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BACKGROUND. Normalization of medicinal and recreational marijuana use has increased the importance of fully understanding effects of marijuana use on individual- and population-level health, including prenatal exposure effects on child development. We undertook a systematic review of the literature to examine the long-term effects of prenatal marijuana exposure on neuropsychological function in children aged 1–11 years. METHODS. Primary research publications were searched from Medline, Embase, PsychInfo, CINAHL EbscoHost, Cochrane Library, Global Health, and ERIC (1980–2018). Eligible articles documented neuropsychological outcomes in children 1–11 years who had been prenatally exposed to marijuana. Studies of exposure to multiple prenatal drugs were included if results for marijuana exposure were reported separately from other substances. Data abstraction was independently performed by two reviewers using a standardized protocol. RESULTS. The eligible articles (n=21) on data from seven independent longitudinal studies, had high quality based on the Newcastle-Ottawa Scale. Some analyses found associations (p

The goal of this special section is to highlight progress made and primary research reports on the relation between Attention Deficit Hyperactivity Disorder (ADHD), impulsivity, and alcohol use disorders (AUDs) utilizing a diverse range of methods. The four papers examine various psychological processes underlying the broad construct of impulsivity that are related largely to impairments in inhibitory control. The section addresses the influences of reward sensitivity, working memory/attention control, and social functioning in the development and persistence of AUDs among individuals with ADHD. These papers are important because they approach the relation between ADHD and AUDs, and the role of impulsivity, from varied perspectives.

Cognitive control has long been a validated construct to explain risk for drug abuse. Research evidence suggests that cognitive-control interventions show promise for future preventive intervention and treatment efforts across development. Biomarkers of the efficacy of these interventions have also been identified. To examine the potential of utilizing developmental cognitive neuroscience to guide cognitive-control interventions for the prevention and treatment of substance use disorders, the National Institute on Drug Abuse held a research roundtable in Rockville, Maryland, in May 2010. The research presented at the roundtable and reviewed in this Special Section of Child Development Perspectives highlights the promise of cognitive-control interventions for enhancing, or ameliorating deficits in, executive functions relevant to substance use disorders, as well as the promise of neuroscience techniques for guiding the conceptualization of these interventions.

The Wisconsin Card Sorting Test (WCST) has been argued to be a sensitive indicator of frontal lobe function. However, several recent studies have failed to find a consistent relationship between structural damage to this cortical area and perseveration on the test. In the present study, positron emission tomography (PET) imaging with 18F-fluorodeoxyglucose was used to examine the relationship of regional brain metabolism to perseverative responding on the WCST in patients with a history of closed-head injury. An inverse relationship was found between perseverative responses and metabolism in the right, but not the left, dorsolateral prefrontal cortex and caudate nucleus. Perseverative responding was not related to metabolism in several other regions of the frontal lobes and basal ganglia, including the putamen and the frontal poles bilaterally. These data suggest that the functional integrity of the right dorsolateral frontal-subcortical circuit is critical for WCST performance.

The effects of two memory-impairing drugs, ethanol and triazolam, on proactive interference (PI) in memory were studied. Following ingestion of either one of these drugs or a placebo, subjects studied an A-B list (e.g., BEE-WASP) of paired associates, followed by an A-C list (e.g., BEE-HONEY) on the interference trial, and a D-E list (e.g., KING-QUEEN) followed by an A-C list on the control trial. A PI effect was found in the data, such that subjects produced fewer correct second list targets on the interference trial than on the control trial. Neither ethanol nor triazolam was found to influence the size of the PI effect. However, both drugs were found to increase B intrusions on the test of the A-C list, to impair subjects' ability to produce more than one studied response for each cue word, and to impair the subjective experience of retrieved memory information. These data suggest that ethanol and triazolam impair an inhibitory process that normally operates as one component of intentional retrieval, playing an important role in the suppression of unwanted information during a memory task.

Emerging brain-imaging findings suggest that developmental differences in the structure and activity of brain regions involved in motivation and behavior control may contribute to risky behavior in adolescence. Adolescence may be characterized by robust motivational neurocircuitry that is relatively unhindered by developing cognitive control neurocircuitry. However, how developmental differences in brain structure or function depend on task features or other experimental contexts, or whether observed differences are functionally relevant for real-world risky behavior, is not well understood. The challenge of attributing adolescent risk taking to developmental patterns of brain morphology and brain activity underscores the need for future research sensitive to development and the contexts of adolescence.

Fifteen normal volunteers were administered placebo, 0.250, 0.375 and 0.500 mg of triazolam in a double- blind cross-over design. Triazolam induced robust dose-dependent impairments in explicit memory of information presented after drug administration. Subjects were unaware of their memory deficit (an impairment in meta-cognition). In contrast, memory for information presented prior to the administration of triazolam was facilitated following the administration of low doses of triazolam. Implicit memory and access to knowledge memory was unaltered by this benzodiazepine. An analysis of these results controlling for concurrent sedation as measured subjectively, through the use of self rating scales and objectively, based upon psychomotor performance, demonstrated that the amnestic effects of triazolam are largely independent of sedative effects. The pattern of memory changes induced by benzodiazepines, such as triazolam, is similar to the memory inpairment expressed in amnestic patients but unlike the pattern of impaired memory evident in dementia such as Alzheimer's disease.

The ability to monitor the source of remembered information and related reflective cognitive processes was examined in normal volunteers and detoxified alcoholics. Normal volunteers were very accurate judges of whether remembered events were presented as stimuli or were self-generated, even when memory was tested 2 days later. In contrast, a subgroup of otherwise cognitively unimpaired alcoholics demonstrated impairments in the ability to track the source of remembered knowledge and were also less able to inhibit intrusion errors in recalling information from memory. These findings provide preliminary evidence of an impairment in cognitive control functions in certain alcoholics. This conclusion is supported by associated findings indicating that, among alcoholics, performance on explicit memory tasks that required reflective cognitive operations were positively correlated with glucose utilization rates in left prefrontal, temporal, and posterior orbital frontal cortical regions.