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)

After reviewing the literature on personality and Parkinsonism and recalling the two concepts which conflict on the etiology of their personality, the author has examined Rorschach charts of 20 Parkinsonians. This was done through formal analysis and content analysis in order to show the various dynamic aspects of personality, the psychic mechanisms preferentially used and the possible relations between psyche and soma. The results reveal a modification of personality in the direction of global narrowing, on ideas and affect, a reduction of relational investments, a narcissitic and hypochondriac retrieval and an important reduction of affects. Two different types of personality appear out of this common branch. The first is characterized by rigidity and stereotipy, the second characterized by some smoothness and a wider opening toward the external world. The psychodynamic study reveals that personality reorganization takes place through libidinal retrieval, through defensive and narcissisic move. After the completion of the study, the somatopsychic hypothesis remains most produce; however the premorbid personality and in particular the aggressive problem can integrate with the behavioral modifications due to Parkinson's disease in order to finally bring a original psycho-affective picture.
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PMID:[Psychodynamic aspects of personality of patients with Parkinsonism]. 102 Jun 90

Metoclopramide is an antiemetic drug which occasionally produced acute dystonic reactions. Although known to interfere with central dopamine mechanisms, it is frequently used in Parkinson's disease to prevent levodopa-induced nausea and vomiting. In this study metoclopramide did not increase Parkinsonism or reduce levodopa-induced involuntary movements in patients with Parkinson's disease. Pimozide, by contrast, increased Parkinsonism and reduced involuntary movements. The capacity of metoclopramide to produce acute dyskinesias while being apparently free of Parkinsonism effects is pharmacologically unique and differentiates this drug from the phenothiazines and butyrophenones.
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PMID:Metoclopramide and pimozide in Parkinson's disease and levodopa-induced dyskinesias. 109 89

Twenty-two patients with Parkinsonism were treated with levoamphetamine and 12 of these with dextroamphetamine. Levoamphetamine resulted in a significant improvement in disability from Parkinsonism, although the reduction in total disability, tremor, akinesia, and rigidity scores was slight (ca 20 percent). Dextroamphetamine in lower dosage also reduced disability by some 17 percent. The most disabled patients, including those also on levodopa, showed the greatest response to amphetamines. Previously, amphetamines have been reported to be a selective treatment for the oculogyric crises of post-encephalitic Parkinsonism. Amphetamines are thought to cause the release of catecholamines from central neurones. Their action in Parkinson's disease may be limited because of pre-existing striatal dopamine deficiency. Side-effects of amphetamines, anorexia, and CNS stimulation are different from those caused by levodopa in patients with Parkinson's disease.
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PMID:Amphetamines in the treatment of Parkinson's disease. 109

Two patients with severe Parkinson's disease were treated with electroconvulsive therapy for a supervening depression. Not only did the symptoms of depression clear up after only four treatments, but the parkinsonian signs also showed striking and sustained improvement. This may be related to ECT-induced changes in dopamine and norepinephrine metabolism. Parkinsonism does not appear to be a contraindication to ECT. On the contrary, ECT may be the treatment of choice for certain patients with Parkinson's disease, whether nor not it is complicated by intractable depression.
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PMID:Improvement of Parkinsonism in depressed patients treated with ECT. 111 72

Judgment of the visual vertical and horizontal in the upright body position was abnormal in 19 (29 percent) of 66 patients with Parkinson's disease. The magnitude of errors correlated with the degree of rigidity and of tremor in the limbs, but not with bradykinesia or other clinical features. The results suggest that the effect on visual perception of the vertical and horizontal coordinates in patients with parkinsonism is brought about by specific changes in the basal ganglia and is not, as in the case of other visual-motor tasks, determined merely by the overall severity of cerebral pathology.
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PMID:Judgment of the visual vertical and horizontal in patients with Parkinsonism. 116 8

Levodopa-induced dyskinesias frequently limit the clinical efficacy of levodopa therapy in Parkinson's disease. Deanol recently has been reported to be of value in relieving the dyskinesias by acting through a central cholinergic mechanism. Seventeen outpatients with levodopa-induced dyskinesias were given deanol in dosages of 300 to 900 mg per day. The dyskinesias improved in four of the patients, remained unchanged in five, and worsened in eight. In all four patients who showed improvement after institution of deanol therapy, the improvement continued after the patients were switched to a placebo. One of these patients also demonstrated improvement in his parkinsonism, while two others experienced a worsening in their parkinsonism. Deanol does not appear to be effective in the treatment of levodopa-induced dyskinesias.
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PMID:Deanol in the treatment of levodopa-induced dyskinesias. 116 39

