This perspective article argues that the theoretical landscape of nonsuicidal self-injury (NSSI) has long been stabilized by the “hydraulic” model of Automatic Negative Reinforcement, which conceptualizes self-harm primarily as a mechanism to down-regulate aversive hyper-arousal. While this framework successfully elucidates the etiology of self-injury driven by high-intensity negative affect, it fails to account for a substantial, treatment-resistant phenotype: adolescents driven by profound anhedonia and ventral striatal hypofunction. This perspective article argues for the formal recognition of an “Anhedonic Subtype” of NSSI. Synthesizing recent epidemiological data identifying “emptiness” as a central symptom network bridge, alongside neurobiological evidence of reward blunting, we posit that for this subtype, NSSI functions not as a sedative, but as a mechanism of “forced activation.” We propose a preliminary differential diagnostic framework distinguishing defensive dissociation from anhedonic deficit and outline the theoretical rationale for exploring a shift in clinical intervention from distress tolerance toward positive affect up-regulation. The clinical utility of this framework remains to be evaluated in future empirical research.

