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)

Plasma renin activity (PRA) of patients with Parkinson's disease was measured in recumbency, upright position, and after frusemide administration. The results show that the renin responses to both stimuli are significantly reduced as compared with those obtained in a group of normal subjects, while recumbent PRA levels of Parkinsonism patients are not significantly lower than those found in recumbent normal subjects. Levodopa treatment, alone or in combination with two different dopa-decarboxylase inhibitors, benserazide and carbidopa, does not modify the renin response to posture or to frusemide. Although the reduced activity of the renin-angiotensin system can play some role in the genesis of orthostatic hypotensive episodes encountered in patients with Parkinsonism, the greater incidence of orthostatis hypotension in patients treated with levodopa seems to be unrelated to any effect of this drug on the renin release.
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PMID:Effects of levodopa alone and in combination with dopa-decarboxylase inhibitors on plasma renin activity in patients with Parkinson's disease. 73 Dec 41

Clinical and neuropharmacological evidence indicates the involvement of dopaminergic mechanisms in Parkinson's disease and schizophrenia, as well as in iatrogenic Parkinsonism and drug-induced schizophrenia-like syndrome. The evidence hitherto presented stresses the existence of a reversed relationship between Parkinson's disease and schizophrenia and implicates the possibility that dysfunction of dopamine-receptors may be a central phenomenon in both diseases. In view of the recent demonstration of two separate dopamine-receptors, it is postulated that a striatal receptor blockade may cause Parkinson's disease, whereas a limbic receptor blockade may result in schizophrenia. The recent discovery that several autoimmune diseases, such as myasthenia gravis, are the result of an immunopharmacological block at receptor sites, together with several observations of immunological disorders in Parkinson's disease and schizophrenia, suggests the possibility that certain types of Parkinson's disease and schizophrenia might be the consequence of an autoimmune blockade of striatal or limbic dopamine-receptors, respectively.
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PMID:Automimmune response to dopamine-receptor as a possible mechanism in the pathogenesis of Parkinson's disease and schizophrenia. 73 51

Since it is was first described by James Parkinson in 1817 much has been learnt about Parkinson's disease. The complete picture is not clear, however, and a new impulse has been given to the study of the physiopathology of the basal ganglia by the therapeutic employment of L-Dopa with a peripheral inhibitor of the decarboxylase. This treatment is the best available particularly for akinetic-hypertonic forms. In certain cases, however, patients developed a dyskinetic long-term L-Dopa syndrome, depending on the amount of L-Dopa given and individual sensitivity. The syndrome occurs in Parkinsonism only and can be prevented by thalamolysis. It would appear to be a specific expression of the effect of L-Dopa on the striatonigral system rather than of generic hypersensitivity due to denervation. A personal case is presented.
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PMID:[Long-term levodopa syndrome. Report of a clinical case]. 75 26

The prognostic value of electroencephalograms in patients with early or mild Parkinson's disease treated with L-dopa is discussed. Fifteen patients with early or mild Parkinson's disease were studied clinically and electroencephalographically while receiving L-dopa or placebo treatment. Only a low incidence (four patients, 27%) of EEG abnormality was found. These patients showed only mild improvement: in three cases, the improvement followed an initial worsening in the first three months. Only one (13%) of the patients with a normal EEG became worse or failed to improve. The potential use of EED data in parkinsonism is discussed.
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PMID:Electroencephalographic findings in patients with mild Parkinson's disease treated with L-dopa and placebo. 76 69

Although the mortality of Parkinsonism is negligible, it is one of the major causes of progressive and often pitiful disability in the elderly. Treatment of the condition, whether medical or surgical, is still only palliative. The successes and limitations of the various forms of treatment are discussed. Despite the spectacular gains which have been achieved during the past 25 years by sterotactic thalamotomy and treatment with levodopa, the patient's disabilities tend to progress slowly and the fundamental enigma of Parkinson's disease and of its cure still awaits solution.
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PMID:Treatment of parkinsonism. 77 Jan 32

