From the, Neurodevelopmental Laboratory on Addictions and Mental Health, McLean Hospital, Belmont, Massachusetts.
Department of Psychiatry, Harvard Medical School, Boston, Massachusetts.
Alcohol Clin Exp Res. 2019 Nov;43(11):2354-2366. doi: 10.1111/acer.14201. Epub 2019 Oct 8.
BACKGROUND: While many adolescents exhibit risky behavior, teenagers with a family history (FH+) of an alcohol use disorder (AUD) are at a heightened risk for earlier initiation of alcohol use, a more rapid escalation in frequency and quantity of alcohol consumption and developing a subsequent AUD in comparison with youth without such family history (FH-). Neuroanatomically, developmentally normative risk-taking behavior parallels an imbalance between more protracted development of the prefrontal cortex (PFC) and earlier development of limbic regions. Magnetic resonance imaging (MRI)-derived volumetric properties were obtained for these structures in FH+ and FH- adolescents. METHODS: Forty-two substance-naïve adolescents (13- to 14-year-olds), stratified into FH+ (N = 19, 13 girls) and FH- (N = 23, 11 girls) age/handedness-matched groups, completed MRI scanning at 3.0T, as well as cognitive and clinical testing. T1 images were processed using FreeSurfer to measure PFC and hippocampi/amygdalae subfields/nuclei volumes. RESULTS: FH+ status was associated with larger hippocampal/amygdala volumes (p < 0.05), relative to FH- adolescents, with right amygdala results appearing to be driven by FH+ boys. Volumetric differences also were positively associated with family history density (p < 0.05) of having an AUD. Larger subfields/nuclei volumes were associated with higher anxiety levels and worse auditory verbal learning performance (p < 0.05). CONCLUSIONS: FH+ risk for AUD is detectable via neuromorphometric characteristics, which precede alcohol use onset and the potential onset of a later AUD, that are associated with emotional and cognitive measures. It is plausible that the development of limbic regions might be altered in FH+ youth, even prior to the onset of alcohol use, which could increase later risk. Thus, targeted preventative measures are warranted that serve to delay the onset of alcohol use in youth, particularly in those who are FH+ for an AUD.
背景:虽然许多青少年表现出冒险行为,但有家族酗酒史(FH+)的青少年比没有家族酗酒史(FH-)的青少年更早开始饮酒,饮酒频率和数量增加更快,并随后发展成酗酒障碍。从神经解剖学角度来看,发展中正常的冒险行为与前额叶皮层(PFC)发育迟缓与边缘区域发育提前之间的不平衡有关。对这些结构进行了基于磁共振成像(MRI)的体积特性测量。
方法:42 名药物-naïve 青少年(13-14 岁),按 FH+(N=19,13 名女孩)和 FH-(N=23,11 名女孩)分为年龄/惯用手匹配组,在 3.0T 下完成 MRI 扫描,以及认知和临床测试。使用 FreeSurfer 处理 T1 图像,以测量 PFC 和海马体/杏仁核亚区/核体积。
结果:FH+状态与更大的海马体/杏仁核体积相关(p<0.05),与 FH-青少年相比,右侧杏仁核的结果似乎是由 FH+男孩驱动的。体积差异也与酗酒障碍家族史密度呈正相关(p<0.05)。更大的亚区/核体积与更高的焦虑水平和更差的听觉言语学习表现相关(p<0.05)。
结论:通过神经形态测量特征可以检测到 FH+患酗酒障碍的风险,这些特征先于饮酒开始和潜在的酗酒障碍发作,并与情绪和认知测量相关。FH+青少年的边缘区域发育可能会发生改变,即使在饮酒开始之前,这可能会增加以后的风险。因此,有必要采取有针对性的预防措施,延缓青少年饮酒的开始,特别是对于 FH+酗酒障碍的青少年。
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