Martin Bryn A, Labuda Richard, Royston Thomas J, Oshinski John N, Iskandar Bermans, Loth Francis
Integrative Bioscience Institute, Ecole Polytechnique Fédérale de Lausanne, Lausanne, Switzerland.
J Biomech Eng. 2010 Nov;132(11):111007. doi: 10.1115/1.4000089.
Full explanation for the pathogenesis of syringomyelia (SM), a neuropathology characterized by the formation of a cystic cavity (syrinx) in the spinal cord (SC), has not yet been provided. It has been hypothesized that abnormal cerebrospinal fluid (CSF) pressure, caused by subarachnoid space (SAS) flow blockage (stenosis), is an underlying cause of syrinx formation and subsequent pain in the patient. However, paucity in detailed in vivo pressure data has made theoretical explanations for the syrinx difficult to reconcile. In order to understand the complex pressure environment, four simplified in vitro models were constructed to have anatomical similarities with post-traumatic SM and Chiari malformation related SM. Experimental geometry and properties were based on in vivo data and incorporated pertinent elements such as a realistic CSF flow waveform, spinal stenosis, syrinx, flexible SC, and flexible spinal column. The presence of a spinal stenosis in the SAS caused peak-to-peak cerebrospinal fluid CSF pressure fluctuations to increase rostral to the stenosis. Pressure with both stenosis and syrinx present was complex. Overall, the interaction of the syrinx and stenosis resulted in a diastolic valve mechanism and rostral tensioning of the SC. In all experiments, the blockage was shown to increase and dissociate SAS pressure, while the axial pressure distribution in the syrinx remained uniform. These results highlight the importance of the properties of the SC and spinal SAS, such as compliance and permeability, and provide data for comparison with computational models. Further research examining the influence of stenosis size and location, and the importance of tissue properties, is warranted.
脊髓空洞症（SM）是一种神经病理学疾病，其特征是脊髓（SC）中形成囊性空洞（空洞），目前尚未对其发病机制给出完整解释。有假说认为，蛛网膜下腔（SAS）血流阻塞（狭窄）导致的脑脊液（CSF）压力异常是患者空洞形成及随后疼痛的潜在原因。然而，详细的体内压力数据匮乏使得对空洞的理论解释难以统一。为了了解复杂的压力环境，构建了四个简化的体外模型，使其在解剖学上与创伤后脊髓空洞症和与Chiari畸形相关的脊髓空洞症相似。实验几何结构和特性基于体内数据，并纳入了相关要素，如逼真的脑脊液流动波形、脊髓狭窄、空洞、柔性脊髓和柔性脊柱。SAS中存在脊髓狭窄会导致脑脊液（CSF）峰峰值压力波动在狭窄部位的头侧增加。同时存在狭窄和空洞时的压力情况较为复杂。总体而言，空洞与狭窄的相互作用导致了舒张瓣膜机制和脊髓的头侧张紧。在所有实验中，阻塞均显示会增加并分离SAS压力，而空洞内的轴向压力分布保持均匀。这些结果突出了脊髓和脊髓SAS特性（如顺应性和渗透性）的重要性，并为与计算模型进行比较提供了数据。有必要进一步研究狭窄大小和位置的影响以及组织特性的重要性。
