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)

Groups of patients with idiopathic Parkinson's disease, either medicated or unmedicated, were compared with matched groups of normal controls on a computerized battery previously shown to be sensitive to frontal lobe dysfunction, including tests of planning, spatial working memory and attentional set-shifting. In a series of problems based on the 'Tower of London' test, medicated patients with Parkinson's disease were shown to be impaired in the amount of time spent thinking about (planning) the solution to each problem. Additionally, an impairment in terms of the accuracy of the solution produced on this test was only evident in those patients with more severe clinical symptoms and was accompanied by deficits in an associated test of spatial short-term memory. Medicated patients with both mild and severe clinical symptoms were also impaired on a related test of spatial working memory. In contrast, a group of patients who were unmedicated and 'early in the course' of the disease were unimpaired in all three of these tests. However, all three Parkinson's disease groups were impaired in the test of attentional set-shifting ability, although unimpaired in a test of pattern recognition which is insensitive to frontal lobe damage. These data are compared with those previously published from a group of young neurosurgical patients with localized excisions of the frontal lobes and are discussed in terms of the specific nature of the cognitive deficit at different stages of Parkinson's disease.
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PMID:Fronto-striatal cognitive deficits at different stages of Parkinson's disease. 148 58

Cognitive deficits which may occur following chronic low-dose exposure to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) were studied in monkeys who remained motor asymptomatic for parkinsonism throughout the study. The tasks used to assess cognitive functioning are those which have proved in the past to be sensitive to disruption of frontal cortical and or striatal integrity (delayed response and delayed alternation) or sensitive to inferior temporal lobe dysfunction (visual pattern discrimination). Since Parkinson's disease patients have been described as exhibiting frontal signs, we were interested to examine whether MPTP-treated monkeys might exhibit deficits on frontally-mediated tasks, without the confound of motor disturbances. We found that macaque nemistrina monkeys exposed to cumulative doses of 14.94-75.42 mg of MPTP over periods ranging from 5 to 13 months never developed parkinsonian motor signs. However, all 4 animals examined showed significant post-MPTP deficits in delayed response and delayed alternation performance, while visual pattern discrimination performance remained intact. These animals also developed other behavioral problems including irritability and decreased attentiveness. These results show that MPTP can cause specific cognitive deficits independent of the motor deficits which can be produced by this toxin.
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PMID:Chronic exposure to low doses of MPTP. I. Cognitive deficits in motor asymptomatic monkeys. 239 1

Patients with Parkinson's disease (PD) displayed a different pattern of cognitive deficit from patients with dementia resulting from Alzheimer's disease (AD). Specifically, PD patients, whether or not impaired on a mental status examination, had deficient Picture Arrangement but normal Vocabulary test scores whereas AD patients were impaired on both measures. Furthermore, PD patients with impaired mental status examination scores showed a deficit in set formation on Picture Arrangement not seen in the AD patients. Finally, when recent memory performance, as measured by the Wechsler Memory Scale, was predicted from an estimated IQ, 71% of PD patients who had normal mental status examination scores were seen to have at least a mild memory impairment.
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PMID:Different cognitive profiles on standard behavioral tests in Parkinson's disease and Alzheimer's disease. 259 25

Even in nonfamilial cases of dementia there is some evidence of a genetic factor. This may be linked to defective expression of neurofilament protein and also abnormal phosphorylation of cytoskeletal proteins. In this respect there may be a link with accumulation of tangles and amyloid which have some degree of homology. It may be speculated that neurons containing tangles or undergoing granulovacuolar degeneration would not be able to release trophic factors and that transneuronal degeneration would result. However, the environmental or aetiological factors associated with Alzheimer's disease are not known. Although there has been a failure to transmit Alzheimer's disease to primates, it is possible that as in postencephalitic Parkinson's disease virus may be implicated at some stage in the pathogenesis. Finally, free radical formation has been considered as an alternative mechanism for death of large neurons within the CNS. Although tangles are found in several other dementing conditions (e.g. dementia puglistica, Parkinson-dementia complex of Guam), Alzheimer-type plaques and tangles are not invariably found in cases of cognitive deficit. For example, in dementia of Parkinson's disease there is a low neuritic plaque count and normal population of tangles. In addition, memory loss is not necessarily associated with defects in the cholinergic system and/or loss of nucleus basalis nerve cells. We have proposed that damage to or loss of cortical cells may be a more general finding in dementing illness.
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PMID:Pathophysiology of ageing brain. 330 42

