Home-based EEG and MEG for detection of subclinical epileptiform activity in Alzheimer’s disease

  • out-of-lab
  • neural oscillations

Can home-based EEG recorded with portable EEG devices help us detect and follow the progression of Alzheimer’s disease?

Alzheimer’s disease (AD) remains one of the most prevalent neurodegenerative disorders, affecting millions worldwide. While the hallmark symptoms of AD include memory loss and cognitive decline, recent research has shed light on a potential link between AD and subclinical epileptiform activity (SEA).

The group of scientists from Belgium, led by Amber Nous published a study in Alzheimer’s Research & Therapy that delves into this intriguing connection. The study explores the prevalence of SEA across the AD continuum and its impact on disease progression and cognitive function.

Understanding Subclinical Epileptiform Activity: Epileptic seizures have long been recognized as a comorbidity of AD. However, researchers have begun to uncover evidence of SEA, which refers to abnormal electrical activity in the brain detected by home-based EEG or magneto-encephalography (MEG) without accompanying clinical seizures.

This subclinical activity is of particular interest due to its potential role in accelerating cognitive decline in AD patients.

Research Objectives

The study aimed to achieve several key objectives:

  1. Estimate the prevalence of SEA and interictal epileptic discharges (IEDs) in individuals along the AD continuum, ranging from preclinical AD to advanced dementia, compared to cognitively healthy controls.
  2. Evaluate the efficacy of different detection methods, including long-term home-based EEG (LTM-EEG), high-density EEG (hd-EEG), and MEG, in identifying SEA in AD.
  3. Characterize AD patients with SEA based on clinical, neuropsychological, and neuroimaging parameters to gain insights into the impact of epileptiform activity on disease progression and cognitive function.

Research Procedure

Long time home-based EEG recording (LTM-EEG)

The study involved 49 subjects from the AD continuum (8 patients with dementia due to AD, 33 patients with mild cognitive impairment – MCI and 8 patients with preclinical AD) diagnosed according to 2011 National Institute on Ageing and Alzheimer’s disease (NIA-AA) criteria, and 24 cognitively healthy controls.

Seventy-one participants (8 dementia, 32 MCI, 8 preclinical AD and 23 healthy controls) underwent LTM-EEG monitoring with a median EEG time of 23.5 h and with a median artefact-free time of 18 h. Part of the participants (44 of them)  underwent this EEG monitoring at home, using Smarting wireless EEG device connected to a mobile phone.

Time between neuropsychological testing and LTM-EEG was maximally 9 months

High density EEG recording (hd-EEG)

Thirthy nine participants underwent high density EEG recording. 50 min of resting-state hd-EEG-monitoring in a sleep promoting environment (darkened room, laying down, encouraged to fall asleep) at the CUB Hôpital Erasme (Brussels, Belgium), some of them simultaneously with MEG (n = 10).

Time between neuropsychological testing and hd-EEG was maximally 16 months.

Magnetoencephalography (MEG)

Twenty-three participants underwent 50 min of resting-state MEG in a sleep-promoting environment (darkened room, laying down, encouraged to fall asleep) at the CUB Hôpital Erasme (Brussels, Belgium).


Results revealed a significantly higher prevalence of SEA in AD subjects (31%) compared to controls (8%). Furthermore, the prevalence of SEA increased as the disease advanced, with rates of 50% in dementia, 27% in mild cognitive impairment (MCI), and 25% in preclinical AD.

Prevalence of Subclinical Epileptiform Activity (SEA) in Alzheimer Disease (AD) continuum patients and healthy volunteers
Prevalence of Subclinical Epileptiform Activity (SEA) in Alzheimer Disease (AD) patients compared to healthy controls (A) and dementia, MCI or Preclinical AD compared to healthy controls (B)

In terms of detection methods, MEG did not demonstrate a higher prevalence of SEA compared to LTM-EEG and hd-EEG. MEG was still statistically better in detecting spikes per 50minute recordings. Additionally, AD patients with SEA exhibited worse performance on visuospatial and attention tasks and had larger volumes in specific brain regions compared to those without SEA.

There were no significant differences in the prevalence of SEA or spike number found by LTM-EEG versus 50-min hd-EEG in AD. However, in those AD participants in whom they found SEA and both LTM-EEG and hd-EEG were available, hd-EEG was able to detect SEA in 5 AD participants in whom LTM-EEG did not, and LTM-EEG was able to detect SEA in 4 AD participants in whom hd-EEG did not. Therefore, the scientists concluded that these techniques remain complementary in detecting SEA in AD (check out our high-density wireless EEG systems Smarting PRO X).

An example of the spike discharge left and right, recorded with long-term home-based EEG recordings using Smarting wireless EEG in a home-based environment.
An example of the left fronto-temporal spike (left) and left temporal spike (right) recorded with long term EEG recordings using Smarting wireless EEG in a home-based environment.

Implications and Future Directions

These findings have significant implications for both the diagnosis and management of AD. The identification of SEA in individuals along the AD continuum highlights the need for comprehensive neurological assessments, including EEG or MEG, to detect epileptic activity even in the absence of clinical seizures. Early detection of SEA may offer insights into disease progression and facilitate targeted interventions aimed at slowing cognitive decline.

Moreover, the superior efficacy of MEG in detecting epileptic spikes suggests its potential as a valuable tool in clinical practice for assessing epileptiform activity in AD patients. Future research endeavors should further explore the mechanistic links between epileptiform activity and AD pathology, potentially uncovering novel therapeutic targets for addressing both conditions.


In conclusion, the study underscores the importance of considering subclinical epileptiform activity in the evaluation and management of individuals with AD. The detection of SEA in AD patients is equally good using home-based EEG and MEG methods. The prevalence of SEA across the AD continuum, coupled with its association with cognitive decline, highlights the complex interplay between epilepsy and AD pathology.

Moving forward, continued research efforts in this area hold promise for advancing our understanding of disease mechanisms and improving patient outcomes through targeted interventions.

The full paper can be found on this link: https://link.springer.com/article/10.1186/s13195-023-01373-9 

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