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 a study of oesophageal motility in 20 patients with Parkinson's disease, intravenous atropine produced marked disruption of co-ordination in response to swallows, when compared with control subjects. This suggests that cholinergic rather than dopaminergic mechanisms are more important in the control of swallowing in patients with Parkinsonism. No conclusive evidence of peripheral dopamine depletion or autonomic neuropathy was found, although minor changes suggestive of the former were found in severely affected patients.
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PMID:Evidence for a change in neurotransmitter affecting oesophageal motility in Parkinson's disease. 2 87

The uptake of tritiated dopamine and 5-hydroxytryptamine by platelets from 11 patients with Parkinsonism who were not receiving any medication, and from 11 control subjects matched for sex and for age within a decade was compared. No significant differences were found in the uptake of either amine. Our findings, therefore, provide no support for the belief that there is a generalised defect of dopamine systems in Parkinson's disease.
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PMID:Uptake of dopamine and 5-hydroxytryptamine by platelets of patients with Parkinsonism. 69 Jun 35

Plasma renin activity (PRA) of patients with Parkinson's disease was measured in recumbency, upright position, and after frusemide administration. The results show that the renin responses to both stimuli are significantly reduced as compared with those obtained in a group of normal subjects, while recumbent PRA levels of Parkinsonism patients are not significantly lower than those found in recumbent normal subjects. Levodopa treatment, alone or in combination with two different dopa-decarboxylase inhibitors, benserazide and carbidopa, does not modify the renin response to posture or to frusemide. Although the reduced activity of the renin-angiotensin system can play some role in the genesis of orthostatic hypotensive episodes encountered in patients with Parkinsonism, the greater incidence of orthostatis hypotension in patients treated with levodopa seems to be unrelated to any effect of this drug on the renin release.
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PMID:Effects of levodopa alone and in combination with dopa-decarboxylase inhibitors on plasma renin activity in patients with Parkinson's disease. 73 Dec 41

Intrapelvic migration of a threaded Steinmann pin complicated internal fixation of a displaced femoral neck fracture in an elderly man with untreated Parkinson's disease. Parkinsonian tremors may have contributed to this unusual complication. This case, in the light of a review of the literature, suggests that transfixation pins and wires should not be used in patients with Parkinson's disease. Endoprosthetic replacement combined with chemotherapy is better tolerated by femoral neck fractures in patients with Parkinsonism.
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PMID:Intrapelvic migration of a threaded Steinmann pin in Parkinson's disease. 99 98

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

The major symptoms of Parkinson's disease (PD) are due to degeneration of the nigrostriatal pathway and depletion of dopamine (DA). Tyrosine hydroxylase (TH), norepinephrine (NE), serotonin (5-HT), and melanin pigments are also decreased and acetylcholinergic activity increased. Biochemically, increased methylation can cause the depletion of DA, NE, 5-HT, and melanin pigments and also an increase of acetylcholine; thus, increased methylation can present a biochemical picture that resembles the biochemical changes that occur in PD. During the therapy of PD with L-dopa, it is well known that L-dopa reacts avidly with S-adenosyl-L-methionine (SAM), the biologic methyl donor, to produce 3-O-methyl-dopa. Correspondingly, L-dopa has been shown to deplete the concentration of SAM, and SAM has been found to induce PD-like motor impairments in rodents; therefore, an excess of SAM-dependent methylation may be associated with Parkinsonism. To further study the effects of methylation, SAM was injected into the lateral ventricle of rats. SAM caused tremors, rigidity, abnormal posture, and dose-related hypokinesia. Doses of 9.38, 50, and 400 nM/rat caused 61.9, 73.4, and 94.8% reduction, respectively, of motor activity. A 200-mg/kg IP dose of L-dopa, given before 50 nM SAM, blocked the SAM-induced hypokinesia. SAM also caused a decrease in TH immunoreactivity, apparent degeneration of TH-containing fibers, loss of neurons, and the accumulation of phagocytic cells in the substantia nigra. These results showed that excess SAM in the brain, probably due to its ability to increase methylation, can induce symptoms that resemble some of the changes that occur in PD.
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PMID:Parkinson's disease-like effects of S-adenosyl-L-methionine: effects of L-dopa. 135 75

