健康与遗传心理学研究室知识库

物质滥用和成瘾是当今世界最严重的公共卫生问题之一,禁毒与戒毒已成为全球关注的社会热点.根据DSM-5定义,物质成瘾是一种慢性复发性精神疾病,表现为强迫性药物寻求、无法控制药物使用而无视其潜在的严重危害.超过80%的成瘾个体没有寻求治疗,这部分反映出物质成瘾个体存在认知功能方面的缺陷与障碍.以此为出发点,本研究回顾了近年来关于物质成瘾者在注意、抑制控制、决策和内感受等方面认知功能缺陷的研究,总结了行为和神经影像学方面的成果,探讨和论证物质成瘾背后的认知神经机制,以便更准确地了解物质成瘾的成因、发展、戒断和复发的本质.最后,本研究提出未来的相关研究应致力于推动多技术融合,关注共病问题,构建和完善生物标记,开发基于脑的干预方法,以便深化该领域的研究,有助于完善成瘾病人的干预与治疗机制.

As one of the most serious public health problems that extract a high toll on individuals and the society as a whole, substance abuse/addiction has attracted much attention from both researchers and the public. According to the DSM-5, substance addiction is a chronically relapsing psychiatric disorder that has been characterized by compulsion to seek and use drugs, loss of control in limiting intake despite serious negative consequences. However, more than 80% of the individuals with addiction fail to seek treatment, perhaps reflecting their cognitive function impairments. Previous studies have showed that most drugs of abuse exert their reinforcing effects and produce euphoria by inducing dopamine surges in limbic regions, which then have cascading effects on other neurotransmitter systems, leading to characteristic plastic adaptions; significant changes in neural circuits implicated in reward, attention, inhibitory control, decision making and interoception; and cognitive dysfunctions. However, much is still to be learned about the neural mechanisms involved in drugs' effects on cognitive functions and the vicious cycle of “drug abuse - withdrawal - recovery - relapse". For a better understanding of the causes of substance addiction and its underlying neural mechanisms, we provide an integrative review of behavioral and neuroimaging studies in substance addiction, introduce a neurobiological model of substance addiction, and finally propose future directions for research and clinical treatment. First, we summarize the research on the cognitive and neural mechanisms involved in substance addiction. (1) Drug-related cues can enhance the activities in the mesocorticolimbic system implicated in reward and drug motivation, which then result in increased attention to the drug-related stimuli. Thus, the neural changes in the frontolimbic system may be a potential neural basis for attentional bias toward drugs in individuals with addiction. (2) The deficit in inhibitory control typically observed in individuals with substance addiction may be due to a dysfunction in their prefrontal cortex-striatothalamic circuitry. (3) These individuals' poor decision making may be a product of an imbalance between three separate, but interacting, neural systems: the amygdala-striatum (an impulsive system); the prefrontal cortex (a reflective system); and the insula (the interoceptive system). (4) Emerging evidence shows that individuals with drug addiction have interoceptive processing deficits, perhaps due to dysfunctions in brain systems such as the insula and the anterior cingulate cortex. Second, we introduce a neurobiological model of substance addiction that depicts addiction as a result of an imbalance of six interactive circuits (i.e., reward, motivation/drive, memory, executive control, mood, and interoception). These brain circuits interact with one another to attain proper inhibitory control and hence good decision making. During addiction, however, the enhanced activities of six circuits (i.e., reward, motivation, memory, executive control, mood, and interoception) overwhelm the PFC's inhibitory control and hence lead to craving. Finally, we propose that future studies should (1) use multi-modal imaging techniques, (2) pay attention to comorbidity and clarify the association between addiction and other psychiatric disorders, (3) discover more biomarkers and optimize the diagnostic system using both behavioral and neuroimaging information, and (4) develop brain-based intervention techniques. Such studies should deepen our understanding of substance addiction and provide insights to its treatment.