“The Spine” is often thought of a single unit, as is “the liver” or “the intestines,” but the concept is somewhat misleading. “The Spine” is really a structure with two parts. The first part, the bony spine, serves dually to support the body and to protect the vulnerable neurological structures inside. The second of the two parts of the spine, the neurological spine, is more than just a “coaxial cable” connecting the brain to the remainder of the body. The neurological spine, the spinal cord, is a complex extension of the central nervous system, capable of learning and adapting. When the bony protection fails, the spinal cord (and possibly the cervical-medullary brainstem or the cauda equina) is traumatized with multiple systemic consequences. These consequences may result in a catastrophic injury. To better develop treatments for spinal cord injury, the pathophysiology of the injury continues to be thoroughly studied [1,2,3,4,5,6,7,8]. In this chapter, traumatic forces are emphasized, but the reader should keep in mind that vascular, infectious, or toxic/metabolic/ischemic damage to the spinal cord may present in a patient with a similar profile of deficits and clinical challenges.

Injury to the spine can be thought of in two phases. The first phase called “Primary Injury” is the moment when excessive kinetic energy is transmitted to the spinal cord in the moment of trauma. The “Secondary Injury” follows immediately after that as the damage from the primary injury creates biologic sequelae. Secondary injury in spinal cord injury (SCI) is believed
to involve the release of neurotoxic chemicals, creation of free radicals, recruitment/activation of macrophages, disruption of the blood-spinal cord barrier, generation of lipid peroxidation, presence of oxidative cell stress, and other events [9]. Even without a complete understanding of all of the variety of events in spinal cord injury, it is believed that secondary injury can be modulated with appropriate therapeutic interventions. These include, but are not limited to, decompressive surgery [10,11] steroids [12,13,14,15,16,17], hypothermia [18,19,20,21,22,23], immunomodulation [24,25,26], nutrition [27,28], and other therapies.

Given the tremendous socioeconomic and psychosocial impact of spinal cord injury, there have been several human clinical trials [12,15,29,30,31,32] to date in an effort to limit the secondary injury, but there is no one therapeutic strategy that is clearly effective in affecting outcome.

Surgical management of spinal cord injury is also still under debate, especially in terms of the timing and utility of the surgical intervention [11,33,34]. Fortunately, there are treatments available for the spinal cord injured patients such as physical therapy, outpatient therapy, and adaptive therapies [35,36,37,38,39,40].

The future of treatment for spinal cord injured patients will likely involve a combination of techniques, such as applying neurotrophic factors, nerve grafting, cellular injection, hypothermia, tissue engineering, neuromodulation, and other innovative approaches. This chapter addresses the many problems unique to the management of a spinal cord-injured patient. The specific surgical treatments for each pathologic entity are beyond the scope of this chapter.

The Edward Smith Papyrus [41,42,43] represents one of the earliest records of spinal cord injury. Dating back approximately to 2500 B.C.E., there is a case report by Imhotep, a physician and architect to the Pharoh Zoser III. In this Papyrus, he describes 48 trauma cases, 6 of which involve vertebral column injury. In the most famous case, Imhotep describes a case of “crushed vertebra” where “incontinence, paralysis, and loss of sensation” follow. In his medical opinion, treatment was not to be pursued. The Greek Physician Galen, some 3000 years later, conducted animal experiments noting the difference in effects between longitudinal and horizontal cord transactions [41]. Only 500 years after Galen, the laminectomy was introduced by Paulus. In 1543, Vesalius then introduced remarkably detailed anatomical drawings of human anatomy. In the early twentieth century, despite significant scientific and engineering advancements, the opinion of Imhotep still reigned true and traumatic SCI was felt to be a terminal condition.

The recognition that spinal cord injury should not be viewed as a terminal condition owes much to the insights of Sir Ludwig Guttmann (UK) and Sir George Bedbrook (Australia). In the aftermath of World War II, these two physicians were at the forefront of refusing to accept the inevitable prognosis for SCI [44,45]. They pioneered the idea that the sequelae of SCI do not need to be fatal and that an intensive regiment of physical therapy and care may be life-saving and life-improving.

