Laboratory exposure to cocaine cues does not increase cocaine use by outpatient subjects.

Sixty-nine cocaine-dependent outpatients were exposed to cocaine-related stimuli and to non-drug events on separate days. Cocaine cue sessions were always followed by a meeting with a trained clinician designed to eliminate any craving that remained following cue presentations. Urine samples were collected before each laboratory session and 1 to 3 days later. Neither rates of cocaine use nor average urine metabolite values differed following the two sessions. Nearly 90% of subjects had the same urine test result both before and after the cocaine cue session. Thus, laboratory presentation of cocaine cues to outpatient subjects did not increase their risk of subsequent drug-taking. These results suggest that with proper clinical protections, cue exposure can be used as a treatment outcome measure and a behavioral intervention in outpatient settings without increasing the risk of drug use.

Cue reactivity and cue reactivity interventions in drug dependence.

Despite a venerable history dating back to Pavlov and countless testimonials from patients such as those in the opening paragraphs of this chapter, there is much that remains to be learned about drug signals and, particularly, about ways of reducing their adverse effects on human drug users. There is a substantial amount of data showing increased craving and signs of physiological arousal to drug-related versus neutral cues in drug users for both drug classes reviewed here. Additional controlled studies will be useful in refining which responses among those studied are, in fact, conditioned in origin and therefore can be subjected reasonably to learning-based interventions. Most attempts to modify cue responsivity for clinical benefit have met with only modest success, and there is ample room for creative, but controlled, treatment-outcome studies. In recent years, several other groups have joined in the effort to understand drug-related cue reactivity, extending the research area to alcohol and nicotine (Monti et al. 1987; Niaura et al. 1988, 1989; Cooney et al. 1984; Hodgson and Rankin 1982; Drummond 1990; Laberg 1990). The interested reader is referred to several additional reviews of cue reactivity and cue exposure research related to alcohol and nicotine (Niaura 1988; Drummond 1990; Laberg 1990), opiates (Powell 1990), opiates and cocaine (Childress et al. 1988b; O'Brien et al. 1990), and all the preceding areas (Rohsenow et al. 1991).