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Radiating Upper Limb Pain in the Contact Sport Athlete: An Update on Transient Quadriparesis and Stingers

Concannon, Leah G. MD1; Harrast, Mark A. MD1,2; Herring, Stanley A. MD, FACSM1,2,3,4

doi: 10.1249/JSR.0b013e318240dc3f
Spine Conditions
Free

Participation in contact sports exposes the athlete to a risk of cervical spine injury. Temporary neurological injuries manifesting as radiating arm pain or paresthesias, such as transient quadriparesis and stingers, present unique challenges for the sports medicine physician and will be reviewed in detail. The initial management of these conditions must recognize signs and symptoms of spinal cord injury and prevent further neurological sequelae. Evaluation will often include advanced imaging of the cervical spine in addition to serial neurological examinations. This review concludes with rational return-to-play guidelines for contact sport athletes.

1Department of Rehabilitation Medicine, University of Washington, Seattle, WA; 2Department of Orthopaedics and Sports Medicine, University of Washington, Seattle, WA; 3Spine, Sports and Musculoskeletal Medicine, University of Washington, Seattle, WA; and 4Seattle Sports Concussion Program, University of Washington, Seattle, WA

Address for correspondence: Leah Concannon, MD, Department of Rehabilitation Medicine, University of Washington, Box 359721, 325 Ninth Avenue, Seattle, WA 98014 (E-mail: lgconcan@uw.edu).

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Introduction

Participation in contact sports exposes the athlete to a risk of cervical spine injury. These can range from simple cervical sprains to permanent spinal cord injury. Temporary neurological injuries, such as those seen in transient quadriparesis (TQ) and stingers, present unique challenges for the sports medicine physician in terms of initial management, evaluation, and eventual return to play.

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Transient Quadriparesis

In the United States, 10% of spinal cord injuries occur during participation in sports (17). TQ has been known by many other names, including cervical cord neurapraxia, burning hands syndrome, commotio spinalis, and spinal cord concussion. TQ, by definition, is a transient neurological episode encompassing sensory symptoms with or without motor changes. A survey of National Collegiate Athletic Association (NCAA) football players in the 1984 season found an incidence of TQ of 7.3 per 10,000, with 6 per 10,000 with sensory symptoms only and 1.3 per 10,000 with motor and sensory symptoms (29). A more recent study from 1989 to 2002 found a significantly lower incidence, with a rate of 0.17 per 100,000 for high school and 2.05 per 100,000 for college athletes, with a combined rate of 0.9 per 100,000 (2). It is unclear how much of this difference is due to insufficient reporting of transient symptoms versus a true decrease in the incidence.

TQ can be divided into three types: plegia (complete loss of motor function), paresis (motor weakness), and paresthesia (sensory symptoms only). Three grades also have been described. Grade 1 involves symptoms lasting less than 15 min, grade 2 symptoms last 15 min to 24 hours, and grade 3 symptoms last longer than 24 h. Symptoms also can be described by their anatomical distribution: quad (all four limbs), upper (both arms), lower (both legs), and hemi (one arm and one leg) (32). TQ is most commonly seen in contact sports such as American football, wrestling, and ice hockey, but it can occur in any sport where collisions occur. It is important for athletes, coaches, and medical personnel to distinguish between TQ and stingers, which are discussed in detail below. Any time an athlete complains of neurological symptoms in more than one extremity, an injury to the cervical spine must be considered first.

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Mechanism of Injury

There are three primary mechanisms for cervical spine injury. These include hyperextension, hyperflexion, and axial loading. Hyperextension of the neck creates a functional spinal stenosis due to infolding of the ligamentum flavum into the spinal canal. The sagittal diameter of the spinal canal is decreased by up to 30% in this position. Penning (24) described the pincer mechanism of injury in hyperextension in which the cord is compressed by the inferior portion of the superior vertebral body anteriorly and the spinolaminar line of the inferior vertebral body posteriorly. In flexion, the reverse occurs, with the lamina of the superior vertebral body and the posterior superior aspect of the inferior vertebral body approximating each other, again resulting in compression of the spinal cord. Thus, a narrow spinal canal, whether congenital or secondary to disc herniation or other causes, can potentially predispose to injury in either of these positions (6).

