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 have recorded movement-related cortical potentials (MRCPs) preceding voluntary finger extension from 10 subjects with Parkinson's disease and compared the results with those obtained from groups of young and old subjects described in the previous paper in this volume (Barrett et al. 1986). Three separate potential shifts preceding voluntary movement were identified in the wave forms of all subjects. There were no differences between the healthy aged subjects and those with Parkinson's disease in terms of the onset latencies or gradients of these potential shifts. The potential shift associated with the final phase of preparation (NS') was significantly less widespread over central scalp for the older subjects compared with the young. Equivalent results for a 35-year-old subject with Parkinson's disease were indistinguishable from those obtained from the young subjects suggesting that this restriction in the distribution of NS' is related to normal ageing rather than the disease process of parkinsonism. There were no differences within the group of parkinsonian subjects with respect to potential shifts associated with differing degrees of movement disability between the two hands. Our results contradict previous reports of abnormal MRCPs in Parkinson's disease (Deecke et al. 1977; Deecke and Kornhuber 1978; Shibasaki et al. 1978). We attribute this primarily to an improved method of recording MRCP which compensates for time jitter between EMG onset and the production of a trigger pulse for averaging (Barrett et al. 1985).
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PMID:Cortical potential shifts preceding voluntary movement are normal in parkinsonism. 241 91

Cognitive problems are a major factor determining quality of life of patients with Parkinson's disease. These include deficits in inhibitory control, ranging from subclinical alterations in decision-making to severe impulse control disorders. Based on preclinical studies, we proposed that Parkinson's disease does not cause a unified disorder of inhibitory control, but rather a set of impulsivity factors with distinct psychological profiles, anatomy and pharmacology. We assessed a broad set of measures of the cognitive, behavioural and temperamental/trait aspects of impulsivity. Sixty adults, including 30 idiopathic Parkinson's disease patients (Hoehn and Yahr stage I-III) and 30 healthy controls, completed a neuropsychological battery, objective behavioural measures and self-report questionnaires. Univariate analyses of variance confirmed group differences in nine out of eleven metrics. We then used factor analysis (principal components method) to identify the structure of impulsivity in Parkinson's disease. Four principal factors were identified, consistent with four different mechanisms of impulsivity, explaining 60% of variance. The factors were related to (1) tests of response conflict, interference and self assessment of impulsive behaviours on the Barrett Impulsivity Scale, (2) tests of motor inhibitory control, and the self-report behavioural approach system, (3) time estimation and delay aversion, and (4) reflection in hypothetical scenarios including temporal discounting. The different test profiles of these four factors were consistent with human and comparative studies of the pharmacology and functional anatomy of impulsivity. Relationships between each factor and clinical and demographic features were examined by regression against factor loadings. Levodopa dose equivalent was associated only with factors (2) and (3). The results confirm that impulsivity is common in Parkinson's disease, even in the absence of impulse control disorders, and that it is not a unitary phenomenon. A better understanding of the structure of impulsivity in Parkinson's disease will support more evidence-based and effective strategies to treat impulsivity.
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PMID:Multiple modes of impulsivity in Parkinson's disease. 2446 78