Idiopathic Scoliosis as a Conversion Reaction to Stress with the Neural Effect of a “Distorting Mirror”

TL;DR

This paper explores how stress and brain asymmetry might contribute to adolescent idiopathic scoliosis, suggesting a new framework for understanding and treating the condition.

Contribution

The paper proposes a novel integrative framework linking AIS with stress mechanisms, neuroanatomical asymmetry, and mental disorders.

Findings

Atypical hemispheric lateralization may increase susceptibility to AIS.

Stress-related coping strategies and body schema disturbances are linked to AIS progression.

Gender differences in stress responses correlate with AIS development and progression.

Abstract

Objective: To synthesize current evidence on the relationships between adolescent idiopathic scoliosis (AIS), stress-related mechanisms, neuroanatomical asymmetry, and mental disorders, and to propose an integrative conceptual framework describing their interaction. Materials and Methods: A comprehensive literature review was conducted using the PubMed, Web of Science, and Scopus databases. Search terms targeted the etiology and pathogenesis of adolescent idiopathic scoliosis, hemispheric lateralization, stress responses, body schema disturbances, and associated mental disorders. The review was reported in accordance with PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) recommendations. A structured qualitative synthesis of 225 relevant publications was performed. Results: The analyzed studies revealed several complementary conceptual approaches to AIS pathogenesis. Emerging evidence suggests that atypical hemispheric lateralization, potentially associated with right-hemisphere (RH) dysfunction, may contribute to susceptibility to AIS. Such patterns of lateralization have been linked to specific stress-related coping strategies, including harm avoidance, as well as to disturbances of body schema and an increased prevalence of certain mental disorders. Gender-related differences in stress responses and in the development and progression of AIS were consistently reported across studies. Collectively, these findings support the hypothesis that neuropsychological and stress-related mechanisms, including phenomena described as the “distorting mirror effect”, may contribute to the persistence and progression of spinal deformity in vulnerable individuals. Conclusions: AIS appears to be a multifactorial condition in which atypical neuroanatomical asymmetry, stress-related processes, and altered body representation interact. This integrative perspective generates hypotheses suggesting that prevention and treatment strategies for AIS could benefit from incorporating approaches aimed at modulating stress responses and enhancing brain neuroplasticity. Further interdisciplinary studies integrating clinical, neuroimaging, and neurobiological methods are warranted to clarify underlying mechanisms.

Figures