Abnormalities in Occipital Cortical Sources of Resting‐State EEG Rhythms in Patients with Epileptiform Activity and Mild Cognitive Impairment due to Alzheimer’s Disease

Abstract

AbstractBackgroundAlzheimer’s Disease (AD) patients present a higher risk of developing epilepsy compared to the age‐matched general population. Neurodegenerative cognitive disorders in general are closely linked with epilepsy and subclinical Epileptiform Electroencephalographic Activity (EEA). Furthermore, AD with Mild Cognitive Impairment (MCI) patients present abnormalities in posterior cortical sources of resting‐state eyes‐closed EEG rhythms at delta (< 4 Hz) and low‐frequency alpha (8‐10 Hz) rhythms. This retrospective study tested the hypothesis that ADMCI patients with EEA (ADMCI‐EEA) may be characterized by specific disease‐related abnormalities in delta and alpha rsEEG source activities compared with ADMCI patients without EEA (ADMCI‐noEEA) and noADMCI controls.MethodWe analysed data from an international database (www.pdwaves.org) comprising clinical, neuropsychological, rsEEG (25‐30 minutes), cerebrospinal fluid (CSF), and structural magnetic resonance imaging (sMRI) data in n = 42 ADMCI and n = 32 noADMCI patients without a diagnosis of epilepsy. The database also included clinical, neuropsychological, and rsEEG data of n = 38 matched cognitively unimpaired elderly (Nold) persons, used as additional controls in the present study. The rsEEG traces were reviewed by expert epileptologists blinded to the diagnostic status. EEA was detected in n = 8 ADMCI and n = 13 no‐ADMCI patients (Table 1). Individual alpha frequency peak (IAF) was used to determine the rsEEG delta, theta, and alpha bands. Regional rsEEG cortical sources were estimated using the eLORETA freeware.ResultCompared to the Nold and noADMCI‐noEEA groups, the noADMCI‐EEA group showed greater temporal rsEEG delta cortical source activity. Conversely, compared to the Nold and ADMCI‐noEEA groups, the ADMCI‐EEA group showed greater temporal and occipital rsEEG delta cortical source activity (Figure 1). Notably, CSF amyloid (but not sMRI‐based cortical atrophy) burden was greater in the ADMCI‐EEA than in ADMCI‐noEEA patients (Table 2).ConclusionThe abnormal temporal rsEEG delta cortical source activity in the ADMCI‐EEA and noADMCI‐EEA groups may reflect an unspecific susceptibility of the temporal lobe to slowing rsEEG activity for several neuropathological processes. Instead, the abnormal occipital rsEEG delta cortical source activity in the ADMCI‐EEA over the control groups may reflect a specific susceptibility of the occipital lobe to slowing rsEEG activity for AD‐related neuropathological processes in the cholinergic tract to the occipital cortex.