Authors
Simone Hauck, Luciana Terra de Oliveira
Published in
Neuroscience and biobehavioral reviews. Pages 106992. Sep 20, 2026. Epub Sep 20, 2026.
Abstract
Current neurodevelopmental classifications partition autism, ADHD, developmental coordination disorder (DCD), dyslexia, twice-exceptionality, and high-ability phenotypes into ostensibly separate clinical entities.
This narrative conceptual review aims to develop the phenotype-level clinical implications of an extracellular matrix (ECM)-based mechanobiological account of atypical neural topology, formulated in prior work, through the High Processing Cost Phenotypes (HPCPh) framework: these presentations are proposed to be phenotype-specific topological expressions of a shared developmental substrate.
Within this model, a more permissive and insufficiently stabilized neural architecture is proposed to give rise to a recurrent geometry of Islands (high-gain domains of efficient local capture and integration), Deserts (weakly stabilized domains of serial implementation, gating, timing, and sensorimotor translation), and Bridges (energetically expensive compensatory pathways linking them). This Island-Desert-Bridge (IDB) topology is used to organize recurrent clinical paradoxes across neurodivergent presentations, including sensory talent with severe overload, preserved intention with dyspraxic execution, semantic richness with reading bottlenecks, salience-driven hyperfocus with routine failure, and high abstract capacity sustained by exhausting masking. The framework proposes a thermodynamic interpretation of some burnout- and depression-like states as load-related reductions in functional throughput when the allostatic cost of bridging exceeds metabolic and autonomic tolerance; this formulation does not exclude primary mood disorders and requires empirical differentiation. Functional Iron Blockade (FIB) is introduced as one candidate, hypothesis-level containment mechanism.
By shifting emphasis from symptom-based deficits to topological cost, the HPCPh framework provides a falsifiable, transdiagnostic account that reconnects neurodevelopmental phenotypes with developmental biology, systems neuroscience, and allostatic physiology.
PMID:
42764047
Bibliographic data and abstract were imported from PubMed on 21 Sep 2026.
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