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)

Neuronal loss in the substantia nigra (SN) in Parkinson's disease (PD) shows a topographical organisation where the lateral part of the SN is more affected. This is--due to projection of the lateral SN mainly to the putamen--reflected in more complete loss of dopamine content in the putamen than in the caudate nucleus. Of the parkinsonian symptoms rigidity and hypokinesia are associated with neuronal loss in the lateral substantia nigra and the resulting dopamine loss in the putamen. Neuronal mechanisms other than degeneration of the nigrostriatal system seem to be involved in the pathophysiology of tremor. Cognitive impairment and dementia in PD is related to dysfunction of the cortical cholinergic system, especially in the frontal cortex. The brain dopaminergic system, however, contributes as a subcortical component to cognitive impairment in PD. Clinical studies have shown that selegiline may slow down the progression of PD. We studied postmortem samples of patients treated with selegiline and levodopa and those with levodopa alone. The number of medial nigral neurons was significantly higher in the selegiline group. Treatment with selegiline might retard the death of nigral neurons, but further studies are needed to confirm the preliminary findings.
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PMID:Nigral degeneration in Parkinson's disease in relation to clinical features. 180 43

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

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

Oropharyngeal functional impairment increases with age so that radiologists frequently are asked to determine the cause of aspiration in elderly patients. Neuromuscular and cognitive impairment often make it difficult to perform and interpret videofluoroscopic deglutition examinations in these patients. We retrospectively reviewed the barium swallow examinations in 50 elderly patients (mean age, 87 years) who were known to aspirate. We looked for specific patterns of oropharyngeal dysfunction that resulted in bolus misdirection. Analysis revealed that aspiration was due to abnormalities of the oral stage in 23, pharyngeal stage in 10, and both stages in 17. Dysfunction in the oral stage was due to ingestion of large volumes or rapid acquisition rates in nine, failure of containment during processing (bolus manipulation) in 18, and dissociation of lingual delivery and swallowing initiation in the transitional phase in 13. Dysfunction in the pharyngeal stage was due to incomplete transport (bolus retention) in 21 and defective closure of the laryngeal vestibule in 11. No significant relationship between conditions known to cause oropharyngeal dysfunction (dementia, stroke, Parkinson disease, disuse deconditioning) and the specific pattern of dysfunction was identified. These results indicate that an accurate and valid assessment of oropharyngeal dysfunction in elderly patients with aspiration is possible if specific patterns of dysfunction are sought. Our study indicates the importance of evaluating the oral and pharyngeal stages of deglutition in elderly patients who aspirate.
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PMID:Videofluoroscopy in elderly patients with aspiration: importance of evaluating both oral and pharyngeal stages of deglutition. 187 55

Current knowledge of cognitive dysfunction in Parkinson's disease (PD) has largely been obtained from studies of chronically treated patients in whom effects of disease chronicity, treatment, depression and dementia are confounding factors. Studies of untreated patients have examined few cognitive domains and relationships between cognition, depression and motor disability have been incompletely explored. Accordingly, we studied 60 consecutive patients with newly diagnosed, untreated, idiopathic PD and 37 matched, healthy control subjects; no subject had clinical dementia or depression. All subjects received tests of specific processes of memory and cognition, including working memory, verbal and non-verbal short- and long-term memory, language, visuospatial capacity, set-formation and shifting and sequencing. Patients also received quantitative global clinical measures of severity of dementia, depression and motor disability. The PD group as a whole showed deficits in immediate recall of verbal material, language production and semantic fluency, set-formation, cognitive sequencing and working memory and visuomotor construction. However, this group was unimpaired in immediate memory span, long-term forgetting, naming, comprehension and visual perception. Language deficits and more severe frontal lobe impairments were confined to those PD patients scoring abnormally on a Mini Mental State examination. Motor disability correlated strongly with severity of depression but weakly with cognitive impairment. Cognitive sequencing, set-formation and set-shifting deficits tended to associate with depression, but otherwise there was no association between cognition and depression. The results indicate dissociation of cognition and motor control in early PD which suggests that cognitive dysfunction is largely independent of frontostriatal dopamine deficiency underlying motor disability. Some, but not all, of the frontal lobe deficits of chronic disease are detectable in early, untreated PD. The pathogenesis of the cognitive deficits shown here appears to involve extrastriatal dopamine systems or non-dopaminergic pathology. Longitudinal study is necessary to determine whether increasing disease duration exacerbates the early cognitive deficits and affects new cognitive domains, in addition to producing increasing motor disability.
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PMID:Cognitive impairment in early, untreated Parkinson's disease and its relationship to motor disability. 193 36

