Neurophysiologic processes underlie the uncontrolled, compulsive behaviors defining the addicted state. These"hard-wired"changes in the brain are considered critical for the transition from casual to addictive drug use. This review of preclinical and clinical (primarily neuroimaging) studies will describe how the delineation between pleasure, reward, and addiction has evolved as our understanding of the biologic mechanisms underlying these processes has progressed. Although the mesolimbic dopaminergic efflux associated with drug reward was previously considered the biologic equivalent of pleasure, dopaminergic activation occurs in the presence of unexpected and novel stimuli (either pleasurable or aversive) and appears to determine the motivational state of wanting or expectation. The persistent release of dopamine during chronic drug use progressively recruits limbic brain regions and the prefrontal cortex, embedding drug cues into the amygdala (through glutaminergic mechanisms) and involving the amygdala, anterior cingulate, orbitofrontal cortex, and dorsolateral prefrontal cortex in the obsessive craving for drugs. The abstinent, addicted brain is subsequently primed to return to drug use when triggered by a single use of drug, contextual drug cues, craving, or stress, with each process defined by a relatively distinct brain region or neural pathway. The compulsive drive toward drug use is complemented by deficits in impulse control and decision making, which are also mediated by the orbitofrontal cortex and anterior cingulate. Within this framework, future targets for pharmacologic treatment are suggested.

/pdf/neurobiologic-processes-in-drug-reward-and-addiction-54j181in75.pdf

Neurobiologic Processes in Drug Reward and Addiction

Background Cocaine dependence is associated with high rates of relapse. Stress and drug cue exposure are known to increase cocaine craving and stress arousal, but the association between these responses and cocaine relapse has not been previously studied. Objective To examine whether stress-induced and drug cue–induced cocaine craving and hypothalamic-pituitary-adrenal axis responses evoked in the laboratory are associated with subsequent cocaine relapse. Design Prospective study design assessing cocaine relapse and drug use during a 90-day follow-up period after discharge from inpatient treatment and research. Data were analyzed by Cox proportional hazards regression and multiple regression. Setting Inpatient treatment and research unit in a community mental health center. Patients Forty-nine treatment-seeking cocaine-dependent individuals. Main Outcome Measures Time to cocaine relapse, number of days of cocaine use, and amount of cocaine used per occasion in the follow-up phase. Results Greater stress-induced, but not drug cue–induced, cocaine craving was associated with a shorter time to cocaine relapse. Stress-induced corticotropin and cortisol responses predicted higher amounts of cocaine use per occasion in the 90-day follow-up. Conclusions These results demonstrate that stress-related increases in cocaine craving and hypothalamic-pituitary-adrenal axis responses are each associated with specific cocaine relapse outcomes. The findings support the use of stress-induced drug craving and associated hypothalamic-pituitary-adrenal axis responses to evaluate cocaine relapse propensity. Furthermore, treatments that address stress-induced cocaine craving and hypothalamic-pituitary-adrenal responses could be of benefit in improving relapse outcomes in cocaine dependence.

https://jamanetwork.com/journals/jamapsychiatry/articlepdf/209411/yoa50307.pdf

Stress-Induced Cocaine Craving and Hypothalamic-Pituitary-Adrenal Responses Are Predictive of Cocaine Relapse Outcomes

Stress has long been suggested to be an important correlate of uncontrolled drinking and relapse. An important hormonal response system to stress-the hypothalamic-pituitary-adrenal (HPA) axis-may be involved in this process, particularly stress hormones known as glucocorticoids and primarily cortisol. The actions of this hormone system normally are tightly regulated to ensure that the body can respond quickly to stressful events and return to a normal state just as rapidly. The main determinants of HPA axis activity are genetic background, early-life environment, and current life stress. Alterations in HPA axis regulation are associated with problematic alcohol use and dependence; however, the nature of this dysregulation appears to vary with respect to stage of alcohol dependence. Much of this research has focused specifically on the role of cortisol in the risk for, development of, and relapse to chronic alcohol use. These studies found that cortisol can interact with the brain's reward system, which may contribute to alcohol's reinforcing effects. Cortisol also can influence a person's cognitive processes, promoting habit-based learning, which may contribute to habit formation and risk of relapse. Finally, cortisol levels during abstinence may be useful clinical indicators of relapse vulnerability in alcohol-dependent people.

Stress and the HPA axis: role of glucocorticoids in alcohol dependence

Enhanced negative emotion and alcohol craving, and altered physiological responses following stress and cue exposure in alcohol dependent individuals.

Stress is an important factor known to increase alcohol and drug relapse risk. This paper examines the stress-related processes that influence addiction relapse. First, individual patient vignettes of stress- and cue-related situations that increase drug seeking and relapse susceptibility are presented. Next, empirical findings from human laboratory and brain-imaging studies that are consistent with clinical observations and support the specific role of stress processes in the drug-craving state are reviewed. Recent findings on differences in stress responsivity in addicted versus matched community social drinkers are reviewed to demonstrate alterations in stress pathways that could explain the significant contribution of stress-related mechanisms on craving and relapse susceptibility. Finally, significant implications of these findings for clinical practice are discussed, with a specific focus on the development of novel interventions that target stress processes and drug craving to improve addiction relapse outcomes.

The role of stress in addiction relapse.

Komorbiditat und Strefireaktion als ruckfallpradlktive Faktoren bei Alkoholabhanqlqkelt

Wir wissen heute aus einer Vielzahl von epidemiologischen Studien, das bei Alkoholabhangigen eine erhebliche Komorbiditat besteht. Dabei ist das Ausmas an Komorbiditat um so hoher, je spezieller die untersuchte Stichprobe gewahlt wird. So fanden Wittchen et al. (1992) eine Lebenszeitpravalenz von 32% Komorbiditat unter Alkoholabhangigen in der Allgemeinbevolkerung, wahrend Tomasson und Vaglum (1995), die die Alkoholabhangigen in alkoholspezifischen klinischen Einrichtungen naher untersuchten, eine Lebenszeitpravalenz fur Komorbiditat fanden, die in etwa doppelt so hoch war (Abb. 1). Arolt und Driessen (1996) untersuchten die Patienten in einem Allgemeinkrankenhaus in Lubeck auf psychiatrische Storungen und fanden mit einer Lebenszeitpravalenz von 41% Pravalenzwerte, die zwischen den beiden anderen Studien lagen.

Komorbidität und Streßreaktion als rückfallprädiktive Faktoren bei Alkoholabhängigkeit

— Aims: to investigate a possible association of cortisol stress response during early abstention with relapse. Methods: Thirty-six alcohol-dependent males, half of them with a comorbid anxiety disorder, and 15 healthy controls were exposed to a standardized psychosocial stress test. Thirty-one of the patients were assessed for relapse 6 weeks after discharge. Results: The relapsers showed almost no cortisol responses in the stress test. Comorbid anxiety disorder influenced neither stress response nor relapse. Conclusions: During early abstention from alcohol, reduced stress-responsivity of the hypothalamo–pituitary–adrenocortical axis seems to be connected to early relapse.

/pdf/impaired-serum-cortisol-stress-response-is-a-predictor-of-3cca03fus9.pdf

Impaired serum cortisol stress response is a predictor of early relapse.

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Komorbiditat und Strefireaktion als ruckfallpradlktive Faktoren bei Alkoholabhanqlqkelt

Komorbidität und Streßreaktion als rückfallprädiktive Faktoren bei Alkoholabhängigkeit

Impaired serum cortisol stress response is a predictor of early relapse.