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)

EEG-findings of a group of 95 patients suffering from Parkinson's disease were related to accompanying diseases inducing cerebral hypoxic hypoxidosis. The EEG in 59 to 74 per cent of our patients was abnormal but the changes were not specific. There was a correlation between age and EEG-abnormalities. On the other hand no association could be seen between EEG-changes and duration of the Parkinson's disease. At least 74 per cent of the patients suffered from concomitant cardiovascular complications and 36 of them had a severe pathologic EEG as well as a pathologic ECG. The results lead to the conclusion that in treatment of parkinsonian patients attention is to be paid to accompanying diseases as heart failure, angiopathy or anemia.
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PMID:[EEG in Parkinson's disease and cerebral hypoxia (author's transl)]. 41 49

Vascular pseudoparkinsonism may be confused with idiopathic Parkinson's disease. Patients may be unnecessarily treated with anti-parkinsonian drugs while their underlying vascular disease is ignored. We investigated 250 parkinsonian patients seen in our Movement Disorders Clinic for a possible vascular etiology. After excluding those with a known secondary cause such as drug-induced parkinsonism, progressive supranuclear palsy, multiple system atrophy and hyperparathyroidism, brain computed tomography and/or magnetic resonance imaging were performed on those who showed poor or no response to levodopa. In those with an ischemic lesion demonstrated on neuroimaging, anti-parkinsonian drugs were stopped and the patients were reassessed. Eleven patients (4.4%) had ischemic brain lesions accounting for their parkinsonism. All were initially diagnosed as Parkinson's disease because of the prominence of bradykinesia and rigidity. Gait disturbance was also common, but resting tremor was distinctly absent. Three anatomical patterns with different prognosis were identified. Three patients with basal ganglia lacunar infarct recovered spontaneously, three with frontal lobe infarcts remained static and five with periventricular and deep subcortical white matter lesions had progressive deterioration. Autopsy in one patient confirmed bilateral frontal lobe watershed infarcts and the absence of brain stem Lewy bodies. Parkinsonian patients with poor or no response to levodopa therapy should be investigated for a vascular etiology.
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PMID:Vascular pseudoparkinsonism. 148 45

Few detailed clinico-pathological correlations of Parkinson's disease have been published. The pathological findings in 100 patients diagnosed prospectively by a group of consultant neurologists as having idiopathic Parkinson's disease are reported. Seventy six had nigral Lewy bodies, and in all of these Lewy bodies were also found in the cerebral cortex. In 24 cases without Lewy bodies, diagnoses included progressive supranuclear palsy, multiple system atrophy, Alzheimer's disease, Alzheimer-type pathology, and basal ganglia vascular disease. The retrospective application of recommended diagnostic criteria improved the diagnostic accuracy to 82%. These observations call into question current concepts of Parkinson's disease as a single distinct morbid entity.
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PMID:Accuracy of clinical diagnosis of idiopathic Parkinson's disease: a clinico-pathological study of 100 cases. 835 Jan 22

Amyloid P (AP) component is present in all types of systemic amyloid deposits. Recently, it has been shown to be also present in cerebral amyloid lesions of Alzheimer's disease (AD). In this study, we used immunocytochemical methods to extend these findings at the electron microscope level and characterize the spectrum of AP immunoreactivity in neurofibrillary pathology (NFP) of AD and other neurodegenerative disorders including Down's syndrome (DS), Creutzfeldt-Jakob, Parkinson's, Pick's and diffuse Lewy body diseases and progressive supranuclear palsy. In AD and DS, AP immunoreaction product was evident in all the classical amyloid lesions and NFP in a large sample of all cortical areas examined. The distribution and relative intensity of immunostaining was similar to that of thioflavin S staining in serial sections. In many cases, however, plaques and vessels stained by anti-AP serum were not apparent with thioflavin S. Serial sections immunostained with antiserum to amyloid A, C-reactive protein or to other proteins involved in systemic amyloidoses and the acute phase response showed no evidence of staining in any of the cerebral lesions. Electron microscopy confirmed that AP immunoreactivity was associated with the abnormal filaments characteristic of NFP as well as amyloid fibrils found in plaques and vessels showing congophilic amyloid angiopathy. Plaques of Creutzfeldt-Jakob disease, Pick bodies of Pick's disease, tangles and Lewy bodies in Parkinson's disease and a subpopulation of Lewy bodies in the diffuse Lewy body disease coexistent with AD were also stained. With the exception of vessels in two of the five cases, AP was not detected in age-matched controls. Our observations indicate AP to be a consistent feature of cerebral NFP and amyloid deposits.
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PMID:Widespread serum amyloid P immunoreactivity in cortical amyloid deposits and the neurofibrillary pathology of Alzheimer's disease and other degenerative disorders. 189 Oct 63

