Wernicke's encephalopathy.

A 35 year o ld chronic a lcohol ic presented wi th progress ive ly increas ing e r ra t i c behaviour and emotional instability for the preceding 72 hours. On examination, he was afebrile and had normal vitals (BP: 110/86 mm of Hg). Neurological examination revealed disorientation to time and place, indifference and inattention. He also had impaired memory with poor recall. The pupils were unequal and had a sluggish reaction. The extra-ocular muscle movements were normal with fine nystagmus on horizontal gaze. The gait was slow, wide based with short spaced steps. He had no asterixis and plantars were downgoing. The random capillary glucose was 58 mg/dl and he was given 25 gm. of glucose intravenously and maintained o n g l u c o s e s a l i n e d r i p . B a s e l i n e investigations including complete blood count and comprehensive metabolic panel were non-contributory. CT scan brain, CSF analysis, serum ammonia, HIV serology and thyroid study didn’t reveal any abnormality. The patient developed progressive clinical deterioration over the course of next 48 hours in the form of increased drowsiness and stupor. He developed hypotension (BP: 88/64 mm of Hg). Pupils became small and unreactive. Plantars remained flexors bilaterally. MRI brain (T2 weighted FLAIR images) revealed hyperintense signal changes in both the thalamus (Figure 1) and peri-aqueductal gray matter (Figure 2) symmetrically without contrast enhancement. The history, clinical findings and neuroimaging suggested Wernicke’s encephalopathy (WE). The patient was given thiamine (100 mg IV daily), with marked clinical improvement in the next four days. However, residual memory defects persisted to some extent. Thiamine (vitamin B-1) deficiency can result in WE, a serious neurological disorder. The components of the classic triad of WE are encephalopathy, ataxic gait, and some variant of oculomotor