A series of compensatory mechanisms within the dopaminergic system have been shown to maintain clinical function in the presence of dopamine loss. Experimental evidence for increased presynaptic dopamine turnover owing to increased dopamine synthesis, release, and reduced reuptake exists. Direct evidence that these mechanisms maintain extracellular dopamine levels is provided by intracerebral microdialysis techniques. Postsynaptic denervation supersensitivity clearly occurs with D2 dopamine receptors, although this is less evident with D1 receptors. Similarly, mechanisms of plasticity have been shown to be relevant in human postmortem and Positron Emission Tomographic studies of patients with Parkinson's disease. However, although presynaptic increases in dopamine turnover are well documented, postsynaptic D1 and D2 receptor changes have been more difficult to establish, mainly because of methodological difficulties. D2, but not D1, receptor increases have been documented in drug naive Parkinsonian patients with PET techniques. In transplantation of adrenal gland to striatum in animal models and patients with Parkinsonism where clinical improvement occurs, plasticity of host response may be as important as plasticity of the graft. Although some elements of the compensatory mechanism of dopamine plasticity may be deleterious, such as dyskinesias owing to dopamine receptor supersensitivity, the overall effect of delay and minimization of the clinical expression of disease is advantageous. An even greater understanding of the mechanisms involved may assist in developing future therapeutic strategies.
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PMID:Evidence for plasticity of the dopaminergic system in parkinsonism. 182 44

The Kraepelinian subtypes, developed early in the century, recognize the heterogeneity of schizophrenia but do not reliably predict differences in response to classical neuroleptics. The newer distinction of positive and negative syndromes in schizophrenia carry promise as an approach to identifying meaningful clinical and neurobiological dimensions. The present review summarizes the supportive evidence from a series of investigations using the Positive and Negative Syndrome Scale (PANSS), and a hypothesis on the pathophysiology of negative and positive symptoms is advanced. Our data suggest that: (a) positive and negative syndromes in schizophrenia represent stable, independent dimensions and not co-exclusive subtypes; (b) both are unrelated to the progression of illness; (c) they are differentially related to fundamental aspects of schizophrenia, including premorbid adjustment, cognitive development, family psychiatric history, the cognitive and neuropsychiatric profiles, dopaminergic functions, drug response, and subsequent course; (d) together with depression and excitement, they comprise the fundamental symptomatic components of schizophrenia, which, in their interaction, can account for the specific Kraepelinian subtypes. We have proposed that negative symptoms represent the core pathology in schizophrenia and may be understood as a variant of parkinsonism, hence characterized by dopaminergic deficiency and increased cholinergic activity. This view is supported by the striking overlap with Parkinsonism in regard to clinical features, neurochemistry, pharmacology, neuropathology, and neuroradiology. Positive symptoms are thought to reflect increased dopaminergic activity, which may arise as a compensatory adaptive mechanism to overcome the progressive dopamine loss in the maturing brain. The early onset of schizophrenia by comparison to Parkinson's disease may explain why schizophrenia entails more pronounced positive symptoms, development deficits, and cognitive, social, and emotional impairments. We describe evidence that pineal calcification, which may reflect disturbance of melatonin functions, appears to be a nongenetic factor in schizophrenia associated with perinatal injury. This may in part underlie the negative syndrome and its response to antipsychotic compounds with serotonergic (5-HT) antagonism.
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PMID:Experimental models of schizophrenia. 193 75

The positive-negative distinction of schizophrenia has emerged as a valid means of clarifying its heterogeneity. Despite evidence that the two symptom classes may reflect different dimensions of the disease, there is presently no integrated model for understanding of the pathophysiology of these symptoms and their co-occurrence in schizophrenia. We propose that negative phenomena of schizophrenia may be a variant of Parkinsonism. This view is supported by the overlap with Parkinsonism in terms of clinical features, neurochemistry, pharmacology, as well as neuroradiological and neuropathological aspects. As such, negative symptoms may be a manifestation of disease of the basal ganglia and constitute the core pathology in schizophrenia. Positive symptoms, conversely, may reflect an "accessory" process related to a compensatory increase in striatal and limbic dopamine activity following an injury to the dopaminergic system. In the present communication we present a series of studies that support the association of negative schizophrenia and Parkinsonism. Based on this evidence, we suggest that schizophrenic patients with prominent negative symptoms might be managed like patients with Parkinson's disease, namely, with dopaminergic drugs and MAO-B inhibitors. Finally, the association of negative schizophrenia with Parkinsonism raises the possibility that adrenal medullary tissue transplantation, which may benefit a selected group of Parkinsonian patients, may be a future promising therapy for refractory negative schizophrenia.
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PMID:The relationship of negative schizophrenia to parkinsonism. 214 20

Multiple system atrophy (MSA) is generally considered a rare disease, but may account for up to 10% of patients with Parkinsonism. The profusion of names for this disease, which may present to general physicians, psychiatrists, cardiologists, autonomic specialists, general neurologists and those with a special interest in Parkinsonism (this author's own perspective) or cerebellar disorders, together with ignorance of its protean manifestations, may account for its underrecognition and misdiagnosis. In this article, the history and nosology of the condition are considered, and provisional diagnostic criteria are advanced. The usefulness (or otherwise) of ancillary investigations is addressed, and the shortcomings of current methods of treatment are stressed. As with idiopathic Parkinson's disease, the ultimate goal of eradicating the disease entails better diagnosis in order to establish the cause, and thence to develop a radical treatment capable of preventing or arresting the disease process.
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PMID:Multiple system atrophy--the nature of the beast. 266 81


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