The spinal column is comprised of 33 vertebrae: 7 cervical vertebrae, 12 thoracic vertebrae, 5 lumbar vertebrae, sacrum (5 fused vertebrae), and coccyx (4 fused vertebrae). Each vertebra, except C1, has a vertebral body, bilateral pedicles, bilateral lamina, bilateral transverse processes, a spinous process, and 4 articular processes. Vertebrae connect to each other via superior and inferior facets and inter-vertebrae disks. Two posterior lamina, two lateral pedicles and vertebra body anteriorly form the vertebral canal where the spinal cord lies. C1 (Atlas) lacks vertebrae body and consists of an anterior arch and tubercle, posterior arches, spinous process, and lateral masses. C2 (Axis) has a strong odontoid process that articulates with C1.

The spinal cord is a continuation of the medulla at the foramen magna and extends to the conus medullaris at the first or second lumbar vertebra in the vertebral canal in adults. On a cross-sectioned view, the cord is composed of gray matter and white matter. The gray matter resembles the shape of the letter H, surrounds the central canal, and contains cell bodies of neurons. It is divided into four main columns: the dorsal horn, intermediate horn, ventral horn, and lateral horn (see Fig. 18.1) [1]. The white matter contains myelinated and unmyelinated nerve fibers that carry information through the cord. The white matter is divided into the dorsal column (or funiculus), lateral column and ventral column. The cord has four regions (cervical, thoracic, lumbar and sacral) and two bulges at the cervical and lumbar region. The dorsal roots and ventral roots join together to form 31 pairs of spinal nerves that exit from spinal foramen. The spinal cord is surrounded with three meninges: pia, arachnoid, and dura.

The anterior spinal artery, two posterior spinal arteries, and radicular arteries are the main arteries that supply blood to the spinal cord. The vertebral arteries at the medulla level branch off to form the anterior spinal artery, which supplies the anterior two-thirds of the cord, while the posterior spinal arteries arising from either vertebral arteries or posterior inferior cerebellar arteries on the same side supply the posterior one-third. The radicular arteries that originate from the segmental arteries of aorta further augment the blood supply to spinal cord. The Artery of Adamkiewicz is the largest segmental feeder in the thoracolumbar region. Injury to those segmental arteries can cause anterior spinal cord ischemia, resulting in paralysis.

The spinal cord blood flow (SCBF) is autoregulated and kept relatively constant. Average SCBF is about 60 ml/100 g/min, but the blood flow to gray matter is four times higher than in white matter. SCBF is well maintained at the mean arterial blood pressure (MAP) between 60 and 120 mmHg [1]. Blood pressure that is lower than the autoregulation lower limit causes ischemia to the spinal cord. Hypoxia and hypercarbia increase SCBF, while hypocarbia reduces SCBF.

Spine surgery is indicated for following conditions:

Cervical spondylotic myelopathy (CSM) is a syndrome produced by central spinal canal stenosis and compression of the spinal cord due to cervical spondylosis, a progressive degenerative process affecting the vertebral body and disk. CSM is the most common cause of myelopathy in older adults.

The common possible manifestations are summarized [2] as following:

Magnetic Resonance Imaging is used to confirm the diagnosis. The Nurick grading system [3] classifies the severity of CSM from the least severe, grade 1, to the most severe, grade 5 based on gait abnormality (see Table 18.1).

Central Cord Syndrome (CCS) is the most common incomplete spinal cord injury and is characterized by a disproportionately greater motor impairment in the upper extremities than in lower extremities, bladder dysfunction, and various sensory losses below the level of injury. The mechanism involves the compression of the cord by osteophytes and infolded ligamentum flavum. Patients with CSM can suffer CCS after minor neck injury without evidence of spinal fracture. Hyperextension of neck should be avoided during direct laryngoscope in patients with CSM to prevent neurological damage.

Anterior cord syndrome (ACS) results from injury to the anterior spinal artery or compression of the anterior cord. It is characterized by variable motor impairment, pain, and temperature sensation impairment with preservation of proprioception below the level of injury.

Brown-Sequard syndrome an incomplete spinal cord injury and results from hemisection of spinal cord. It is manifested as ipsilateral loss of motor and proprioception with contralateral loss of pain and temperature sensation. It usually occurs after penetrating trauma.

Spinal shock is a neurogenic shock caused by an interruption of sympathetic output from the spinal cord and unopposed parasympathetic activity after acute spinal cord injury (SCI). The severity of spinal shock is related to the severity and completeness of SCI. Loss of sympathetic activity below the level of injury results vasodilation and decrease in venous return, leading to hypotension. Bradycardia can occur if the SCI is above T6 level. Treatment includes fluid therapy and the use of vasopressors to support blood pressure in order to maintain MAP > 85 mmHg for the first week following the initial injury.

