Are There Different Routes to a Delusion? A Mechanistic Framework for Convergent Psychosis

Abstract

Delusions occur in disorders with markedly different etiologies, including schizophrenia, medication-induced psychosis, postpartum psychosis, neurodegenerative disease, and metabolic encephalopathy. This convergence poses a basic clinical problem: the phenomenology of a delusion may provide limited information about the mechanism that produced it or the prognosis that follows. This article examines five routes to a fixed false belief using the ARCH × Φ framework, in which biological execution depends on the conjunction of architecture (A), drive (D), context (C), and a permissive phase or gating state (Φ). The central proposal is that, in a conjunctive system, severe disruption of different required components can converge on a common clinical endpoint. A second distinction separates current execution from the persistent neural substrate that constrains future execution. Transient state disturbances may therefore produce severe but reversible psychosis, whereas developmental mis-writing or progressive substrate loss may produce persistent or worsening illness. Schizophrenia, corticosteroid psychosis, postpartum psychosis, Alzheimer's disease, and homocystinuria illustrate distinct versions of this problem. The framework is presented as a mechanistic organizing hypothesis rather than a completed theory of delusion; several mappings remain inferential, and the homocystinuria case identifies a failure mode not represented by the original equation. Its value lies in making clinically relevant distinctions among convergent symptoms and in generating falsifiable predictions across molecular, circuit, and clinical levels.