Efforts to develop, test and refine theoretical models are critical to enhancing the understanding and prevention of relapse [1,2,14]. A major development in this respect was the reformulation of Marlatt's cognitive-behavioral relapse model to place greater emphasis on dynamic relapse processes [8]. Whereas most theories presume linear relationships among constructs, the reformulated model (Figure 2) views relapse as a complex, nonlinear process in which various factors act jointly and interactively to affect relapse timing and severity. Similar to the original RP model, the dynamic model centers on the high-risk situation. Against this backdrop, both tonic (stable) and phasic (transient) influences interact to determine relapse likelihood. Tonic processes include distal risks--stable background factors that determine an individual's "set point" or initial threshold for relapse [8,31]. Personality, genetic or familial risk factors, drug sensitivity/metabolism and physical withdrawal profiles are examples of distal variables that could influence relapse liability a priori. Tonic processes also include cognitive factors that show relative stability over time, such as drug-related outcome expectancies, global self-efficacy, and personal beliefs about abstinence or relapse. Whereas tonic processes may dictate initial
