PATHOPHYSIOLOGY AND MORTALITY OF STATUS EPILEPTICUS

描述(由研究人员提供)：癫痫持续状态(SE)与显著的死亡率有关，但对死亡的病理生理学基础知之甚少。此外，没有预后标准来预测SE死亡的概率。本研究将探讨SE和非惊厥性SE(NCSE)死亡率的预测因素。初步结果(PR)表明，我们为SE和NCSE制定了预测死亡率的结果量表，具有高度的特异性和敏感性。这些结果量表将在这项研究中进行前瞻性的验证和改进。我们的公关发现SE发作后放电(ASID)是SE患者死亡率和心脏异常的主要预测因子。建议进行研究以确定ASID在引起心脏电生理和功能异常中的作用。PR提示ASID可引发急性心脏失代偿和死亡。这项研究将检验我们的初步观察，即ASID的频率和持续时间的增加与死亡率的增加有关。我们还将通过持续的脑电和心电监测来确定ASID是否及时与心脏电生理异常相关，并可能引发死亡。我们还建议对监测的SE患者和对照组的脑和心脏进行尸检研究。我们的PR表明SE可引起海马区和丘脑区的急性脑缺血和胶质细胞改变，并与特定的心脏病理有关。假设将在以下5个具体目标中得到检验。目的1：前瞻性验证NCSE预后量表对NCSE死亡率的预测。目的2：探讨自发性睡眠呼吸暂停综合征的发生频率和持续时间对病死率的影响。目的3：确定ASID与心脏电生理和/或功能异常及死亡的时间关系。目的4：在生前确定中枢和心血管系统功能异常，并与脑和心脏病理结果相关联。目的5：前瞻性验证SE结局量表预测SE死亡率的能力。这项研究可能会对SE的死亡原因提供重要的见解，并开发SE和NCSE的结果量表，可以在床边使用来识别高危病例。识别高危SE和NCSE病例的能力将为开发新的高危病例治疗策略提供新的希望，以防止SE死亡，并为咨询家庭预后提供指导。

DESCRIPTION (provided by investigator): Status Epilepticus (SE) is associated with significant mortality, yet little is known concerning the pathophysiological basis of death. Furthermore, there are no outcome scales to predict the probability of mortality in SE. This study will investigate predictors of mortality for SE and non convulsive SE (NCSE). Preliminary results (PR) indicate that we developed Outcome Scales for both SE and NCSE that predict mortality with a high degree of specificity and sensitivity. These Outcome Scales will be prospectively validated and improved in this study. Our PR identified After SE Ictal Discharges (ASIDS) as a major predictor of mortality and cardiac abnormalities in SE. Studies are proposed to determine the role of ASIDS in causing cardiac electrophysiological and functional abnormalities. PR indicates that ASIDS can trigger acute cardiac decompensation and death. This study will test our initial observations that increased frequency and duration of ASIDS are associated with increased mortality. We will also determine by continuous EEG and ECG monitoring whether ASIDS are associated in time with cardiac electrophysiological abnormalities and can trigger death. We also propose to conduct postmortem studies on the pathological findings in brain and heart in monitored SE patients and controls. Our PR indicated that SE causes acute ischemic and gliotic changes in the hippocampus and thalamus and is associated with specific cardiac pathology. Hypotheses will be tested in the following 5 Specific Aims. AIM 1: Prospectively validate the NCSE Outcome Scale to predict mortality in NCSE. Aim 2: Determine the effect of frequency and duration of ASIDS on mortality in SE. Aim 3: Determine the temporal relationship of ASIDS and cardiac electrophysiological and/or functional abnormalities and death. AIM 4: Determine CNS and CVS functional abnormalities prior to death and correlate with brain and heart pathologic findings. AIM 5: Prospectively validate the ability of the SE Outcome Scale to predict mortality in SE. This study may provide significant insights into the causes of mortality in SE and also develop Outcome Scales for both SE and NCSE that can be used at the bedside to identify high risk cases. The ability to recognize high risk SE and NCSE cases will offer new hope for the development of new treatment strategies for high risk cases to prevent death in SE and provide guidelines to counsel families regarding prognosis.