- Email: [email protected]
Ligamentous Injuries
Cervical Spine Injuries in Athletes: Cervical Disk Herniations and Fractures/Ligamentous Injuries Brian W. Su, MD,* and Alan S. Hilibrand, MD† Cervical spine injuries in the athlete range from a simple stinger to cervical cord neuropraxia and in some cases complete spinal cord injuries. These injuries can be a result of a herniated disk or fracture dislocation of the spine. Treatment is tailored to the degree of neurological injury and location of neural compression as well as the desire to return to sports. Radiographic criteria of ligamentous instability and characteristics of fractures that are known to progress to instability are critical for treatment decision-making. The mainstay of surgical treatment is decompression and fusion with many patients allowed to return to contact sports after a healed single level fusion. Although the results of cervical disk replacements are promising in the general population, in athletes who wish to return to collision sports, a cervical disk replacement is not recommended. Semin Spine Surg 22:198-205 © 2010 Elsevier Inc. All rights reserved. KEYWORDS cervical spine, athletes, fractures, ligamentous injury
A
thletic injuries to the cervical spine account for 10% of the 10,000 cervical spine injuries in the United States.1 The severity of neurological injury can range from a single episode of radiculopathy to complete quadriplegia secondary to a fracture or dislocation. Contact and collision sports, such as football, have been specifically implicated in catastrophic injuries. The incidence of complete quadriplegia among high school and college football athletes has been reported to range between 2.5 per 100,000 (reported in 1976) and 0.5 per 100,000 (reported in 1991).2 This discrepancy is at least in part the result of system-wide changes for protective equipment and rule changes, such as the banning of spear tackling, which has been implicated in causing neurological injuries in football.3 Two of the most commonly reported and studied neurological injuries in contact athletes are “stingers” and cervical cord neuropraxia (CCN). Although a herniated disk can cause either phenomenon, it is important to clearly differentiate the 2 entities on the basis of clinical presentation because they have differing pathophysiology and clinical management. CCN is a transient neurological phenomenon that presents as temporary bilateral burning paresthesias and is associated with various degrees of bilateral extremity weakness. There
*Mt. Tam Spine Center, Larkspur, CA. †The Rothman Institute, Philadelphia, PA. Address reprint requests to Alan S. Hilibrand, MD, The Rothman Institute, 925 Chestnut St, Philadelphia, PA 19107. E-mail: ahilibrand@gmail. com
198
1040-7383/$-see front matter © 2010 Elsevier Inc. All rights reserved. doi:10.1053/j.semss.2010.06.008
can be varying degrees of neurological involvement affecting 2 or 4 limbs. The duration of symptoms is typically only 10 to 15 minutes, but some patients can have residual symptoms up to 36 hours.4 The incidence in college football players is 1.3 per 100,000,5 and the mechanism of injury is thought to be hyperflexion, hyperextension, and axial compression forces.6 Torg et al7 described and classified CCN in 110 cases and found that it was not associated with permanent neurological injury, and no permanent morbidity occurred in patients who returned to contact activities. Evaluation of athletes who had CCN revealed a consistent finding of developmental narrowing of the canal, protrusion of a disk, or instability of the cervical spine.7 Torg et al5 proposed a ratio of canal to vertebral body depth of less than 0.8 as a risk factor for CCN with a sensitivity of 90%. However, Herzog et al8 found that approximately 33% of asymptomatic and 49% of all players have low Torg ratios, leading to low positive predictive values (PPV 0.2%) for determining future neuropraxic injuries and effacement of the subarachnoid space on magnetic resonance image (MRI; PPV 13%). Maroon et al9 recently examined the pathologic findings in 5 elite football players who had cervical neuropraxia. In all cases, MRI demonstrated marked focal cord compression secondary to a herniated disk and degenerative changes at a single level (Fig. 1).9 A “stinger” is descriptive of a unilateral upper extremity sensory disturbance and commonly motor weakness an athlete experiences at the time of injury. Stingers or burners are extremely common and can occur in as many as 50% of athletes involved in contact or collision sports.10,11 It occurs
Cervical disk herniations and fractures/ligamentous injuries
199
Figure 1 Five examples of focal neural compression secondary to disk disease in professional football players. (Reprinted with permission from Maroon et al.9)
