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 studied 60 patients with idiopathic Parkinson disease with motor and neuropsychologic tests to ascertain whether the severity of motor symptoms was associated with the degree of neuropsychologic deficity. Significant correlations were found between the severity of brady kinesia and impaired performance on tests assessing visual-spatial reasoning and psychomotor speed. More severe tremor was associated with better performance on a spatial orientation memory test. There relationships remained when age, age at onset, and self-rated depression were controlled. The findings suggested that cognitive impairment may result from the same subcortical lesions that cause motor symptoms.
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PMID:Relationship of motor symptoms to intellectual deficits in Parkinson disease. 719 40

Two psychiatric screening instruments, the Mini-Mental State (MMS), a test for cognitive disturbance, and the General Health Questionnaire (GHQ), were administered to 197 neurological in-patients. The results suggest a high rate of psychiatric disturbance. The highest rate of cognitive disturbance detected by the MMS was found in patients with Parkinson's disease. The highest rates of emotional disturbance indicated by GHQ scores were related to myasthenia gravis and multiple sclerosis. MMS scores but not GHQ scores were related to standard tests of cognition, the diagnosis of cerebral pathology, and CAT scan abnormality. The results also demonstrate that the GHQ does not adequately detect patients with cognitive impairment. It is concluded that in populations at high risk for cognitive impairment a tandem screening procedure utilizing tests for both cognitive and emotional disorders is needed.
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PMID:Psychiatric screening on a neurological ward. 738 13

Lesions of the subthalamic nucleus (STN) have been found to reduce the severe akinetic motor symptom produced in animal models of Parkinson's disease, such as in monkeys treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) or in monoamine-depleted rats. However, little is known about the effect of STN exclusion on subtle motor deficits induced by moderate dopaminergic lesions in complex motor tasks. The present study was thus performed on rats trained in a reaction time (RT) task known to be extremely sensitive to variations of dopamine transmission in the striatum. Animals were trained to release a lever after the onset of a visual stimulus within a time limit to obtain a food reward. Discrete dopamine depletion produced by infusing the neurotoxin 6-hydroxydopamine (6-OHDA) bilaterally into the dorsal part of the striatum, produced motor initiation deficits which were revealed by an increase in the number of delayed responses (lever release after the time limit) and a lengthening of RTs. In contrast, bilateral excitotoxic lesion of the STN with ibotenic acid induced severe behavioral deficits which were opposite to those produced by the dopaminergic lesion, as shown by an increase in the number of premature responses (lever release before the onset of the visual stimulus) and a decrease of RTs. Surprisingly, the performance of the animals bearing a double lesion (striatal dopaminergic lesion followed 14 d later by STN ibotenic lesion) was still impaired 40 d after the ibotenic lesion. As expected, the 6-OHDA-induced motor initiation deficits were reversed by a subsequent STN lesion. However, the dramatic increase of premature responses contributing to major behavioral deficits induced by the STN lesion remained unchanged. Thus, the bilateral lesion of the STN was found to alleviate the motor deficits in this model of parkinsonism, but essentially produced over time, long lasting deficits that might be related to dyskinesia or cognitive impairment. The present results strongly support the recent concept of a predominant control of the STN on basal ganglia output structures.
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PMID:In a rat model of parkinsonism, lesions of the subthalamic nucleus reverse increases of reaction time but induce a dramatic premature responding deficit. 747 15

Intellectual changes observed in progressive supranuclear palsy (PSP) are sometimes seen with lesser intensity in Parkinson's disease (PD). Cognitive impairment of PSP has been attributed to a frontal lobe dysfunction explaining the frontal cortex hypometabolism detected by PET. To establish whether this frontal hypometabolism is more pronounced in PSP than in PD, we compared frontal and temporo-parietal cerebral blood flow (CBF) indexes studied by SPECT using Tc99m HmPAO in 18 PSP, 18 PD and 8 control subjects. For each patient neuropsychological performances were also assessed. A significant left frontal hypoperfusion was observed in PSP (mean index value: 0.78 +/- 0.03, p < 0.01) and PD (0.78 +/- 0.04, p < 0.05) as compared to controls (0.84 +/- 0.03), whereas there was no difference between PSP and PD. No correlation was discovered between neuropsychological performances and frontal cortical index changes. This frontal uptake reduction of Tc99m HmPAO in PSP and PD could result from a disconnection phenomenon secondary to subcortical lesions. In both groups mean frontal indexes showed only a left frontal hypoperfusion suggesting that subcortical structures might be asymmetrically involved in early stages of the diseases. The lack of difference for indexe values between PSP and PD might be explained by the difference between the mean disease duration: 4.3 years for the PSP and 7.8 years for the PD. It might also suggest that frontal CBF reduction exists in the same proportions in PD and PSP, but at a later stage in the former case.
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PMID:Tomographic measurements of regional cerebral blood flow in progressive supranuclear palsy and Parkinson's disease. 748 78

