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Consensus-Based Review

High-Energy Contact Sports and Cervical Spine Neuropraxia Injuries: What Are the Criteria for Return to Participation?

Dailey, Andrew, MD*; Harrop, James S., MD†‡; France, John C., MD§

Author Information
doi: 10.1097/BRS.0b013e3181f32db0
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Athletes who participate in contact sports may experience a syndrome called “transient neuropraxia” or “cervical cord neuropraxia (CCN)” in which they have transient bilateral motor and/or sensory symptoms that are referable to the cervical spinal cord.1,2 The sensory symptoms can include burning, numbness, or loss of sensation, and can be associated with motor weakness that ranges from mild to complete. The symptoms are present for a time frame that can last from minutes up to 36 hours, but recovery is usually thought to be complete. The underlying condition associated with this injury is cervical spinal stenosis that predisposes the athlete to a transient compression or concussive type of injury to the spinal cord.2–6

In the United States, football is the most prevalent contact sport in which cervical spinal cord injuries have been characterized. However, other sports, including hockey, rugby, diving, gymnastics, and snow sports, bring the participant at risk for cervical injury. The proposed mechanism for CCN was described initially by Penning,7 who described a pincer mechanism on the spinal cord in the setting of spinal canal narrowing. With the neck in flexion, the lamina of the cephalad vertebra forces the cord against the posterior superior margin of the caudal vertebral body. In extension, the posterior inferior margin of the cephalad vertebra pinches against the lamina of the lower vertebra, causing compression of the cord and a resultant conduction block with transient cord dysfunction.8,9

Initial evaluation of the athlete with bilateral symptoms includes immobilization followed by clinical and radiographic evaluation. A catastrophic cervical spinal cord injury from a fracture, fracture dislocation, or traumatic disc herniation must be excluded. Fortunately, the rates of fracture with subsequent quadriplegia have dropped substantially over the last several decades since the work of Torg and the National Football Head and Neck Injury Registry has led to rule changes in football.9–11 In 1975, the rate of cervical fractures was 4.1 per 100,000 participants at both the high school and college level, and the rate of permanent quadriplegia was 2.2 per 100,000 high school players and 8.4 per 100,000 college players. Elimination of spearing and axial-loading blocking and tackling techniques lowered the rate of quadriplegia to 0.43 per 100,000 at the high school level and 0 at the college level by 1984,11 and the rate remains low over the most recent period that has been reported (1989–2002). Boden et al12 and Langer et al8 reported data from the National Center for Catastrophic Sports Injury Research with a rate of quadriplegia at 0.50 per 100,000 high school players and 0.82 per 100,000 college athletes over this period. As the rate of fractures and permanent quadriplegia have dropped, attention has turned to transient injury and CCN, which was initially estimated to occur in 70 per 100,000 participants at the high school and college levels.2 Although the first estimates of CCN are much higher in comparison to other catastrophic cervical injuries, recent data from the National Center for Sports Injury Research reported a rate of 0.17 per 100,000 high school players and 2.05 per 100,000 college athletes.12

CCN must be differentiated from the stinger and burner, which are unilateral injuries to the brachial plexus or a cervical nerve root in a contact athlete (Table 1).13,14 The athlete describes unilateral shoulder and arm burning or paresthesias associated with weakness in the proximal arm muscles, specifically the deltoid, biceps, supraspinatus, and infraspinatus muscles. Stingers and burners represent peripheral nerve injuries either of the cervical nerve root at the level of the neural foramen or at the trunk or division level in the brachial plexus. The incidence of stingers has been reported to be much higher than that of CCN, with up to 65% of football players experiencing a stinger during their careers14,15 and more than 50% of patients having multiple episodes throughout their careers. Several different mechanisms for stingers have been proposed: (1) contralateral flexion of the neck with depression of the ipsilateral arm is referred to as the brachial plexus type of stretch injury; (2) extension compression of a nerve root at the cervical foramen results from ipsilateral flexion with simultaneous extension of the neck, compressing an existing nerve root at the neural foramen; or (3) a direct blow to the brachial plexus. Extension compression injuries that occur in the older athlete are generally associated with cervical stenosis.16,17

Table 1
Table 1:
Comparison of the Characteristics of Transient NeuropraxiaVersusBurner, Stinger Syndromes

Although CCN usually resolves within minutes, the spinal cord concussion that occurs may portend a more serious underlying condition such as congenital, developmental, or degenerative stenosis. As a result, athletes who have an episode of CCN want to know if it is safe to return to play or if there is a chance they may develop permanent neurologic sequelae after another injury. A systematic evidence-based medical review provides insight to better define the clinical syndrome and optimize treatment strategies. Therefore, 2 clinically relevant questions for CCN pertaining to the athlete were proposed by a multidisciplinary panel consisting of fellowship-trained neurologic and orthopedic spine surgeons.