To determine the possible role of Wallerian degeneration secondary to the grey matter neuronal loss in the pathogenesis of "leuko-araiosis", computerised tomography (CT) of the brain was studied in 98 normotensive and non diabetic subjects free of cardiac diseases: 32 with Alzheimer's disease, 36 with Parkinson's disease, eight with progressive supranuclear palsy, and 22 controls. In Alzheimer's disease, leuko-araiosis scores were greater than in control subjects. Leuko-araiosis was more prominent in anterior periventricular areas in Parkinson's disease and progressive supranuclear palsy, and in posterior periventricular areas in Alzheimer's disease. In two patients with Alzheimer's disease and leuko-araiosis, necropsy revealed diffuse white matter pallor, mild fibrillary astrocytosis, and in one patient limited hyaline thickening of small white matter vessels, without any infarction or hypertensive change. Changes were more severe in white matter close to cortical areas with a great density of neurofibrillary tangles. Leuko-araiosis was more severe or more widespread in Alzheimer's disease than in Parkinson's disease, progressive supranuclear palsy and normal ageing. Differences in the location of leuko-araiosis between the four groups might be due to differences in the location of the grey matter disorder and Wallerian degeneration rather than amyloid in Alzheimer's disease, Parkinson's disease, progressive supranuclear palsy and normal ageing. Wallerian degeneration might be another cause of leuko-araiosis in neuro-degenerative disorders beside previously reported extra-cerebral predisposing factors and amyloid angiopathy.
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PMID:Could Wallerian degeneration contribute to "leuko-araiosis" in subjects free of any vascular disorder? 201 Jul 59

Fifty brains from patients prospectively studied in a geriatric hospital (Charles Richet Study) were examined pathologically. The patients were senile (mean age: 85) and demented and had been clinically diagnosed as senile dementia of Alzheimer type (SDAT), vascular or multi-infarct dementia (VD), mixed dementia (MD). The whole brain was studied after formalin fixation and coronal sections. The senile changes were quantified in 6 neocortical areas, hippocampus and amygdala and subcortical structures after staining by thioflavine--S and Bodian's method. The other vascular and degenerative lesions were semiquantitatively studied. Three groups of patients were identified after microscopic examination: 1. SDAT (n = 27), 2. VD (n = 6), 3. MD (n = 15), 2 patients had no significant pathological correlate for dementia. Comparison of thioflavine S and Bodian's method in 30 cases showed the former to be more sensitive for the identification of senile plaques. In SDAT, 13/27 brains lacked neurofibrillary tangles in the neocortex. Amyloid angiopathy was observed in 78% of the brains but lacked in 5/6 cases affected by pure VD. Significant lesions of the substantia nigra were observed in 13 cases with typical features of Parkinson's disease in 2 cases. The locus coeruleus was affected mainly in SDAT cases (20/27) and in some cases of VD or MD (6/21). The raphe nuclei showed neuronal loss in 18% of the cases, mostly SDAT. In this series of cases, neocortical neurofibrillary tangles could be lacking in SDAT. Amyloid angiopathy was almost always present in SDAT and MD. Subcortical structures involved in cholinergic, noradrenergic and serotoninergic innervation of the cortex were more severely impaired in SDAT and MD than in VD. Mixed dementia was frequent in these very old demented patients. Clinical and pathological criteria are needed to identify this group of patients.
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PMID:[Neuropathologic study of 50 cases of senile dementia]. 207 18

