Debbané Martin, Salaminios George, Luyten Patrick, Badoud Deborah, Armando Marco, Solida Tozzi Alessandra, Fonagy Peter, Brent Benjamin K
Faculty of Psychology and Educational Sciences, University of GenevaGeneva, Switzerland; Research Department of Clinical, Educational and Health Psychology, University College LondonLondon, UK; Office Médico-PédagogiqueGeneva, Switzerland.
Research Department of Clinical, Educational and Health Psychology, University College London London, UK.
Front Hum Neurosci. 2016 Aug 22;10:406. doi: 10.3389/fnhum.2016.00406. eCollection 2016.
In this review article, we outline the evidence linking attachment adversity to psychosis, from the premorbid stages of the disorder to its clinical forms. To better understand the neurobiological mechanisms through which insecure attachment may contribute to psychosis, we identify at least five neurobiological pathways linking attachment to risk for developing psychosis. Besides its well documented influence on the hypothalamic-pituary-adrenal (HPA) axis, insecure attachment may also contribute to neurodevelopmental risk through the dopaminergic and oxytonergic systems, as well as bear influence on neuroinflammation and oxidative stress responses. We further consider the neuroscientific and behavioral studies that underpin mentalization as a suite of processes potentially moderating the risk to transition to psychotic disorders. In particular, mentalization may help the individual compensate for endophenotypical impairments in the integration of sensory and metacognitive information. We propose a model where embodied mentalization would lie at the core of a protective, resilience response mitigating the adverse and potentially pathological influence of the neurodevelopmental cascade of risk for psychosis.
在这篇综述文章中,我们概述了从精神障碍的病前阶段到其临床形式,将依恋逆境与精神病联系起来的证据。为了更好地理解不安全依恋可能导致精神病的神经生物学机制,我们确定了至少五条将依恋与患精神病风险联系起来的神经生物学途径。除了其对下丘脑-垂体-肾上腺(HPA)轴的充分记录的影响外,不安全依恋还可能通过多巴胺能和5-羟色胺能系统导致神经发育风险,并对神经炎症和氧化应激反应产生影响。我们进一步考虑了神经科学和行为学研究,这些研究将心理化作为一组潜在地调节向精神障碍转变风险的过程。特别是,心理化可能有助于个体弥补感觉和元认知信息整合中的内表型损伤。我们提出了一个模型,其中体现性心理化将处于保护性、复原力反应的核心,减轻精神病风险的神经发育级联的不利和潜在病理影响。