because of an overload to the cervical spine and is not a result of spinal cord injury.12 Mechanisms proposed for a stinger include traction to the brachial plexus, compression to the brachial plexus from a direct blow, or compression of the nerve root within the cervical foramen from an extension injury. Mundt et al13 examined the association between participation in noncontact sports and herniated cervical intervertebral disks and found that most noncontact sports are not associated with an increased risk of herniation. The mechanism of protection was hypothesized to be secondary to improved muscular conditioning that protected the disk from stresses placed on the spine.13 On the contrary, Levitz et al14 studied 55 contact athletes with recurrent burners and found that 83% had a mechanism of injury of extension combined with ipsilateral-lateral deviation, with 70% exhibiting a positive Spurling’s sign.14 Twentynine patients (53%) had developmentally narrowed cervical canals, and 48 patients (87%) had evidence of disk disease by magnetic resonance imaging.14 They defined “disk disease” as either a disk bulge, disk protrusion, or a frank disk herniation deforming the cord. Fifty-one patients (93%) had disk disease or narrowing of the intervertebral foramina secondary to degenerative disk disease.14 The authors concluded that nerve root compression in the intervertebral foramina secondary to disk disease is a common cause in athletes with recurrent or chronic burner syndromes.14 Similarly, Meyer et al15 studied 266 football players and found that 15% reported a symptomatic stinger with most football players having an extension compression mechanisms rather than a brachial plexus stretch mechanism implying that foraminal compression led to the stinger. Although the Torg ratio was developed to examine stenosis in patients with cervical neuropraxia, Meyer et al15 evaluated the relationship of cervical stenosis in 40 football players who had stingers. The mean Torg ratio was significantly smaller for the stinger group compared with the asymptomatic group and the Torg ratio was less than 0.8 at one or more levels in
47.5% of the stinger group; players with a Torg ratio less than 0.8 had 3 times the risk of incurring stingers.15 This study agrees with that by Levitz et al,14 which indicates that there may be a relationship between central stenosis and the development of foraminal stenosis leading to “stingers” from root compression. The combination of disk disease and cervical spinal canal stenosis that leads to shortened pedicles may lead to an alteration in normal cervical spine mechanics that may make these athletes more prone to chronic burner syndromes secondary to foraminal stenosis. Because of their inherent mobility, the fifth, sixth, and seventh nerve roots are the most susceptible to injury.12 Fractures and ligamentous injuries have also been well described in collision sports. Albright et al16 examined the incidence of nonfatal neck injuries in high school football players with an injury significant enough to have caused the athlete to miss at least 1 practice or game. The incidence of radiographic evidence of neck injuries (compression fracture, abnormal motion, abnormal disk space, and neural arch fracture) was as high as 32% and was related to years of experience with a significant increase in injury after the junior high school year.16 Cantu and Mueller17 found that catastrophic football injuries resulted from either a combined fracture-dislocation (33%) or an anterior compression fracture (22%). In a study of 193 catastrophic cervical spine injuries in high school and college football players, Boden et al6 found that 95 athletes had a fracture, dislocation, or major ligamentous injury in the subaxial cervical level, 9 athletes at the C1 or C2 levels, and 7 athletes at combined upper and lower levels. The importance of recognizing injuries with subtle presentations, such as an anterior vertebral compression fracture but result in instability is outlined by Webb et al who described 7 patients who developed late vertebral deformity after flexion injuries of the cervical spine.18 All of these cases were associated with an anterior vertebral compression fracture.18 They described a radiological tetrad that suggested damage to the posterior interspinous complex of the cervical
200 spine: (1) interspinous widening, (2) vertebral subluxation, (3) vertebral compression fracture, and (4) loss of cervical lordosis.18 One important type of fracture of particular concern in athletes participating in contact sports is the teardrop fracture. In 1956, Kahn and Schneider19 described a teardrop fracture as a triangular fracture fragment at the anterior-inferior corner of a cervical vertebral body. Their description was determined solely by analysis of lateral radiographs and did not mention a sagittal body or posterior arch fracture; both subsequently recognized as important components of the fracture type.19 Torg et al20 subsequently analyzed 58 teardrop fractures included in the National Football Head and Neck Injury Registry (Fig. 2). Most of The fractures were at C5 with 2 types of teardrop fractures described; (1) an isolated fracture of the anterior-inferior corner of the vertebral body (2) an additional sagittal fracture of the vertebral body, ie, a three-part, two-plane fracture pattern through the lamina. In the absence of a fracture, it is also critical to rule out ligamentous instability of the cervical spine. In a classic 1975 biomechanical analysis by White et al,21 the stability of the cervical spine was described in relationship to the ligaments and facets. The authors defined the anterior elements to include the posterior longitudinal ligament (PLL) and all the anatomic structures anterior to it, including the intervertebral disk.21 The posterior elements included the structures posterior to the PLL (Fig. 3).21 The ligaments were transected from anterior to posterior as well as posterior to anterior and then tested biomechanically in flexion and extension.21 Displacement with all ligaments intact were very small with no horizontal displacement exceeding 2.7 mm and no angular displacement exceeding 10.7 degrees.21 On the basis of magnification of a standard cervical spine radiograph, this led to greater than 3.5 mm of horizontal displacement as evidence of instability in a clinical setting.21 This detail regarding horizontal displacement is important to emphasize particularly in the era of digital radiographs because displacement is now commonly measured with a precalibrated scale on a com-
