al., 2009; Tzilos et al., 2005). On the other hand, while previous reports on the effects of PSUD on brain GM volumes are sparse, they are at least consistent: GM volumes were reduced compared to age-matched drug-free controls in prefrontal and temporo-parietal cortices of active cocaine dependent individuals, many of whom were dependent also on other drugs (Ersche et al., 2011; Ersche et al., 2012), in the orbitofrontal cortex of polysubstance abusers abstinent for at least15 days (Liu et al., 1998), and in prefrontal cortex of polysubstance dependent individuals abstinent for more than 2 years (Tanabe et al., 2009). This suggests GM atrophy in active, short-term and long-term abstinent polysubstance users. We found appreciable GM volume loss in our one-month-abstinent PSU only in the temporal cortex, lenticular and thalamic GM. The apparent “normal” frontal and parietal cortical GM volume in our PSU sample could be the result of reactive astrogliosis described above (where actual cortical GM loss in the PSU may be masked by a comparable amount of volume gain from inflamed astrocytes), or where GM loss is offset by a neuroadaptive response to the need for greater cognitive control over substance use (e.g., see Koehler et al., 2013). The
