Diffusion abnormalities and Wernicke encephalopathy

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To the Editor: Doherty et al.1 shed new light on Wernicke encephalopathy (WE) and emphasized important but often-forgotten points on this fatal yet preventable entity. I wish to make a few relevant clinical and pathological points. Their second case illustrates that WE is not seen only in alcoholics but also in other forms of malnutrition (e.g., thiamine deficiency). I would add other circumstances, such as (but not limited to) anorexia nervosa, peritoneal dialysis or hemodialysis,2 and HIV infection,3 in which WE has occurred. In addition, I wish to emphasize that although the ocular signs are considered the hallmark of WE, it is now more recognized that the classic triad is neither consistently nor frequently encountered.4 I believe that every clinician should remember the many clinical circumstances in which WE may develop and that the classical clinical triad is not always present. Further, autopsy studies have shown that WE prevalence in both nonalcoholics and alcoholics far exceeds its recognition in living persons.4 On macroscopic examination, the involved areas are slightly shrunken and show brown discoloration due to hemosiderin deposition, typically but not limited to the mamillary bodies, and the periventricular and periaqueductal lesions often spare a slender strip of subependymal tissue.3 Microscopic sections might be needed to make the diagnosis of WE. Twenty-five percent of cases can have normal mamillary bodies on macroscopic examination, and visible hemorrhages are seen in only 5% of cases.5 # Diffusion abnormalities and Wernicke encephalopathy {#article-title-2} To the Editor: We read with great interest the paper from Doherty et al.,1 describing diffusion-weighted MR findings in two patients with WE. Typical MR alterations were found in both patients, including T2 hyperintensities …