The concentrations of delta sleep-inducing peptide (DSIP)-like (DSIP-LI) and P-DSIP-like (phosphorylated, Ser7) immunoreactivity (P-DSIP-LI) were measured by specific radioimmunoassay in the cerebrospinal fluid (CSF) of patients with senile dementia of the Alzheimer type [SDAT, subdivided into early (S1), middle (S2) and late dementia (S3)], multi-infarct dementia (MD), Parkinson's disease (PD), vascular disease (VD) and communicating hydrocephalus (H), as well as in control patients (C1, C2). Mean DSIP-LI and P-DSIP-LI concentrations were found to be significantly higher in the elderly control group (C1, mean age 83 +/- 5 years) than in the middle-aged control group (C2, mean age 40 +/- 16 years). DSIP-LI and P-DSIP-LI were positively correlated with age in both control groups. Significant decreases of DSIP-LI compared with age-matched controls (C1) were observed for S2, S3, MD, PD, VD and H. In contrast, no significant differences corresponding to pathology were found for P-DSIP-LI.
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PMID:Comparison of DSIP- (delta sleep-inducing peptide) and P-DSIP-like (phosphorylated) immunoreactivity in cerebrospinal fluid of patients with senile dementia of Alzheimer type, multi-infarct syndrome, communicating hydrocephalus and Parkinson's disease. 244 24

One hundred fifty autopsy brains from patients with clinically diagnosed Alzheimer's disease (AD) were examined pathologically. The brains were received consecutively over a 3-year period from numerous sources as part of a research program in which one brain half was frozen for biochemical studies and the other half was fixed in formalin. One hundred thirty-one (87%) of the 150 cases fulfilled histological criteria for AD, with or without additional findings, such as Parkinson's disease or stroke. At least a minimal degree of amyloid angiopathy was found in every brain showing histopathological abnormalities of AD. Twenty-three (18%) of the 131 AD brains had Lewy bodies in neurons of the substantia nigra. Thirteen of the 19 non-AD cases were diagnosed as other neurodegenerative disorders. In only 2 cases was no histological correlate for the patient's dementia found. We conclude that (1) the many physicians who diagnosed these cases did so highly accurately; (2) degenerative changes in the substantia nigra were more common in patients with AD than has been reported for the general aged population; (3) amyloid angiopathy was a constant accompaniment of AD, although its severity varied widely; (4) vascular dementia was rarely clinically misdiagnosed as AD; (5) neuropathological findings were insufficient to account for the clinical syndrome of dementia in less than 2% of cases; (6) the histological criteria established by the National Institutes of Health/American Association of Retired Persons Workshop on the Diagnosis of Alzheimer's Disease worked well in assessing this large series.
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PMID:Clinically diagnosed Alzheimer's disease: autopsy results in 150 cases. 255 94

In 58 patients with progressive supranuclear palsy (PSP), 19 (32.8%) had CT, MRI, or autopsy evidence of a multi-infarct (MI) state. The clinical findings in the infarct syndrome were similar to idiopathic PSP. Five MI-PSP patients had had a stroke, four had focal dystonia, two had hemiparesis, and one had an intention tremor of recent onset. In contrast, only 5.9% (12.9% of those with CT or MRI) of 426 Parkinson's disease patients had evidence of strokes. One case of PSP studied pathologically was attributed to cerebral amyloid angiopathy.
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PMID:Progressive supranuclear palsy and a multi-infarct state. 356 71

In a case control study of the relationship between smoking habits and Parkinson's disease a negative association was demonstrated with a relative risk of 0 x 52. A history of smoking up to 20 years earlier was associated with a risk of developing Parkinson's disease equal to about half that in non-smokers. The type of disease, age of onset and rate of progression were associated with a similar reduction in risk implying that in respect of smoking history the disease is homogeneous. The positive correlation of degenerative vascular disease with smoking is further evidence that arteriosclerosis is not involved in the causation of Parkinson's disease. The negative association between Parkinson's disease and smoking is confirmed and is independent of other associated factors. The known and serious risks of smoking far outweigh the possible benefit of lowered risk of Parkinson's disease.
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PMID:Smoking and Parkinson's disease. 711 26


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