It is controversial if early onset Parkinson's disease (EOPD) (onset at < 41 years of age) is Parkinson's disease (PD) occurring at a younger age or a different disease. This controversy is due to some clinical and pathological differences between EOPD and PD. Within EOPD, there appear to be two groups namely: young onset Parkinson's disease (YOPD), with onset between 21 and 40 years, and juvenile parkinsonism (JP), with onset at < 20 years. The two major clinical differences between these groups are a higher familial occurrence of PD and dystonia in JP. In this study, we determine if the two groups have the classical features of PD, namely rest tremors, rigidity, bradykinesia, and postural instability, and have a meaningful response to levodopa. Furthermore, we compare their other clinical features, autonomic and cognitive functions, and levels of CSF monoamine metabolites to determine differences between these groups. We observe that all YOPD (100%) and JP (85%) patients had rest tremors. Most of these patients also had a meaningful response to levodopa (YOPD: 72%; JP: 100%). The prevalence of family history of PD was similar, whereas dystonia was more frequent in JP (43%) compared to YOPD (9%). Autonomic symptoms were twice as common in JP (42%) compared to YOPD (17%). However, bedside autonomic functions were abnormal in similar proportions and, like in PD, suggest involvement of parasympathetic nervous system. Cognitive dysfunction does occur but with no difference in severity between the two groups. The difference in number of patients between YOPD and JP groups makes statistical comparison of the occurrence of clinical features like dystonia and autonomic dysfunction difficult.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Early onset Parkinson's disease: are juvenile- and young-onset different? 752 83

The Mattis Dementia Rating Scale (DRS) was used to distinguish between 50 dementia of the Alzheimer's type (DAT) and 50 Parkinson's disease (PD) subjects matched for age, education, and DRS total score. Despite a similar level of overall cognitive impairment, the DAT group earned significantly lower scores than did the PD group on the Memory subscale, while the PD group displayed lower scores than did the DAT subjects on the Construction subscale. Ajackknifed, stepwise, linear discriminant function using the five DRS subscales revealed that the Memory, Construction, and Initiation subtests significantly distinguished the groups. These results suggest qualitative differences in the dementias of DAT and PD patients and reveal that such differences can emerge on brief mental status examinations.
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PMID:Differentiation of the dementias of Alzheimer's and Parkinson's disease with the dementia rating scale. 757 44

Measurement of regional cerebral blood flow (rCBF) in 30 patients with Parkinson's disease using single-photon emission computed tomography and 123I-IMP demonstrated that hypoperfusion was relatively severer in the parietal cortex than other cortices before and after a 1-year follow-up period. The decline in the scores of the Mini-Mental State Examination was significantly correlated with the decrease in rCBF in the parietal cortex during the follow-up period. Our findings suggest that the parietal cortex is involved in the cognitive impairment in patients with Parkinson's disease.
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PMID:Twelve-month follow-up study of regional cerebral blood flow in Parkinson's disease. 760 85

Cognitive impairment in Parkinson's disease is accompanied by a marked decrease of cerebrocortical nicotinic receptors. To study the putative site of impaired receptor synthesis, frontal cortices of Parkinson patients with cognitive dysfunction have been screened for the expression of the nicotinic receptor alpha 4 subunit gene. Quantitative assessment of alpha 4 mRNA-expressing neurons did not show significant differences between patients and controls. Therefore, decreased nicotinic receptor sites cannot be attributed to alterations at the transcriptional level of the alpha 4 gene. Alternative causes have to be searched for at the translational and/or postranslational level.
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PMID:Gene expression of the nicotinic acetylcholine receptor alpha 4 subunit in the frontal cortex in Parkinson's disease patients. 762 20

Chronic or contingent electrical stimulation at various sites in the region of the ventrolateral nucleus of the thalamus can suppress contralateral intention tremor and the resting tremor seen in Parkinson's disease and idiopathic tremor. The procedure appears to carry less risk, in producing physical or cognitive impairment, than stereotactic ablation. However, the procedure has been tried in few centres to date and long term follow-up studies are needed to place this treatment in its true clinical perspective. It is important to assess patients' needs very carefully to ensure that their functional objectives will be best met by treatments of this kind, and that the requirement for regular monitoring and periodic reassessment can be fully met during long term follow-up.
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PMID:Implants for tremor. 763 78

Patients with Parkinson's disease can suffer from neuropsychological deficits which, in most cases, are already demonstrated at the very beginning (53). Primarily, they are characterized by impairments associated with frontal lobe function affecting psychomotor speed and mental flexibility. Furthermore they show circumscribed impairment of memory functions as well as deficits of visuospatial information processing. Sets of neuropsychological dysfunction of that kind are called subcortical dementia in the American literature. In addition, Parkinson's disease is quite often associated with depressive states which are independent of the neuropsychological deficits. Application of L-Dopa helps to improve the cognitive impairment.
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PMID:[Neuropsychological aspects in idiopathic Parkinson disease]. 770 41


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