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Quality Control of Diffusion Weighted Images.扩散加权图像的质量控制
Proc SPIE Int Soc Opt Eng. 2010 Mar 11;7628:76280J-. doi: 10.1117/12.844748.
2
Interactive specialization: a domain-general framework for human functional brain development?交互式专业化:人类功能性大脑发育的一般性领域框架?
Dev Cogn Neurosci. 2011 Jan;1(1):7-21. doi: 10.1016/j.dcn.2010.07.003. Epub 2010 Jul 30.
3
Involvement of the anterior thalamic radiation in boys with high functioning autism spectrum disorders: a Diffusion Tensor Imaging study.前丘脑辐射在高功能自闭症谱系障碍男孩中的作用:一项弥散张量成像研究。
Brain Res. 2011 Oct 12;1417:77-86. doi: 10.1016/j.brainres.2011.08.020. Epub 2011 Aug 16.
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Hyperconnectivity and slow synapses during early development of medial prefrontal cortex in a mouse model for mental retardation and autism.精神发育迟缓和自闭症小鼠模型内侧前额叶皮质早期发育过程中的超连接和突触传递缓慢。
Cereb Cortex. 2012 Jun;22(6):1333-42. doi: 10.1093/cercor/bhr224. Epub 2011 Aug 19.
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Recurrence risk for autism spectrum disorders: a Baby Siblings Research Consortium study.自闭症谱系障碍的复发风险:婴儿兄弟姐妹研究联盟研究。
Pediatrics. 2011 Sep;128(3):e488-95. doi: 10.1542/peds.2010-2825. Epub 2011 Aug 15.
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Control of local protein synthesis and initial events in myelination by action potentials.动作电位对局部蛋白质合成和髓鞘形成初始事件的控制。
Science. 2011 Sep 16;333(6049):1647-51. doi: 10.1126/science.1206998. Epub 2011 Aug 4.
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Early specialization for voice and emotion processing in the infant brain.婴儿大脑中对声音和情感处理的早期专业化。
Curr Biol. 2011 Jul 26;21(14):1220-4. doi: 10.1016/j.cub.2011.06.009. Epub 2011 Jun 30.
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Disrupted neural synchronization in toddlers with autism.自闭症幼儿的神经同步中断。
Neuron. 2011 Jun 23;70(6):1218-25. doi: 10.1016/j.neuron.2011.04.018.
9
Early brain overgrowth in autism associated with an increase in cortical surface area before age 2 years.自闭症早期大脑过度生长与2岁前皮质表面积增加有关。
Arch Gen Psychiatry. 2011 May;68(5):467-76. doi: 10.1001/archgenpsychiatry.2011.39.
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Abnormal white matter integrity in young children with autism.自闭症儿童的异常脑白质完整性。
Hum Brain Mapp. 2011 Apr;32(4):534-43. doi: 10.1002/hbm.21042.

自闭症婴儿在 6 至 24 个月时出现的白质纤维束发育差异。

Differences in white matter fiber tract development present from 6 to 24 months in infants with autism.

机构信息

Carolina Institute for Developmental Disabilities and the Department of Psychiatry, University of North Carolina, Chapel Hill, USA.

出版信息

Am J Psychiatry. 2012 Jun;169(6):589-600. doi: 10.1176/appi.ajp.2011.11091447.

DOI:10.1176/appi.ajp.2011.11091447
PMID:22362397
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3377782/
Abstract

OBJECTIVE

Evidence from prospective studies of high-risk infants suggests that early symptoms of autism usually emerge late in the first or early in the second year of life after a period of relatively typical development. The authors prospectively examined white matter fiber tract organization from 6 to 24 months in high-risk infants who developed autism spectrum disorders (ASDs) by 24 months.

METHOD

The participants were 92 high-risk infant siblings from an ongoing imaging study of autism. All participants had diffusion tensor imaging at 6 months and behavioral assessments at 24 months; a majority contributed additional imaging data at 12 and/or 24 months. At 24 months, 28 infants met criteria for ASDs and 64 infants did not. Microstructural properties of white matter fiber tracts reported to be associated with ASDs or related behaviors were characterized by fractional anisotropy and radial and axial diffusivity.

RESULTS

The fractional anisotropy trajectories for 12 of 15 fiber tracts differed significantly between the infants who developed ASDs and those who did not. Development for most fiber tracts in the infants with ASDs was characterized by higher fractional anisotropy values at 6 months followed by slower change over time relative to infants without ASDs. Thus, by 24 months of age, those with ASDs had lower values.

CONCLUSIONS

These results suggest that aberrant development of white matter pathways may precede the manifestation of autistic symptoms in the first year of life. Longitudinal data are critical to characterizing the dynamic age-related brain and behavior changes underlying this neurodevelopmental disorder.

摘要

目的

来自高危婴儿前瞻性研究的证据表明,自闭症的早期症状通常在经历一段相对典型的发育后,于 1 岁或 2 岁早期出现。作者前瞻性地检查了在 24 个月时发展为自闭症谱系障碍(ASD)的高危婴儿从 6 个月至 24 个月的白质纤维束组织。

方法

参与者是正在进行的自闭症成像研究中的 92 名高危婴儿兄弟姐妹。所有参与者在 6 个月时进行弥散张量成像,在 24 个月时进行行为评估;大多数人在 12 个月和/或 24 个月时提供了额外的成像数据。在 24 个月时,28 名婴儿符合 ASD 标准,64 名婴儿不符合。与 ASD 或相关行为相关的白质纤维束的微观结构特性通过分数各向异性和径向及轴向扩散率来描述。

结果

在发展为 ASD 的婴儿和未发展为 ASD 的婴儿之间,有 15 条纤维束中的 12 条的分数各向异性轨迹有显著差异。在患有 ASD 的婴儿中,大多数纤维束的发育特征是在 6 个月时具有较高的分数各向异性值,随后相对于没有 ASD 的婴儿,随时间的变化较慢。因此,到 24 个月时,这些婴儿的分数各向异性值较低。

结论

这些结果表明,白质通路的异常发育可能先于生命第一年自闭症症状的出现。纵向数据对于描述这种神经发育障碍的大脑和行为随年龄变化的动态特征至关重要。