儿童青少年非自杀性自伤影响因素及生物学机制研究进展

Research progress on influencing factors and biological mechanisms of non-suicidal self-injury in children and adolescents

摘要

非自杀性自伤（non-suicidal self-injury, NSSI）是儿童青少年常见的心理行为问题，也是自杀行为的重要预测因素。研究表明，情绪调节障碍、冲动控制缺陷、精神疾病共病及家庭与社会环境逆境等可增加儿童青少年发生NSSI的风险，而家庭、学校与同伴支持可对该行为发挥保护作用。其生物学机制涉及遗传与表观遗传易感性、应激反应及内分泌紊乱、阿片系统与疼痛调节功能异常、免疫炎症失衡，以及情绪调节、执行功能、奖赏加工相关神经通路异常。该文系统综述儿童青少年NSSI的相关影响因素及生物学机制，以期为NSSI的早期识别、预防及干预提供参考。

Abstract

Non-suicidal self-injury (NSSI) is a common psychological and behavioral problem among children and adolescents and an important predictor of suicidal behavior. Studies indicate that emotion regulation difficulties, impaired impulse control, psychiatric comorbidities, family adversity, and adverse social environments increase the risk of NSSI, while family, school, and peer support exert protective effects. The biological mechanisms underlying NSSI include genetic and epigenetic susceptibility, stress response and endocrine dysregulation, abnormalities in the opioid system and pain modulation, immune-inflammatory imbalance, and dysfunction of neural circuits related to emotion regulation, executive function, and reward processing. This review systematically summarizes the influencing factors and biological mechanisms of NSSI in children and adolescents to provide a reference for early identification, prevention, and intervention of NSSI.

关键词

非自杀性自伤 / 影响因素 / 生物学机制 / 儿童 / 青少年

Key words

Non-suicidal self-injury / Influencing factor / Biological mechanism / Child / Adolescent

非自杀性自伤（non‑suicidal self‑injury, NSSI）指在无自杀意图的情况下，故意、直接对身体组织实施不被社会认可的自我伤害，常见方式包括切割、刮擦、刺伤等。大量研究表明，青少年是NSSI的高危人群，该行为是未来自杀行为的重要预测因子。Farkas等^［1］通过对2015—2020年相关文献的Meta分析发现，NSSI的总体患病率约为16%，其中女性（21%）高于男性（16.5%），亚洲地区（19.5%）高于其他地区（14.7%）。我国儿童青少年NSSI总体患病率约为22.37%^［2］。近年来，全球NSSI患病率持续上升，发病年龄呈低龄化趋势。Geoffroy等^［3］总结12岁以下儿童NSSI患病率可达6.2%~54.5%。基于NSSI对儿童青少年造成的严重心理痛苦体验及其潜在不良后果，深入探讨其影响因素及生物学机制对有效预防和干预具有重要意义。本文就生物、个人和社会因素在NSSI中的作用进行综述，以期为NSSI的防治提供理论依据与实践指导。

1 NSSI发生的影响因素

1.1　个人因素

情绪失调与发育非同步性：多项研究证实，情绪调节功能障碍与NSSI存在显著关联^［4］。儿童期个体因心理发育不成熟，自我保护机制欠缺，易受外界环境刺激诱发情绪失调^［5］。Warne等^［6］的前瞻性队列研究显示，儿童期情绪调节困难可预测青春期自伤风险，其机制可能涉及社会认知偏差与欺凌暴露等中介路径。进入青春期后，受性激素波动、身体意象改变、自我评价体系重构等影响，情绪易感性显著增加，而情绪认知和调节能力的滞后则进一步促进了NSSI的发生^［7］。此外，青春期存在“奖赏/情绪反应系统与顶层控制系统发育不同步”的现象，表现为冲动性增加及风险评估能力不足，这被认为是NSSI的高危发育特征^［8］。

