Relative incidence of seizures and myoclonus in Alzheimer’s disease, dementia with lewy bodies, and frontotemporal dementia.
Open accessAbstract
BACKGROUND: Patients with Alzheimer's disease (AD) are more prone to seizures and myoclonus, but relative risk of these symptoms among other dementia types is unknown. OBJECTIVE: To determine incidence of seizures and myoclonus in the three most common neurodegenerative dementias: AD, dementia with Lewy bodies (DLB), and frontotemporal dementia (FTD). METHODS: Our institution's medical records were reviewed for new-onset unprovoked seizures and myoclonus in patients meeting criteria for AD (n = 1,320), DLB (n = 178), and FTD (n = 348). Cumulative probabilities of developing seizures and myoclonus were compared between diagnostic groups, whereas age-stratified incidence rates were determined relative to control populations. RESULTS: The cumulative probability of developing seizures after disease onset was 11.5% overall, highest in AD (13.4%) and DLB (14.7%) and lowest in FTD (3.0%). The cumulative probability of developing myoclonus was 42.1% overall, highest in DLB (58.1%). The seizure incidence rates, relative to control populations, were nearly 10-fold in AD and DLB, and 6-fold in FTD. Relative seizure rates increased with earlier age-at-onset in AD (age <50, 127-fold; 50-69, 21-fold; 70+, 2-fold) and FTD (age <50, 53-fold; 50-69, 9-fold), and relative myoclonus rates increased with earlier age-at-onset in all groups. Seizures began an average of 3.9 years after the onset of cognitive or motor decline, and myoclonus began 5.4 years after onset. CONCLUSIONS: Seizures and myoclonus occur with greater incidence in patients with AD, DLB, and FTD than in the general population, but rates vary with diagnosis, suggesting varied pathomechanisms of network hyperexcitability. Patients often experience these symptoms early in disease, suggesting hyperexcitability could be an important target for interventions.
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Seizures and hyperexcitability occur more frequently in primary tauopathies than in the general population.
“However, the possibility of seizures and hyperexcitability in primary tauopathies should not be ruled out, as they occur more frequently in these diseases than in the general population (Beagle et al., 2017; Sanchez et al., 2018).”
From Tauopathy and Epilepsy Comorbidities and Underlying Mechanisms (2022) · cites this paper as Beagle et al., 2017
The Results report seizure incidence six times higher in the FTD cohort than in age-matched controls, and the Methods show that this cohort included PSP and corticobasal degeneration. But the paper does not establish an elevated seizure rate specifically for primary tauopathies: the Discussion instead identifies higher myoclonus propensity in those disorders. The claim extends the cohort-level seizure finding to a narrower disease group. (LLM, conf=0.85)
Experimental — accuracy not yet measuredSeizures are more common in Alzheimer's disease and dementia with Lewy bodies than in primary tauopathies, such as frontotemporal dementia and progressive supranuclear palsy.
“Seizures are more common in AD and dementia with Lewy bodies than in primary tauopathies, such as frontotemporal dementia and progressive supranuclear palsy (Beagle et al., 2017).”
From Tauopathy and Epilepsy Comorbidities and Underlying Mechanisms (2022) · cites this paper as Beagle et al., 2017
The Results and Discussion report a higher cumulative incidence of seizures in AD and DLB than in FTD. The paper includes PSP among the FTD-spectrum disorders studied, but the passages do not establish a separate AD/DLB-versus-PSP comparison. They also do not characterize FTD as uniformly a primary tauopathy. (LLM, conf=0.86)
Experimental — accuracy not yet measuredA mechanism by which epileptogenesis gives rise to tau hyperphosphorylation may underlie the high incidence of tauopathy and epilepsy co-pathology found in diseases such as Alzheimer's disease and dementia with Lewy bodies.
“A mechanism by which epileptogenesis gives rise to tau hyperphosphorylation may underlie the high incidence of tauopathy and epilepsy co-pathology that is found in diseases such as AD and dementia with Lewy bodies (Vossel et al., 2016, 2017; Beagle et al., 2017).”
From Tauopathy and Epilepsy Comorbidities and Underlying Mechanisms (2022) · cites this paper as Beagle et al., 2017
The Introduction links epileptiform activity in AD to potentially increased tau production, and the Discussion reports seizures in AD and DLB alongside pathological tau. Neither section says that epileptogenesis causes tau hyperphosphorylation or establishes that mechanism as an explanation for the co-pathology. Page numbers are unavailable in our copy. (LLM, conf=0.84)
Experimental — accuracy not yet measured
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- Authors
- Beagle, A. J., Darwish, S. M., Ranasinghe, K. G., La, A. L., Karageorgiou, E., & Vossel, K. A.
- Affiliations
- University of California, San Francisco (US)
- University of Minnesota (US)
- Corresponding author
- Vossel, Keith A.
- Venue
- Journal of Alzheimer's Disease
- Publisher
- SAGE Publications
- Published
- 2017-08-29
- Volume
- 60
- Issue
- 1
- Pages
- 211-223
- ISSN
- 1387-2877 (ISSN-L)
- 1875-8908
- PMC
- PMC5608587
- OpenAlex
- W2746678792
- Cited by
- 173
- References
- 62
- Citations by year
- 2026: 18 · 2025: 24 · 2024: 27 · 2023: 17 · 2022: 17 · 2021: 25 · 2020: 27 · 2019: 10 · 2018: 8
- FWCI
- 10.11
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Journal of Alzheimer s Disease (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- University of California, San Francisco
- National Institute on Aging (K23AG038357, F32AG050434)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Health Sciences › Medicine › Psychiatry and Mental health › Epilepsy research and treatment
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Keywords
- Alzheimer's disease, dementia with Lewy bodies
- MeSH terms
- Aged, Alzheimer Disease, Female, Humans, Male, Middle Aged, Myoclonus, Psychiatric Status Rating Scales, Retrospective Studies, Seizures, Severity of Illness Index, Incidence, Age Distribution, Lewy Body Disease, Frontotemporal Dementia
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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