An axial load to the head when the neck is either straightened or slightly flexed also can put one at risk for injury. When the normal cervical lordosis is lost, the cervical spine functions as a segmented column and is less able to tolerate axial loads. In this position, the spine will fail in flexion. Oftentimes a fracture-dislocation results, and there is some degree of permanent spinal cord injury (11). When a fracture does not occur, the presence of spinal stenosis, either congenitally or from a disc herniation or disc-osteophyte complex, can still lead to transient compression of the cord, though with potentially less devastating results.

Spear tackler’s spine is defined by the development of stenosis of the cervical canal, with loss or reversal of the normal cervical lordosis, and prior evidence of posttraumatic changes on radiographs. There is a prior history of using a spear tackling technique. The classification of “spear tackler’s spine” originated from a report of 15 cases during a 4-year period (30). Eleven of these athletes had transient symptoms and four developed permanent neurological deficits. Contact sport athletes with spear tackler’s spine are at increased risk for both transient and permanent spinal cord injury. In 1976, a football rule change was implemented, banning spear tackling or using the helmet as the initial point of contact, which causes axial compression of a straight or slightly flexed cervical spine. This led to an immediate decrease in the incidence of cervical spinal injuries in 1977 (34). In 2007 and 2008, both the National Federation of State High School Associations and the NCAA, respectively, tightened their rules against spear tackling even further. More recent studies have demonstrated stability at this lower rate of spinal cord injury for both high school and collegiate athletes (Table 1).

Table 1

Table 1

A recent case of a Canadian professional hockey player who developed TQ after being struck in the back of the neck by a puck indicates that an additional mechanism may be involved in the development of TQ. It may be that an indirect force was imparted to the cord via a transfer of kinetic energy from the puck, causing symptoms in the absence of underlying stenosis and without a hyperflexion, extension, or axial loading moment (39).

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Presentation and Initial Management

An athlete with TQ may complain of symptoms in two to four limbs. The most common complaint is the so-called burning hands syndrome, with painful paresthesias in both hands, which is suggestive of a central cord syndrome. Sensory changes include burning, tingling, and diminished or absent sensation. Motor changes may or may not be present and can range from mild weakness to full paralysis. There may be dysethesias in the neck area, but typically, there is no other neck pain at the time of injury. Symptoms generally last less than 10 to 15 min but may last as long as 36 to 48 hours. Athletes should be treated with full cervical spine precautions to prevent progression of the injury (37). Establishment and maintenance of an airway may be necessary. In cases of more severe spinal cord injury, neurogenic shock may occur and should be appropriately managed.

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Evaluation

Diagnostic imaging should begin with cervical spine radiographs, potentially including flexion and extension views if the patient is neurologically stable. Advanced imaging with computed tomography (CT) can more readily diagnose a cervical fracture or dislocation, but in cases of TQ, there is generally no bony injury. Further imaging with magnetic resonance imaging (MRI) should then be performed to evaluate for intrinsic spinal cord abnormalities or ongoing spinal cord or nerve root compression. MRI may occasionally show spinal cord edema, but this is not generally seen in TQ. MRI may, however, identify a disc herniation or disc-osteophyte complex causing a functional spinal stenosis. Dynamic MRI in flexion and extension can also be used to further evaluate for any functional stenosis, although its clinical utility has not yet been proven. Somatosensory evoked potentials (SSEPs) may be considered to evaluate for myelopathy and, more specifically, dorsal column dysfunction. SSEPs are an electrodiagnostic study that consists of repetitive stimulation of a peripheral nerve, generally the tibial nerve, with cutaneous recording of the ascending sensory potentials in the limb, spinal cord, and over the sensory cortex. These potentials ascend through the dorsal columns of the spinal cord, so a lesion that spares the dorsal columns will result in a normal SSEP. Latencies of the responses can be compared to known normal values to identify a site of dysfunction along the pathway. The SSEP is a test of nerve function that can be used as an extension of the physical examination and imaging findings.

