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Query: UMLS:C0030567 (Parkinson's disease)
 63,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The prevalence of overt dementia in 27 studies representing 4,336 Parkinson's disease (PD) patients was 39.9%. The studies reporting the highest incidence of intellectual impairment (69.9%) used psychologic assessment techniques, whereas studies identifying the lowest prevalence of dementia (30.2%) depended on nonstandardized clinical examinations. Neuropsychologic investigations reveal that PD patients manifest impairment in memory, visuospatial skills, and set aptitude. Language function is largely spared. Intellectual deterioration in PD correlates with age, akinesia, duration, and treatment status. Neuropathologic and neurochemical observations demonstrate that PD is a heterogeneous disorder: the classic subcortical pathology with dopamine deficiency may be complicated by atrophy of nucleus basalis and superimposed cortical cholinergic deficits, and a few patients have the histopathologic hallmarks of Alzheimer's disease. Mild intellectual loss occurs with the classic pathology, and the more severe dementia syndromes have cholinergic alterations or Alzheimer's disease. Thus, PD includes several syndromes of intellectual impairment with variable pathologic and neurochemical correlates.
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PMID:Intellectual impairment in Parkinson's disease: clinical, pathologic, and biochemical correlates. 290 99

An understanding of the causes, nature, and course of intellectual impairment in Parkinson's disease (PD) is essential for the correct development of therapy. This article reviews the causes of the dementia of PD, its primary clinical and pathological features, and its course.
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PMID:The dementia of Parkinson's disease. 306 60

Disruption of neural activity within the basal ganglia of experimental animals causes selective learning deficits in tasks requiring switching between response strategies. These data along with reports of both general and specific intellectual impairment in patients with neurodegenerative disorders such as Parkinson's disease, appear to support the theory of cognitive functions of the basal ganglia. Recent studies have failed to confirm general cognitive or memory deficits in parkinsonian patients, but have identified deficiencies in devising and executing certain cognitive strategies. Following the lead of theorists such as Squire and Mishkin, this brief review emphasizes the distinction between procedural and declarative knowledge and examines the possible role of the basal ganglia in the acquisition and retention of procedural knowledge.
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PMID:Cognition and the basal ganglia: a possible substrate for procedural knowledge. 331 45

Speech and language alterations were assessed in 51 patients with Parkinson's disease (PD) and 10 patients with dementia of the Alzheimer type (DAT). Thirty-five of the PD patients had no evidence of intellectual impairment on a conventional mental status questionnaire and 16 of the PD patients had dementia syndromes of comparable severity to the DAT patients. DAT produced significantly greater language disturbances, including anomia, decreased information content of spontaneous speech, and diminished word list generation. PD patients had significantly decreased phrase length, impaired speech melody, dysarthria, and agraphia. The results suggest that the dementia of PD is distinguishable from that of DAT:PD patients have prominent motor speech abnormalities, whereas DAT patients exhibit more profound language alterations.
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PMID:Alzheimer's disease and Parkinson's disease: comparison of speech and language alterations. 336 62

The relationship between severity of disease, intellectual impairment, and depression was examined in 50 patients with Parkinson's disease. A significant correlation between severity of disease and intellectual impairment suggests that both may result from the same subcortical lesions. Depression was not significantly related either to severity of disease or to intellectual impairment. This suggests that the relationship between severity of disease and intellectual impairment was not an artifact of increasing depression. Severity of rigidity and of bradykinesia did predict severity of intellectual decline, but severity of tremor predicted better intellectual status. Patients with a predominance of tremor may have a more benign clinical course as well as better intellectual function than patients with a predominance of rigidity and bradykinesia.
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PMID:Relationship of motor symptoms, intellectual impairment, and depression in Parkinson's disease. 340 93

A contribution of cerebral cortical damage to the development of intellectual impairment in patients with Parkinson's disease (PD) has been suspected. We studied the relationship between intellectual impairment and cerebral cortical blood flow in 28 treated idiopathic parkinsonian patients. Mean IQ score as evaluated by applying the Suzuki-Binet test in patients with PD was 70.7 (+/- 12.7) and 78.6% of the patients showed abnormal score (below 80). The intellectual deficits were characterized by impairment of memory and abstract thinking, and showed a significant correlation with the severity of motor symptoms. Mean hemispheric cortical blood flow measured by using the 133xenon intravenous injection technique in patients with PD was significantly lower than that for 18 age-matched controls. Prefrontal cortical blood flow in PD was also significantly reduced compared with that in age-matched controls, showing a partial loss of hyperfrontal pattern. However, there was no significant correlation between IQ score and either mean hemispheric cortical blood flow or prefrontal cortical blood flow values. These results suggest that, although the patients with PD demonstrated a high prevalence of intellectual impairment, the impairment is not necessarily of cortical origin.
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PMID:Intellectual impairment in Parkinson's disease--correlation with cerebral cortical blood flow. 367 65

