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)

Six patients with fluctuating Parkinson's disease received single rising oral doses of the nonergot dopamine agonist CV 205-502 in an open experimental study. Doses of 0.5 mg produced antiparkinsonian effects of comparable intensity but longer duration than 200 mg of L-DOPA. CV 205-502, which combines structural features common to both ergolines and apomorphine, thus revealed interesting antiparkinsonian properties, but nausea and vomiting were dose-limiting side effects in all patients tested.
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PMID:Antiparkinsonian activity of a non-ergot dopamine agonist, CV 205-502, in patients with fluctuating Parkinson's disease. 238 46

CQA 206-291, a new D2 dopamine receptor agonist with a biphasic dopaminergic profile, was given to six patients with idiopathic Parkinson's disease after overnight drug withdrawal. With incremental single oral doses of CQA, a dose-related, clinically significant, and prolonged antiparkinsonian effect was observed. Most subjects experienced drowsiness after the drug while a minority of subjects experienced nausea and/or vomiting or postural hypotension. Further study of this drug in humans is indicated.
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PMID:The antiparkinsonian activity of CQA 206-291, a new D2 dopamine receptor agonist. 256 66

Fluctuations in motor performances are the major problem in the longterm management of Parkinson's disease. In this study the clinical effects of L-dopa intravenous infusion were evaluated in 18 parkinsonian patients with fluctuations. 14 out of these were given Lisuride intravenous infusion in a following study. Lisuride is a potent dopamine agonist and it is highly soluble in water. The results obtained with L-dopa were very good and we found a close correlation between oral and intravenous dosage. The dosage of L-dopa infusion ranged between 360-1,250 mg for 12 hours. Lisuride proved to be able to give prolonged mobile state in 8 patients out of 14. The other 6 patients showed a different response to the drug. The dosage used ranged between 0.6 and 2.4 mg per day. No severe side-effects were observed during both studies except for nausea and vomiting occurring during Lisuride infusion.
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PMID:Problems in daily motor performances in Parkinson's disease: the continuous dopaminergic stimulation. 346 72

A clinical trial of the combination of naloxone in a low dose (1-1.5 micrograms X kg-1 body weight) with physostigmine (0.5-1.0 mg i.v.) was made to elucidate whether this combination could reverse postanaesthetic overdosing in neurosurgical patients without increasing postoperative pain. The investigation was made following previous findings that physostigmine has analgesic properties in addition to its systemic antisedative and anticholinergic effects as well as a stimulatory effect on morphine-depressed ventilation. Altogether 198 neurosurgical patients were investigated. The results showed that postanaesthetic over-sedation can be safely treated by a combination of naloxone and physostigmine in the dosages named above, resulting in the rapid reversal of sedation, where opiates, neuroleptics and benzodiazepines have been used. In contrast, this combination has very little effect on sedation following the administration of agents such as halothane and isoflurane. In the great majority of patients (95%), the treatment resulted in excellent analgesia during the first postoperative hour. The incidence of nausea and vomiting was increased somewhat by this treatment, but these side-effects could be minimized by decreasing the rate of drug administration. Physostigmine is contra-indicated in patients having symptoms and signs similar to those of Parkinson's disease, and the dose of physostigmine should also be reduced to 0.5 mg i.v. in all patients over the age of 65.
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PMID:Reversal of sedation and respiratory depression after anaesthesia by the combined use of physostigmine and naloxone in neurosurgical patients. 376 92

In a comparison of the effects of domperidone and carbidopa during levodopa treatment, 20 patients with idiopathic Parkinson's disease were treated with fixed dose regimens of either levodopa 500 mg-domperidone 20 mg or levodopa 100 mg-carbidopa 25 mg; each for 8 weeks. Clinical response, incidence of side effects, and plasma levodopa concentration resulting from each treatment were compared. Overall, in the dosages used, Parkinson's disease was less well controlled with levodopa-domperidone than with levodopa-carbidopa. In eight subjects there was a severe deterioration 2 to 7 days after changing from a fixed dose of levodopa-carbidopa to levodopa-domperidone. In nine subjects who completed the trial, the clinical response, occurrence of dyskinesias and of nausea and vomiting, were similar with both treatments, although peak plasma levodopa concentration and levodopa bioavailability were greater on levodopa-domperidone than on levodopa-carbidopa.
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PMID:Comparison of levodopa with carbidopa, and levodopa with domperidone in Parkinson's disease. 376 66

Thirty patients with Parkinson's disease were treated for four weeks with levodopa combined with an inhibitor of extracerebral dopa decarboxylase, L-alpha-methyldopahydrazine (MK 486). The therapeutic results were compared with the effects of treatment of a group of 40 patients with levodopa alone. Patients treated with the combined therapy improved more rapidly, had less nausea and vomiting, and required a much smaller dose of levodopa than patients treated with levodopa by itself.
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PMID:Treatment of Parkinson's disease with levodopa combined with L-alpha-methyldopahydrazine, an inhibitor of extracerebral DOPA decarboxylase. 469 82

