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)

Levodopa is at present the most effective treatment of Parkinson's disease. Its use in combination with a peripheral decarboxylase inhibitor prolongs the elevation of plasma levels and decreases the incidence of peripheral side effects. Severe psychiatric and neurologic side-effects may necessitate reduction or cessation of the drug.
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PMID:Levodopa in the treatment of Parkinson's disease. 26 29

L-DOPA-psychosis is a frequent side effect of the combined treatment of Parkinson's disease with L-DOPA and peripherally active decarboxylase inhibitors. Regional human post-mortem brain studies showed a significant increase of noradrenaline and serotonin particularly in extrastriatal areas, whereas the lenticular nuclei were not involved. The significance of extrastriatal neurotransmitter dysfunctions for psychiatric disorders is discussed.
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PMID:Toxic delirium after L-dopa medication. 29 Jul 36

The pathophysiology, anticholinergic therapy and dopaminergic therapy of Parkinson's disease are reviewed; an emphasis is placed on the structure and function of the basal ganglia because of their importance in understanding the pharmacotherapy of parkinsonism. The pharmacologic management of Parkinson's disease is limited primarily to manipulation of the dopamine-acetylcholine system. Levodopa, with or without a peripheral dopa decarboxylase inhibitor, is the current drug of choice in the management of idiopathic and postencephalitic Parkinson's disease. Modification of the serotonin-histamine system via the use of antihistamines may be useful in some patients. There are also many adjunctive agents which may be employed in combination with or in place of levodopa. Levodopa clearly has no place in the treatment of neuroleptic-induced Parkinson's disease; anticholinergics and antihistamines are the agents of choice.
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PMID:Pharmacotherapy of Parkinson's disease. 32 45

The treatment of Parkinson's disease is discussed. Levodopa is the most effective drug in this therapy. The place of other agents is discussed.
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PMID:The treatment of Parkinson's disease. 34 79

A sixteen-week study examined the effect of Madopa and Sinemet on patients with Parkinson disease disease suffering nausea or vomiting as side-effects of levodopa therapy and compared the efficacy of the three preparations in controlling the symptoms of Parkinson disease. Following a control period on levodopa, 20 patients underwent four consecutive four-week regimens as follows: (1) double-blind, in which a randomized half received levodopa and half received Madopa; (2) single-blind, in which all received Madopa; (3) double-blind, in which a re-randomized half received Madopa and half Sinemet; and (4) single-blind, in which all received Sinemet. Levodopa administration via Sinemet and Madopa was held to a fixed 20% of prior levodopa dosage. Almost all patients showed great reduction in nausea and vomiting with both Madopa and Sinemet. Seventy percent of the patients showed improvement in disability compared to their levodopa baseline levels. Group means showed no difference between the improvement seen on Madopa and that seen on Sinemet. However, examination of individual responses showed that the majority of patients fared distinctly better on either Sinemet or Madopa.
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PMID:A double-blind comparison of levodopa, Madopa, and Sinemet in Parkinson disease. 35 36

Twenty-two patients entered a double-blind trial to test the efficacy of bromocriptine therapy in patients with Parkinson's disease who were already stabilized on conventional L-Dopa therapy. Of these, three patients who were receiving placebo withdrew when no improvement occurred and control became complicated. Another four patients taking active drug withdrew because of side effects, but only in one case was the symptom (nausea and vomiting) thought to be a true effect of the drug. Of the 15 patients who completed the trial, nine were taking active drug and six took placebo. Although more than half the patients in each group were subjectively improved, measurement scales of functional disability and physical examination revealed no significant change in either group. Side effects encountered included nausea, dyskinesia, and hallucinations. It was concluded that bromocriptine does not offer any additional benefit to patients with Parkinson's disease who are stabilized on L-Dopa therapy, but may have a place in those patients who encounter side effects due to fluctuations in serum and tissue levels of L-Dopa.
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PMID:A double-blind trial of bromocriptine in Parkinson's disease. 37 May 27

