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Background and aimsRecently, we demonstrated that a distinct pattern of structural covariance networks (SCN) from magnetic resonance imaging (MRI)-derived measurements of brain cortical thickness characterized young adults with alcohol use disorder (AUD) and predicted current and future problematic drinking in adolescents relative to controls. Here, we establish the robustness and value of SCN for identifying heavy alcohol users in three additional independent studies.Design and settingCross-sectional and longitudinal studies using data from the Pediatric Imaging, Neurocognition and Genetics (PING) study (n = 400, age range = 14-22 years), the National Consortium on Alcohol and Neurodevelopment in Adolescence (NCANDA) (n = 272, age range = 17-22 years) and the Human Connectome Project (HCP) (n = 375, age range = 22-37 years).CasesCases were defined based on heavy alcohol use patterns or former alcohol use disorder (AUD) diagnoses: 50, 68 and 61 cases were identified. Controls had none or low alcohol use or absence of AUD: 350, 204 and 314 controls were selected.MeasurementsGraph theory metrics of segregation and integration were used to summarize SCN.FindingsMirroring our prior findings, and across the three data sets, cases had a lower clustering coefficient [area under the curve (AUC) = -0.029, P = 0.002], lower modularity (AUC = -0.14, P = 0.004), lower average shortest path length (AUC = -0.078, P = 0.017) and higher global efficiency (AUC = 0.007, P = 0.010). Local efficiency differences were marginal (AUC = -0.017, P = 0.052). That is, cases exhibited lower network segregation and higher integration, suggesting that adjacent nodes (i.e. brain regions) were less similar in thickness whereas spatially distant nodes were more similar.ConclusionStructural covariance network (SCN) differences in the brain appear to constitute an early marker of heavy alcohol use in three new data sets and, more generally, demonstrate the utility of SCN-derived metrics to detect brain-related psychopathology.

AimsTo understand processes placing individuals at risk for stimulant (amphetamine and cocaine) use disorder.DesignLongitudinal study.SettingUniversity of California, San Diego Department of Psychiatry, CA, USA.ParticipantsOccasional stimulant users (OSU; n = 184) underwent a baseline clinical interview and a functional magnetic resonance imaging (fMRI) session. On the basis of a follow-up clinical interview completed 3 years later, OSU (n = 147) were then categorized as problem stimulant users (PSU: n = 36; those who developed stimulant use disorders in the interim) or desisted stimulant users (DSU: n = 74; those who stopped using). OSU who did not meet criteria for PSU or DSU (n = 37) were included in dimensional analyses.MeasurementsfMRI blood oxygen level-dependent (BOLD) contrast percentage signal change from baseline collected during a Paper-Scissors-Rock task was examined during three decision-making conditions, those resulting in: (1) wins, (2) ties and (3) losses. These data were used as dependent variables in categorical analyses comparing PSU and DSU, as well as dimensional analyses including interim drug use as predictors, controlling for baseline drug use.FindingsPSU exhibited lower anterior cingulate, middle insula, superior temporal, inferior parietal, precuneus and cerebellum activation than DSU across all three conditions (significant brain clusters required > 19 neighboring voxels to exceed F(1,108)  = 5.58, P  0.83). Higher interim marijuana use was linked to lower pre-central and superior temporal activation during choices resulting in wins (> 19 neighboring voxels to exceed t = 2.61, P  0.11).ConclusionsIndividuals who transition from stimulant use to stimulant use disorder appear to show alterations in neural processing of stimulus valuation and outcome monitoring, patterns also evident in chronic stimulant use disorder. Attenuated anterior cingulate and insular processing may constitute a high-risk neural processing profile, which could be used to calculate risk scores for individuals experimenting with stimulants.

AimsAdolescents with substance use disorders (SUD) exhibit hyposensitivity to pleasant internally generated (interoceptive) stimuli and hypersensitivity to external rewarding stimuli. It is unclear whether similar patterns exist for aversive interoceptive stimuli. We compared activation in the insular cortex and other brain regions during the anticipation and experience of aversive stimuli between adolescents with SUD and those without.DesignCross-sectional experimental study with two groups.ParticipantsAdolescents (ages 15-17 years) with an alcohol or marijuana SUD (n=18) and healthy comparison subjects (CON, n=15). Participants were recruited by distributing flyers at local high schools.SettingKeck Imaging Center, University of California San Diego, CA, USA.MeasurementsBehavioral and neural responses to a continuous performance task with inspiratory breathing load recorded during an fMRI session. Questionnaires assessed life-time drug use, anxiety, sensation-seeking, impulsivity, affect and bodily awareness. Visual analog scales assessed drug craving and breathing load responses.FindingsAcross subjects, experience of breathing load elicited greater bilateral anterior and posterior insula (AI and PI, respectively) activation than anticipation (F(1,31)=4.16, P

