Some discordant twin studies have supported a two-hit (diathesis-stress) model of disease expression, in which posterior parietal brain regions may be vulnerable to environmental stressors in those at risk for schizophrenia, and after psychosis onset, the trajectory of deficits may proceed to engulf regions where a genetic liability for deficits has been found, such as the frontal lobes, leading to deficits in executive function and working memory (Cannon et al., 2002).
