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June 2019 - July 1959

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May 2, 2011, Vol 68, No. 5, Pages 440-533

This Month in Archives of General Psychiatry

Archives Of General Psychiatry

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Arch Gen Psychiatry. 2011;68(5):441. doi:10.1001/archgenpsychiatry.2011.30
Art and Images in Psychiatry

Arcimboldo's Vertumnus: A Portrait of Rudolf II

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Arch Gen Psychiatry. 2011;68(5):442-443. doi:10.1001/archgenpsychiatry.2011.41
Original Article

Epidemiology of Autism Spectrum Disorders in Adults in the Community in England

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Arch Gen Psychiatry. 2011;68(5):459-465. doi:10.1001/archgenpsychiatry.2011.38

Early Brain Overgrowth in Autism Associated With an Increase in Cortical Surface Area Before Age 2 Years

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Arch Gen Psychiatry. 2011;68(5):467-476. doi:10.1001/archgenpsychiatry.2011.39

Common Proteomic Changes in the Hippocampus in Schizophrenia and Bipolar Disorder and Particular Evidence for Involvement of Cornu Ammonis Regions 2 and 3

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Arch Gen Psychiatry. 2011;68(5):477-488. doi:10.1001/archgenpsychiatry.2011.43

Neuroanatomical Abnormalities That Predate the Onset of Psychosis: A Multicenter Study

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Arch Gen Psychiatry. 2011;68(5):489-495. doi:10.1001/archgenpsychiatry.2011.42

Preinjury Psychiatric Status, Injury Severity, and Postdeployment Posttraumatic Stress Disorder

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Arch Gen Psychiatry. 2011;68(5):496-504. doi:10.1001/archgenpsychiatry.2011.44

Effect of Bupropion Treatment on Brain Activation Induced by Cigarette-Related Cues in Smokers

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Arch Gen Psychiatry. 2011;68(5):505-515. doi:10.1001/archgenpsychiatry.2010.193
ContextNicotine-dependent smokers exhibit craving and brain activation in the prefrontal and limbic regions when presented with cigarette-related cues. Bupropion hydrochloride treatment reduces cue-induced craving in cigarette smokers; however, the mechanism by which bupropion exerts this effect has not yet been described.ObjectiveTo assess changes in regional brain activation in response to cigarette-related cues from before to after treatment with bupropion (vs placebo).DesignRandomized, double-blind, before-after controlled trial.SettingAcademic brain imaging center.ParticipantsThirty nicotine-dependent smokers (paid volunteers).InterventionsParticipants were randomly assigned to receive 8 weeks of treatment with either bupropion or a matching placebo pill (double-blind).Main Outcome MeasuresSubjective cigarette craving ratings and regional brain activations (blood oxygen level-dependent response) in response to viewing cue videos.ResultsBupropion-treated participants reported less craving and exhibited reduced activation in the left ventral striatum, right medial orbitofrontal cortex, and bilateral anterior cingulate cortex from before to after treatment when actively resisting craving compared with placebo-treated participants. When resisting craving, reduction in self-reported craving correlated with reduced regional brain activation in the bilateral medial orbitofrontal and left anterior cingulate cortices in all participants.ConclusionsTreatment with bupropion is associated with improved ability to resist cue-induced craving and a reduction in cue-induced activation of limbic and prefrontal brain regions, while a reduction in craving, regardless of treatment type, is associated with reduced activation in prefrontal brain regions.