  1. Can a patient with transient neuropraxia and radiographic stenosis return to full participation in high-energy contact sports?
  2. Can a patient with transient neuropraxia but with NO radiographic stenosis return to full participation in high-energy contact sports?
  3. In addition, because anterior cervical discectomy and fusion of a single-level stenosis or disc herniation may treat the condition that caused the CCN, the question was posed,
  4. Should patients who have undergone successful single-level anterior cervical fusion be allowed to return to high-energy contact sports?

Materials and Methods

Optimal management for sport-related transient neuropraxia was analyzed through an evidence-based systematic published review further supported with clinical expert opinion. Specifically, the analysis considered how the degree of radiographic evidence of cervical stenosis influenced the decision to “clear” a patient to return back to play full contact sports. Questions (listed previously) were formulated and edited through a Delphi process by a multidisciplinary panel consisting of fellowship-trained neurologic and orthopedic spine surgeons with expertise in the treatment of spinal trauma.

Keywords pertinent to the proposed questions were selected from Medical Subject Headings, and a literature search was conducted through MEDLINE (1950–May 2009), EMBASE, and the Cochrane Database of Systematic Reviews. The initial query was further refined to limit the findings to studies that provided evidence to answer the specific questions. The abstracts of the identified articles were obtained and assessed to limit the articles to clinical series with original data. Several articles were case reports and small case series but were included because of the paucity of original data on the subject.

Each abstract was then specifically reviewed to identify articles that concentrated on the detailed study questions. The search was further supplemented with articles found in the reference sections of the index literature as well as articles independently proposed by the expert panel. The quality of the evidence of the literature was then scored as high, moderate, low, or very low based on the Grading of Recommendations Assessment, Development and Evaluation approach.18 The focus questions in conjunction with the graded literature were again analyzed by the multidisciplinary panel Spine Trauma Study Group, which provided a treatment recommendation based on the benefits, harms, and costs of the proposed interventions. This recommendation was then rated as either strong or weak based on the strength of the literature and clinical experience.


The article search using Medical Subject Headings terms limited to articles that included the keyword “sports AND spine injury” resulted in 1850 articles, and this was refined with searches of “transient quadriparesis” (153 articles) and “transient neuropraxia” (33 articles). A separate search using the terms “cervical AND sports” found 900 articles. This group was limited by searches using the terms “cervical AND sports AND stenosis” (59 articles), and finally “cervical AND neuropraxia“ (9 articles). Among the identified articles, there were no randomized studies or large multicenter series comparing treatment methods. Because this is a relatively rare condition, a true randomized, controlled, prospective study is unlikely to ever be available and the strongest literature is likely to remain as case series. The literature consisted of only limited case series and case reports. After eliminating duplicates, reviews, non-English language articles, articles with insufficient patient data, and expert opinions, 16 articles that were pertinent to the research question were included in the evidentiary table. Eleven of the 16 articles were graded as very low quality evidence whereas 5 articles were rated as low quality evidence (Table 2).

Table 2
Table 2:
Evidentiary Table
Table 2
Table 2:


Can Athletes With Neuropraxia Return to Play?