There are more than 200,000 people in the United States living with a chronic SCI. Each year, approximately 11,000 Americans are afflicted with this condition [46]. More than half of the people who sustain SCIs are 15 to 29 years old (CDC data: http://www.cdc.gov/ncipc/factsheets/scifacts.htm). Approximately 80% of the injured are male [46]. There is a growing trend of seeing SCI among middle-aged and elderly patients due to improved lifestyle habits and improved survivability of injuries. Data collected from North America, Europe, and Australia confirm similar results [47]. The cervical spine is the most commonly injured site, with the remaining injury sites divided between thoracic, thoracolumbar, and lumbosacral levels [48].

The mechanism of injury can be blunt (e.g., motor vehicle accident, fall, assault) or penetrating (e.g., gunshot wound, knife, and other sharp object). Approximately 50% of the injuries derive from a motor vehicle accident, with the remainder primarily from falls (23%), violence (14%), and sports (9%) [46].

As a trauma patient is assessed through the initial “ABCDE” of Advanced Trauma Life Support, the physician must perform a neurologic examination. The neurologic examination is of paramount importance localizing the probable site of injury as well as to assess the severity of injury to the spinal cord. Once the SCI is identified, the physician can classify the injury by mechanism (e.g., penetrating vs. blunt), level (cervical, thoracic, lumbar), and degree of neurological impairment (often through the American Spinal Injury Association [ASIA] scale).

To assess the degree of neurologic injury, particular attention is paid to the motor, sensory, reflex, and rectal examinations. Based on the degree of functional impairment, the ASIA has proposed an easily used scoring system (Table 163.1). The neurologic injury is categorized using this score and by noting lowest normal segmental level. (When referring to the “level” of injury, it is important to note that the level is the corresponding “neurological level” or dermatological level and not the “bony level.” For example, consider a patient shot in the spine. A neurosurgeon evaluates the patient and states that the patient has a complete neurological injury at the “L4” level. This means that the lowest spinal level with completely normal function is at the L4 neurons of the spinal cord. The bony disruption, however, may be at approximately T12, which corresponds to the locations of neurons that innervate L5 and below.)

In this classification scheme, the severity of injury is denoted by Grade, followed by letters A-E. The letters serve as shorthand to classify the severity of injury as it relates to sensory and motor function. Grade A (complete) denotes a complete injury with no sensory or motor function preserved in sacral segments S4–5. Grade B (incomplete) denotes sensory, but not motor function preserved below the neurologic level and extends through sacral segments S4–5. Grade C (incomplete) denotes motor function preserved below the neurologic level with muscle strength graded below antigravity strength. Grade D (incomplete) denotes motor function preserved below neurologic level with muscle strength graded more than or equal to antigravity strength, but not normal. Grade E denotes a normal
sensory and motor exam [49,50]. The grades have a prognostic feature. Complete recovery of function after a Grade A injury is unlikely. However, improvement of one or two grades is seen in more than 10% of patients. Some recovery is most likely to occur in Grade D injuries [51].

SCI may be also classified as complete or incomplete. In complete SCI, there is no preservation of motor function and/or sensation for three spinal segments below the level of injury. Complete injuries above T6 are usually associated with spinal shock. Spinal shock is characterized by: hypotension from interruption of sympathetics, bradycardia from unopposed vagal (parasympathetic) output, hypothermia, and transient loss of all neurologic function resulting in a flaccid paralysis and areflexia. Incomplete SCI may be further subclassified into specific neurological symptoms based on the anatomy of the injury.

Specific neurologic syndromes have been described for particular incomplete spinal cord injuries [52,53]. These syndromes include the anterior cord syndrome, the central cord syndrome, the posterior cord syndrome, Brown-Sequard (hemisection cord syndrome), conus medullaris syndrome, cauda equina syndrome, and cord concussion syndrome.

The anterior cord syndrome is characterized by complete paralysis and hypoalgesia (to pain and temperature) from damage to anterior and anterolateral column function below the level of injury, with preservation of proprioception (vibration and position sense) and light touch from posterior column function. This syndrome occurs most commonly after trauma focused at the anterior spinal cord as well as ischemia in the territory supplied by the anterior spinal artery, which supplies the corticospinal and spinothalamic tracts in the anterior 2/3 of the spinal cord. It is classified as an ASIA B injury.

