Another step forward in relating facial and brain dysmorphologies associated with prenatal alcohol exposure.
Another step forward in relating facial and brain dysmorphologies associated with prenatal alcohol exposure.
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DOI：
10.1111/j.1530-0277.2012.01849.x
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发表时间：
2012-07
期刊：
影响因子：
--
通讯作者：
Fryer SL
中科院分区：
文献类型：
--
作者：
Fryer SL
Yang及其同事（2012）最近的研究是一项进行得很好、样本很好的神经影像学研究，研究胎儿酒精对与面部畸形有关的胼胝体结构的影响。研究结果包括观察特定颅面畸形与胼胝体面积和厚度的减少与产前酒精暴露史的年轻人。这项工作的部分价值在于多站点采样，这使得数据能够在洛杉矶和圣地亚哥的美国站点以及南非开普敦的国际站点进行汇总。作为胎儿酒精谱系障碍合作倡议（CIFASD）的一部分，本研究源于将跨文化评估与新方法和跨学科框架相结合的更大努力，以促进对胎儿酒精暴露相关后遗症的理解。CIFASD的一个中心目标是推动一项研究议程，为与产前酒精接触有关的所有出生缺陷制定更好的诊断标准。颅面畸形（例如，短睑裂、平滑的中心、薄朱红色边界）是产前酒精暴露的标志性特征，并与生长缺陷和中枢神经系统（CNS）异常一起，形成了诊断胎儿酒精综合征（FAS）所需的三个特征（Bertrand etal ., 2004）。然而，FAS发生在胎儿酒精连续效应的最严重的一端，许多被认为是由于产前酒精暴露导致的认知和行为缺陷的年轻人可能没有全部或任何符合FAS诊断标准所需的面部畸形。据估计，除FAS外，胎儿酒精相关病理（包括酒精相关神经发育障碍）的发生率比单独FAS高数倍（Sampson等，1997）。为了认识到暴露相关影响的连续性，胎儿酒精谱系障碍（FASD）被用作非诊断性总称（Bertrand等人，2004年）。然而，FASD是一个描述性术语，而不是临床诊断。迄今为止，除了胎儿酒精综合症以外，对胎儿酒精相关病理的循证诊断指南尚无共识。目前的诊断框架促使人们关注那些表现出与FAS患者相似的行为表型，但缺乏满足FAS诊断标准所需的颅面和/或生长特征的年轻人。
The recent study by Yang and colleagues (2012) is a well-conducted, well-sampled neuroimaging investigation into fetal alcohol effects on corpus callosum structure, in relation to facial dysmorphology. Results of the study include observations of specific craniofacial malformations correlating with decrements in corpus callosum area and thickness in youth with prenatal alcohol exposure histories. Part of the value of this work rests on multisite sampling, which enabled data to be pooled across US sites in Los Angeles and San Diego, as well as an international site in Capetown, South Africa. As part of the Collaborative Initiative on Fetal Alcohol Spectrum Disorders (CIFASD), this study stems from a larger effort to combine cross-cultural assessment with novel methodologies and an interdisciplinary framework to advance understanding of fetal alcohol exposureassociated sequelae. A central CIFASD aim entails driving a research agenda to generate improved diagnostic criteria for the entire range of birth defects associated with prenatal alcohol exposure.Craniofacial malformations (eg, short palpebral fissures, smooth philtrum, thin vermillion border) are hallmark features of prenatal alcohol exposure, and along with growth deficiency and central nervous system (CNS) abnormalities, form a triad of characteristics required for the diagnosis of the fetal alcohol syndrome (FAS)(Bertrand et al., 2004). However, FAS falls at the severe end of the continuum of fetal alcohol effects, and many youth with cognitive and behavioral deficits believed to be attributable to prenatal alcohol exposure may not bear all, or any, of the facial dysmorphia necessary to meet FAS diagnostic criteria. Fetal alcohol-related pathologies other than FAS, including alcohol-related neurodevelopmental disorders, are estimated to occur at rates several-fold higher than FAS alone (Sampson et al., 1997). In recognition of the continuum of exposure-related effects, fetal alcohol spectrum disorders (FASD) is used as a nondiagnostic umbrella term (Bertrand et al., 2004). However, FASD is a descriptive term, not a clinical diagnosis. To date, there is no consensus on evidence-based diagnostic guidelines for fetal alcohol-related pathologies other than FAS. The diagnostic framework presently in place motivates concern that youth who exhibit a similar behavioral phenotype to individuals with FAS, but who lack the requisite craniofacial and/or growth characteristics required to meet FAS diagnostic criteria,
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