Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Case Reports
. 2024 Dec 18;24(1):478.
doi: 10.1186/s12883-024-03979-4.

A case report about focal status epilepticus as first presentation in Alzheimer's disease: finding the culprit

Astrid Devulder  1   2 , Greet Vanderlinden  3 , Evy Cleeren  4   5 , Valerie Goovaerts  4 , Tom Theys  6   5 , Koen Van Laere  3   7 , Wim Van Paesschen  8   4
Affiliations
Case Reports

A case report about focal status epilepticus as first presentation in Alzheimer's disease: finding the culprit

Astrid Devulder et al. BMC Neurol. .

Abstract

Background: Neuronal hyperexcitability has been proposed to play a key role in Alzheimer's disease (AD). Understanding the relation between this enhanced excitability and AD pathology could provide a window for therapeutic interventions. However epileptiform activity is often subclinical, hidden on scalp EEG and very challenging to assess with current diagnostic modalities.

Case presentation: A woman in her sixties presented with acute confusion. Despite a normal scalp electroencephalogram (EEG), magnetic resonance imaging (MRI) showed cytotoxic edema of the right mesial temporal lobe and hippocampal hypermetabolism was present on ([18F]-fluoro-2-deoxyglucose positron emission tomography (PET). Bilateral foramen ovale (FO) electrodes were placed to directly record mesial temporal activity and revealed continuous mesial temporal epileptic activity, while scalp EEG remained normal. After recovery, a new diagnosis of AD was established on cerebrospinal fluid. The lateralization of the epileptiform activity was congruent with the predominant side of tau pathology in the mesial temporal cortex on 18F-MK6240 PET. On follow-up MRI, two and five months later, the right hippocampus became atrophic.

Conclusion: This case highlights the significant role of neuronal hyperexcitability in early AD pathogenesis and how shared mechanisms between AD and epilepsy can complicate clinical management.

Keywords: Alzheimer’s disease; Case report; Hippocampal atrophy; Tau pathology; Temporal lobe epilepsy.

PubMed Disclaimer

Conflict of interest statement

Declarations. Ethics approval and consent to participate: Written informed consent was obtained for all procedures from the participant and caregiver. The study was approved by the Ethical Committee of University Hospitals Leuven (clinical.trials.gov NCT03617497). Consent for publication: Patient gave written informed consent for publication of the manuscript. Competing interests: K.V.L. has contract research through Leuven Research and Development with BMS, Cerevel and Janssen Pharmaceuticals and is advisory board member for 18F-MK6240 for Cerveau-Enigma. W.V.P. has grant for Toegepast Biomedisch Onderzoeks-Fonds voor Wetenschappelijk Onderzoek (FWO-TBM) (T000423N) and receives consulting fees from Angeline Pharma, UCB Pharma and Byteflies. The other authors have nothing to report.

Figures

Fig. 1
Fig. 1
Imaging and EEG data. (A): Sequential brain MRI: axial FLAIR images. From left to right: Cytotoxic edema of the right hippocampus and amygdala (arrow) at presentation (MTA right 0/1); Decreased edema of the right hippocampus and amygdala (arrow) 20 days later (MTA right 1); Atrophy of the right hippocampus (arrow) with increased T2/FLAIR signal consistent with hippocampal sclerosis two months later (MTA right 2); Stable atrophy of right hippocampus with hippocampal sclerosis (arrow) five months later (MTA right 2). (B): Axial and coronal images of 18F-FDG PET at presentation with hypermetabolism of the right hippocampus (arrow). (C): Axial and coronal image of 18F-MK6240 tau PET one month later shows increased SUVR in the hippocampus (R > L) (arrow) and typical Braak neocortical brain regions, a pattern consistent with AD. (D): Intracranial EEG (bottom panel) obtained from FO electrodes and spectrogram (top panel) on day 2. Subclinical electrographic mesial temporal lobe seizure on right FO electrode (under treatment with levetiracetam): LPDs on right FO electrode with evolution in frequency and morphology and abrupt end. Spectrogram reveals first increased delta activity (LPDs) with evolution to faster activity on the right FO electrode at the time of seizure onset (white arrow). Continuous EEG of 60 s. A referential montage is shown where the upper four channels represent the four contact points (from anterior to posterior) of the right FO electrode, and the lower four channels represent the left FO electrode. Filters at 0.53–15.0 Hz, 300µV/cm. The top panel represents a one hour spectrogram where the upper spectrogram corresponds to the third contact of the right FO electrode, and the lower spectrogram to the third contact of the left FO electrode
See this image and copyright information in PMC

References

    1. Braak H, Braak E. Neuropathological stageing of Alzheimer-related changes. Acta Neuropathol. 1991;82:239–59. - PubMed
    1. Ossenkoppele R, Schonhaut DR, Scholl M, et al. Tau PET patterns mirror clinical and neuroanatomical variability in Alzheimer’s disease. Brain. 2016;139:1551–67. - PMC - PubMed
    1. Wu JW, Hussaini SA, Bastille IM, et al. Neuronal activity enhances tau propagation and tau pathology in vivo. Nat Neurosci. 2016;19:1085–92. - PMC - PubMed
    1. Schultz MK Jr., Gentzel R, Usenovic M, et al. Pharmacogenetic neuronal stimulation increases human tau pathology and trans-synaptic spread of tau to distal brain regions in mice. Neurobiol Dis. 2018;118:161–76. - PubMed
    1. Franzmeier N, Neitzel J, Rubinski A, et al. Functional brain architecture is associated with the rate of tau accumulation in Alzheimer’s disease. Nat Commun. 2020;11:347. - PMC - PubMed

Publication types

MeSH terms

LinkOut - more resources