine receptor blocker (domeperidone) was administered to four parkinsonian patients in a double-blind placebo-controlled study. The therapeutic efficacy of apomorphine was not reduced by domperidone, while nausea, drowsiness, sedation, and arterial hypotension were prevented. Combination of domperidone with dopamine agonists may result in more effective treatment of Parkinson's disease.
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PMID:Therapeutic efficacy of apomorphine combined with an extracerebral inhibitor of dopamine receptors in Parkinson's disease. 8 20

A sixteen-week study examined the effect of Madopa and Sinemet on patients with Parkinson disease disease suffering nausea or vomiting as side-effects of levodopa therapy and compared the efficacy of the three preparations in controlling the symptoms of Parkinson disease. Following a control period on levodopa, 20 patients underwent four consecutive four-week regimens as follows: (1) double-blind, in which a randomized half received levodopa and half received Madopa; (2) single-blind, in which all received Madopa; (3) double-blind, in which a re-randomized half received Madopa and half Sinemet; and (4) single-blind, in which all received Sinemet. Levodopa administration via Sinemet and Madopa was held to a fixed 20% of prior levodopa dosage. Almost all patients showed great reduction in nausea and vomiting with both Madopa and Sinemet. Seventy percent of the patients showed improvement in disability compared to their levodopa baseline levels. Group means showed no difference between the improvement seen on Madopa and that seen on Sinemet. However, examination of individual responses showed that the majority of patients fared distinctly better on either Sinemet or Madopa.
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PMID:A double-blind comparison of levodopa, Madopa, and Sinemet in Parkinson disease. 35 36

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

22 patients entered a double-blind trial to test the efficacy of bromocriptine therapy in patients with Parkinson's disease already established on conventional levodopa therapy. 3 patients on placebo withdrew when no improvement occurred and control became complicated. 4 patients on active drug withdrew because of various symptoms, but in only 1 case were these (nausea and vomiting) thought to be a real drug effect. Of the 15 patients who completed the trial, 9 were on active drug and 6 were on 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, dyskinesiae and hallucinations. It is concluded that bromocriptine does not offer any additional benefit in most patients with Parkinson's disease who are well stabilised on levodopa therapy, but may have a place in those patients who encounter side effects due to fluctuations in serum and tissue levels of levodopa.
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PMID:An evaluation of bromocriptine in the treatment of Parkinson's disease. 38 7

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

The broad results of the treatment of patients with idiopathic Parkinson's disease who have received levodopa or its variants are reported. 50 patients, 24 males and 26 females, with a mean age of 66.5 years were treated with levodopa, in daily doses ranging from 0.25g to 6.0g or 'Sinemet' in daily doses of 300mg to 750mg. Periods of treatment ranged from 4 months to 8 years, with a mean of 4.02 years. The relationships of patients' age, onset of Parkinsonian symptoms and interval between initial treatment with levodopa and the current clinical state were studied. Patients were classified according to their clnical response into 3 categories: satisfactory response, progressive deterioration or intolerance of levodopa. The proportion of patients in each category was 66%, 22% and 12% respectively. The clinical results of treatment correlated with those of Webster Disability Testing Scale. Analysis showed that the majority of patients tolerated levodopa and showed an initially satisfactory response. Patients who responded well were considerably younger than those who failed to respond. Patients receiving the drug for a shorter period (less than 3 years) showed a better response. After 3 years' treatment, the response declined. Patients who had had Parkinson's disease for more than 4 years appeared to do less well than those with recently diagnosed disease, but many patients responded well even when treatment was initiated 10 years after the onset of symptoms. Patients discontinued levodopa treatment because of psychoses, nausea, dyskinesia or exacerbation of urinary incontinence. The commonest side effects were nausea (34%), postural hypotension (22%), psychoses (10%) and 'on-off' phenomena in 12% of patients.
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PMID:Patterns of response to levodopa in Parkinson's disease. 75 20

