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)

Seventy-eight subjects suffering from idiopathic Parkinson's disease were studied in 2 separate groups to test the hypothesis that benzhexol affects memory. In study A, 54 subjects were tested by means of a free recall technique; in study B, 24 subjects were given a signal detection memory task. Both studies yielded significant correlations between memory impairment and dosage levels of benzhexol. No correlation was found between memory status and dosage of levodopa, duration of illness or Hamilton depression scores. The implications of these findings are discussed.
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PMID:The adverse effect of benzhexol on memory in Parkinson's disease. 368 79

A patient with severe variant angina that was refractory to conventional treatment became symptom free when she was treated with benzhexol (trihexyphenidyl hydrochloride), a cholinergic blocking agent used in the management of Parkinson's disease. There was a brief psychotic reaction when a large dose was taken and some memory impairment on the maintenance dose. Benzhexol should be used with caution but may prove to be an additional therapeutic agent in the management of severe variant angina.
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PMID:Management of a case of refractory variant angina with benzhexol hydrochloride (trihexyphenidyl hydrochloride). 405 85

Disruption of cholinergic neurotransmission may result in memory impairment. In this study the anticholinergic drug, trihexyphenidyl, at low doses when administered chronically for one month to Parkinson disease patients caused a decrease in performance on recent but not immediate memory tests. Awareness of possible deterioration of memory function of parkinsonian patients on anticholinergic medication is necessary.
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PMID:Disturbance of recent memory function in parkinsonian patients on anticholinergic therapy. 674 1

A detailed analysis of the mnestic deficits associated with Parkinson's disease (PD) contributes to explaining the cognitive disorders and their well documented consequences. This study was designed to show that, in PD declarative as well as procedural memory is severely impaired. Three tests designed to explore this aspect of mnestic functioning were proposed to a group of 16 parkinsonian patients whose motoricity was controlled: inverted reading, braille reading, sound form association. The results obtained, compared with those of young and aged controls, show that PD is associated with marked deficits in both declarative and procedural memory. Declarative memory impairment was similar to that observed in the control population (healthy elderly subjects, age-matched with the PD patients) but more marked in PD subjects. The procedural memory deficit was linked with age and pathology. Procedural memory involves a variety of processing modules dedicated to the type of information (visual, auditive, tactile codes). The deficits observed were more like a loss of automatism than procedural impairment stricto sensu ('knowing how'). It would be worth pursuing research by studying akinesia and motor disorders from the angle of automatic memory impairment.
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PMID:Procedural memory and Parkinson's disease. 762 May 31

Patients with Huntington's disease (HD) and Parkinson's disease (PD) show different patterns of preserved and impaired memory performance. This study investigates explicit memory for movements in HD and PD with a linear positioning apparatus using Dick et al.'s procedure (J. Gerontol. 43, 127-135, 1988). In the first experiment, 12 HD patients were compared to 12 matched-controls. HD patients were more impaired than the controls by the delay between criterion and recall movements, whether the delay was filled or unfilled. Switching the limb between criterion and recall movements did not lead to more effects in HD patients and in controls. In the second experiment, 12 non-demented PD patients were compared to matched-controls. PD patients were more impaired than controls when the recall movement was executed with the contralateral hand, but were not more affected by the delay. In both experiments, HD and PD patients, as well as the controls, recalled self-generated preselected movements better than imposed movements. These results suggest the existence of distinct forms of motor memory impairment in some subcortical neurodegenerative diseases.
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PMID:Motor memory and the preselection effect in Huntington's and Parkinson's disease. 796 69

We investigated the profile of cognitive and memory deficits of 22 Parkinson's disease (PD), 24 amyotrophic lateral sclerosis (ALS) patients and 26 age-matched controls. The patients were at the early phase of the disease and untreated. The ALS patients exhibited deficits in simple visuoperceptual functions and in complex visuoperceptual reasoning (Digit Symbol and Block Design tests), whereas the PD patients showed deficits only in simple visuoperceptual functions. Moreover, both ALS and PD patients had impairment in tasks requiring set shifting from one reaction to another that may suggest frontal lobe dysfunction. The ALS and PD patients also showed impairment in the task of learning a word list with effort-demanding organization of the material to be remembered. However, preserved delayed recall of logical passages suggests that memory, per se, is not impaired in ALS or in PD. The patterns of errors in a test of recognition of learned words imply, at least partially, different underlying deficits in the two diseases. An inability to inhibit irrelevant information may contribute to memory impairment in ALS patients, whereas the memory deficit in PD may derive from lowered motivation or initiating behaviour.
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PMID:Cognitive and memory deficits in untreated Parkinson's disease and amyotrophic lateral sclerosis patients: a comparative study. 811 9

