Authors :
Presenting Author: Peiyu Wang, MD – West China Hospital, Sichuan University
Lu Lu, MD – West China Hospital, Sichuan University
Jiani Chen, MD – West China Hospital, Sichuan University
Weixi Xiong, MD – West China Hospital, Sichuan University
Xintong Wu, MD – West China Hospital, Sichuan University
Dong Zhou, MD – West China Hospital, Sichuan University
Rationale: Late-onset epilepsy (LOE) has gained much attention due to its association with cognitive impairment and accelerated cognitive decline. Furthermore, a bidirectional relationship between LOE and Alzheimer's disease (AD) is suggested. Scalp electroencephalography (EEG) is a non-invasive tool that is popular in the research of epilepsy and cognitive impairment due to AD and other dementing diseases. However, few studies have explored the use of EEG in predicting the risk of cognitive decline in LOE.
Methods:
In this cross-sectional study, we retrospectively collected VEEG recordings from 142 cognitively normal participants with LOE (LOE-CN), 67 participants with LOE and cognitive decline (LOE-CD), and 132 cognitively normal elderly healthy controls (HC). LOE was defined as having the first seizure after the age of 55. In the LOE-CD group, a subgroup of 42 participants with cognitive decline related to AD (LOE-CDAD) was further divided. The electrodes were placed according to the International 10-20 system, extended by inferior temporal lobe electrodes FT9/FT10 and TP9/TP10. VEEGs were visually reviewed by two epileptologists; disagreement was mediated by a third reviewer to reach a consensus conclusion.
Results:
There was a trend of an increasing proportion of overall abnormal EEGs and an increasing presence of generalized delta activities, focal delta and theta activities, and subclinical epileptiform activities (SEAs) across the HC, LOE-CN, and LOE-CD groups. Between the LOE-CN and LOE-CD groups, binominal logistic regression revealed that depressed mood, abnormal neuroimaging findings, overall abnormal EEGs, presence of generalized delta activities and focal slowing (especially left temporal slowing) were associated with an increased risk for cognitive decline. These EEG markers remained significant after controlling for age, sex, years of education, seizure frequency, depressed mood and neuroimaging abnormalities. In the subgroup analysis, SEAs in both right and left temporal regions (Bi-temporal SEAs) and SEAs with a maximal voltage at FT9 or FT10 (FT9/10 SEAs) were more frequent in the LOE-CDAD group compared to LOE-CN (35.71% versus 12.68%, 47.62% versus 21.13%, respectively). Overall abnormal EEGs, generalized delta activities, Bi-temporal SEAs, and FT9/10 SEAs were independently associated with an elevated risk of cognitive decline due to AD. Stepwise regression was performed. Diabetes, lipidemia, regular alcohol consumption, depressed mood, focal slowing, generalized delta activities, presence of SEAs, Bi-temporal SEAs, and SEAs with a maximal voltage at FT9 were included in the predictive model, which performed well in distinguishing LOE-CDAD participants from their LOE-CN counterparts with an AUC of 0.83.
Conclusions: Generalized delta slowing and specific features of SEAs are associated with cognitive decline in LOE. Medial temporal lobe SEAs are specifically related to AD-related cognitive decline in LOE, warranting further investigation. Considering the mutual facilitatory effect between LOE and AD, these EEG features could provide guiance on which patients with LOE are at higher risk for cognitive decline.
Funding: No funding was received in support of this abstract.