Alcoholics suffer several neurological problems, including alcoholic dementia, cerebellar atrophy, and thiamine deficiency related to Wernicke's-Korsakoff encephalopathy. Cytokine-mediated neuroinflammation and oxidative damage may play a role in brain atrophy of uncomplicated alcoholics. Therefore, selenium and zinc deficiency, involved in antioxidative capacity, or iron excess, acting as a pro-oxidant, may all be involved. In this study on 61 alcoholic patients and 12 controls we found a more intense degree of atrophy in the former, differences affecting Huckmann (t = 2.95), bicauda (t = 3.93) and cella indices (t = 3.75) and cortical atrophy (t = 5.45, p < 0.001 in all cases). Differences were also observed between patients with cerebellar atrophy and those without, regarding copper (854 μg/l ± 181 μg/l vs. 1,088 μg/l ± 269 μg/l, p = 0.014), zinc (971 μg/l ± 696 μg/l vs. 1,817 μg/l ± 1,298 μg/l, p = 0.03), and serum ferritin, higher among patients with cerebellar atrophy (529 ± 370 ng/ml vs. 308 ± 209 ng/ml, p = 0.044). Serum ferritin showed a significant correlation with bicaudate index (rho = 0.3, p = 0.029) and Huckmann index (rho = 0.32, p = 0.02), and serum transferrin, an inverse one with Huckmann index (rho = -0.30, p = 0.031). However, selenium showed a direct, (opposite of what was expected) significant, correlation with the Huckmann index (rho = 0.35, p = 0.046). Thus, besides ferritin, higher among those with more intense atrophy, trace elements are only poorly related to brain atrophy, but patients with cerebellar atrophy do have lower serum copper and zinc levels.