Severe psychiatric disorders — major depression, bipolar disorder, borderline personality disorder, and post-traumatic stress disorder — share phenomenological features of dissociation, emotional dysregulation, and cognitive fragmentation that respond incompletely to monoaminergic treatment. This paper proposes that these syndromes converge on a common pathophysiological principle: high-metabolic-cost integrative cortical circuits are selectively disengaged when the energetic cost of maintaining functional architecture is not offset by the adaptive return of environmental coupling. Building a structural analogy between the drift-barrier formalism of evolutionary bioenergetics (extending the author’s prior drift-barrier analysis of GPCR-class signalling, submitted to PLOS ONE, PONE-D-26-40793, Zenodo 10.5281/zenodo.21916009) and the maintenance economics of large-scale neural networks, the model generates falsifiable predictions about regional metabolic vulnerability, connectivity restoration preceding symptomatic recovery, and the relationship between late-life depression and neurodegeneration. Section 3.4 extends the framework with an explicit boundary condition: dopaminergic reward-prediction signalling carries information in its variance rather than its mean, and interventions that stabilise network configuration by compressing that variance may purchase state stability at the cost of motivational capacity. Section 5 proposes that glutamatergic plasticity-inducing agents (e.g., ketamine) act by lowering the transition barrier between pathological and functional network configurations, rather than by correcting a monoamine deficit. No treatment protocol is proposed; therapeutic implications are stated as hypotheses requiring controlled trials. Version 2 removes an earlier unsafe drug-protocol section present in v1.
Sidário Rodrigues Malheiros-junior (Fri,) studied this question.