Neurology：脑脊液α突触核蛋白含量预测创伤性脑损伤预后的价值较高

创伤性脑损伤是影响健康的常见疾病之一，其往往产生继发性的脑损伤。来自意大利的Stefania Mondello等医生研究了创伤性脑损伤的临床预后生物标记物，发表在2013年4月30日的Neurology杂志上。该研究的目的是检验重度创伤性脑损伤患者脑脊液中α突触核蛋白的含量及其与临床特征和长期预后的关系。研究发现：脑脊液α突触核蛋白含量预测创伤性脑损伤预后的价值较高。

该前瞻性病例对照研究纳入的重度创伤性脑损伤患者（格拉斯哥评分小于等于8分）接受脑室引流治疗。每一例创伤性脑损伤患者在入院时及损伤后8天内每天留取脑脊液样本，并随后用ELISA检测。对照组患者的脑脊液标本来源于因其他原因进行腰椎穿侧的患者人群。研究采用描绘不同时间脑脊液α突触核蛋白含量曲线的方法与临床预后相对比。

创伤性脑损伤患者损伤后脑脊液α突触核蛋白的含量较对照组明显增加(p = 0.0008)。总体来说，在损伤后8天的观察期内，死亡患者的标本含量（曲线下面积表示）相比那些损伤后生存6月多的患者相比，浓度更高(p = 0.002)。研究随着时间的推移记录了两个不同时间段的α突触核蛋白含量。死亡患者相比生存下来的患者，脑脊液α突触核蛋白含量明显增高，而生存患者的α突触核蛋白浓度与对照组相似。高脑脊液α突触核蛋白含量预测死亡风险的敏感度为83%，特异性为100%。

总的来说，这些数据显示重度脑损伤患者脑脊液α突触核蛋白浓度明显增加，预示广泛的神经变性，反应出损伤后继发的神经病理改变。该研究显示脑脊液α突触核蛋白为预后的良好预测指标，与临床症状综合分析可以为尽早的临床干预提供有力证据。
与脑损伤相关的拓展阅读：

• NEJM：外伤性脑损伤治疗中颅内压监测并无明显作用
• Diabetes：降糖药linagliptin可能减少中风后脑损伤
• Neural Regen Res：揭示缺氧缺血性脑损伤的天然神经保护系统
• 轻度外伤性脑损伤的远期影响大
• Europace：不间断抗凝的AF消融患者仍有无症状性脑损伤风险
• 对于高血压患者β受体阻滞剂可减少阿尔茨海默型脑损伤
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α-Synuclein in CSF of patients with severe traumatic brain injury.
OBJECTIVE
The study aims to examine α-synuclein in the CSF of patients with severe traumatic brain injury (TBI) and its relationship with clinical characteristics and long-term outcomes.
METHODS
This prospective case-control study enrolled patients with severe TBI (Glasgow Coma Score ≤8) who underwent ventriculostomy. CSF samples were taken from each TBI patient at admission and daily for up to 8 days after injury and successively assessed by ELISA. Control CSF was collected for analysis from subjects receiving lumbar puncture for other medical reasons. We used trajectory analysis to identify distinct temporal profiles of CSF α-synuclein that were compared with clinical outcomes.
RESULTS
CSF α-synuclein was elevated in TBI patients after injury as compared to controls (p = 0.0008). Overall, patients who died had higher concentrations (area under the curve) over 8 days of observation compared to those who survived at 6 months postinjury (p = 0.002). Two distinct temporal α-synuclein profiles were recognized over time. Subjects who died had consistently elevated α-synuclein levels compared to those who survived with α-synuclein levels near controls. High-risk trajectory was a strong and accurate predictor of death with 100% specificity and a very high sensitivity (83%).
CONCLUSIONS
Taken together, these data support the hypothesis that in severe TBI patients, substantial increase of CSF α-synuclein may indicate widespread neurodegeneration and reflect secondary neuropathologic events occurring after injury. The determination of CSF α-synuclein may be a valuable prognostic marker, adding to the clinical assessment and creating opportunities for medical intervention.