Supersensitivity psychosis is a subdiagnosed clinical reality. This entity, however, is insufficiently elucidated from the point of view of the neurobiochemical mechanisms involved in the pathogenesis. The combination of an antipsychotic with a high D2 receptor blocking capacity and a neuroleptic-like substance such as cinnarizine trigger the dopaminergic hypersensitivity mechanisms. This stimulates the sensitivity for dopamine in the prefrontal cortex, ameliorating the negative and cognitive symptoms at the thalamic level, remodeling sensory integration and decreasing tinnitus, as well as in the cerebral tonsil, consequently decreasing the risk of antisocial behavior.