Deanna M Barch

Washington University in St. Louis, San Luis, Missouri, United States

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Publications (379)2092.39 Total impact

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    ABSTRACT: Maternal major depressive disorder (MDD) increases risk for MDD and predicts reduced reward responding in adolescent offspring. However, it is unclear whether alterations in neural response to reward can be detected in school-aged children at high risk prior to the typical increase in reward response observed in adolescence.
    No preview · Article · Feb 2016
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    Michael S Gaffrey · Deanna M Barch · Joan L Luby
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    ABSTRACT: Background: Elevated negative affect is a highly salient risk factor for later internalizing disorders. Very little is known about the early neurobiological correlates of negative affect and whether they associate with developmental changes in negative emotion. Such information may prove critical for identifying children deviating from normative developmental trajectories of negative affect and at increased risk for later internalizing disorders. The current study examined the relationship between amygdala activity and negative affect measured concurrently and approximately 12 months later in preschool-age children. Method: Amygdala activity was assessed using functional magnetic resonance imaging in 31 medication-naive preschool age children. Negative affect was measured using parent report both at the time of scan and 12 months later. Results: Negative affect at baseline was positively correlated with right amygdala activity to sad faces, right amygdala activity to happy faces, and left amygdala activity to happy faces. Right amygdala activity to sad faces also positively predicted parent-reported negative affect 12 months later even when negative affect reported at baseline was controlled. Conclusions: The current findings provide preliminary evidence for amygdala activity as a potential biomarker of persistent negative affect during early childhood and suggest future work examining the origins and long-term implications of this relationship is necessary.
    Full-text · Article · Feb 2016 · Developmental Cognitive Neuroscience
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    ABSTRACT: Objective: In this study, the authors tested the hypothesis that poverty experienced in early childhood, as measured by income-to-needs ratio, has an impact on functional brain connectivity at school age, which in turn mediates influences on child negative mood/depression. Method: Participants were from a prospective longitudinal study of emotion development. Preschoolers 3-5 years of age were originally ascertained from primary care and day care sites in the St. Louis area and then underwent annual behavioral assessments for up to 12 years. Healthy preschoolers and those with a history of depression symptoms underwent neuroimaging at school age. Using functional MRI, the authors examined whole brain resting-state functional connectivity with the left and right hippocampus and amygdala. Results: Lower income-to-needs ratio at preschool age was associated with reduced connectivity between hippocampus and amygdala and a number of regions at school age, including the superior frontal cortex, lingual gyrus, posterior cingulate, and putamen. Lower income-to-needs ratio predicted greater negative mood/depression severity at school age, as did connectivity between the left hippocampus and the right superior frontal cortex and between the right amygdala and the right lingual gyrus. Connectivity mediated the relationship between income-to-needs ratio and negative mood/depression at the time of scanning. Conclusions: These findings suggest that poverty in early childhood, as assessed by at least one measure, may influence the development of hippocampal and amygdala connectivity in a manner leading to negative mood symptoms during later childhood.
    No preview · Article · Jan 2016 · American Journal of Psychiatry
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    ABSTRACT: Background: There has been little available data to inform the predictors and outcomes of latent class trajectories of depressive symptoms beginning during preschool and continuing throughout school age. Further, the extant literature in this domain has been limited by the use of parent report checklists of nonspecific 'internalizing' psychopathology rather than diagnostic interviews for depression. Methods: To address these gaps in the literature, this study applied growth mixture modeling to depressive symptom severity endorsed by children and/or their caregivers (N = 348) during a structured clinical interview in a 10-year longitudinal dataset spanning from preschool into late school age. Results: Three distinct trajectories of depressive symptom severity were found in boys and girls. For boys, but not girls, the high depression severity latent class increased in depressive symptoms from preschool through school age, followed by a decline in depressive symptom severity during later school age. For girls, the high depression severity latent class remained stable across time. Early childhood social adversity, familial history of affective disorder, preschool-onset ODD/CD, and school age functional impairment differentiated high-risk trajectory classes among both boys and girls. Conclusions: Extending the literature on trajectories of depressive symptoms to the preschool period, these findings incorporate structured clinical interviews of depressive symptom severity and indicate gender differences as well as psychosocial predictors and functional outcomes among children in high severity latent classes. The findings from this study suggest that increased attention to screening for depressive symptoms in early childhood is of significant public health importance.
