Studies of neurobiological risk factors suggest that COS is continuous with the adult-onset illness (R. Nicolson et al., 2000; R. Nicolson & Rapoport, 1999), so it would be expected that the GM changes in COS might eventually evolve into a pattern similar to that seen in the adult onset illness. Adult-onset studies using VBM or cortical thickness mapping methods, show predominantly cortical GM loss in prefrontal and superior temporal cortices (Kuperberg et al., 2003; Narr et al., 2005; White, Andreasen, Nopoulos, & Magnotta, 2003; Wiegand et al., 2004). In one study (P. M. Thompson et al., 2008), two time-lapse films were created from groups of first-episode adult-onset patients scanned 4 times over a year, after they were randomized to haloperidol or olanzapine treatment. In a convincing replication of the childhood-onset trajectory, the adult patients also exhibited a back-to-front wave of cortical gray matter loss, with greatest losses in the 3 months after psychosis onset, but proceeding into the frontal cortices a year later. Olanzapine-treated patients showed significant progressive gray matter reductions but in a more restricted anatomical pattern than in
