Imaging description

Wernicke’s encephalopathy (WE) is an acute neuropsychiatric syndrome that develops secondary to nutritional deficiency of thiamine (vitamin B1), which is seen in alcoholics and non-alcoholics with nutritional deficiency as a result of a variety of gastrointestinal problems including anorexia nervosa, bariatric surgery, malabsorption, and hyperemesis.

Typical imaging findings include T2 signal increase in the medial and posterior thalami, mammillary bodies, tectal plate, and periaqueductal area (Fig. 41.1) [1]. Symmetric signal abnormality in the medial thalami is the most characteristic finding, seen in 80% of patients. Mammillary body involvement is seen in all patients in autopsy series but only in 50% of MRIs. Petechial hemorrhage within lesions has been reported to occur in autopsies but this is not a common finding on MRI.

Although there is no significant difference in their clinical presentation, alcoholic and non-alcoholic patients may have differences in their pattern of imaging abnormalities. Non-alcoholic patients show atypical MR imaging features including increased T2 signal in the cranial nerve nuclei, cerebellum dentate nuclei, vermis, red nuclei and caudate nuclei, splenium, cerebral cortex, and fornix [2,3]. These atypical findings are always seen with more typical findings. Depending on the timing of imaging and severity of damage the DWI signal is variable. Enhancement on post-contrast T1-weighted images is also seen in approximately half of the patients, and more frequently in alcoholic patients (Fig. 41.2) [2,4].