Carolien Zeetsen

122 have shown that such personalized treatment approaches can be efficacious in patients with SUD and cognitive impairment (Eack et al., 2016). To what extent this might also benefit patients with GUD remains to be studied. The results of this study should be viewed in the light of several limitations. First, the MoCA is not a diagnostic tool for cognitive impairment. While the MoCA has been shown to be a valid screening instrument in patients with SUD (Bruijnen, Jansen, et al., 2019), no extensive neuropsychological assessment was used in the current study. Therefore, future studies should confirm the current findings, using more detailed neuropsychological assessment across different cognitive domains. Another limitation is that most patients with primary GUD have poly substance use, often stimulants (Dijkstra et al., 2017; Beurmanjer et al., 2019). It is therefore impossible to disentangle GHB effects on cognitive impairment from the effects of other substances. In addition, the observed persistent cognitive impairments could have been present before the use of GHB (or other substances) started. As a result, no causal inferences can be made on the relationships between GHB use/GUD and cognitive impairment in the current study. In conclusion, in the current study about half of all included patients with GUD had an indication for cognitive impairment before detoxification, decreasing to about one third after detoxification. Cognitive impairment before detoxification, particularly memory problems, were associated with a higher relapse risk after detoxification. Current findings warrant clinical attention for cognitive impairment in patients with GUD, for instance by screening for cognitive impairment using the MoCA, and full neuropsychological assessment after a sufficient period of abstinence following detoxification where appropriate. Future studies should confirm these findings and explore whether GUD patients with cognitive impairment require specific treatment adaptations.