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)

We evaluated pergolide in 22 patients with Parkinson's disease and 3 with progressive supranuclear palsy (PSP). After achieving an optimal dose of pergolide and Sinemet, a matching placebo was substituted in double-blind manner. The mean dose of levodopa (in Sinemet) was reduced by 68%; in eight patients, pergolide completely replaced levodopa. In parkinsonian patients, the mean Hoehn-Yahr stage decreased from 3.2 to 1.6, and the mean total disability score decreased from 48.3 to 17.8. In 10 patients with on-off phenomenon, the time on increased 174% with pergolide. There was little effect in PSP. Postural light-headedness and reversible mental changes were seen.
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PMID:Controlled trial of pergolide mesylate in Parkinson's disease and progressive supranuclear palsy. 633 85

Twenty-eight patients with Parkinson disease (PD) were treated with bromocriptine for at least 2 years (mean, 2.8 years; range, 2 to 5 years). All of them had first been treated with levodopa (alone or combined with carbidopa, as Sinemet) for 7.4 years (range, 1 to 10 years). At the time bromocriptine was started, all were showing increasing disability. In these patients, attempts to increase levodopa resulted in adverse effects, and attempts to decrease levodopa resulted in increased parkinsonism. Bromocriptine (mean daily dose, 56 mg) was added to levodopa and resulted in improvement of at least one stage (Hoehn and Yahr scale) in 21 of the patients. After 2 years, five of these patients continue to maintain this improvement. The remaining patients, although there has been deterioration, maintain some of their original improvement. Bromocriptine, when added to levodopa, results in improvement that is maintained, in part, for at least 2 years. The ratio of bromocriptine to levodopa has to be periodically readjusted.
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PMID:Long-term efficacy of bromocriptine in Parkinson disease. 676 3

The thyrotrophin (TSH) and prolactin (Prl)-releasing effects of TSH-releasing hormone (TRH) were investigated in 20 subjects with Parkinson's disease (PD), unmedicated, on chronic treatment with a combination levodopa-benserazide (Madopar) or levodopa-carbidopa (Sinemet) or withdrawn from therapy. Administration of TRH (200 micrograms iv) induced in unmedicated patients TSH and Prl responses significantly lower than those of sex-and age-matched controls. In patients on Madopar therapy the TSH and Prl responses to TRH were greater than in unmedicated patients and comparable to those of controls, while in patients on Sinemet therapy the pituitary responses were undistinguishable from those of unmedicated subjects. Withdrawal of Madopar therapy resulted in a marked diminution of the TSH response but did not affect the Prl response to TRH. Withdrawal of Sinemet therapy did not alter the TSH and Prl responses to TRH. Concomitant evaluation of growth hormone (GH) levels, in none of the subjects evidenced non-specific changes in plasma GH following TRH. Since TSH and Prl responses to TRH are inhibited by an enhancement of the dopaminergic tone, it would appear that the latter is preserved in the tuberoinfundibular system of unmedicated subjects and subjects on chronic Sinemet therapy, but is defective in subjects on chronic Madopar therapy.
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PMID:Thyrotrophin and prolactin responses to thyrotrophin-releasing hormone in patients with Parkinson's disease. 680 85

We studied the dopaminergic control of lactotroph cells in the anterior pituitary of parkinsonian patients and age-matched normal subjects. The resting levels of prolactin and the TRH-induced rise in prolactin were normal in Parkinson disease. Levodopa elicited a normal suppression of prolactin concentrations in parkinsonian subjects; the major abnormality to emerge was attenuation of the response to thyrotropin-releasing hormone (TRH) in the parkinsonian patients following administration of Sinemet (levodopa plus carbidopa) or bromocriptine. These findings imply pathology of extrastriatal dopamine systems in Parkinson disease. Since the addition of carbidopa enhanced the suppression of prolactin induced by levodopa, exogenous levodopa probably acts predominantly through the formation of dopamine in the hypothalamus, but inside the blood-brain barrier, rather than as a direct effect of circulating dopamine on the anterior pituitary or areas of the hypothalamus outside the blood-brain barrier.
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PMID:Prolactin secretion in Parkinson disease. 681 Feb 4

Thirty-seven patients with advanced Parkinson's disease who initially tolerated, and responded to bromocriptine therapy were followed for 12 to 50 (mean 28) months. Using a method of gradual increase of bromocriptine, with concomitant levodopa reduction, the peak effect of the drug was apparent by three months, at which time the mean daily dose of bromocriptine was 23.9 mg and Sinemet (levodopa + carbidopa) had been reduced by 34 percent. Eight patients had sustained improvement without further drug changes for an average of 29 (range 14-50) months. After periods of improvement varying between 3 and 30 months, 29 patients had a fall-off from peak effect. Peak effect was regained in 21 of these 29 patients for an average of 16 additional months by initially increasing bromocriptine or Sinemet, or by eventually increasing both drugs. The main adverse effect was a confusional state which necessitated late withdrawal of bromocriptine in four patients. The best results were in younger patients with end-of-dose deterioration and levodopa induced dyskinesias. With cautious introduction, and intermittent dosage adjustment, bromocriptine can be of long-term benefit to patients with advance Parkinson's disease. The majority of patients have a gradual late fall-off in effect which can frequently be reversed with dosage adjustment.
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PMID:Bromocriptine in the long-term management of advanced Parkinson's disease. 686 Oct 13

