Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0030567 (Parkinson's disease)
63,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. In the human brain, DA was found in appreciable amounts in most of the examined basal telencephalic limbic regions, with the nucleus accumbens having the highest mean level (3.38 microgram/g). In the cortical areas of the limbic lobe of Broca, DA could be measured with certainty only in the parolfactory gyrus (0.35 microgram/g). 2. In patients with Parkinson's disease, the DA concentration in the parolfactory gyrus and nucleur accumbens was markedly reduced, whereas little change was seen in the olfactory areas. Quantitatively, the DA decrease in the nucleus accumbens was of the same magnitude as in the caudate nucleus, being, in both regions, distinctly less severe than in the putamen. 3. In three cases of paranoid schizophrenia, there were no statistically significant changes of the mean levels of DA or HVA in the nucleus accumbens. However, the DA/HVA ratio was shifted noticeably in favor of HVA, possibly indicating an increase in DA turnover. This change was less pronounced in the putamen of these cases and was absent in the caudate nucleus. 4. The possibility of the substantia nigra contributing to the dopaminergic innervation of the human nucleus accumbens, as well as the significance of the observations on DA metabolism in the schizophrenic cases, is discussed.
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PMID:Dopamine in thelimbic regions of the human brain: normal and abnormal. 88 59

In brain capillary endothelium and catecholaminergic terminals a single decarboxylation step effected by aromatic amino-acid decarboxylase converts phenylalanine to phenylethylamine, at a rate comparable to that of the central synthesis of dopamine. Phenylethylamine, however, is not stored in intra-neuronal vesicles and is rapidly degraded by monoamine oxidase-B. Despite its short half-life, phenylethylamine attracts attention as an endogenous amphetamine since it can potentiate catecholaminergic neurotransmission and induce striatal hyperreactivity. Subnormal phenylethylamine levels have been linked to disorders such as attention deficit and depression; the use of selegiline (Deprenyl) in Parkinson's disease may conceivably favour recovery from deficient dopaminergic neurotransmission by a monoamine oxidase-B inhibitory action that increases central phenylethylamine. Excess phenylethylamine has been invoked particularly in paranoid schizophrenia, in which it is thought to act as an endogenous amphetamine and, therefore, would be antagonized by neuroleptics. The importance of phenylethylamine in mental disorders is far from fully elucidated but the evolution of phenylethylamine concentrations in relation to symptoms remains a worthwhile investigation for individual psychotic patients.
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PMID:Does phenylethylamine act as an endogenous amphetamine in some patients? 1128 91

A 52-year-old patient with treatment-resistant paranoid schizophrenia developed severe parkinsonian features after more than 20 years of antipsychotic drug therapy. The role of this therapy was thought to have been a contributing factor to the patient's clinical presentation, although Parkinson's disease could not be ruled out. Originally, parkinsonian symptoms developed acutely and progressed to hand tremor, sialorrhea, upper body rigidity, masked facies, striatal hand, bradykinesia, and a severe, unsteady, shuffling gait. Tremor and rigidity were the only parkinsonian symptoms that responded to anticholinergic therapy. After converting from a first- to a second-generation antipsychotic drug, the patient maintained psychiatric stability, with some improvement in motor functioning-most notably decreased upper body rigidity. Our findings are consistent with the literature on quetiapine therapy in patients with Parkinson's disease in terms of adequately controlling psychosis without worsening motor symptoms. The difference, however, was that in most cases reported, psychotic features were the result of dopamine-enhancing treatments and not schizophrenia.
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PMID:Quetiapine use in a patient with chronic schizophrenia and severe parkinsonism. 1623 27

The Capgras syndrome (CS) is a rare psychiatric disorder. CS is classified as a delusional misidentification syndrome. Initially, CS was described in paranoid schizophrenia and schizoaffective disorders. CS has also been reported in neurodegenerative diseases such as Alzheimer's disease and Lewy body dementia. To date, there are very few descriptions of the occurrence of CS in idiopathic Parkinson's disease (PD), with or without dementia. Considering the recent observation of two new cases in PD patients, a systematic overview of the literature published between 1976 and 2016 reporting CS in PD was conducted. The purpose of this article is to examine the phenomenon in people with PD with and without dementia, the psychopathologic context in which it happened, the role played by the dopaminergic medications and to define useful therapeutic strategies. Our CS cases occurred in two elderly patients with advanced PD and cognitive impairment, respectively, after an acute stressor event and after an increase of the total daily dose of levodopa. In light of our observations and the cases reported in the literature, we argue that CS is an acute or subacute psychotic disorder occurring mostly in PD with dementia. Besides, the increase in brain dopamine levels induced by acute stressful events and/or dopamine-enhancing medications should be considered as a possible causal mechanism of CS in patients with advanced stages of PD and cognitive decline.
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PMID:Capgras syndrome in Parkinson's disease: two new cases and literature review. 2784 17

Comorbidity of idiopathic Parkinson's disease (IPD) and schizophrenia is an uncommon and rare scenario, which often poses a difficult and challenging situation for management. Both the disorders have completely opposite pathophysiology and treatment of one disorder with available pharmacological agents can pose a threat to the other disorder. The situation becomes graver and risk of adverse side effects increases when an individual presents at a later age with both these disorders along with compromised physical and mental health. Of all the available psychopharmacological agents, clozapine has been found to be quite helpful for the management of psychosis without deterioration of existing movement problems of Parkinson's disease. In this case report, we present the case of a 60-year-old female with long-standing paranoid schizophrenia for the last 30 years, who later developed IPD and discuss the various management issues encountered during her treatment.
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PMID:Schizophrenia with Comorbid Idiopathic Parkinson's Disease: A Difficult Clinical Management Scenario. 2928 23