The ASIA impairment scale is used to define the severity of a spinal cord injury. It combines the sensory and motor deficits with completeness of the injury to classify the injury into five grades from Grade A to grade E. The ASIA impairment scale evaluates and scores 10 key muscle groups and 28 dermatomes for both light touch and pin prick.

Spinal surgery poses potential risks to the spinal cord, nerve roots, caudal equina, and peripheral nerves. Although the overall incidence of NND is small, the consequence of neurological complications, such as spinal cord paralysis, could be disastrous for both patient and family. Revision surgery, spinal fusion, use of implants, and surgical approach may affect the rate of NND. The most recent data from the Scoliosis Research Society shows that the overall rates of new nerve roots, cauda equina, and spinal cord deficits for 108,419 patients were 0.61, 0.07, and 0.27% [4].

The mortality of spinal surgery is low and varies depending on the location of the procedure. Lumbar spine (range from 0.07 to 0.52%) and cervical spine surgery (range from 0.1 to 0.8%) carry lower mortality compared to thoracic spine surgery (range from 0.3 to 7.4%) [5]. Recent studies from the Scoliosis Research Society Morbidity and Mortality database showed that the overall mortality rate is 1.8–1.9 per 1000 spinal deformity procedures [6, 7]. However, mortality increases in patients over 60 years of age. High ASA scores, fusion and implants are associated with an increased mortality rate. The main causes are respiratory (respiratory failure, pneumonia, pulmonary embolism, etc.), cardiac (cardiac failure, myocardial infarction, or cardiac arrest), sepsis, multi-system organ failure, stroke, and blood loss. Although mortality due to intraoperative blood loss accounted for 4% of all mortality, it can be prevented if careful planning and intraoperative management are implemented.

There are three goals of IONM during spine surgery. The principle goal of IONM is to prevent injury to the spinal cord and nerve roots by way of surgical manipulation and instrumentation. Secondly, IONM is used to prevent ischemia due to hypoperfusion to the spinal cord. The third goal is to prevent peripheral nerve injury by way of inappropriate positioning.

SSEPs are electric responses from peripheral nerve stimulations. It was introduced in the 1980s and is indicated for monitoring spinal cord integrity in scoliosis correction, spinal cord tumor, spinal decompression, and instrumentation surgeries. SSEPs can be recorded along sensory pathways. Cortical SSEPs are recorded from the electrodes placed on scalp according to the international 10–20 system. The most common peripheral stimulating sites are the ulnar or medium nerve for upper extremity SSEPs, and the posterior tibia nerve or common peroneal nerve for lower extremity SSEPs. SSEPs voltage is very small compared to EKG and EEG; it requires averages to obtain high quality waveforms for monitoring by reducing 60 Hz interferences. SSEP is characterized as amplitude and latency that are affected by many factors. SSEP waveforms P14 and N20 from upper extremity and N34 and P37 from lower extremity are commonly used for monitoring. The baseline SSEPs must be obtained before the surgical incision.

SSEPs are primarily mediated by the dorsal column-medial lemniscal system. The anatomy of this sensory pathway includes peripheral nerves, first-order neurons in the dorsal ganglion, second-order neurons with nucleus gracilis and cuneatus, third-order neurons in the thalamus, and sensory cortex. Peripheral nerves enter the dorsal root ganglion where primary sensory neurons receive sensory input. The central axons of sensory neurons ascend ipsilaterally within the fasciculus gracilis and fasciculus cuneatus to the caudal medulla where the neuron fibers synapse with second-order neurons within the nucleus cuneatus and nucleus gracilis. The axons of second-order neurons decussate and ascend as medial lemniscus to third-order neurons in the ventral posterior lateral nucleus of the thalamus. The third-order neurons in the thalamus project axons to the primary somatosensory cortex in the contralateral posterior gyrus. When the peripheral nerves are stimulated, action potentials propagate along the pathway and generate the SSEPs that can be recorded. Any disruption to the sensory pathway can lead to loss of SSEP production. Surgical manipulation and instrumentation during spinal surgery could result in spinal cord and nerve root injury. SSEP monitoring will alert both the surgeons and anesthesiologists for any impending spinal cord injury, thus allowing surgeons to correct reversible causes in time, while the anesthesiologists affirm physiological and anesthesia stability.

Anesthetics affect cortical SSEPs but have minimal effect on subcortical SSEPs. The deeper the anesthesia is, the more SSEPs are suppressed. It is very important to keep anesthetic level steady state while SSEP’s are recorded.