“Transient neuropraxia” or CCN was the term coined by Torg et al to describe a transient loss of motor or sensory function lasting from seconds to 36 hours after a compressive, flexion, or extension injury of the cervical spine. The injury is categorized by the bilateral nature of the signs and symptoms and is different than the injury alternately called “stinger” or “burning,” which is unilateral in character. These injuries have an incidence of 7.3 per 10,000 participants as quantified by a questionnaire sent to schools that had active football programs in the National Collegiate Athletic Association. Motor weakness was found less commonly in 1.3 per 10,000 players and sensory disturbances alone in 6 per 10,000.2

The most recent data from the National Center for Catastrophic Sports Injury Research database suggest an overall decline in the prevalence of CCN over a 13-year period ending in 2002.12 Forty-three patients over this period were reported to have experienced an episode of CCN. Mean incidence was 0.17 per 100,000 for high school and 2.05 for college athletes, which indicates a 12-fold increase at the more competitive level. Although significant rule changes with elimination of spear tackling techniques and allowing lineman to use hands for blocking have contributed to this decline, it is very difficult to judge the true incidence of CCN.4,28,29 The Center for Catastrophic Sports Injuries relies on sports physicians and trainers to report the injuries and may significantly under-report the incidence of CCN. Follow-up is also a problem for this database, as the records on fewer than 50% of athletes with CCN had any information on return to participation, although none of the 17 athletes that returned to participation had a more serious cervical spine injury with permanent neurologic sequelae.

Much of the literature on CCN is in the form of case reports or case series, which were retrospectively analyzed. As a result, our references were graded as low or very low in quality; however, we felt that we could make stronger recommendations regarding return to play based on the potentially catastrophic spine injury that could occur when athletes return to play without a full evaluation or with evidence of critical cervical stenosis and loss of any cerebrospinal fluid (CSF) space surrounding the cord.3,29,30

In the initial report describing this injury, Torg et al2 described a retrospective case series of 32 patients with transient neurologic symptoms. Seventeen patients were diagnosed with congenital stenosis and 6 of these returned to play. Three of these patients had further episodes, although none had permanent neurologic sequelae, leading the authors to conclude that athletes with instability, those with acute or chronic degenerative changes who have transient quadriparesis, or those with congenital fusions should not be allowed to return to play but those with congenital stenosis could return without risk of permanent injury.

After the initial description of the clinical entity,2 Torg et al5,31 suggested a screening method to determine whether an athlete had spinal stenosis. The Torg or Pavlov ratio is the distance from the midpoint of the posterior aspect of the vertebral body to the nearest point on the corresponding spinolaminar line, divided by the anteroposterior width of the vertebral body, measured through the midpoint of the body (spinal canal/vertebral body or SC/VB ratio). The normal ratio was approximately 1, with a ratio less than 0.8 indicative of cervical spinal stenosis. In a report of 23 patients, the mean sagittal ratio from C3–C6 was 0.69 whereas that in an asymptomatic population was 0.99.31 Subsequent measurements in a group of symptomatic players were then compared with those in a group of asymptomatic football players. Although the sensitivity of a lateral radiograph was high (93%), 41% of asymptomatic players had a ratio below 0.80, and therefore, the positive predictive value of this method was low (0.2%). The authors did note that in the group of 45 patients with CCN, none had permanent neurologic injury as a result of return to play.5

Several clinical reports support the assertion that CCN is associated with radiographic stenosis. Grant and Puffer22 reported the case of an 18-year-old football player who experienced a third episode of neuropraxia. Air myelography showed narrowing at the C3–C4 level. The player was advised not to return to sports because of the repeated episodes of neuropraxia in the setting of stenosis. Ladd and Scranton1 reported 2 cases of transient quadriparesis in National Football League players with hyperflexion injuries. Although only mild stenosis was found on plain radiographs, a computed tomography (CT) myelogram revealed significant stenosis in both patients, and retirement was recommended. Other authors have also suggested that football players are particularly prone to CCN and a decision to return to play needs to be addressed on a case-by-case basis.24–26,32

Criteria for return to play include normal neurologic function, pain-free motion, no evidence of instability, and adequate space for the spinal cord within the canal. The use of SC/VB ratio as a screening method for cervical stenosis in athletes who had neuropraxic injury or as a routine screening technique has been questioned by some authors. Odor et al33 examined 124 professional football players without complaints of neck pain or any history of arm numbness or weakness and found that 30% had a SC/VB ratio less than 0.8. Likewise in a group of rookie football players screened for a variety of complaints, 34% had a ratio less than 0.8. Herzog et al34 compared plain radiographs with either CT or magnetic resonance imaging (MRI) in 80 elite athletes. The SC/VB ratio was very sensitive (92%) for determining stenosis if stenosis was defined as a value less than 2 standard deviations below the normal mean; however, the positive predictive value was only 22%. These authors recommended that patients undergo further evaluation, preferably with MRI, if radiographs or medical history were indicative of stenosis. Others have suggested that a ratio of 0.70 is more indicative of true cervical stenosis, although this has never been examined in the clinical setting of CCN.4,35

