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

P300 latency is often delayed in dementia but some authors have questioned its value in clinical practice, because of the relatively low specificity and sensibility of the method. Numerous parameters (latency, duration, amplitude and surface) of N100, N200 and P300 waves were therefore studied in patients with senile dementia, subjects suffering from Parkinson's disease with dementia, and non-demented elderly patients. Using discriminant analysis, more than 90% of the patients were correctly classified. This method could thus be contributory in diagnosing dementia in clinical practice.
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PMID:[Cognitive evoked potentials in the diagnosis of senile dementia and dementia of Parkinson's disease: significance of multivariate analysis]. 180 2

We examined the effects of anticholinergic medication on memory function in 113 patients with idiopathic Parkinson's disease (PD). Subjects were divided into three disease duration groups: early, middle, and advanced. The battery consisted of three tasks assessing memory of logical discourse, semantically related words, and figural material. We found no evidence of anticholinergic-induced memory dysfunction in any of the three groups. Analysis of covariance indicated that age was not a significant variable; however, dementia may have influenced the relationship between anticholinergic medication and memory scores. Our results indicate that anticholinergic medication does not uniformly compromise memory function in PD patients.
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PMID:A retrospective analysis of the effects of anticholinergic medication on memory performance in Parkinson's disease. 182 Dec 62

The increasing availability of single-photon emission computed tomography (SPECT) perfusion brain scans has led to the investigation of a variety of neuropsychiatric conditions including the movement disorders such as Huntington's and Parkinson's disease. In general, observers have noted that Huntington patients have bilaterally decreased uptake of technetium 99m HM-PAO and iodine 123 IMP in the basal ganglia regions involving the heads of the caudate nucleic and adjacent structure, which reflects decreased neuronal function. These functional changes precede the morphological changes due to caudate nucleus atrophy that are observed on computed tomography and magnetic resonance imaging. Cortical changes occur in severely diseased Huntington's patients but are more nonspecific. Prediction of individuals at risk for Huntington's disease using SPECT scans should be done with caution and in association with other clinical data. In contrast, in Parkinson's disease mild diffusely decreased perfusion is commonly noted throughout the cerebral structures, except for the cerebellum. In Parkinson's disease, there is less agreement among observers as to whether the basal ganglia are abnormal. Some observers report that there are no specific basal ganglia perfusion defects in excess of those changes seen elsewhere in the brain. Others report diminished basal ganglia uptake associated with L-dopa therapy in some Parkinson's patients, and in patients with hemi-parkinsonism there have been perfusion deficits reported in the contralateral basal ganglia. In some Parkinson patients, bilateral Alzheimer's-like posterior temporoparietal cortical perfusion defects have been observed in association with progressive dementia. Basal ganglia and cortical perfusion changes also have been reported in a few patients with a variety of other less common movement disorders.
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PMID:The scintigraphic evaluation of Huntington's disease and other movement disorders using single photon emission computed tomography perfusion brain scans. 182 59

To investigate differences in severity and specificity of cognitive impairment among various neurodegenerative diseases, we tested groups of patients presenting with senile dementia of the Alzheimer type (SDAT; 44), progressive supranuclear palsy (PSP; 45), Huntington's disease (HD; 35) and Parkinson's disease (PD; 164), with an extensive neuropsychological battery. We found dementia, as defined by a global intellectual performance 2 standard deviations lower than mean control values, in 93% of SDAT, 66% of HD, 58% of PSP, and 18% of PD patients. Specific features of cognitive impairment distinguished the four groups of patients once they were matched for level of intellectual deterioration: remote memory and linguistic disorders in SDAT, frontal lobe-like abnormalities in PSP, concentration and acquisition disorders in HD. There was no specific alteration in demented PD patients. This study demonstrates the frequency of dementia in predominantly subcortical degenerative diseases and indicates that "subcortical dementia," rather than being a homogeneous entity, should be divided into specific subtypes of cognitive impairment related to different underlying specific lesions of each disease.
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PMID:Severity and specificity of cognitive impairment in Alzheimer's, Huntington's, and Parkinson's diseases and progressive supranuclear palsy. 182 13

