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

In 14 untreated informed patients (5 M, 9 F, mean age 62 yrs) with initial idiopathic Parkinson's disease AEPs, early (BAEPs) and long latency components (LLCs) were studied. In 10 subjects experimental session were carried out before treatment (L-Dopa plus Carbidopa, 0.25-0.50 g/die) and at 2, 6 and 12 months intervals. At the same time all patients underwent clinical assessment by Webster Rating Scale evaluation. BAEPs. The IPLs prolonged (greater than 2.5 SD) in 6 patients: in 3 the III-V, in 2 the I-V and in 1 the I-III. The absolute latencies were abnormally prolonged in 11 subjects: V wave in 4, III wave in 3, II wave in 2 and I wave in 3. The absence of one or more components were observed in 12 out of 14 patients, the most frequently absent was the II wave (12 patients). LLCs. The absolute latencies of P1 and N1 waves were prolonged respectively in 4 and in 3 subjects. The P1-N1 IPL was prolonged only in one patient. A follow-up study demonstrated transitory improvement of the AEPs previously observed abnormalities. The improvement was partially in agreement with clinical assessment.
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PMID:Auditory evoked potentials (AEPs), early (BAEPs) and long latency components (LLCs) in Parkinson's disease: a 12 month follow-up study. 368 83

A 60 year old woman with idiopathic Parkinson's disease had been prescribed thioridazine for schizophrenia. Five months after this was stopped, Sinemet also considered of dubious therapeutic value, was withdrawn. One week later she developed features of the neuroleptic malignant syndrome (NMS) accompanied by myoglobinuric renal failure. Post-mortem examination confirmed Lewy body degeneration in the substantia nigra. It is proposed that NMS may be caused by levodopa withdrawal in Parkinson's disease, and that it is withdrawal of dopaminergic drive that causes the syndrome.
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PMID:Levodopa withdrawal syndrome identical to neuroleptic malignant syndrome. 379 65

Eight Parkinson patients with response fluctuations completed an open-label trial of a controlled-release carbidopa/levodopa preparation (Sinemet CR3). At the end of 6 weeks, percent "on" time and mean interdose interval increased, the number of daily doses and "off" periods was decreased, and the variability of plasma levodopa levels and disability scores was reduced. However, response fluctuations continued to occur, day-to-day consistency was poor, and the bioavailability of levodopa appeared less than that of standard Sinemet. Overall benefit waned over the next 3 to 6 months. Oral controlled-release carbidopa/levodopa is capable of reducing fluctuations in plasma levodopa levels and clinical performance in Parkinson's disease. The response to this particular controlled-release formulation was suboptimal and unsustained.
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PMID:Controlled-release levodopa/carbidopa. I. Sinemet CR3 treatment of response fluctuations in Parkinson's disease. 380 4

Pergolide mesylate, a dopamine agonist, was studied as adjunctive therapy in a 6-month double-blind trial in 20 patients with Parkinson's disease who were achieving less than optimal response from Sinemet. As pergolide or placebo was administered in increasing dosage, Sinemet was reduced if side effects developed. Both the pergolide and placebo groups improved significantly (p less than 0.05). The pergolide group improved 30% at the end of 24 weeks, and the placebo group 23%. There was no significant difference between drug and placebo groups, possibly due to a fortuitous support group and the side effects that may have burdened the pergolide group. Nevertheless, pergolide had a definite antiparkinsonian effect.
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PMID:Double-blind trial of pergolide for Parkinson's disease. 388 32

The efficacy of low-dose bromocriptine mesylate administration (20 mg daily or less) was evaluated in a double-blind study. Nine of 16 individuals receiving bromocriptine completed the 40-week study. Modest, but significant, improvement was derived from bromocriptine therapy. Improvement was most evident in tremor. Maximum improvement was achieved with doses between 7.5 and 15.0 mg daily, with some decline in efficacy as doses approached 20 mg. Adverse effects were common, but were generally mild in severity. Our results suggest that bromocriptine in low doses may be an effective adjunct to carbidopa and levodopa (Sinemet) in the treatment of Parkinson's disease.
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PMID:Low-dose bromocriptine therapy in Parkinson's disease. 400 3

In a general practice population of 57 000, 32 patients suffering from Parkinson's disease were identified from repeat prescription indexes and direct questioning of all members of the primary health care team. Of these patients 26 were receiving an L-dopa preparation and 10 an anticholinergic drug. The only newer drug found to be in use was bromocriptine and three patients were receiving this treatment.Of the 26 patients receiving an L-dopa preparation one received L-dopa alone, six L-dopa with benserazide (Madopar, Roche) and 19 L-dopa with carbidopa (Sinemet, Merck, Sharp and Dohme). The patients treated with Sinemet were receiving inadequate doses of carbidopa - three quarters received less than 75 mg per day which was in part a reflection of the low doses of L-dopa the patients received, the average dose being 468 mg per day. The L-dopa preparations were given in adequately spaced doses.The general practitioner made the diagnosis in 20 of the 32 cases and was in control of the drug therapy in 15 cases, however 25 cases were referred for specialist advice.
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PMID:Audit of the drug treatment of Parkinson's disease in general practice. 403 54

In five patients with initial idiopathic Parkinson disease AEPs (early and late components of auditory evoked potentials), SEPs (somatosensory evoked potentials) and arm ballistic movements (abduction of the humerus) were studied. Experimental sessions were conducted before starting treatment (L-Dopa plus Carbidopa) and at two and six month intervals. Before treatment evoked potential abnormalities were found in four out of five patients; EMG patterns underlying ballistic arm abduction movements were altered in all patients; corresponding prolonged duration of initial movements and low mean velocities were found. After treatment AEP and SEP showed a reduction of previously observed abnormalities and both EMG patterns and kinematic variables consistently improved. It is suggested that the electrophysiological investigations employed in this preliminary study may be a useful tool in clinical and pharmacological researches on Parkinson disease.
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PMID:Auditory and somatosensory evoked potentials (AEPs and SEPs) and ballistic movements in Parkinson disease. 406 68

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


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