To characterize the full spectrum of injury occurring with CCN, Torg et al19 retrospectively reviewed 110 patients (mean age: 21 years) who were referred after an episode of neuropraxia. Of the injuries, 87% were football-related. The authors classified the injuries based on the severity of the neurologic injury at presentation and whether the patient experienced plegia, paresis, or paresthesias alone. Plain radiographs (104/110) were reviewed in 104/110 patients, and MRI studies in 53/110 patients. The authors noted that 40% of the patients had complete plegia, 25% had an incomplete paresis, and 35% presented with sensory symptoms alone. The upper extremities were usually involved symmetrically, with 80% of the patients having a quadriparesis and 17% having upper extremity involvement alone. Most (74%) of the patients recovered within 15 minutes, but 15% took up to 24 hours to recover, and 11% took more than 24 hours. Patients were monitored for a mean follow-up of 3.3 years, including at least 12 months for all players who returned to play and did not retire. Overall, 63 players (57%) returned to play, 42 (38%) retired, and 5 (5%) were lost to follow-up.

In this study,19 the rate of recurrent episodes in athletes returning to play was 56%. The authors correlated 3 radiographic parameters with recurrence: SC/VB ratio; spinal canal diameter at the disc level; and space available for the cord as calculated by subtracting spinal cord diameter from canal diameter. All radiographic parameters were significantly lower in the patients who suffered recurrence (SC/VB, 0.65 vs. 0.72; canal diameter, 8.7 vs. 10.1 mm; space available for the cord, 1.1 vs. 2 mm) than in those players who did not. However, none of the patients with recurrence suffered permanent sequelae. The authors concluded that patients with neuropraxia may return to play if there was no evidence of instability or disc herniation, although logistic regression analysis showed increased risk of recurrence inversely correlated with canal diameter and SC/VB ratio.

As a result of the poor positive predictive value of plain radiographs, the concept of functional spinal stenosis as evaluated by MRI has been introduced. Cantu et al3,30 defined functional spinal stenosis as loss of the CSF space around the spinal cord or deformation of the spinal cord as defined on MRI or CT myelography. The importance of full evaluation for patients with CCN is illustrated in a case report by Brigham and Adamson23 in which a 22-year-old football player had persistent mild weakness and burning in the hands after an episode of CCN. A previous episode and a preinjury MRI study suggested stenosis, but the player was allowed to continue to play. He subsequently sustained another neck injury, he developed permanent sequelae. Bailes21 retrospectively reviewed MRI data in 10 patients with transient spinal cord injury lasting 15 minutes to 48 hours. All of these patients had stenosis of 7 to 12 mm over 3 levels on MRI. Three had no CSF space and were told to retire and did so voluntarily. Of the 4 athletes with preserved CSF who returned to contact sports, none had additional episodes of CCN. As a result, it seems as though radiographic work-up with plain radiographs and MRI give the optimal information on these players concerning return to play. If an athlete has no evidence of fracture or ligamentous instability and has preservation of CSF space around the cord on MRI imaging, return to contact sports appears to be a safe option unless the athlete is having repeated episodes of neuropraxia.

Because of the inconsistencies of the plain radiographic measurements, it is recommended that all patients who suffer a transient neuropraxia undergo a more detailed imaging of the canal dimensions, preferably with MRI, using CT/myelography if there are MRI contraindications. Radiographic stenosis then can be better defined as the lack of spinal fluid surrounding the spinal cord for the purposes of return to play decisions. There are a variety of conditions that may be identified radiographically (Table 3) that would be considered contraindications to return to play, only spinal stenosis is addressed in this review. In addition to plain radiographs to include flexion/extension and MRI imaging, these patients should be evaluated by a physician with expertise in the evaluation of subtle neurologic deficiencies, has a thorough understanding of the radiographic criteria that constitutes stenosis or other at-risk conditions, and understands the management of spine and spinal cord trauma.

