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)

Six patients autopsied by the neuropathology service at UMDNJ-Robert Wood Johnson Medical School between 1985 and 1988 had pathologically typical Lewy-body Parkinson's disease (PD). Review of their clinical records revealed that none had clinically typical PD. Atypical clinical features included juvenile onset, retrocollis, strong family history, and absence of tremor, flexed posture, or levodopa response. One patient had dementia without parkinsonism. We conclude that the clinical spectrum of Lewy-body PD is wider than is generally assumed and that the diagnosis of pathologically typical Parkinson's disease cannot be excluded on clinical grounds alone.
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PMID:Clinically atypical expression of pathologically typical Lewy-body parkinsonism. 168 15

A comparative topographical immunohistochemical analysis was performed on the basal ganglia (including the substantia nigra) in Guamanian parkinsonism-dementia complex, idiopathic Parkinson's disease (PD), and Alzheimer's disease (AD). The striatal projection neurons and their efferent fibers were examined by using antibodies to calcineurin, methionine-enkephalin, and substance P. Tyrosine hydroxylase served as a marker for nigrostriatal dopaminergic neurons. The basal ganglia of patients with parkinsonism-dementia complex reacted strongly with all of the antibodies and the reaction products exhibited a normal distribution pattern. These findings suggest that the striatal output system is well preserved in patients with this disease. Similar results were obtained in patients with AD or PD. However, as compared to the patients with AD or PD, patients with parkinsonism-dementia complex showed severe reduction (greater than 90%) in the number of dopaminergic neurons in both the lateral and the medial portions of the substantia nigra. In view of the functional cortico-subcortical loops, these findings could explain the parkinsonian features and in part the cognitive impairment that occur in parkinsonism-dementia complex on Guam.
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PMID:Immunohistochemical study of the striatal efferents and nigral dopaminergic neurons in parkinsonism-dementia complex on Guam in comparison with those in Parkinson's and Alzheimer's diseases. 169 18

EEG studies of Parkinson's disease (PD) have shown that the incidence of EEG abnormalities is higher than in normal old individuals. The most common alteration in PD is generalized slowing of the EEG. We studied 18 patients with Parkinson dementia, 18 age-matched Parkinson patients without dementia and 20 controls. The absolute and relative amplitudes of delta, theta, alpha and beta bands and the peak and mean frequency were calculated from EEG spectra recorded from the T6-O2 derivation. All variables differed significantly in Parkinson dementia patients compared to controls. The most conspicuous finding was the increase of delta activity. Parkinsonian patients without dementia had more theta activity and the frequencies were slow compared to controls. We conclude that parkinsonian subgroups have distinct patterns of abnormality in EEG spectra: Parkinson patients with dementia have distinctly slower EEGs than patients without dementia.
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PMID:Slowing of EEG in Parkinson's disease. 171 7

Cholinergic and monoaminergic (dopaminergic and serotonergic) activities have been examined in postmortem brain tissue in senile dementia of Lewy body type, Parkinson's disease, and Alzheimer's disease. Quantitative data suggest that although extrapyramidal symptoms relate to striatal levels of dopamine, cognitive impairment is most closely associated with cholinergic (but not monoaminergic) deficits in temporal and archicortical areas. Hallucinations, which are most frequent in Lewy body dementia, appear to be related to an extensive cholinergic deficit in temporal neocortex and the resulting imbalance between decreased cholinergic and relatively preserved serotonergic activities. Topographic analyses such as these including consideration of quantitative "threshold" effects, may be relevant to the future anatomic focus of neurochemical investigations in dementia and to the development of appropriate experimental models.
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PMID:Topography, extent, and clinical relevance of neurochemical deficits in dementia of Lewy body type, Parkinson's disease, and Alzheimer's disease. 172 56

The ability to identify smells was tested in nine males and six females with motor neuron disease (MND) of varying severity, using the University of Pennsylvania Smell Identification Test (UPSIT). The olfactory impairment found in MND patients compared with age and sex matched controls is statistically significant at the 0.005 level. The relationship with Parkinson's disease, with Alzheimer's dementia and the possible aetiological implications of this new aspect of the MND are discussed.
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PMID:Olfactory impairment in motor neuron disease: a pilot study. 174 50

Clinical and neuropathologic data in 45 patients with Parkinson's disease (PD) were compared. Twenty-seven patients suffered from marked akinesia and rigidity (AR-type) and 18 patients from predominant resting tremor (T-type). Dementia, depression, and psychosis occurred in 26, 18, and 18 patients, respectively. Neuronal counts were performed in defined areas of the medial and lateral substantia nigra (SNM, SNL), locus ceruleus (LC), and dorsal raphe nucleus (DRN). The AR-type (compared with the T-type) showed higher neuronal loss of LC, SNL, SNM, and more severe gliosis, extraneuronal melanin deposits, and neuroaxonal dystrophy in substantia nigra. Demented PD patients showed more intense cortical Alzheimer lesions and higher neuronal depletion in the SNM, whereas PD subjects with moderate or marked dementia differed from mildly or not demented ones only in the higher degree of cortical Alzheimer lesions. More severe neuronal cell loss of DRN was observed in PD patients with depression. Occurrence of psychosis was not associated with any pathologic feature. Our findings indicate that some major clinical features of PD are related to distinct neuropathologic lesions.
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PMID:The neuropathologic basis of different clinical subgroups of Parkinson's disease. 174 81

