The freeze-arrest model of catatonia: a critical neuroimaging review with evo-neurobiological integration.

Abstract

Catatonia is a heterogeneous and poorly defined entity. Akinetic catatonia shares core phenomenology with the adaptive freeze-to-tonic immobility response, a threat-defense system conserved across evolution. It has been suggested that catatonia may be the maladaptive counterpart of the freeze-to-tonic immobility response. While similar brain structures are implicated in both entities, no theory-driven synthesis of neuroimaging evidence has been conducted to provide mechanistic support for this hypothesis. In this critical review, we cross-referenced available neuroimaging studies in human freezing and catatonia studies across etiologies. Both independent literatures implicate failure of the orbitofrontal-medial prefrontal cortices, dysregulation of the salience network, and basal ganglia-midbrain mediated motor block. Based on this review's findings, we developed the freeze-arrest model of catatonia (FAMC), a unified mechanistic framework that integrates evolutionary, neurobiological, and clinical data. The three entry points into the FAMC are overwhelming emotions, toxic-metabolic network disruption, and subcortical short-circuiting. Neurodegenerative, neurodevelopmental, and structurally mediated catatonia represent a mechanistically distinct category. FAMC is a testable evo-neurobiological model that explains the heterogeneity of acute akinetic catatonia, proposes unified diagnostic criteria, and treatment implications per presentation.