The Superposition-Collapse Model: A Unified Framework for Differential Diagnosis of Neurodevelopmental vs. Attachment-Mediated Attention Dysregulation

Background: Attention Deficit Hyperactivity Disorder (ADHD) is conventionally modeled as a neurodevelopmental condition characterized by dopaminergic hypofunction in the prefrontal cortex (PFC). However, converging evidence from attachment theory, computational neuroscience, evolutionary psychiatry, and autonomic physiology indicates that a significant subset of individuals meeting DSM-5 criteria for ADHD exhibit symptom profiles that are functionally indistinguishable from the autonomic defense responses associated with disorganized attachment—specifically, the Systemic Acquired Disorganized Attachment (SADA) phenotype described in Bust (2026a). Objective: This paper proposes the Superposition-Collapse Model (SCM), a unified diagnostic framework that differentiates neurodevelopmental ADHD (ND-ADHD) from attachment-mediated attention dysregulation (AM-ADHD) by analyzing the pattern and context-dependency of attentional collapse from a state of chronic multidirectional vigilance ("superposition"). Methods: The model integrates four convergent lines of evidence: (1) Karl Friston’s Free Energy Principle and the role of weak priors in generating high neural entropy states; (2) columnar activation patterns in the Periaqueductal Gray (PAG) and their mapping onto Limbic Friction profiles; (3) P50 auditory gating data as a biomarker for the sentinel phenotype; and (4) Life History Theory’s Fast/Slow Strategy framework as an evolutionary explanation for the persistence of ADHD-like traits. Results: The SCM proposes three differential diagnostic markers: (a) context-dependency of symptom expression (stable vs. stress-modulated), (b) narrative coherence pattern on the Adult Attachment Interview ("web" vs. "block" pattern), and (c) the stimulant paradox (paradoxical calming vs. arousal escalation). These markers are mapped onto measurable physiological parameters via the SADA-Entropy Protocol (Bust, 2026b). Conclusions: The Superposition-Collapse Model provides clinicians with a theoretically grounded and empirically testable framework for distinguishing between dopamine-deficit ADHD and neuroception-driven attentional dysregulation. This distinction carries immediate treatment implications: stimulant medication may ameliorate ND-ADHD while potentially exacerbating AM-ADHD by increasing sympathetic arousal without addressing the underlying Limbic Friction generated by the PAG-ECS axis. The model positions ADHD not as a unitary disorder but as a final common pathway with divergent etiologies requiring differential intervention.