Parkinson's disease, cognition and aging Clinical, neuropsychological, electrophysiological and cranial computerized tomographic assessment
Introduction
The occurrence of cognitive impairment in Parkinson's disease (PD) as the disease progressed was frequently reported (Charcot and Vulpian, 1861; Charcot, 1875; Mjones, 1949; Walshe, 1955; Reitan and Boll, 1971; Shaw et al., 1980).
This cognitive impairment could be either global or specifically involving certain aspects such as visual discrimination, visuospatial orientation, verbal fluency, memory, frontal lobe functions and conceptual abilities (Girotti et al., 1988).
The frequency of cognitive impairment increases with increased duration of the disease and severity of motor disability, and has been attributed to the possible role of advancing age (Dubois et al., 1990).
Whereas dementia in PD ranged from 10 to 40% (Girotti et al., 1988; Mayeux et al., 1990), depression, mild or moderate, occurred in 40% (Hamilton, 1960). However, 25% experienced depression before motor symptoms of PD became manifest, associated later with mild intellectual dysfunction (Starkstein et al., 1992).
Impairment in intellectual functions involved mainly complex language comprehension, visuospatial factors and attention in parkinsonian patients with the highest depression levels (Vilert et al., 1991).
The aim of this work was to evaluate the influence of aging on the cognitive domain in PD and to assess points of similarities as well as differences between PD and normal aging. It was hoped that this study would clarify whether such changes were specifically due to the disease process of PD or to an underlying age process, and to clarify the relationship between cognitive decline in PD and parkinsonian motor disability or depression.
Section snippets
Subjects and methods
Forty-three consecutive patients diagnosed as idiopathic Parkinson's disease (PD) (Group I), attending the Neurology outpatient clinic in a public hospital, the Kasr El Aini Hospital, were submitted to the present study.
Clinical results
Group I of parkinsonian patients were all right-handed. Sixteen patients were below the age of 60, i.e., middle-aged (mean age = 54.4 ± 3.3 years) while 27 patients were above the age of 60 i.e. elderly (mean age = 66.2 ± 5.12 years).
At the time of examination, the duration of illness (duration of motor disability) ranged from one month up to 15 years with a mean of 28.6 ± 33.3 months.
The H + Y grading scale for PD denoted that the severity of the motor disability was mild in ten patients
Discussion
When Parkinson first described PD (Parkinson, 1817), he stated that the cognitive abilities were ‘uninjured’. Later it was evident that as the disease progressed, mental deterioration supervened (Charcot and Vulpian, 1861). The introduction of levodopa, led to a longer life expectancy of parkinsonian patients and so intellectual impairment was reported in association with the disease (Lees and Smith, 1983). The intellectual impairment in PD was attributed to slowing of thought processes,
Conclusion
Global cognitive impairment in PD could be attributed to complex cognitive changes rather than to the process of aging. These cognitive changes were considered as a part of the disease process, though not directly related to duration or degree of parkinsonian motor disability nor to depression. PD and normal aging differed as regards the effect of age on the specific cognitive functions, where in PD patients, age was related to intentional memory, while in normal controls, it was related to
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2020, Clinical NeurophysiologyCitation Excerpt :However, results of P3 changes in non-demented PD vary among studies. In the present study, we found prolonged P3b latency, similar to earlier reports on non-demented PD groups (Aotsuka et al., 1996; Elwan et al., 1996; Wright et al., 1996; Tachibana et al., 1997; Wang et al., 1999). However, this finding is not supported by other groups (Stanzione et al., 1991; Toda et al., 1993; Rumbach et al., 1993; Green et al., 1996).
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2015, Acta PsychologicaCitation Excerpt :Despite important differences in the processes underlying P3a and P3b evoked potentials and their assumed dependence on dopamine, many of the studies of PD focused exclusively on the P3b potential evoked by the standard two-stimulus oddball paradigm. Some of these studies (Elwan et al., 1996; Graham, Yiannikas, Gordon, Coyle, & Morris, 1990; Green et al., 1996; Karayanidis, Andrews, Ward, & Michie, 1995) found no differences between PD patients and healthy controls, whereas others reported reduced P3b amplitude (Koberskaia, Zenkov, and Iakhno (2003)), or prolonged P3b latency (Stanzione et al. (1998)) in PD patients compared to healthy controls. Additionally, Bodis-Wollner et al. (1995) have found that the P3b latencies in both auditory and visual oddball tasks significantly but differentially correlate with scores on cognitive tests.
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