Prior to the advent of more advanced imaging, radiographs were used to evaluate for spinal stenosis. This was done by simply measuring the anteroposterior diameter of the spinal canal from the posterior aspect of the vertebral body to the most anterior point on the spinolaminar line. Values greater than 15 mm are considered normal, while 13 mm or less is considered consistent with stenosis (6).

An alternative measurement, mainly of historical interest, is the ratio method, also commonly referred to as the Torg ratio or the Torg-Pavlov ratio. This method was developed before MRI was in common use. By using a ratio, this method is independent of variations in the technique used in obtaining plain radiographs. The Torg ratio is measured at the C3-C6 levels and is the ratio between the sagittal diameter of the spinal canal measured from the mid height of the posterior aspect of the vertebral body to the spinolaminar line divided by the anterior-to-posterior diameter of the corresponding vertebral body. A normal ratio is 1.0, and values less than 0.8 are consistent with stenosis (29). This ratio is very sensitive for identifying what Torg described as “significant spinal stenosis.” He found that the sensitivity was 93% for transient neurapraxia; however, its low positive predictive value of 0.2% for identifying athletes at risk of transient neurapraxia or cervical spinal cord injury led him to conclude that the ratio itself should not be used as a screening method to exclude athletes from participation in contact sports (31). Another difficulty with the ratio method is the larger size of the vertebral body in professional football players. This will skew the denominator and decrease the ratio even if the true diameter of the spinal canal is normal (21).

A more useful measurement is the amount of “functional” spinal stenosis seen on MRI. The “functional reserve” of the spinal canal refers to cerebrospinal fluid (CSF) that is able to flow freely around the cord in the absence of stenosis. Factors that can lead to stenosis include a congenitally narrow canal, disc herniation or disc-osteophyte complexes, other degenerative changes, and posttraumatic instability. When there is a loss of CSF around the cord or, in more severe cases, indentation of the cord, this represents more significant stenosis. This functional reserve cannot be evaluated on plain radiographs and requires the use of MRI or CT myelogram. It has been determined that the ratio method described above has a low positive predictive value, ranging from 12% to 33%, for identifying patients who truly have functional spinal stenosis on MRI (14,21). Thus, any high-risk athlete with neurological symptoms in more than one limb, no matter how transient, should be evaluated with a cervical spine MRI to determine a potential source of the transient symptoms and measure the functional reserve. Lateral flexion and extension plain radiographs are necessary for evaluation as well before returning an athlete to play.

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Treatment

High-dose methylprednisolone has been used for the initial management of acute traumatic spinal cord injury, although its use remains somewhat controversial (23,36). It may work by decreasing inflammatory mediators and inhibiting lipid peroxidation that can lead to secondary neurological injury. It has been associated with increased infections (4). There is no role for steroids in the athlete with TQ who shows resolution of symptoms. Depending on policies of the treating hospital, it may be considered in cases where neurological signs persist. The Bracken, or National Acute Spinal Cord Injury Study II, protocol is often followed, continued for either 24 or 48 hours (3,4).

Moderate systemic hypothermia also has been used in the treatment of TQ, although its use is still considered experimental and is not recommended for routine care. Hypothermia is thought to decrease tissue metabolism and limit secondary hypoxic injury. However, it can be complicated by hypotension, cardiac arrhythmias, coagulopathy, infections, and sepsis. Therapeutic hypothermia gained media attention after its use in a professional football player (9). A recent retrospective review of 14 patients with complete spinal cord injury demonstrated similar complication rates at 1 year to matched controls, but continued studies are needed to determine efficacy before its widespread use can be endorsed (15).