Animal experiments and human neuropsychological studies have provided evidence for the hypothesis that skill acquisition may be regulated by the basal ganglia. In the present studies, perceptual and cognitive skill acquisition as well as a number of explicit verbal memory functions were investigated in patients in early and more advanced stages of Parkinson's disease (PD) and in patients with frontal lobe lesions. Patients in more advanced stages of PD were impaired at cognitive skill acquisition as well as during recall conditions that involved active semantic organisation of the stimulus material. Similar explicit memory deficits were present in frontally lesioned patients. PD patients with unilateral symptoms showed a selective impairment in acquiring a cognitive skill. Perceptual skill acquisition was preserved in all groups. The overall pattern of memory impairment in PD is largely consistent with dysfunction of fronto-striatal circuitry.
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PMID:Memory and skill acquisition in Parkinson's disease and frontal lobe dysfunction. 853 73

Are the striato-frontal neuronal circuits implicated in learning of item-specific spatial coordinates? To answer this question, we compared the performance of 20 patients with Parkinson's disease to that of 14 controls matched for age, global cognitive efficiency and mood, on a visuo-spatial learning task with little involvement of motor and constructive functions, allowing control of encoding and comparison of free recall, cued recall and recognition. Compared to controls, patients showed a severe memory impairment for visuo-spatial location of pictures, contrasting with relative preservation of verbal memory, and mild difficulties in perceptive visuo-spatial and executive functions. These results implicate striato-frontal neuronal circuits in memory for spatial location.
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PMID:Memory for spatial location is affected in Parkinson's disease. 885 95

To evaluate the efficacy of chronic nicotine administration in dementia, electrical field distributions of event-related potentials (ERPs) and midlatency response (MLR) were recorded and were analyzed in terms of time and space. The study was carried out on 22 normal individuals and 17 patients with dementia (vascular dementia, Alzheimer disease and Parkinson disease). Nicotine was delivered transdermally from a nicotine patch (22.5 to 52 mg/day) for 2 or 4 weeks. Dementing patients showed abnormal ERPs in latency, amplitude and electrical field on the scalp. Decreased amplitude and electrical field abnormality of P1 in MLR was also seen in some patients with dementia. These abnormal ERPs and MLR of the patients improved after administration of nicotine especially in P300 latency of ERPs and P1 amplitude of MLR. These data suggest that nicotine administration might be useful as a cognitive enhancer in memory impairment.
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PMID:[The role of nicotinic receptor in memory impairment: a study using event-related potentials and midlatency responses]. 912 92

Studies with single photon emission computed tomography (SPECT) have shown temporoparietal (TP) hypoperfusion in patients with Alzheimer's disease (AD). We evaluated the utility of this findings in the diagnosis of AD. SPECT images with 123I-iodoamphetamine were analyzed qualitatively by a rater without knowledge of the subject's clinical status. Sixty-seven of 302 consecutive patients were judged as having TP hypoperfusion by SPECT imaging. This perfusion pattern was observed in 44 of 51 patients with AD, in 5 with mixed dementia, 8 with cerebrovascular disease (including 5 with dementia), 4 with Parkinson's disease (including 2 with dementia), 1 with normal pressure hydrocephalus. 1 with slowly progressive aphasia. 1 with progressive autonomic failure, 2 with age associated memory impairment, and 1 with unclassified dementia. The sensitivity for AD was 86.3% (44 of 51 AD), and the specificity was 91.2% (229 of 251 non-AD). Next, we looked for differences in perfusion images between patients with AD and without AD. Some patients without AD had additional hypoperfusion beyond TP areas: deep gray matter hypoperfusion and diffuse frontal hypoperfusion, which could be used to differentiate them from the patients with AD. Other could not be distinguished from patients with AD by their perfusion pattern. Although patients with other cerebral disorders occasionally have TP hypoperfusion, this finding makes the diagnosis of AD very likely.
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PMID:[Single photon emission computed tomography in the diagnosis of Alzheimer's disease]. 930 Dec 61


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