STAA or LTAA with comorbid stimulant dependence had subcortical volumes which did not differ from NSAC. In STAA, DASD showed larger subcortical volumes than DAO; in LTAA, no such differences were evident, yet the lower volumes in LTAA DAO vs. NSAC were no longer present in LTAA DASD. This set of results is consistent with either of the two hypotheses. In the first hypothesis, comorbid stimulant abuse/dependence protects individuals from alcohol dependence induced atrophy. In the second hypothesis, comorbid stimulant abuse/dependence causes inflammation of the already atrophied tissue, masking the effects of alcohol dependence induced subcortical atrophy, with the inflammatory effect diminishing with long-term abstinence. Our cognitive data is highly supportive of the inflammation hypothesis. If stimulants were protective, we would have expected alcoholics DASD to show less cognitive impairments than alcoholics DAO – the results showed DASD evidenced numerically (but not statistically) more impairment than DAO. The lack of associations of subcortical volumes with cognitive performance measures in STAA DAO is consistent with subjects DAO having reached a threshold of subcortical volume reduction that negatively impacts cognitive function.
