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)

Ventricular fluid concentrations of homovanillic acid (HVA) and 5-hydroxyindoleacetic acid (5-HIAA), the respective metabolites of dopamine and serotonin, were measured in 57 patients undergoing thalamotomy for relief of movement disorders. The diseases included were Parkinson disease, dystonia, cerebral palsy, multiple sclerosis, and posttraumatic or posthypoxic encephalopathy. Untreated parkinsonian patients had the lowest mean HVA level (119 ng per milliliter). Patients with multiple sclerosis or with posttraumatic or posthypoxic encephalopathy with both intellectual impairment and bilateral motor involvement had lower mean HVA levels (197 and 177 ng per milliliter, respectively) than cerebral palsy patients with bilateral motor disease (233 ng per milliliter), dystonia patients (246 ng per milliliter), or multiple sclerosis patients with normal intellect (376 ng per milliliter). The data suggest that diffuse cerebral disease may lead to diminished dopaminergic activity. Ventricular fluid 5-HIAA levels were similar in all groups of patients. Chronic cerebellar stimulation markedly increased ventricular fluid HVA and 5-HIAA levels, indicating that cerebellar stimulation affected cerebral dopaminergic and serotonergic systems.
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PMID:Ventricular fluid homovanillic acid and 5-hydroxyindoleacetic acid concentrations in patients with movement disorders. 56 83

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

A number of neurological disorders including Alzheimer and Parkinson disease have been suggested to be caused by processes leading to lipid peroxidation. Other theories implicate the accumulation of damaged DNA, resulting from a defect in DNA repair, in the pathogenesis of these disorders. I suggest that these theories might be related, since the hydroxy free radical is known to attack DNA and inactivate enzymes so that oxygen metabolism has the potential to interfere with the maintenance of genomic integrity. Since psychometric intelligence correlates highly with erythrocyte glutathione peroxidase activity, a free radical scavenger, perhaps this might explain the marked intellectual impairment caused by chemotherapeutic agents such as cytosine arabinoside, as well as in Alzheimer disease.
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PMID:Dementia in cancer patients undergoing chemotherapy: implication of free radical injury and relevance to Alzheimer disease. 189 Sep 72

Twenty patients with Parkinson's disease and marked intellectual impairment or dementia participated in a double-blind placebo controlled trial of the nootropic, piracetam. A standardized neurological examination, a neuropsychological test battery, and a functional scale, The Sickness Impact Profile, were completed for all patients. They were then assigned by blind randomization to drug or placebo conditions receiving 3.2 g of piracetam or an identical amount of placebo for 12 weeks. The dose was increased to 4.8 g for an additional 12 weeks. Neurological, psychological, and functional measures were rated as improved, unchanged, or worsened in comparison to baseline performance. Twenty-five percent of the patients did not complete the trial for reasons unrelated to the medication. Although there was a significant improvement on one subtest of the functional scale, no significant effects were demonstrated in cognitive or neurological measures.
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PMID:A controlled trial of piracetam in intellectually impaired patients with Parkinson's disease. 238 39

Experimental evidence has shown that the amount of 5-HIAA in the CSF reflects the metabolism of serotonin in the brain if this metabolite is eliminated from the brain and flows into the CSF at a constant rate. We studied the concentration of 5-HIAA in the lumbar CSF in several neurological diseases to elucidate the alteration in abnormalities of serotonin metabolism. The concentration of 5-HIAA in the CSF was measured in 94 patients with cerebral infarction, 30 with vascular dementia, 25 with dementia of the Alzheimer type, 28 with Parkinson's disease and 6 with hypoxic encephalopathy. Patients with cerebral infarction were classified into 24 with a solitary cerebral infarct and 70 with multiple cerebral infarcts. Patients with Parkinson's disease were subdivided into 12 with various psychiatric symptoms including depressive state, hallucination and/or intellectual impairment and 16 without psychiatric symptoms. Patients with hypoxic encephalopathy consisted of 5 with apallic syndrome and one patient with Lance-Adams syndrome. The concentration of 5-HIAA in solitary cerebral infarct, multiple cerebral infarcts and vascular dementia did not exhibit a significant difference from that in control cases (54.6 +/- 23.1 ng/ml). But patients with dementia of the Alzheimer type (34.5 +/- 10.9, p less than 0.001) showed a significantly lower concentration. This fact seems to reflect the pathological finding that the number of large neurons is decreased and neurofibrillary tangles are increased in the nucleus raphe dorsalis of patients with Alzheimer type dementia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Study on the concentration of 5-hydroxyindoleacetic acid (5-HIAA) in the lumbar cerebrospinal fluid (CSF) in neurological diseases]. 248 Aug 63