Figure 2 Tear drop fracture which includes an anterior-inferior vertebral body fracture, sagittal fracture, and posterior arch fracture. (Reprinted with permission from Torg et al.20)
B.W. Su and A.S. Hilibrand
Figure 3 Diagram of anatomy of cervical motion segment demonstrating the anterior and posterior elements. Anterior elements include the PLL and all the anatomic structures anterior to it, including the intervertebral disk. The posterior elements included the structures posterior to the PLL. (Reprinted with permission from White et al.21)
puter monitor rather than by hand from a printed radiograph. As such, no normal adult spine free of degenerative changes should demonstrate horizontal motion of more than 2.7 mm between vertebrae on either flexion or extension.21 Because angulation is not effected by magnification, the authors set ⬎11 degrees of angulation more than either normal adjacent vertebra as unstable (Fig. 4).21 Notably, with some ligaments cut and just before complete failure, the maximum displacement recorded was 4.9 mm, and the maximum angular displacement was 15.7 degrees, indicating that only modest displacement occurs before complete and sudden failure. There was not a stepwise increase in deformation of the spine with each ligament transected but rather very small changes in displacement before complete catastrophic failure with no predictable “prefailure” phase.21 Examination of the importance of ligamentous structures led to the conclusion that if a motion segment has all of its anterior elements “plus one” additional posterior structure, or all of its posterior elements “plus one” of the additional anterior structures then the spine would be stable under physiological loads.21 If any one of the following 3 condition exists, then
Cervical disk herniations and fractures/ligamentous injuries
Figure 4 (A) On a neutral, flexion, or extension lateral x-ray, no normal adult spine should permit horizontal motion of more than 2.7 mm (3.5 mm if measured on a printed radiograph) or (B) greater than 11 degrees of angulation more than either normal adjacent vertebra. (Reprinted with permission from White et al.21)
the spine is unstable or on the brink of instability: (1) either all the anterior or all the posterior elements are destroyed; (2) more than 2.7 mm (3.5 mm on a printed radiograph) of horizontal displacement of 1 vertebra in relation to an adjacent vertebra anteriorly or posteriorly measured on a neutral, flexion, or extension radiograph; or (3) more than 11 degrees of rotational difference to that of either adjacent vertebra, measured on a neutral, flexion, or extension radiograph.21
Management In football players with radiological abnormalities, at the time of injury, approximately 1 of 3 players experience more than
201 neck pain.16 This often includes upper extremity weakness and numbness, headaches, or transient visual disturbances.16 Management of players with stingers, CCN, and fractures or ligamentous injury always begins with a detailed assessment on the sideline with particular attention to mechanism of injury, distribution and duration of symptoms, evaluation of cervical range of motion within pain tolerance, palpation for muscle spasm, localized bony tenderness, and a detailed neurological examination. Interestingly, in a series of athletes with cervical spine injuries presented by Albright et al,16 a licensed physician examined only 55% of injured players, while another 11% were seen by a chiropractor. The management of a “stinger” has been well described by several authors.12,22,23 The duration of pain can vary from seconds to hours, rarely persisting longer than several days, although specific myotomal weakness can persist even longer. Athletes should not return to play in the same game if there is loss of cervical range of motion or persistent pain and weakness. If weakness persists for more than 2 weeks or worsens over the first few days, electromyography is reasonable as early as 7 days after the onset of symptoms. Imaging studies should include flexion and extension views for evaluation of any fractures or instability. Central stenosis as measured by the Torg ratio in the setting of a “stinger” may prompt obtaining an MRI, which is useful for evaluating the presence of central stenosis, foraminal stenosis, and any cord compromise. Some authors have advocated that an acute disk herniation be ruled out before return to play if significant pain and weakness occurs in the setting of a stinger.12 In a series of professional football players presented by Maroon et al,9 a linebacker experienced 8 to 9 episodes of upper-extremity paraesthesia that resolved and were thought to be stingers. A subsequent MRI demonstrated marked cord compression from a disk herniation.9 If an MRI does not