Executive Dysfunction in Parkinson’s Disease

Executive Dysfunction in Parkinson’s Disease

Satoshi Kamei (Nihon University School of Medicine, Japan)
DOI: 10.4018/978-1-4666-2113-8.ch002
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Executive dysfunction (ExD) constitutes a core feature of the cognitive impairment in Parkinson’s disease (PD). ExD in non-demented PD was evaluated using the Behavioral Assessment of the Dysexecutive Syndrome (BADS), which provided for the first time a broad assessment of ExD in PD patients. ExD in non-demented PD patients are predisposed to a greater severity of PD, particularly in impairments in activities of daily living. Patients with non-demented PD exhibited a wide range of ExD symptoms. All components of ExD were correlated with severity of PD, but correlation patterns differed across components. The first quantitative EEG evaluation of the differences between PD with and without ExD was also described. PD with ExD exhibited an increase in slow wave activity and a decrease in alpha and fast wave activities in frontal pole and frontal locations. These findings suggest that the ExD in PD is caused by frontal dysfunction.
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Definition of Participants

Of 146 patients consecutively diagnosed with sporadic form PD at the neurology clinic of our hospital, 96 gave informed written consent to participate in this study. The clinical diagnosis of sporadic PD was made according to the UK PD Brain Bank criteria (Gibb, W. R. & Lees, A. J., 1988). Based on clinical features and neuroradiological findings from brain computed tomography (CT) and magnetic resonance imaging (MRI) at later than 12 months post-onset, we excluded other forms of parkinsonism, which included (1) dementia with Lewy bodies (DLB) (Geser, F. et al., 2005; McKeith, I. G. et al., 1996), (2) drug-induced parkinsonism, (3) vascular parkinsonism, and (4) atypical parkinsonism with absent or minimal responses to anti-parkinsonian drugs. The subjects included in the study had thus exhibited good responses to anti-parkinsonian drugs and did not have a history of visual hallucinations or fluctuations in cognitive ability suggestive of the clinical diagnosis of DLB at 12 months post-onset.

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