SUMMARY Addiction is a global health problem with a chronic relapsing nature for which there are few treatment options. In the past few decades, neuroimaging has allowed us to better understand the neurobiology of addiction. Functional neuroimaging paradigms have been developed to probe the neural circuits underlying addiction, including reward, inhibitory control, stress, emotional processing and learning/memory networks. Functional neuroimaging has also been used to provide biological support for the benefits of psychosocial and pharmacological interventions, although evidence remains limited and often inconclusive in this area, which may contribute to the variability in treatment efficacy. In this article, we discuss the changing definitions and clinical criteria that describe and classify addictive disorders. Using examples from functional neuroimaging studies we summarise the neurobiological mechanisms that underpin drug use, dependence, tolerance, withdrawal and relapse. We discuss the links between functional neuroimaging and treatment, outline clinical management in the UK and give an overview of future directions in research and addiction services.

Opioid use disorder (OUD) has gained increasing publicity and interest during recent years, with many countries describing problems of epidemic proportions with regard to opioid use and deaths related to opioids. While opioids are not themselves acutely neurotoxic, the chronic relapsing and remitting nature of this disorder means that individuals are often exposed to exogenous opioids for lengthy periods of time (either illicit or prescribed as treatment). We are increasingly characterizing the effect of such long‐term opioid exposure on the brain. This narrative review aims to summarize the literature regarding OUD and the brain from a clinical perspective. Alterations of brain structure and function are discussed, as well as neurological and psychiatric disorders in OUD. Finally, we review current and new directions for assessment and treatment.

SUMMARY Despite record-breaking numbers of opiate related deaths in the UK in 2019, pharmacological management of opiate dependence has evolved little since the advent of methadone in 1965. Along with harm minimisation and psychosocial interventions, the mainstay of pharmacological treatment remains opioid substitution therapy (OST) using methadone or buprenorphine, with many patients receiving OST for many years. Even with these treatments, opiate users continue to face mortality risks 12 times higher than the general population, and emerging evidence suggests that individuals who remain on long-term OST present with a range of physical and cognitive impairments. Therefore, with a growing ageing opiate dependent population who would benefit from detoxification from OST, this article provides an overview of the current state of opiate dependence in clinical practice, explores the reasons why availability and acceptability of detoxification pathways are declining, and discusses emerging pharmacological therapies that could provide benefit in relapse prevention.

Background Opiate addiction is a major health challenge with substantial societal cost. Though harm minimisation strategies have been effective, there is a growing need for new treatments for detoxification and relapse prevention. Preclinical research has found neurokinin 1 (NK 1 ) receptors have prominent effects on opiate reward and reinforcement, and human studies have found NK 1 antagonism led to reductions in craving and withdrawal. However, its effect on brain mechanisms in opiate addiction has not yet been examined. Methods This study aims to assess the impact of NK 1 antagonist aprepitant on heroin cue-elicited changes in blood-oxygenation level dependent (BOLD) signal in opiate dependent individuals undergoing detoxification. Participants will attend two scanning sessions and receive a single dose of aprepitant (320 mg) and a placebo in a randomised, cross-over design. During functional magnetic resonance imaging participants will undergo two runs of a cue reactivity task, which consists of passive viewing of drug cues or neutral cues in a block design fashion. We hypothesise that NK 1 antagonism will attenuate the BOLD response to drug cues in the caudate nucleus and amygdala. Regions of interest were selected based on NK 1 receptor density and their role in cue reactivity and craving.

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