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)

The effect of levodopa on the mortality of patients with Parkinson's disease was investigated in 349 patients treated with levodopa or levodopa combined with decarboxylase inhibitor during 1969-1975 inclusive. During the study period, 61 patients died. The expected mortality was 32.99 resulting in a ratio of actual to expected deaths of 1.85. The excess mortality was accounted for by patients with a severe disease at entry and especially, by the less favorable effect of levodopa treatment than in the living patients. In comparison with the prelevodopa era, the reduction of mortality and the increase of life expectancy of patients with Parkinson's disease during levodopa treatment possibly reflect the decrease of the early mortality due to Parkinson's disease.
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PMID:Mortality of patients with Parkinson's disease treated with levodopa. 7 32

Parkinson's disease can present as a progressive hemiparesis without tremor. The presence of mild cogwheel rigidity in a hemiparetic patient may suggest the diagnosis, as may the normal findings on brain scan and electroencephalogram in a patient with gradually evolving hemiparesis. The response to appropriate medication has been prompt and excellent. It is important that Parkinson's disease be considered in the differential diagnosis of a progressively evolving hemiparesis.
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PMID:A pseudohemipharetic form of Parkinson's disease. 7 43

Computed tomographic examinations of parkinsonian patients revealed a high incidence of cerebral atrophy, in most cases a combination of cortical atrophy and ventricular enlargement. The present study considered the relationship between cerebral atrophy and physical signs indicating or promoting arteriosclerosis such as overweight, electrocardiographic changes, hypertension, calcification of the internal carotid artery and aorta as well as elongation of the aorta. The study is based on 173 treated and untreated parkinsonian patients (89 men, 84 women) aged from 37--84 years (mean 64.6), on whom CT was performed about 5.4 years after the onset of the first symptoms of the illness. The results demonstrate an increase of pathological CT findings as well as of calcification in the carotid siphon with advanced age. No correlation was found between the other items and increasing age. Further analysis of the relationship between cerebral atrophy and signs of arteriosclerosis revealed only a statistically relevant correlation with calcification of the carotid siphon, especially with calcification of the media. Since pathological CT findings and calcification of the internal carotid artery are both related to advanced age, whereas all the other items which may be considered to be indications of arteriosclerosis do not have any clear relationship, it is concluded that the cerebral atrophy in Parkinson's disease is not caused by arteriosclerosis.
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PMID:Relationship between arteriosclerosis and cerebral atrophy in Parkinson's disease. 7 48

Six patients with Parkinson's disease developed nocturnal myoclonic attacks after prolongued treatment with L-Dopa which were electroencephalographically recorded. These symptoms persisted after treatment with 2 bromo-alpha-ergocryptin (Bromocryptin), a dopamine receptor agonist, which was substituted for L-Dopa. Bromocryptin is known to have no pre- or postsynaptic effect on serotonin metabolism. It is proposed that these myoclonic phenomena are the expression of the hypersensitivity of denervated catecholamine receptors in the brainstem to the stimulation of L-Dopa and Bromocryptin. This thesis differs with previous suggestions that serotonin plays a major role in the genesis of myoclonic seizures in Parkinsonian patients treated with L-Dopa.
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PMID:Myoclonic attacks induced by L-dopa and bromocryptin in Parkinson patients: a sleep EEG study. 7 16

In order to investigate the influence of basal ganglia and cerebellar involvement on the preparatory state of the cerebral cortex for voluntary movement, the cortical potential preceding finger movement was studied in 20 patients with Parkinson's disease and 20 patients with cerebellar ataxia. Readiness potential (RP) was abnormal in 90% of the Parkinson group and in 55% of the cerebellar ataxia group. The most frequent abnormality was a depressed amplitude and earlier onset of RP in both groups. The most remarkable finding in the present study was the complete absence of RP with dyssynergia cerebellaris myoclonica (presumed Ramsay Hunt syndrome) whereas normal RP was obtained with cerebellar cortical degeneration. In addition, RP was absent or severely depressed in patients with a unilateral vascular lesion of the midbrain (Benedikt's syndrome) and in patients with Parkinson's disease who underwent unilateral intermedioventral (Vim) thalamotomy. These facts suggest a possible important role of the dentatorubrothalamic or dentatothalamic pathway in the physiogenesis of RP.
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PMID:Clinical studies of the movement-related cortical potential (MP) and the relationship between the dentatorubrothalamic pathway and readiness potential (RP). 8 Dec 81

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

Cysteamine-induced duodenal ulcers in rats were prevented by the dopamine agonists bromocriptine, lergotrile, and apomorphine, whereas both the severity of duodenal ulcers and the mortality among cysteamine-treated rats were raised by the dopamine receptor antagonist, haloperiodol. Bromocriptine and lergotrile greatly reduced gastric-acid output in cysteamine-treated rats. A review of the literature shows a high incidence of duodenal ulcers in patients with Parkinson's disease (associated with dopamine deficiency) and a low occurrence in schizophrenics (associated with dopamine excess and/or hyperactivity). Thus, changes in peripheral and/or central dopamine concentrations and/or receptor activity may have a role in the pathogenesis of duodenal ulceration.
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PMID:Dopamine disorder in duodenal ulceration. 9 Sep 70

The term 'long term neurological cripple' is an unattractive and yet an all embracing one, covering a wide spectrum of disorders from spina bifida or cerebral palsy with or without associated epilepsy and behavioural and learning problems, through muscular dystrophy, multiple sclerosis, and motor neurone disease, to the effects of head injury, cerebrovascular lesions and the degenerative disorders of later life such as Parkinson's disease and the senile and presenile dementias. Whilst many of the problems are common to several of these entities, each has its own particular aspects.
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PMID:The support of the long term neurological cripple. 10 16

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


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