During the years 1970-1974, a total of 44 patients referred by neurologists to the Urological Laboratory were classified in the following groups: paralysis agitans (27), postencephalitic parkinsonism (5), cerebral arteriosclerosis and parkinsonism (7) and cerebral arteriosclerosis and parkinsonism, suspected (5). Bladder function was assessed on the basis of cystometry and urodynamic investigation. A high frequency of supranuclear bladder paresis (SNP) was found, although unequally distributed in the different diagnostic groups. Stereotactic operations on the thalamic nuclei seemed to be correlated with SNP. The question was raised whether SNP was part of the parkinsonian syndrome or merely signs and symptoms related to ageing.
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PMID:Disturbances of micturition in Parkinson's disease. 126 66

We report a sporadic case of Dopa responsive dystonia and two families with different combinations of parkinsonism and dystonia. The possible relationships between Dopa responsive dystonia and early onset Parkinson's disease are discussed.
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PMID:Dopa responsive dystonia and juvenile Parkinson's disease: two subtypes of the same disorder? 129 88

A 77-year-old man developed syncope after meals at the age of 75. He had been treated with anti-Parkinson's drugs such as levodopa for 18 years as a patient with idiopathic Parkinson's disease (PD). The medications had been very effective to his parkinsonism. Ambulatory blood pressure was recorded every 20 minutes throughout one day by indirect measurement using a Colin medical instrument monitor (ABPM-630). The subsequent data disclosed that postprandial hypotension (PPH) was associated with the frequent after-meal syncope. It was also found that oral ingestion of a solution containing 50 grams of glucose caused a marked and prolonged hypotension during the resting supine position. Plasma norepinephrine failed to show any increment. Plasma vasopressin slightly increased while pulse rate, plasma renin activity, osmolality, and hematocrit did not change despite the production of severe hypotension of a relative acute onset. Signs of glucose intolerance and hyperinsulinemic response were observed. Indications of systemic autonomic nervous dysfunctions were revealed in various autonomic nervous function tests. Physical treatment combined with medication such as droxidopa, midodrine and especially caffeine and fludrocortisone proved to be effective on PPH. The authors confirmed the existence of PD with symptomatic PPH. In addition, we considered this present case as an example of "progressive autonomic failure with PD" (Bannister, 1988).
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PMID:[Parkinson's disease with syncope as a chief complaint induced by prominent postprandial hypotension]. 130 Feb 58

It is now well recognized that the hypothalamus is an important site of neuropathology in Parkinson's disease (PD). Lewy bodies, a marker of nerve cell degeneration and a pathological hallmark of PD, have been observed frequently in the hypothalamus of PD patients by Lewy (1923) and other investigators and confirmed by more recent systematic studies by Langston & Forno (1978). Both Lewy and Langston & Forno found a predilection of Lewy body formation in specific hypothalamic nuclei with the tuberomammillary, lateral, and posterior areas containing by far the highest average counts per nucleus. Selective vulnerability of the tuberomammillary, lateral, and posterior hypothalamic cell groups to degeneration has been observed also in aging, postencephalitic Parkinsonism, Alzheimer's disease, and schizophrenia. The susceptibility of these particular nuclei to degenerative changes including Lewy body formation is not presently understood nor are the mechanisms by which Lewy bodies are formed in PD and other CNS disorders. Accumulation of amines, a pathological process which follows degeneration of catecholamine-containing neurons in experimental animals, also occurs most frequently in the lateral and posterior hypothalamic areas. In the present communication we propose that in PD, amine accumulation may be a precursor to Lewy body formation and that the susceptibility of certain hypothalamic areas to Lewy body formation may be related to their propensity to accumulate amines. Furthermore, the frequent co-existence of Lewy bodies and Alzheimer's neurofibrillary tangles in the lateral and posterior hypothalamic nuclei suggest that they may share a common pathogenetic etiology. If confirmed, this hypothesis may provide an experimental model by which the formation of Lewy bodies and neurofibrillary tangles may be investigated.
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PMID:Amine accumulation: a possible precursor of Lewy body formation in Parkinson's disease. 130 71


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