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Query: UMLS:C0030567 (Parkinson's disease)
 63,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Alzheimer's and Parkinson's diseases are associated with cognitive impairment, although the pattern of cognitive dysfunction is not identical. We investigated the recall and recognition memory of 18 patients with idiopathic Parkinson's disease (PD) and of 32 patients with probable Alzheimer's disease (AD). In the list-learning test using Buschke's selective reminding method, PD patients showed superior delayed recognition memory capability compared to AD patients, whereas immediate recall did not differ in the two groups. In the delayed story recall, PD patients were also able to benefit from rehearsal and probe more than AD patients. The results suggest that PD patients are able to bind information better into long-term storage than are AD patients. This may be due to better function in PD of the entorhinal cortex and hippocampus.
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PMID:Recall and recognition memory in patients with Alzheimer's and Parkinson's diseases. 317 77

We compared the neuropsychological performance of patients with Parkinson's disease who were young at onset of the disease (mean age, 41.4 years) and had received prolonged L-dopa treatment (mean, 52.1 months) with nontreated patients of the same age. A similar comparison was made for patients who were older at onset of the disease (mean, 62.1 years). There were no significant differences in cognitive and memory functions between the L-Dopa-treated and untreated young patients, whereas the L-Dopa-treated patients in the older age group performed more poorly than untreated patients in some memory tests (Wechsler Memory Scale I: logical and visual) and cognitive functions (Wechsler Adult Intelligence Scale: similarities, block design, and cognitive flexibility). Treatment duration, disease duration, and mean L-Dopa dose were comparable for the two age groups. After linear effects of age and disease duration had been eliminated, the duration of L-Dopa treatment did not correlate with the cognitive variables studied. These observations suggest that treatment with L-Dopa may not be the cause of cognitive impairment in Parkinson's disease.
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PMID:Dementia and treatment with L-dopa in Parkinson's disease. 319 64

The neuropathologic and pathophysiological relationship of specific to more generalized cognitive dysfunction in Parkinson's disease (PD) remains incompletely understood. This issue was examined in a study of 39 patients with PD, utilizing standardized clinical measures, computerized neuropsychological tests, and quantitative computed tomography. Disorders of visuospatial discrimination and perceptual-motor function closely paralleled motor scores, suggesting a common neuropathologic basis. Caudate nuclear and mesocortical dopamine depletion play a role in this context. More generalized cognitive dysfunction occurred in older patients with a somewhat longer disease duration, more advanced parkinsonism, and computed tomographic evidence of subcortical and frontal cortical atrophy but without significant cerebral atrophy when compared with age-matched controls. Further prospective clinicopathologic studies will be required to clarify the relative contribution of the primary dopaminergic dysfunction, age-related changes, Alzheimer-type pathologic condition, and other coexisting neurotransmitter deficits to the dementia seen in PD.
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PMID:Cognitive and motor dysfunction in Parkinson's disease. Clinical, performance, and computed tomographic correlations. 329 55

In recent years, several attempts have been made to characterize the nature of the cognitive deficits shown by patients with Parkinson's disease. It has been suggested variously that they have difficulty in switching cognitive set, in performing effortful (or controlled) as opposed to automatic tasks, or that their impairment is found in tasks which maximize the amount of 'self-directed task specific planning'. It is proposed that this latter distinction may be reformulated in terms of the degree of internal versus external attentional control which is required by the task. An experiment is described which attempted to manipulate this parameter. A version of the Stroop colour-word test was used, in which the words 'red' and 'green' were presented in the complementary coloured 'ink'. Subjects responded either to the colour of the ink in which the word was written or the colour named by the word. The relevant attribute changed at intervals during the course of the experiment. In one condition, the relevant stimulus attribute was cued before each trial. In another condition, subjects had to remember which attribute was currently relevant. Results revealed that patients with Parkinson's disease were impaired mainly on the second version of the task which required internal attentional control. The results are discussed in relation to the models of Working Memory (Baddeley, 1986), and attentional control (Norman and Shallice, 1980). Exploration of these models leads to the formulation of a theory in which the crucial determinant of cognitive impairment in Parkinson's disease is reduced resources in the Supervisory Attentional System. Provided the demands of the task are within the patient's available attentional resources the patient may not show any deficit. If, however, the attentional demands exceed available resources, as in tasks which depend upon internal cues, then deficits will be observed.
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PMID:Internal versus external cues and the control of attention in Parkinson's disease. 337 39

