A lcohol induces rest and relaxation, is a means of sharing, and plays an indispensable role in celebrations of many cultures. A little alcohol may stimulate original thoughts and many of us appreciate a spirited dinner conversation with a lively companion. However, there is no question that excessive and prolonged consumption of alcohol results in brain damage. The most dramatic alcohol-related neurologic disorders are central pontine myelinolysis (this can occur without hyponatremia), cerebellar degeneration, subdural hematomas associated with frequent falls, and the rare Marchiafava-Bignami syndrome. More common, in alcoholics, is the emergence of brain atrophy. A study in 30 alcoholics, ages less than 45 years, found that drinking of at least 125 g of alcohol per day for 10 years or more resulted in 30% sulcal atrophy on computed tomography (CT) scan. Brain shrinkage was also associated with a variety of neuropsychological test abnormalities. 1 The pathological feature in alcoholic brain damage is a decreased brain weight, when compared with controls, specifically caused by loss of white matter. [2][3][4][5] A more recent study suggested that neocortical nerve cell death does not occur and, thus, it may be speculated that loss of neuronal connections can be reestablished or restore their function after abstinence. 2 Harper and Kril hypothesize that only minor changes occur in myelin lamellae rather than extensive demyelination or axonal loss. The gray matter appears to be somewhat resistant to injury, but selective frontal lobe damage in the superior frontal association cortex has been documented. 4 An alternative explanation for white matter changes may be brain tissue rehydration, but serial magnetic resonance imaging (MRI) studies have not confirmed this. Harper 4 suggests that metabolites of ethanol, nitric oxide, or free radicals are involved in alcoholinduced neurotoxicity, but alcohol interference with thiamine absorption or storage may be operational as well.The serial CT scans in this issue of Liver Transplantation are of considerable interest. The images clearly show reduction in the number of sulci after a period of abstinence from alcohol, implicating reversibility of brain atrophy. There is no preferential change in the frontal or parietal lobe in this patient. The image, however, does not show a clear view of possible changes in the cerebellum. The publication of these CT scans should rekindle the interest in this phenomenon, particularly in the liver transplantation population.The images are, however, not novel because reversible brain shrinkage has been documented earlier by MRI in prior alcohol-dependent patients and may continue up to a year after cessation. 6 It would be of interest to see whether grafting of a healthy liver promotes reversibility and whether liver transplantation in itself facilitates remyelination. Future longitudinal studies using MRI scan in recovered alcoholics and recovered alcoholics with liver transplantation may answer this important question. Moreover, these stud...