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Reversible Cytotoxic Edema?

Kon Chu, MD; Dong-Wha Kang, MD, PhD; Han-Joon Kim, MD; Yong-Seok Lee, MD, PhD; Seong-Ho Park, MD, PhD

Arch Neurol. 2002;59:123-127.

Background  Wernicke encephalopathy (WE) is a metabolic disorder of the central nervous system resulting from vitamin B₁ deficiency. The exact mechanisms underlying the pathogenesis of the lesions in WE are not completely understood. Vitamin B₁ deficiency is associated with intracellular and extracellular edema by glutamate_{N-methyl-D-aspartate} receptor–mediated excitotoxicity. Conventional magnetic resonance imaging (MRI) cannot differentiate the types of edema. Diffusion-weighted imaging (DWI) has been reported to detect early ischemic damage (cytotoxic edema) as bright areas of high signal intensity (SI) and vasogenic edema as areas of heterogeneous SI.

Objectives  To describe the DWI findings and to characterize the types of edema in WE using DWI.

Setting  Tertiary referral center.

Design and Methods  Two patients with WE underwent DWI and conventional MRI with gadolinium enhancement. Wernicke encephalopathy was diagnosed with salient conventional MRI findings (high SIs in the paramedian thalamus, periaqueductal gray matter, and mamillary bodies) and typical clinical history and symptoms. Apparent diffusion coefficient (ADC) values were measured in abnormal lesions by visual inspection of DWIs and T2-weighted echo planar images.

Results  T2-weighted and fluid-attenuated inversion recovery MRIs showed high SIs in the bilateral paramedian thalamus, mamillary bodies, and periaqueductal gray matter. The DWIs showed bright high SI in the corresponding lesions, and ADC values were decreased (patient 1: 512-545 x 10^-6mm²/s; patient 2: 576-612 x 10^-6mm²/s). The ADC decrease and the DWI high SI were normalized in 2 weeks with administration of thiamine hydrochloride.

Conclusions  Abnormalities on DWI and ADC decrease became normalized with adequate therapy. The MRI abnormalities in WE might be owing to the "reversible cytotoxic edema" caused by vitamin B₁ deficiency.

From the Department of Neurology and Clinical Research Institute, Seoul National University Hospital, Neuroscience Research Institute of Seoul National University Medical Research Center (Drs Chu, Kang, and Kim), and the Department of Neurology, Seoul Boramae Municipal Hospital (Drs Lee and Park), Seoul, Korea; and Section on Stroke Diagnostics and Therapeutics, National Institute of Neurological Disorders and Stroke (Dr Kang), Bethesda, Md.

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