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围生期卒中后丘脑失联络与临床残疾有关。

Thalamic diaschisis following perinatal stroke is associated with clinical disability.

机构信息

Hotchkiss Brain Institute, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada; Calgary Pediatric Stroke Program, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada; Alberta Children's Hospital Research Institute, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada.

Hotchkiss Brain Institute, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada; Calgary Pediatric Stroke Program, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada; Alberta Children's Hospital Research Institute, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada.

出版信息

Neuroimage Clin. 2019;21:101660. doi: 10.1016/j.nicl.2019.101660. Epub 2019 Jan 4.

DOI:10.1016/j.nicl.2019.101660
PMID:30639178
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6412070/
Abstract

BACKGROUND

Perinatal stroke causes most hemiparetic cerebral palsy and leads to lifelong disability. Understanding developmental neuroplasticity following early stroke is increasingly translated into novel therapies. Diaschisis refers to alterations brain structures remote from, but connected to, stroke lesions. Ipsilesional thalamic diaschisis has been described following adult stroke but has not been investigated in perinatal stroke. We hypothesized that thalamic diaschisis occurs in perinatal stroke and its degree would be inversely correlated with clinical motor function.

METHODS

Population-based, controlled cohort study. Participants were children (<19 years) with unilateral perinatal stroke (arterial ischemic stroke [AIS] or periventricular venous infarction [PVI]), anatomical magnetic resonance imaging (MRI) >6 months of age, symptomatic hemiparetic cerebral palsy, and no additional neurologic disorders. Typically developing controls had comparable age and gender proportions. T1-weighted anatomical scans were parcellated into 99 regions of interest followed by generation of regional volumes. The primary outcome was thalamic volume expressed as ipsilesional (ILTV), contralesional (CLTV) and thalamic ratio (CLTV/ILTV). Standardized clinical motor assessments were correlated with thalamic volume metrics.

RESULTS

Fifty-nine participants (12.9 years old ±4.0 years, 46% female) included 20 AIS, 11 PVI, and 28 controls. ILTV was reduced in both AIS and PVI compared to controls (p < .001, p = .029, respectively). Ipsilesional thalamic diaschisis was not associated with clinical motor function. However, CLTV was significantly larger in AIS compared to both controls and PVI (p = .005, p < .001, respectively). CLTV was inversely correlated with all four clinical motor assessments (all p < .003).

CONCLUSION

Bilateral thalamic volume changes occur after perinatal stroke. Ipsilesional volume loss is not associated with clinical motor function. Contralesional volume is inversely correlated with clinical motor function, suggesting the thalamus is involved in the known developmental plasticity that occurs in the contralesional hemisphere after early unilateral injury.

摘要

背景

围产期中风导致大多数偏瘫性脑瘫,并导致终身残疾。对早期中风后发育神经可塑性的理解正逐渐转化为新的治疗方法。远隔失联络是指远离中风病变但与之相连的脑结构的改变。成人中风后已描述了同侧丘脑远隔失联络,但尚未在围产期中风中进行研究。我们假设围产期中风会发生丘脑远隔失联络,其程度与临床运动功能呈负相关。

方法

基于人群的对照队列研究。参与者为患有单侧围产期中风(动脉缺血性中风 [AIS] 或脑室周围静脉梗死 [PVI])、年龄大于 6 个月、有症状性偏瘫性脑瘫且无其他神经障碍的儿童(<19 岁)。正常发育的对照组具有相似的年龄和性别比例。T1 加权解剖扫描被分割成 99 个感兴趣区,然后生成区域体积。主要结果是用同侧(ILTV)、对侧(CLTV)和丘脑比(CLTV/ILTV)表示的丘脑体积。对标准化临床运动评估与丘脑体积指标进行了相关性分析。

结果

59 名参与者(12.9 岁±4.0 岁,46%为女性)包括 20 例 AIS、11 例 PVI 和 28 例对照组。与对照组相比,AIS 和 PVI 的同侧丘脑体积均减少(p<0.001,p=0.029)。同侧丘脑远隔失联络与临床运动功能无关。然而,AIS 的对侧丘脑体积明显大于对照组和 PVI(p=0.005,p<0.001)。对侧丘脑体积与所有四项临床运动评估均呈负相关(均 p<0.003)。

结论

围产期中风后双侧丘脑体积发生变化。同侧体积减少与临床运动功能无关。对侧体积与临床运动功能呈负相关,这表明丘脑参与了已知的发育可塑性,即早期单侧损伤后对侧半球发生的发育可塑性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6514/6412070/005a2f8ca8bb/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6514/6412070/6725d106404b/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6514/6412070/92b11b114145/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6514/6412070/eb7252950d76/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6514/6412070/1907f347e422/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6514/6412070/005a2f8ca8bb/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6514/6412070/6725d106404b/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6514/6412070/92b11b114145/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6514/6412070/eb7252950d76/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6514/6412070/1907f347e422/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6514/6412070/005a2f8ca8bb/gr5.jpg

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