The Valence Conflict Model of Pathological Rumination: The Deadlock Mechanism of the ACC–DMS Circuit

Abstract Existing theories define pathological rumination as repetitive cognitive processing of negative memories. However, this unipolar definition fails to explain why individuals continue to experience cognitive gridlock and circular idling even when they "logically know there is no solution." This paper proposes the valence conflict hypothesis: the essence of rumination is not the singular replay of negative memories, but the mandatory coexistence and co-activation of positive and negative memories within the same cognitive scenario. This simultaneous activation of bidirectional valences creates an irreconcilable cognitive gap in the anterior cingulate cortex (ACC). The ACC identifies this gap as a persistent prediction error and consequently refuses to issue "action execution permission" to the dorsomedial striatum (DMS). Deprived of valid instructions, the DMS becomes trapped in a "jamming" cycle of repeated initiation attempts repeatedly overruled by the ACC. Building on this framework, this paper further proposes that chronic valence conflict leads to sustained cortisol elevation through hyperactivation of the hypothalamic-pituitary-adrenal (HPA) axis, exerting neurotoxic damage on prefrontal-hippocampal structures and thereby consolidating functional rumination into pathological rigidity at the personality structure level. This hypothesis provides a novel neural circuit explanation for the formation and maintenance of rumination, and suggests that clinical intervention should shift from "modifying thought content" to "resolving valence conflict." Keywords: pathological rumination; valence conflict; anterior cingulate cortex; dorsomedial striatum; cortisol; prediction error