Abstract Details

Title Wernicke’s Encephalopathy: Ophthalmologic and Neuroanatomic Correlates in Multiple Etiologies

Topic General Neurology

Presentation(s) P1 - Poster Session 1 (8:00 AM-9:00 AM)

Poster/Presentation
Number 7-009

Objective To characterize the clinical, ocular, and radiologic spectrum of Wernicke’s encephalopathy (WE), emphasizing atypical ocular findings and MRI correlates that may facilitate earlier recognition.

Background Wernicke’s encephalopathy (WE) is a neurological emergency caused by thiamine deficiency, classically presenting with confusion, gait ataxia, and ophthalmoplegia. Although historically linked to alcoholism, thiamine depletion occurs in numerous settings such as hyperemesis, bariatric surgery, malignancy, and dialysis. Since diagnosis often precedes laboratory confirmation, recognizing characteristic ocular and imaging findings is critical for timely treatment and prevention of irreversible deficits.

Design/Methods A systematic literature search was performed using PubMed, Embase, and Scopus through October 2025. Case reports and case series were included if WE was confirmed clinically, biochemically, or radiographically. Extracted data included demographics, precipitating etiology, neurologic and ophthalmologic features, MRI findings, thiamine treatment (dose and route), and outcomes.

Results A total of 108 unique cases met inclusion criteria. Non-alcoholic etiologies accounted for 56%, primarily postoperative malnutrition, hyperemesis gravidarum, and malignancy-related cachexia. Ocular motor dysfunction was present in 91% of cases: nystagmus (upbeat 48%, downbeat 27%), abducens palsy 33%, and internuclear ophthalmoplegia 11%. Optic neuropathy or retinal hemorrhage occurred in 7%. MRI demonstrated bilateral medial thalamic and periaqueductal lesions in over 60%, with mammillary body or cerebellar involvement in about 40%. Intravenous thiamine typically produced neurologic improvement within 48 hours, but treatment delays beyond 5 days were associated with persistent ocular or cognitive deficits.

Conclusions WE is frequently underrecognized outside alcoholic populations. Early ocular manifestations, particularly vertical or gaze-evoked nystagmus and abducens palsy, serve as critical diagnostic clues. Immediate administration of high-dose parenteral thiamine yields rapid recovery, whereas diagnostic delay increases residual morbidity. Integrating ocular and MRI findings into diagnostic protocols can improve early detection and outcomes.

Authors/Disclosures
Dean Neutel PRESENTER	Mr. Neutel has nothing to disclose.
Matthew J. Thomas, ScM	Mr. Thomas has nothing to disclose.
Nasser Mohammed, MBBS (MD Anderson Cancer center)	Dr. Mohammed has nothing to disclose.

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