Schettino Martino, Parrillo Chiara, Gazzellini Simone, Cairone Luca, Baldassari Giulia, Thayer Julian F, Giove Federico, Napolitano Antonio, Ottaviani Cristina
Department of Psychology, Sapienza University of Rome, Rome, Italy.
IRCCS Istituto Delle Scienze Neurologiche di Bologna, Bologna, Italy.
J Neural Transm (Vienna). 2025 Sep 4. doi: 10.1007/s00702-025-02992-2.
Unwanted intrusive thoughts play a key role in the onset, maintenance, and relapse of stress-related psychopathological conditions and are usually accompanied by a physiological fight-or-flight response. However, the mechanisms underlying the persistence of this maladaptive process remain unclear. This study employed a multimodal approach, integrating proton magnetic resonance spectroscopy, resting-state functional connectivity, and heart rate monitoring, to investigate gamma-aminobutyric acid (GABA) and glutamate-mediated neurometabolism during intrusive thinking, alongside central and peripheral autonomic nervous system activity. In individuals meeting diagnostic criteria for Generalized Anxiety Disorder (n = 29), an experimental induction of intrusive thoughts was associated with an increase in anterior cingulate cortex (ACC) GABA+ (macromolecular-contaminated), which correlated with suppressed autonomic reactivity. This relationship was mediated by the dispositional tendency to engage in intrusive thinking and was accompanied by reduced resting-state activation of the central autonomic network. Conversely, age- and sex-matched healthy controls (n = 29) exhibited a reduction in ACC GABA + and increased autonomic reactivity during intrusive thinking. While limited by a cross-sectional design, these findings suggest that pathological intrusive thinking may be maintained through neurometabolic negative reinforcement mechanisms involving both the central and autonomic nervous systems. If corroborated, current results may inform the development of targeted treatments aimed at disrupting such reinforcement processes.
不必要的侵入性思维在应激相关精神病理状态的发作、维持和复发中起关键作用,并且通常伴随着生理上的战斗或逃跑反应。然而,这种适应不良过程持续存在的潜在机制仍不清楚。本研究采用多模态方法,整合质子磁共振波谱、静息态功能连接和心率监测,以研究侵入性思维过程中γ-氨基丁酸(GABA)和谷氨酸介导的神经代谢,以及中枢和外周自主神经系统活动。在符合广泛性焦虑症诊断标准的个体(n = 29)中,侵入性思维的实验诱导与前扣带回皮质(ACC)中GABA+(大分子污染)增加有关,这与自主反应性抑制相关。这种关系由参与侵入性思维的倾向性介导,并伴随着中枢自主网络静息态激活的降低。相反,年龄和性别匹配的健康对照(n = 29)在侵入性思维过程中表现出ACC GABA+减少和自主反应性增加。虽然受横断面设计的限制,但这些发现表明,病理性侵入性思维可能通过涉及中枢和自主神经系统的神经代谢负强化机制得以维持。如果得到证实,目前的结果可能为旨在破坏这种强化过程的靶向治疗的开发提供信息。