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Epileptic Seizures in Alzheimer Disease: A Review

Horváth, András MD; Szűcs, Anna MD, PhD; Barcs, Gábor MD; Noebels, Jeffrey L. MD, PhD; Kamondi, Anita MD, PhD

Alzheimer Disease & Associated Disorders: April-June 2016 - Volume 30 - Issue 2 - p 186–192
doi: 10.1097/WAD.0000000000000134
Review Article
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Alzheimer disease (AD) is the most frequent cause of major neurocognitive disorders with a huge economical and medical burden. Several studies pointed out that AD is associated with a high risk for developing epileptic seizures. The aims of our review were to evaluate and to summarize the current literature (ending in September 2015) of animal and human studies in the relation of AD and epileptic seizures. It seems likely that epileptic hyperexcitation could be partially responsible for the progression of AD due to the increased rate of amyloid deposition. Pathologic changes in animal models of AD are similar to those seen in human temporal lobe epilepsy. Antiepileptic treatment had a positive effect on cognitive function in animal and human studies. Because the detection of seizures in patients with cognitive decline is extremely difficult because of methodological problems, the true prevalence of seizures has remained unclear. Nonconvulsive seizures with no overt clinical symptoms may be frequent seizure types in AD. These are difficult to detect by clinical observation and with standard scalp electroencephalogram (EEG) methods. We propose that long-term EEG recording and video-EEG monitoring is necessary to prove the presence of epileptiform activity in demented patients.

*National Institute of Clinical Neurosciences

János Szentágothai Doctoral School of Neurosciences, Semmelweis University School of PhD Studies

§Department of Neurology, Semmelweis University, Budapest, Hungary

Baylor College of Medicine, Houston, TX

Supported by National Brain Research Program (KTIA_NAP_13-1-2013-0001) and MET Hungary Ltd.

The authors declare no conflicts of interest.

Reprints: András Horváth, MD, National Institute of Clinical Neurosciences, 57 Amerikai út, Budapest 1145, Hungary (e-mail: andras.horvath.semmelweis@gmail.com).

Received November 27, 2014

Accepted December 2, 2015

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