Neurosurg Focus 31 (5):E7, 2011 Cervical spinal stenosis and sports-related cervical cord neurapraxia AARON J. CLARK, M.D., PH.D.,1 KURTIS I. AUGUSTE, M.D.,1,2 AND PETER P. SUN, M.D.1,2 1Department of Neurological Surgery, University of California, San Francisco; and 2Division of Pediatric Neurosurgery, Children’s Hospital and Research Center, Oakland, California Cervical cord neurapraxia is a common sports-related injury. It is defined as a transient neurological deficit following trauma localizing to the cervical spinal cord and can be caused by hyperextension, hyperflexion, or axial load mechanisms. Symptoms usually last less than 15 minutes, but can persist up to 48 hours in adults and as long as 5 days in children. While a strong causal relationship exists between cervical spine stenosis and cervical cord neurapraxia in adult patients, this association has not been observed in children. Likewise, while repeated episodes of neurapraxia can be commonplace in adult patients, recurrences have not been reported in the pediatric population. Treatment is usually supportive, but in adults with focal cervical lesions or instability, surgery is an option. Surgery for neurapraxia in children is rarely indicated. (DOI: 10.3171/2011.7.FOCUS11173) KEY WORDS • neurapraxia • cervical spine • spinal cord • cervical stenosis • sports ERVICAL cord neurapraxia is defined as a transient following sections will describe current information re- neurological deficit following cervical spinal cord garding the contribution of cervical spinal stenosis to cer- trauma.24 It is a common sports-related injury, oc- vical cord neurapraxia in the adult and pediatric athlete. curringC in 1.3–6 per 10,000 athletes, but there have been few studies that thoroughly describe the phenomenon.5,24 In a large series of 110 patients with cervical cord neura- Pathophysiology of Neurapraxia praxia, the vast majority of cases (87%) occurred during Underyling the motor/sensory manifestations of neur- football.22 In the largest pediatric series with cervical cord apraxia is a temporary derangement of axonal permeabil- neurapraxia (13 patients), once again football was the ity. 25 Hyperextension or hyperflexion causes a mechanical most common sport (4 cases, 31%).6 Case reports do exist injury that depolarizes the axon membrane in a reversible of cervical cord neurapraxia following nonsports-related but sustained manner. Laboratory studies reveal that the injury.1 The mechanism of injury is typically hyperexten- rapid stretch experienced by the strained axon results in sion, but cervical cord neurapraxia can occur after hyper- calcium influx, hyperpolarization, then prolonged depolar- flexion and axial loading as well.5,24 ization, during which the axon is no longer excitable. In There is a wide range of clinical presentations of cer- addition, anatomical strain experienced during this type vical cord neurapraxia. Sensory symptoms (paresthesias) of insult can result in microvascular constriction and vaso- can include burning pain, numbness, or tingling, and can spasm. As a result, local and regional blood flow is altered involve both arms (upper), both legs (lower), ipsilateral and the threat of ischemia becomes prominent. The tran- arm and leg (hemi), or all 4 extremities (quad).22 Motor sient nature of these physiological changes distinguished symptoms can occur in a similar anatomical distribution neurapraxia from irreversible neurological damage. and ranges from weakness (paresis) to complete paraly- 22 sis (plegia). Symptoms generally resolve in less than 15 Cervical Spinal Stenosis minutes, but have been reported to persist for up to 48 hours after injury.24 By definition, a patient with neura- Cervical spinal stenosis is common in pediatric and praxia completely returns to their baseline neurological adult athletes.4 Several methods to screen for cervical functional status with no residual weakness or paresthe- spinal stenosis in the setting of cervical cord neurapraxia sias. Torg et al.22 developed a grading system based on have been proposed. Sagittal spinal canal diameter can be duration of symptoms: Grade I (< 15 minutes), Grade II measured on lateral cervical plain radiographs and com- (15 minutes to 24 hours), and Grade III (> 24 hours). The pared with standard measurements (< 14 mm in the adult Neurosurg Focus / Volume 31 / November 2011 1 Unauthenticated | Downloaded 10/01/21 08:16 AM UTC A. J. Clark, K. I. Auguste, and P. P. Sun cervical spine is considered stenotic).11 The Torg ratio is proposed to evaluate functional stenosis, although not all calculated as the ratio of the spinal canal diameter to the centers may be capable of performing these studies.2 vertebral body diameter at the C3–7 levels as measured on lateral plain radiographs of the cervical spine (Fig. 1).19 It was developed as a measure of congenital spinal canal Cervical Cord Neurapraxia in Adult Athletes stenosis that theoretically minimizes the effect of varia- A large epidemiological study23 compared athletes tions in landmarks and radiographic technique. A Torg who reported