Table 3
Table 3:
Radiographic Features Identifiable on Plain Radiographs, CT, or MRI Imaging That Should Be Taken Into Account When Making a Return to Play Decision and Constitute Varying Degrees of Contraindication

Although spinal stenosis is thought to be a risk factor for CCN, the concept remains debated, particularly in children. Bookvar et al20 reported on 13 patients aged 7 to 15 years who presented to an emergency room during a 1-year period. The injuries occurred during football (4), wrestling (2), hockey (2), and soccer, gymnastics, baseball, kickball, and pogo-sticking (1 each). All patients had resolution of symptoms in 5 minutes to 5 days, and all had normal Torg ratios (mean: 1.20) or spinal canal diameters (mean: 17.58 mm, range: 15–20.5 mm). Of the 10 children who had follow-up examination at a mean of 14 months, none had recurrent episodes of CCN. These authors suggested that CCN in children may be due to hypermobile ligaments and muscles in the absence of spinal stenosis. Rathbone et al27 previously reported on 12 children presenting over a 14-year period, ranging in age from 8 to 16 years. All of these patients had para- or quadriparesis, from which they recovered by 72 hours. None had instability demonstrated on radiographic imaging, but using various methods to measure stenosis, the authors found 7 of 12 patients may have had stenosis. Although the authors acknowledged that hypermobility might play a role in the CCN experienced by patients in this pediatric group, they still believed spinal stenosis might be a predisposing factor in pediatric CCN and recommended a more cautious approach to allowing a return to play.

In summary, the literature-based evidence regarding return to play after transient neuropraxia is based on case series and thus is graded as very low quality. However, it would clearly support the return to play, including contact sports, for patients with transient neuropraxia without existing cervical stenosis, and would tend to support caution if there is radiographic evidence of canal compromise. With those general concepts in mind one must remain cognizant of the values and circumstances of the individual patient. For example, a high school athlete whose future career potential does not include professional sports perhaps would not want to put them self at any future risk of neurologic injury, whereas the professional athlete who stands to make a substantial financial gain by return to play would be more willing to accept some degree of risk. On the basis of this data and clinical experience extracted from Orthopedic and Neurosurgeons participating in the Spine Trauma Study Group, with a practice heavy in spine trauma, the following recommendations can be made at this time.

  1. A weak recommendation that patients with transient neuropraxia and radiographic evidence of cervical canal compromise should be withheld from participation in contact sports that place the neck at risk,
  2. A strong recommendation that patients with transient neuropraxia and without cervical stenosis can return to full sports activities.

Return to Play After Single-Level Anterior Cervical Decompression and Fusion (ACDF)

Numerous authors have reported a direct correlation between the degree of spinal canal stenosis and the incidence of traumatic spinal cord injury, particularly with high-energy or contact sports.3,36,37 Therefore, recommendations have evolved such that in the setting of cervical stenosis athletes should not return to an environment with increased risk of high-energy collisions and potential for cervical spinal cord trauma.1,30,36,38

Repetitive loading on the spinal axis such as occurs in collisions or contact sports may result in the propagation and development of spinal osteophytes, disc degeneration, and stenosis. These alterations in the cervical spine often lead to spondylosis and restricted range of motion.39–42 Lark and McCarthy39 analyzed the influence of a single game of rugby on the range of motion of a player's cervical spine in 21 professional players. The authors reported that even a single game resulted in a significant reduction in the players' range of motion, and this effect was most pronounced in the higher impact positions, where the greatest degree motion was lost. Therefore, the cumulative effects of numerous games and impacts would most likely result in considerable deterioration of the cervical spine in terms of stenosis and reduced range of motion.

The relationship between cervical stenosis, high-energy mechanisms of injury, and neurologic injuries has been detailed in the literature.3,23,38,43–47 However, does the converse situation, in which an athlete has a procedure to eliminate stenosis, provide a safe environment to return back to collision sports? However, there is very sparse literature on this topic, and we were only able to identify a single retrospective review related to return to sports after anterior cervical discectomy and fusion. Nonetheless, several authors have reported through guidelines and management algorithms that there is no contraindication after a single-level anterior cervical fusion to return to contact sports if an individual has a solid arthrodesis, no neurologic deficit, and normal cervical range of motion.43,48,49