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Return to Play

Controversy continues to exist over return-to-play guidelines for athletes who have suffered an episode of TQ. Part of the controversy stems from the relative lack of long-term data. With such a small incidence of both TQ and SCI in athletes, it would take a study of enormous proportions to truly determine the risk of catastrophic spinal cord injury after an episode of TQ. Torg et al. (32) in 1997 reported on 110 athletes who had suffered an episode of TQ. In this survey, 57% of the athletes returned to contact sports, and of these, 56% later developed a second episode of TQ. None of them sustained a permanent neurological injury, although no physical examination data were presented. Narrowing of the spinal canal as determined by MRI was the only predictive factor in identifying those athletes who suffered a second episode of TQ, although MRI was not performed on more than half of the athletes. In a separate study, they surveyed 117 athletes with permanent quadriplegia and found that none of them recalled a prior episode of TQ. Conversely, none of the athletes with TQ in this study went on to develop permanent neurological injury. In addition, none of the athletes with permanent spinal cord injury had evidence of spinal stenosis on imaging (29).

There are two reports in the literature of an athlete with transient neurological symptoms who subsequently developed permanent neurological injury. Cantu (7) reports on a case of a young football player with an episode of TQ and stenosis based on x-rays but did not undergo further imaging. He later went on to develop Brown-Sequard syndrome and permanent spastic tetraplegia after a tackle, with imaging demonstrating a C3-C4 disc herniation with cord displacement and edema.

Brigham and Adamson (5) reported a case of a young football player with a complaint of tingling in all four extremities when he performed neck flexion, without a prior history of injury. He was evaluated and allowed to continue playing, although imaging did reveal the presence of functional spinal stenosis. Two years later, he suffered an axial load while tackling and developed bilateral C6 paresthesias, with cord signal changes at C5. Symptoms remained 2 years after the incident, with continued dysethesias and weakness of elbow flexion and wrist extensors bilaterally.

There are differing opinions regarding return-to-play criteria after TQ. On the conservative end, Castro (10) recommends that a single episode of TQ is an absolute contraindication for return to contact sports; however, this view is not generally accepted. More widely agreed upon absolute contraindications include cervical fracture or ligamentous injury, any persistent neurological signs or symptoms, and cord signal changes or edema, although it is known that there are some professional athletes who return to play with persistent cord signal changes without obvious neurological deficit. Any incidentally discovered congenital abnormality that would normally preclude contact sports, such as os odontoideum, Klippel-Feil fusion greater than two levels, any atlanto-occipital fusion, or brain stem signs to include Arnold-Chiari malformation or basilar invagination, is an absolute contraindication. Cervical spine segmental instability, including C1-C2 hypermobility (anterior dens interval ≥4 mm) and more caudal vertebral segments (>3.5 mm of translatory displacement on dynamic flexion or extension plain radiographs or >11 degrees of kyphotic deformity) is also an absolute contraindication. Cantu (6) also argues that functional spinal stenosis seen on MRI or CT myelogram is an absolute contraindication for return to contact sports. Studies with the National Center for Catastrophic Sports Injury Research have demonstrated that in those athletes who suffer a spinal cord injury, those who have underlying spinal stenosis have a poorer prognosis for recovery of function than in those without cervical stenosis (6). A second episode of TQ requires a repeat complete evaluation and is considered either an absolute or relative contraindication for return (8,35). Spear tackler’s spine also is considered either an absolute or a relative contraindication (8,35). A well-healed single-level fusion is not a contraindication for return to play. Maroon et al. (18) reported on five professional football players who underwent cervical surgery and advocated that a fusion in and of itself should not represent a contraindication but that any level of fusion with loss of functional reserve should be considered a contraindication. Multilevel fusions are generally considered a contraindication for return to contact sports (33). Absolute and relative contraindications for return to play are summarized in Tables 2 and 3, respectively.