Thirty-one patients with Parkinson's disease were treated with the ergot alkaloid bromocriptine, a drug which stimulates dopamine receptors. Bromocriptine had a slight therapeutic effect in patients on no other treatment and an additional effect in patients on levodopa. The mean optimum dosage of bromocriptine, established over a 12 week period, was 26 mg daily. In 20 patients bromocriptine was compared with placebo in a double-blind controlled trial. Active treatment caused a significant (P less than 0.02) reduction in total disability and akinesia scores. The least disabled patients showed the greatest response. Side-effects of bromocriptine--nausea, vomiting, hallucinations, and abnormal involuntary movements--were similar to nature to those of levodopa. In most normal subjects, bromocriptine causes an increase in plasma growth hormone concentration. This was determined in 20 patients with Parkinson's disease after 1-15 mg bromocriptine. Only a single patient showed an obvious increase up to 120 minutes after dosage. Bromocriptine was not effective treatment in two patients who had not previously responded to levodopa and replacement of this drug by bromocriptine in patients with end-of-dose akinesia after chronic levodopa treatment did not totally abolish response swings.
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PMID:Bromocriptine treatment in Parkinson's disease. 77 75

The effect of a new dopaminergic agonist, piribedil, was studied in 16 patients with Parkinson's disease and compared with placebo and L-DOPA. Piribedil appeared to have a moderate therapeutic effect that was significantly less than that of L-DOPA. Tremor appeared to be the main clinical feature to benefit. Nausea, vomiting, and somnolence were most frequent during the buildup of treatment and confusion and hallucinations during long-term treatment. Piribedil caused a significant decrease in probenecid-induced accumulation of HVA in the CSF, suggesting reduced turnover of endogenous dopamine in the brain. There was a significant relationship between dopamine receptor activation by piribedil and improvement of parkinsonian disability.
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PMID:Dopaminergic agonist effects on Parkinsonian clinical features and brain monamine metabolism. 109 75

The further therapeutic benefit of piribedil when combined with amantadine or Levodopa was studied by a double-blind, cross-over trial in 15 patients with Parkinson's disease. A significant improvement at the 5 per cent level for akinesia, gait, speech disorder and facial expression occurred when piribedil was added to Levodopa; and a more highly significant improvement at the 1 per cent level for akinesia, facial expression and finger dexterity occurred with piribedil and amantadine. No significant improvement occurred for special timed tests. Improvement was associated with side effects in both groups of patients. Side effects occurred with both placebo and active piribedil. Only nausea during piribedil and Levodopa treatment reached statistical significance when compared with the placebo. Piribedil did not give rise to any haematological or biochemical complications. Our findings suggest that piribedil is of further therapeutic benefit when added to amantadine or Levodopa. It was suggested that the improvement which occurred together with amantadine could be due to the combined action of both drugs on dopamine receptors.
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PMID:Piribedil (ET 495) in the treatment of Parkinson's disease combined with amantadine or levodopa. 109 59

A double-blind study comparing the effects of carbidopa and levodopa combined in a single tablet with levodopa alone was undertaken in 50 patients with Parkinson's disease. After 6 months, there was a statistically significant improvement over baseline in total score, rigidity, and tremor only in the patients randomized to carbidopa/levodopa. In addition, 40 percent of the patients treated with carbidopa/levodopa showed obvious clinical improvement (a greater than 50 percent reduction in their total score) over treatment with levodopa alone. However, after 2 years, only 20 percent continued to show this improvement. Nausea, vomiting, and anorexia developed in 56 percent of patients on levodopa but in only 27 percent of patients on carbidopa/levodopa. However, abnormal involuntary movements, observed in 48 percent of patients on levodopa, were present in 77 percent of patients on carbidopa/levodopa. Despite the increase in abnormal involuntary movements, carbidopa/levodopa is more effective than levodopa.
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PMID:Comparison of dopa decarboxylase inhibitor (carbidopa) combined with levodopa and levodopa alone in Parkinson's disease. 110 Oct 99


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