Stress-related neuroplasticity and developmental vulnerability in functional neurological disorder: from adverse experience to maladaptive overlearning

Functional Neurological Disorder (FND) is increasingly understood as a disorder of brain functioning rather than structural damage. While contemporary predictive coding models have provided important insights into the generation of functional symptoms, they offer limited explanations for vulnerability, developmental risk, and the striking association between FND and adverse life experiences. A substantial body of evidence indicates that early-life stress, trauma, and chronic adversity are overrepresented in individuals with FND and are associated with enduring neurobiological alterations in brain systems central to emotional processing, interoception, and motor control. In this paper, we propose that stress-related neuroplasticity constitutes a key developmental substrate that predisposes the brain to maladaptive learning processes, increasing the likelihood that salient bodily states become rigidly encoded and persist as functional symptoms. We review evidence linking trauma exposure to long-lasting changes in limbic, paralimbic, and sensorimotor circuits implicated in FND, including the amygdala, anterior cingulate cortex, insula, orbitofrontal cortex, and supplementary motor areas. We further examine autonomic and neuroendocrine abnormalities and gender-related biological factors that may amplify these effects. We argue that these convergent findings support a model in which FND emerges from excessive, stress-biased neuroplasticity that promotes overlearning of bodily predictions, rather than from a primary failure of belief updating. This framework provides a coherent account of vulnerability, symptom persistence, and heterogeneity in FND, and offers a biologically grounded bridge between developmental risk factors and contemporary computational models of functional symptoms.