an episode of cervical cord neurapraxia ratio < 0.8 is considered evidence of congenital stenosis. to athletes and nonathletes who had never experienced A criticism of this technique is that it does not take into neurapraxia and found that those with previous neura- consideration disproportionate differences in vertebral praxia had significantly smaller cervical spinal canals body size; football players commonly have larger verte- and lower Torg ratios, suggesting an association between bral bodies relative to the other spinal elements.10 Mag- stenosis and neurapraxia. A smaller series21 of 9 rugby netic resonance imaging has surpassed plain radiographs players with cervical cord neurapraxia demonstrated 4 and is the accepted method for evaluating spinal stenosis. athletes with Torg ratios < 0.8 and an additional 2 athletes Magnetic resonance imaging provides visualization of with congenital vertebral body fusions. Another series12 the vertebral column and intervertebral discs in relation- of 2 professional football players, each with an episode ship to the spinal cord, nerve roots, and surrounding CSF of cervical cord neurapraxia, reported normal Torg ra- within the spinal canal. Magnetic resonance imaging tios in both, but significant stenosis on myelography. In demonstrates bone and discogenic encroachment on the the largest series to date of cervical cord neurapraxia in spinal canal and spinal cord compression. The “function- athletes,22 110 patients were evaluated after 1 episode of al reserve” of the spinal canal is indicated by the presence cervical cord neurapraxia. In this series, 80% presented or absence of CSF signal surrounding the spinal cord.13 with symptoms in all 4 extremities, and 40% were com- This can be quantified by subtracting the spinal cord di- pletely plegic; 74% were Grade I (symptoms lasting < 15 ameter on a midsagittal MR image from the disc-level minutes). On subsequent evaluation of 104 radiographs of spinal canal diameter (Fig. 2).22 Dynamic flexion and ex- the athletes with cervical cord neurapraxia, 86% had Torg tension cervical spine MR imaging modalities have been ratios < 0.8,22 and of these patients, 53 underwent MR imaging. More than 81% of these patients had evidence FIG. 1. Lateral plain radiograph of the cervical spine of a 10-year-old boy who experienced transient paresthesias in both legs lasting less than 24 hours after a hyperextension injury during football practice. The Torg ratio is calculated as the ratio of the spinal canal diameter (SC, FIG. 2. Midsagittal MR image of the patient in Fig. 1. There is no distance from the midpoint of the posterior vertebral body to the nearest evidence of a structural lesion. Presence of CSF signal surrounding point on the spinolaminar line) to the vertebral body diameter (VB). The the spinal cord indicates good “functional reserve” of the spinal cord. Torg ratio at C-4 in this patient is > 0.8 and therefore demonstrates no Quantification can be performed by subtracting the diameter of the spi- evidence of cervical spinal stenosis. nal canal (CA) from the diameter of the spinal cord (CO). 2 Neurosurg Focus / Volume 31 / November 2011 Unauthenticated | Downloaded 10/01/21 08:16 AM UTC Cervical cord neurapraxia of cervical disc herniation, 25% had evidence of efface- tures to protrude into the spinal canal, further decreasing ment of the thecal sac, and 34% had frank cervical cord the canal reserve with the neck extended. Torg et al.22 ex- compression. In the largest modern series,2 10 athletes trapolated these findings to explain that, during flexion, the who experienced cervical cord neurapraxia underwent spinal cord is compressed between the lamina of the supe- MR imaging that demonstrated cervical stenosis in all rior level and the posterior superior aspect of the inferior patients and frank cord compression in 3 (33%). vertebral body. In the stenotic canal of an adult, the pincer For patients with cervical cord neurapraxia, sur- mechanism is likely more profound. Experimental studies gery should be considered in the setting of focal lesions in a giant squid axon model of cord deformation demon- and associated cord compression or instability on plain strated that during injury there was an increase in intracel- radiographs and MR imaging. In two combined series, lular calcium.25 Depending on the strength and duration of 12 (8.5%) of 142 patients underwent surgery for cord the injury, the chemical disturbance can be either reversible compression or spinal instability.22,24 The authors did or irreversible, leading to permanent cellular damage. This not make general recommendations regarding surgical can be applied to the phenomenon of sports-related cervi- decision-making as they believed the number of patients cal neurapraxia that results from a short duration injury of was too small. Instead, they proposed that the decision to moderate magnitude that causes the spinal cord to be de- pursue surgery should be individualized based on imag- formed by the “pincers mechanism,” which causes revers- ing findings and patient wishes.