Imaging brain response to reward in addictive disorders
Imaging brain response to reward in addictive disorders
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DOI：
10.1111/j.1749-6632.2010.05898.x
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发表时间：
2011-01-01
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影响因子：
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通讯作者：
Gilman, Jodi M.
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文献类型：
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作者：
Hommer, Daniel W.;Bjork, James M.;Gilman, Jodi M.
我们比较了来自人类神经影像学研究的证据，支持和反对两个主要的假设，即大脑奖励系统的改变是成瘾的基础。其中之一，冲动假说，提出成瘾的特点是过度敏感的奖励结合失败的抑制。另一种是奖励缺乏假说，认为成瘾者对非药物奖励的反应降低，导致他们优先于社会可接受的目标寻求药物。多巴胺受体密度和多巴胺释放的正电子发射断层扫描（PET）研究强烈支持奖赏缺乏假说，而最近和大量的功能性磁共振成像（fMRI）研究目标导向行为提供了支持和矛盾的每一个假设。PET和fMRI进行测量的时间尺度的差异可能解释了结果的差异，至少部分是这样。冲动假说和奖励缺乏假说所描述的大脑功能的各个方面可能对成瘾的病理生理学有贡献。
We compare the evidence from human neuroimaging studies for and against two of the major hypotheses of how alterations in the brain's reward system underlie addiction. One of these, the impulsivity hypothesis, proposes that addiction is characterized by excessive sensitivity to reward combined with a failure of inhibition. The other, the reward-deficiency hypothesis, proposes that addicted individuals have a reduced response to nondrug rewards that leads them to seek drugs in preference to more socially acceptable goals. Positron emission tomographic (PET) studies of dopamine receptor density and dopamine release strongly support the reward-deficiency hypothesis, while the more recent and numerous functional magnetic resonance imaging (fMRI) studies of goal-directed behavior provide both support and contradiction for each of the hypotheses. Differences in the time scale on which PET and fMRI make measurements probably account for differences in results, at least in part. It is likely that aspects of brain function described by both the impulsivity and reward-deficiency hypotheses contribute to the pathophysiology of addiction.