ABSTRACT
Introduction
In past years, a possible bidirectional link between epilepsy and Alzheimer’s disease (AD) has been proposed: if AD patients are more likely to develop epilepsy, people with late-onset epilepsy evidence an increased risk of dementia. Furthermore, current research suggested that subclinical epileptiform discharges may be more frequent in patients with AD and network hyperexcitability may hasten cognitive impairment.
Areas covered
In this narrative review, the authors discuss the recent evidence linking AD and epilepsy as well as seizures semeiology and epileptiform activity observed in patients with AD. Finally, anti-seizure medications (ASMs) and therapeutic trials to tackle seizures and network hyperexcitability in this clinical scenario have been summarized.
Expert opinion
There is growing experimental evidence demonstrating a strong connection between seizures, neuronal hyperexcitability, and AD. Epilepsy in AD has shown a good response to ASMs both at the late and prodromal stages. The new generation ASMs with fewer cognitive adverse effects seem to be a preferable option. Data on the possible effects of network hyperexcitability and ASMs on AD progression are still inconclusive. Further clinical trials are mandatory to identify clear guidelines about treatment of subclinical epileptiform discharges in patients with AD without seizures.
Article highlights
Recent findings suggest a possible bidirectional link between epilepsy and Alzheimer’s disease (AD).
Seizures are more frequent in both sporadic and genetically determined forms of AD.
In patients with AD and mild cognitive impairment (MCI) due to AD, interictal and subclinical epileptiform activity was common, suggesting that neuronal hyperexcitability characterizes AD and may affect progression.
Epilepsy in AD has shown a good response to anti-seizure medications (ASMs).
Second- and third-generation ASMs with fewer cognitive adverse effects seem to be a preferable option.
Existing data on the possible effects of network hyperexcitability and ASMs on AD progression are still inconclusive; further clinical trials are needed to identify clear guidelines about treatment of subclinical epileptiform discharges in AD patients without seizures.
Declaration of interest
The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.
Reviewer disclosures
Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.