Lisuride, a semisynthetic ergoline and potent central dopamine and serotonin agonist, was combined with levodopa in 20 patients with advanced Parkinson disease who were no longer responding satisfactorily to levodopa, including 14 patients with "on-off' phenomena. Every patient who completed the 8-week trial improved significantly (p greater than or equal to 0.01), with a decrease in all symptoms. The mean dose of lisuride was 2.4 mg per day. The dose of levodopa (mg of levodopa in Sinemet) was reduced from 1030 to 920 mg. Among the patients with "on-off' phenomena, there was a significant increase in the time in which they were 'on' (mobile) from 4.6 to 9.6 hours. In 5 of 10 patients who have been on lisuride for at least 1 year, there has been no decline in efficacy.
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PMID:Lisuride combined with levodopa in advanced Parkinson disease. 703 4

We conducted a prospective study of thyroid function in 46 patients with Parkinson disease and 46 age- and sex-matched controls with other neurologic disease. There was no statistical difference in serum thyroxine (T4) and T3 resin uptake (T3U) between the two groups. Neither the duration nor the quantity of L-dopa or carbidopa/L-dopa (Sinemet) therapy influenced these assessments of thyroid function. However, 3 of 46 Parkinson patients were hypothyroid, whereas none of 46 controls was hypothyroid. There was one hyperthyroid individual in each group. Early evaluation of thyroid function in all patients with Parkinson disease is recommended because of the unexpected frequency of hypothyroidism and because hypothyroid symptoms may be masked.
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PMID:Thyroid function in Parkinson disease. 719 33

1. A randomized, placebo controlled, double-blind cross-over study was conducted to evaluate the clinical efficacy of the anticholinergic agent, benztropine mesylate (CogentinR) in 29 patients with mild to moderate, idiopathic Parkinson disease. 2. Patients were maintained on a stable, therapeutically optimal dosage and schedule of levadopa-carbidopa (Sinemet) throughout the study. 3. Both the neurologist's and the patient's global assessments of treatment efficacy indicated that Sinemet plus benztropine mesylate resulted in significantly greater improvement than Sinemet plus placebo. 4. Qualitative and quantitative evaluations of relevant neurologic functions showed small, but statistically significant improvements for rigidity, finger tapping speed and activities of daily living in patients during the Sinemet plus benztropine mesylate treatment period. 5. At the completion of the study 16 patients chose to continue taking benztropine mesylate as an adjuvant to Sinemet. 6. No important adverse side effects occurred during the study.
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PMID:Parkinson's disease: Cogentin with Sinemet, a better response. 720 30

Using a method of a gradual increase of bromocriptine with a concomitant reduction of Sinemet (levodopa 250 mg + carbidopa 25 mg), 19 patients with advanced Parkinson's disease have been treated for periods of up to 22 months and 16 of them have shown improvements of varying degrees. Eighteen patients were able to tolerate bromocriptine addition, with early transient adverse effects occurring in seven cases. In contrast to several previously reported studies, it was found necessary to withdraw bromocriptine in only one case. With the drugs currently available, bromocriptine has a role in the management of patients with advanced Parkinson's disease. The method described here may allow a greater number of patients to be given a trial with this drug.
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PMID:Method of addition of bromocriptine to the drug regime of patients with advanced Parkinson's disease. 722 54

The authors report the results of treatment of hereditary extrapyramidal diseases with new preparations acting upon neurotransmitter systems. Patients with torsion dystonia, Huntington's chorea, Parkinson's disease, hereditary tremor, myoclonic epilepsy were followed-up for several years.. The best results in akinetic-rigidity syndromes (Parkinson's disease, rigid froms of torsion dystonia, Hallevorden-Spatz disease) were obtained with L-DOPA (including Sinemet, Nacom, Madopar) and in many patients these preparations were given in combination with other drugs (cholinolytic agents, Midantan) which contributed to compensation of the disturbed equilibrium of neurotransmitter systems and reduction of side effects. For decreasing the side effects of L-DOPA (hyperkineses of dystonic type, chorea and myoclonia) preparations from the group of phenothiazine and diazepine were given. In many cases improvement was achieved by slover increase of L-DOPA doses. In the hyperkinetic syndromes (Huntington's chorea, idiopathic tremor, myoclonic epilepsy, hyperkinetic torsion dystonia) preparations of phenothiazine, butyrophenone and new drugs active on the GABAergic system (Baclophen, Lyoresal, Pantogam) and diazepine (Clonazepam) were used. The analysis of the results shows that disturbed equilibrium of central neurotransmitters plays and important role in the pathogenesis of hereditary extrapyramidal system diseases.
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PMID:[Pathogenetic treatment of various hereditary extrapyramidal disorders with new drugs]. 732 7


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