Cardiorespiratory modulation of cerebrospinal fluid flow in the presence of spinal subarachnoid space obstruction

Traumatic injury to the spinal cord disrupts cerebrospinal fluid (CSF) flow in the spinal subarachnoid space (SAS) and can precipitate cystic accumulation of fluid within the tissue - syringomyelia. The dynamic processes that lead to syringomyelia from an obstruction to CSF flow are not clearly defined. Investigations into CSF circulation have revealed that physiological variables, including respiration, heart rate, and blood pressure, influence CSF flow. Spinal cord injury affects each of these variables, however it is unknown how these variables influence CSF flow when the SAS is obstructed.

We examined the separate effects of respiratory pressure (spontaneous breathing and positive pressure ventilation), heart rate (tachycardia), and blood pressure (hypertension) on CSF flow in a rodent model of SAS obstruction. A C7 - T1 laminectomy was performed in male Sprague-Dawley rats, followed by a suture tied around the spinal dura to obstruct CSF flow. SAS and intraparenchymal hydrodynamics of intracisternally-infused fluorescent tracers were investigated through real-time intraoperative and epifluorescence imaging, respectively.

A SAS obstruction significantly reduced spinal CSF flow. In the presence of SAS obstruction, tachycardia may initially reduce spinal CSF flow whilst hypertension reduces CSF influx above the obstruction. In the brain, both hypertension and spontaneous breathing increased CSF tracer influx. SAS obstruction reduced tracer influx into the brain in spontaneously breathing animals only.

Acute changes to respiratory pressure, heart rate, and blood pressure have spatial- and time-dependent effects on CSF flow in the spinal cord and brain. Correcting for cardiorespiratory dysfunction in people living with SCI may disrupt the processes leading to syringomyelia, but further investigations are required.