Defensive‑Timing Disorders: A Neuroevolutionary Model of the Bipolar‑Psychotic Spectrum
James Le Bas
Research Square March 26, 2026 preprint DOI: 10.21203/rs.3.rs-9205460/v1 (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Theoretical or philosophical paper |
|---|---|
| Key points | Proposes that the bipolar-psychotic spectrum reflects a unified class of "Defensive-Timing Disorders" arising from graded losses of parvalbumin-mediated inhibitory precision and hippocampal temporal-context stability. Argues that as this coupled scaffold weakens, defensive responses distort, salience becomes disordered, and counterfactual representations gain excessive weight, with an extreme high-arousal immobility state termed "reverted escape". Suggests the same timing vulnerability may underlie schizophrenia's persistent cognitive impairments. |
Abstract
Abstract Mammalian social life oscillates between two broad modes: an agonic mode organised around dominance, tension, and defensive collapse, and a hedonic mode characterised by low arousal, reciprocity, and prestige-based coordination. Archaeological and anthropological evidence suggests that some Upper Palaeolithic groups moved fluidly between these modes, with ritual specialists (shamans) occupying a sanctioned niche in which brief psychotic-like states – often hallucinogen-facilitated – were tolerated and even valued. From a cognitive-neuroscience perspective, these altered states can be understood as transient perturbations of the timing architecture that normally aligns perception, simulation, and contextual inference. I propose that the bipolar-psychotic spectrum reflects a unified class of Defensive-Timing Disorders (DTD), arising from graded losses of parvalbumin-mediated inhibitory precision and hippocampal temporal-context stability. As this coupled scaffold weakens, defensive responses distort, salience becomes disordered, counterfactual representations gain excessive weight, and at the extreme, reverted escape emerges: a high-arousal immobility state representing a distinct pathophysiology. The same timing vulnerability may underlie the persistent cognitive impairments of schizophrenia, which can be viewed adds the cognitive expression of the same PV-hippocampal timing collapse. This paper integrates evolutionary anthropology, ethology, and cognitive neurodynamics to articulate a mechanistic account of the bipolar-psychotic spectrum that has not previously been formulated.