demonstrate significant central or foraminal stenosis, the patient with a resolved stinger should focus on neck strengthening and stretching in a comprehensive program that is aggressive but does not cause further injury to the patient.22,23 By contrast, if an MRI demonstrates significant stenosis secondary to a disk herniation, the patient should be managed more cautiously and largely as any nonathlete patient who presents with a first-time disk herniation. If foraminal stenosis is present and correlates to the patient’s clinical symptoms/examination, it is our preference to begin with a selective nerve root injection at the affected level followed by range of motion and strengthening exercises. Bush and Hillier24 reported clinical success and avoidance of surgery using selective cervical nerve root injections. If symptoms persist after 6 weeks of nonoperative treatment, the patient is offered surgical intervention. The management of a player with CCN includes immediate removal from sporting that particular event.4 A complete neurological and radiographic examination should be performed on a timely basis. If the patient complains of neck stiffness and constant neck pain, the patient has a fracture unless proven otherwise. Following stabilization, the patient should be taken to a medical facility and undergo appropriate imaging studies, including X-ray, computed tomography
202 (CT), and MRI for evaluation of fracture, ligamentous injury, or a disk herniation. It is critical to be able to see the C7/T1 junction which often requires a CT scan. In the absence of a fracture or ligamentous injury leading to instability or a persistent neurological deficit, surgical intervention is not indicated in patients who have focal cord compression secondary to a herniated disk. A central disk herniation should be treated similarly to the nonathlete with conservative care. However, if a player desires to return to play, surgical treatment should be considered, as focal spinal cord compression from a disk herniation is a contraindication to play. Surgery for a herniated disk can be approached from an anterior or posterior approach. A posterior laminoforaminotomy is limited to a smaller cohort of patients as it requires the disk herniation to be lateral to the boundary of the spinal cord. A posterior approach would only be suitable for a patient with a herniated disk leading to foraminal stenosis and recurrent stingers. Plain radiographs must also demonstrate no disk narrowing, osteophyte formation, or motion of flexion extension films. One potential advantage is that a laminoforaminotomy may allow a faster return to play because a fusion procedure is not performed. As such, some authors have suggested expanding the indications for a posterior procedure in this subset of patients.25 Our procedure of choice in an athlete with a herniated disk is an anterior cervical diskectomy and fusion (ACDF) with allograft. In long-term studies, an ACDF has been shown to result in relief of radicular pain in approximately 90% of patients with an equally high fusion rate.26 One benefit of anterior surgery in this setting is the avoidance of any muscle dissection, which is required with any posterior procedure. It is our preference to use plate fixation for all ACDFs, particularly in athletes who have an increased biomechanical demand on the construct and to minimize postoperative immoblilization. Plating has been shown to increase fusion rates, particularly for 2 or more level ACDFs with Wang et al27 reporting an increase in fusion rates from 75% to 100%. When allograft is used, plating significantly increases fusion rates in both 1 and 2 level ACDF.28 Use of a cervical disk replacement (CDR) in an athlete with a cervical disk herniation is discussed later in this manuscript. In all athletes with persistent neck pain, it is imperative to rule out a fracture or ligamentous injury with a CT or MRI scan. Mazur and Stauffer29 reported on 27 patients who had seemingly stable compression cervical vertebral fractures. Although most patients healed without problems, 6 patients demonstrated persistent progressive postinjury instability related to posterior ligament rupture.29 As muscle spasm diminished, the patients could be given a more reliable flexion-extension radiographic examination, unmasking the hidden posterior instability.29 Close follow-up of patients with simple compression fractures of the cervical spine is mandatory.29 In the series of teardrop fractures described by Torg et al,20 45 patients in the series were permanently quadriplegic, and 10 had transient neurologic symptoms.20 All but 1 patient with an isolated corner fracture had no serious neurologic injury. Of the 49 patients with a documented 3-part, 2-plane injury, 44 (90%) were quadriplegic.20 It is therefore critical to study
B.W. Su and A.S. Hilibrand advanced imaging, ie, CT scan to determine whether the injury is an isolated corner fracture or a 2-plane fracture that includes a sagittal split of the vertebral body and a fracture of the posterior neural arch, which is usually associated with neurologic sequelae.20 The treatment of fractures and dislocations in athletes is similar to that for nonathletic cervical spine trauma. Patients with fractures, dislocation, or ligamentous injuries in the setting of a spinal cord injury should be decompressed and stabilized as soon as possible.