    No preview · Article · Jan 2016 · Journal of Child Psychology and Psychiatry
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    ABSTRACT: Importance The trajectory of cortical gray matter development in childhood has been characterized by early neurogenesis and volume increase, peaking at puberty followed by selective elimination and myelination, resulting in volume loss and thinning. This inverted U-shaped trajectory, as well as cortical thickness, has been associated with cognitive and emotional function. Synaptic pruning–based volume decline has been related to experience-dependent plasticity in animals. To date, there have been no data to inform whether and how childhood depression might be associated with this trajectory.Objective To examine the effects of early childhood depression, from the preschool age to the school age period, on cortical gray matter development measured across 3 waves of neuroimaging from late school age to early adolescence.Design, Setting, and Participants Data were collected in an academic research setting from September 22, 2003, to December 13, 2014, on 193 children aged 3 to 6 years from the St Louis, Missouri, metropolitan area who were observed for up to 11 years in a longitudinal behavioral and neuroimaging study of childhood depression. Multilevel modeling was applied to explore the association between the number of childhood depression symptoms and prior diagnosis of major depressive disorder and the trajectory of gray matter change across 3 scan waves. Data analysis was conducted from October 29, 2014, to September 28, 2015.Main Outcomes and Measures Volume, thickness, and surface area of cortical gray matter measured using structural magnetic resonance imaging at 3 scan waves.Results Of the 193 children, 90 had a diagnosis of major depressive disorder; 116 children had 3 full waves of neuroimaging scans. Findings demonstrated marked alterations in cortical gray matter volume loss (slope estimate, −0.93 cm3; 95% CI, −1.75 to −0.10 cm3 per scan wave) and thinning (slope estimate, −0.0044 mm; 95% CI, −0.0077 to −0.0012 mm per scan wave) associated with experiencing an episode of major depressive disorder before the first magnetic resonance imaging scan. In contrast, no significant associations were found between development of gray matter and family history of depression or experiences of traumatic or stressful life events during this period.Conclusions and Relevance This study demonstrates an association between early childhood depression and the trajectory of cortical gray matter development in late school age and early adolescence. These findings underscore the significance of early childhood depression on alterations in neural development.
    No preview · Article · Dec 2015 · JAMA Psychiatry
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    Julia M. Sheffield · Deanna M. Barch
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    ABSTRACT: Individuals with schizophrenia consistently display deficits in a multitude of cognitive domains, but the neurobiological source of these cognitive impairments remains unclear. By analyzing the functional connectivity of resting-state functional magnetic resonance imaging (rs-fcMRI) data in clinical populations like schizophrenia, research groups have begun elucidating abnormalities in the intrinsic communication between specific brain regions, and assessing relationships between these abnormalities and cognitive performance in schizophrenia. Here we review studies that have reported analysis of these brain-behavior relationships. Through this systematic review we found that patients with schizophrenia display abnormalities within and between regions comprising 1) the cortico-cerebellar-striatal-thalamic loop and 2) task-positive and task-negative cortical networks. Importantly, we did not observe unique relationships between specific functional connectivity abnormalities and distinct cognitive domains, suggesting that the observed functional systems may underlie mechanisms that are shared across cognitive abilities, the disturbance of which could contribute to the "generalized" cognitive deficit found in schizophrenia. We also note several areas of methodological change that we believe will strengthen this literature.
