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)

In an attempt to determine the mechanism of action of L-proly-L-leucyl-glycine amide (MIF-I) in the treatment of Parkinson's disease, various parameters of dopaminergic neuronal function were studied in rats. It was found that the active uptake of 3H-dopamine (3H-DA) by synaptosome-rich homogenates of the striatum of rats treated with MIF-I (1 mg/kg IP X 3, 24 hr intervals) was unaltered 1 hr after final treatment with MIF-I. Also, neither tyrosine hydroxylase nor dopa decarboxylase activity was altered in the striatum and substantia nigra of rats treated with MIF-I (20 mg/kg IP X 3, 24 hr intervals). Thus, vital functional processes associated with dopaminergic neurons apparently are not altered by MIF-I under the conditions studied. These findings illustrate the importance of concurrent DOPA administration in observing an effect of MIF-I on dopaminergic neuronal function.
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PMID:Effects of L-prolyl-L-leucyl-glycine amide (MIF-I) on dopaminergic neurons. 1 12

The writers present some physiological (and not therapeutic) acute and sub-acute trials with tripeptide: L-propyl-L-leucyl-glycine amide (M.I.F.-I) in Parkinson's Disease. This work confirms the earlier observation that M.I.F.-I employed alone or in combination with Levodopa is active against Parkinson's disease. The writers evoke the hypothesis that this action takes place at the postsynaptic receptors, whose configuration may be modified in the sense of a hypersensitivity. These studies justify undertaking a series of controlled therapeutic trials when the cost of the product permits and as well instituting development work on analogues active orally.
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PMID:[Physiological trials with MIF-I in Parkinson's disease (author's transl)]. 2 30

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

23.3 per cent out of 180 old patients (age above 60 years, 71 y in the mean) suffering from chronic cerebral disorders (3 large groups of disease) developed pharmacotoxic psychoses. This relative high percentage can be explained by psychotoxic side effects of the modern antiparkinson-therapy. The incidence to psychotoxicity of combined L-Dopa seems to be less marked in patients without Parkinson's disease when compared to patients with progredient nigrostriatal degeneration. Toxic delirium as a result of treatment with antidepressants, diuretics and digitalis was observable only in a few percentage. This occurance was even less pronounced in comparison to acute developing exogene psychoses in the same group of patients when drugs were not administered.
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PMID:[Pharmacotoxic psychoses in patients with neurological disorders during old age (author's transl)]. 4 22

Clinical EEG evaluation and power spectral analysis were performed on 12 parkinsonian patients before and during L-DOPA treatment. The EEG evaluation did not disclose any significant effects of L-DOPA treatment. Spectral analysis disclosed normal interlobar and interhemispheric power differences and an increase in delta and slow-theta power in the right temporal as compared to the right occipital lobe before L-DOPA treatment was initiated. L-DOPA treatment significantly increased alpha power in both occipital lobes, decreased theta power in the right temporal lobe, accentuated power differences in the theta and alpha bands between temporal and occipital lobes and attenuated beta power differences in those areas. This work is intended as a pilot study in the quantitative EEG evaluation of Parkinson's disease and L-DOPA treatment.
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PMID:EEG power spectral changes secondary to L-DOPA treatment in parkinsonian patients: a pilot study. 6 67

In a double-blind crossover trial, (-)-deprenyl, a fast-acting selective monoamine-oxidase-B inhibitor without a "cheese effect", was given to 41 patients with idiopathic Parkinson's disease who were receiving maximum tolerated doses of levodopa either alone or combined with carbidopa ("Sinemet"). In a dose of 10 mg, daily or on alternate days, (-)-deprenyl prolonged the therapeutic effect of levodopa and was effective in mild "on-off" disabilities with end-of-dose akinesia; the majority of patients with nocturnal and early-morning akinesia also improved. No statistically significant improvement occurred in diurnal akinesia, and there was no improvement in patients with severe on-off disabilities with freezing and rapid oscillations ("yo-yo" effect). Levodopa-induced dyskinesias were aggravated in 14 patients. In 5 previously untreated patients, (-)-deprenyl alone gave no benefit, but when it was used with levodopa and carbidopa a mean dosage reduction of 200 mg levodopa daily was possible. Depression, present in 15 patients, was unchanged. (-)-Deprenyl in combination with smaller total daily doses of levodopa and a peripheral decarboxylase inhibitor may prove useful in reducing the frequency and severity of some types of on-off effect with overall benefit comparable to that obtained with larger doses of levodopa.
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PMID:Deprenyl in Parkinson's disease. 7 2

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

Levodopa administered alone or in combination with a peripheral decarboxylase inhibitor is at present the best means available for the control of Parkinson symptoms. It has proved particularly effective in Parkinson's disease and postencephalitic parkinsonism. In these disorders its continued administration for periods that now exceed five years has resulted in sustained therapeutic responses and a significant decrease in mortality rate. Levodopa has been shown to be a safe pharmacologic agent even after long-term usage. However, its potential for inducing side effects makes it essential that patients be carefully screened before use and monitored throughout the period of administration. Though not fully established and lacking FDA approval at this time, levodopa appears to be useful in reversing the symptoms of hepatic encephalopathy and as a diagnostic aid in assessing pituitary disorders as well as uncovering presymptomatic Huntington's chorea.
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PMID:Levodopa. 12 8

The effect of a new dopamine receptor stimulating agent, piribedil (ET 495), was studied in 10 patients with Parkinson's syndrome, who had had no or a poor response to previous L-DOPA treatment, or had displayed marked side effects during L-DOPA administration. Piribedil produced significant improvement of the functions of activity of daily living (ADL), and appeared to have a preferential effect on parkinsonian tremor. However, treatment was difficult to control primarily because of severe psychiatric side effects.
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PMID:Piribedil in Parkinson's syndrome: a clinical study. 18 60

Clinical data demonstrate that there is a significant difference between at least two types of idiopathic Parkinsonian patients; a benign type of Parkinson's disease and a malignant type. They can be distinguished by the time course of a disability-score, independent of the duration of the disease. The benign cases respond very well to L-Dopa (Madopar) treatment and show a long lasting (7 years) drop in the disability, whereas the improvement of disability in the malignant cases is much smaller and lasts for about one year, followed by an increase of disability. The duration of the disease is 12,5 +/- 0,4 years in the benign type but only 4,0 +/- 0,3 years in the malignant type. Akinetic crises, off-phases, hyperkinetic crises and toxic deliria after Madopar treatment can be observed later in the benign than in the malignant cases. These results suggest that the degeneration of the dopaminergic nigrostriatal system occurs much more rapidly in malignant cases than in benign cases of Parkinson's disease.
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PMID:Distinction between benign and malignant type of Parkinson's disease. 23 Sep 30


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