神经行为成瘾的方法:对阿片类药物的流行和成瘾的心理的影响

心理科学的公共利益(20卷2)
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近年来,海洛因等阿片类药物死亡危机升级,加强循证建议教育的必要性和政策宣传,防止滥用阿片类药物和其他物质。了解药瘾行为的神经生物学机制来创建这些预防活动至关重要。全面提供成瘾的神经行为的观点,重要的是要回答两个主要问题:(a)为什么人们在第一时间寻求药物?和(b)为什么有些吸毒的人最终成为无法抵制毒品的诱惑,成为“上瘾”?

在这个问题上心理科学的公共利益(20卷,问题2),安东尼贝沙拉Kent Berridge,沃伦·k . Bickel何塞·a·莫罗́n,西德尼·b·威廉姆斯和Jeffrey s . Stein审查一些成瘾理论,聚焦于阿片类药物的情况。他们特别注意疼痛和交叉opioid-use障碍和认知的低风险的作用采取法律药用阿片类药物(如氢可酮),通常规定的卫生专业人员,在决定使用阿片类药物。Bechara)和他的同事们还审查前额叶皮层和脑岛的角色在决定使用药物和可能倾向的个体差异或易受药物成瘾(即。,为什么有些人吸毒上瘾,而其他人不)。他们还描述了一些新颖的治疗策略和政策思想,可以帮助防止阿片类药物和其他物质滥用。

在阿片类药物使用的特定情况下,它是重要的占其镇痛属性和强烈的愉悦的感觉。阿片类药物如海洛因、吗啡、芬太尼和羟考酮具有镇痛属性与大脑中疼痛通路,但他们也有上瘾的特性与影响多巴胺系统(即。他们改变所谓的想要系统,神经结构负责突出激励去追求一定的奖励,和这些变化增加药物的欲望)。尽管有证据表明阿片类药物的有效性治疗急性疼痛(如手术后),他们似乎没有有效的治疗慢性疼痛。而不是帮助慢性疼痛,长期阿片类药物使用可能引起宽容和痛觉过敏(增加对疼痛的敏感性)。此外,患者在阿片类药物似乎超过90天的风险继续服用阿片类药物和物质使用障碍。鉴于慢性疼痛和opioid-use障碍的发展随着时间的推移可能会改变对阿片类药物的神经生物学反应,作者呼吁更多的研究在人们经历慢性疼痛。

Bechara)和他的同事们还描述如何上瘾可能导致大脑功能异常的三个系统:在amygdala-striatum(“冲动”系统),脑额叶前部皮层(“执行官”系统)和脑岛(一个区域参与越来越多的冲动和欲望)。他们讨论个体差异及其对预后的影响,以及未来研究的重要性如何具体的大脑功能异常可能与不同的模式在复苏成瘾和随后的禁欲。探索这些机制的个体差异可以解释为什么有些人不发展成瘾或成为功能性成瘾者(即。,individuals who take drugs but have suffered minimal social and psychological harm as a result of their drug use, usually because they stop procuring or using drugs when it is no longer worth the cost).

成瘾的上述机制产生影响来确定有效的治疗方法。贝沙拉等人提出一种链接机制和治疗的方法,如competing-neurobehavioral-decision-systems(组合),可以指导今后的临床干预措施降低成瘾。根据组合,一个人的选择源于一个冲动地决定系统之间的交互和行政决策系统(即。、控制系统)和那些上瘾,冲动地决定系统主导。因此,任何干预,恢复两个决策系统之间的平衡,通过减少冲动地决定系统的主导地位或增加行政决策系统的优势,可以促进物质禁欲。未来情景思维(即等干预措施。,mentally simulating future events), transcranial magnetic stimulation of the prefrontal cortices (i.e., TMS; noninvasive brain stimulation that can have analgesic effects), and working memory training might increase the dominance of the executive-decision system. TMS might also reduce the dominance of the impulsive-decision system by reducing the activation of the dopamine circuit, which is associated with drug craving. Overall, the authors emphasize the promise of scientific, neurobehavioral approaches to addiction for helping researchers, practitioners, and policy makers better understand the mechanisms of addiction and develop clinical interventions and policies to prevent and treat opioid abuse.

t·w·罗宾斯在发表的一篇评论文章,剑桥大学的认知神经科学教授,同意需要神经行为的研究来调查毒品滥用的潜在机制,尤其是及时在美国阿片类药物流行病。然而,而贝沙拉和同事回顾了opponent-motivational-processing视角(即。,a drug activates reward processes and creates euphoria, which counteractivates an unpleasant process that will eventually persist over the pleasant process and create withdrawal syndromes) and dismissed it as a complete explanation of addiction because it cannot handle the vulnerability to relapse after withdrawal, Robbins suggests that this might be a valid theory of addiction. He argues that broadening the theory to include voluntary behavior (e.g., an individual with addiction will seek heroin in anticipation of withdrawal to prevent its negative effects of withdrawal, which as an example of a hard to extinguish avoidance behavior) would strengthen its explanatory power. Robbins also points out the role of Pavlovian conditioning in addiction and how environmental stimuli (e.g., locations, people, or paraphernalia associated with drug use), as well as the action of the drug itself, can stimulate drug-seeking behavior. He suggests further clarification of some aspects of the research, such as the role of motivation in habits or the different predisposing factors for different drugs (e.g., impulsive behavior seems to predict future cocaine-seeking but not future heroin-seeking). In addition, Robbins suggests that, besides the interventions suggested by Bechara et al., a neurosurgical procedure called deep-brain stimulation may be a viable intervention.

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