With a lack of a consensus, any return-to-play decisions must obviously include a lengthy discussion with the athlete, parents, and coach on the potential risks and must be made on a case-by-case basis.

Table 2

Table 2

Table 3

Table 3

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Stingers

Stingers, or burners, are a common but often under reported peripheral nerve injury. As mentioned above, stingers should not be confused with burning hands syndrome, which is indicative of a central cord injury. Simultaneous bilateral stingers are quite rare, and any athlete with symptoms in more than one extremity should be evaluated for a spinal cord injury. Stingers are a unilateral peripheral nerve injury occurring at a point from the cervical nerve root to the brachial plexus. Up to 50% to 65% of collegiate football players report at least one prior episode of a stinger, and recurrences have been reported to be as high as 87% (16,25).

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Mechanism of Injury

Controversy exists over the exact mechanism of injury involved in stingers, as well as the exact location of the lesion. It may well be that different mechanisms and locations of the injury are present in different age groups. The three commonly reported mechanisms include traction or tensile stretch injury, compressive injury, and direct trauma.

Traction results from ipsilateral shoulder depression with flexion of the neck to the contralateral side, which leads to stretch on the nerve roots and the brachial plexus. This more commonly occurs in younger athletes with less experience and weak neck and shoulder musculature, who lack radiographic evidence of cervical spondylosis (26). Compression stems from extension and lateral bending to the ipsilateral side, with compression often occurring within a narrowed neural foramina and is more common in older players (16,19). Direct compression can occur at Erb’s point and stems from improper padding. The brachial plexus is most superficial at this point and vulnerable to direct compressive forces.

The cervical nerve roots are at higher risk than the brachial plexus for both tensile and compressive injury for several reasons. The linear, as opposed to plexiform, orientation of the cervical nerve roots and their relative lack of perineurium and epineurium increase their susceptibility to injury. The C5 nerve root is the shortest and is in direct alignment with the brachial plexus and is therefore the most vulnerable. In addition, the ventral motor root lacks the dampening effect of the dorsal root ganglion, which may help explain why motor symptoms may be more persistent than sensory symptoms (38).

Despite these anatomic factors, the literature slightly favors brachial plexus stretch injury over nerve root stretch, nerve root compression, and direct compressive forces. As mentioned above, this may relate to the age and experience of the player (13).

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Presentation

Stingers are a transient episode of unilateral pain and/or paresthesias in an upper extremity. They may or may not present with weakness. Symptoms are most commonly in the C5 or C6 distribution. However, sensory symptoms may be present in a circumferential, rather than a dermatomal pattern. The athlete generally has full, pain-free cervical neck range of motion (ROM), without tenderness to palpation. They may have a positive Spurling maneuver on examination, particularly if the mechanism of injury was one of compression. As mentioned, there is a preponderance for C5 or C6 and upper trunk symptoms. Shoulder abduction, external rotation, and elbow flexion strength should be given special attention during the examination of the athlete to evaluate carefully for weakness in this distribution. Serial assessments are necessary because the duration of symptoms can be quite variable, generally lasting seconds to minutes, but may persist for days or longer.

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Evaluation

The first step in evaluation of the athlete is to rule out the presence of symptoms in more than one extremity, no matter how transient, because this raises concern for a cervical spine injury.

After a first stinger, cervical radiographs and MRI may be recommended to evaluate for potential etiologies. This is particularly important if symptoms last for more than 1 hour, if there is concomitant neck pain, or if neurological symptoms and signs are in a particular nerve root distribution (6). Stingers that resolve within minutes without any residual signs or symptoms may not require further evaluation. X-ray can identify bony foraminal stenosis or instability on flexion or extension. MRI can be used to identify disc herniation or disc-osteophyte complexes that may be contributing to any neural foraminal narrowing that is present and is recommended in the evaluation of any athlete with persistent weakness. Chronic stingers are often associated with foraminal narrowing or cervical disc disease (16). Imaging of the brachial plexus with MRI also can be considered to evaluate for a more peripheral injury.

