Serum S-100B protein and neuron-specific enolase after traumatic acute subdural hematoma in the rat

急性硬膜下血肿（SDH）的高死亡率在很大程度上是由于其经常与包括挫伤和脑肿胀在内的原发性脑损伤相关。然而，创伤性脑损伤后脑肿胀的性质和原因是多因素的，并且知之甚少。S-100 B蛋白和神经元特异性烯醇化酶（NSE）被认为是脑损伤的神经生化标志物。血清S-100 B蛋白和NSE浓度及动力学变化可作为急性SDH后原发性脑损害的评价指标。本研究通过建立SDH、SDH合并弥漫性脑损伤（DBI）、SDH + DBI +低氧血症的实验动物模型，观察了血清S-100 B蛋白和NSE浓度及动力学变化对脑水肿形成和生理后果的影响。血清S-100 B蛋白和NSE与损伤程度显著相关。S-100 B与NSE呈显著正相关。SDH + DBI +缺氧组血清S-100 B蛋白和NSE水平明显高于单纯SDH组和SDH + DBI组。血清标志物的继发性升高与继发性损伤（如缺氧或低血压）的存在相关。根据我们的研究结果，急性SDH的不良结局可能不仅取决于血肿本身的特征，还取决于是否存在额外的脑实质损伤和继发性损伤。因此，与急性SDH相关的脑肿胀可能主要是由细胞毒性脑水肿引起的，细胞毒性脑水肿因额外的二次损伤而加重。在未来，S100 B和NSE测量可能可靠地预测继发性脑损伤，并用于监测治疗效果。

The high mortality of acute subdural hematoma (SDH) is largely explained by its frequent association with primary brain damage consisting of contusion and brain swelling. However, the nature and causes of brain swelling after traumatic brain injury are multifactorial and poorly understood. S-100B proteins and neuron specific enolase (NSE) are considered to be neurobiochemical markers for the brain damage. Serum concentration and kinetics of S-100B protein and NSE provide the assessment of the primary brain damage after acute SDH. In the present study, we examined serum concentration and kinetics of S-100B protein and NSE on the physiological consequence and brain edema formation in the experimental animal model of SDH alone, SDH associated with diffuse brain injury (DBI), and SDH + DBI + hypoxemia. Serum S-100B protein and NSE were significantly correlated with injury severity. The significant correlation was found between the initial S-100B and NSE. In the group of SDH + DBI + hypoxia, the serum value of S-100B protein and NSE was significantly higher compared with SDH alone and SDH + DBI. Secondary increase of serum markers was associated with the presence of secondary insult such as hypoxia or hypotension. Given our findings, it is possible that the poor outcome of acute SDH depends not only on the characteristics of the hematoma itself, but also on the presence of additional cerebral parenchymal injury and secondary insult. Thus, it is possible that the brain swelling associated with acute SDH is mainly caused by cytotoxic brain edema aggravated by an additional secondary insult. In the future, S100B and NSE measurements might reliably predict secondary brain injury and also be used to monitor the efficacy of treatments.