The central cord syndrome is characterized by motor dysfunction more pronounced in the distal upper extremities than in the lower extremities (“man in a barrel”), accompanied by varying degrees of sensory loss and bladder dysfunction. The injury occurs characteristically after a hyperextension injury in elderly patients with acquired cervical stenosis from spondylosis or in athletes with congenital cervical stenosis. The injury can be seen in the absence of any clear radiographic disruption of the bones or ligaments. Most patients recover the ability to walk, with partial restoration of upper-extremity strength. It is associated with severe allodynia of the hands. (Allodynia is pain from stimuli that are not normally painful.)

The posterior cord syndrome is an uncommon presentation in which position sense, vibration sense, and crude touch are impaired due to injury to the dorsal columns or injury directed to the posterior of the spinal cord.

The Brown-Sequard syndrome, or hemisection cord syndrome, presents with ipsilateral paresis and loss of proprioception, touch, and vibration below the level of the lesion and the contralateral loss of pain and temperature sensation. This can be the result of penetrating injuries or asymmetrical lateral closed injuries resulting in a spinal cord hemisection, and is usually not seen in the pure form. Asymmetrical, lateral closed injuries are often confused with an ipsilateral brachial plexus injury.

The conus medullaris syndrome occurs with injuries at the thoracolumbar junction. This syndrome has components of both spinal cord and nerve root injury due to the dense population of nerve roots emerging from the caudal end of the spinal cord. Symmetric lower-extremity motor impairment and anesthesia with bowel, bladder, and sexual dysfunction are typically seen. There is typically a symmetric “saddle” area loss of sensory function. Spinal cord function recovery from this syndrome is less likely than recovery from nerve root injury. In cases of the cauda equina syndrome, partial recovery is possible with decompression [54]. Cauda equina injuries occur at spinal levels below the termination of the cord, typically at L1 or below.

Cord concussions present with transient neurologic symptoms followed by rapid resolution. These injuries are seen most commonly in athletes with low velocity hyperflexion or extension injuries of the cervical spine. Complete recovery is the rule; however, patients should be evaluated meticulously for severe stenosis or occult spinal instability and intraspinal hematomas. This is in contrast to “stingers or burners” that involve cervical nerve roots only. The issue of “return to play” [55,56,57,58,59,60] is especially important in the field of athletics. Currently, there is no agreed upon measure to predict which athletes are most at risk of further injury. However, “functional” stenosis [61] and anatomic measurements [56] may both play a role.

The injury to the spinal column and spinal cord involves the transfer of energy sufficient to disrupt the cell membranes and mechanical attachments of the ligaments, muscles, and joints. This results from movement and stressing of the spine beyond its biomechanical/physiological limits in hyperflexion/hyperextension, rotation, compression, or a combination thereof. Injury may result in retropulsion of materials (e.g., bone, cartilage, blood, foreign body) into the spinal canal. Disruption of the vertebral column may also damage the spinal cord within the canal (e.g., dislocation injuries) by reducing the spinal column diameter and compressing the spinal cord. The spinal cord may also be injured by direct laceration or transaction of the cord (e.g., bullet or knife injury). Direct crush, stretch, and shear injury to neurons within the spinal cord leads to immediate cell death.

Secondary injury occurs as the body responds to the damage from the primary injury. There are many mechanisms that initiate secondary injury. These include systemic hypoxia (e.g., hypotension from neurogenic shock or hypovolemic shock, hypoperfusion, etc), local vascular insufficiency (local hypoxia) from trauma, direct penetrating trauma, and spinal compression.

The secondary injury involves biochemical changes and the release of neurotoxic substances. Toxic substances, such as glutamate and free radicals contribute to cell damage and death. These biochemical changes lead to excitotoxicity, neurotransmitter accumulation, arachidonic acid release, free radical production, eicosanoid production, and lipid peroxidation. There are electrolytic shifts such as increased intracellular calcium, increased extracellular potassium, and increased intracellular sodium. The disruption in electrolytes is compounded with the loss of energy metabolism, as the neurons are unable to produce adenosine triphosphate (ATP). Within minutes to hours, oxidative stress leads to cell necrosis. Apoptosis follows further depletion of cells. Over the following days to months, demyelination occurs with the loss of oligodendrocytes. Glial scar formation and axonal degeneration/retraction follow [9]. The damage of the cord may be visualized as edema.