Electrodiagnostic testing can be considered in the athlete with persistent symptoms and, in general, is more helpful for evaluating motor weakness rather than sensory changes only. Electrodiagnostics can help to differentiate a cervical nerve root injury from a brachial plexus injury. They may also help to differentiate a neurapraxic versus an axonal injury, helping to predict prognosis and time frame for recovery. It often takes up to 3 wk for signs of denervation to be seen on an electrodiagnostic study; however, reduced recruitment may be seen immediately. In addition, findings on electrodiagnostics can remain abnormal even after full clinical recovery of strength and should not necessarily preclude a return to competition, particularly if the examination demonstrates evidence of reinnervation (38).

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Treatment

Initial treatment consists of rest and pain control. A comprehensive rehabilitation program focused on ROM, posture, muscular imbalances, and other predisposing factors should follow to decrease the risk of recurrent injury. Because stingers are generally self-limited, further treatment would be unusual but could include fluoroscopically guided epidural steroid injections for pain relief or even surgical decompression of a narrowed foramen or fusion for continued or progressive weakness (13).

Cervical collars are sometimes used in an effort to decrease the risk of recurrent injury. They are intended to decrease extension and lateral flexion, although research to demonstrate their effectiveness is lacking (12). In addition, limiting extension may have the unwanted effect of placing the player’s head in a more flexed position, thereby potentially increasing the risk of severe cervical spine injury. Reducing cervical ROM also may affect a player’s abilities on the field. The Cowboy collar has added padding over Erb’s point and may be used to prevent recurrent direct trauma to the brachial plexus.

B vitamins are occasionally used in the treatment of stingers and other nerve injuries. While vitamin B deficiencies have been linked to the development of peripheral neuropathies, the literature does not clearly support their use in peripheral neuropathies that do not have an underlying vitamin B deficiency. There is not sufficient evidence to support its use in alcoholic and diabetic neuropathy (1) and it is no better than placebo in the treatment of carpal tunnel syndrome (22). Practitioners who elect to prescribe B vitamins should be careful not to exceed the recommended daily upper limit because pyridoxine (B6) toxicity also can present with peripheral neuropathy and excess of either thiamine (B1) or pyridoxine can deplete other B vitamins.

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Return to Play

Athletes should not return until they have full, pain-free cervical neck ROM, no neck tenderness to palpation, no residual symptoms, and no suspicion of underlying cervical injury (7). If symptoms resolve rapidly and the athlete has a normal neurological examination with full, pain-free cervical ROM, he or she may be considered for return to play in the same game if this is his or her first stinger. Recurrent stingers in the same game or season, or any evidence of neck pain or neurological changes require the player to undergo further workup before returning to competition (27).

Absolute contraindications for return to play include persisting weakness, cervical anomalies identified on imaging, persisting electrodiagnostic abnormalities (with the exception of reinnervation), evidence of myelopathy, continued pain, and reduced cervical ROM (Table 4) (27).

Table 4

Table 4

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Conclusions

Evaluation and management of any suspected cervical spine injury require a well-managed team of medical professionals. In the case of TQ, the first priority is prevention of further neurological injury. Only after symptoms have resolved and a complete evaluation has been performed can the focus shift to questions of return to play. When evaluating a stinger, the first priority is identifying those athletes who may actually have an injury to the spinal cord. Any athlete with bilateral symptoms, no matter how transient, should be treated as a suspected spinal cord injury. They should be placed in a cervical collar, on a backboard, and taken to the emergency department for full evaluation. Athletes with persistent unilateral symptoms also require a more detailed evaluation before considering return to play.

The authors declare no conflicts of interest and do not have any financial disclosures.

