Opioid use disorder and the brain: a clinical perspective.

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.

Functional evaluation of NK1 antagonism on cue reactivity in opiate dependence; An fMRI study.

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 (NK1) receptors have prominent effects on opiate reward and reinforcement, and human studies have found NK1 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 NK1 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 NK1 antagonism will attenuate the BOLD response to drug cues in the caudate nucleus and amygdala. Regions of interest were selected based on NK1 receptor density and their role in cue reactivity and craving.