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创伤性脑损伤后非惊厥性脑电图发作会导致颅内压延迟性、持续性升高及代谢危机。

Nonconvulsive electrographic seizures after traumatic brain injury result in a delayed, prolonged increase in intracranial pressure and metabolic crisis.

作者信息

Vespa Paul M, Miller Chad, McArthur David, Eliseo Mathew, Etchepare Maria, Hirt Daniel, Glenn Thomas C, Martin Neil, Hovda David

机构信息

Department of Neurosurgery, University of California Los Angeles, Los Angeles, CA, USA.

出版信息

Crit Care Med. 2007 Dec;35(12):2830-6.

Abstract

OBJECTIVE

To determine whether nonconvulsive electrographic post-traumatic seizures result in increases in intracranial pressure and microdialysis lactate/pyruvate ratio.

DESIGN

Prospective monitoring with retrospective data analysis.

SETTING

Single center academic neurologic intensive care unit.

PATIENTS

Twenty moderate to severe traumatic brain injury patients (Glasgow Coma Score 3-13).

MEASUREMENTS AND MAIN RESULTS

Continuous electroencephalography and cerebral microdialysis were performed for 7 days after injury. Ten patients had seizures and were compared with a matched cohort of traumatic brain injury patients without seizures. The seizures were repetitive and constituted status epilepticus in seven of ten patients. Using a within-subject design, post-traumatic seizures resulted in episodic increases in intracranial pressure (22.4 +/- 7 vs. 12.8 +/- 4.3 mm Hg; p < .001) and an episodic increase in lactate/pyruvate ratio (49.4 +/- 16 vs. 23.8 +/- 7.6; p < .001) in the seizure group. Using a between-subjects comparison, the seizure group demonstrated a higher mean intracranial pressure (17.6 +/- 6.5 vs. 12.2 +/- 4.2 mm Hg; p < .001), a higher mean lactate/pyruvate ratio (38.6 +/- 18 vs. 27 +/- 9; p < .001) compared with nonseizure patients. The intracranial pressure and lactate/pyruvate ratio remained elevated beyond postinjury hour 100 in the seizure group but not the nonseizure group (p < .02).

CONCLUSION

Post-traumatic seizures result in episodic as well as long-lasting increases in intracranial pressure and microdialysis lactate/pyruvate ratio. These data suggest that post-traumatic seizures represent a therapeutic target for patients with traumatic brain injury.

摘要

目的

确定非惊厥性脑电图型创伤后癫痫发作是否会导致颅内压升高及微透析乳酸/丙酮酸比值升高。

设计

前瞻性监测并进行回顾性数据分析。

地点

单中心学术性神经重症监护病房。

患者

20例中重度创伤性脑损伤患者(格拉斯哥昏迷评分3 - 13分)。

测量指标及主要结果

伤后7天进行持续脑电图监测和脑微透析。10例患者发生癫痫发作,并与一组匹配的无癫痫发作的创伤性脑损伤患者进行比较。癫痫发作呈重复性,10例患者中有7例构成癫痫持续状态。采用受试者自身对照设计,创伤后癫痫发作导致癫痫发作组颅内压呈发作性升高(22.4±7 vs. 12.8±4.3 mmHg;p <.001)以及乳酸/丙酮酸比值呈发作性升高(49.4±16 vs. 23.8±7.6;p <.00)。采用受试者间比较,癫痫发作组与无癫痫发作患者相比,平均颅内压更高(17.6±6.5 vs. 12.2±4.2 mmHg;p <.001),平均乳酸/丙酮酸比值更高(38.6±18 vs. 27±9;p <.001)。癫痫发作组颅内压和乳酸/丙酮酸比值在伤后100小时后仍持续升高,而非癫痫发作组则无此现象(p <.02)。

结论

创伤后癫痫发作会导致颅内压以及微透析乳酸/丙酮酸比值出现发作性和持续性升高。这些数据表明,创伤后癫痫发作是创伤性脑损伤患者的一个治疗靶点。

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