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 carried out a neuropsychological study on cognitive impairment in 57 subjects affected by idiopathic Parkinson's Disease (PD) and 32 subjects affected by Alzheimer's Disease (AD). First, we found two different subgroups of Parkinsonian patients, the first one with and the second without dementia. We clearly identified these two distinct subclinical entities regardless of mean age, age of onset, duration of treatment; on the contrary, the type of treatment seems to play a specific role in the appearance of dementia in PD, anticholinergics being assumed almost exclusively by demented Parkinsonian patients. Second, we observed two main differences for cognitive impairment between PD with dementia and AD. In fact, cognitive impairment is consistently more evident in Alzheimer patients than in Parkinsonian ones with dementia; in addition, demented Parkinsonians show a pattern of impairment similar to that exhibited by patients affected by frontal lobe lesions. This result supports neuroanatomical and neurochemical data on the involvement of the whole dopaminergic system in PD and the role played by the ventromedial tegmental area projecting to the frontal cortex in causing cognitive dysfunction in this disease.
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PMID:Dementia in Parkinson's disease: possible specific involvement of the frontal lobes. 399 82

In Parkinson's disease, there is high prevalence of dementia, reduction of the regional cerebral blood flow (rCBF), and neuronal loss and Alzheimer-like pathologic changes in cerebral cortex. Since rCBF is also decreased in Alzheimer's dementia, it is theoretically possible that both decreases in rCBF and cognitive impairment in parkinsonians are caused by a similar mechanism, eg, reduced metabolic demand or loss of cholinergic neurons innervating cortex and microvessels. We therefore measured rCBF using the 133Xenon inhalation technique and evaluated cognitive function with a detailed neuropsychological test battery in 48 patients with Parkinson's disease. Mean brain, hemispheric, and regional flows were decreased in parkinsonians as compared with those in age-matched controls. Most of the cognitive functions were impaired in patients as compared with those in normal subjects. However, there was no correlation between the magnitude of rCBF reduction and the presence and severity of intellectual deterioration in parkinsonians, suggesting that each may be caused by a different mechanism.
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PMID:Cerebral blood flow and cognitive impairment in Parkinson's disease. 402 47

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

The effects of levodopa on tests measuring auditory and visual perception, auditory, and visual short-term memory, verbal learning, and on attention and concentration were studied in 29 patients with Parkinsonism. Thirty-two control subjects matched with the Parkinsonism patients on age, educational level, and verbal IQ were administered the same tests to control for practice effects. Significant improvement occurred for the Parkinsonism patients in verbal learning (an intermediate memory test) and in auditory perception. These improvements were unrelated to changes in anticholinergic medications, increases in alertness or concentration, lessening of depression, or improved motor ability or control. There was no test evidence of levodopa improving visual perception, short-term auditory or visual memory, alertness or concentration. Thus, there is no objective test evidence for levodopa producing a generalized awakening or an alerting effect in Parkinsonism patients who are intellectually alert and well-orientated. Interpretation of the test findings suggests a specific awakening effect, that of improvement in intermediate memory but not in short-term memory. Overall, the Parkinsonism group scored below the control group on all tests, suggesting that cognitive impairment accompanies Parkinson's disease even in patients who are intellectually intact and well oriented.
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PMID:Levodopa's awakening effect on patients with Parkinsonism. 439 42

Eleven post-thalamotomy Parkinson's disease patients, and 11 post-operative, age matched, spinal control subjects, were tested on three visual discrimination matching tasks, two of which involved a delay in response. Error and reaction time scores were recorded. The former produced no differentiation but reaction time scores were significantly faster for the control group on the two tasks involving delay in response but not for the `no-delay' task. Since the motor components of all three tasks were the same, this significant difference in reaction time scores was attributed to the factor of delay in response, and treated as evidence that basal ganglia damage in humans can produce a purely cognitive impairment. The role of sensorimotor interactions, as another factor in this deficit, was also discussed.
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PMID:Performance on delayed response tasks by patients with parkinsonism. 557 3