Because spinal cord-injured patients frequently also suffer polytrauma, they are susceptible to derangements of homeostasis. Cardiovascular and pulmonary compromise may affect perfusion and oxygen delivery to the spinal cord, exacerbating the damage. Recent work in animal models of SCI suggests that SCI itself may further disrupt homeostasis. There is evidence from animal models of SCI for a systemic inflammatory response capable of disrupting the cardiopulmonary and renal system [62]. Vasoactive substances released by injured cells
and endothelin released from damaged capillaries may also disrupt the spinal cord microcirculation. Ischemia may thus cause neurologic deficits to extend rostrally beyond the initially injured area [63,64].

Because cell death due to secondary injury is an ongoing process, it is believed that early pharmacologic intervention and maintenance of adequate tissue perfusion can salvage these neurons. Given that only 5% to 10% of the descending pathways are necessary for retention of some neurological function [4], even a modest preservation of axons during an injury could have a profound impact on the life of a person with spinal cord injury.

Care of the spinal injury patient begins in the field with Emergency Medical Services personnel. The “ABCDE” (Airway, Breathing, Circulation, Disability, Exposure) of Advanced Trauma Life Support are followed. Attention to maintaining a patent airway and the management of shock take precedence. The patient is immobilized with a rigid cervical collar and backboard for transportation to a trauma center. Intubation and helmet removal should be attempted only with strict attention to maintaining neck alignment. This is particularly important in unresponsive patients, as 3% to 5% of comatose patients have a coexisting cervical spine injury. Additionally, there may be a second site spinal injury, which occurs in 15% of SCI patients.

In the trauma center, the priority remains the maintenance of tissue oxygenation and perfusion, with particular attention to maintaining an adequate mean arterial blood pressure. In this regard, the spinal injury patient presents particular challenges. Immobilization of the cervical spine during intubation is essential and is best accomplished with fiberoptic or awake nasotracheal maneuvers. Mechanical respiratory efforts may be minimal when the injury level is C5 or higher. In these patients, muscular expansion of the rib cage is absent and diaphragmatic breathing may be weakened. Thus, intubation with inline stabilization using two physicians may be the only option to quickly establish airway control and ventilation. Caution should be exercised in suctioning the oropharynx, as this may stimulate autonomic reflex arcs, causing profound bradycardia and even cardiac arrest. The emergent cricothyroidotomy for airway access must also be considered.

Cervical and high thoracic injuries may result in spinal shock, which can severely complicate the management of a patient already in hypovolemic shock. The clinical picture is hypotension with an associated bradycardia and often hypothermia. Treatment is with mild fluid resuscitation and continuous intravenous inotropic infusions possessing alpha-adrenergic properties to increase the heart rate, cardiac output, and vasomotor tone. Dopamine, because of its mixed alpha-and beta-adrenergic effects, is a useful medication to treat spinal shock. Acutely symptomatic bradycardia should be treated with intravenous atropine. Monitoring with pulmonary atrial catheters (e.g., Swan-Ganz catheters) can help determine the adequacy of perfusion and cardiac output.

Associated extraspinal injuries are common and must also be ruled out. This would be assessed in the “D” and “E” sections of the assessment. Because spinal column injuries are typically the result of severe traumatic mechanisms, the incidence of associated cranial, thoracic, abdominal, and orthopedic injuries is high. Priority must be given to the most life-threatening injuries. If the patient is stable and cooperative, an exam to determine the level of injury (e.g., the ASIA scale) is performed.

The diagnosis of a spinal column injury is based on the clinical examination and radiologic investigations. In an awake, non-intoxicated patient, the absence of pain along the spinal axis is useful to rule out injury. In these patients, a low-velocity injury may require no x-rays, and a high-velocity injury requires only limited plain x-rays. It is essential that radiographic evidence of spinal column injury be correlated with the clinical examination, as 15% of patients have injuries at multiple spinal segments. X-ray, computed tomography, and magnetic resonance imaging investigations are needed in patients who are not able to fully cooperate with the neurologic examination.