认知异常：NSSI青少年常伴有低自尊、注意力缺陷、情绪面部识别障碍等问题^［9］，导致其在学习与社会交往中面临更多阻碍。在多重应激源的协同作用下，个体经历的心理与躯体痛苦程度加剧，进而增加了NSSI的发生频率。

共病风险：精神障碍共病亦显著增加了NSSI的发生。抑郁障碍青少年倾向于利用NSSI行为进行情绪代偿或舒缓情绪^［7］。而共病焦虑障碍、双相情感障碍、进食障碍及睡眠障碍等均是青少年NSSI发生的独立危险因素^［10］。此类共病情况增加了临床诊疗的复杂性，提示未来应建立系统化、多维度的整合性评估体系，以期制定精准的个性化治疗方案。

1.2　社会环境因素

1.2.1　社会因素

逆境经历与脆弱性：不良的社会环境对NSSI具有显著的预测作用，包括不良的童年成长经历（如情感、性或身体虐待，父母忽视、离异，丧亲，家庭暴力等）、负性生活事件、家庭功能失调、低水平的社会支持等^［10］。此类经历可能削弱个体内在心理韧性并增强人际脆弱性，使其倾向于通过NSSI来调节情感或社会失调^［11］。其中，童年期情感虐待的风险关联度最高，其次是情感忽视^［12］。

数字化生活环境：随着社交网络的飞速发展，网络欺凌引发的社会隔离感和无助感常诱发抑郁、焦虑等内化症状，促使受害者通过NSSI缓解痛苦和压力^［13］。社交媒体平台上关于NSSI的分享、讨论甚至展示可能引发易感人群的模仿效应。同时媒体呈现的理想化形象和青少年参与社会比较，容易诱发青少年的自卑感和负面自我认知^［14］。此外，网络成瘾则通过情绪逃避机制和冲动控制能力的减弱，进一步增加了NSSI的发生风险^［15］。

1.2.2　学校因素

学校作为核心微系统，是儿童青少年日常生活的重要场所，其内部应激与支持因素共同影响NSSI的发生。而校园负性生活事件（如校园欺凌受害、同伴排斥、学业高压等）是NSSI发生的高风险因素^［16］。与之相对，高质量的同伴支持与友谊通过降低应激敏感性表现出保护效应^［17］。学校联结感和支持体系能有效改善情绪困扰，发挥间接保护作用^［18］，也为校园心理干预提供了明确方向。

1.2.3　家庭因素

家庭经济情况、家庭结构、父母教养方式、父母的心理健康状态等与NSSI的发生高度相关。纵向研究显示，低社会经济条件家庭中成长的个体，发生NSSI的风险更高^［19］。Meta分析发现，多孩家庭青少年NSSI的发生率（27%）高于独生子女家庭（25.8%），单亲家庭青少年NSSI发生率（30%）高于双亲家庭（23.5%）^［20］。极端矛盾和消极的教养方式（如严厉惩罚、拒绝否认、过度干涉、过度保护）是NSSI发生的重要诱因^［21］。父母的物质滥用、注意缺陷和多动症状、低亲和力及责任心亦与子女NSSI有关^［22］。相反，积极的亲子沟通可以提供安全感和情感支持，可以直接和间接减少青少年NSSI行为^［23］。

