Quantitative EEG (qEEG) findings in Parkinson disease (PD) have been reported in only five previous studies. In these studies, the sample size was small and the distribution of qEEG changes was not estimated. This is the first qEEG evaluation not only employing multiple logistic regression analysis but also estimating the distribution of qEEG changes. The subjects comprised 45 PD patients without remarkable dementia and 40 age-adjusted normal controls. The lack of ischemic lesions in all subjects was confirmed by MRI. Absolute power values were measured for four frequency bands from delta to beta. The electrodes were divided into six, viz. frontal pole, frontal, central, parietal, temporal, and occipital locations. We calculated the spectral ratio, i.e., the sum of the power values in the alpha and beta waves divided by the sum of the values in the slow waves. The dependent variable was either PD or normal control; the independent variables were the spectral ratios, age, sex, and Mini-Mental State Examination score. The significant predictive variables in PD were the spectral ratios at all electrode locations except for the frontal pole (frontal location: P = 0.025, other locations: P < 0.01). PD presented diffuse slowing in the qEEG when compared with age-adjusted normal controls.

Quantitative EEG evaluation in Parkinson disease (PD) reveals diffuse slowing. This is the first quantitative EEG evaluation of the differences between PD with and without executive dysfunction (ExD). The subjects were 32 PD patients without remarkable dementia. The lack of ischemic lesions was confirmed by magnetic resonance imaging. ExD was defined as <70 points on the age-controlled standardized score of the Behavioral Assessment of the Dysexecutive Syndrome. Absolute power was measured for four frequency bands from delta to beta. Electrodes were placed at frontal pole, frontal, central, parietal, occipital, and temporal locations. Spectral ratio was calculated as the sum of power values for alpha and beta waves divided by the sum of values for the slow waves. In multiple logistic regression analysis of each electrode location, the dependent variable was ExD or not, and the independent variables were spectral ratio, age, and Unified Parkinson Disease Rating Scale. The only significant predictor of ExD was spectral ratio at the frontal pole (P = 0.031) and frontal (P = 0.048) locations. PD with ExD exhibited an increase in slow wave activity and a decrease in alpha and fast wave activities in these locations. These findings indicated that the ExD in PD was caused by frontal dysfunction.

The previous association study confirmed that diffuse slowing of EEGs was present in Parkinson's disease (PD), demonstrated with the use of the quantitative EEG technique. This study was the first to assess the relationship between progression of PD and quantitative EEG. A total of 106 patients with PD with a mean Hoehn-Yahr stage of 2.73 were serially enrolled. Lack of ischemic lesions was confirmed in all patients by magnetic resonance imaging. Absolute power values were measured for four frequency bands from delta to beta. The electrodes were divided among six locations: frontal pole, frontal, central, parietal, temporal, and occipital locations. Spectral ratio was calculated as the sum of power values for the alpha and beta waves divided by the sum values for the slow waves. The relationship between the progression of PD and spectral ratio was assessed by the Jonckheere-Terpstra trend test. At all electrode locations, spectral ratio significantly decreased with progression of Hoehn-Yahr stage (frontal pole, P = 0.007; frontal, P = 0.005; central, P = 0.031; parietal, P = 0.017; temporal, P = 0.005; occipital, P = 0.010). This shows that the slowing of EEGs became more obvious with PD progression.