创伤性脑损伤
神经炎症
阿片类药物使用障碍
神经科学
脑震荡
医学
萧条(经济学)
焦虑
心理学
类阿片
精神科
毒物控制
伤害预防
疾病
内科学
受体
经济
宏观经济学
环境卫生
作者
Maya Jammoul,Dareen Jammoul,Kevin Wang,Firas Kobeissy,Ralph G. DePalma
标识
DOI:10.1016/j.biopsych.2023.05.013
摘要
Traumatic brain injury (TBI) and opioid use disorder (OUD) comprise twin plagues causing considerable morbidity and mortality worldwide. As interactions between TBI and OUD are to our knowledge uncharted, we review the possible mechanisms by which TBI may stimulate the development of OUD and discuss the interaction or crosstalk between these two processes. Central nervous system damage due to TBI appears to drive adverse effects of subsequent OUD and opioid use/misuse affecting several molecular pathways. Pain, a neurological consequence of TBI, is a risk factor that increases the likelihood of opioid use/misuse after TBI. Other comorbidities including depression, anxiety, posttraumatic stress disorder, and sleep disturbances are also associated with deleterious outcomes. We examine the hypothesis that a TBI "first hit" induces a neuroinflammatory process involving microglial priming, which, on a second hit related to opioid exposure, exacerbates neuroinflammation, modifies synaptic plasticity, and spreads tau aggregates to promote neurodegeneration. As TBI also impairs myelin repair by oligodendrocytes, it may reduce or degrade white matter integrity in the reward circuit resulting in behavioral changes. Along with approaches focused on specific patient symptoms, understanding the CNS effects following TBI offers a promise of improved management for individuals with OUD.
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