2 NSSI发生的生物学机制

2.1　遗传与表观遗传易感性

表观遗传学为解析环境因素如何通过生物学途径塑造NSSI表型提供了理论框架。从机制全过程角度看，早期逆境暴露（儿童期不良经历、不良育儿方式、严重人际压力等），可能通过表观遗传调控（如DNA甲基化）在不改变序列的前提下调节基因表达，在情绪调节通路上形成可测量的生物学变化。如NAD依赖性蛋白去乙酰化酶sirtuin‑1（SIRT1）基因启动子区域CpG5位点甲基化改变，以及阿片黑皮质素原（POMC）基因启动子区域CpG1位点甲基化异常，提示其与青少年抑郁症合并NSSI的病理过程相关^［24-25］。在遗传学层面，神经递质代谢及情绪调节相关基因，如色氨酸羟化酶（TPH）基因、儿茶酚-O-甲基转移酶（COMT）基因及胶质细胞高亲和力谷氨酸转运体（SLC1A3）基因等，也被认为可能参与NSSI的遗传易感性机制^［26］。基因-环境交互研究显示，携带5-HTTLPR短等位基因、BDNF多态性、FKBP5变异或COMT Val158Met相关基因型的个体在面临环境压力时，更易出现NSSI行为^［27-29］。目前的研究仅探讨了少数候选基因对于NSSI的作用，且样本多来自抑郁障碍共病NSSI等特定诊断群体。未来研究应进一步拓展基因研究范围，并纳入更多独立诊断的NSSI个体，以验证目前研究结果的可靠性。

2.2　应激反应与内分泌系统失调

2.2.1　下丘脑-垂体-肾上腺轴

下丘脑-垂体-肾上腺轴（hypothalamic-pituitary-adrenal axis, HPA）是调节应激反应的核心神经内分泌通路。研究发现，NSSI青少年在应激诱导期间（如创伤访谈期间）存在唾液皮质醇水平显著降低及反应性钝化，提示既往童年逆境相关经历可能与应激情境下HPA轴功能下调有关^［30］。Klimes-Dougan等^［31］研究发现，抑郁障碍共病反复NSSI的青少年在特里尔社会应激测试情境下表现出较低的唾液皮质醇水平，并呈现相对钝化的皮质醇反应和恢复轨迹，提示HPA轴应激低反应性可能与自伤行为的反复性及严重程度相关。

2.2.2　自主神经系统

自主神经系统（autonomic nervous system, ANS）包括交感神经系统和副交感神经系统，在NSSI青少年的情绪调控中起关键作用。NSSI青少年在急性应激状态下表现出积极情绪受损、消极情绪增加、心率增加、心率变异下降不明显等特点^［32］。Goreis等^［33］的Meta分析同样证实，NSSI人群基础副交感神经活性较低，应激恢复期交感和副交感神经活性也较低。由此可见，ANS功能的失调可能影响个体采取NSSI来调节情绪与应对压力。此外，迷走神经自我刺激假说认为，NSSI行为可能通过增强迷走神经张力来诱导平静状态，从而达成情绪调节，保持更加平静的情绪状态^［34］。然而，ANS功能失调与NSSI之间的因果关系尚不明确，未来需通过纵向研究进一步检验二者在情绪调节和应激应对中的相互作用机制。

2.2.3　青春期性腺轴

青春期启动后，下丘脑-垂体-性腺轴（hypothalamic-pituitary-gonadal axis, HPG）被激活，促性腺激素、雌二醇、睾酮等性激素水平升高，这一内分泌转变与情绪反应性增强、奖赏敏感性改变及内化情绪症状增加同步出现^［35］。Luking等^［36］研究发现，9~10岁时即报告青春期提前（如女性月经初潮偏早、乳房发育提前等）的儿童，在后续随访中出现自伤行为^［36］，提示青春期HPG轴较早激活及性激素水平变化可能增加青少年NSSI风险。

2.3　阿片系统、疼痛调节与应激反应异常

内源性阿片系统是由阿片受体、内源性阿片类物质及负责其储存、释放的相关神经元共同组成，参与疼痛控制、伤口愈合、情绪调节等。研究显示，NSSI青少年中枢神经与外周组织（如脑脊液、血浆）内源性阿片物质（如β-内啡肽、脑啡肽）水平普遍较低^［37］。Störkel等^［38］研究发现，NSSI行为可提高β-内啡肽水平，且与行为严重程度呈正相关，与主观疼痛感受无明显关联。提示NSSI行为可促进β-内啡肽释放以恢复正常的生理平衡，且这种生化改变并不直接影响个体疼痛感知。影像学与分子研究表明杏仁核μ阿片受体及下丘脑前脑啡肽表达下降与NSSI相关^［39］。

