Minimal hepatic encephalopathy and extrapyramidal signs in patients with cirrhosis.
ABSTRACT Two types of neurological dysfunction can occur in compensated cirrhosis: 1) extrapyramidal signs related to the accumulation of manganese in the basal ganglia and 2) milder degrees of cognitive impairment known as minimal hepatic encephalopathy (mHE). We assessed whether there was any relationship between both disorders in 42 patients with compensated cirrhosis.
Minimal hepatic encephalopathy was diagnosed using a battery of manual neuropsychological tests. Cognitive functioning was assessed by the Mini-Mental State Examination. Extrapyramidal signs were evaluated by the Columbia scale.
Minimal hepatic encephalopathy was diagnosed in 15 (35.7%) patients. A total of 52.4% of patients showed significant extrapyramidal signs. Scores for the Columbia scale were higher in the presence of mHE (mean +/- SD, 16.0 +/- 10.9 vs 5.3 +/- 7.1, p = 0.0004). In the bivariate analysis, mHE, Child-Pugh score, and Mini-Mental State Examination score were significantly associated with extrapyramidal signs, whereas in the multivariate analysis, mHE was the only independent variable related to extrapyramidal signs.
There was a link between extrapyramidal signs and diagnosis of mHE based on manual neuropsychological testing. This finding may be explained by the influence of extrapyramidal manifestations on test performance or by a real pathophysiological relationship between both disorders. Further studies are necessary to resolve this question.
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ABSTRACT: We explored the nature of the visuospatial deficit in Parkinson's disease (PD) and its progression as a function of disease duration. We compared the performance of 183 patients with idiopathic PD and 90 control subjects matched for age and education on six visuospatial measures. We divided patients into three groups according to the disease duration: early (1 to 4 years), middle (5 to 10 years), and advanced (greater than 10 years). Performance deteriorated in five of the six visuospatial measures, as a function of disease duration. However, the pattern of visuospatial decline depended on whether dementia was present. The results were not influenced by age or anticholinergic medication. These findings support the presence of visuospatial deficits in PD patients, with a changing pattern of impairment related to dementia and progression of the disease.Neurology 04/1991; 41(3):365-9. · 8.25 Impact Factor
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ABSTRACT: Neuropsychological investigations of patients with Parkinson's disease have shown specific impairments even in the early stages of the disease, which include deficit of behavioural regulation in sorting or planning tasks, defective use of memory stores, and impaired manipulation of internal representation of visuospatial stimuli. These deficits, reported in a disease which predominantly involves subcortical structures, have drawn attention to a potential role of the basal ganglia in cognitive processes. Given the modulatory role of the basal ganglia, these disorders might result from more fundamental deficits concerning the allocation of attentional resources, the temporal organization of behaviour, the maintenance of representations in working memory or the self-elaboration of internal strategies, all of which resemble dysfunctions of processes that are commonly considered to be controlled by the frontal lobes. This suggests a functional continuity or complementarity between the basal ganglia and association areas of the prefrontal cortex. The recent description in primates of segregated loops that interconnect discrete regions of the caudate nucleus to the dorsolateral and orbitofrontal regions of the prefrontal cortex via the thalamus may give some support to this hypothesis. Alternatively, degeneration of the ascending cholinergic and catecholaminergic neuronal systems may contribute, at least in part, to the occurrence of this frontal-lobe-like symptomatology associated with Parkinson's disease.Journal of Neurology 02/1997; 244(1):2-8. · 3.58 Impact Factor
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