Effects of Varenicline on Smoking Cue–Triggered Neural and Craving Responses

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Arch Gen Psychiatry. 2011;68(5):516-526. doi:10.1001/archgenpsychiatry.2010.190
ContextVarenicline, an effective smoking cessation medication, functions as an α4β2 nicotinic acetylcholine receptor partial agonist. It indirectly affects the dopaminergic reward system by reducing withdrawal symptoms during abstinence and by decreasing the reinforcement received from nicotine while smoking. We hypothesize that varenicline would have a third mechanism to blunt responses to smoking cues in the reward-related ventral striatum and medial orbitofrontal cortex and would be associated with a reduction in smoking cue–elicited craving.DesignA laboratory model of conditioned responding and arterial spin-labeled perfusion functional magnetic resonance imaging, a biomarker of regional brain activity, was used to test our hypothesis. Perfusion functional magnetic resonance imaging is quantitative and stable across time, facilitating the measurement of medication-induced neural modifications in the brain in response to a challenge (smoking cue exposure) and in the brain in the resting condition (without provocation). Smokers were imaged during rest and during smoking cue exposure before and after a 3-week randomized placebo-controlled medication regimen. Subjects were nonabstinent to explicitly examine the effects of varenicline on cue reactivity independent of withdrawal.SettingCenter for the Study of Addictions, University of Pennsylvania, Philadelphia.SubjectsSubjects were nicotine-dependent smokers who responded to advertisements placed on local radio and Listservs to participate in a medication-related research study that specifically stated “this is not a Quit Smoking Study” and “smokers may be contemplating but not currently considering quitting.”ResultsPrerandomization smoking cues vs nonsmoking cues activated the ventral striatum and medial orbitofrontal cortex (t = 3.77) and elicited subjective reports of craving (P = .006). Craving reports correlated with increased activity in the posterior cingulate (t = 4.11). Administration of varenicline diminished smoking cue–elicited ventral striatum and medial orbitofrontal cortex responses (t values from −3.75 to −5.63) and reduced self-reported smoking cue–elicited craving, whereas placebo-treated subjects exhibited responses similar to those observed prior to randomization. Varenicline-induced activation of lateral orbitofrontal cortex in the brain at rest (t = 5.63) predicted blunting of smoking cue responses in the medial orbitofrontal cortex (r = −0.74).ConclusionsVarenicline's reciprocal actions in the reward-activated medial orbitofrontal cortex and in the reward-evaluating lateral orbitofrontal cortex underlie a diminished smoking cue response, revealing a distinctive new action that likely contributes to its clinical efficacy.

Distinguishing Between Major Depressive Disorder and Obsessive-Compulsive Disorder in Children by Measuring Regional Cortical Thickness

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Arch Gen Psychiatry. 2011;68(5):527-533. doi:10.1001/archgenpsychiatry.2011.36
Meta-analysis

The Serotonin Transporter Promoter Variant (5-HTTLPR), Stress, and Depression Meta-analysis Revisited: Evidence of Genetic Moderation

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Arch Gen Psychiatry. 2011;68(5):444-454. doi:10.1001/archgenpsychiatry.2010.189
ContextTwo recent meta-analyses assessed the set of studies exploring the interaction between a serotonin transporter promoter polymorphism (5-HTTLPR) and stress in the development of depression and concluded that the evidence did not support the presence of the interaction. However, even the larger of the meta-analyses included only 14 of the 56 studies that have assessed the relationship between 5-HTTLPR, stress, and depression.ObjectiveTo perform a meta-analysis including all relevant studies exploring the interaction.Data SourcesWe identified studies published through November 2009 in PubMed.Study SelectionWe excluded 2 studies presenting data that were included in other larger studies.Data ExtractionTo perform a more inclusive meta-analysis, we used the Liptak-Stouffer z score method to combine findings of primary studies at the level of significance tests rather than the level of raw data.Data SynthesisWe included 54 studies and found strong evidence that 5-HTTLPR moderates the relationship between stress and depression, with the 5-HTTLPR s allele associated with an increased risk of developing depression under stress (P = .00002). When stratifying our analysis by the type of stressor studied, we found strong evidence for an association between the s allele and increased stress sensitivity in the childhood maltreatment (P = .00007) and the specific medical condition (P = .0004) groups of studies but only marginal evidence for an association in the stressful life events group (P = .03). When restricting our analysis to the studies included in the previous meta-analyses, we found no evidence of association (Munafò et al studies, P = .16; Risch et al studies, P = .11). This suggests that the difference in results between meta-analyses was due to the different set of included studies rather than the meta-analytic technique.ConclusionContrary to the results of the smaller earlier meta-analyses, we find strong evidence that the studies published to date support the hypothesis that 5-HTTLPR moderates the relationship between stress and depression.
Commentary

Genes and Environment in Psychiatry: Winner's Curse or Cure?

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Arch Gen Psychiatry. 2011;68(5):455-456. doi:10.1001/archgenpsychiatry.2011.35

Genetic Indeterminism, the 5-HTTLPR, and the Paths Forward in Neuropsychiatric Genetics

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Arch Gen Psychiatry. 2011;68(5):457-458. doi:10.1001/archgenpsychiatry.2011.34
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