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The reinstatement model and relapse prevention: a clinical perspective

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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.

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Notes

  1. In this commentary, lapse indicates any use of a drug by an individual who has been abstaining from that drug; relapse indicates a return to compulsive or harmful patterns of use. Operational definitions of these terms vary across studies

  2. The alcohol literature also includes at least two relapse-prevention trials using acamprosate (Sass et al. 1996; Tempesta et al. 2000), which has been screened (with positive results) in the alcohol-deprivation model (Spanagel et al. 1996; Holter et al. 1997; Heyser et al. 1998). The alcohol-deprivation model differs from the reinstatement model in that there is no operant extinction procedure and alcohol is available again during the postdeprivation session (Lê and Shaham 2002)

  3. ABT-431 and ecopipam are, respectively, an agonist and an antagonist at D1 receptors. The seeming paradox of their common effectiveness is discussed by Alleweireldt et al. (2002)

  4. The EMA study by Freedman et al. (2002) focused on the feasibility of issuing and recovering equipment; no data on the process of relapse were reported

  5. This suggested model is admittedly unsatisfying in several respects. The most obvious is that most animals would continue to self-administer some amount of drug throughout the experiment, thus sacrificing one of the major strengths of the reinstatement model: its ability to separate drug-seeking behavior from the pharmacological effects of the drug. The suggested model would also be unsuitable for assessment of priming-induced reinstatement. Still, this line of research could be useful for determining whether reinstatement in laboratory animals differs depending on the circumstances of cessation

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Acknowledgements

We thank David Gorelick, M.D., for helpful comments on the manuscript.

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  1. NIDA/IRP Treatment Section, Intramural Research Program, National Institute on Drug Abuse, 5500 Nathan Shock Drive, Baltimore, MD 21224, USA

    David H. Epstein & Kenzie L. Preston

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Correspondence to David H. Epstein.

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Epstein, D.H., Preston, K.L. The reinstatement model and relapse prevention: a clinical perspective. Psychopharmacology 168, 31–41 (2003). https://doi.org/10.1007/s00213-003-1470-6

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