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)

We analyzed the results of the Sickness Impact Profile, a self-reporting measure of sickness-related dysfunction in 753 essential tremor (ET) patients, 87 controls from the general population, and 145 patients with Parkinson's disease (PD). Compared with the general population, ET patients had significantly greater dysfunction in all but one category. Communication, Work, Emotional Behavior, Home Management, and Recreation and Pastimes were particularly impaired in ET. The PD patients had significantly higher dysfunction in all categories as compared with ET patients. We conclude that significant disability can occur in ET and, compared with PD, ET tends to be less severe but causes relatively greater psychosocial dysfunction.
Neurology 1991 Dec
PMID:Is essential tremor benign? 174 59

There is substantial evidence that electroconvulsive therapy (ECT) can ameliorate the symptoms of Parkinson's disease independent of any antidepressant activity. ECT thus presents a treatment alternative for the severely impaired, medication-resistant Parkinson's patient. In this article, we review the literature on this subject and present our recommendations for current clinical practice.
Psychiatr Clin North Am 1991 Dec
PMID:Treatment of Parkinson's disease with electroconvulsive therapy. 177 Nov 54

Recent studies have suggested that deprenyl may exert a neuroprotective influence and thus retard progression of Parkinson's disease (PD). On the other hand, the data do not disprove that deprenyl is primarily another form of symptomatic therapy like levodopa. Longitudinal Gompertzian analysis demonstrates the absence of beneficial alteration of intrinsic or environmental influences on the epidemiology of PD mortality after the introduction of levodopa. Moreover, this method demonstrates the basis for the enhanced survival in PD that resulted from the efficacy of levodopa as symptomatic therapy. If deprenyl becomes standard therapy in PD and exerts a beneficial (neuroprotective) influence on intrinsic and environmental pathogenic mechanisms, this will become evident by a decrease in the PD mortality rate in the United States in men at age 73.4 years and in women at age 79.1 years. The ability to accurately assess the overall impact of new therapies on the general population is increasingly important in an era of upward spiraling health care costs. Longitudinal Gompertzian analysis is a simple method of detecting and distinguishing between symptomatic (competitive) and protective (intrinsic and environmental) influences on disease mortality at the population level after the introduction of new therapies.
Clin Neuropharmacol 1991 Dec
PMID:Parkinson's disease: an epidemiologic method for distinguishing between symptomatic and neuroprotective treatments. 177 20

A series of computational models were developed to better understand basal ganglia functions and the effects of levodopa pharmacodynamics in Parkinson's disease. The models employed a relatively new computational approach known as a neural network, which is a small number of simple processing units interconnected with designated constraints. A key difference from traditional computational modeling is that the networks are "trained" rather than programmed with experimental input and output data. After training, only a limited number of these models, could explain the pharmacodynamic data observed by Mouradian et al. in different groups of Parkinsonian patients. These successful models strongly argue for at least two pharmacologic mechanisms to explain the antiparkinsonian effect and dyskinesia tendency for the different classes of Parkinson's patients: never-treated, stable, wearing-off, and on-off. They suggest different roles for the striatal units by examining predictions of motor and dyskinesia tendency through theoretical blockade of each kind of unit. The models show that the antiparkinsonian effect in Parkinson's disease cannot be explained by the action of dopaminergic neurons on striatal neurons alone. Although the models necessarily oversimplify basal ganglia function, they provide a useful quantitative insight into how motor and dyskinesia behaviors may develop in different Parkinsonian subgroups.
Clin Neuropharmacol 1991 Dec
PMID:A computational model of levodopa pharmacodynamics in Parkinson's disease. 177 21

Several hypotheses have explained the beneficial effect of adding bromocriptine (BR) to levodopa (LD) in Parkinson's disease (PD) by interaction at the striatal level. In the present study we show the influence of BR on plasma LD values in an acute loading experiment (125 mg LD + 12.5 mg carbidopa [DCI] given alone and together with 2.5 mg BR at 0 time; 4 h observation). On the basis of this influence we have been able to differentiate between three groups of patients: (a) in six patients (five of them with frequent off episodes) LD values were significantly lower (p less than 0.05) when both drugs were given together (area under the curve [AUC] +/- SE 2.10 +/- 0.42 micrograms/ml/h vs. 4.96 +/- 1.10 micrograms/ml/h); (b) in eight patients (one with frequent akinesia) LD levels were significantly higher (p less than 0.003) when both drugs were given together (AUC +/- SE 4.05 +/- 0.51 micrograms/ml/h vs. 1.94 +/- 0.19 micrograms/ml/h); (c) in six patients (without motor fluctuations) no difference in LD levels was noted (AUC +/- SE 3.91 + 0.62 micrograms/ml/h vs. 3.81 +/- 0.70 micrograms/ml/h). The clinical evaluation (Webster scale) did not show substantial differences, except for increased dyskinesia, which correlated with higher LD levels. In summary, we suggest that the diminution of motor fluctuations and the occurrence of dyskinesias when BR is added to LD may stem from changes in LD plasma levels. These findings would be taken into consideration in the interpretation of therapeutic response fluctuations under combined treatment.
Clin Neuropharmacol 1991 Dec
PMID:The influence of bromocriptine on the pharmacokinetics of levodopa in Parkinson's disease. 177 22

