Wilson’s disease (WD) is a rare, genetic disorder. The main defect of hepatocellular copper deposition is caused by pathogenic variants in the copper-transporting gene, ATP7B. Abnormal deposition of free copper occurs in various organs but mainly in the liver and brain. The changes found on brain magnetic resonance imaging are hyperintensity signal lesions in the basal ganglia, thalamus, cortex, and in other structures. As well as movement disorders, brain damage causes psychiatric symptoms (depression, mania, anxiety, etc.) and behavioral disturbances, such as apathy, irritability, cognitive deficits, limited control of cognitive and social behavior, etc. These dysfunctions are primarily thought to result from frontobasal neural loops pathology. The loops regulate activation, supervisory cognitive, self-regulation, and metacognitive functions. Additionally, some behavioral symptoms may be adaptive in their nature, arising as a reaction to stress caused by the disease that can severely disable the patient in an unpredictable way. Not all WD patients have behavioral dysfunctions if they are properly and systematically treated.