The reinstatement model and relapse prevention: a clinical perspective

Abstract

Objectives-This commentary assesses the degree to which the reinstatement model is homologous to the human experience of relapse.Results-A review of the literature suggests that the relationship is less clear than is often assumed, largely due to a lack of prospective data on the precipitants and process of relapse (especially relapse to heroin or cocaine abuse). However, reinstatement does not need to resemble relapse to have immediate clinical value; predictive validity as a medication screen would be sufficient. Whether the model has predictive validity is unknown, because, to date, very few clinical trials have tested medications that are effective in the reinstatement model, and even fewer have used designs comparable to those of reinstatement experiments. A clinical trial comparable to a reinstatement experiment would enroll participants who are already abstinent, and its main outcome measure would be propensity to undergo a specific type of relapse (e.g., relapse induced by stress or cues).Conclusions-Until clinical and preclinical work are more comparable, criticisms of the reinstatement model's presumed shortcomings are premature.The reinstatement model has generated a body of preclinical data that grows increasingly substantial and impressive (Shaham et al. 2003). Yet opinions remain divided about its relation to clinical realities (Marlatt 1996;Bergman and Katz 1998). In this commentary, we address the issues of whether reinstatement resembles relapse, whether it can be useful without resembling relapse, and why neither of those questions can yet be answered satisfactorily. We have drawn on clinical literature and on our own experiences working with substance abusers. Does reinstatement resemble relapse? MaybeIn most published discussions of the reinstatement model, attention is drawn to the fact that the most widely studied precipitants of reinstatement in rats (drug priming, drug-associated cues, and stress) are provocatively similar to the precipitants of relapse in humans. This is typically taken as a point of commonality between the reinstatement model and the real-life experiences of recovered addicts. It is tempting to agree without further consideration; the assertion that priming, cues, and stress precipitate relapse is intuitively appealing and seems to accord with clinical experience. But how strong is the evidence that most relapses are precipitated by any of those three factors?No definitive answer can be found in the clinical literature. Relapse is usually described retrospectively, with weeks or months intervening between the event and its recollection. This leaves ample time for the introduction of recall bias and the formation of post hoc explanations for the reporter's behavior. As an only slightly tangential illustration of the problem, consider the intuitively plausible prediction that abused children are at increased risk for later addiction. The prediction is confirmed when adult addicts are asked retrospectively about their childhoods -but not when abused and nonabused c...

Blockade of mesolimbic dopamine D3 receptors inhibits stress-induced reinstatement of cocaine-seeking in rats

“…At the same time, caution along these lines is warranted. The seeming face validity of the reinstatement animal model has not been shown to have predictive validity for human relapse (Epstein and Preston 2003;Katz and Higgins 2003; however, for more sanguine views of the utility of the reinstatement model, see Shaham and Miczek 2003;.…”

Conceptual framework for the etiology of alcoholism: a ?kindling?/stress hypothesis

“…Withdrawal from a single 5-day exposure to alcohol is without effect on social interaction behavior (Overstreet et al 2002). This protocol of reintroducing chronic alcohol to uncover functional change is reminiscent of previous work in which priming injections of drugs of abuse altered responding for the drug that would not otherwise be apparent (de Wit and Stewart 1981), an approach suggested to be related to drug relapse (see reviews by Shaham et al 2003;Katz and Higgins 2003;Epstein and Preston 2003).…”

Incubation of Methamphetamine and Palatable Food Craving after Punishment-Induced Abstinence

“…A common feature of these studies and related studies (Pacchioni et al, 2011;Van den Oever et al, 2008;Van den Oever et al, 2010) is that abstinence is forced either by removing the rats from the drug self-administration environment or by conducting extinction training. However, in humans, abstinence is typically self-imposed, despite drug availability, because the drug's rewarding effects are outweighed by the aversive consequences of seeking or using them (Burman, 1997;Epstein and Preston, 2003;Klingemann, 1991;Marlatt, 1996). This form of abstinence can be modeled in laboratory animals by punishment of the drug self-administration response, typically in the form of response-contingent presentation of mild intermittent footshock (Marchant et al, 2013a;Panlilio et al, 2003).…”