Radiographs are useful not only for the detection of but also for the classification of injuries. The fracture types, as well as the degree of cord compression, are particularly important aspects of the injury that determine the management strategy. For the cervical spine, plain lateral x-rays must include the C7-T1 junction, as 31% of injuries occur between C6 and T1. In large, bulky patients, downward traction on the shoulders, a swimmer’s view, or a computed tomography scan of the cervical spine may be needed to properly visualize the cervicothoracic junction. Lateral x-rays allow evaluation of vertebral alignment (> 3 mm subluxation suggests instability), canal diameter (normal is > 12 mm), angulation of the intervertebral space (normal is < 11°), width of the interspinous gap, and the atlantodental interval (the distance between the anterior margin of the dens and the closest point on the anterior arch of C1, which should be 3 mm in adults). Soft tissue swelling in the prevertebral space is an indirect indicator of cervical spine injury (maximum prevertebral space in adults at C1 is 10 mm, C2–4 is 5 to 7 mm, and C5–7 is 22 mm).

In the thoracic and lumbar spine, anterior compression fractures and fracture dislocations are usually clearly visible on lateral x-rays. Splaying of the interspinous ligaments is indicative of disruption of the posterior tension band, comprised of the spinous processes and the interspinous ligament. Burst fractures may be difficult to detect on a lateral x-ray but are evident from an abnormally increased intrapedicular space when compared to adjacent levels. Computed tomography is particularly useful in burst fractures for assessing the degree of canal compromise by retropulsed bone fragments from the vertebral body.

If the patient is otherwise systemically stable, cervical traction using a halo frame or Gardner-Wells tongs may be used to restore alignment of the cervical spine and to reduce neural compression. Traction must be initiated with caution, however, as neurologic deterioration can occur from overdistraction or movement of acutely herniated disk material [65]. Before traction is initiated, a full set of x-rays and a magnetic resonance imaging scan help to reduce the likelihood of worsening deficits. In the subaxial spine, it is prudent to begin with 10 lbs and to add weight until reduction is achieved or a total of 5 lbs per cervical level has been used. Serial lateral x-rays or fluoroscopic images should be taken and repeat physical exams performed after each addition of weight to ensure that the neck and spine have not been overdistracted. Of note, not all spine surgeons advocate the routine use of MRI in all cervical spine injuries [66]. Care should be also taken to avoid traction when possible in patients with ankylosing spondylitis because further fracture and· distraction of the vertebral column is likely.

Early intervention to prevent delayed sequelae should also be initiated at this point. This would include use of good respiratory therapy (e.g., incentive spirometry), GI prophylaxis (e.g., H-blockers), and pulmonary embolism prophylaxis (e.g., heparin derivatives, supportive stockings, and sequential compression devices).

The human vertebral column consists of 7 cervical, 12 thoracic, 5 lumbar, and 1 fused sacrococcygeal vertebrae. A plum line
dropped from the C7 vertebra, tracing an imaginary line of gravity, runs anterior to the vertebral column in the thoracic and somewhat posterior in the lumbar regions. The line should normally fall near the sacral promontory. This is known as “sagittal balance” (Fig. 163.1).

The cervical canal is wider at the Cl and C2 levels, below which the canal diameter slowly tapers caudally. The lumbar canal is slightly wider than the thoracic canal. The greatest degree of flexion and extension occurs at the atlanto-occipital junction, and the greatest rotatory capability occurs at the atlantoaxial joint. Cervical vertebrae have transverse foramina that transmit the vertebral artery, which usually enters between C6 and C7.

The rib cage and costovertebral ligaments afford an additional element of stability compared with either the cervical or the thoracolumbar junction. Therefore, more force is required to produce a fracture in the mid thoracic spine region than the cervical or lumbar region. By the same token, less mobility is afforded in the thoracic spine [67]. The facet joint plane in the thoracic region is more sagittal than the cervical spine, but more coronal than the typical lumbar spine. The combination of these factors protects against rotational injury and allows somewhat more axial rotation.

