Abstract Details

Title Post-injury Autoimmune Encephalitis in Older Adults: A Shift from Classical Demographics

Topic Autoimmune Neurology

Presentation(s) P9 - Poster Session 9 (5:00 PM-6:00 PM)

Poster/Presentation
Number 1-008

Objective Report a series of individuals with onset of AE in the setting of an antecedent neurovascular event or neurologic comorbidity.

Background Autoimmune encephalitis (AE) is classically attributed to idiopathic autoimmune, paraneoplastic, or iatrogenic etiologies, including oncologic-directed immunotherapy. We report an observational cohort of older adults who experienced a neurovascular event or active central neurologic comorbidity closely preceding AE diagnosis. Whether prior CNS insult may unmask neuronal epitopes and permit AE development warrants further exploration.

Design/Methods

We retrospectively reviewed cases (2000–2024) from Massachusetts General Hospital and Hadassah Medical Center meeting:

1. Antibody-positive AE or probable seronegative AE (Graus et al., 2016), and

2. Documented neurologic insult or active central neurologic comorbidity within 12 months prior to AE diagnosis.

Data on demographics, insult type, antibody status, clinical features, imaging, CSF, and treatment were collected.

Results

Ten patients met inclusion criteria. All were male, with a mean age of 70.5 years (range 40–91). All were antibody-positive: LGI1 (n=6), NMDA receptor (n=3), and anti-Ma (n=1). Prior neurologic insults included neurodegenerative disease (4/10), cerebrovascular injury (3/10), epilepsy (2/10), and ALS (1/10).

Predominant clinical manifestations were cognitive decline (9/10), epileptic or paroxysmal events (7/10), and psychiatric/behavioral disturbances (6/10). Movement disorders occurred in 5/10, and autonomic features in 2/10. CSF was generally acellular with normal or mildly elevated protein. EEG most often showed focal slowing or epileptiform activity. MRI was normal at initial evaluation in 4/10. All patients received acute immunotherapy, and 9/10 subsequently required maintenance immunosuppression.

Conclusions This series raises the possibility that post-CNS injury mechanisms may contribute to AE pathogenesis, particularly in older seropositive males. Prior insults may expose neuronal epitopes, triggering secondary autoimmunity in individuals not traditionally considered at risk.

Authors/Disclosures
Giovanna Manzano, MD PRESENTER	Dr. Manzano has received personal compensation in the range of $500-$4,999 for serving as a Consultant for Gilead Sciences. Dr. Manzano has received personal compensation in the range of $500-$4,999 for serving on a Speakers Bureau for InfuCare Rx.
Tal Friedman Korn, MD	Dr. Friedman Korn has received personal compensation in the range of $500-$4,999 for serving on a Speakers Bureau for Roche.
tal benoliel, MD	Dr. benoliel has received personal compensation in the range of $500-$4,999 for serving as a Speaker at conference with Dexel pharma.
Benjamin Uliel, MD	Dr. Uliel has nothing to disclose.
Adi Vaknin-Dembinsky, MD	Dr. Vaknin-Dembinsky has received personal compensation in the range of $500-$4,999 for serving on a Scientific Advisory or Data Safety Monitoring board for Medison Pharma. Dr. Vaknin-Dembinsky has received personal compensation in the range of $500-$4,999 for serving on a Scientific Advisory or Data Safety Monitoring board for neopharm group. Dr. Vaknin-Dembinsky has received personal compensation in the range of $500-$4,999 for serving on a Speakers Bureau for medisone . Dr. Vaknin-Dembinsky has received personal compensation in the range of $500-$4,999 for serving on a Speakers Bureau for alexion.

��ɫ��

��ɫ��