    Full-text · Article · Dec 2015 · Neuroscience & Biobehavioral Reviews
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    ABSTRACT: The large impact of loss of reward on behavior has been well documented in adult populations. However, whether responsiveness to loss relative to gain is similarly elevated in child versus adult populations remains unclear. It is also unclear whether relations between incentive behaviors and self-reported reward/punishment sensitivity are similar within different developmental stages. To investigate these questions, 7- to 10-year-old children (N = 70) and young adults (N = 70) completed the Behavioral Inhibition System/Behavioral Activation System (BIS/BAS) scale, along with 2 probabilistic incentive tasks assessing gain approach and loss avoidance behavior. BIS/BAS subscales were calculated per Pagliaccio et al. (2015), which established an age invariant model of the BIS/BAS. Bias toward responses more frequently followed by gain feedback and away from responses more frequently followed by loss feedback, approach, and avoidance behavior, respectively, were quantified via signal detection statistics. Gain approach behavior did not differ across age groups; however, children exhibited significantly elevated loss avoidance relative to adults. Children also showed greater reductions in accuracy and slower RTs specifically following loss feedback relative to adults. Interestingly, despite age group differences in loss avoidance behavior, relations between self-report measures and approach/avoidance behaviors were similar across age groups. Participants reporting elevated motivation (BAS Drive) showed both elevated gain approach and elevated loss avoidance, with both types of behavior predicting unique variance in BAS Drive. Results highlight the often-neglected developmental and motivational roles of responsiveness to loss of reward. (PsycINFO Database Record
    Full-text · Article · Nov 2015 · Emotion
  • Yu Sun Chung · Deanna M. Barch
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    ABSTRACT: Schizophrenia is characterized by deficits of context processing, thought to be related to dorsolateral prefrontal cortex (DLPFC) impairment. Despite emerging evidence suggesting a crucial role of the DLPFC in integrating reward and goal information, we do not know whether individuals with schizophrenia can represent and integrate reward-related context information to modulate cognitive control. To address this question, 36 individuals with schizophrenia (n = 29) or schizoaffective disorder (n = 7) and 27 healthy controls performed a variant of a response conflict task (Padmala & Pessoa, 2011) during fMRI scanning, in both baseline and reward conditions, with monetary incentives on some reward trials. We used a mixed state-item design that allowed us to examine both sustained and transient reward effects on cognitive control. Different from predictions about impaired DLPFC function in schizophrenia, we found an intact pattern of increased sustained DLPFC activity during reward versus baseline blocks in individuals with schizophrenia at a group level but blunted sustained activations in the putamen. Contrary to our predictions, individuals with schizophrenia showed blunted cue-related activations in several regions of the basal ganglia responding to reward-predicting cues. Importantly, as predicted, individual differences in anhedonia/amotivation symptoms severity were significantly associated with reduced sustained DLPFC activation in the same region that showed overall increased activity as a function of reward. These results suggest that individual differences in motivational impairments in schizophrenia may be related to dysfunction of the DLPFC and striatum in motivationally salient situations. (PsycINFO Database Record
    No preview · Article · Nov 2015 · Journal of Abnormal Psychology
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    Yu Sun Chung · Deanna M. Barch

    Full-text · Article · Nov 2015 · Journal of Abnormal Psychology
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    Dov B. Lerman-Sinkoff · Deanna M. Barch
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    ABSTRACT: A growing body of literature suggests functional connectivity alterations in schizophrenia. While findings have been mixed, evidence points towards a complex pattern of hyper-connectivity and hypo-connectivity. This altered connectivity can be represented and analyzed using the mathematical frameworks provided by graph and information theory to represent functional connectivity data as graphs comprised of nodes and edges linking the nodes. One analytic technique in this framework is the determination and analysis of network community structure, which is the grouping of nodes into linked communities or modules. This data-driven technique finds a best-fit structure such that nodes in a given community have greater connectivity with nodes in their community than with nodes in other communities. These community structure representations have been found to recapitulate known neural-systems in healthy individuals, have been used to identify novel functional systems, and have identified and localized community structure alterations in a childhood onset schizophrenia cohort. In the present study, we sought to determine whether community structure alterations were present in an adult onset schizophrenia cohort while stringently controlling for sources of imaging artifacts. Group level average graphs in healthy controls and individuals with schizophrenia exhibited visually similar network community structures and high amounts of normalized mutual information (NMI). However, testing of individual subject community structures identified small but significant alterations in community structure with alterations being driven by changes in node community membership in the somatosensory, auditory, default mode, salience, and subcortical networks.
