Vilella Laura, Lacuey Nuria, Hampson Johnson P, Zhu Liang, Omidi Shirin, Ochoa-Urrea Manuela, Tao Shiqiang, Rani M R Sandhya, Sainju Rup K, Friedman Daniel, Nei Maromi, Strohl Kingman, Scott Catherine, Allen Luke, Gehlbach Brian K, Hupp Norma J, Hampson Jaison S, Shafiabadi Nassim, Zhao Xiuhe, Reick-Mitrisin Victoria, Schuele Stephan, Ogren Jennifer, Harper Ronald M, Diehl Beate, Bateman Lisa M, Devinsky Orrin, Richerson George B, Ryvlin Philippe, Zhang Guo-Qiang, Lhatoo Samden D
From the NINDS Center for SUDEP Research (L.V., N.L., S.O., M.O.-U., S.T., M.R.S.R., R.K.S., D.F., M.N., C.S., L.A., B.K.G., J.S.H., S.S., J.O., R.M.H., B.D., L.M.B., O.D., G.B.R., P.R., G.-Q.Z., S.D.L.) and Department of Neurology (L.V., N.L., J.P.H., S.O., M.O.-U., S.T., M.R.S.R., N.J.H., J.S.H., G.-Q.Z., S.D.L.), McGovern Medical School, and Biostatistics and Epidemiology Research Design Core (L.Z., G.B.R.), Division of Clinical and Translational Sciences, University of Texas Health Science Center at Houston; Departament de Medicina (L.V.), Universitat Autonoma de Barcelona, Spain; University of Iowa Carver College of Medicine (R.K.S., B.K.G.), Iowa City; NYU Langone School of Medicine (D.F., O.D.), New York; Sidney Kimmel Medical College (M.N.), Thomas Jefferson University, Philadelphia, PA; Division of Pulmonary (K.S.), Critical Care and Sleep Medicine, University Hospitals Medical Center, Cleveland, OH; Institute of Neurology (C.S., L.A., B.D.), University College London, UK; Case Western Reserve University (N.S., X.Z., V.R.-M.), Cleveland, OH; Feinberg School of Medicine (S.S.), Northwestern University, Chicago, IL; Department of Neurobiology and the Brain Research Institute (J.O., R.M.H.), University of California, Los Angeles; Department of Neurology (L.M.B.), Columbia University, New York, NY; and Department of Clinical Neuroscience (P.R.), Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland.
Neurology. 2021 Jan 19;96(3):e352-e365. doi: 10.1212/WNL.0000000000011274. Epub 2020 Dec 2.
To analyze the association between peri-ictal brainstem posturing semiologies with postictal generalized electroencephalographic suppression (PGES) and breathing dysfunction in generalized convulsive seizures (GCS).
In this prospective, multicenter analysis of GCS, ictal brainstem semiology was classified as (1) decerebration (bilateral symmetric tonic arm extension), (2) decortication (bilateral symmetric tonic arm flexion only), (3) hemi-decerebration (unilateral tonic arm extension with contralateral flexion) and (4) absence of ictal tonic phase. Postictal posturing was also assessed. Respiration was monitored with thoracoabdominal belts, video, and pulse oximetry.
Two hundred ninety-five seizures (180 patients) were analyzed. Ictal decerebration was observed in 122 of 295 (41.4%), decortication in 47 of 295 (15.9%), and hemi-decerebration in 28 of 295 (9.5%) seizures. Tonic phase was absent in 98 of 295 (33.2%) seizures. Postictal posturing occurred in 18 of 295 (6.1%) seizures. PGES risk increased with ictal decerebration (odds ratio [OR] 14.79, 95% confidence interval [CI] 6.18-35.39, < 0.001), decortication (OR 11.26, 95% CI 2.96-42.93, < 0.001), or hemi-decerebration (OR 48.56, 95% CI 6.07-388.78, < 0.001). Ictal decerebration was associated with longer PGES ( = 0.011). Postictal posturing was associated with postconvulsive central apnea (PCCA) ( = 0.004), longer hypoxemia ( < 0.001), and Spo recovery ( = 0.035).
Ictal brainstem semiology is associated with increased PGES risk. Ictal decerebration is associated with longer PGES. Postictal posturing is associated with a 6-fold increased risk of PCCA, longer hypoxemia, and Spo recovery. Peri-ictal brainstem posturing may be a surrogate biomarker for GCS severity identifiable without in-hospital monitoring.
This study provides Class III evidence that peri-ictal brainstem posturing is associated with the GCS with more prolonged PGES and more severe breathing dysfunction.
分析全面性惊厥发作(GCS)发作期脑干姿势体征与发作后期广泛性脑电图抑制(PGES)及呼吸功能障碍之间的关联。
在这项针对GCS的前瞻性多中心分析中,发作期脑干体征分为:(1)去大脑强直(双侧对称的强直性上肢伸展);(2)去皮层强直(仅双侧对称的强直性上肢屈曲);(3)半去大脑强直(单侧强直性上肢伸展伴对侧屈曲);(4)无发作期强直相。还评估了发作后期姿势。通过胸腹带、视频和脉搏血氧饱和度监测呼吸。
分析了295次发作(180例患者)。295次发作中观察到发作期去大脑强直122次(41.4%),去皮层强直47次(15.9%),半去大脑强直28次(9.5%)。295次发作中有98次(33.2%)无强直相。295次发作中有18次(6.1%)出现发作后期姿势。发作期去大脑强直(优势比[OR]14.79,95%置信区间[CI]6.18 - 35.39,<0.001)、去皮层强直(OR 11.26,95% CI 2.96 - 42.93,<0.001)或半去大脑强直(OR 48.56,95% CI 6.07 - 388.78,<0.001)时,PGES风险增加。发作期去大脑强直与更长的PGES相关(P = 0.011)。发作后期姿势与惊厥后中枢性呼吸暂停(PCCA)相关(P = 0.004)、更长时间的低氧血症相关(P<0.001)以及血氧饱和度恢复相关(P = 0.035)。
发作期脑干体征与PGES风险增加相关。发作期去大脑强直与更长的PGES相关。发作后期姿势与PCCA风险增加6倍、更长时间的低氧血症以及血氧饱和度恢复相关。发作期前后脑干姿势可能是无需住院监测即可识别的GCS严重程度的替代生物标志物。
本研究提供了III级证据,即发作期前后脑干姿势与GCS相关,伴有更长时间的PGES和更严重的呼吸功能障碍。