Late-onset Epilepsy of Unknown Etiology Is More Likely to Be Treatment-responsive Than Lesional Late-onset Epilepsy
Abstract number :
2.212
Submission category :
4. Clinical Epilepsy / 4A. Classification and Syndromes
Year :
2024
Submission ID :
18
Source :
www.aesnet.org
Presentation date :
12/8/2024 12:00:00 AM
Published date :
Authors :
Presenting Author: L. Brian Hickman, MD, MSc – University of California, Los Angeles
Mohit Bandla, MS, BS – University of California, Los Angeles
Alexander Fish, BA – University of California, Los Angeles
Adnan Husein, MD – University of California, Los Angeles
Corinne Allas, BS – University of California, Los Angeles
Harika Kottakota, BS – University of California, Los Angeles
Lauren Herzog, MD – University of California, Los Angeles
Bhavya Pandey, Undergraduate Student – University of California, Los Angeles
Keith Vossel, MD, MSc – University of California, Los Angeles
John Stern, MD – University of California Los Angeles
Rationale: While most older adults with new incidence of epilepsy have a detectable, lesional etiology, 25-50% of late-onset epilepsy cases do not have an identifiable cause. These cases, known as late-onset epilepsy of unknown etiology (LOEU), are associated with an elevated subsequent incidence of dementia. Proposed causes of LOEU include undetected age-related neurodegenerative pathology and occult cerebrovascular disease. We compared medical comorbidities and epilepsy evaluation/treatment history between LOEU and lesional late-onset epilepsy to assess for clinical features suggestive of LOEU beyond lack of identifiable lesion.
Methods: We performed a retrospective chart review of patients with onset of epilepsy at or above age 55 years and either epilepsy-protocol brain MRI or epilepsy monitoring unit (EMU) evaluation at UCLA from April 2013 to April 2023. Cases meeting criteria were reviewed for identified etiology of epilepsy from neurologist/epileptologist evaluations, described lesions on neuroradiology reports, comorbidities, and medical history. Cases without an identifiable etiology, including hippocampal sclerosis without known etiology, were categorized as LOEU. Patients with pre-existing dementia, amyloid angiopathy, autoimmune encephalitis, and lesions with uncertain significance (e.g., cerebral microhemorrhages, possible demyelinating lesions) were excluded. Analyses were performed using multivariate logistic regression controlling for sex, age of onset, and epilepsy duration.
Results: We identified 61 cases consistent with LOEU and 56 cases with lesional late-onset epilepsy. Of lesional cases, etiologies included ischemic stroke (n=15), cerebral tumor (n=15), developmental anomaly (n=9), infectious meningitis/encephalitis (n=6), post-traumatic (n=6), and intracranial hemorrhage (n=5). Age of onset (median: 63) and age at most recent evaluation (median: 70) were not significantly different between groups. LOEU was less likely to have a documented history of status epilepticus compared to lesional epilepsy (6.6% vs 23.2%, aOR: 0.21, 95% CI: 0.06-0.72, p< 0.02). Furthermore, patients with LOEU were less likely to be prescribed two or more concurrent ASMs than lesional epilepsy (29.5% vs 48.2%, aOR: 0.37, 95% CI: 0.17-0.83, p< 0.02) and were less likely to have undergone an EMU evaluation (21.3% vs 35.7%, aOR: 0.38, 95% CI: 0.16-0.91, p< 0.04). Comorbid hyperlipidemia was less frequently observed in LOEU (41.0% vs 58.9%, aOR: 0.47, 95% CI: 0.22-0.99, p=0.046), though rates of hypertension and diabetes mellitus were not significantly different between groups (p=0.11 and p=0.07, respectively).
Clinical Epilepsy