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

Reductions in the numbers of binding sites for the serotonergic S2-receptor antagonist, ketanserin, are, as previously reported, evident in Alzheimer's disease. New findings indicate that these sites are not affected in the cortex of patients with Parkinson's disease despite the presence of cognitive impairment. In contrast S1-receptor binding sites were reduced to a small but significant extent in both Alzheimer's and Parkinson's disease with cognitive deficit. The S2-receptor binding loss was not related to the cholinergic deficit (decreased choline acetyltransferase) common to both disorders nor to the presence of cortical senile plaques but did relate to the extent of cortical neurofibrillary tangle formation, evident in Alzheimer's but not generally in Parkinson's disease. These observations suggest that S2- but not S1-receptor binding abnormalities may reflect an important intrinsic cortical involvement specifically associated with the Alzheimer disease process.
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PMID:Cortical serotonin-S2 receptor binding abnormalities in patients with Alzheimer's disease: comparisons with Parkinson's disease. 652 62

An extensive set of neuropsychological measures was administered to 60 Parkinson's disease patients and age-, sex-, and education-matched controls in order to investigate the nature and prevalence of the cognitive deficit in the disease. Parkinsonian patients performed significantly poorer on all measures with the exception of tests for apraxia and object recognition, and on a test of vocabulary knowledge. Discriminant analysis of the test data revealed that over 93% of patients are impaired relative to matched controls, but that assigning a prevalence rate for dementia in the disease may be difficult due to the continuous distribution of cognitive deficits.
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PMID:Dementia in Parkinson disease: a neuropsychological analysis. 692 55

Studies of cognition and motor control have independently suggested that patients with Parkinson's disease show deficits in both attentional control and the preprogramming of movement. However, few studies have examined directly the involvement of cognitive processes in the origin of their slowed response. We examined the performance of 100 Parkinson's disease patients on simple reaction time (SRT) and a series of go/no-go cross-modality choice reaction time (CRT) tasks, in which motor response was constant; correct positive responses required attention to a progressively increasing number of dimensions of visual and auditory stimuli. The results showed that Parkinson's disease patients became increasingly impaired in response speed as choice complexity increased. Slowed response speed in Parkinson's disease involved two factors: (i) a 'perceptuomotor' factor which was constant across conditions and independent of choice complexity. Depression affected this factor selectively and independently of confounding associations with impoverished motor control; (ii) a 'cognitive-analytical' factor, which played an increasingly important role as complexity of choice increased. The characteristics of the relationship between response latency and cognitive complexity indicate that the deficit was due to a constant proportional slowing in cognitive speed across all SRT and CRT conditions. A cognitive deficit affecting the monitoring of stimulus-response compatibility may contribute to delayed response in Parkinson's disease. This cognitive-analytical deficit is present in early, untreated cases and, in contrast to perceptuomotor processes, is weakly related to depression.
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PMID:Slowed central processing in simple and go/no-go reaction time tasks in Parkinson's disease. 803 62

Auditory event-related potentials were recorded using the oddball paradigm in 26 patients with Parkinson's disease, all treated with L-Dopa. The latency of the P3 wave was significantly greater than in an age-matched controls, and was also correlated with the disease duration, but not with scores on two scales measuring cognitive deficit. One year later, when treatment with a dopaminergic agonist, bromocriptine 20-30 mg/day, had been added to the therapeutic regimen, N2 and P3 latencies had increased, whereas several clinical parameters had improved. Thus a longer P3 latency does not seem to be linked to a global cognitive deficit. The use of neuropsychological tests exploring more limited tasks should show the prospective utility of event-related potentials in Parkinson's disease.
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PMID:Event-related potentials in Parkinson's disease: a 12-month follow-up study. 833 61

The term "brain failure" implies only dysfunction of a major organ system, not that an exact diagnosis has been made. Assessment and treatment of older patients with diminished cognitive ability can be challenging; however, the experience can also be extremely rewarding when a reversible condition is alleviated and the patient is given added years of productive life. The first step in patient evaluation is to rule out delirium. The presence of delirium is a medical emergency in a patient of any age. Abrupt onset of cognitive deficit, waxing and waning of symptoms, and worsening of symptoms at night are the hallmarks of delirium. The second step is careful history taking and physical examination to rule out "apparent dementia," a potentially reversible form of brain failure that can mimic irreversible dementia. The third step is to treat what is treatable. Finally, extreme care must be taken in making the diagnosis of true dementia. Diagnosis of such a condition (eg, Alzheimer's disease, multi-infarct dementia, dementia of Parkinson's disease) has a profound effect on the patient and the family. These conditions are largely nontreatable, but physicians still have an important role in helping caregivers find appropriate assistance and support.
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PMID:Brain failure in older patients. Uncovering treatable causes of a diminished ability to think. 865 80


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