Background and aimsIndividuals with methamphetamine dependence (MD) exhibit dysfunction in brain regions involved in goal maintenance and reward processing when compared with healthy individuals. We examined whether these characteristics also reflect relapse vulnerability within a sample of MD patients.DesignLongitudinal, with functional magnetic resonance imaging (fMRI) and clinical interview data collected at baseline and relapse status collected at 1-year follow-up interview.SettingKeck Imaging Center, University of California San Diego, USA.ParticipantsMD patients (n = 60) enrolled into an in-patient drug treatment program at baseline. MD participants remaining abstinent at 1-year follow-up (abstinent MD group; n = 42) were compared with MD participants who relapsed within this period (relapsed MD group; n = 18).MeasurementsBehavioral and neural responses to a reinforcement learning (paper-scissors-rock) paradigm recorded during an fMRI session at time of treatment.FindingsThe relapsed MD group exhibited greater bilateral inferior frontal gyrus (IFG) and right striatal activation than the abstinent MD group during the learning of reward contingencies (Cohen's d range: 0.60-0.83). In contrast, the relapsed MD group displayed lower bilateral striatum, bilateral insula, left IFG and left anterior cingulate activation than the abstinent MD group (Cohen's d range: 0.90-1.23) in response to winning, tying and losing feedback.ConclusionsMethamphetamine-dependent individuals who achieve abstinence and then relapse show greater inferior frontal gyrus activation during learning, and relatively attenuated striatal, insular and frontal activation in response to feedback, compared with methamphetamine-dependent people who remain abstinent.

AimsTo determine if methamphetamine-dependent (MD) individuals exhibit behavioral or neural processing differences in risk-taking relative to healthy comparison participants (CTL).DesignThis was a cross-sectional study comparing two groups' behavior on a risk-taking task and neural processing as assessed using functional magnetic resonance imaging (fMRI).SettingsThe study was conducted in an in-patient treatment center and a research fMRI facility in the United States.ParticipantsSixty-eight recently abstinent MD individuals recruited from a treatment program and 40 CTL recruited from the community completed the study.MeasurementsThe study assessed risk-taking behavior (overall and post-loss) using the Risky Gains Task (RGT), sensation-seeking, impulsivity and blood-oxygenation-level-dependent activation in the brain during the decision phase of the RGT.FindingsRelative to CTL, MD displayed decreased activation in the bilateral rostral anterior cingulate cortex (ACC) and greater activation in the left insula across risky and safe decisions (P

Aims: To examine whether moderate adolescent cannabis use has neurocognitive effects that are unexplained by familial confounds, which prior family‐controlled studies may not have identified. Design A quasi‐experimental, sibling‐comparison design was applied to a prospective, observational study of adolescents with moderate cannabis use. Participants were recruited from 2001 to 2006 (mean age = 17 years). A second wave of data was collected from 2008 to 2013 (mean age = 24 years). Setting: Two US metropolitan communities. Participants: A total of 1192 adolescents from 596 families participated in this study. Participants were primarily male (64%) and racially and ethnically diverse (non‐Hispanic white = 45%). A sibling in each family was a clinical proband identified due to delinquent behaviors. Whereas prior family‐controlled studies have used samples of primarily infrequent cannabis users (mean = 1–2 days/month), participants here endorsed levels of cannabis use comparable to findings from epidemiological cohort studies (mean = 7–9 days/month). Measurements Semi‐structured clinical interviews assessed drug use, and a neuropsychological battery assessed cognitive abilities. Covariates included age at assessment, gender and alcohol use. Findings After correcting for multiple testing, a greater frequency and earlier onset of regular cannabis use were associated with poorer cognitive performance, specifically on tests of verbal memory. Further, after accounting for familial factors shared by siblings and alcohol use, poorer verbal memory performance was still associated with greater life‐time frequency of cannabis use at wave 1 [b = −0.007 (−0.002, −0.012), adjusted P = 0.036]; earlier cannabis use at wave 2 [b = −0.12 (−0.05, −0.19), adjusted P = 0.006; b = −0.14 (−0.06, −0.23), adjusted P = 0.006]; and greater frequency of past 6 months use at wave 2 [b = −0.02 (−0.01, −0.03), adjusted P = 0.002; b = −0.02 (−0.01, −0.03), adjusted P = 0.008]. Conclusions: Moderate adolescent cannabis use may have adverse effects on cognitive functioning, specifically verbal memory, that cannot be explained by familial factors. [ABSTRACT FROM AUTHOR]