Inflammation after Trauma: Microglial Activation and Traumatic Brain Injury
Inflammation after Trauma: Microglial Activation and Traumatic Brain Injury
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DOI：
10.1002/ana.22455
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发表时间：
2011-09-01
影响因子：
11.2
通讯作者：
Sharp, David J.
中科院分区：
文献类型：
--
作者：
Ramlackhansingh, Anil F.;Brooks, David J.;Sharp, David J.
目的：创伤性脑损伤（TBI）后的患者预后差异很大。其潜在的病理生理学机制了解甚少，但炎症可能是一个重要因素。小胶质细胞在这种反应的多个方面起协调作用。可以使用正电子发射断层扫描（PET）配体[11C](R)PK11195（PK）在体内研究它们的激活情况。在本研究中，我们调查对TBI的炎症反应是否持续存在，以及这种反应是否与脑结构异常和认知功能有关。
方法：10名在中度至重度TBI后至少11个月接受研究的患者，进行了PK PET和结构磁共振成像（包括弥散张量成像）检查。计算了局灶性脑损伤部位及其周围以及选定的远隔和皮质下脑区的PK结合电位。进行了标准化的神经心理学测试。
结果：TBI后，丘脑、壳核、枕叶皮质和内囊后肢的PK结合显著增加。在局灶性脑损伤的原发部位，PK结合没有增加。丘脑的高PK结合与更严重的认知障碍相关，尽管结合与受伤后的时间以及脑结构损伤的程度均无关。
解释：我们证明在TBI后长达17年仍可能存在小胶质细胞激活增加。这表明TBI引发了一种慢性炎症反应，特别是在皮质下区域。这凸显了将对TBI的反应视为随时间演变的重要性，并表明在创伤后的较长时间间隔内进行干预可能比以前认为的更有益。《神经病学年鉴》2011年；70：374 - 383
Objective: Patient outcome after traumatic brain injury (TBI) is highly variable. The underlying pathophysiology of this is poorly understood, but inflammation is potentially an important factor. Microglia orchestrate many aspects of this response. Their activation can be studied in vivo using the positron emission tomography (PET) ligand [11C](R)PK11195 (PK). In this study, we investigate whether an inflammatory response to TBI persists, and whether this response relates to structural brain abnormalities and cognitive function.Methods: Ten patients, studied at least 11 months after moderate to severe TBI, underwent PK PET and structural magnetic resonance imaging (including diffusion tensor imaging). PK binding potentials were calculated in and around the site of focal brain damage, and in selected distant and subcortical brain regions. Standardized neuropsychological tests were administered.Results: PK binding was significantly raised in the thalami, putamen, occipital cortices, and posterior limb of the internal capsules after TBI. There was no increase in PK binding at the original site of focal brain injury. High PK binding in the thalamus was associated with more severe cognitive impairment, although binding was not correlated with either the time since the injury or the extent of structural brain damage.Interpretation: We demonstrate that increased microglial activation can be present up to 17 years after TBI. This suggests that TBI triggers a chronic inflammatory response particularly in subcortical regions. This highlights the importance of considering the response to TBI as evolving over time and suggests interventions may be beneficial for longer intervals after trauma than previously assumed. ANN NEUROL 2011;70:374-383