The diagnosis, management, interpretation, and implications of cervical stenosis have caused significant debate and controversy over the past several decades. The concept of cervical stenosis is simple; the spinal canal is narrow. However, the answer to the question of how narrow is too narrow is quite complex.
Figure 15-2 Radiographic assessment of cervical spine alignment. A, The anterior vertebral line, posterior vertebral line, spinolaminar line, and spinous process line should be smooth and continuous without step-off. B, Sagittal displacement greater than 3.5 mm or angular deformity greater than 11 degrees indicates an unstable injury of the cervical spine.
The definition of stenosis has generated considerable debate. Originally, stenosis was diagnosed from measurements of the transverse spinal canal diameter on plain radiographs.20 Wolfe et al21 and Penning22 recognized the relations between radiographic measurements and myelopathy as early as 1956 and 1962, respectively. Gore et al13 understood that technique factors in obtaining plain radiographs could cause significant discrepancies in absolute measurements obtained from them. Torg and Pavlov in 1987 put forth the Pavlov ratio as a method to avoid problems of magnification when evaluating for possible stenosis.23 This is the ratio of the spinal canal to the vertebral body. A Pavlov ratio of less than 0.85 qualified as stenosis and a ratio of more than 0.8 was reported to place athletes at risk of catastrophic neurologic injury. Herzog et al24 recognized that football players generally have larger vertebral bodies and that even if these athletes had normal canal measurements, the Pavlov ratio could be less than 0.8, a false-positive result that may prevent an asymptomatic athlete from participating in contact sports. Computed tomography and MRI have been subsequently used to determine ranges of "normal" canal diameter. The average spinal cord diameter ranges from 5.0 to 11.5 mm (mean, 10mm).20 The average canal diameter from C3-C7 is 15 to 25 mm (mean, 17 mm).25,26 A canal diameter less than 13 mm is considered stenotic and absolute stenosis considered to be less than 10mm.27,28 Blackley et al29 showed a poor correlation between Pavlov's ratio and computed tomography scan measurements of canal diameter. Prasad et al30 demonstrated that Pavlov's ratio correlated poorly with MRI measurements of the space available for the cord. Matsuura et al31 demonstrated that the anteroposterior diameter of the spinal canal on computed tomography was less in patients with spinal cord injury than in controls. Of importance in this topic is that the overall space available for the cord is dependent on the sagittal and transverse diameters of the canal. Cantu,32 expounding Burrows'33 ideas, proposed the concept of "functional stenosis." This concept takes into account the variability in anatomy of the canal and cord among athletes and states that the more important factor is whether there is enough spinal fluid surrounding the cord to protect it from injury. Functional stenosis must be determined on a case-by-case basis, as the predictability of absolute measurements and ratios is moderate at best.
Stenosis may be either acquired, congenital, or a combination of both. Acquired causes include disk pathology, osteophytes, degenerative subluxation, hypertrophic ligamentum flavum, fracture, or ossification of the posterior longitudinal ligament. Congenital causes may vary from shortened pedicles, Klippel-Feil syndrome, or other congenital anomalies.
Previously, stenosis alone was thought to be a contraindication to contact sports, but more recent literature has suggested a revision of that doctrine.4,34 Currently, the use of Pavlov's ratio should not be used as a screen for prediction of spinal cord injury given its low positive predictive value (0.2%). A ratio of less than 0.8 has, however, been demonstrated to have reasonable predictive value for a recurrent episode of either transient neu-rapraxia or burner syndrome but not catastrophic injury.35,36 Kang et al37 demonstrated that the canal diameter at the time of injury was positively correlated to the severity of the neurologic injury sustained. Higher energy injuries were associated with smaller canal diameters and more severe neurologic injuries. This study raises concern for athletes with severe stenosis who wish to participate in collision sports.37 Some authors continue to recommend that asymptomatic athletes with stenosis not participate in contact sports.38 A proven screening tool for prediction of catastrophic injury remains elusive. In the existing literature, quadriplegia has been more closely associated with axial loading from poor tackling techniques, such as spearing, that lead to catastrophic vertebral body fracture than to stenosis.39
Temporary paralysis after a collision in sports with rapid and complete resolution of symptoms within 10 to 48 hours after injury has been termed transient quadriparesis or cervical cord
neurapraxia.23 The incidence in collegiate football players has been estimated to be 7.3 in 10,000 athletes. The mechanism of injury is usually axially loading of the cervical spine in flexion or extension. Penning22 described the pathoanatomy of the "pincer mechanism" of hyperextension on the cervical cord. Taylor reported that infolding of the ligamentum flavum can reduce canal diameter up to 30%. The cervical spinal cord gets pinched between the inferior aspect of the superior vertebral body and the anterosuperior aspect of the spinolaminar line of the inferior adjacent vertebra. Similarly, with hyperflexion the cervical cord gets pinched between the anterosuperior aspect of the spin-olaminar line of the superior vertebrae and the posterior superior aspect of the vertebral body of the inferior vertebrae.22,40
Although the precise etiology of transient quadriparesis remains elusive, Torg has postulated that cord function is disrupted because of local cord anoxia and the increased concentration of intracellular calcium.41 Zwimpfer and Bernstein42 described a "postconcussive state" of the spinal cord after brief conduction block causing axon dysfunction.
Transient quadriparesis encompasses a spectrum of neurologic dysfunction. Motor dysfunction ranges from bilateral upper and lower extremity weakness to complete paralysis. Sensory dysfunction ranges from dysesthesias to complete absence of sensation. Deficits may resolve in as little as 10 minutes but may persist for up to 48 hours. Deficits lasting longer than 48 hours are not due to transient quadriparesis.43
Radiographic evaluation of patients with transient quadri-paresis or an abnormal neurologic examination includes plain radiographs and MRI. Imaging is negative for fractures but may reveal congenital anomalies (Klippel-Feil), congenital stenosis (canal diameter <13mm), acquired stenosis, a herniated disk, or cervical instability. As previously stated, considerable controversy currently exists regarding the use of spinal canal measurements to predict risk of catastrophic neurologic injury. Torg et al43 reported that 56% of players of contact sports with transient quadriparesis experienced a recurrence; however, none suffered a permanent neurologic injury. Risk factors for recurrence included a small Torg ratio (<0.8) as well as acquired stenosis from spondylotic changes.43 For a first-time occurrence, if the athlete's symptoms resolve quickly and he or she is asymptomatic and imaging studies do not demonstrate contraindications, the athlete should be allowed to return to play. Prolonged quadriparesis of 24 to 48 hours, two or more previous episodes of transient neuropraxia, or an increase in baseline neck discomfort are relative contraindications to return to play. Absolute contraindications include persistent pain, abnormal neurologic examination, spear tackler's spine, instability, acute fracture, or malalignment.44
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