Patients with disorders of the basal ganglia, such as Parkinson’s disease, Huntington’s disease and Tourette’s Syndrome, exhibit characteristic motor symptoms and less obvious cognitive deficits. These deficits can be understood with reference to the model of cortico-striato-thalamo-cortical circuitry proposed by Alexander et al. (1986) which highlights how the basal ganglia can affect the functioning of the whole of the frontal lobe. This thesis explored the possibility that patients with these disorders also have difficulties with social cognition. Patients with Parkinson’s exhibited deficits in reasoning about mental states. These deficits can largely be attributed to executive dysfunction which results from disordered activity in the circuitry linking the dorsolateral prefrontal cortex and the basal ganglia. Patients with Huntington’s exhibited reduced fear responses which most likely results from abnormal amygdala activity. Patients with Tourette’s exhibited deficits on a wide range of social cognitive tasks involving reasoning about mental states, non-literal language interpretation and economic decision making. These difficulties probably reflect dysfunction in circuitry linking the anterior cingulate and insula with the basal ganglia. These studies offer insight into the neuroanatomical basis of the behavioural symptoms associated with these conditions whilst highlighting the necessity to develop more precise and inclusive models of frontostriatal circuitry.