Subcutaneous apomorphine is a useful treatment for refractory motor fluctuations in Parkinson's disease. We have now clinically evaluated a formulation of sublingual apomorphine (57 mg) and performed preliminary pharmacokinetic studies. In acute studies, all 10 patients switched "on" after a mean latency of 25 min with a mean duration of motor benefit of 118 min. In three patients followed for a mean of 4.7 months, we have shown that chronic sublingual use can be effective, safe, and convenient in controlling motor fluctuations. The pattern of clinical response followed closely the plasma profile of apomorphine with a mean Cmax of 76 pmol/ml (50-106 pmol/ml) and a mean Tmax of 60 min (45-80 min), with moderate interpatient variability in bioavailability. Sublingual apomorphine is a practical alternative to subcutaneous use in selected patients with severe motor fluctuations.
Clin Neuropharmacol 1991 Dec
PMID:Sublingual apomorphine in the treatment of Parkinson's disease complicated by motor fluctuations. 177 24

In this review the experimental background for treatment of patients with Parkinson's disease by intracerebral transplantation is presented. Intracerebral transplantation has been performed either with the patients own adrenal medulla or with human fetal dopaminergic neurons obtained from abortions. Intracerebral transplantation of adrenal chromaffin cells to rodents has shown poor cell survival and minor, transient effects on experimentally induced parkinson-like symptoms. Intracerebral autotransplants of medullary adrenal tissue to patients with Parkinson's disease have shown corresponding, minor improvements in the parkinson status. Animal experiments with grafting of developing fetal dopaminergic neurons have been more rewarding and resulted in reversal of parkinson-like symptoms. Experimental transplantations with human fetal dopaminergic neurons to patients with Parkinson's disease have not entirely lived up to these expectations. At a recent meeting, arranged to set up a European network for research and information, it was agreed that more animal experiments, in particular including non-human primates are needed. Regarding the clinical trials with transplantation of human fetal dopaminergic tissue coordination of neurological test procedures performed pre- and posttransplantation was strongly recommended.
Ugeskr Laeger 1991 Dec 09
PMID:[Experimental clinical transplantation in patients with Parkinson disease. Experimental background and clinical picture]. 177 97

An autopsy case of spinal arteriovenous malformation (AVM) was reported. The patient was a 75-year-old male and his initial neurologic symptoms were paraplegia, paresthesia below the umbilical level and urination difficulty. Subsequently night delirium and parkinsonism also appeared. The clinical and pathological findings in this case are identical with those in the spinal AVM except for Parkinson's disease. In addition, the lateral funiculus of the spinal cord in the middle thoracic segment showed pallor: Under light microscopy, the funiculus was spongiform, with a thinner wall of the myelin sheath, enlargement of the axon and the perivascular infiltration of phagocytes without plasma exudation. The changes in the lateral funiculus seemed to indicate early congestive changes.
Acta Med Okayama 1991 Dec
PMID:An autopsy case of spinal arteriovenous malformation (Foix-Alajouanine syndrome). 178 2

Twelve patients with idiopathic Parkinson's disease had acoustic speech analysis of sentence utterances to provide information on speech tempo and accuracy of articulation. As a measure of rate of speech the duration of opening-closing movements during articulation was determined from speech wave variables. The intensity of sound emission during articulatory closure as required for stop consonant production, for example, magnitude of p, magnitude of t, magnitude of k, was used as an index of the degree of closure. Speech tempo was not significantly different from normal. The patients, however, had a reduced capacity of completing articulatory occlusion. This was interpreted as reflecting a reduction in movement amplitude of the articulators. Articulatory "undershoot" was not uniform but influenced by linguistic demands in that the closures associated with a stressed syllable were performed at the expense of unstressed ones. Furthermore, switching between opening and closing movements of the articulators in sentence production seemed undisturbed. These results indicate that motor planning of speech differs from arm movement control.
J Neurol Neurosurg Psychiatry 1991 Dec
PMID:Articulatory deficits in parkinsonian dysarthria: an acoustic analysis. 178 24

Harding et al. suggested at first that an increase of P2 latency in flash VEP without an increase of P2 latency in pattern reversal VEP may be a diagnostic marker of Alzheimer's disease. Up to now there is no convincing evidence for this hypothesis. The purpose of the present study was to examine this hypotheses in an extended group of patients with Alzheimer's disease (n = 36). In addition, a group of patients with Parkinson's disease (n = 8) without dementia syndrome and a group of healthy elderly controls (n = 46) was investigated in order to determine the sensitivity and specificity of these VEP parameters. The results confirmed significant group differences between patients with Alzheimer's disease and healthy controls concerning the increase of Flash P2 latency and unchanged latency of P2 in the pattern reversal VEP. No significant correlations were found between duration of illness and mental test scores. The group differences of P2 latency in the flash VEP for patients with Parkinson's disease and healthy controls were also significant. Therefore, the increase of flash P2 latency in VEP does not seem to be specific for Alzheimer's disease nor for dementia syndrome. The pathological mechanism causing the flash P2 latency increase in a remarkable number of neuropsychiatric patients should be elucidated in further experimental investigations.
EEG EMG Z Elektroenzephalogr Elektromyogr Verwandte Geb 1991 Dec
PMID:[Visual evoked potentials in Alzheimer's and Parkinson disease]. 178 86


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