Sofuoglu Mehmet, DeVito Elise E, Waters Andrew J, Carroll Kathleen M
a Department of Psychiatry , Yale University School of Medicine , West Haven , Connecticut , USA.
b VA Connecticut Healthcare System , West Haven , Connecticut , USA.
J Dual Diagn. 2016;12(1):90-106. doi: 10.1080/15504263.2016.1146383.
Stimulant use disorder is an important public health problem, with an estimated 2.1 million current users in the United States alone. No pharmacological treatments are approved by the U.S. Food and Drug Administration for stimulant use disorder and behavioral treatments have variable efficacy and limited availability. Most individuals with stimulant use disorder have other comorbidities, most with overlapping symptoms and cognitive impairments. The goal of this article is to present a rationale for cognition as a treatment target in stimulant use disorder and to outline potential treatment approaches. Rates of lifetime comorbid psychiatric disorders among people with stimulant use disorders are estimated at 65% to 73%, with the most common being mood disorders (13% to 64%) and anxiety disorders (21% to 50%), as well as non-substance-induced psychotic disorders (<10%). There are several models of addictive behavior, but the dual process model particularly highlights the relevance of cognitive impairments and biases to the development and maintenance of addiction. This model explains addictive behavior as a balance between automatic processes and executive control, which in turn are related to individual (genetics, comorbid disorders, psychosocial factors) and other (craving, triggers, drug use) factors. Certain cognitive impairments, such as attentional bias and approach bias, are most relevant to automatic processes, while sustained attention, response inhibition, and working memory are primarily related to executive control. These cognitive impairments and biases are also common in disorders frequently comorbid with stimulant use disorder and predict poor treatment retention and clinical outcomes. As such, they may serve as feasible transdiagnostic treatment targets. There are promising pharmacological, cognitive, and behavioral approaches that aim to enhance cognitive function. Pharmacotherapies target cognitive impairments associated with executive control and include cholinesterase inhibitors (e.g., galantamine, rivastigmine) and monoamine transporter inhibitors (e.g., modafinil, methylphenidate). Cognitive behavioral therapy and cognitive rehabilitation also enhance executive control, while cognitive bias modification targets impairments associated with automatic processes. Cognitive enhancement to improve treatment outcomes is a novel and promising strategy, but its clinical value for the treatment of stimulant use disorder, with or without other psychiatric comorbidities, remains to be determined in future studies.
兴奋剂使用障碍是一个重要的公共卫生问题，仅在美国估计就有210万当前使用者。美国食品药品监督管理局未批准用于治疗兴奋剂使用障碍的药物治疗方法，行为治疗的疗效各异且可及性有限。大多数患有兴奋剂使用障碍的个体还患有其他合并症，大多数合并症具有重叠症状和认知障碍。本文的目的是阐述将认知作为兴奋剂使用障碍治疗靶点的基本原理，并概述潜在的治疗方法。兴奋剂使用障碍患者中终生合并精神障碍的发生率估计为65%至73%，最常见的是情绪障碍（13%至64%）和焦虑障碍（21%至50%），以及非物质所致精神障碍（<10%）。有几种成瘾行为模型，但双过程模型特别强调认知障碍和偏差与成瘾的发展及维持的相关性。该模型将成瘾行为解释为自动过程和执行控制之间的平衡，而这又与个体（遗传学、合并症、心理社会因素）和其他（渴望、触发因素、药物使用）因素相关。某些认知障碍，如注意力偏差和趋近偏差，与自动过程最为相关，而持续注意力、反应抑制和工作记忆主要与执行控制相关。这些认知障碍和偏差在经常与兴奋剂使用障碍合并的疾病中也很常见，并预示着治疗依从性差和临床预后不良。因此，它们可能是可行的跨诊断治疗靶点。有一些有前景的药物、认知和行为方法旨在增强认知功能。药物治疗针对与执行控制相关的认知障碍，包括胆碱酯酶抑制剂（如加兰他敏、卡巴拉汀）和单胺转运体抑制剂（如莫达非尼、哌甲酯）。认知行为疗法和认知康复也能增强执行控制，而认知偏差矫正针对与自动过程相关的障碍。通过认知增强来改善治疗效果是一种新颖且有前景的策略，但其对于治疗有或没有其他精神合并症的兴奋剂使用障碍的临床价值仍有待未来研究确定。