The severity of intellectual impairment of 89 patients with Parkinson's disease was evaluated with the Osaka Intelligence Scale for the Aged (OISA). Based on their intelligence levels, the patients were divided into three groups: normal, slight dementia and dementia. EEGs, psychiatric complications such as hallucination, degree of motor disability, history of medication, relationship between changes in intelligence and total amount of administered drugs were also examined. There was no significant correlation between the length of duration of the illness and the degree of intellectual impairment. Two characteristic subgroups were found among our subjects: a group of patients who rapidly became demented after the onset of Parkinsonism, and a group of patients whose intelligence was preserved for a longer period. The mean age of the onset of the disease in the former group was older than that of the latter. Patients of the former group exhibited psychiatric complications and EEG abnormalities more frequently. The severity of motor disability and medications administered at the time of the OISA examination did not differ between the two groups. Deterioration of the intelligence of the patients with Parkinson's disease did not correlate with the total amount of the administered antiparkinsonian drugs.
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PMID:A clinical study on intellectual impairment in parkinsonian patients during long-term treatment. 175 58

The etiology of the nigrostriatal pathway degeneration in Parkinson's disease (PD) is unknown but there is a growing pool of evidence that environmental factors may be involved in the genesis of this disorder. The discovery of the N-Methyl 4-Phenyl 1,2,3,6-Tetrahydro-Pyridine (MPTP)-induced injury in late 1970s provided the first experimental model of PD and stimulated dramatically the epidemiological research. An excitotoxic amino acid contained in Cycadales, which is thought to be responsible for the amyotrophic lateral sclerosis-parkinsonism-dementia complex of Guam, provides another example of toxin-induced parkinsonism. This amino acid is present in most seeds common in the Western diet. In developed countries, prevalence of PD is 2 to 5 times as high than in developing countries. PD patients in developed countries are more likely than controls to have lived in rural environment. Case control studies have suggested that this positive association is possibly related to pesticides and herbicides exposures or well water drinking. Dietary surveys are now going on and several hypothesis are tested including high MPTP-structural analogs or seeds consumption in PD patients and low antioxidants consumption. The negative association between smoking habits and PD has been recognized for more than 20 years. There is evidence that this association is not an artefact due to the disease affecting smoking habits. Its origin is unknown but it could provide important aetiological clues for PD. The most recent hypothesis concerning the relationships between these environmental factors and PD are reviewed and pertinent suitable surveys for the future are discussed.
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PMID:[Parkinson's disease and environmental factors]. 175 3

Neuropathologic examination in elderly individuals and patients with Parkinson's disease with and without dementia reveals abundant isocortical amyloid deposits with no or only a few neuritic plaques, neuropil threads (NT), and neurofibrillary tangles (NFT), whereas NT and NFT may be present only in the entorhinal region of the parahippocampal cortex. In Down's syndrome, Alzheimer's disease, and Parkinson's disease, early neuronal degeneration with deposition of NT and NFT may selectively involve layer pre-alpha (II) of the entorhinal region (Brodmann 26 area) forming the origin of the glutamatergic perforant pathway. Its bilateral destruction isolates the hippocampus from isocortical influx. Comparative studies in a series of aged subjects and those with Parkinson's disease show that psychostatus correlates better with the number of NT and NFT in the entorhinal region than in hippocampal area CA-1 and isocortex. This pattern of neuronal degeneration may explain cognitive impairment in early stages of both Alzheimer's and Parkinson's diseases.
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PMID:Alzheimer lesions in the entorhinal region and isocortex in Parkinson's and Alzheimer's diseases. 177 40

Many diseases of the brain leading to impairment of intellectual capacities are associated with morphological changes in the anteromedial portions of the temporal lobe. Among these are Alzheimer's disease, Parkinson's disease and the syndrome of dementia with argyrophilic grains. The hallmarks of Alzheimer's disease are intraneuronal neurofibrillary changes and extracellular amyloid deposits. The neurofibrillary changes consist of neurofibrillary tangles, neuritic plaques and neuropil threads. The distribution pattern of neurofibrillary changes differs from the distribution of amyloid deposits. The neurofibrillary changes exhibit a distinct but varying distribution pattern in different areas of the cerebral cortex. In fully developed Alzheimer's disease, both the hippocampal formation and isocortical association areas are severely involved while the brunt of the pathology is found in the entorhinal region. The entorhinal region receives information from various isocortical association areas and limbic circuits and projects to the hippocampal formation via the perforant path. This fibre tract is mainly generated by projection neurons within the superficial entorhinal cell layer. In Alzheimer's disease virtually all projection neurons within this layer are destroyed by neurofibrillary tangles. In cases of Parkinson's disease with progressive cognitive decline the neurofibrillary changes are confined to the outer cellular layer of the entorhinal region. In cases of "dementia with argyrophilic grains" the argyrophilic grains are predominantly encountered in the hippocampal formation and in the outer layers of the entorhinal region.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Morphological changes in the human cerebral cortex in dementia]. 177 31


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