The vascular supply of the spinal cord comprises the single anterior spinal artery, the paired posterior spinal arteries, and the segmental radicular arteries. The anterior spinal artery supplies the anterior two thirds of the cord, and the posterior spinal arteries supply the posterior third of the cord. In the cervical cord, the main vascular supplies come from the spinal arteries, but in the thoracic and lumbar regions, the segmental radicular arteries are the major contributors of blood supply. In the upper thoracic cord, the vascular supply may be sparse, especially between the fourth and eighth vertebrae, creating the watershed zone [68], which may be prone to hypotensive and hypoxic insults. The artery of Adamkiewicz (artery of lumbar enlargement) usually arises from T8 to T12 on the left side, most commonly arising from T10 to T12 on the left.

At the thoracolumbar junction and distally, the vertebral bodies allow a greater degree of motion. The lack of rib cage support, the increased room for flexion-extension, and the change in disc size and shape may all contribute to the relatively greater mobility of the lumbar spine. However, the additional degree of mobility at the thoracolumbar junction, especially from Tll to L2, makes this region more susceptible to injury than other adjacent portions of the spine. Because the middle and upper thoracic regions are relatively fixed, the thoracolumbar junction acts as a zone of mechanical stress concentration. The conus medullaris usually resides between the Tll and the Ll-2 disc space, and could be compromised by injuries at this level.

Because the neural and musculoskeletal components of the human spine are intimately associated, any discussion regarding blunt traumatic spinal cord injury requires an understanding of the vertebral column. Concepts of stability in the vertebral column are complex. This reflects the intricate nature of the arrangements of joints in the spinal column. Each vertebra has multiple sites of articulation and interaction with the neighboring vertebra (intervertebral disks, facet joints, connecting ligaments). To maintain the stability of this naturally flexible structure, the body must incorporate a complex array of muscles and ligaments.

The vertebral column serves to transmit loads, to permit motion, and to protect the spinal cord. Instability of the spinal column may then be defined as its failure to perform any of these functions under physiologic levels of mechanical loading. This failure may occur acutely or in a progressive, delayed manner. In cases of traumatic spinal cord injury, the vertebral column acutely fails to shield the neural elements from external forces as a result of being stressed beyond its mechanical tolerances.

Various classification schemes have been devised to predict if the spine is unstable. The most common of these is the three-column
theory introduced by Denis [69,70] (Fig. 163.2). Although these concepts were originally based on studies of thoracolumbar fractures, these principles have been applied successfully to other regions of the spine. This classification system divides the spine into anterior, middle, and posterior columns. The anterior column consists of the anterior half of the vertebral body, the anterior half of the intervertebral disk, and the anterior longitudinal ligament. The middle column consists of the posterior half of the vertebral body, the posterior half of the intervertebral disk, and the posterior longitudinal ligament. The posterior column consists of the posterior arch, the facet joint complex, the interspinous ligament, the supraspinous ligament, and the ligamentum flavum. The diagnosis of instability is made if two or more of the columns are compromised.

External forces placed on the spine include axial compression, distraction, flexion, extension, and translation. Axial compression in the cervical spine results in disruptions of the ring of Cl and burst fractures of the remaining vertebrae. Axial compression in the thoracolumbar spine results in burst fractures. When compressive forces are applied anterior to the spinal column and result in a component of flexion, anterior compression fractures result. Severe flexion is the most common injury mechanism in the cervical spine. This can cause odontoid fractures, teardrop fractures of the vertebral bodies, dislocations of the vertebral bodies, and jumped facets. In the thoracolumbar spine, severe flexion results in compression of the anterior vertebral body. If the fulcrum of force is anterior to the vertebral column, as occurs when a seat-belted passenger is involved in a motor vehicle accident, a flexion-distraction injury of the thoracolumbar junction may result. If the injury passes through the disk space or through the vertebral body, a “chance fracture” may occur (Fig. 163.3).

White and Panjabi [67] recommended a systematic approach to stability, and devised a checklist to determine it. In an adult cervical spine, horizontal subluxation more than 3 mm or an angulation more than 11 degrees is considered unstable [71]. Fractures or alignment patterns that suggest substantial disruption of the bony/ligamentous structures on radiographs suggest injury. Other more complex systems to measure spine stability have also been developed [72].

Instability of the spinal column requires maintenance of spinal precautions and bracing. In many instances, surgical realignment, fixation, and fusion will be necessary. Of note, missile injuries do not usually destabilize the spine.