The influence of coughing on cerebrospinal fluid pressure in an in vitro syringomyelia model with spinal subarachnoid space stenosis

BACKGROUND: The influence of coughing, on the biomechanical environment in the spinal subarachnoid space (SAS) in the presence of a cerebrospinal fluid flow stenosis, is thought to be an important etiological factor in craniospinal disorders, including syringomyelia (SM), Chiari I malformation, and hydrocephalus. The aim of this study was to investigate SAS and syrinx pressures during simulated coughing using in vitro models and to provide information for the understanding of the craniospinal fluid system dynamics to help develop better computational models. METHODS: Four in vitro models were constructed to be simplified representations of: 1) non-communicating SM with spinal SAS stenosis; 2) non-communicating SM due to spinal SAS stenosis with a distensible spinal column; 3) non-communicating SM post surgical removal of a spinal SAS stenosis; and 4) a spinal SAS stenosis due to spinal trauma. All of the models had a flexible spinal cord. To simulate coughing conditions, an abrupt CSF pressure pulse (~ 5 ms) was imposed at the caudal end of the spinal SAS by a computer-controlled pump. Pressure measurements were obtained at 4 cm intervals along the spinal SAS and syrinx using catheter tip transducers. RESULTS: Pressure measurements during a simulated cough, showed that removal of the stenosis was a key factor in reducing pressure gradients in the spinal SAS. The presence of a stenosis resulted in a caudocranial pressure drop in the SAS, whereas pressure within the syrinx cavity varied little caudocranially. A stenosis in the SAS caused the syrinx to balloon outward at the rostral end and be compressed at the caudal end. A >90% SAS stenosis did not result in a significant Venturi effect. Increasing compliance of the spinal column reduced forces acting on the spinal cord. The presence of a syrinx in the cord when there was a stenosis in the SAS, reduced pressure forces in the SAS. Longitudinal pressure dissociation acted to suck fluid and tissue caudocranially in the SAS with a stenosis. CONCLUSIONS: Pressures in the spinal SAS during a simulated cough in vitro had similar peak, transmural, and longitudinal pressures to in vivo measurements reported in the literature. The pressure wave velocities and pressure gradients during coughing (longitudinal pressure dissociation and transmural pressure) were impacted by alterations in geometry, compliance, and the presence of a syrinx and/or stenosis.