30 patients with Parkinson disease were investigated with computed tomographic (CT) scanning and neuropsychological tests. The CT data proved to be of scant interest whereas tests of intelligence, verbal and visual memory and visuomotor abilities were all informative. Parkinsonian patients with cognitive impairment seem to constitute a separate group in which akinesia and gait disturbances predominate.
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PMID:Cognitive performance and Parkinson disease: neuropsychological and CT study. 359 51

Forty-three neurologically and psychiatrically assessed patients with idiopathic Parkinson's disease (PD) underwent detailed cognitive assessment. Cognitive deficits typical of senile dementia of Alzheimer's type (SDAT) were found in 7% but the majority showed definite impairments not typical of SDAT. Cognitive impairment was significantly more likely in those with more severe PD symptoms. There was substantial agreement between psychiatric diagnosis and psychological picture of SDAT and some links were found between other diagnostic categories and nature of cognitive functioning. However, cognitive deficits were also found in two-thirds of patients with no psychiatric diagnosis.
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PMID:Cognitive functioning in Parkinson's disease: in relation to prevalence of dementia and psychiatric diagnosis. 379 Aug 70

The reliability of primitive reflexes as monitors of dementia, depression, and severity of Parkinson's disease were studied. The results indicated that the proportion of certain reflexes increased with severity of disease and cognitive impairment, but no relationship was seen between any of the reflexes and degree of depression.
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PMID:Relationship between primitive reflexes and severity in Parkinson's disease. 379 36

Drug-induced psychiatric symptoms are usually reversible within days. However, if the patient also has cognitive impairment of a more permanent nature, improvement may not be seen for weeks or even months. During the year preceding the diagnosis of Parkinson's disease, the incidence of depression, hyperirritability, and instability of emotions is significant. After the onset of Parkinson's disease, depression is very common.
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PMID:Parkinson's disease in the elderly: psychiatric manifestations. 388 40

There is an urgent need for efficient, non-invasive measures of neurotoxic insult in humans. The late positive component (LPC) of the event-related cortical potential may be such a measure. The latency and amplitude of the LPC have been related to both memory and response speed, two aspects of behavior which are indicators of neurological status. The LPC has been found to be altered in cases of known neurophysiological insult, including Alzheimer's disease, cerebrovascular disease, Parkinson's disease, surgical and traumatic damage, hyperkinesis, chronic alcoholism, mental retardation, and in schizophrenia. Further development of the LPC as a possible indicator of both the cognitive impairment due to neurotoxic substances as well as the site of neurological damage is warranted.
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PMID:The late positive component of the evoked cortical potential: application to neurotoxicity testing. 390 31

Although Parkinson's disease has traditionally been considered as a motor disorder, there has been much recent interest in the nature and the neural substrates of parkinsonian dementia and cognitive dysfunction. These disabilities, which can induce visuospatial impairment and visual 'neglect', may also have a bearing on the controversy about the normal functions of the nigrostriatal dopamine (DA) projection and the basal ganglia. The observations that neurones in both substantia nigra and striatum respond to sensory events in terms of neuronal firing or DA release, also suggest a role for striatum in sensorimotor integration. An important behavioural correlate of this integration is the 'sensorimotor neglect' syndrome in animals with unilateral lesions of the nigrostriatal projection who fail to orient to contralateral sensory events. However, this neglect may arise not from contralateral sensory inattention, but from an inability to express this sensory selection via motor output. We present here two lines of evidence that unilateral striatal DA depletion in the rat does not affect sensory attention to visual signals of reward, but rather impairs the initiation (though not the completion) of contralateral motor acts. These results not only help to clarify the function of the nigrostriatal DA projection, but also show that depletion in this system is linked specifically to a process of response initiation, which may be the fundamental impairment in Parkinson's disease.
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PMID:Depletion of unilateral striatal dopamine impairs initiation of contralateral actions and not sensory attention. 397 1


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