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References

1. Ang CD, Alviar MJ, Dans AL, et al.. Vitamin B for treating peripheral neuropathy. Cochrane Database Syst. Rev. 2008: CD004573.
2. Boden BP, Tacchetti RL, Cantu RC, et al.. Catastrophic cervical spine injuries in high school and college football players. Am. J. Sports Med. 2006; 34: 1223–32.
3. Bracken MB, Shepard MJ, Collins WF, et al.. A randomized, controlled trial of methylprednisolone or naloxone in the treatment of acute spinal-cord injury. Results of the Second National Acute Spinal Cord Injury Study. N. Engl. J. Med. 1990; 322: 1405–11.
4. Bracken MB, Shepard MJ, Hofford TR, et al.. Administration of methylprednisolone for 24 or 48 hours or tirilazad mesylate for 48 hours in the treatment of acute spinal cord injury. Results of the Third National Acute Spinal Cord Injury Randomized Controlled Trial. National Acute Spinal Cord Injury Study. JAMA. 1997; 277: 1597–604.
5. Brigham CD, Adamson TE. Permanent partial cervical spinal cord injury in a professional football player who had only congenital stenosis. J. Bone Joint Surg. Am. 2003; 85-A: 1553–6.
6. Cantu RC. Stingers, transient quadriplegia, and cervical spinal stenosis: return to play criteria. Med. Sci. Sports Exerc. 1997; 29 (Suppl. 7): S233–5.
7. Cantu RC. Cervical spine injuries in the athlete. Semin. Neurol. 2000; 20: 173–8.
8. Cantu RV, Cantu RC. Current thinking: return to play and transient quadriplegia. Curr. Sports Med. Rep. 2005; 4: 27–32.
9. Cappuccino A, Bisson LJ, Carpenter B, et al.. The use of systemic hypothermia for the treatment of an acute cervical spinal cord injury in a professional football player. Spine. 2010; 35: E57–62.
10. Castro FP. Stinger, cervical cord neurapraxia, and stenosis. Clin. Sports Med. 2003; 22: 483–92.
11. Chao S, Marisa JP, Torg JS. The pathomechanics, pathophysiology and prevention of cervical spinal cord and brachial plexus injuries in athletics. Sports Med. 2010; 40: 59–75.
12. Gorden JA, Straub SJ, Swanik CB, Swanik KA. Effects of football collars on cervical hyperextension and lateral flexion. J. Athl. Train. 2003; 38: 209–15.
13. Harrast M, Weinstein S. The cervical spine. In: Orthopedic Knowledge Update: Sports Medicine. Rosemont (IL): AAOS; 2009; Chapter 25. p. 295–303.
14. Herzog RJ, Weins MF, Dillingham MF, Sontag MJ. Normal cervical spine morphometry and cervical spinal stenosis in asymptomatic professional football players. Spine. 1991; 16: 178–86.
15. Levi AD, Casella G, Green BA, et al.. Clinical outcomes using modest intravascular hypothermia after acute cervical spinal cord injury. Neurosurgery. 2010; 66: 670–7.
16. Levitz CL, Reilly PJ, Torg JS. The pathomechanics of chronic, recurrent cervical nerve root neurapraxia. The chronic burner syndrome. Am. J. Sports Med. 1997; 25: 73–6.
17. Maroon JC, Bailes JE. Athletes with cervical spine injury. Spine. 1996; 21: 2294–9.
18. Maroon JC, El-Kadi H, Abla AA, et al.. Cervical neurapraxia in elite athletes: evaluation and surgical treatment. Report of five cases. J. Neurosurg. Spine. 2007; 6: 356–63.
19. Meyer SA, Schulte KR, Callaghan JJ, et al.. Cervical spinal stenosis and stingers in collegiate football players. Am. J. Sports Med. 1994; 22: 158–66.
20. 20. Mueller FO, Cantu RC. Catastrophic Football Injuries Annual Report 2010. Available from: http://www.unc.edu/depts/nccsi. Accessed September 27, 2011.