    Preview · Article · Nov 2015 · Clinical neuroimaging
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    ABSTRACT: Objective: Behavioral inhibition (BI) during early childhood predicts risk for anxiety disorders and altered cognitive control in adolescence. Although BI has been linked to variation in brain function through adulthood, few studies have examined relations between early childhood BI and adult brain structure. Method: The relation between early childhood BI and cortical thickness in adulthood was examined in a cohort of individuals followed since early childhood (N = 53, mean age 20.5 years). Analyses tested whether anxiety and/or cognitive control during adolescence moderated relations between BI and cortical thickness. Cognitive control was measured with the Eriksen Flanker Task. Initial analyses examined cortical thickness in regions of interest previously implicated in BI, anxiety disorders, and cognitive control: dorsal anterior cingulate (dACC), anterior insula (aI), and subgenual anterior cingulate (sgACC); and volumes of the amygdala and hippocampus. Exploratory analyses examined relations across the prefrontal cortex. Results: BI during early childhood related to thinner dACC in adulthood. Neither anxiety nor cognitive control moderated this relation. A stronger congruency effect on the Eriksen Flanker Task during adolescence independently related to thinner dACC in adulthood. Higher anxiety during adolescence related to thicker cortex in the right ventrolateral prefrontal cortex (VLPFC) in adulthood among those with low BI as children. Conclusion: Temperament in early childhood and the interaction between temperament and later anxiety relate to adult brain structure. These results are consistent with prior work associating BI and anxiety with functional brain variability in the dACC and VLPFC.
    No preview · Article · Nov 2015 · Journal of the American Academy of Child and Adolescent Psychiatry
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    ABSTRACT: Major Depressive Disorder (MDD) is characterized by poor emotion regulation. Rumination, a maladaptive strategy for dealing with negative emotions, is common in MDD, and is associated with impaired inhibition and cognitive inflexibility that may contribute to impaired emotion regulation abilities. However, it is unclear whether rumination is differently associated with emotion regulation in individuals with MDD history (MDD-ever) and healthy individuals. In this study, children (8-15 years old) performed a cognitive reappraisal task in which they attempted to decrease their emotional response to sad images during fMRI scanning. Functional connectivity (FC) between both the amygdala and subgenual anterior cingulate (sACC) increased with cortical control regions during reappraisal as rumination increased in MDD-ever, while connectivity between those regions decreased during reappraisal as rumination increased in healthy controls. As the role of cortical control regions is to down-regulate activity of emotion processing regions during reappraisal, this suggests that rumination in MDD-ever, but not controls, is associated with inefficient regulation. This finding suggests that rumination may be particularly associated with poor emotion regulation in MDD-ever, and may also indicate qualitative group differences in whether rumination is maladaptive. These differences in rumination may provide important insight into depressive risk and potential avenues for treatment.