Case-control studies of Alzheimer's disease were re-analysed to examine the association of Alzheimer's disease with family history in first degree relatives of dementia, Down's syndrome and Parkinson's disease. Overall, the relative risk of Alzheimer's disease for those with at least one first degree relative with dementia was 3.5 (95% confidence interval 2.6-4.6). Stratification according to age of onset of Alzheimer's disease showed that the relative risk decreased with increasing onset age. However, among patients with an onset of disease after 80 years, there were still significantly more subjects with one or more first degree relatives with dementia as compared to controls (relative risk 2.6; 95% confidence interval 1.3-5.2). The relative risk of Alzheimer's disease was significantly lower in patients who had one first degree relative with dementia (relative risk 2.6; 95% confidence interval 2.0-3.5) as compared to those who had two or more affected relatives (relative risk 7.5; 95% confidence interval 3.3-16.7). Furthermore, the re-analysis showed a significant association between Alzheimer's disease and family history of Down's syndrome (relative risk 2.7; 95% confidence interval 1.2-5.7), which was strongest in those patients who had a positive family history of dementia. The relative risk of Alzheimer's disease for those with a positive family history of Parkinson's disease was 2.4 (95% confidence interval 1.0-5.8).
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PMID:Familial aggregation of Alzheimer's disease and related disorders: a collaborative re-analysis of case-control studies. 183 49

To investigate differences in severity and specificity of cognitive impairment among various neurodegenerative diseases, we tested groups of patients presenting with senile dementia of the Alzheimer's type (SDAT) (n = 44), progressive supranuclear palsy (PSP) (n = 45), Huntington's disease (HD) (n = 35), and Parkinson's disease (PD) (n = 164), with an extensive neuropsychologic battery. We found dementia, as defined by a global intellectual performance 2 SD lower than mean control values, in 93% of patients with SDAT, 66% of patients with HD, 58% of patients with PSP, and 18% of patients with PD. Specific features of cognitive impairment distinguished the four groups of patients once they were matched for level of intellectual deterioration. This study shows the frequency of dementia in predominantly subcortical degenerative diseases and indicates that "subcortical dementia," rather than being a homogeneous entity, should be divided into specific subtypes of cognitive impairment related to different underlying pathology.
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PMID:Severity and specificity of cognitive impairment in Alzheimer's, Huntington's, and Parkinson's diseases and progressive supranuclear palsy. 183 77

Ten patients with advanced Parkinson's disease, presenting with tremor, rigidity and akinesia had autologous adrenal medullary transplantation taken from the left adrenal gland to the head of the right caudate nucleus. Particular attention was taken to avoid prolonged exposure of the adrenal tissue before transplantation and to separate the medullary from the cortical adrenal tissues. Postoperative CT scans confirmed the correct position of the transplants. Differences between pre- and 1-year postoperative clinical conditions were statistically evaluated, with patients under medical (L-dopa) treatment and after the medication was temporarily discontinued. Performance of motor tasks was tested to differentiate slowness of movements imposed by excessive muscular tension (rigidity) from that secondary to delayed reaction time to sensory demands (akinesia). Two deaths occurred 35 and 69 day after surgery for causes not related to the surgical procedures. One of those patients had remained stable neurologically and the other had deteriorated to progressive dementia and catatonia. At autopsy, no lesions in the CNS other than those expected from the surgical procedure were evident, and histological examination failed to reveal chromaffin cells in the head of the right caudate nucleus. Evaluation of the 8 cases that survived for 1 year revealed no significant improvement in their clinical or motor task performance, when considered as a group. However, cases with mild akinesia did better than cases with moderate to advanced akinesia, suggesting that transplantation is indicated in cases with rigidity, but not in cases with 'negative' symptoms of Parkinson's disease. All cases required postoperative medication.
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PMID:Autologous adrenal medullary transplants in advanced Parkinson's disease with particular attention to the selective improvement in symptoms. 184 77

A total of 240 patients of Parkinson's disease (PD) were studied (125 male, 115 female). The age of onset was 60.0 +/- 9.9 years(Y) (mean +/- S.D.) (range 30-87). A 0-4 rating score was applied on each of 6 major symptoms: i.e. tremor, rigidity, bradykinesia, gait, activities of daily living and fluctuation with maximum score of 24. According to the Hoehn and Yahr's stages, there were 44 cases in stage I, 141 in stage II, 31 in stage III, 19 in stage IV and 5 in stage V. Fluctuation in symptoms occurred in 42.9%, dyskinesia in 7.1%, psychosis in 9.6%, depression in 4.6%, and dementia in 2.9%. The mean duration of PD was 4.9 +/- 4.5 Y with 40% 5 years or longer. Significantly longer duration of PD was seen in the patients suffering from fluctuation (6.7 +/- 4.7 Y), dyskinesia (10.7 +/- 6.7 Y) and psychosis (9.4 +/- 6.5 Y). The mean duration of L-dopa treatment was 4.1 +/- 3.4 Y. The patients showing fluctuation (6.2 +/- 4.0 Y) or dyskinesia (7.6 +/- 4.7 Y) had significantly longer duration of L-dopa treatment. The mean daily dose of L-dopa was 370 +/- 203 mg. The patients with fluctuation (430 +/- 187 mg) or dyskinesia (545 +/- 265 mg) received significantly higher dose of L-dopa. Dementia tended to occur in the patients having later age of onset of PD (71.2 +/- 11.2 Y). The symptom score was significantly worse in those with fluctuation, dyskinesia, psychosis and dementia. It was well correlated with the Hoehn and Yahr's staging system.
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PMID:Abbreviated rating score for Parkinson's disease. 184 38

