Dysautonomia after severe traumatic brain injury
Dysautonomia after severe traumatic brain injury
复制标题
DOI：
10.1111/j.1468-1331.2010.02989.x
复制
发表时间：
2010-09-01
影响因子：
5.1
通讯作者：
Vos, P. E.
中科院分区：
文献类型：
--
作者：
Hendricks, H. T.;Heeren, A. H.;Vos, P. E.
背景：外伤性脑损伤（TBI）后的自主神经障碍的特征是心率、呼吸频率、体温、血压、肌肉张力、去皮质或去皮质姿势以及大量出汗。本研究探讨了严重TBI后自主神经异常的发生率、与自主神经异常相关的临床变量以及自主神经异常患者的功能结局。方法：对严重TBI患者进行历史性队列研究[入院时格拉斯哥昏迷评分(GCS) < 8]。结果：119例患者中76例存活，符合随访条件。自主神经异常发生率为11.8%。自主神经异常发作的平均时间为20.1天（范围3-68天），通常由不适引起。自主神经异常患者的昏迷时间（24.78天和7.99天）和机械通气时间（22.67天和7.21天）明显更长。自主神经异常与弥漫性轴索损伤（DAI）[相对危险度（RR） 20.83, CI 4.92-83.33]和痉挛的发生相关（RR 16.94, CI 3.96-71.42）。自主神经异常患者有更多的继发并发症。他们的结果往往较差。结论：自主神经异常发生在大约10%的严重TBI患者中，并与DAI和随访时痉挛的发展有关。由不适引发的自主神经异常支持兴奋：抑制比模型作为病理生理机制。
Background:Dysautonomia after traumatic brain injury (TBI) is characterized by episodes of increased heart rate, respiratory rate, temperature, blood pressure, muscle tone, decorticate or decerebrate posturing, and profuse sweating. This study addresses the incidence of dysautonomia after severe TBI, the clinical variables that are associated with dysautonomia, and the functional outcome of patients with dysautonomia.Methods:A historic cohort study in patients with severe TBI [Glasgow Coma Scale (GCS) < 8 on admission].Results:Seventy-six of 119 patients survived and were eligible for follow-up. The incidence of dysautonomia was 11.8%. Episodes of dysautonomia were prevalent during a mean period of 20.1 days (range 3-68) and were often initiated by discomfort. Patients with dysautonomia showed significant longer periods of coma (24.78 vs. 7.99 days) and mechanical ventilation (22.67 vs. 7.21 days). Dysautonomia was associated with diffuse axonal injury (DAI) [relative risk (RR) 20.83, CI 4.92-83.33] and the development of spasticity (RR 16.94, CI 3.96-71.42). Patients with dysautonomia experienced more secondary complications. They tended to have poorer outcome.Conclusions:Dysautonomia occurs in approximately 10% of patients surviving severe TBI and is associated with DAI and the development of spasticity at follow-up. The initiation of dysautonomia by discomfort supports the Excitatory: Inhibitory Ratio model as pathophysiological mechanism.