The spinal cord is composed of the neurons and supporting glial tissue transmitting information to and from the brain to the remainder of the body. The spinal cord begins rostrally at the base of the skull at the region of the foramen magnum, continues through the cervical and thoracic region, and terminates as the conus medullaris. The conus medullaris typically ends at the L1-L2 interspace but varies in individuals from T10 to the sacrum (1).

The spinal cord parenchyma is composed of central gray matter with white matter tracts circumferentially around the periphery. The spinal cord is enveloped inside the dural sac and in turn is surrounded by cerebral spinal fluid (CSF). The spinal cord transmits motor information through the corticospinal tracts to the upper and lower extremities providing muscle strength. In addition, it receives and transmits sensory input through multiple tracts including the posterior columns and lateral spinothalamic tracts. These tracts are believed to each transmit unique sensory modalities (i.e., pain transmitted through the spinothalamic tracts) (2). In addition, the spinal cord also provides control of the bowel, bladder, and sexual function via the autonomic nervous system.

Injury to the spinal cord itself can result in a variable and numerous clinical symptoms. Spinal cord injury can range in severity from mild or no motor dysfunction, sensory dysfunction, or neuropathic symptoms to the most severe pattern of complete spinal cord injury. A “complete” spinal cord injury (ASIA A) results in loss of all sensory and voluntary motor function caudal to the lesion, including loss of bowel and bladder function (3,4).

The blood supply to the spinal cord parenchyma, much like the cerebral neurologic tissue, is controlled through autoregulation processes (5,6). It is composed of a complex arterial and venous network. There is typically a single anterior spinal artery and two paired posterior spinal arteries that supply the ventral and dorsal portions, respectively, of the spinal cord. These arteries are directly supplied through the spinal radicular arteries, which are branches off the thoracic and lumbar segmental vessels. In the cervical region, these arteries arise from the vertebral arteries, carotid and subclavian system, while in the thoracic spine segmental arteries arise from intercostal arteries. Once penetrating the dura, these arteries divide and form an arterial network over the median sulcus and the ventral portion of the column in addition to two posterior lateral arteries over the posterolateral columns and dorsal nerve roots. These arterial networks have greater variability and abundance over the cervical and thoracolumbar spinal cord enlargements where there are the greatest metabolic needs for the nervous tissue.

Dommisse (7) reported that 80% of cervical medullary radicular feeders to the cervical spinal cord are composed of vertebral artery branches, while the remaining 20% are off the deep cervical superior intercostal vessels. This is as opposed to the thoracic and lumbar spinal cord medullary arteries that arise exclusively from the aortic segmental arteries. In Dommisse’s manuscript, the microsurgical dissection of 35 cadavers showed that on average patients had 8 ventral and 12 dorsal radicular arteries supplying their longitudinal spinal arteries. However, the number of spinal arteries has been shown by others to be quite variable, ranging between 2 to 17 ventrally and 6 to 25 dorsally (8, 9 and 10).

The venous system of the spinal cord surrounds the spinal cord’s periphery and has a similar distribution to the arterial system. It differs in the distribution of the three longitudinal trunks consisting of a single anterior medial and anterior lateral vein into which the sulcal vein drains. Additionally, there is a dorsal longitudinal venous trunk that drains the dorsal portion of the spinal cord. One unique feature of the spinal canal’s epidural venous plexus is that it is a valveless system, and thus, retrograde flow or reflux through spinal venous system can occur (11).

The majority of literature concerning iatrogenic spinal cord injury relates to treatment of pediatric spinal deformities such as idiopathic adolescent scoliosis. However, there is some of literature concerning cervical surgery and spinal cord injury. Flynn noted in a paper reviewing 82,114 ventral cervical operations that the onset of a new postoperative neurologic deficit had an incidence of 0.3% (12). In addition, Lee et al. (13) reviewed 1,445 ventral cervical cases in a large academic spinal cord injury center. There were two patients (0.1%) with new postoperative neurologic deficits due to spinal cord injuries. Both of these patients’ deficits were after cervical corpectomies. Both patients had preoperative neurologic deficits as well as one patient having severe ossification of posterior longitudinal ligaments. It should be noted as a distinction in that in the cervical population there appears to be the risk of applying traction to the spinal cord due to the increased mechanical flexibility given the absence of the rigid thoracic cavity. On the other hand, the cervical spinal cord appears to be much more resistant to hypotension most likely due to its abundant vascular supply.

It appears that there are multiple etiologies of intraoperative neurologic losses and monitoring alerts. One cause may be spinal cord hypoperfusion due either to direct blood supply interruption or hypotension. This appears to be much more common in the thoracic spinal cord region than in the cervical spinal cord. There is always the possibility of a direct traumatic effect due to instrumentation or blunt forces directly onto the spinal cord. This could also be induced by surgical manipulations. Finally, spinal cord compression or distraction can result from deformity correction as seen in the thoracic spine.

The overall incidence of iatrogenic cervical spinal cord injuries is difficult to define or calculate. There are numerous possible etiologies or mechanisms from which a spinal cord injury can occur, and several of these have been reported in the literature (14). For example, during the intubation of a patient with a severely spondylitic and stenotic cervical spinal canal, the hyperextension required for intubation can cause compression of the spinal cord resulting in a central cord injury (15). Another example is the inadvertent injection into the spinal cord itself or into the epidural venous or arterial system during an epidural steroid injection or during an image-guided biopsy or myelogram (16). There is also the possibility of an acute spinal cord injury during ventral or dorsal surgical decompression of the spinal cord (12,17). Overall, the incidence of a significant neurologic injury after spinal cord or canal surgery is considered to be rare due to the limited number of case reports or series of these occurrences (12,14, 15, 16, 17 and 18). In order to have a more focused outlook, the scope of this chapter will be on iatrogenic spinal cord injuries as a direct result of operative treatments of all spinal disorders.

In 1998, Bridwell et al. (19) performed a retrospective study of 1,090 spinal deformity patients. In this series, the majority of patients were treated for idiopathic adolescent scoliosis and all had normal neurologic exams of their lower extremities with normal bowel and bladder function preoperatively. The authors reported four cases (0.38%) that developed a major neurologic deficit postoperatively. These authors then performed a multivariant analysis of the potential etiologies of these neurologic deficits. This analysis noted that all four patients had anterior-posterior surgical procedures performed (p = 0.009) and preoperative hyperkyphosis of the spine (p = 0.0006), as well as unilateral convex segmental vessel ligation during exposure (19). It thus appears that the injured patients were likely to be more complex cases, therefore having a potentially higher risk of neurologic injury due to a higher complexity of the procedure. Hyperkyphosis was also identified as a predictor of neurologic deficit; however, this disorder is typically treated from a ventral approach, which can result in lengthening of the spinal column, with secondary stretching or lengthening of the spinal cord, which has been shown to potentially cause damage to neurologic tissue (20, 21 and 22).