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

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

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

Bladder function was studied in 24 patients with a diagnosis of parkinsonism using cystometry, sphincter electromyography, flowmetry and electromyelography. A high incidence of disturbances in detrusor function and sphincter control was documented and the signal tracing studies showed prolonged conduction times, giving evidence of peripheral neuropathy. The abnormalities of detrusor function were ascribed to the lesion of the basal ganglia, whereas the sphincter disturbances indicate impairment of the corticospinal tract as a result of Parkinson's disease.
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PMID:Cystometric, sphincter and electromyelographic abnormalities in Parkinson's disease. 13 35

The habituation index is a quantitative expression of the ability of the orbicularis oculi (blink reflex) to adapt to a series of electrical stimuli applied to the supraorbital region. This parameter has been studied in a group of normal control subjects, and the results compared with those in cases of idiopathic and drug-induced Parkinsonism, states of dementia, and dyskinesias such as Huntington's chorea and senile chorea. Patients with Huntington's chorea showed a tendency for the reflex to habituate readily in contrast to patients with dementia caused by cortical atrophy and those with Parkinson's disease. Younger patients with Huntington's chorea had indices within the normal range. It seems unlikely that this test will prove of value in the detection of clinically unaffected relatives. Where dementia was associated with a reversible intracranial lesion, the habituation index was studied before and after treatment. Failure of habituation in this condition appears to be due to the release of a primitive protective reflex.
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PMID:Habituation of the orbicularis oculi reflex in dementia and dyskinetic states. 15 Nov 27

The characteristic oily skin in individuals with parkinsonism has long been observed by clinicians. The oiliness seems to be associated with periods when the disease is most active. This seborrhea has been observed particularly in post-encephalitic parkinsonism, as well as in idiopathic paralysis agitans. It also occurs in phenothiazine-induced parkinsonism.
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PMID:The skin in Parkinson's disease. 16 45

A systematic study of the central and peripheral nervous systems in 3 cases of Parkinson's disease has demonstrated that Lewy bodies are present in 27 nuclei. Of these 20 nuclei (12 pigmented and 8 unpigmented) are involved in 2 or all 3 cases. It is noticed that the distribution of Lewy bodies in Parkinson's disease described here corresponds surprisingly well to that of monoamine (dopamine, noradrenaline and serotonin) cell bodies demonstrated in rats by the histochemical fluorescence method. This correlation is similar to that of Alzheimer's neurofibillary changes in postencephalitic Parkinsonism as described by Ishii. Inasmuch as these viewpoints are also in agreement with preciously reported biochemical data on Parkinsonism, it is suggested that Parkinsonism (idiopathic and postencephalitic) should represent a system degeneration of monoamine neuron systems.
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PMID:Parkinson's disease: distribution of Lewy bodies and monoamine neuron system. 17 63

Necropsy studies were done on six patients with idiopathic paralysis agitans, one with multiple system atrophy including features of Parkinsonism, and one control. Autonomic functions had been evaluated during life to a varying degree. Intra-arterial blood pressure studies were carried out on two patients with paralysis agitans (cases 4 and 6) and the one with multiple system atrophy (case 7). Lewy bodies with or without cell loss were seen in the sympathetic ganglia of five cases of paralysis agitans. Three of these had orthostatic hypotension and the severity of the lesion approximately correlated with the degree of hypotension. It is concluded that the lesions of the sympathetic ganglia may play a major role in the production of orthostatic hypotension in idiopathic paralysis agitans.
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PMID:Dysautonomia in Parkinsonism: a clinicopathological study. 18 90

Paralysis agitans may be mimicked by other disease processes and drugs which disturb the structural or functional integrity of the dopaminergic nigrostriatal system. In another group of patients, isolated symptoms or signs such as tremor or increased muscle tone are considered out of the context of the total clinical picture and may suggest parkinsonism.
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PMID:Differential diagnosis of paralysis agitans. 26 20

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


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