Association between EEG Abnormalities and CSF Biomarkers in a Memory Clinic Cohort

Abstract

Background: The aim of the study was to describe distinct electroencephalogram (EEG) phenotypes defined after routine visual EEG analysis in a large memory clinic cohort and to investigate their relationship to cerebrospinal fluid (CSF) biomarkers. Methods: Patients with Alzheimer's disease (n = 131), mild cognitive impairment (n = 285), subjective cognitive impairment (n = 310), and mixed dementia (n = 29) were assessed clinically with neuroimaging, EEG and CSF investigations. EEG phenotypes were based on frequency of background activity (BA) and presence and degree of episodic abnormalities (EA). Results: BA and EA differed significantly (p < 0.001) between diagnostic groups. A lower CSF amyloid β42/phospho-tau ratio and higher total tau were associated with slower BA (p < 0.01) and a higher degree of EA (p < 0.04). Conclusions: Slowing of BA in combination with EA seems to be related to biological markers of neurodegeneration.

Electroencephalography Is a Good Complement to Currently Established Dementia Biomarkers

“…Although not statistically significant, this subgroup also showed higher Aβ 42 levels and less atrophy in the medial temporal lobe and posterior cortex. The association between CSF biomarkers and EEG abnormalities has been shown in previous studies [50]. Nonetheless, our CSF findings should be taken with caution due to the small sample size.…”

Electromagnetic signatures of the preclinical and prodromal stages of Alzheimer’s disease

“…Moreover, their non-invasive nature allows for repeated measurements to monitor the disease status or to evaluate the effects of intervention. Patients with Alzheimer’s disease and MCI generally show slowing of oscillatory brain activity ( Stam, 2010 ; Lizio et al , 2011 ; López et al , 2014 b ; Engels et al , 2016 ), and this slowing is associated with several factors such as cognitive status, risk of progression to dementia ( Fernández et al , 2006 b ; Prichep, 2007 ; López et al , 2016 ), hippocampal atrophy ( Fernández et al , 2003 ), hypometabolism ( Rodriguez et al , 1998 ), CSF tau levels ( Jelic et al , 1998 ; Stomrud et al , 2010 ; Kramberger et al , 2013 ), APOE4 genotype ( Lehtovirta et al , 1996 ; de Waal et al , 2013 ; Cuesta et al , 2014 ), and low cholinergic activity ( Riekkinen and Sirviö, 1990 ). However, the usefulness of EEG/MEG characteristics as biomarkers for the evaluation of predementia stages of Alzheimer’s disease is not yet fully established.…”

“…However, the usefulness of EEG/MEG characteristics as biomarkers for the evaluation of predementia stages of Alzheimer’s disease is not yet fully established. One main reason is that only a few studies of predementia stages of Alzheimer’s disease have been performed in which EEG/MEG was combined with amyloid-β biomarker information ( Jelic et al , 1998 ; Stomrud et al , 2010 ; Kramberger et al , 2013 ; Gouw et al , 2017 ; Nakamura et al , 2017 ). Therefore, the main objective of this study was to explore potential electrophysiological signatures that may act as surrogate markers of the pathophysiological changes that occur in the predementia stages of Alzheimer’s disease.…”

Amyloid Associated Intermittent Network Disruptions in Cognitively Intact Older Subjects: Structural Connectivity Matters

“…Only about 2% of the patients diagnosed with mild cognitive impairment (MCI) or dementia due to sporadic AD show overt epileptiform discharges during routine EEG recordings though. Intermittent unspecific EEG abnormalities, e.g., episodic focal or diffuse slowing of the background activity, indicative for low level focal or diffuse paroxysmal hypersynchrony are more common in MCI and AD and can be found in 20–45% of the routine EEGs (Liedorp et al, 2009 , 2010 ; Kramberger et al, 2013 ). If paroxysmal hypersynchrony severe enough to be detected by routine EEG occurs in the more advanced stages, it is very well-possible that it is already present in a more subtle form in the preclinical stage and contributes to the conflicting resting state findings depending on its severity and frequency in the study population.…”