“…Alcoholics are at special risk for thiamine deficiency because of the poor diet associated with their lifestyle and because chronic alcoholism compromises thiamine absorption from the gastrointestinal tract, impairs storage, and may reduce thiamine phosphorylation, essential for cellular function (Lieber, 2003a;Martin et al, 2003;Thomson et al, 1987;Todd and Butterworth, 1999). Parenteral thiamine treatment given in the early symptomatic stages largely reverses the classical neurological signs of ophthalmoplegia, nystagmus, ataxia of gait, and amnesia for new information (Caine et al, 1997;Victor et al, 1971Victor et al, , 1989, although severe or undertreated cases may show enduring memory impairment and ataxia defining Korsakoff's syndrome (Butters and Cermak, 1980;Kopelman, 1995;Talland, 1965;Victor et al, 1959). Neuroradiological studies of WE since the 1970s report in vivo signs of hyperintensity in thalamus, periventricular gray matter, inferior colliculi, and occasionally in cerebellum, observations consistent with post-mortem reports (eg, Baker et al, 1999;Kril, 1988, 1990;Kril et al, 1997;Torvik et al, 1982Torvik et al, , 1986, with partial lesion resolution with treatment.…”