Wernicke encephalopathy after bariatric surgery: Losing more than just weight D. Foster, DO; M. Falah, MD; N. Kadom, MD; and R. Mandler, MD Bariatric surgery is a frequent treatment for obesity. Neurologic complications after surgery include encephalopathy, behavioral abnormalities, seizures, cranial nerve palsies, ataxia, plexopathy, myelopathy, polyneuropathy, mononeuropathy (carpal tunnel syndrome, meralgia paresthetica), compartment syndrome, neuropathy, and myopathy. In particular, Wernicke encephalopathy, caused by vitamin B1 deficiency, can result in permanent neurologic deficit. 1,2 We report unusual clinical and imaging findings in a postgastric bypass patient with Wernicke encephalopathy.Case report. A 35-year-old woman underwent gastric bypass surgery for obesity. Subsequently, she reported anorexia, nausea, vomiting, and generalized fatigue, resulting in hospitalization. The patient continued to develop progressive hearing loss, psychomotor slowing, apathy, forgetfulness, ataxia, and bilateral hand paresthesias. In the 12th postoperative week, she had lost 40 lbs, was lethargic and confused, and had difficulty walking. She was awake but not attentive, speech was fluent, and comprehension was decreased. Pupils were equal and reactive to light, extraocular movements were intact, there was no nystagmus, and hearing was diminished. Strength was 3/5 in the lower extremities and normal in upper extremities, vibratory sense was diminished in feet, deep tendon reflexes were absent, plantar reflexes were down-going, and gait was wide-based. Laboratory tests were normal for blood count, thyroid function, vitamin B 12 , and CSF. Abnormal results included a slight elevation in liver enzymes, high serum glucose (163 mg/dL), and low serum potassium (2.6 MEq/L). EEG and head CT were normal.The patient's mental status continued to decline despite treatment for dehydration. Upon admission to our hospital, the heart rate was 125 beats/min; she opened her eyes to nail bed pressure but followed no commands and was nonverbal. The pupils were round and fixed at 3 mm, oculocephalic and deep tendon reflexes were absent, plantar reflexes were down-going, and general muscle tone was flaccid without spontaneous movements or withdrawal to painful stimuli. Abnormal test results were as follows: serum glucose (256 mg/dL), CSF protein (90 mg/dL), and diffuse slowing on EEG. Pretreatment red blood cell transketolase and serum thiamine levels were not down. The first MRI showed bilateral symmetric hyperintense signal on T2-weighted and fluidattenuated inversion recovery (FLAIR) images at the floor of the fourth ventricle, periaqueductal gray matter, the medial portions of both thalami, and the premotor and motor cortices (figure, A through C). All T2 hyperintense regions demonstrated contrast enhancement. Restricted diffusion was seen in the same regions on diffusionweighted imaging (DWI) and apparent diffusion coefficient maps.Initially, thiamine 100 mg IV showed no clinical improvement. Subsequently, high-dose thiamine (100 mg ...