Abstract
Chronic pain involves maladaptive plasticity of the insular cortex, a key hub for both pain and affective touch. While C-tactile (CT) afferent stimulation shows analgesic potential, its efficacy is limited by altered touch processing in chronic pain populations. This review integrates neuroimaging and behavioural evidence to propose a novel, stratified therapeutic framework targeting the insula. A narrative review of PubMed and Scopus was performed. Two literature streams were synthesized: (1) neuroimaging studies characterizing structural and functional insular abnormalities in chronic pain and (2) studies examining behavioural and neural responses to affective touch in chronic pain populations. The synthesis identifies a core ‘dysfunctional insula’ phenotype marked by structural atrophy, persistent hyperactivity and reorganized network connectivity (e.g. salience, default mode). This is paralleled by altered affective touch processing, often manifesting as anhedonia. Neuroimaging supports a ‘neural hijacking’ model, where insular activity during gentle touch decouples from pleasantness and instead correlates with pain-related metrics. Critically, findings are heterogeneous: some cohorts retain hedonic discrimination, suggesting the underlying neural circuits are suppressed rather than permanently damaged. We propose a stratified model where CT-based interventions are personalized to a patient’s neurofunctional phenotype: either by normalizing ‘hijacked’ pain-related circuits or by strengthening intact hedonic pathways. This approach moves beyond a one-size-fits-all strategy, establishing the insula as a nuanced target for personalized, non-pharmacological pain therapies.
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This post is Copyright: | July 4, 2026
Neuro-General