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)

269 patients suffering from progredient, chronic either primary or secundary cerebral diseases (Parkinson's disease, cerebral vascular diseases, cerebral atrophic dystrophy, Huntington's chorea, muliple sclerosis have been studied in the last two years. 44 of these patients developed pharmaco-toxic psychoses during drug treatment (low and medium dosis). The psycho-pathological rating resulted in an acute organic brain syndrome with predominance of confusion, sometimes progressing to delirium. EEG was changed during the psychotic stage. These changes cannot be decided from organic psychoses, which are not related to drugs. Patients with Parkinson's disease showed a relatively high incidence to psychoses during drug treatment (51.47%). In patients without Parkinson's disease, but on treatment with antidepressants, neuroleptics, diuretics and digitalis, pharmacotoxic psychoses only could be observed in 4.4% of the patients. However, the same group of patients showed an acute organic brain syndrome in 12.43%, when not on treatment. Combined treatment with L-DOPA plus peripherally acting decarboxylase inhibitors resulted in a high incidence to psychoses in idiopathic Parkinsonism but the same dosis produced this side effect only in a few patients with cerebral atrophic dystrophy. The ratio was 5:1 between the former group and the later one. That means, that L-DOPA is a much more psychotoxic substance in Parkinsonism when compared to other cerebral diseases. These pharmacotoxic psychoses could be correlated with the progredience of the disease. These pharmacotoxic psychoses are not only dependent from age and duration of treatment. Evidence exist, that there might be a correlation between the incidence for pharmacotoxic psychoses and the lack of surviving dopaminergic neurons in the nigro-striatal areas. Treatment with very low doses of neuroleptics suppresses pharmacotoxic psychoses but allow a further anti-Parkinson therapy which is of vital necessity.
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PMID:[Acute pharmacotoxic psychoses in patients with chronic cerebral disorders]. 3 35

In contrast to antipsychosis drugs which inhibit the dopamine-activated adenylate cyclase [ATP pyrophosphate-lyase (cyclizing), EC 4.6.1.1] of caudate nucleus, dopaminergic drugs for treatment of Parkinson's disease stimulate this cyclase. Stimulants and inhibitors of cholinergic neurons inhibited this adenylate cyclase activity competitively and specifically. Thus, the mechanism by which dopaminergic medications ameliorate the effects of Parkinson's disease includes activation of the dopamine-sensitive adenylate cyclase. Excessive activation might be present during the psychotic episodes seen in patients with parkinsonism who are overtreated. The enzymatic effects of the drugs that affect cholinergic mechanisms seem to be generally in keeping with the pharmacological reciprocity between psychoses and extrapyramidal function, except for the anticholinergic ones which inhibited this cyclase although they can be hallucinogenic.
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PMID:Opposing effects of dopaminergic to cholinergic compounds on a cerebral dopamine-activated adenylate cyclase. 26 41

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

A review of the effects of using bromocriptine in Parkinson's disease showed that it rarely helps patients not primarily improved by levodopa. Patients who show late failure with levadopa and whose response to treatment is declining are helped by combining the two drugs. High cost and severe psychosis are the main disadvantages of bromocriptine, and, although it is not recommended for patients who are doing well on levodopa, it is the best available drug for hospital use in patients who show late failure with levodopa.
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PMID:Bromocriptine in Parkinsonism. 34 61

Dopamine and its specific receptors are widely distributed in man. Body regions where dopaminergic activity is of special pharmacologic interest include the basal ganglions, hypothalamus, chemoreceptor trigger zone, other less well defined areas in the central nervous system, and the renal and cardiovascular systems. The search for dopaminergic agents to modify these systems in disease states has depended heavily on in vitro and in vivo bioassays. These assays involving receptor binding, enzyme activation, smooth muscle and neuronal excitation, and modification of animal behavior have provided physicians with important therapeutic tools. Indeed, the introduction of levodopa for the treatment of Parkinson's disease and of the phenothiazines and related drugs for schizophrenia and psychosis has been a hallmark of neuropharmacologic research. However, the maximal benefits that these drugs may afford have not yet been realized due to an inadequate understanding of disease processes and a relative lack of specificity of drug action.
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PMID:Clinical aspects of dopamine agonists and antagonists. 35 76

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

Of 88 patients with idiopathic Parkinson's disease, without prior psychotic symptoms, and without significant dementia, nearly half had experienced vivid dreams, hallucinations, illusions, and nonconfusional as well as confusional psychoses as side effects of chronic levodopa therapy within the previous year of treatment. It was found that 61.3% of all hallucinations were associated with preexistent or concurrent vivid dream phenomena, that all psychotic states were associated with preexistent or concurrent vivid dreams and/or hallucinations, and that nonconfusional psychotic states tended to become confusional. These findings raise the possibility that chronic levodopa therapy may result in dopaminergic kindling and support the hypothesis that chronic dopaminergic agonism may, via such a kindling mechanism, play a role in the development of some types of psychoses.
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PMID:Levodopa-induced psychosis: a kindling phenomenon. 65 76

Acturial methods are used to study the correlation between the initial condition and early therapeutic results, and the present condition of 164 parkinsonian patients treated with L. dopa for 4 to 8 years. There is an ineluctable deterioration in motility. There is a lower risk in patients who are autonomous and only slightly akinetic at the beginning of treatment. Intellectual deterioration is seen in some patients only. The risk factors are: males, the clinical forms of Parkinson's disease in which tremor is not predominant, onset of the disease before 60 years of age, and depression and transitory psychotic disorders during the first year of treatment. This deterioration appears 3 to 5 years after starting dopatherapy, which could be the cause. Life expectancy is still reduced by the disease at the present time. It is longer in patients in whom the disease started with isolated tremors, absence of Babinski's sign, and no loss of autonomy, and those in whom a good initial therapeutic result was obtained.
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PMID:[Long-term prognostic factors in Parkinson's disease (author's transl)]. 72 3

Forty patients have been treated with Sinemet (L-carbidopa/L-dopa) for a period of up to two years. The results are in agreement with those in the literature. In two-thirds of cases a good to very good improvement was obtained. The principal side effects were dyskinesia, hypotonia, and gastrointestinal and psychotic symptoms, though they seldom necessitated treatment interruption. L-carbidopa/L-dopa affords a real alternative therapy in the modern treatment of Parkinson's disease with L-dopa and a decarboxylase inhibitor. Generally the dosage range was up to a maximum of one tablet three times daily. Sinemet tablets are simple and convenient to handle for both doctor and patient. Dosage titration to therapeutic efficacy can be achieved in one week to ten days without complications, though we recommended a slower titration based on individual patient reaction and requirements.
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PMID:[Treatment of Parkinson's disease with the combination drug L-carbidopa/L-dopa. Report on a 2 years study]. 84 50

Biperiden hydrochloride has been used in the treatment of Parkinson's disease and related disorders within two drugs: --Akinophyl, --and Akineton which is chemically similar but has a slower effect. The first French publications upon its use as a neuroleptic corrector date from 1972. Our study deals with 55 chronic psychotic patients treated with neuroleptics and varied correctors of resulting Parkinson disorders. Akineton has been substituted for the preceding antiparkinson drugs. We may come to the following conclusions = Akineton is effective upon neuroleptic syndrom, gives few or no untoward reactions, has no toxicologic effects, shows no incompatibility with any other drug. It is very satisfactory to have at our disposal a drug effective in small doses and having a slow effect within average of 24 hours.
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PMID:[Treatment of the neuroleptic syndrome by biperiden hydrochloride under its delayed-action form. A 9-month study on 55 hospitalized patients]. 100 Dec 42


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