Harmen Beurmanjer

58 Chapter 4 study did not observe a relationship between the number of self-reported GHB-induced comas and cognitive impairment. Several methodological limitations hamper strong conclusions concerning the (causal) relationship between GHB-induced coma and cognitive impairment. First, studies, including ours, commonly rely on self-reported comas. A detailed and reliable account of the total number of GHB-induced comas is hard to obtain due to its frequency (usually on a daily basis (Beurmanjer et al., 2019), amnesia (as this might be an aspect of GHB-induced coma itself ) (Sumnall et al., 2008), and the observed memory impairment in patients with GUD. Second, as seen in other samples, patients with GUD often also use other substances. These might also contribute to cognitive impairment in these patients. Finally, it may also be that it is not the number of GHB-induced comas or substance use levels that contribute to cognitive impairment. Similar to patients with other SUDs our data did not find a relationship between MoCA scores and years of regular use, (GHB) dose, severity of dependence and coma’s (Bruijnen, Dijkstra, et al., 2019). This suggests that other factors might be involved, for instance lack of sleep, malnutrition or other psychiatric or somatic comorbidities. Future studies should explore mechanisms contributing to cognitive impairment in patients with GUD and other SUDs. The current study shows that MoCA scores, in particular performance on the memory domain, were associated with the risk of relapse. This is in line with studies in other SUD, such as alcohol (Czapla et al., 2016), cocaine (Turner et al., 2009) and opioids (Ma et al., 2019), where cognitive impairment is associatedwith the risk of relapse and poor treatment retention. Cognitive functions are crucial to direct behaviour and obtain control over impulses and emotions (Loughead et al., 2015), including substance use. Cognitive impairment in patients with SUD (including GUD) might thus interfere with taking control of substance use, to change behaviour, and reach treatment goals (Loughead et al., 2015; Volkow & Morales, 2015). SUD patients with cognitive impairment might require treatment adaptations focussing on cognitive enhancement (Rensen, Egger, Westhoff, Walvoort, & Kessels, 2019; Verdejo-Garcia, 2016). Indeed, several studies have shown that such personalized treatments approaches can be efficacious in patients with SUD and cognitive impairment(34). 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, Dijkstra, et al., 2019; Bruijnen, Jansen, et al., 2019), no extensive neuropsychological assessments were used in the current study. Therefore, future studies should confirm the current findings, using more detailed neuropsychological assessments across different cognitive domains. Another limitation is that most patients with primary GUD have poly substance use, often stimulants (Beurmanjer et al., 2019; Dijkstra et al., 2017; Kamal et al., 2016). It is therefore impossible to disentangle GHB effects on cognitive impairment from the effects of other