Thygesen Mathias Møller, Entezari Seyar, Houlind Nanna, Nielsen Teresa Haugaard, Olsen Nicholas Østergaard, Nielsen Tim Damgaard, Skov Mathias, Tankisi Alp, Rasmussen Mads, Einarsson Halldór Bjarki, Orlowski Dariusz, Dyrskog Stig Eric, Thorup Line, Pedersen Michael, Rasmussen Mikkel Mylius
Department of Clinical Medicine Comparative Medicine Lab, Aarhus University, Palle Juul Jensens Blvd 99, DK8200, Aarhus, Denmark.
Department of Neurosurgery, Aarhus University Hospital, Aarhus, Denmark.
Neurocrit Care. 2024 Dec 11. doi: 10.1007/s12028-024-02181-1.
It has been suggested that intraspinal pressure (ISP) below the dura is elevated following traumatic spinal cord injury (TSCI). The dura can maintain the pressure, and hence a subdural compartment syndrome has been hypothesized to develop regardless of bony decompression. This study aimed to evaluate whether a such intradural compartment syndrome develops during the first 72 h in a porcine TSCI model.
First, in a randomized sham controlled-trial design, longitudinal ISP measurements were performed over a period of 72 h from onset of TSCI. TSCI was inflicted by a weight-drop contusion regime: 75-g rod, 75-mm free fall, and 5-min compression of the spinal cord. Second, in a sham-controlled dose-response design longitudinal ISP measurements were performed over a period of 16 h from the onset of TSCI, using two other contusion regimes: 75-g rod, 125-mm free fall, and 5-min compression; and 75-g rod, 75-mm free fall, and 240-min compression. Animals were kept sedated for the entire course of the study using propofol, fentanyl, and midazolam.
Intraspinal pressure increased in TSCI and sham animals alike, but we found no significant increases in ISP following TSCI compared with the sham group, and we found no relationship between the ISP increase and larger impacts or increased time of compression.
These findings suggest that the subdural swelling of the spinal cord following thoracic TSCI is not responsible for the ISP increase measured in our TSCI model, but that the ISP increase was caused by the surgical procedure or the reconstitution of normal cerebrospinal fluid pressure.
有人提出,创伤性脊髓损伤(TSCI)后硬脊膜下的脊髓内压力(ISP)会升高。硬脊膜可维持压力,因此有人推测,无论是否进行骨性减压,都会发生硬脊膜下腔综合征。本研究旨在评估在猪TSCI模型的最初72小时内是否会发生这种硬脊膜内综合征。
首先,在随机假手术对照试验设计中,从TSCI发作开始的72小时内进行纵向ISP测量。TSCI通过重物坠落挫伤方案造成:75克棒,75毫米自由落体,脊髓压缩5分钟。其次,在假手术对照剂量反应设计中,从TSCI发作开始的16小时内进行纵向ISP测量,使用另外两种挫伤方案:75克棒,125毫米自由落体,脊髓压缩5分钟;以及75克棒,75毫米自由落体,脊髓压缩240分钟。在整个研究过程中,使用丙泊酚、芬太尼和咪达唑仑使动物保持镇静。
TSCI组和假手术组动物的脊髓内压力均升高,但与假手术组相比,我们发现TSCI后ISP没有显著升高,并且我们发现ISP升高与更大的撞击或更长的压缩时间之间没有关系。
这些发现表明,胸段TSCI后脊髓的硬脊膜下肿胀并非我们TSCI模型中测量到的ISP升高的原因,而是ISP升高是由手术操作或正常脑脊液压力的恢复引起的。