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)

Parkinson's disease (PD) is frequently associated with psychiatric problems. Depression generally responds to antidepressant medications or to electroconvulsive therapy (ECT). The nondepressive psychoses generally require a reduction in parkinsonian medications, or possibly a "drug holiday." In patients whose psychosis fails to respond to a reduction in medication or who cannot tolerate the worsening parkinsonism, an antipsychotic drug should be added. Clozapine is probably the drug of choice, with low potency neuroleptics being second-line options.
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PMID:The management of the levodopa psychoses. 168 May 56

The introduction of levodopa in the treatment of Parkinson's disease had modified both the prognosis and the current concepts of the disease, Although levodopa remains the most potent drug for the treatment of Parkinson's disease, its long-term use is associated with fluctuations in motor performance, abnormal movements and psychotic hallucinations. These late side-effects remain difficult to treat and thus raise questions as to the benefits and risks of first-time treatment with levodopa. Levodopa mainly alleviates akinesia and rigidity and to a lesser extent, tremor. Levodopa increases life expectancy. This paper reviews some recent developments in the pharmacology of Parkinson's disease. Recent findings indicate that not only central dopamine but also several other central neurotransmitter and receptor changes are involved in the pathophysiology of Parkinson's disease. New data on autonomic dysfunction in Parkinson's disease are presented. New methods of investigation (clinical rating scales, pharmacological tests, imaging techniques, etc.) are reviewed. Finally, future strategies, e.g. the development of potent new symptomatic drugs (selective D2 and D1 agonists, new formulations of apomorphine, COMT inhibitors, new routes of administration, etc.) and etiopathogenic agents (antioxidative and anti-free radical drugs, etc.) are discussed.
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PMID:Recent advances in the clinical pharmacology of Parkinson's disease. 168 24

There is evidence to suggest that glutamate and other excitatory amino acids play an important role in the regulation of neuronal excitation. Glutamate receptor stimulation leads to a non-physiological increase of intracellular free Ca2+. Disturbed Ca2+ homeostasis and subsequent radical formation may be decisive factors in the pathogenesis of neurodegenerative diseases. Decreased glutamatergic activity appears to contribute to paranoid hallucinatory psychosis in schizophrenia and pharmacotoxic psychosis in Parkinson's disease. It has been suggested that a loss of glutamatergic function causes dopaminergic over-activity. Imbalances of glutamatergic and dopaminergic systems in different brain regions may result in anti-akinetic effects or the occurrence of psychosis. The simplified hypothesis of a glutamatergic-dopaminergic (im)-balance may lead to a better understanding of motor behaviour and psychosis.
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PMID:Glutamate receptor antagonism: neurotoxicity, anti-akinetic effects, and psychosis. 168 83

A case report and a review of the literature concerning electroconvulsive therapy (ECT) in the treatment of Parkinson's disease with special reference to the therapy of "on-off" phenomena is given. The first report of positive effect appeared in 1959 and, with a single exception, all published articles on this topic point to a positive outcome of ECT. There seems to be a specific anti-Parkinsonian effect alongside the well-known effect on various psychotic conditions. ECT thus must be considered a valuable intervention when drug therapy is insufficient, when prolonged medication leads to decreased efficacy, or when patients develop neuro-psychiatric manifestations. A short review of the pathophysiological mechanisms which may underly the effect of ECT in Parkinson's disease is given.
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PMID:[Electric stimulation (ECT) in Parkinson disease]. 173 41

Clinical and neuropathologic data in 45 patients with Parkinson's disease (PD) were compared. Twenty-seven patients suffered from marked akinesia and rigidity (AR-type) and 18 patients from predominant resting tremor (T-type). Dementia, depression, and psychosis occurred in 26, 18, and 18 patients, respectively. Neuronal counts were performed in defined areas of the medial and lateral substantia nigra (SNM, SNL), locus ceruleus (LC), and dorsal raphe nucleus (DRN). The AR-type (compared with the T-type) showed higher neuronal loss of LC, SNL, SNM, and more severe gliosis, extraneuronal melanin deposits, and neuroaxonal dystrophy in substantia nigra. Demented PD patients showed more intense cortical Alzheimer lesions and higher neuronal depletion in the SNM, whereas PD subjects with moderate or marked dementia differed from mildly or not demented ones only in the higher degree of cortical Alzheimer lesions. More severe neuronal cell loss of DRN was observed in PD patients with depression. Occurrence of psychosis was not associated with any pathologic feature. Our findings indicate that some major clinical features of PD are related to distinct neuropathologic lesions.
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PMID:The neuropathologic basis of different clinical subgroups of Parkinson's disease. 174 81

A total of 240 patients of Parkinson's disease (PD) were studied (125 male, 115 female). The age of onset was 60.0 +/- 9.9 years(Y) (mean +/- S.D.) (range 30-87). A 0-4 rating score was applied on each of 6 major symptoms: i.e. tremor, rigidity, bradykinesia, gait, activities of daily living and fluctuation with maximum score of 24. According to the Hoehn and Yahr's stages, there were 44 cases in stage I, 141 in stage II, 31 in stage III, 19 in stage IV and 5 in stage V. Fluctuation in symptoms occurred in 42.9%, dyskinesia in 7.1%, psychosis in 9.6%, depression in 4.6%, and dementia in 2.9%. The mean duration of PD was 4.9 +/- 4.5 Y with 40% 5 years or longer. Significantly longer duration of PD was seen in the patients suffering from fluctuation (6.7 +/- 4.7 Y), dyskinesia (10.7 +/- 6.7 Y) and psychosis (9.4 +/- 6.5 Y). The mean duration of L-dopa treatment was 4.1 +/- 3.4 Y. The patients showing fluctuation (6.2 +/- 4.0 Y) or dyskinesia (7.6 +/- 4.7 Y) had significantly longer duration of L-dopa treatment. The mean daily dose of L-dopa was 370 +/- 203 mg. The patients with fluctuation (430 +/- 187 mg) or dyskinesia (545 +/- 265 mg) received significantly higher dose of L-dopa. Dementia tended to occur in the patients having later age of onset of PD (71.2 +/- 11.2 Y). The symptom score was significantly worse in those with fluctuation, dyskinesia, psychosis and dementia. It was well correlated with the Hoehn and Yahr's staging system.
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PMID:Abbreviated rating score for Parkinson's disease. 184 38

