Traumatic brain injury (TBI) is a leading cause of injury-induced disability in young children worldwide, and social behavior impairments in this population are a significant challenge for affected patients and their families. The protracted trajectory of secondary injury processes triggered by a TBI during early life-alongside ongoing developmental maturation-offers an extended time window when therapeutic interventions may yield functional benefits. This mini-review explores the scarce but promising pre-clinical literature to date demonstrating that social behavior impairments after early life brain injuries can be modified by drug therapies. Compounds that provide broad neuroprotection, such as those targeting neuroinflammation, oxidative stress, axonal injury and/or myelination, may prevent social behavior impairments by reducing secondary neuropathology. Alternatively, targeted treatments that promote affiliative behaviors, exemplified by the neuropeptide oxytocin, may reduce the impact of social dysfunction after pediatric TBI. Complementary literature from other early life neurodevelopmental conditions such as hypoxic ischemic encephalopathy also provides avenues for future research in neurotrauma. Knowledge gaps in this emerging field are highlighted throughout, toward the goal of accelerating translational research to support optimal social functioning after a TBI during early childhood.

中文翻译：

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亲社会药丸？药物治疗改善小儿创伤性脑损伤后社会结果的潜力。

创伤性脑损伤 (TBI) 是全球幼儿损伤性残疾的主要原因，该人群的社会行为障碍是受影响患者及其家人面临的重大挑战。在早期生命期间由 TBI 触发的继发性损伤过程的长期轨迹 - 以及持续的发育成熟 - 提供了一个延长的时间窗口，当治疗干预可能产生功能益处时。这篇小型综述探讨了迄今为止稀缺但有希望的临床前文献，这些文献证明早期脑损伤后的社会行为障碍可以通过药物治疗来改变。提供广泛神经保护的化合物，例如靶向神经炎症、氧化应激、轴突损伤和/或髓鞘形成的化合物，可以通过减少继发性神经病理学来预防社交行为障碍。或者，促进亲和行为的靶向治疗，例如神经肽催产素，可能会减少小儿 TBI 后社会功能障碍的影响。来自其他生命早期神经发育状况（如缺氧缺血性脑病）的补充文献也为未来的神经创伤研究提供了途径。这一新兴领域的知识差距贯穿始终，旨在加速转化研究，以支持儿童早期 TBI 后的最佳社会功能。来自其他生命早期神经发育状况（如缺氧缺血性脑病）的补充文献也为未来的神经创伤研究提供了途径。这一新兴领域的知识差距贯穿始终，旨在加速转化研究，以支持儿童早期 TBI 后的最佳社会功能。来自其他生命早期神经发育状况（如缺氧缺血性脑病）的补充文献也为未来的神经创伤研究提供了途径。这一新兴领域的知识差距贯穿始终，旨在加速转化研究，以支持儿童早期 TBI 后的最佳社会功能。