Subjects
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, including brain computed tomography (CT) and MRI, which were obtained at > 12 months after onset, we excluded other forms of parkinsonism, such as (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. All patients were scanned to obtain T1- and T2-weighted images, fluid-attenuated inversion recovery (FLAIR) images, and diffusion images by a cranial MRI (1.5-T Siemens Magnetom Symphony, Münich, Germany). We also included patients without any intracerebral ischemic changes, including asymptomatic lacuna or slight periventricular hyperintensity on T2 and FLAIR images, in accordance with the reported classification of PVH (Fazekas, F. et al., 1987). At more than 12 months after onset, the subjects had exhibited good responses to anti-Parkinsonian drugs and did not have a history of visual hallucinations or fluctuations in their cognitive ability, which suggested clinical diagnosis of DLB.
PD progression was assessed by the Hoehn and Yahr staging scale (Hoehn, M. M. & Yahr, M. D., 1967). Cognitive function in PD patients was assessed using the Mini-Mental State Examination (MMSE), which is based on the Diagnostic and Statistical Manual of Mental Disorders, 4th ed. (DSM-IV) criteria for dementia in accordance with a previously reported study (Burn, D. J. et al., 2006).
The CTRL subjects were also defined as participants without any organic intracerebral disease who were ≥ 60 years old and exhibited no intracerebral ischemic lesions on a cranial MRI.
Participants who were being treated with drugs that influenced qEEG, such as anti-anxiety or psychotropic drugs, were excluded prior to the study.