CHAPTER 317 Transient Quadriparesis and Athletic Injuries of the Cervical Spine
Epidemiology and Significance
Sporting events rank as the fourth most common cause of spinal cord injury, behind motor vehicle crashes, violence, and falls, and up to 7% of all spinal cord injuries have been reported to be related to athletics.1–4 These injuries most commonly occur in younger patients and are the second most common cause of spinal cord injury in the first three decades of life.4,5
The National Center for Catastrophic Sports Injury Research (NCCSIR) has defined a catastrophic sports injury as “any severe spinal, spinal cord, or cerebral injury incurred during participation in a school/college sponsored sport.”3 Sporting injuries may be broadly classified as either direct or indirect. Direct injuries result from participating in the sport, whereas indirect injuries result from systemic failure caused by exertion while participating in the sport.3,4 Indirect injuries are frequently related to underlying cardiopulmonary conditions, including cardiac arrhythmia, coronary artery disease, and hypertrophic cardiomyopathy. Within each category, injuries can be subclassified as serious, nonfatal, and fatal.6 Serious injuries include significant injuries that do not result in a permanent functional disability, such as a spinal fracture that does not result in neurological deficit. Nonfatal injuries include injuries that are severe and have resulting permanent functional disability.
According to the NCCSIR, the incidence of direct and indirect catastrophic injuries for all sports is about 1 of every 100,000 high school and 4 of every 100,000 college athletes.3 These injuries result in fatality rates of 0.40 of every 100,000 high school and 1.42 of every 100,000 college athletes.3
Cervical spine injuries related to sports have been reported at many different levels of participation, ranging from unsupervised activities to organized contact and collision sports.7 Cervical trauma has the potential to lead to devastating and irreversible neurological consequences for the player-athlete. Improvements in protective equipment, rule changes, and immediate postinjury care have lowered the incidence of complete quadriplegia among high school and college athletes from 2.5 per 100,000 in 1976 to 0.5 per 100,000 in 1991.8
Although athletic injuries have been reported in a variety of sports, including weightlifting, rugby, diving, surfing, skiing, gymnastics, and boxing, football is associated with the greatest number of direct, catastrophic injuries of all team sports.4 Up to 15% of football players experience a cervical spine injury at some point during play or practice, which may include injuries of the spinal column, spinal cord, or nerve roots.4,9 Linemen, defensive ends, and linebackers are disproportionately prone to these injuries. An increased number of cervical injuries are also encountered among players on special teams, in which players are frequently subject to high-speed collisions.10 In addition, up to 50% of football players with a history of neck trauma have been demonstrated to have radiographic changes, including compression fractures, abnormal motion segments, and disk disease.11
Predisposing Factors
Certain conditions may predispose the athlete to injury. Athletes with a congenitally narrow cervical vertebral canal may be at higher risk for transient quadriplegia. The Torg ratio, a radiographic measure comparing the spinal canal diameter to the vertebral body width, was developed as a marker of spinal stenosis, with a ratio of 0.8 or less indicating severe cervical stenosis and suggesting that a participant was at increased risk for neurological injury.9,12,13 However, among 124 professional football players and 100 rookie football players, 32% of the professional football players and 34% of the rookies had a sagittal canal–to–vertebral body ratio of less than 0.80 at one or more levels from C3 to C6.9 Herzog and colleagues have reported that the Torg ratio has a poor positive predictive value for the presence of true spinal stenosis.14 Because of this factor, as well as the fact that the Torg ratio was studied primarily in professional athletes, it is not commonly used today to determine safety for athletic competition.7
A number of syndromic disorders have been reported to predispose to increased risk for cervical injury. Up to 40% of athletes with Down syndrome demonstrate occipitocervical and atlantoaxial instability owing to increased ligamentous laxity, which would be expected to place them at increased risk for cervical spinal cord injury. However, this theoretically increased risk has not been confirmed in reports of children with Down syndrome in sporting activities when compared with age-matched controls.15,16 Patients with achondroplasia often have multiple levels of cervical spine stenosis, which may be particularly prominent at the foramen magnum. Individuals with achondroplasty have been reported to be at increased risk for spinal cord injury with hyperflexion and hyperextension.15 In addition, atlantoaxial instability is associated with type VI mucopolysaccharidosis (Maroteaux-Lamy syndrome), and atlantoaxial rotatory subluxation may be seen in patients with Marfan’s syndrome.16,17
Anatomic Considerations and Biomechanics
A basic understanding of spinal developmental anatomy and biomechanics is important in managing the injured athlete. The first two cervical vertebrae have characteristic patterns of development.18 Three primary ossification sites contribute to the formation of the atlas (C1). These include a single anterior arch and two neural arches, which subsequently fuse to form the posterior arch. Ossification of the anterior arch typically occurs by 1 year of age but is present in up to 20% of cases at birth.18 Although the neural arches develop in the seventh fetal week, they do not fuse with the anterior arch until later in childhood, typically by 7 years of age. Before these arches fuse, forming the complete C1 ring, this apparent lack of fusion may be readily mistaken for a fracture.18–20 Posterior fusion of the neural arches typically occurs by 3 years of age. In the event that the anterior ossification center fails to form, the neural arches may attempt to fuse anteriorly. This anomaly typically can be distinguished from a fracture based on the presence of sclerotic margins.18,21
Development of the axis (C2) is the most complex of all vertebrae.18 At birth, the axis consists of four ossification centers, including two for the neural arches and one each for the body and odontoid process. The ossification center for the odontoid process forms in utero from the fusion of two ossification centers by the seventh fetal month. In addition, between 3 and 6 years of age, a secondary ossification center forms at the tip of the odontoid process (os terminale) and typically fuses by 12 years of age.18 Fusion of the odontoid process to the body of C2 typically occurs by 3 to 6 years of age. A remnant of this fusion line, termed the subdental synchondrosis, may be apparent at up to 11 years of age and may easily be mistaken for a fracture. By 3 years of age, the neural arches typically fuse posteriorly, and between 3 and 6 years of age, these arches fuse with the body and odontoid process.18
The vertebrae of the subaxial cervical spine share a similar developmental pattern.18 Each vertebra develops from three primary ossification centers, one for the body and one each for two neural arches. Typically, by 2 to 3 years of age, the neural arches fuse, and over the next 3 years, the arches fuse with the body. Secondary ossification centers contribute to the formation of the transverse and spinous processes and may also be present at the superior and inferior edges of the bodies. Secondary ossification centers may be mistaken for fractures because they may remain unfused into the third decade of life.
