Pain and suicidality: insights from reward and addiction neuroscience.
Pain and suicidality: insights from reward and addiction neuroscience.
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DOI：
10.1016/j.pneurobio.2013.06.003
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发表时间：
2013-10
影响因子：
6.7
通讯作者：
Volkow ND
中科院分区：
文献类型：
--
作者：
Elman I;Borsook D;Volkow ND
自杀在疼痛患者中非常普遍。尽管这种联系的病理生理学尚不清楚，但它可能潜在地与身体和情感疼痛系统的部分一致性有关。在社会依恋背景下遭受挫折和损失时，后一种制度在自杀中的作用也很明显。在这里，我们提出了一个基于调节奖赏和反奖赏的神经通路(即，对奖赏回路反复激活的平衡调节)的模型；两者都是疼痛、自杀和社会依恋的相关病因因素。对疼痛和自杀的神经生物学进行了全面的文献检索。对收集到的文章进行了严格的回顾，并在四个关键领域提取和总结了相关数据：(1)身体和情感痛苦，(2)情感痛苦和社会依恋，(3)与成瘾相比，与疼痛和自杀相关的奖赏和反奖赏回路的改变，这是这些回路功能障碍的主要探索，以及(4)共生疼痛和自杀的机械信息治疗。疼痛、应激和止痛药物诱导的中边缘多巴胺能通路的反对者和支持者状态可能使奖赏和反奖赏系统容易敏化、交叉敏化和异常学习与自杀行为和行为相关的内容和背景。这些发现表明，疼痛患者的大脑回路显示出调节奖赏(抑郁功能)和反奖赏(敏化功能)的变化，这可能会影响他们的自杀倾向，并支持疼痛和自杀分类，以及其他“奖赏缺乏综合症”和“增强的反奖赏综合症”的新提议。我们建议，旨在恢复慢性疼痛患者奖赏和反奖赏网络之间平衡的干预措施可能有助于降低他们的自杀风险。
Suicidality is exceedingly prevalent in pain patients. Although the pathophysiology of this link remains unclear, it may be potentially related to the partial congruence of physical and emotional pain systems. The latter system’s role in suicide is also conspicuous during setbacks and losses sustained in the context of social attachments. Here we propose a model based on the neural pathways mediating reward and anti-reward (i.e., allostatic adjustment to recurrent activation of the reward circuitry); both are relevant etiologic factors in pain, suicide and social attachments. A comprehensive literature search on neurobiology of pain and suicidality was performed. The collected articles were critically reviewed and relevant data were extracted and summarized within four key areas: (1) physical and emotional pain, (2) emotional pain and social attachments, (3) pain-and suicide-related alterations of the reward and anti-reward circuits as compared to addiction, which is the premier probe for dysfunction of these circuits and (4) mechanistically informed treatments of co-occurring pain and suicidality. Pain-, stress- and analgesic drugs-induced opponent and proponent states of the mesolimbic dopaminergic pathways may render reward and anti-reward systems vulnerable to sensitization, cross-sensitization and aberrant learning of contents and contexts associated with suicidal acts and behaviors. These findings suggest that pain patients exhibit alterations in the brain circuits mediating reward (depressed function) and anti-reward (sensitized function) that may affect their proclivity for suicide and support pain and suicidality classification among other “reward deficiency syndromes” and a new proposal for “enhanced anti-reward syndromes”. We suggest that interventions aimed at restoring the balance between the reward and anti-reward networks in patients with chronic pain may help decreasing their suicide risk.