Teaching NeuroImages: The full-blown neuroimaging of Wernicke encephalopathy
M. Luigetti, MD,
S. De Paulis, MD,
P. Spinelli, MD,
M. Sabatelli, MD,
P. Tonali, MD,
C. Colosimo, MD and
A. Cianfoni, MD
From the Departments of Neurology (M.L., P.S., M.S., P.T.), Cardiovascular Medicine (S.D.P.), and Radiology (C.C.), Catholic University of Sacred Heart, Rome; Don Carlo Gnocchi ONLUS Foundation (P.T.), Rome, Italy; and Neuroradiology Section (A.C.), Radiology Department, Medical University of South Carolina, Charleston.
Address correspondence and reprint requests to Dr. Marco Luigetti, Institute of Neurology, Largo F. Vito 1, 00168 Rome, Italy mluigetti{at}gmail.com.
A 55-year-old man presented in a global confusional state andafter 24 hours fell into deep coma. Laboratory findings, includingalcohol level, were normal. MRI showed abnormalities typicalof Wernicke encephalopathy (figure).1,2 Thiamine was administeredimmediately, but the patient died 2 weeks later. The diagnosiswas confirmed by measurement of blood thiamine level (19.3 ng/mL;normal range 27.2–42.2), obtained after initiation oftreatment. Nonalcoholic Wernicke encephalopathy is probablyunderestimated; typical radiologic manifestations allow diagnosis.2Cortical involvement is indicative of irreversible lesions withpoor prognosis.2 Thiamine should be administered to reduce riskof clinical worsening.
Axial T2–fluid-attenuated inversion recovery images show abnormal high signal distributed symmetrically in the floor of fourth ventricle (arrows on A), periaqueductal gray matter and colliculi (arrows on B), hypothalamus and mammillary bodies (arrowheads on B), splenium (arrow on C), mesial thalami (arrowheads on C), and perirolandic cortex (arrowheads on D).
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