    21. Odor JM, Watkins WH, Dillin S, et al.. Incidence of cervical spinal stenosis in professional and rookie football players. Am. J. Sports Med. 1990; 18: 507–9.
    22. Piazzini DB, Aprile I, Ferrara PE, et al.. A systematic review of conservative treatment of carpal tunnel syndrome. Clin. Rehabil. 2007; 21: 299–314.
    23. Pandya KA, Weant KA, Cook AM, Smith KM. High-dose methylprednisolone in acute spinal cord injuries: proceed with caution. Orthopedics. 2010; 33: 327–31.
    24. Penning L. Some aspects of plain radiography of the cervical spine in chronic myelopathy. Neurology. 1962; 12: 513–9.
    25. Sallis RE, Jones K, Knopp W. Burners: offensive strategy for an underreported injury. Physician Sportsmed. 1992; 20: 47–55.
    26. Shannon B, Klimkiewicz JJ. Cervical burners in the athlete. Clin. Sports Med. 2002; 21: 29–35.
    27. Standaert CJ, Herring SA. Expert opinion and controversies in musculoskeletal and sports medicine: stingers. Arch. Phys. Med. Rehabil. 2009; 90: 402–6.
    28. Torg JS, Quedenfeld TC, Burstein AH, et al.. National Football Head and Neck Injury Registry: report on cervical quadriplegia 1971 to 1975. Am. J. Sports Med. 1979; 7: 127–32.
      29. Torg JS, Pavlov H, Genaurio SE, et al.. Neurapraxia of the cervical spinal cord with transient quadriplegia. J. Bone Joint Surg. Am. 1986; 68: 1354–70.
      30. Torg JS, Sennett B, Pavlov H, et al.. Spear tackler’s spine. An entity precluding participation in tackle football and collision activities that expose the cervical spine to axial energy inputs. Am. J. Sports Med. 1993; 21: 640–9.
      31. Torg JS, Naranja RJ Jr, Pavlov H, et al.. The relationship of developmental narrowing of the cervical spinal canal to reversible and irreversible injury of the cervical spinal cord in football players. J. Bone Joint Surg. Am. 1996; 78: 1308–14.
      32. Torg JS, Corcoran TA, Thibalt LE, et al.. Cervical cord neurapraxia: classification, pathomechanics, morbidity, and management guidelines. J. Neurosurg. 1997; 87: 843–50.
      33. Torg JS, Ramsey-Emrhein JA. Suggested management guidelines for participation in collision activities with congenital, developmental or postinjury lesions involving the cervical spine. Med. Sci. Sport Exerc. 1997; 29: S256–72.
      34. Torg JS, Guille JT, Jaffe S. Injuries to the cervical spine in American football players. J. Bone Joint Surg. Am. 2002; 84-A: 112–22.
      35. Torg JS. Cervical spinal stenosis with cord neurapraxia: evaluations and decisions regarding participation in athletics. Curr. Sports Med. Rep. 2002; 1: 43–6.
      36. Walsh KA, Weant KA, Cook AM. Potential benefits of high-dose methylprednisolone in acute spinal cord injuries. Orthopedics. 2010; 33: 249–52.
      37. Waninger KN, Swartz EE. Cervical spine injury management in the helmeted athlete. Curr. Sports Med. Rep. 2011; 10: 45–9.
      38. Weinstein SM. Assessment and rehabilitation of the athlete with a “stinger.” A model for the management of noncatastrophic athletic cervical spine injury. Clin. Sports Med. 1998; 17: 127–35.
      39. Winder MJ, Brett K, Hurlbert RJ. Spinal cord concussion in a professional ice hockey player. J. Neurosurg. Spine. 2011; 14: 677–80.
      © 2012 American College of Sports Medicine