No clear general view has emerged from the many recent studies devoted to cognitive disorders in Parkinson's disease. Disparity of the populations and methods, as well as interference from motor disorders and possible psychiatric disorders account for the variability of epidemiological data. Subtle cognitive disorders can be found in most patients at the very beginning of the disease. Recent memory is disturbed in free recall tests, but recognition capacities are preserved. Individualization of visuospatial disorders is discussed. Alteration of conceptual capacities is the predominant disorder. Clinically obvious cognitive disorders appear only in some patients after several years of neurological disease. Some risk factors are agreed upon. The bradyphrenia concept is debated, and the term dementia is not accepted by all authors. The major cognitive alterations in Parkinson's disease differ from those observed in Alzheimer dementia, but the latter is more frequent in parkinsonian patients than in the general population. Patients with Parkinson's disease are also exposed to the risk of transient psychotic episodes. Where parkinsonian cognitive pathology is concerned, modern imaging methods are of no help to clinicians. The anatomical and biochemical changes observed in these patients are reviewed, and their responsibility in the genesis of cognitive disorders is discussed: lesions of brainstem nuclei and alterations in their cortical projections on one side, Alzheimer type dementia lesions and Lewys' bodies on the other side. The diverse and inconstant cognitive disorders of patients with Parkinson's disease cannot be explained by lesions of one single structure; they probably result from variable combinations of multiple known or unknown neuronal and biochemical changes.
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PMID:[Cognitive deficits in Parkinson's disease]. 185 32

The subjects were 20 patients with Parkinson's disease. They were aged 52 to 76 years and the duration of the disease ranged from four to 25 years (mean, 12.5 years). All the patients were receiving levodopa alone or in combination with tricyclic antidepressants, amantadine, bromocriptine, anticholinergic agents, or lisuride. Each patient received 1,000 mg of citicoline intramuscularly daily for 15 days and then 500 mg daily for 15 days. After 30 days of treatment, the scores on the Columbia rating scale improved 7.3%; rigidity was improved 18.8%; times to walk 10 m and turn over were reduced 17.5% and 37.4%; and the handwriting test scores improved 19.7%. No side effects were reported. Four patients with advanced parkinsonian symptoms and psychotic side effects received 2,000 mg of citicoline subcutaneously or intravenously for seven days. No improvements in symptoms or treatment side effects were noted.
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PMID:Citicoline in the treatment of Parkinson's disease. 186 39

It is known that the anticholinergic drug causes acute psychosis and memory disturbance, which may be due to cholinergic dysfunction. But it has not been well described that the anticholinergic drug causes chronic dementia after long administration. We describe six cases of chronic dementia, which is thought to be induced by anticholinergic drug. We conducted detailed neuropsychological and neuroradiological examination in these six cases. All of them were Parkinson's disease, and had used anticholinergic drug for more than six months without any side effect, and then their initial symptom of dementia appeared, followed by chronic dementia. All cases recovered reversibly from dementia within a few weeks after stoppage of taking anticholinergic drug. And any of our cases had no possibility in the cause of chronic dementia other than the side effect of anticholinergic drug. Detailed neuropsychological examinations (WAIS, WMSR, and so on) were conducted in all cases, SPECT was in two cases, and PET was in one case, before and after stoppage of the anticholinergic drug. And in all cases, brain MRI was conducted. The indices of attention, verbal memory, visual memory, and delayed recall were significantly elevated after stoppage of drug. And both verbal IQ and performance IQ were increased after stoppage of drug, too. SPECT and PET revealed significant improvement, which showed diffuse and generalized change, not localized change.
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PMID:[Chronic dementia in Parkinson disease treated by long-term administration of anticholinergic drug--evaluation of neuropsychological test, PET, and SPECT]. 193 77

A variety of neuropharmacologic agents, including anticholinergic drugs, amantadine hydrochloride, levodopa, selegiline, bromocriptine, and pergolide, are now available for the treatment of Parkinson's disease. Of patients treated with dopaminergic agents, 30% develop visual hallucinations, 10% exhibit delusions, 10% have euphoria, 1% have mania, 10% to 15% experience increased anxiety, 15% have confusional periods, and a few exhibit altered sexual behavior. Anticholinergic drugs have a greater tendency to produce confusional states than dopaminergic compounds. Elderly patients and those with underlying dementia are most likely to have untoward side effects with anti-parkinsonism treatment. Dosage reduction is the optimum management strategy, although anti-psychotic agents may be necessary in patients with delusions, and lithium may help control drug-induced mania. Dopaminergic agents share the property of stimulation of D2 dopamine receptors, and this action may play an essential role in mediating their neuropsychiatric effects.
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PMID:Behavioral complications of drug treatment of Parkinson's disease. 206 39


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