In a effort to better define the role cholinergic basal forebrain neurons play in human cognitive processes, a quantitative assessment of cholinergic nucleus basalis (Ch4) neurons was carried out in 5 patients with Parkinson's disease (PD; 4 non-demented and 1 demented) and 4 age-matched controls using nerve growth factor (NGF) receptor immunohistochemistry as a direct marker for cholinergic basal forebrain neurons. Virtually all (greater than 90%) NGF receptor-containing neurons co-localize with the specific cholinergic marker choline acetyltransferase (ChAT) within the nucleus basalis in PD. NGF receptor-containing neurons were reduced on average by 68% (range 38.6-87.4%) in the non-demented PD cases and by 88.6% in the demented PD patient. Loss of these neurons was heterogeneous across the nucleus basalis subfields with only the anterolateral and posterior Ch4 subregions demonstrating significant reductions of NGF receptor-containing neurons. The reduction in NGF receptor-containing neurons was accompanied by a decrease of acetylcholinesterase (AChE) containing fibers within temporal cortex and in some cases ChAT immunoreactivity in the basolateral amygdaloid nucleus. The numerous non-cholinergic AChE-rich pyramidal cells which were observed throughout the cortex of aged controls were also virtually absent in PD. Although PD patients exhibited severe reductions in Ch4 neurons, few neuritic plaques or neurofibrillary tangles were observed within the PD cortex or Ch4 and similar numbers of these AD-type pathologies were seen within age-matched controls. This suggests that Ch4 degeneration alone is not sufficient to induce such cytoskeletal abnormalities and that the neuron loss seen within Ch4 in AD and PD may be mediated through different processes. These results, coupled with the extensive basic and clinical literature linking acetylcholine and memory function, further indicate that Ch4 degeneration without additional cortical and/or subcortical pathology is not sufficient to impair cognition in PD. Perhaps additional pathology must be superimposed upon nucleus basalis degeneration to induce dementia in humans.
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PMID:Nerve growth factor receptor immunoreactivity within the nucleus basalis (Ch4) in Parkinson's disease: reduced cell numbers and co-localization with cholinergic neurons. 184 79

No clear general view has emerged from the many recent studies devoted to cognitive disorders in Parkinson's disease. Disparity of the populations and methods, as well as interference from motor disorders and possible psychiatric disorders account for the variability of epidemiological data. Subtle cognitive disorders can be found in most patients at the very beginning of the disease. Recent memory is disturbed in free recall tests, but recognition capacities are preserved. Individualization of visuospatial disorders is discussed. Alteration of conceptual capacities is the predominant disorder. Clinically obvious cognitive disorders appear only in some patients after several years of neurological disease. Some risk factors are agreed upon. The bradyphrenia concept is debated, and the term dementia is not accepted by all authors. The major cognitive alterations in Parkinson's disease differ from those observed in Alzheimer dementia, but the latter is more frequent in parkinsonian patients than in the general population. Patients with Parkinson's disease are also exposed to the risk of transient psychotic episodes. Where parkinsonian cognitive pathology is concerned, modern imaging methods are of no help to clinicians. The anatomical and biochemical changes observed in these patients are reviewed, and their responsibility in the genesis of cognitive disorders is discussed: lesions of brainstem nuclei and alterations in their cortical projections on one side, Alzheimer type dementia lesions and Lewys' bodies on the other side. The diverse and inconstant cognitive disorders of patients with Parkinson's disease cannot be explained by lesions of one single structure; they probably result from variable combinations of multiple known or unknown neuronal and biochemical changes.
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PMID:[Cognitive deficits in Parkinson's disease]. 185 32


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