Cortical atrophy in Alzheimer's disease unmasks electrically silent sulci and lowers EEG dipolarity.

Abstract

Alzheimer's disease (AD) patients show lower dipolarity (goodness-of-fit) for dipole localizations of alpha or other dominant electroencephalography (EEG) frequency components in the occipital cortex. In the present study, we performed computer simulations to discover which of distributions of dipole activity lower dipolarity in a manner similar to that seen in severe AD. Dipolarity was estimated from simulations of various electric dipole generator configurations within the occipital cortex under conditions of widened cortical sulci (a severely demented AD case) or no sulcal widening (a normal subject). The cortical and scalp surfaces, derived from the subjects' MRI's, were assumed to be uniformly electrically conducting. Randomly placed, nonoverlapping lesions ranging from 1 to 4 mm2 per lesion were used in both the normal and AD models to simulate the electrical effect of neuropathological AD lesions. In both models, dipolarity decreased as total lesion size increased. However, the AD model showed lower dipolarity than the normal model for both individual lesion sizes and for larger total lesion sizes. The larger decline in dipolarity in the AD model appears to be due to sulcal widening which unmasks the effect of lesions buried within sulci. These simulations identify a possible mechanism explaining why sulcally-located neuropathological changes plus progressive cortical atrophy in AD brains (and presumably other cortical disorders producing atrophy) alter EEG patterns and dipolarity differently from normal cortex damaged by similar lesions.