在疼痛感知层面，NSSI的群体通常表现出更高的疼痛阈值、疼痛耐受性，以及更低的自评疼痛强度^［40］。Lalouni等^［41］基于疼痛调节理论，发现NSSI个体在条件性疼痛调节测试中表现出更有效的疼痛抑制，提示该群体可能具有较强的疼痛感知调节与抑制能力。Boyne等^［42］开展的纵向研究，发现基线疼痛耐受性高可预测随访期间NSSI频率和方式多样性的增加，而反向预测则不成立，这表明高疼痛耐受性可能是NSSI的致病因子而非其结果。然而，Kao等^［43］的纵向研究发现，随着NSSI频率降低个体疼痛阈值可趋于正常化。基线高疼痛耐受性可以预测1年后更低的NSSI发生频率，提示疼痛加工与NSSI的关系可能受个体差异、行为阶段或共病等因素共同调节。

此外，疼痛和应激系统紧密关联。van der Venne等^［44］研究表明，NSSI的严重程度与疼痛介导的HPA轴及ANS反应异常相关，表现为交感神经活动减弱、副交感神经活动增强。综上，内源性阿片系统、疼痛调节及应激反应异常可能是促发NSSI的重要生物学因素，需要进一步研究和验证其因果关系。

2.4　炎症反应的改变

免疫激活可能参与了NSSI的病理生理过程。有证据表明，炎症与精神障碍和自杀相关行为密切相关。Kim等^［45］研究发现，在伴有NSSI行为的情绪障碍患者中，促炎细胞因子（如肿瘤坏死因子-α）等水平升高。Kindler等^［46］发现，NSSI青少年白细胞的绝对计数和白细胞/皮质醇比值明显升高，提示免疫系统紊乱可能与NSSI相关。在基于丹麦全国纵向登记数据的研究发现，接受抗感染药物治疗的感染者NSSI发生风险增加，且该风险与感染或抗感染药物暴露的时间及剂量呈相关^［47］。此外，基于微生物-肠-脑轴理论，与健康青少年相比，NSSI青少年存在肠道菌群多样性下降，菌群结构发生改变的特点，进一步揭示了微生态失调的潜在影响^［48］。上述研究加深了对炎症、免疫、微生态失衡及感染因素与NSSI关系的理解，然而炎症与NSSI的直接关联性研究证据仍较有限。

2.5　神经影像学与神经认知机制

Lai等^［49］通过任务态功能磁共振成像研究发现，NSSI个体额叶、前扣带回、岛叶等参与情绪调节和奖赏加工相关环路呈现激活异常，提示青少年NSSI行为可能由情绪调节困难与奖赏加工缺陷共同驱动。Başgöze等^［50］针对青少年认知控制开展的多层次研究证实，青少年NSSI的严重程度与情绪依赖抑制控制和认知控制缺陷相关，尤其是前额叶脑区功能和神经连接异常，提示青少年在高强度情绪刺激下难以有效抑制自伤冲动。综上，青少年NSSI的发生可能反映了情绪调节障碍、奖赏加工缺陷以及认知控制功能受损的综合神经机制，这些脑区功能和连接异常与青春期边缘系统反应性增强而前额叶调控尚未成熟的发育特点相吻合，可能共同增加了儿童青少年NSSI的易感性。

3 小结与展望

综上所述，儿童青少年NSSI的病理机制具有高度的复杂性与多维性，涉及心理学、社会环境及生物学机制的深度交互。当前的研究仍多局限于横断面水平，未来需依托大样本纵向追踪队列，整合多组学分析，进一步揭示NSSI的因果路径与作用机制，从而为个性化干预与精准预防策略的制定提供科学依据。

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