Seventeen patients with either Parkinson's disease or post-encephalitic parkinsonism were treated with Piribedil, an apomorphine-like drug, in single blind conditions for a period ranging from five weeks to twenty-four months. The analysis of the results shows that Piribedil modifies the extrapiramidal symptomatology being specially effective against the tremor either when used alone or in association with L-Dopa. The side effects noticed during treatment with Piribedil are similar to those of Apomorphine, and are dose-dependent.
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PMID:[Piribedil in the treatment of Parkinson disease (author's transl)]. 77 98

Amantadine is a putative dopaminergic compound known to be therapeutically effective in idiopathic and postencephalitic Parkinson's disease. In a double-blind placebo-controlled crossover study of 39 psychiatric inpatients, amantadine and trihexyphenidyl were equally effective in treating drug-induced parkinsonism, and amantadine produced fewer and less severe side effects. The authors suggest that amantadine is an effective alternative to atropine-like agents, with fewer implications for long-term risk of tardive dyskinesia.
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PMID:Amantadine versus trihexyphenidyl in the treatment of neuroleptic-induced parkinsonism. 78 62

Twenty-three patients with Parkinson's disease participated in long-term, double-blind evaluations of the effectiveness and side effects of amantadine in combination with levodopa therapy. Sixteen patients completed the year-long study, which consisted of randomized crossover of amantadine and placebo before levodopa was begun and again after 5 and 11 months of continuous levodopa therapy. Initially, 16 of 23 patients (70 percent) had a favorable response to amantadine during the first crossover period. After 1 year of levodopa, at least eight of 16 patients (50 percent) responded favorably to amantadine compared with placebo. Some of the amantadine responders previously had been nonresponders, and vice versa. The response to amantadine was quantitatively similar in the responders even after the patients had been receiving levodopa therapy. Amantadine should be tried as a therapeutic agent in addition to levodopa for parkinsonism if more beneficial effect is desired, even if amantadine was previously ineffective in the same patient.
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PMID:Long-term evaluation of amantadine and levodopa combination in parkinsonism by double-blind corssover analyses. 80 69

The author reviews the association between Parkinson's disease and depression and presents evidence to support the hypothesis that depression may be not only reactive but biochemically related to the disease. A psychotically depressed patient with parkinsonism responded positively to ECT as shown by improvement on a depression rating scale, two extrapyramidal rating scales, and handwriting samples. The beneficial effect on parkinsonian signs occurred before the improvement in depression, which suggests that ECT has a specific antiparkinsonian effect. Possible explanations for this observation based on biochemical theories of depression are discussed.
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PMID:Parkinson's disease, depression, and ECT: a review and case study. 83 44

The clinical, biochemical, and pharmacologic responses to L-dopa were studied in 87 patients with Parkinson's disease. Eleven of the 87 patients had a long-duration response, 39 had a short-duration response, and 37 had a combination of both. Thirty-four of the 39 patients with short-duration response to L-dopa experienced a consistent and reproducible sequence of clinical and biochemical events after each dose, characterized by improvement of parkinsonism and a single phase of dystonia occurring during or shortly after the peak of dopa concentration in plasma and during maximal clinical improvement. We have called this the I-D-I- response, for Parkinsonism-Improvement-Dystonia-Improvement-Parkinsonism. The remaining five patients all had the onset of the disease at an unusually young age and showed a distinctly different response pattern consisting of a first phase of dystonia, before there was any improvement, followed by a phase of improvement without dystonia and then by a second phase of dystonia before the abrupt return of parkinsonism. We have called this the D-I-D response, for Parkinsonism-Dystonia-Improvement-Dystonia-Parkinsonsim. Dystonia occurs in the D-I-D- response when the concentration of dopa in plasma passes through a critical but relatively low level, whereas it remains absent as long as the concentration of dopa remains above that level. In the I-D-I- response, dystonia is avoided by keeping the plasma concentration of dopa low, in the D-I-D- response by keeping it high. It is postulated that in the D-I-D response postsynaptic depolarization blockade due to supramaximal stimulation of the neuronal system mediating dystonia occurs, whereas in the I-D-I response the postsynaptic members of the same neuronal population respond with excitation but not with depolarization blockade.
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PMID:Patterns of dystonia ("I-D-I" and "D-I-D-") in response to l-dopa therapy for Parkinson's disease. 83 64


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