Bromocriptine (CB-154) and the 8-alpha-ergoline CU 32-085, two dopamine receptor agonists, were administered at different times to two series of 22 patients with Parkinson's disease, most of whom took levodopa (plus benserazide) at optimum dosage. The addition of bromocriptine (mean daily dose 32 mg; after 6 months 40 mg) led to a 38.5% reduction of levodopa, while CU 32-085 (mean daily dose 15.2 mg; after 6 months 17.5 mg) permitted a 33.7% reduction in levodopa. The mean dose in two patients on CU 32-085 monotherapy was 55 mg/day. A total of 15 patients tolerated adequate doses of bromocriptine (5-75 mg/day, mean duration of treatment 7.5 months) and 15 patients long-term treatment up to 14 months with CU 32-085 (dose range 1-60 mg/day; mean duration 8.8 months). Both groups showed a significant improvement of "total disability score' at 6 months by 56% and 67%, respectively, and after 6 months by 69% and 69.4%, respectively, with a significant decrease of all types of disability. All patients with fluctuations and "on-off' effects rapidly improved on both compounds. Bromocriptine and CU 32-085 were discontinued in seven patients each (32%) because of adverse effect including mental changes (for with bromocriptine, two with CU 32-085), nausea and vomiting (one and two, respectively), hypotension (one each) and increased tremor plus vomiting (one with CU 32-085). Although adverse effects were similar to those observed with levodopa, CU 32-085 in general showed less severe dyskinesia and mental changes but more frequent nausea than bromocriptine and levodopa. While the results of treatment with bromocriptine and CU 32-085 were comparable, the antitremor effect of the latter drug developed more rapidly, even at low dosage. Both compounds were useful in the management of patients with advanced Parkinson's disease, CU 32-085 having a stronger effect on tremor, bradykinesia, fluctuations and "on-off' effects than bromocriptine.
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PMID:Adjuvant treatment of Parkinson's disease with dopamine agonists: open trial with bromocriptine and CU 32-085. 618 Jan 42

Twenty-six patients with late-stage Parkinson disease were given 0.4 to 15 mg of pergolide mesylate daily in addition to, or as replacement for, levodopa or bromocriptine therapy. Despite treatment with individually determined optimum doses of levodopa, bromocriptine, and anticholinergics, they had shown response failure or fluctuating response. Forty percent (11 patients) were unable to tolerate pergolide. Nausea and vomiting, somnolence, and psychiatric disturbances were the most frequent side effects. Eleven of the remaining patients improved on pergolide, 2 were unchanged, and 2 were slightly worse. Among the patients who benefited, pergolide improved dose-related response fluctuations more than non-dose-related fluctuations, with a reduction in number and duration of "off" periods and improvement in quality of sleep and early morning akinesia but little change in freezing episodes. Despite treatment failure in many cases, pergolide is at present the best available drug for specific late-stage management problems.
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PMID:Pergolide in late-stage Parkinson disease. 675 30

In a single-blind trial of therapy in 20 patients with idiopathic Parkinson disease, domperidone prevented nausea and vomiting induced by bromocriptine without diminishing beneficial central effects. Combination of the two drugs permitted rapid increase in bromocriptine dosage from 22.5 mg per day to 148 mg per day, with 71% mean clinical improvement over baseline score; continuing efficacy of the regimen was evident for a mean follow-up of 2 months.
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PMID:Bromocriptine and domperidone in the treatment of Parkinson disease. 719 83

Levodopa-induced motor fluctuations (MF) is a disabling complication of Parkinson's disease (PD) and is usually refractory to conventional treatment. Apomorphine, a dopamine agonist with affinity for both D1 and D2 receptors, has been emerged as an useful alternative in the management of MF of PD. The frequency of nausea and vomiting prevented its use in the past, but the simultaneous administration of domperidone has proved to be able to control these side effects. Although apomorphine has been successfully used to control levodopa-induced MF in other countries, it has not been considered in the management of PD in Brazil. We report here our initial experience with subcutaneous injections of apomorphine combined to oral domperidone. We administered apomorphine in doses ranging from 1.5 to 3 mg in four PD patients with MF of our outpatient clinic. All the doses administered switched the "off" state to a motor response qualitatively similar to what is seen in the "on" phase induced by levodopa, including the occurrence of dyskinesia. The latency to turn "on" after apomorphine ranged from 7 to 30 minutes and the duration of the response ranged from 60 to 85 minutes. We observed yawning in all four patients, labial paresthesia in one patient and an inspecific unpleasant sensation in another patient. These side effects were not significant in our four patients. Our data show that the use of apomorphine adds a reliable and effective strategy in the management of MF of PD patients.
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PMID:[Apomorphine: an alternative in the control of motor fluctuations in Parkinson's disease]. 748 31


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