to explore the potentially modulating effects of other individual characteristics; of particular interest are the impact of co-morbid disorders (for example, depression may exacerbate deficits in addicted individuals152) and of the recency of drug use and duration of abstinence (for example, cocaine may reduce or mask underlying cognitive153 or emotional154 impairments in cocaine-addicted individuals). Longitudinal studies would enable examination of these issues, which are of particular importance to those who abstain from drugs in the hope that PFC functioning will recover. Furthermore, comparison between different types of abused substances would allow differentiation between factors that are specific to certain drugs from factors that could be common across addiction populations. Instead of treating the heterogeneity of neural and behavioural changes in addiction as noise, studies could explore it with the goal of answering key questions: is PFC dysfunction in iRISA more prominent in certain addicted individuals than in others? Does self-medication drive drug taking more in some individuals than in others? How does co-morbid drug use, which is more the rule than the exception (for example, most alcoholics are nicotine-addicted), affect the neurobiology in addiction? What is the implication of this variability to treatment outcome and recovery? Most importantly, how can