In the single article related to these finding, Andrews et al50 retrospectively reviewed 19 professional rugby players that underwent anterior cervical discectomy and fusions over a 5-year period. The aim of the article was to assess the safety and efficiency of this procedure during the postoperative period in a high-energy contact sport setting and document if athletes were able to return to this physically demanding arena. Seventeen of the 19 players had a single-level anterior cervical discectomy and fusion, and 2 had a 2-level procedure. Both of the patients that had a 2-level discectomy and fusion had difficulties after surgery and did not return to play high-impact sports. However, 13 of the 17 players who underwent a single-level procedure did return to contact sports, and the majority returned within 6 months of the procedure. Although the authors concluded, “a return to playing rugby union after surgery and fusion of the anterior cervical spine is both likely and safe and need not end a career in the game,” it should be noted that 15% (2/13) of these players suffered further symptoms in the neck and 1 eventually retired as the result of the injury.50 Moreover, the authors discussed the safety of returning to sports after an anterior cervical discectomy and fusion procedure but did not address or confirm that any stenotic region of the spinal canal was decompressed. In addition, the operative procedures based on the patients' medical histories and symptoms appear to have been performed for radicular pain rather than myelopathic symptoms. Therefore, the article does not directly address whether there was a stenotic region when the athletes returned to the sports arena.

Numerous management algorithms report that there is no restriction on returning to sports after a single-level anterior cervical discectomy and fusion if the stenotic region of the canal is removed and the patient does not have restricted range of motion after the procedure.38,43,48,50–52 The original reference from which these recommendation arises appears to be the 1997 guidelines by Torg and Ramsey-Emrhein regarding returning to sports with postinjury lesions.51 In this article, there is a discussion on the management of patients with Klippel-Feil syndrome that have 1 or 2 fused segments distal to the C3 vertebra. Torg and Ramsey-Emhrein comment that “with full cervical range of motion and an absence of occipital cervical anomalies, instability, disc disease, or degenerative changes, should present no contraindication” to return back to sports.51 This recommendation is based on the work by Pizzutillo,53 who reported that children with these types of congenital cervical spinal fusions, Klippel-Feil, rarely develop neurologic signs or symptoms.

Morganti et al54 analyzed 113 detailed questionnaires completed by spine physicians on the management of 10 clinical vignettes of athletes with cervical spine trauma. The authors concluded that there is “no consensus on the postinjury management of many cervical spine-injured patients.” However, they do note the association between stenosis, restricted range of motion, and neurologic injury in the athlete. There is very weak literature supporting returning to sports after an anterior cervical discectomy and fusion in particular; however, the overall recommendation to allow a return is based on the expert opinion resulting from experience from clinical practice and indirect literature on the topic. Therefore, surgical fixation with single-level ACDF and no residual cervical stenosis is a strong recommendation as a treatment option to return to full contact sport play. The pathology addressed by the ACDF may include radicular as well as myelopathic syndromes as long as the canal dimensions are restored and the neurologic compromise was at a single level.


  1. It is a weak recommendation that patients with transient neuropraxia should not return to full participation in high-energy contact sports if they have radiographic stenosis demonstrated on MRI.
  2. It is a strong recommendation that patients with transient neuropraxia may consider return to full participation in high-energy contact sports if radiographic studies show no radiographic stenosis demonstrated on MRI.
  3. Surgical fixation with single-level ACDF to eliminate single level neurologic compression causing radiculopathy or myelopathy is a strong recommendation as a treatment option to return to full-contact sport play.

Key Points

  • There is only low and very low quality evidence concerning treatment of cervical spine sport-related injuries resulting in transient neurologic symptoms (neuropraxia) and no prospective or randomized studies.
  • A weak recommendation can be given for patients that suffer transient neuropraxia who also have radiographic stenosis should not return to full participation in high-energy contact sports.
  • A strong recommendation can be given for patients with transient neuropraxia who have no underlying radiographic stenosis as defined by MRI to consider return to full participation in high-energy contact sports.
  • When surgical fixation with single-level anterior cervical discectomy and fusion is used eliminate a single-level cervical neurocompression a strong recommendation can be given to allow return to full-contact sport play.


The authors thank Kristin Kraus for her editorial assistance with the manuscript.


