Abstract

Parkinson’s disease (PD) is caused by a disruption of dopaminergic neurotransmission in the basal ganglia, which serve as an integrative centre for the sensory and cognitive processing of information and as a mutual link between this processing and disturbed motor performance. The basal ganglia and the cerebellum transmit information via the thalamus to the cerebral cortex in order to regulate movement. The neurotransmitter changes affect the output of the striatum into the globus pallidus as well as into the thalamus and cerebral cortex beyond. The disease is a common and disabling disorder of movement characterized by poverty, slowness and impaired scaling of voluntary movements (akinesia and bradykinesia), muscle rigidity, and tremor of the limbs at rest. Alterations of the basal ganglia with proven neuronal degenerative disorders of dopaminergic neurons and a reduction in activity in frontostriatal neural circuitry have been suggested to play a role in the executive dysfunction of PD (Taylor et al., 1990; Innis et al., 1993; Lewis et al., 2003; Owen, 2004; Leblois et al., 2006; Anik et al., 2007). The slowed information processing, insufficient encoding strategies and planning, and attentional setshifting are related to memory deficits and cognitive impairment in PD (Daum et al., 1995; Pillon et al., 1997; Knoke et al., 1998; Robertson & Empson, 1999; Sawamoto et al., 2002; Cools, 2006). Neuropsychological studies of PD patients report cognitive deficits even during the early stages of the disease (van Spaendonck et al., 2006). The primary working memory deficit in PD is associated with impaired free recall performances (Higginson et al., 2003). Many electroencephalographic (EEG) studies on PD have used the event-related potential (ERP) method, where the early modal dependent and obligatory N1 and P2 components permit analysis of sensory events while the later N2 and P3 potentials reflect the cognitive processes involving the assessment of stimuli, decision making, strategy selection and recognition memory. ERP investigations have shown P3 predominantly with prolonged latencies and/or diminished amplitudes for Parkinsonian patients (PP) when compared to healthy subjects (HS) (Evarts et al., 1981; Tachibana et al., 1992; Philipova et al., 1997; Wascher et al., 1997; Minamoto et al., 2001; Antal et al., 2002; Wang et al., 2002). Such results have been interpreted as electrophysiological signs of cognitive slowing with respect to stimulus classification and attentional processing (Robertson & Empson, 1999). One valuable means of assessing deviations from the normal state in PD is to study oscillatory brain processes. In the ERP method, however, the functional significance of the

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