According to their mental status, patients with Parkinson's disease can be subdivided into three groups: (1) mentally normal patients; (2) patients with severe cognitive impairment and Alzheimer-type brain pathology (neuritic plaques, neurofibrillary tangles, granulovacuolar changes); and (3) demented patients without any evidence of Alzheimer changes. Neurochemically, irrespective of the presence or absence of Alzheimer-type brain pathology, demented Parkinson patients seem to have the same disturbance of cortical cholinergic neuron function as patients with Alzheimer-type dementia (Alzheimer's disease), namely, reduced levels of cortical acetylcholine esterase and choline acetyltransferase activity. At present, the question whether the "cortical cholinergic deficiency" is the only (or sufficient) neurochemical basis for the cognitive impairment in Parkinson patients with dementia cannot be answered with certainty; the additional role of other neurotransmitter changes known to occur in the Parkinson brain, especially loss of cortical, hippocampal and subcortical noradrenaline and/or dopamine cannot be ruled out.
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PMID:Neurochemical basis of dementia in Parkinson's disease. 614 10

Reductions in the numbers of binding sites for the serotonergic S2-receptor antagonist, ketanserin, are, as previously reported, evident in Alzheimer's disease. New findings indicate that these sites are not affected in the cortex of patients with Parkinson's disease despite the presence of cognitive impairment. In contrast S1-receptor binding sites were reduced to a small but significant extent in both Alzheimer's and Parkinson's disease with cognitive deficit. The S2-receptor binding loss was not related to the cholinergic deficit (decreased choline acetyltransferase) common to both disorders nor to the presence of cortical senile plaques but did relate to the extent of cortical neurofibrillary tangle formation, evident in Alzheimer's but not generally in Parkinson's disease. These observations suggest that S2- but not S1-receptor binding abnormalities may reflect an important intrinsic cortical involvement specifically associated with the Alzheimer disease process.
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PMID:Cortical serotonin-S2 receptor binding abnormalities in patients with Alzheimer's disease: comparisons with Parkinson's disease. 652 62

Cerebrospinal fluid levels of homovanillic acid (HVA) in unmedicated patients with Parkinson's disease were 45% of levels in control subjects. Levels of 3-methoxy-4-hydroxyphenylglycol (MHPG) and platelet monoamine oxidase activity (MAO) did not differ. Within the Parkinson's disease group platelet MAO B activity correlated with HVA (an MAO B substrate) but not MHPG (an MAO A substrate). A mild global dementia was found that did not correlate with the more severe motor deficit. There was a negative correlation between the motor deficit and HVA levels but not with MHPG. Cognitive functioning correlated positively with platelet MAO, and the ratio of HVA to MHPG levels and negatively with MHPG alone. It is postulated that dopaminergic and noradrenergic activity or the functional balance between these systems may contribute to the observed cognitive dysfunction.
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PMID:Central catecholamine metabolism in vivo and the cognitive and motor deficits in Parkinson's disease. 664 14

Tests of cognitive functions were carried out in a group of patients with Parkinson's disease and repeated after a three-year interval. Comparison was made with a control group drawn from a population of psychiatric patients, matched for age and sex. No differences in cognitive functions were found between the groups, either initially, or between those surviving for three years. Deaths among the index group included a high proportion of patients with cognitive impairment and there was an increasing prevalence and severity of dementia in the index group which exceeded that observed in the control group. Requirements for a methodologically sound study of dementia in Parkinson's disease are discussed.
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PMID:A controlled study of dementia in Parkinson's disease. 717 41

To determine the prevalence of depression in Parkinson disease (PD) we evaluated 55 consecutive patients without dementia and 31 of their spouses. All subjects completed the Beck depression inventory and a quantitative mini-mental state examination. Using the Beck criteria, 47% of the patients and 12% of the spouses rated themselves as significantly depressed. Mental state scores were significantly lower in the patients. There was a correlation between the severity of depression and cognitive impairment, particularly for calculation, digit span, and visuomotor skills. The severity of parkinsonism, particularly bradykinesia, also paralleled cognition. There was a slight but significant relationship between parkinsonism and depression. These results confirm the high incidence of depression in PD, and suggest that depression in Parkinson patients may be accompanied by mild intellectual impairment and inattention which is independent of the severity of the illness.
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PMID:Depression, intellectual impairment, and Parkinson disease. 719 81


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