Spinal cord injury: is monitoring from the injury site the future?

Pressure reactivity and compensatory reserve

Pressure reactivity is the ability of smooth muscle in the walls of arteries and arterioles to respond to changes in arterial pressure to keep blood flow constant. We define spinal pressure reactivity index (sPRx) as the running correlation coefficient between ISP and MAP. Therefore, ^–1???sPRx???⁺1. When sPRx ?0, spinal cord pressure reactivity is intact and when sPRx 0, pressure reactivity is impaired. sPRx for TSCI is analogous to the pressure reactivity index (PRx) for TBI [25, 35].

The Monro-Kellie doctrine states that inside the adult skull there is blood, cerebrospinal fluid (CSF), and brain tissue in a state of volume equilibrium; an increase in volume of one component is compensated by an equivalent decrease in volume of another. A small increase in brain volume does not lead to increases in ICP because CSF and venous blood are displaced into the spinal canal. Once the ICP is ~25 mmHg, small increases in brain volume cause marked elevations in ICP. This is the basis of an exponential relationship between ICP and intracranial volume and the concept of RAP, which is a running correlation coefficient (R) between mean ICP amplitude (A) and ICP pulse amplitude (P). RAP ~0 indicates good compensatory reserve, whereas RAP ~1 indicates that ICP rises greatly with a small increase in volume [25]. Here, we argue that the Monro-Kellie doctrine may also apply to the injured cord. After severe TSCI, the pia is damaged, evidenced by the observations that the injured cord appears swollen on MRI [16] and, at the injury site, subdural ISP equals intraparenchymal ISP [17]. Spinal cord swelling may generate forces radially and rostro-caudally. Since most neuronal fibers run rostro-caudally, cord edema will produce radial rather than rostro-caudal cord expansion. The denticulate ligaments and nerve roots may also restrict rostro-caudal cord expansion. If rostro-caudal spinal cord expansion were possible, then the spinal cord above the injury would be displaced upward whereas the spinal cord below the injury would be displaced downward. Such displacements are not seen on MRI scans; instead, there is radial swelling of the injured cord against the dura. The observations that, after a laminectomy, the dural sac diameter at the injury site appears the same as above or below, and that ISP at the injury site remains high, suggest that the spinal dura is non-distensible. Thus, as the injured cord swells, the compensatory mechanisms of displacing CSF and venous blood become exhausted and ISP rises. This means that the injury site probably obeys the Monro-Kellie doctrine and the concept of compensatory volume reserve likely applies, quantified using spinal RAP (sRAP) by analogy with brain RAP [13, 14]. sRAP ~0 indicates good pressure-volume compensatory reserve and, when RAP ~1, the swollen spinal cord is on the steep part of the pressure-volume curve. We showed that as ISP rises 10 mmHg, sRAP increases, and as SCPP rises 40 mmHg, sRAP decreases [13, 14].