    Preview · Article · Nov 2015 · Developmental Cognitive Neuroscience
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    ABSTRACT: Goal maintenance is an aspect of cognitive control that has been identified as critical for understanding psychopathology according to criteria of the NIMH-sponsored CNTRICS (Cognitive Neuroscience Treatment Research to Improve Cognition in Schizophrenia) and Research Domain Criteria (RDoC) initiatives. CNTRICS proposed the expectancy AX-CPT, and its visual-spatial parallel the dot probe expectancy (DPX), as valid measures of the cognitive and neural processes thought to be relevant for goal maintenance. The goal of this study was to specifically examine the functional neural correlates and connectivity patterns of both goal maintenance tasks in the same subset of subjects to further validate their neural construct validity and clarify our understanding of the nature and function of the neural circuitry engaged by the tasks. Twenty-six healthy control subjects performed both the letter (AX) and dot pattern (DPX) variants of the CPT during fMRI. Behavioral performance was similar between tasks. The 2 tasks engaged the same brain networks including dorsolateral prefrontal cortex (DLPFC) and dorsal parietal regions, supporting their validity as complementary measures of the goal maintenance construct. Interestingly there was greater engagement of the frontal opercular insula region during the expectancy AX-CPT (letter) and greater functional connectivity between the PFC and medial temporal lobe in the DPX (dot pattern). These differences are consistent with differential recruitment of phonological and visual-spatial processes by the two tasks and suggest that additional long-term memory systems may be engaged by the dot probe version.
    Full-text · Article · Oct 2015 · Cognitive Affective & Behavioral Neuroscience
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    ABSTRACT: Previous work suggests that individuals with schizophrenia display accelerated aging of white matter integrity, however, it is still unknown whether functional brain networks also decline at an elevated rate in schizophrenia. Given the known degradation of functional connectivity and the normal decline in cognitive functioning throughout healthy aging, we aimed to test the hypothesis that efficiency of large-scale functional brain networks supporting overall cognition, as well as integrity of hub nodes within those networks, show evidence of accelerated aging in schizophrenia. Using pseudo-resting state data in 54 healthy controls and 46 schizophrenia patients, in which task-dependent signal from 3 tasks was regressed out to approximate resting-state data, we observed a significant diagnosis by age interaction in the prediction of both global and local efficiency of the cingulo-opercular network, and of the local efficiency of the fronto-parietal network, but no interaction when predicting both default mode network and whole brain efficiency. We also observed a significant diagnosis by age interaction for the node degree of the right anterior insula, left dorsolateral prefrontal cortex, and dorsal anterior cingulate cortex. All interactions were driven by stronger negative associations between age and network metrics in the schizophrenia group than the healthy controls. These data provide evidence that is consistent with accelerated aging of large-scale functional brain networks in schizophrenia that support higher-order cognitive ability.
    Full-text · Article · Oct 2015 · Schizophrenia Bulletin
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    ABSTRACT: Previous work suggests that individuals with schizophrenia display accelerated aging of white matter integrity, however it is still unknown whether functional brain networks also decline at an elevated rate in schizophrenia. Given the known degradation of functional connectivity and the normal decline in cognitive functioning throughout healthy aging, we aimed to test the hypothesis that efficiency of large-scale functional brain networks supporting overall cognition, as well as integrity of hub nodes within those networks, show evidence of accelerated aging in schizophrenia. Using pseudo-resting state data in 54 healthy controls and 46 schizophrenia patients, in which task-dependent signal from three tasks was regressed out to approximate resting-state data, we observed a significant diagnosis by age interaction in the prediction of both global and local efficiency of the cingulo-opercular network, and of the local efficiency of the fronto-parietal network, but no interaction when predicting both default mode network and whole brain efficiency. We also observed a significant diagnosis by age interaction for the node degree of the right anterior insula, left dorsolateral prefrontal cortex, and dorsal anterior cingulate cortex. All interactions were driven by stronger negative associations between age and network metrics in the schizophrenia group than the healthy controls. These data provide evidence that is consistent with accelerated aging of large-scale functional brain networks in schizophrenia that support higher-order cognitive ability.
