Vanadium, a metallic element of the first transition series is abundant in the environment. Occupational exposure is common with workers at workplaces and among those living near vanadium related industries such as metallurgical plants. Moreover atmospheric concentrations of vanadium have been on the increase in part due to emissions from petrochemical plants and increased combustion of fuel derived products. Despite the significant health problems thought to be associated with vanadium exposure, few studies have looked at the neurotoxic effect of the metal which is reviewed herein. Vanadium easily crosses the blood brain barrier, causing astrogliosis, oligodendrocyte depletion, neuroinflammation, necrosis of ependymal layer and disruption of the Blood Brain Barrier, demyelination and various locomotor deficits. Vanadium enters the brain through inhalation and different parenteral routes. In brain cell cultures, vanadium compounds cause apoptosis, DNA cleavage and promote iron-mediated oxidative stress. It has been proposed that most of the toxic effects of vanadium on the brain are due to the generation of reactive oxygen species and consequent lipid peroxidation. Though novel and an area that is of high current interest, there is still a dearth in the literature on the study of antidotal mechanisms against vanadium induced neurotoxicity.