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

Alzheimer's disease (AD) patients show lower dipolarity (goodness-of-fit) f or 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 dipol e activity lower dipolarity in a manner similar to that seen in severe AD, Dipolarity was estimated from simulations of various electric dipole genera tor configurations within the occipital cortex under conditions of widened cortical sulci (a severely demented AD case) or no sulcal widening (a norma l subject). The cortical and scalp surfaces, derived from the subjects' MRI 's, mere assumed to be uniformly electrically conducting. Randomly placed, nonoverlapping lesions ranging from 1 to 4 mm(2) per lesion were used in bo th the normal and AD models to simulate the electrical effect of neuropatho logical AD lesions. In both models, dipolarity decreased as total lesion si ze 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 sulca l widening which unmasks the effect of lesions buried within sulci. These s imulations identify a possible mechanism explaining why sulcally-located ne uropathological changes plus progressive cortical atrophy in AD brains land presumably other cortical disorders producing atrophy) alter EEG patterns and dipolarity differently from normal cortex damaged by similar lesions.