Larger WM volumes in recently abstinent methamphetamine users were postulated to be a result of tissue inflammation and/or reactive astrogliosis as a response to tissue injury sustained from the chronic substance abuse (Chang et al., 2007; Thompson et al., 2004). A dose-related enhancement of neurological and histological signs of acute encephalomyelitis (brain inflammation) following in vivo administration of amphetamine or cocaine in rats was described (Nunez et al., 2007). Also, in rats administered with cocaine daily for 7 days, increases in glial fibrillary acidic protein and vimentin expressions, the hallmarks of reactive astrocytes and reactive gliosis (Pekny and Nilsson, 2005), were observed in the prefrontal cortex and nucleus accumbens at 3 weeks after substance administration (Bowers and Kalivas, 2003). These findings support the theory of brain tissue enlargement due to reactive astrogliosis. Therefore, it is not out of context to interpret the observed larger lobar WM volumes in our PSU cohort as inflammation and/or glial scarring associated with reactive astrogliosis observed at one month after withdrawal from chronic consumption of both alcohol and illicit substances.