    Full-text · Article · Oct 2015 · Schizophrenia Bulletin
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    ABSTRACT: Investigating brain tissue T2* relaxation properties in vivo can potentially guide the uncovering of neuropathology in psychiatric illness, which is traditionally examined post mortem. We use an MRI-based Gradient Echo Plural Contrast Imaging (GEPCI) technique that produces inherently co-registered images allowing quantitative assessment of tissue cellular and hemodynamic properties. Usually described as R2* (=1/T2*) relaxation rate constant, recent developments in GEPCI allow the separation of cellular-specific (R2*C) and hemodynamic (BOLD) contributions to the MRI signal decay. We characterize BOLD effect in terms of tissue concentration of deoxyhemoglobin, i.e. CDEOXY, which reflects brain activity. 17 control (CON), 17 bipolar disorder (BPD), 16 schizophrenia (SCZ), and 12 unaffected schizophrenia sibling (SIB) participants were scanned and post-processed using GEPCI protocols. A MANOVA of 38gray matter regions ROIs showed significant group effects for CDEOXY but not for R2*C. In the three non-control groups, 71-92% of brain regions had increased CDEOXY. Group effects were observed in the superior temporal cortex and the thalamus. Increased superior temporal cortex CDEOXY was found in SCZ (p=0.01), BPD (p=0.01) and SIB (p=0.02), with bilateral effects in SCZ and only left hemisphere effects in BPD and SIB. Thalamic CDEOXY abnormalities were observed in SCZ (p=0.003), BPD (p=0.03) and SIB (p=0.02). Our results suggest that increased activity in certain brain regions is part of the underlying pathophysiology of specific psychiatric disorders. High CDEOXY in the superior temporal cortex suggests abnormal activity with auditory, language and/or social cognitive processing. Larger studies are needed to clarify the clinical significance of relaxometric abnormalities.
    No preview · Article · Oct 2015 · Schizophrenia Research
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    ABSTRACT: We investigated the relationship between individual subjects' functional connectomes and 280 behavioral and demographic measures in a single holistic multivariate analysis relating imaging to non-imaging data from 461 subjects in the Human Connectome Project. We identified one strong mode of population co-variation: subjects were predominantly spread along a single 'positive-negative' axis linking lifestyle, demographic and psychometric measures to each other and to a specific pattern of brain connectivity.
    No preview · Article · Sep 2015 · Nature Neuroscience
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    ABSTRACT: Objective: Despite research documenting the existence of depression and other psychiatric disorders in early childhood, little is known about the nature and consequences of suicidal cognitions and behaviors (SI) in young children ages 3 to 7 years. The identification of trajectories of SI across childhood is a critical step toward preventing childhood suicide. Method: Participants were 306 children enrolled in a prospective longitudinal investigation of young children and their families. Children and their families completed a baseline assessment between ages 3 and 7 years, and at least 1 follow-up assessment (ages 7-12 years). Child psychopathology, suicidal thoughts, plans, and behaviors were assessed via parent and trained interviewer report before age 9, and also with self-report after age 9. Data on maternal history of psychopathology, as well as maternal and family history of suicide attempts, were also obtained through parent report. Results: Controlling for a range of clinical and demographic variables, early-childhood SI (as defined as suicidal thoughts, behavior, or any expression of plans/attempts occurring before age 7) and suicidal themes in play were concurrently associated with childhood attention-deficit/hyperactivity (ADHD) and oppositional defiant/conduct disorders (ODD/CD). Early-childhood SI also predicted school-age depression and ODD/CD; however, these findings were no longer significant after controlling for the same diagnoses at the childhood baseline. Longitudinal analysis indicated that early-childhood SI was a robust predictor of school-age SI, even after accounting for psychiatric disorders at both time points. Conclusion: Extending current research, these findings demonstrate that early-childhood SI confers significant risk for continuation into school-age SI and is concurrently associated with ADHD and ODD/CD. Although the meaning of early-childhood SI remains unclear, results suggest that it is a clinically important phenomenon that should be carefully assessed and taken seriously as a marker of risk for ongoing suicidal ideation/behavior. These findings suggest that early screening for SI in childhood is indicated in clinical settings, particularly in children less than 7 years of age with depression and externalizing disorders.
