Najda Mikołaj, Mataczyński Cyprian, Burzyńska Małgorzata, Kasprowicz Magdalena, Kędziora Jarosław, Hammarlund Emma, Thelin Eric P, Uryga Agnieszka
Institute of Data Science, Maastricht University, Maastricht, Limburg, The Netherlands.
Faculty of Information and Communication Technology, Wroclaw University of Science and Technology, Wroclaw, Poland.
Acta Neurochir (Wien). 2025 May 30;167(1):158. doi: 10.1007/s00701-025-06566-9.
Overstimulation of the autonomic nervous system (ANS) in the acute phase after traumatic brain injury (TBI) may lead to paroxysmal sympathetic hyperactivity (PSH) syndrome. This study aimed to investigate the impact of the relationship between ANS activity and cerebral hemodynamics on the development of PSH syndrome.
This retrospective study included 41 TBI patients admitted to Wroclaw University Hospital (Poland). Among them, 14 were classified as at risk for PSH based on the probabilistic Paroxysmal Sympathetic Hyperactivity Assessment Measure (PSH-AM), with 10 rated as 'possible' and 4 as 'probable'. High-resolution neuromonitoring data from the first 72 h post-injury included intracranial pressure (ICP), pressure reactivity index (PRx), baroreflex sensitivity (BRS), arterial blood pressure (ABP), and heart rate (HR). The correlation between ANS activity and cerebral hemodynamics was quantified using the mean, standard deviation, and zero-crossing rate (ZCR) across sliding windows of 3, 6, 12, and 24 h. Logistic regression was used to model PSH risk.
The PSH risk model, including ZCR-based variability of ANS-cerebral hemodynamic correlations within a 3-h sliding window and adjusted by clinical metadata, achieved the highest performance (AUC 0.72 ± 0.27), outperforming the clinical metadata-only model (AUC 0.64 ± 0.18). Aggregated feature importance values indicated that the most predictive relationships were observed between HR-ICP and HR-PRx.
Including the early post-injury interactions between ANS and cerebral hemodynamics in the clinical characteristics-based PSH risk model may improve its performance. Further studies in larger cohorts are necessary to validate these findings.
创伤性脑损伤（TBI）急性期自主神经系统（ANS）的过度刺激可能导致阵发性交感神经过度兴奋（PSH）综合征。本研究旨在探讨ANS活动与脑血流动力学之间的关系对PSH综合征发生发展的影响。
这项回顾性研究纳入了波兰弗罗茨瓦夫大学医院收治的41例TBI患者。其中，根据概率性阵发性交感神经过度兴奋评估量表（PSH-AM），14例被归类为有PSH风险，其中10例被评为“可能”，4例被评为“很可能”。伤后72小时内的高分辨率神经监测数据包括颅内压（ICP）、压力反应性指数（PRx）、压力反射敏感性（BRS）﹑动脉血压（ABP）和心率（HR）。通过3、6、12和24小时滑动窗口的均值、标准差和过零率（ZCR）对ANS活动与脑血流动力学之间的相关性进行量化。采用逻辑回归对PSH风险进行建模。
PSH风险模型，包括基于3小时滑动窗口内ANS-脑血流动力学相关性的ZCR变异性，并经临床元数据调整，表现最佳（曲线下面积[AUC]为0.72±0.27），优于仅基于临床元数据的模型（AUC为0.64±0.18）。汇总的特征重要性值表明，HR-ICP和HR-PRx之间的关系具有最强的预测性。
在基于临床特征的PSH风险模型中纳入伤后早期ANS与脑血流动力学之间的相互作用，可能会提高其性能。有必要在更大的队列中进行进一步研究以验证这些发现。