Intellectual deterioration may be observed in the course of Parkinson's disease. Since it had been reported that central cholinergic systems degenerate in senile dementia and Alzheimer's disease, we measured the activity of choline acetyltransferase (C.A.T.) and the number of muscarinic receptors in various cortical regions of 12 control subjects and 20 patients and compared these biochemical results with clinical and neuropathological data concerning the patients. Thirteen of the parkinsonian patients showed signs of intellectual decline (moderate in 8, severe in 5) and neuropathological examination of the cortex revealed in 10 cases large number of Alzheimer type senile changes extending beyond the hippocampus. C.A.T. activity was decreased in the cerebral cortex in every patient. The decrease was greater in intellectually deteriorated patients and in the group with numerous senile changes in the cortex. The number of muscarinic receptors was increased in patients that had been treated with anticholinergic drugs until they died, but also in those who had not received these drugs, suggesting and underlying denervation hypersensitivity. In the caudate nucleus, however, neither C.A.T. activity nor muscarinic receptor number was altered, indicating that the cortical cholinergic lesion was specific. Although in most cases dementia in Parkinson's disease was of the Alzheimer type, the case of a demented parkinsonian patient in whom cortical C.A.T. activity was severely decreased, in spite of the absence of cortical histopathological evidence characteristic of Alzheimer's disease, suggests that a parkinsonian dementia different from the Alzheimer type also exists. In Parkinson's disease as in Alzheimer's disease the decrease in C.A.T. activity in the cerebral cortex results from degeneration of the cholinergic neurones in the nucleus of Meynert which projects to the cortex. Although the severity of intellectual deterioration seems in relationship with the extent of degeneration, this could already begin before intellectual impairment is apparent.
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PMID:[Dementia and Parkinson's disease: biochemical and anatomo-clinical correlation]. 400 6

Clinical examination of 33 consecutive newly diagnosed cases of Steele-Richardson-Olszewski syndrome revealed evidence of cognitive impairment in 20. Eighteen of the 27 right handed patients who underwent neuropsychological assessment had intellectual impairment (mild in nine and marked in nine patients). The pattern of abnormalities was similar to but more severe than those previously reported in Parkinson's disease, with particular difficulties in carrying out tests which are believed to be sensitive to frontal lobe dysfunction.
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PMID:Cognitive deficits in the Steele-Richardson-Olszewski syndrome (progressive supranuclear palsy). 408 98

A literature review shows that patients affected by Parkinson's disease present an intellectual impairment more frequently than the comparably aged population. Such impairment has been related to several factors (age, arteriosclerosis, motor difficulties, depression, dopaminergic therapy, cortical and/or subcortical lesions). Parkinsonian dementia may be caused by the extent of the degenerative process. Our own results show that parkinsonian patients with dementia are different from nondemented ones with the following features: a) a more marked bradykinesia b) a more severe extrapyramidal picture c) a progressive unresponsiveness to levodopa in a shorter time. It seems possible that there is a Parkinson syndrome characterized, clinically, by an intellectual impairment with a poor prognosis quoad valetudinem, and, anatomically, with multiple cortical and subcortical lesions. Such syndrome may be a "transition" form between Parkinson disease and senile-presenile dementia.
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PMID:[Evaluation of intellectual functions in patients with Parkinson's disease. Bibliographic review]. 617 33

Subcortical dementia is a clinical syndrome characterized by slowness of mental processing, forgetfulness, impaired cognition, apathy, and depression. First recognized in progressive supranuclear palsy and Huntington's disease, the concept has been extended to account for the intellectual impairment of Parkinson's disease, Wilson's disease, spinocerebellar degenerations, idiopathic basal ganglia calcification, the lacunar state, and the dementia syndrome of depression. Disorders manifesting subcortical dementia have pathologic changes that involve primarily the thalamus, basal ganglia, and related brain-stem nuclei with relative sparing of the cerebral cortex. Recent studies of neuropsychologic deficits following focal subcortical lesions also support a role for these structures in arousal, attention, mood, motivation, language, memory, abstraction, and visuospatial skills. The clinical characteristics of subcortical dementia differ from those of dementia of Alzheimer's type where prominent cerebral cortical involvement produces aphasia, amnesia, agnosia, and apraxia.
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PMID:Subcortical dementia. Review of an emerging concept. 623 97


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