In this issue of the journal, von Aspern et al. report on an experimental study with the objective of investigating near-infrared spectroscopy (NIRS) as a possible means of intraoperative spinal cord perfusion monitoring [ 1 ]. The underlying hypothesis is that spinal NIRS signals not only indicate paraspinal tissue perfusion, but also allow inferences on actual parenchymal spinal cord perfusion. Thus, NIRS might help by serving as a mode of indirect spinal cord perfusion assessment, detect insufficient spinal cord blood flow and thus lead decision-making, regarding operative steps and neuroprotective measures in the operation theatre.

Paraspinal and intraspinal compartments of the spinal cord collateral network are distinctly different with regard to the characteristics of anatomical collateral vessels [ 2 ]. In the paraspinal muscles, an extensive network of very small, immature, prearteriogenetic arterioles can be found which primarily connect neighbouring segments longitudinally. In contrast to this, the intraspinal system consists of a network of epidural arterial arcades, with one circular or pentagonal arterial connection located on the back of every single vertebral body. These arcades connect segmental flow in a latero-lateral and a longitudinal fashion. They are connected to anterior radiculo-medullary arteries (ARMAs), which in turn arise in a highly variable manner. ARMAs connect the paraspinal collateral inflow, as well as the system of epidural arcades, to the anterior spinal circulation. These anatomical details have been studied and confirmed in human and animal cadaver research [ 3 ].

On the basis of the assumption that the paraspinal arteriolar connections are prearteriogenic—in patients with chronic degenerative calcific aortic pathologies, these form large, cork-screw-shaped arteriogenic collaterals as in the lower limb muscle in the setting of peripheral artery disease—the question of a time-dependent difference between the two systems is obvious. In another recent report (own data, accepted for publication, in press), a study describing the effects of depriving the spinal circulation of its inflow into the system of epidural arcades in 30 animals is presented. It was possible to directly demonstrate the function of the epidural arcades as the immediate backup system: deprived of epidural arcades, and thus depending on paraspinal collateral inflow exclusively, animals showed higher levels of cerebrospinal fluid pressure, marked drops in local spinal cord blood flow levels and were not able to generate reactive spinal cord hyperaemia. In addition, they did not regain sufficient spinal cord perfusion pressures or spinal cord blood flow levels. Most importantly, almost all of these animals suffered clinical paraplegia. The system of epidural arcades, which is part of the intraspinal collateral compartment, is thus the immediate backup system providing spinal cord integrity in the acute setting without chronic degenerative aortic disease, as is the case in all currently known porcine aortic surgical models or also in young acute aortic dissection patients.

If one poses the question if NIRS can be a suitable mode of monitoring spinal cord perfusion, or oxygenation, one needs to realize that NIRS signals will be, to a large extent, reflecting paraspinal muscle oxygenation. The reasons for this are the limited signal tissue depth on the one hand and, on the other hand, the massive muscular and vascular paraspinal muscle volume in pigs as well as in humans. The question thus needs to be phrased: is NIRS monitoring of paraspinal muscle indicative of spinal cord oxygenation? After the occlusion of dorsal segmental inflow acutely in healthy pigs without degenerative aortic pathology, and thus without chronic segmental artery ostia occlusion and consequently without mature paraspinal collateral vessels, one expects a clear drop in muscular NIRS signal. This could be successfully shown by the authors. Cranial and caudal inflow into the system of the epidural arcades is, however, very unlikely to be detected due to the small artery sizes and their intraspinal localization. Were ARMAs perfused during segmental artery occlusion? Were epidural arcades perfused during the procedure? These are questions which need new and innovative ideas developed in large animal models in order to be answered.

The authors successfully demonstrated a correlation of paraspinal NIRS and directly quantified paraspinal muscle and spinal cord tissue. A positive statistical correlation in an animal model, however, does not make an actual predictive value of a monitoring device in the human operating room, which is an intrinsic problem of large animal experimental research. As a consequence, the reported results should be interpreted as an important first step, posing several more questions: what is the predictive value of paraspinal muscle oxygenation with regard to perfusion of the system of epidural arcades and the spinal cord? What is its predictive value in the actual clinical setting? Do chronic degenerative aortic disease and postarteriogenetic paraspinal collaterals as found in most patients impact NIRS findings?

A large prospective trial, with enough clinical adverse end-points in order to be of conclusive value, will hopefully show the true predictive value of paraspinal NIRS in the future.

Funding

There is no Funding specifically for this paper. Regarding the own work cited Funding is: Deutsche Forschungsgemeinschaft, German Research Foundation (DFG) Grant Nr. KA 3872/2-1.

REFERENCES

1

von Aspern
K
,
Haunschild
J
,
Hoyer
A
,
Luehr
M
,
Bakhtiary
F
,
Misfeld
M
et al. .
Non-invasive spinal cord oxygenation monitoring: validating collateral network near-infrared spectroscopy for thoracoabdominal aortic aneurysm repair
.
Eur J Cardiothorac Surg
2016
;
in press
.

2

Etz
CD
,
Kari
FA
,
Mueller
CS
,
Silovitz
D
,
Brenner
RM
,
Lin
HM
et al. .
The collateral network concept: a reassessment of the anatomy of spinal cord perfusion
.
J Thorac Cardiovasc Surg
2011
;
141
:
1020
8
.

3

Gillilan
LA
.
The arterial blood supply of the human spinal cord
.
J Comp Neurol
1958
;
110
:
75
103
.