Theoretical model explores memory dynamics in PTSD, suggesting therapeutic pathways for intervention.
Post-traumatic stress disorder (PTSD) is defined by a specific anomaly in memory dynamics: traumatic events are not stored as retrievable records that fade over time but as configurations that are reactivated — re-experienced — with full perceptual and affective intensity, triggered by stimuli bearing only partial structural resemblance to the original event. We address this gap within the Schrödinger–REK–RGB field-theoretic framework, introducing the concept of pathological crystallization: the regime in which the non-local memory functional ε_REK[Ψ_H] exceeds a critical threshold λ_c, generating a stable attractor from which the holistic field cannot exit spontaneously. We derive λ_c analytically and show that it depends on three neurobiologically interpretable parameters: the coherence length ℓ_z (hippocampal contextual embedding capacity), the integrated kernel weight K̂ (total crystallization capacity), and the crystallized density ρ_c (event intensity). The model provides a formal stability criterion (λ_c), a formal resolution condition (E_min), and a formal account of two distinct therapeutic mechanisms: pharmacological reduction of λ_REK (MDMA-assisted therapy) and graduated exposure increase of ε_k (Prolonged Exposure, EMDR). The model generates four testable predictions including a non-Markovian signature distinguishing it from existing Markovian models of intrusive memory dynamics.
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Andrea Succi (2026) studied this question.
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