Levodopa has become established as the treatment of choice in Parkinson's disease. It is adsorbed by an active mechanism from the small bowel. Its pharmacological activity depends upon the formation of dopamine and possibly other metabolites. Its beneficial effect in Parkinson's disease probably depends upon temporarily restoring the ability of degenerating nigro-striatal cells to release dopamine. Its main side effect, that of dyskinesia, may reflect a direct action of dopamine on striatal receptors. Peripheral decarboxylase inhibitors reduce the incidence of levodopa-induced nausea, probably by lowering the concentration of dopamine in the area postrema. The introduction of levodopa in the treatment of Parkinson's disease is generally regarded as one of the uncommon examples in medicine where effective therapy has resulted from systematic research rather than seredipity. As our knowledge of the pharmacology of levodopa grows, we may be forced to admit that perhaps the right drug was chosen for the wrong reasons.
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PMID:A review of some aspects of the pharmacology of levodopa. 38 8

In a study of 16 psychotic patients with neuroleptic-induced tardive dyskinesia and 16 patients with Parkinson's disease and L-Dopa-induced hyperkinesia it was found that (1) tardive dyskinesia, compared to L-Dopa hyperkinesia, was localized almost exclusively to the oral region (P mean value of 0.01), whereas theL-Dopa hyperkinesia was more pronounced in the neck (P mean value of 0.05) and the extremities (P mean value of 0.05); (2) L-Dopa hyperkinesia showed an increasing tendency to oral preponderance with age, irrespective of the severity ofParkinsonism and extra-oral hyperkinesia, while tardive dyskinesia only itensified with age, without any change in distribution; and (3) extra-oral L-Dopa hyperkinesia was related to the localization and severity of pretreatment Parkinsonism, and more to bradykinesia than to rigidity and tremor. It is concluded that the irreversible neurotoxic effect of neuroleptic drugs may be associated with age-related changes in the oral somatotopic region of the basal ganglia (to be given consideration in any future search for the pathogenetic process underlying irreversible tardive dyskinesia), and that the pathophysiology of involuntary hyperkinesia in neuroleptic-treated psychiatric patients and in L-Dopatreated parkinson patients may consist of a primary dopamine deficiency (pharmacological or structural), and a secondary relative hyperactivity in the dopaminergic system ("dopaminergic hypersensitivity") possibly corresponding to hypoactivity in the cholinergic system.
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PMID:Relationship between tardive dyskinesia, L-Dopa-induced hyperkinesia and parkinsonism. 40 41

N-carbamoyl-2-(2,6-dichlorophenyl) acetamidine hydrochloride (LON 954) causes a reproducible rest tremor in mice, of rapid onset and short duration with no associated rigidity or akinesia and in the absence of any marked changes in body temperature or accompanying peripheral parasympathomimetic effects. This tremor can be antagonised by the dopamine receptor agonists L-Dopa, bromocriptine, nomifensine and piribedil, as well as by anticholinergic anti-Parkinson drugs having an inhibitory effect on dopamine uptake such as benapryzine and benztropine. In contrast, benzhexol, orphenadrine and amantadine had no effect. LON 954 appears to be more specific than oxotremorine for the detection of drugs having therapeutic potential in the treatment of Parkinson's disease, particularly those exerting their effect through dopaminergic systems. An antagonist (BS 100-141), which is a structural isomer of LON 954, is also described.
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PMID:The production of an alternative laboratory model of the Parkinson syndrome using a new benzylimidoylurea derivative LON 954. 40

Our findings in a relatively small series of cases seem to confirm a lack of statistically significant EEG changes when Carbidopa is combined with Levodopa in the therapy of patients with Parkinson's disease. There appears to be a slight increase in basic background frequency which was one of the earlier findings when Levodopa was first used clinically. From the literature surveyed there appears to be a definite lack of consistency in the effects of Levodopa therapy on the electroencephalogram and on the clinical status of the patients followed. We think this well may be explainable by the fact that no large study has been accomplished in which a neuroanatomical (pathological) correlation has been done with both the clinical and the EEG data. Neurological examination and the electroencephalogram are both clinical tools and have yet to be closely reviewed with the added parameter of neuro-pathologic investigation in this new day of therapy for Parkinson's disease.
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PMID:Electroencephalographic change in Parkinsonian patients treated with levodopa-carbidopa. 44 60


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