Psychosocial and pharmacological interventions
G. Hussein Rassool in Alcohol and Drug Misuse, 2017
Cue exposure is aimed at extinguishing conditioned responses such as craving. Childress et al. (1988) recognised that repeated pairings of substance use with particular settings, individuals, affect states, paraphernalia and so on could lead to substantial conditioned craving. They demonstrated “cue reactivity” including both physiologic (changes in skin temperature) and subjective (withdrawal-like symptoms, craving) responses in both opiate and cocaine abusers exposed to drug-related stimuli, such as handling drug paraphernalia etc. The general approach is to expose drug or alcohol users to cues for using (for example, expose a cocaine user to white powder or drug paraphernalia or an alcohol misuser to a beer bottle) while concurrently addressing and attempting to lessen the desire to use. Cue exposure can reduce the desire to use that was caused by the cue, provides the opportunity to practice coping responses (for example, relaxation) realistically and can increase self-efficacy, which will increase the likelihood that the response will be utilised in future real-life cue exposures (Monti et al. 1989).
The principles of behaviourist psychology
Devinder Rana, Dominic Upton in Psychology for Nurses, 2013
The principles of classical conditioning can also in part explain why patients may find it difficult to change their current health behaviours when advised to do so. A nurse who acknowledges possible triggering factors and then addresses these with the patient will increase the chances of a care plan being put together that is individualised and hence more effective in facilitating behaviour change. Studies have shown that nicotine craving tends to occur on presentation of smoking-related stimuli, e.g. drinking in a pub (Payne et al., 1990) which results in an increased desire for a cigarette. This has been referred to as cue reactivity.
Controlled and Automatic Learning Processes in Addiction
Hanna Pickard, Serge H. Ahmed in The Routledge Handbook of Philosophy and Science of Addiction, 2019
Wikler’s early account of cue reactivity argued that drug cues elicit conditioned withdrawal, which automatically primes drug-seeking to ameliorate this state. To quote: ‘abstinence distress . . . may be reactivated long after cure . . . providing an unconscious motivation to relapse’ (Wikler 1984, p. 280). Key support for this claim is that drug cues elicit conditioned withdrawal (O’Brien et al. 1977), and compensatory responses (Siegel et al. 1982), but the assumption that these CRs exert unconscious motivational influences has not been supported (see the section below on p. 332 on incentive learning and self-medication). Another complication was added by positive reinforcement theorists who found that drug cues could elicit dopamine and locomotor activity akin to the drug effect. This positive state arguably energises drug-related cognitions driving behaviour, i.e., an S–S account (Stewart et al. 1984). To quote: ‘Conditioned stimuli associated with these drugs arouse neural states that mimic features of those produced by the drugs themselves and thereby serve to increase . . . the probability of drug-related thoughts and actions’ (p. 251). Later studies found that physiological CRs are not consistently drug-like or drug-opposite and so do not distinguish withdrawal and positive reinforcement accounts (Carter and Tiffany 1999). By contrast, studies that have taken subjective measures reliably suggest that drug cues elicit positive emotional states and craving (Niaura et al. 1988) and that cue-elicited craving is the best predictor of cue-elicited drug consumption (Hogarth et al. 2010), again supporting a controlled S–S positive reinforcement account of cue reactivity.
Three-dimensional virtual reality: Applications to the 12 grand challenges of social work
Published in Journal of Technology in Human Services, 2019
Mark H. Trahan, Kenneth Scott Smith, Amy C. Traylor, Micki Washburn, Nicole Moore, Alberto Mancillas
VR interventions have been piloted to treat substance use disorders using virtual reality cue exposure therapy (VRET; Freeman et al., 2017) which involves exposing participants to common substance use cues, resulting in physiological arousal within the virtual environment. Cue reactivity is a phenomenon experienced by addicted individuals resulting in significant physiological and subjective reactions during exposure to drug-related stimuli (Kuntze et al., 2001). Subjective cue-elicited reactions have been found in literature including withdrawal symptoms, drug-agonistic effects, craving, and physiological responses (Kuntze et al., 2001). Interested researchers have followed suit with the use of virtual environments (VE) in measuring craving and cue reactivity in nicotine alcohol, cannabis, cocaine, opioid, and methamphetamine dependent individuals (Bordnick et al., 2004, 2008; Hone-Blanchet et al., 2014; Pericot-Valverde, Germeroth, & Tiffany, 2016). Participants exposed to these substances within VE experienced consistently higher levels of craving than those exposed to “neutral” or not-substance related cues. While VR exposure elicits cue reactivity, rigorous research on virtual reality exposure therapy including dosage assessment, fidelity, and randomized control methods is still in nascent stages, but necessary to conclusively indicate intervention effectiveness (Ghită & Gutiérrez-Maldonado, 2018; Trahan, Maynard, Smith, Farina, & Khoo, 2019).
When triggers become tigers: taming the autonomic nervous system via sensory support system modulation
Published in Journal of Social Work Practice in the Addictions, 2021
Holly C. Matto, Padmanabhan Seshaiyer, Stephanie Carmack, Nathalia Peixoto, Matthew Scherbel
Several theories of addiction, including the incentive salience sensitization theory (Berridge & Robinson, 2016) and stress surfeit disorder (Koob et al., 2014), suggest that drug cues hold motivational power through the reinforcement learning process, which can lead to relapse when triggered by the cues. Exteroceptive cues, those experienced by stimuli outside the body such as the sensory characteristics of the drug itself (visual, smells, tastes) or rituals used to obtain and consume the substance, can activate autonomic (physiological changes), attention, and motor activity and are hypothesized to lead to substance use (Cofresi et al., 2019). Such cues increase Heart Rate (HR) even when mental imagery is used as the cue-elicited task (Oberlin et al., 2018). Behavior (i.e., drug-seeking) is affected when exposed to cues, even when the cue was not followed by substance ingestion in the past; this can be referred to as drug cue reactivity (Cofresi et al., 2019). While there are many drug treatment options that attempt to address the psychological factors and the surrounding social environment influences that may lead to relapse, they still leave those with SUD vulnerable because they fail to effectively address or limit drug cue reactivity (Cofresi et al., 2019).
Comparing alcohol cue-reactivity in treatment-seekers versus non-treatment-seekers with alcohol use disorder
Published in The American Journal of Drug and Alcohol Abuse, 2020
Alexandra Venegas, Lara A. Ray
Difference scores for measures of heart rate and blood pressure were calculated by subtracting the values obtained during the relaxation period from the values obtained following the presentation of the water and alcohol cues, respectively. ANOVAs did not reveal significant effects of cue on any physiological indicators of cue-reactivity, including cue-induced heart rate (F(1, 64) = 0, p = .97), systolic blood pressure (F(1, 64) = 2.4, p = .13), or diastolic blood pressure (F(1, 64) = 0, p = .95). Similarly, although analyses yielded a significant effect of group on cue-induced heart rate (F(1, 63) = 4.1, p < .05), they did not yield any significant effects of group on systolic blood pressure (F(1, 63) = 0.7, p = .42) or diastolic blood pressure (F(1, 63) = 0.04, p = .84). Lastly, there were no significant group × cue interaction effects on cue-induced heart rate (F(1, 63) = 0.3, p = .61), systolic blood pressure (F(1, 63) = 1.0, p = .33), or diastolic blood pressure (F(1, 63) = 0.2, p = .63).
Related Knowledge Centers
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