    Full-text · Article · Sep 2015 · Journal of the American Academy of Child and Adolescent Psychiatry
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    Full-text · Dataset · Aug 2015
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    ABSTRACT: Prior neuroimaging studies have suggested that alterations in brain structure may be a consequence of cannabis use. Siblings discordant for cannabis use offer an opportunity to use cross-sectional data to disentangle such causal hypotheses from shared effects of genetics and familial environment on brain structure and cannabis use. To determine whether cannabis use is associated with differences in brain structure in a large sample of twins/siblings and to examine sibling pairs discordant for cannabis use to separate potential causal and predispositional factors linking lifetime cannabis exposure to volumetric alterations. Cross-sectional diagnostic interview, behavioral, and neuroimaging data were collected from community sampling and established family registries from August 2012 to September 2014. This study included data from 483 participants (22-35 years old) enrolled in the ongoing Human Connectome Project, with 262 participants reporting cannabis exposure (ie, ever used cannabis in their lifetime). Cannabis exposure was measured with the Semi-Structured Assessment for the Genetics of Alcoholism. Whole-brain, hippocampus, amygdala, ventral striatum, and orbitofrontal cortex volumes were related to lifetime cannabis use (ever used, age at onset, and frequency of use) using linear regressions. Genetic (ρg) and environmental (ρe) correlations between cannabis use and brain volumes were estimated. Linear mixed models were used to examine volume differences in sex-matched concordant unexposed (n = 71 pairs), exposed (n = 81 pairs), or exposure discordant (n = 89 pairs) sibling pairs. Among 483 study participants, cannabis exposure was related to smaller left amygdala (approximately 2.3%; P = .007) and right ventral striatum (approximately 3.5%; P < .005) volumes. These volumetric differences were within the range of normal variation. The association between left amygdala volume and cannabis use was largely owing to shared genetic factors (ρg = -0.43; P = .004), while the origin of the association with right ventral striatum volumes was unclear. Importantly, brain volumes did not differ between sex-matched siblings discordant for use (fixed effect = -7.43; t = -0.93, P = .35). Both the exposed and unexposed siblings in pairs discordant for cannabis exposure showed reduced amygdala volumes relative to members of concordant unexposed pairs (fixed effect = 12.56; t = 2.97; P = .003). In this study, differences in amygdala volume in cannabis users were attributable to common predispositional factors, genetic or environmental in origin, with little support for causal influences. Causal influences, in isolation or in conjunction with predispositional factors, may exist for other brain regions (eg, ventral striatum) or at more severe levels of cannabis involvement and deserve further study.
    No preview · Article · Aug 2015 · JAMA Psychiatry

Publication Stats

25k Citations
2,092.39 Total Impact Points

Institutions

  • 1999-2016
    • Washington University in St. Louis
      • • Department of Psychiatry
      • • Department of Psychology
      San Luis, Missouri, United States
  • 2006-2012
    • Duke University
      • Department of Biomedical Engineering (BME)
      Durham, North Carolina, United States
  • 2010
    • University of Maryland, Baltimore
      Baltimore, Maryland, United States
  • 2008
    • University of Missouri
      • Department of Psychological Sciences
      Columbia, MO, United States
    • Princeton University
      • Department of Psychology
      Princeton, New Jersey, United States
  • 1997-2005
    • University of Pittsburgh
      • Department of Psychiatry
      Pittsburgh, Pennsylvania, United States
  • 2004
    • Washington School of Psychiatry
      Washington, Washington, D.C., United States
  • 2003
    • University of Missouri - St. Louis
      • Department of Psychology
      Сент-Луис, Michigan, United States
  • 1995-1999
    • University of Illinois, Urbana-Champaign
      • Department of Psychology
      Urbana, Illinois, United States
  • 1995-1997
    • Western Psychiatric Institute and Clinic
      Pittsburgh, Pennsylvania, United States