Abstract
The striatum plays an important role in the pathophysiology of psychotic disorders.1 Its function is heavily modulated by dopamine and it contains a rich abundance of D2 receptors—the primary target for most antipsychotic agents.2 Markers of striatal dopamine are robustly elevated (by 14% on average) in patients with schizophrenia, irrespective of medication status.3,4 Similar elevations have been reported in patients’ unaffected relatives5 and individuals in an at-risk mental state (ARMS) for psychosis,6,7 suggesting that striatal dopamine dysregulation represents a risk phenotype for psychotic illness.