The craniocervical junction is vulnerable to traumatic injury, and an appreciation of the bony and ligamentous anatomy of this region is important for understanding the mechanisms of injury.18 The cephalad edge of C1 is connected to the foramen magnum by paired anterior and posterior atlanto-occipital membranes. The anterior aspect of the dens is attached to the anterior arch of C1 by the atlantoaxial ligament. The posterior longitudinal ligament extends in a cephalad direction as the tectorial membrane and provides attachment of the cervical spine to the foramen magnum. The transverse ligament extends laterally from tubercle to tubercle along the inner aspect of the anterior arch of C1 and provides approximation of the atlas to the dens. The apical ligament extends from the tip of the odontoid process to the anterior edge of the foramen magnum. The alar ligaments extend between the sides of the dens and the tubercles on the medial aspects of the occipital condyles. Because the alar ligaments serve to limit the degree of contralateral rotation, a tear produces an increased range of motion to the contralateral side and may result in rotational instability.
Cervical spine injury patterns and vulnerabilities vary between the immature and mature spine.18 The adult cervical spine has a fulcrum of motion centered at the C5-C6 level. In contrast, the pediatric cervical spine has a fulcrum of motion that is centered at C2-C3,18,22,23 resulting in a greater risk for occipitocervical and high cervical injuries. This more cephalad fulcrum predisposes children to injuries in the occiput to C3 region. In addition, the pediatric cervical spine in general is predisposed to instability by a number of factors, including a relatively large head, hypermobility owing to increased ligamentous laxity, incomplete ossification of the dens, relatively weak neck muscles, and shallow facet joints.18,19,23–25 As the cervical spine matures, its fulcrum gradually descends to the C3-C5 level in 8- to 12-year-old children, and ultimately descends to the C5-C6 level in adolescents and adults.
Mechanisms of Injury
Lateral Bending
When excessive lateral bending forces are applied to the cervical spine, exiting nerve roots may be subjected to considerable compressive and tractional forces.26 Although a connective tissue layer surrounds the exiting cervical nerve roots and provides some degree of protection, these roots remain vulnerable and are common sources of symptoms in the injured athlete. When nerve roots are subjected to tractional forces, the force is distributed along the length of the root. However, once the elastic limit of the nerve and associated connective tissue is reached, partial or complete disruption may occur. A stinger, an example of neurapraxia (see later), is a common example of a neurological sporting injury that results from excessive traction on neural tissue.
Axial Loading
Axial loading refers to compressive forces applied along a vector parallel to the axis. Resulting fractures commonly affect the region of the fulcrum, C5-C6 in adults and C2-C3 in children. These injuries are typically stable because it is uncommon for pure axial forces, in the absence of rotational or sheer forces, to produce dislocation.27
Considerable attention has been directed toward addressing excessive axial loading forces in athletics because it remains a common mechanism of cervical injuries. About half of the 209 football injuries resulting in permanent quadriplegia between 1971 and 1975 were attributed to axial loading forces.1 The cervical spine loses considerable buffering capacity when the head is lowered. In the lowered position, the cervical spine loses the lordotic contour that provides maximal ability of the vertebral bodies, disks, and cervical soft tissues to absorb and dissipate force. The result is a biomechanically compromised cervical spine that is vulnerable to angulation or hyperflexion to release energy. The result is often intervertebral disk space injury, vertebral body fractures, or ligamentous injury. Biomechanical studies suggest that the axial load limits of the cervical spine in young adults is between 3340 and 4450 Newtons, which can be readily approached with a fast walk when the head is lowered.28,29
Axial loading injuries are often avoidable and have received the most attention in football, where they can occur when an athlete intentionally uses the crown of the helmet as a point of contact (“spearing”). On this basis, most professional, college, and high school football leagues have banned both deliberate spearing and the use of the top of the helmet as the initial point of contact when making a tackle. After these rule changes, a marked decrease in cervical spine injury rates occurred.30
Rotation
Because of the oblique relationship of the superior and inferior articulating processes of the cervical facets, lateral bending forces in the cervical spine are typically associated with a rotational force. Most rotational motion in the cervical spine is facilitated by the atlas and axis. Extremes of rotation at this interface can produce neurological and vascular compromise. For example, with leftward rotation of the atlas, the right transverse foramen of the atlas moves in a posterior direction. With extremes of rotation, increased stretch is applied to the vertebral arteries and spinal nerves. In severe cases, this may result in compromised brainstem or spinal cord circulation and has most commonly been described in wrestlers.31–35
