Cognitive control in young adults with cannabis use disorder: An event-related brain potential study

Abstract

Contemporary models of substance use disorders emphasize the role of cognitive control, which has been linked to difficulties in resisting the use of substances. In the present study, we measured two aspects of cognitive control, response inhibition (operationalized by a Go/NoGo Task) and performance monitoring (operationalized by an Eriksen Flanker Task), in a group of young cannabis-use disorder (CUD) patients and compared these functions with two control groups (i.e. a group of cigarette smokers and a group of non-smokers). We employed both behavioural and electrophysiological measures. The results indicate that CUD patients displayed reduced NoGo-P3 event-related potentials compared with non-smoking controls, but not compared with smoking controls. In addition, CUD patients were slower on Go trials than both control groups. No other between-group electrophysiological or behavioural differences were observed. These results seem to suggest that CUD patients have problems related to response inhibition, but performance monitoring seems relatively unaffected.

In utero Δ9-tetrahydrocannabinol exposure confers vulnerability towards cognitive impairments and alcohol drinking in the adolescent offspring: Is there a role for neuropeptide Y?

“…Whereas it has been proved that cannabis use during pregnancy is associated with an increased risk of adverse obstetrical outcomes (Gunn et al, 2016), detrimental neuro-behavioural consequences in the progeny are still poorly explored. On the contrary, abnormal activation of the ECS plays a de facto role in emotional dysregulation and cognitive deficits observed in adolescent heavy users of cannabis (Maij et al, 2017). Emerging preclinical evidence demonstrates that adolescent exposure to THC selectively targets molecular and neuropharmacological signalling pathways in both cortical and subcortical regions, including the prefrontal cortex (PFC) and the mesolimbic dopamine (DA) pathway, comprising the ventral tegmental area (VTA) and the nucleus accumbens (NAc; Wenzel and Cheer, 2018).…”

A multimodal investigation of cerebellar integrity associated with high‐risk cannabis use

“…[14][15][16] The integrity of these intrinsic networks is associated with cognitive and behavioral functions that appear to be impaired in individuals with chronic THC exposure, such as response inhibition, attention, and memory. [17][18][19] Cerebellar alterations related to acute and long-term cannabis use have been observed using brain imaging techniques. Positron emission topography (PET) studies have demonstrated that following acute administration of cannabis, there is increased cerebral blood flow to the cerebellum and to the orbitofrontal and temporal pole regions during a dichotic selective attention and listening task.…”

Distress intolerance moderation of neurophysiological markers of response inhibition after induced stress: Relations with cannabis use disorder.

“…Consistent with this interpretation, greater cannabis problem severity was associated with increased errors on go trials regardless of acute stress, suggesting that enhanced ΔP3a in disordered cannabis users may reflect compensatory activity to achieve normative response inhibition performance at the expense of response initiation performance. Given the absence of significant moderation by acute stress, enhanced ΔP3a may be a trait-like neural marker of CUD severity in regular cannabis users, though blunted ΔP3a in conjunction with slowed go reaction time among CUD patients relative to non-user healthy controls has also been found (Maij et al, 2017). Future studies should include a non-user control group to determine the nature of ΔP3a alterations across the cannabis use to CUD spectrum.…”

“…Existing data provides some support for an association between response inhibition and CUD, but findings are mixed. Worse response inhibition task performance has been found in problem cannabis users relative to healthy controls (Behan et al, 2014; Maij, van de Wetering, & Franken, 2017; Moreno et al, 2012), though non-significant group differences have also been reported (Crane, Schuster, & Gonzalez, 2013; Dougherty et al, 2013; Grant, Chamberlain, Schreiber, & Odlaug, 2012; Gonzalez et al, 2012; Hester, Nestor, & Garavan, 2009; Smith et al, 2011; Tapert et al, 2007). Response inhibition-related neural activity’s association with cannabis use is similarly mixed.…”