1.Ladd A, Scranton P. Congenital cervical stenosis presenting as transient quadriplegia in athletes. Report of two cases. J Bone Joint Surg Am 1986;68:1371–4.
2.Torg J, Pavlov H, Genuario S, et al. Neurapraxia of the cervical spinal cord with transient quadriplegia. J Bone Joint Surg Am 1986;68:1354–70.
3.Cantu RC. Stingers, transient quadriplegia, and cervical spinal stenosis: return to play criteria. Med Sci Sports Exerc 1997;29:S233–5.
4.Castro F. Stingers, cervical cord neurapraxia, and stenosis. Clin Sports Med 2003;22:483–92.
5.Torg J, Naranja R, 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.
6.Torg JS. Cervical spinal stenosis with cord neurapraxia and transient quadriplegia. Sports Med 1995;20:429–34.
7.Penning L. Some aspects of plain radiography of the cervical spine in chronic myelopathy. Neurology 1962;12:513–9.
8.Langer P, Fadale P, Palumbo M. Catastophic neck injuries in the collision sport athlete. Sports Med Athrosc 2008;16:7–15.
9.Torg JS, Guille JT, Jaffe S. Injuries to the cervical spine in American football players. J Bone Joint Surg Am 2002;84:112–22.
10.Torg JS, Truex R Jr, Quedenfeld TC, et al. The National Football Head and Neck Injury Registry. Report and conclusions 1978. JAMA 1979;241:1477–9.
11.Torg JS, Vegso JJ, Sennett B, et al. The National Football Head and Neck Injury Registry. 14-year report on cervical quadriplegia, 1971 through 1984. JAMA 1985;254:3439–43.
12.Boden B, Tacchetti R, Cantu R, et al. Catastrophic cervical spine injuries in high school and college football players. Am J Sports Med 2006;34:1223–32.
13.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.
14.Shannon B, Klimkiewicz J. Cervical burners in the athlete. Clin Sports Med 2002;21:29–35.
15.Sallis R, Jones K, Knopp W. Burners offensive strategy for an under reported injury. Phys Sportsmed 1992;20:47–55.
16.Kelly JI, Aliquo D, Sitler M, et al. Association of burners with cervical canal and foraminal stenosis. Am J Sports Med 2000;28:214–7.
17.Meyer S, Schulte K, Calllaghan J, et al. Cervical spinal stenosis and stingers in collegiate football players. Am J Sports Med 1994;22:158–66.
18.Schunemann H, Jaeschke R, Cook D, et al. An official ATS statement: grading of the quality of evidence and strength recommendations in ATS guidelines and recommendations. Am J Respir Crit Care Med 2006;174:605–14.
19.Torg J, Corcoran T, Thibault L, et al. Cervical cord neurapraxia: classification, pathomechanics, morbidity and management guidelines. J Neurosurg 1997;87:843–50.
20.Bookvar J, Durham S, Sun P. Cervical spinal stenosis and sports-related cervical cord neurapraxia in children. Spine 2001;26:2709–13.
21.Bailes J. Experience with cervical stenosis and temporary paralysis in athletes. J Neurosurg Spine 2005;2:11–6.
22.Grant T, Puffer J. Cervical stenosis: a developmental anomaly with quadriparesis during football. Am J Sports Med 1976;4:219–21.
23.Brigham C, Adamson T. Permanent partial cervical spinal cord injury in a professional football player who had only congenital stenosis: a case report. J Bone Joint Surg Am 2003;85:1553–6.
24.Finoff J, Mildenberger D, Cassidy C. Central cord syndrome in a football player with congenital spinal stenosis. Am J Sports Med 2004;32:516–21.
25.Funk F, Wells R. Injuries of the cervical spine in football. Clin Orthop Relat Res 1975;109:50–8.
26.Maroon J. “Burning hands” in football spinal cord injury. JAMA 1977;238:2049–51.
27.Rathbone D, Johnson G, Letts M. Spinal cord concussion in pediatric athletes. J Pediatr Orthop 1992;12:616–20.
28.Allen C, Kang J. Transient quadriparesis in the athlete. Clin Sports Med 2002;21:15–27.
29.Boden B, Jarvis C. Spinal injuries in sports. Neurol Clin 2008;26:63–78.
30.Cantu RC, Bailes JE, Wilberger JE Jr. Guidelines for return to contact or collision sport after a cervical spine injury. Clin Sports Med 1998;17:137–46.
