Compulsivity is a core feature of addictive disorders, including gambling disorder. However, it is unclear to what extent this compulsive behavior in gambling disorder is associated with abnormal compulsivity-related neurocognitive functioning. Here, we summarize and synthesize the evidence for compulsive behavior, as assessed by compulsivity-related neurocognitive tasks, in individuals with gambling disorder compared to healthy controls (HCs). A total of 29 studies, comprising 41 task-results, were included in the systematic review; 32 datasets (n=1072 individuals with gambling disorder; n=1312 HCs) were also included in the meta-analyses, conducted for each cognitive task separately. Our meta-analyses indicate significant deficits in individuals with gambling disorder in cognitive flexibility, attentional set-shifting, and attentional bias. Overall, these findings support the idea that compulsivity-related performance deficits characterize gambling disorder. This association may provide a possible link between impairments in executive functions related to compulsive action. We discuss the practical relevance of these results, their implications for our understanding of gambling disorder and how they relate to neurobiological factors and other 'disorders of compulsivity'.

Deficits in instrumental, goal-directed control, combined with the influence of drug-associated Pavlovian-conditioned stimuli, are thought to influence the development and maintenance of addiction. However, direct evidence has mainly come from animal studies. We sought to establish whether alcohol use disorder (AUD) is characterized by behavioral or neurobiological deficits in (i) the integration of Pavlovian and instrumental values and (ii) goal-directed control; and (iii) whether duration or severity of AUD is associated with such deficits. The influence of cues predicting food rewards on instrumental action was assessed in a Pavlovian-to-instrumental transfer (PIT) test, measuring both specific and general PIT, and goal-directed behavior in an outcome-devaluation test. Brain activity was measured using functional MRI in 38 abstinent individuals with AUD and 22 matched healthy control individuals (HCs). We found significant specific and general PIT and outcomedevaluation effects across groups indicating goal-directed control, mediated by distinct corticostriatal signals, but no significant differences between individuals with AUD and healthy controls. Bayesian analyses provided substantial-to-strong evidence for the absence of group differences for these effects, or any relationship with duration or severity of AUD. These results suggest intact ability to integrate action-outcome associations on specific and general PIT and goal-directed learning in AUD during abstinence. Alcohol use disorder (AUD) is characterized by a loss of control over alcohol consumption. Associative learning mechanisms are proposed to play a crucial role in the development and maintenance of this loss of control 1-4. Habitual and eventually compulsive alcohol use is thought to depend largely on instrumental conditioning 5 : whereas initial drinking is thought to be goal-directed-when actions are governed by associations between actions and outcomes (e.g. drinking is pleasurable)-habitual actions are instead outcome-independent and become controlled through learned stimulus-response associations 6,7. One way to expose which system controls responding is by outcome-devaluation. Such paradigms have been used to reveal distinct corticostriatal neural mechanisms for goal-directed actions, depending on orbitofrontal cortex (OFC), ventromedial prefrontal cortex (mPFC) and the ventral striatum, and habitual behavior depending on the premotor cortex and dorsal striatum 8-10. Concerning AUD, habitual control over alcohol seeking indeed increases with prolonged self-administration in rodents 11 and human AUD patients rely more on stimulus-response habits than HCs 12 .