Thiamine (vitamin B-1) deficiency can result in Wernicke encephalopathy, a serious neurologic disorder. Dr Carl Wernicke, a Polish neurologist, described it in 1881 as a triad of acute mental confusion, ataxia, and ophthalmoplegia. Korsakoff amnestic syndrome is a late neuropsychiatric manifestation of Wernicke encephalopathy with memory loss and confabulation; sometimes, the condition is referred to Wernicke-Korsakoff syndrome or psychosis. Thiamine deficiency is characteristically associated with chronic alcoholism, because it affects thiamine uptake and utilization. However, Wernicke encephalopathy may develop in nonalcoholic conditions, such as prolonged starvation, (AIDS), and can even develop in healthy infants given the wrong formulas. Alcohol abuse, AIDS, malignancy, hyperemesis gravidarum, prolonged total parenteral nutrition, iatrogenic glucose loading in any predisposed patient, and other disorders associated with grossly impaired nutritional status have been associated with Wernicke-Korsakoff syndrome. S.I., A 36-year-old male patient is married, unoccupied and he has 5 children. Patient has been using alcohol since 16 years. His alcohol consumption has increased during the last 3 years. His nutrition was poor. He was treated for alcohol addiction in our clinic a year ago. He was sober for only two weeks after the discharge. He was admitted to our polyclinic with alcohol drinking. Diazepam 50 mg/day was initiated to patient for withdrawal symptoms. Ataxia, confusion and ophthalmoplegia were occurred when diazepam dose was decreased to 30 mg/day. Wernicke’s encephalopathy was diagnosed to patient and thiamine 1200 mg/day and diazepam 60 mg/day treatments were initiated. Thiamine and diazepam doses were decreased during clinical observation and stopped after 15 days. Cranial MRI was normal. Following administration of thiamine, the patient’s symptoms spontaneously resolved. It becomes evident that the diagnosis of Wernicke’s encephalopathy is based mainly on clinical presentation, although the combination of symptoms is present in only 10% to 38% patients, depending on the series and 19% of the patients do not have any of the classical symptoms. Our case also had ataxia, confusion, ophthalmoplegia. Oculomotor dysfunctions are present in about 30% of patients. Unfortunately, the syndrome quite often develops subclinical and it may be overlooked or misdiagnosed. In the patient presented, the symptoms were typical and the diagnosis was confirmed by the rapid improvement and full recovery after thiamine administration. According to the literature, all symptoms and especially ocular palsies, respond so dramatically to treatment, that failure to recover within a few days, should raise doubts about the diagnosis. In this case patient’s symptoms spontaneously resolved. The 3 components of the classic triad of Wernicke encephalopathy are encephalopathy, ataxic gait, and some variant of oculomotor dysfunction. All 3 features of the triad are recognized in only about one third of cases. So assessing the case according to Wernicke differential diagnosis is important, when the clinicians notice one of the three characteristics.