31.Pavlov H, Torg J, Roble B, et al. Cervical spinal stenosis: determination with vertebral body ratio method. Radiology 1987;164:771–5.
32.Stratford J. Congenital cervical spinal stenosis a factor in myelopathy. Acta Neurochir 1978;41:101–6.
33.Odor J, Watkins R, Dillin W, et al. Incidence of cervical spinal stenosis in professional and rookie football players. Am J Sports Med 1990;18:507–9.
34.Herzog R, Wiens J, Dillingham M, et al. Normal cervical spine morphometry and cervical spinal stenosis in aymptomatic professional football players: plain film radiography, multiplanar computed tomography and magnetic resonance imaging. Spine 1991;16:S178–86.
35.Castro FP Jr, Ricciardi J, Brunet ME, et al. Stingers, the Torg ratio, and the cervical spine. Am J Sports Med 1997;25:603–8.
36.Eismont FJ, Clifford S, Goldberg M, et al. Cervical sagittal spinal canal size in spine injury. Spine (Phila Pa 1976) 1984;9:663–6.
37.Kang JD, Figgie MP, Bohlman HH. Sagittal measurements of the cervical spine in subaxial fractures and dislocations. An analysis of two hundred and eighty-eight patients with and without neurological deficits. J Bone Joint Surg Am 1994;76:1617–28.
38.Morganti C. Recommendations for return to sports following cervical spine injuries. Sports Med 2003;33:563–73.
39.Lark SD, McCarthy PW. The effects of a single game of rugby on active cervical range of motion. J Sports Sci 2009;27:491–7.
40.Mehnert MJ, Agesen T, Malanga GA. “Heading” and neck injuries in soccer: a review of biomechanics and potential long-term effects. Pain Physician 2005;8:391–7.
41.Tysvaer AT. Head and neck injuries in soccer. Impact of minor trauma. Sports Med 1992;14:200–13.
42.Tsirikos A, Papagelopoulos PJ, Giannakopoulos PN, et al. Degenerative spondyloarthropathy of the cervical and lumbar spine in jockeys. Orthopedics 2001;24:561–4.
43.Vaccaro AR, Watkins B, Albert TJ, et al. Cervical spine injuries in athletes: current return-to-play criteria. Orthopedics 2001;24:699–703; quiz 704–5.
44.Torg JS. Cervical spinal stenosis with cord neurapraxia and transient quadriplegia. Clin Sports Med 1990;9:279–96.
45.Torg JS. Epidemiology, pathomechanics, and prevention of football-induced cervical spinal cord trauma. Exerc Sport Sci Rev 1992;20:321–38.
46.Torg JS. Cervical spinal stenosis with cord neurapraxia: evaluations and decisions regarding participation in athletics. Curr Sports Med Rep 2002;1:43–6.
47.Torg JS, Pavlov H. Cervical spinal stenosis with cord neurapraxia and transient quadriplegia. Clin Sports Med 1987;6:115–33.
48.Jeyamohan S, Harrop JS, Vaccaro A, et al. Athletes returning to play after cervical spine or neurobrachial injury. Curr Rev Musculoskelet Med 2008;1:175–9.
49.Vaccaro AR, Klein GR, Ciccoti M, et al. Return to play criteria for the athlete with cervical spine injuries resulting in stinger and transient quadriplegia/paresis. Spine J 2002;2:351–6.
50.Andrews J, Jones A, Davies PR, et al. Is return to professional rugby union likely after anterior cervical spinal surgery? J Bone Joint Surg Br 2008;90:619–21.
51.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 Sports Exerc 1997;29:S256–72.
52.Torg JS, Ramsey-Emrhein JA. Management guidelines for participation in collision activities with congenital, developmental, or post-injury lesions involving the cervical spine. Clin Sports Med 1997;16:501–30.
53.Pizzutillo PD. Spinal considerations in the young athlete. Instr Course Lect 1993;42:463–72.
54.Morganti C, Sweeney CA, Albanese SA, et al. Return to play after cervical spine injury. Spine (Phila Pa 1976) 2001;26:1131–6.
55.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.
56.Shelly MJ, Butler JS, Timlin M, et al. Spinal injuries in Irish rugby: a ten-year review. J Bone Joint Surg Br 2006;88:771–5.
57.Scher AT. Spinal cord concussion in rugby players. Am J Sports Med 1991;19:485–8.

neuropraxia; sport; stinger; burner; cervical

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