From:  Rethinking computational models of addiction: toward context-sensitive and psychologically grounded frameworks

 Comparative summary of major computational models of addiction, showing their key mechanisms, behavioral focus, empirical grounding, and limitations.

ModelKey mechanismMain brain systemsBehavioral focusStrengthsLimitationsEmpirical support
TDRL/MF-RLDopaminergic reward-prediction error learning; cached stimulus-response values drive behavior.VTA, ventral/dorsal striatum, OFC.Habit formation, persistence, relapse.Mechanistically precise; explains compulsion and habit strength.Neglects craving, flexible thinking, emotion, recovery, intra-individual variability; dopamine-centric.Rodent neurophysiology & RL behavior; ventral striatum (Keiflin and Janak [36] 2015); OFC & DLS, habit shift (Lucantonio et al. [37] 2014); Rodent RL (Groman et al. [38] 2019).
Dual-system (MB + MF)Arbitration between goal-directed (MB) and habitual (MF) control.Lateral PFC, OFC, ACC, striatum.Transition from voluntary to compulsive use.Captures flexibility vs. habit; links to CBT/CM.Limited account of craving, emotion, and spontaneous recovery.fMRI arbitration (Lee et al. [45] 2014); rodent modeling (Lesaint et al. [46] 2014); behavioral devaluation (Byrne et al. [47] 2019).
Incentive-sensitization theory (IST)Sensitized mesolimbic dopamine amplifies cue-triggered “wanting” independent of pleasure.Nucleus accumbens, VTA, ventral pallidum, PFC.Craving, cue-reactivity, relapse.Distinguishes “wanting” vs. “liking”; explains persistent cue-driven craving.Lacks mechanisms for recovery, cognition, and symbolic meaning; dopamine-centric.VP electrophysiology (Tindell et al. [56] 2004); DAT variation (Singer et al. [57] 2016); Review (Berridge and Robinson [55] 2016).
iRISAExaggerated cue salience + impaired executive inhibition.Insula/ACC (salience), DLPFC/IFG (control), striatum, DMN.Cue-reactivity, craving under weak control, and relapse.Integrates cognition and motivation; strong imaging evidence; recovery correlates.Limited modeling of belief/identity change or natural recovery.Neuroimaging meta-analyses (Zilverstand et al. [23] 2018; Ceceli et al. [61] 2025; Zilverstand and Goldstein [60] 2020).
Bayesian/Active inferenceMaladaptive high-precision priors bias inference about drug relief; craving as predictive belief.Cortical predictive-coding circuits; dopamine/serotonin systems.Cue reactivity, craving, relapse, and recovery as belief updating.Unifies cognition, emotion, and context; models craving without cues. Accounts for natural recovery and identity change.Abstract; limited circuit-level data; early empirical base.Computational & imaging (Gu and Filbey [17] 2017; Harlé et al. [67] 2019; Kulkarni et al. [14] 2023).

ACC: anterior cingulate cortex; CBT: cognitive behavioral therapy; CM: contingency management; DAT: dopamine transporter; DLPFC: dorsolateral prefrontal cortex; fMRI: functional magnetic resonance imaging; iRISA: impaired response inhibition and salience attribution; MB: model-based; MF: model-free; OFC: orbitofrontal cortex; RL: reinforcement learning; TDRL: temporal-difference RL; VTA: ventral tegmental area.