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 haloperidol-treated patients. The spreading wave in the childhood-onset cases was earlier, a pattern that is considered by many researchers to represent the disease process interacting with normal brain development (Pantelis et al., 2003). Even so, in the adult time-lapse study, we also found a strikingly similar trajectory in adult-onset patients receiving haloperidol, despite these subjects being a decade older. As many developmental processes continue until middle age (Bartzokis et al., 2003), late intra-cortical myelination processes that continue throughout life may be derailed in schizophrenia (Peters & Sethares, 2004). Alternatively, these gray matter volume deficits may reflect an active disease process that occurs early in the illness. Whether psychosis onset occurs in adolescence or adulthood, active pathophysiology may be combined with exaggerated or dysregulated neurodevelopment (Lieberman, 1999; Lieberman et al., 2005; Woods, 1998). These structural differences are extremely dynamic in the first year after psychosis onset; this serves as a caveat to researchers seeking an MRI-based biological marker for genetic or
