期刊
HUMAN BRAIN MAPPING
卷 43, 期 1, 页码 399-413出版社
WILEY
DOI: 10.1002/hbm.25114
关键词
addiction; alcohol; cannabis; structural neuroimaging
资金
- National Institutes of Health (NIH) [U54 EB 020403]
- NIDA [1R01DA047119-01]
- Canada Research Chair
- VICI grant from the Netherlands Organization for Scientific Research (NWO) [453.08.01]
- ZonMW grant from the Netherlands Organization for Scientific Research (NWO) [31160003, 31160004, 91676084, 31180002]
- VIDI grant from the Netherlands Organization for Scientific Research (NWO) [016.08.322]
- National Health and Medical Research Council Fellowship [1117188]
- David Winston Turner Endowment Fund
- [R01 MH116147]
- [NIH/NIDA: PL30-1DA024859-01]
- [NIH/NCRR: UL1-RR24925-01]
Alcohol use disorder (AUD) and cannabis use disorder (CUD) are associated with significant brain alterations, particularly in subcortical and cortical regions. The brain abnormalities in AUD are comparable to or larger than those found in other psychiatric disorders, while CUD is most strongly related to reduced cortical thickness in the medial orbitofrontal cortex.
Alcohol use disorder (AUD) and cannabis use disorder (CUD) are associated with brain alterations particularly involving fronto-cerebellar and meso-cortico-limbic circuitry. However, such abnormalities have additionally been reported in other psychiatric conditions, and until recently there has been few large-scale investigations to compare such findings. The current study uses the Enhancing Neuroimaging Genetics through Meta-Analysis (ENIGMA) consortium method of standardising structural brain measures to quantify case-control differences and to compare brain-correlates of substance use disorders with those published in relation to other psychiatric disorders. Using the ENIGMA protocols, we report effect sizes derived from a meta-analysis of alcohol (seven studies,N= 798, 54% are cases) and cannabis (seven studies,N= 447, 45% are cases) dependent cases and age- and sex-matched controls. We conduct linear analyses using harmonised methods to process and parcellate brain data identical to those reported in the literature for ENIGMA case-control studies of major depression disorder (MDD), schizophrenia (SCZ) and bipolar disorder so that effect sizes are optimally comparable across disorders. R elationships between substance use disorder diagnosis and subcortical grey matter volumes and cortical thickness were assessed with intracranial volume, age and sex as co-variates . After correcting for multiple comparisons, AUD case-control meta-analysis of subcortical regions indicated significant differences in the thalamus, hippocampus, amygdala and accumbens, with effect sizes (0.23) generally equivalent to, or larger than |0.23| those previously reported for other psychiatric disorders (except for the pallidum and putamen). On measures of cortical thickness, AUD was associated with significant differences bilaterally in the fusiform gyrus, inferior temporal gyrus, temporal pole, superior frontal gyrus, and rostral and caudal anterior cingulate gyri. Meta-analysis of CUD case-control studies indicated reliable reductions in amygdala, accumbens and hippocampus volumes, with the former effect size comparable to, and the latter effect size around half of that reported for alcohol and SCZ. CUD was associated with lower cortical thickness in the frontal regions, particularly the medial orbitofrontal region, but this effect was not significant after correcting for multiple testing. This study allowed for an unbiased cross-disorder comparison of brain correlates of substance use disorders and showed alcohol-related brain anomalies equivalent in effect size to that found in SCZ in several subcortical and cortical regions and significantly greater alterations than those found in MDD in several subcortical and cortical regions. Although modest, CUD results overlapped with findings reported for AUD and other psychiatric conditions, but appear to be most robustly related to reduce thickness of the medial orbitofrontal cortex.
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