The Centers for Disease Control have recently described opioid use and resultant deaths as an epidemic. At this point in time, treating this disease well with medication requires skill and time that are not generally available to primary care doctors in most practice models. Suboptimal treatment has likely contributed to expansion of the epidemic and concerns for unethical practices. At the same time, access to competent treatment is profoundly restricted because few physicians are willing and able to provide it. This “Practice Guideline” was developed to assist in the evaluation and treatment of opioid use disorder, and in the hope that, using this tool, more physicians will be able to provide effective treatment. Although there are existing guidelines for the treatment of opioid use disorder, none have included all of the medications used at present for its treatment. Moreover, few of the existing guidelines address the needs of special populations such as pregnant women, individuals with co-occurring psychiatric disorders, individuals with pain, adolescents, or individuals involved in the criminal justice system. This Practice Guideline was developed using the RAND Corporation (RAND)/University of California, Los Angeles (UCLA) Appropriateness Method (RAM) – a process that combines scientific evidence and clinical knowledge to determine the appropriateness of a set of clinical procedures. The RAM is a deliberate approach encompassing review of existing guidelines, literature reviews, appropriateness ratings, necessity reviews, and document development. For this project, American Society of Addiction Medicine selected an independent committee to oversee guideline development and to assist in writing. American Society of Addiction Medicine's Quality Improvement Council oversaw the selection process for the independent development committee. Recommendations included in the guideline encompass a broad range of topics, starting with the initial evaluation of the patient, the selection of medications, the use of all the approved medications for opioid use disorder, combining psychosocial treatment with medications, the treatment of special populations, and the use of naloxone for the treatment of opioid overdose. Topics needing further research were noted.

Exposure to cigarette smoking cues can trigger physiological arousal and desire to smoke. The brain substrates of smoking cue-induced craving (CIC) are beginning to be elucidated; however, it has been difficult to study this state independent of the potential contributions of pharmacological withdrawal from nicotine. Pharmacological withdrawal itself may have substantial effects on brain activation to cues, either by obscuring or enhancing it, and as CIC is not reduced by nicotine replacement strategies, its neuro-anatomical substrates may differ. Thus, characterizing CIC is critical for developing effective interventions. This study used arterial spin-labeled (ASL) perfusion fMRI, and newly developed and highly appetitive, explicit smoking stimuli, to examine neural activity to cigarette CIC in an original experimental design that strongly minimizes contributions from pharmacological withdrawal. Twenty-one smokers (12 females) completed smoking and nonsmoking cue fMRI sessions. Craving self-reports were collected before and after each session. SPM2 software was employed to analyze data. Blood flow (perfusion) in a priori-selected regions was greater during exposure to smoking stimuli compared to nonsmoking stimuli (po0.01; corrected) in ventral striatum, amygdala, orbitofrontal cortex, hippocampus, medial thalamus, and left insula. Perfusion positively correlated with intensity of cigarette CIC in both the dorsolateral prefrontal cortex (r 2 ¼ 0.54) and posterior cingulate (r 2 ¼ 0.53). This pattern of activation that includes the ventral striatum, a critical reward substrate, and the interconnected amygdala, cingulate and OFC, is consistent with decades of animal research on the neural correlates of conditioned drug reward. Keywords: cigarette smoking; craving; neuroimaging; ventral striatum; amygdala; DLPFC INTRODUCTION RationaleBoth nicotine and conditioned cues (reminders) maintain cigarette smoking and lead to relapse (Henningfield and Goldberg, 1983;Rose, 2006). Thus, effective smoking cessation treatments should address both factors. Nicotine replacement therapy (NRT) and bupropion are both effective at ameliorating nicotine withdrawal-induced craving, but neither block the craving elicited by learned associations formed between environmental cues and nicotine (Teneggi and Tiffany, 2002;Robinson and Berridge, 1993;Wise, 1988;Hughes et al, 1999;Hurt et al, 1997;Jorenby et al, 1999). Currently, medications that unequivocally prevent or reduce cue-induced craving (CIC) are not available. Further understanding of the underlying neurobiology of CIC would facilitate the development of effective therapies and improve the currently low (10-20% at 6 months to a year) success rates associated with current smoking interventions West et al, 2001). Thus, a major goal of this work is to examine the element of neurobiology underlying CIC distinct from that observed in CIC studies associated with nicotine withdrawal.Craving generated by drug cues may accrue slowly over time, recruiting supplementary neural substrates as...

These data provide new evidence of the feasibility, efficacy, and tolerability of long-lasting antagonist treatments for opioid dependence.