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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 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.

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.