Schneider and Kovelowski (1990) showed that chronic low-dose N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) administration to monkeys caused cognitive dysfunction without significant motor impairment on tasks thought to be related to the caudate-frontal axis. The cognitive difficulties were similar to those seen in monkeys with frontal lesions, normal young monkeys, and normal young children. The caudate-frontal dysfunction is consistent with the cognitive difficulties that are thought to exist in children with attention deficit disorder (ADD). The caudate-frontal dysfunction is also consistent with the distribution of decreased cerebral blood flow and, presumably, decreased metabolism that has recently been found in children with ADD. In monkeys given chronic low-dose MPTP, pilot neurochemical studies have suggested abnormalities in dopamine and norepinephrine metabolism, the two neurotransmitters most frequently linked with ADD. We suggest that chronic low-dose MPTP induced cognitive dysfunction in primates may not only be a model for the cognitive disturbances that accompany Parkinson's disease but may also aid in understanding the cognitive dysfunction seen in children with ADD.
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PMID:Chronic low-dose MPTP in nonhuman primates: a possible model for attention deficit disorder. 200 19

Altered motor or mental skills in Parkinson's disease (PD) could adversely affect driving ability. We interviewed 150 patients regarding their driving habits and compared them with 100 controls. Thirty patients had stopped driving because of PD. PD patients had no more lifetime accidents than controls. With increased disability, however, there was a smaller percentage of patients still driving with fewer miles traveled and with proportionately more accidents occurring. Though disability scores did not correlate well with driving ability, there were significantly more accidents in subjects with more severe PD. The presence of cognitive impairment was associated with an increased accident rate. We conclude that driving in PD may be a public health problem and that some PD patients should not drive.
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PMID:Driving in Parkinson's disease. 201 Dec 49

Two hundred and forty-nine patients with Parkinson's disease previously examined by Mutch et al 1,2 were followed up three and a half years after the original study. Cognitive impairment, age, some postural signs and symptoms of Parkinson's disease and high scores on the Hoehn and Yahr scale predicted premature death. Patients were more likely to die from respiratory infections than controls. Respiratory diseases as cause of death recorded on the death certificate were not related to kyphosis, posture scores or Hoehn and Yahr scores before death. The hypothesis is advanced that death of respiratory causes might be associated with signs of general autonomic dysregulation.
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PMID:Mortality and causes of death in idiopathic Parkinson's disease: results from the Aberdeen whole population study. 207 49

Cognitive disturbances are frequently encountered in advancing Parkinson's disease (PD). Typically there are visuo-spatial disorders, memory impairment and bradyphrenia, defined as 'subcortical dementia' to distinguish it from the dementia that occurs in Alzheimer's disease, where the most prominent dysfunctions are agnosia, apraxia and aphasia. An electrophysiological test to study cognitive processing is the P300 (or P3) of the Event Related Potentials; in particular the latency of the P3 seems to correlate with cognitive decline. Thirty patients affected with idiopathic PD were investigated using a classic auditory "oddball" paradigm (rare tone--"target"--3000 Hz, frequent tone--"non target"--1000 Hz; the patients were instructed to recognize and keep a mental count of the number of rare tones). Electrophysiological findings were compared with those obtained in twenty normal subjects, age and sex matched with the patient's group. The parameters of P300 were correlated with patient's age, duration of the disease, motor and cognitive impairment levels and L-Dopa therapy. The P300 was loss in 16.6% (5 p.) and delayed in 33.3% (10 p.). Significative correlations were found only with age and cognitive impairment scores, but not with other variables analyzed. These results suggest that P300 could be a useful test to identify demented patients among those with PD, despite different motor disabilities.
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PMID:[P300 and Parkinson disease. The role of cognitive changes]. 210 48

The Authors introduce some questions concerning cognitive impairment in Parkinsonian patients and they focus the attention on 'bradyphrenia'. They briefly discuss the methodological difficulties in studying this kind of disturbances in Parkinson's disease (PD) and the approach to this problem with the help of the Event-Related Potentials or ERPs. Finally, they review literature and their data on Contingent Negative Variation (CNV) and P300 in PD and conclude that interesting and useful informations can be obtained by means of the electrophysiological methods.
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PMID:[Parkinson disease and cognitive evoked potentials]. 210 50


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