Intellectual impairment and disease severity tend to parallel one another in patients with Parkinson's disease (PD), but the pattern of development of the neuropsychological impairments contributing to the overall intellectual decline is unknown. This problem was addressed by comparing neuropsychological performance in the early and later stages of PD. Impairment of recent memory, impairment of cognition, and somatic features of depression were seen early and worsened with more advanced disease. Impairment of visuospatial skills, remote memory, language, and mood were observed only in the later stages of PD. These findings suggest that neuropsychological impairments do not develop in a uniform manner with progression of PD.
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PMID:Neuropsychological impairments associated with severity of Parkinson's disease. 252 Oct 56

The intellectual impairment appearing during the Parkinson's disease has been analysed and compared with the severity of the motor deficit respectively with the presence of the cerebral atrophy determined by computed tomography. The organic mental syndrome was more frequently observed in males and well correlated with the degree of cortical and subcortical atrophy.
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PMID:[Cerebral atrophy and dementia in Parkinson disease]. 257 29

The possibility that dementia in Parkinson's disease is associated with specific cerebral abnormalities identifiable by magnetic resonance imaging (MRI) was examined. Sixty eight patients with Parkinson's disease and 28 age and education matched normal controls were evaluated using neuropsychological procedures that included assessment of language, memory, cognition, visuospatial skills and mood. Twenty three patients (34%) were found to have developed significant impairment in at least three of the five areas, thus meeting criteria for a dementia syndrome. Eleven patients (16%) had no intellectual impairment and thirty four patients (50%) had a mild to moderate intellectual disturbance. Patients with (n = 10) and without dementia (n = 20), matched for severity of Parkinson's disease, and normal controls (n = 10) matched for age with the two patients groups, were evaluated by MRI. MRI scans were analysed for evidence of generalised cerebral atrophy, ventricular enlargement, visualisation of the substantia nigra and severity of focal brain lesions. Results indicated that the presence of dementia in patients with Parkinson's disease was not associated with any specific pattern of MRI abnormalities.
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PMID:Magnetic resonance imaging in dementia of Parkinson's disease. 259 66

The purpose of this longitudinal study was to investigate if the presence of frontal motor deficits in parkinsonians without signs of global intellectual impairment may have a predictive value for the development of a progressive dementing process during the course of the illness. An examination of the higher level of motor organization, using skills thought to depend upon the integrity of the frontal regions, was performed by 30 parkinsonian patients who did not present any signs of general intellectual impairment. According to their performance, as compared with controls, they were divided into two subgroups: those with and those without frontal dysfunctions. After a mean period of 4 years, a second neuropsychological examination was carried out to assess any eventual change of mental status. The results suggest that frontal dysfunctions may be observed several years before the appearance of generalized intellectual impairment and may be considered one of the predictive factors for development of dementia in Parkinson's disease. Careful consideration of these defects during examination of motor abilities may be of value in the clinical management of parkinsonian patients.
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PMID:Frontal lobe dysfunction in Parkinson's disease: prognostic value for dementia? 270 95

To evaluate clinically the slowing of cognitive processing in Parkinson's disease, we used a visual discrimination task consisting of 15 superimposed images of objects. The time needed to identify 12 objects increased by 58% in 70 patients withdrawn from levodopa treatment compared with 20 controls matched for age and education. Perceptual, motor, and psycholinguistic factors, as well as mood, only partially accounted for the slowness of performance. The 15-objects test scores of the parkinsonian patients correlated significantly with both their intellectual impairment and the severity of their parkinsonian disability, but not with the duration of the disease. The scores did not correlate with depression. Levodopa had no effect on the score, although the parkinsonian motor disability score was improved by 54%. The results indicate a cognitive slowing in Parkinson's disease which is probably related to abnormalities of nondopaminergic neuronal systems in the brain.
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PMID:Cognitive slowing in Parkinson's disease fails to respond to levodopa treatment: the 15-objects test. 272 68


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