Cervical Disk Replacement in Athletes CDR has been gaining popularity as an alternate to an ACDF for treatment of radiculopathy or myelopathy secondary to a herniated disk at a single level. The advantage of motion preserving technology, such as the CDR, is a possible longterm reduction in rates of adjacent level degeneration. This is particularly interesting in the setting of athletes because Maroon et al9 have demonstrated an increased chance of repeated herniation above or below a fused level after an ACDF. There are no clinical studies related to the outcomes of CDR specifically in athletes. However, it is important to consider that athletes withstand greater loads to the cervical spine, making the biomechanical stability and ingrowth of a specific CDR device a particularly important consideration. As of 2009, the Food and Drug Administration-approved CDRs, which had a minimum of 2 year follow-up, included the Prestige ST (Medtronic Sofamor Danek, Memphis, TN), Bryan (Medtronic Sofamor Danek, Memphis, TN), and Prodisk-C (Synthes Spine, Paoli, PA). The current Food and Drug Administration indication for CDR is the treatment of radiculopathy and/or myelopathy due to neural compression caused by a disk herniation or spondylotic changes at a single level between C3-7 which has been refractory to at least 6 weeks of nonoperative treatment. When the Prestige ST CDR was compared with an ACDF, there were no differences in any functional outcome measure at 2 years.30 Similarly, Murrey et al31 reported on a randomized controlled trial comparing the Prodisk-C CDR to a single-level ACDF and found that at 1 and 2 years, there were no differences in any outcomes between the 2 groups. Heller et al32 reported on the 2-year outcomes of the Bryan CDR and found significant improvements in SF-36 mental component score, physical component score, and arm pain scores at 1 year follow-up in favor of the CDR, but these differences were not maintained at 2 years. However, the CDR group did have statistically lower Neck Disability Index and neck pain scores, that is, 16 versus 19 for Neck Disability Index and 23 versus 30 for neck pain at 2 years.32 Other studies of the Bryan CDR have demonstrated similar improvements in functional outcomes to the U.S. Investigational Device Exemption studies.33-35 In summary, the clinical improvement after CDR at 2-year follow-up seems to be similar to an ACDF. However, it is important to point out that there are no published outcomes with longer than 2-year follow-up after CDR. In addition, it appears that there is
Cervical disk herniations and fractures/ligamentous injuries preservation of range of motion with CDR, as Murrey et al31 have reported that at 2 years, 84% of the Prodisk C CDR group had 4° or greater of motion on flexion/extension radiographs. If the surgeon is considering a CDR, it is critical to follow the strict guidelines for exclusion that have been described in the published Investigational Device Exemption studies. Exclusion criteria are typically: Instability based on flexion/extension x-rays, including translation greater than 3 mm,31 greater than 11 degrees of rotational difference to that of either adjacent level,31 a fused level adjacent to the level treated,31 severe facet joint disease or degeneration,31 spondylosis evidenced by bridging osteophytes,31 reduction of motion at the index segment,32 loss of disk height greater than 50%,31 absence of motion (⬍2°), cervical kyphosis,32 or osteoporosis.31 The axial load placed on the cervical spine during contact sports is larger than the general population. This is an important consideration if an athlete is going to return to contact sports following a CDR. Duggal et al36 analyzed the strength of the normal cervical spine versus the strength after a single level Bryan CDR in a cadaveric model. A pure moment was applied to induce flexion, extension, or axial rotation until the segment failed. The prosthesis provided 63%, 45%, and 69% of the strength of a normal spine during flexion, extension, and rotation, respectively. There were no cases of prosthesis expulsion. This study does not evaluate the strength of a CDR after ingrowth of the implant, which presumably increases the strength profile on the basis of the extent of ingrowth. Jensen et al37 studied end plate ingrowth in retrieved Bryan CDR from 2 humans who had removal of the CDR and revision for failure. Bony ingrowth was quantified at a mean of 30% with no differences between peripheral, intermediate, or central locations. The degree of ingrowth was similar to that for the femoral component of total hip replacements from human retrieval studies (range, 16%-35%). The same study implanted the Bryan CDR in 2 primates and reported a range of 10% to 50% of bony ingrowth at 3 months post operatively at the bone/metal interface.37 On the basis of limited animal and human studies on CDR, it is reasonable to assume that most bone ingrowth occurs in the first 3 months after implantation and that if a patient received a CDR, athletic activities should be limited for the first 3 months. As such, a CDR in an athlete would preclude return to sport sooner than 3 months. On the basis of the uncertain strength profile after a CDR, if an athlete with a cervical disk herniation wishes to return to collision sports, our opinion is that he/she should undergo ACDF. It is logical that a fusion procedure is inherently more stable than a motion sparing procedure. However, an athlete who does not wish to return to contact sports may be an ideal candidate for a CDR because such individuals are younger active patients without posterior facet arthrosis who have a greater potential to benefit over time from a potential decreased risk of adjacent level degeneration.
203
Return-to-Play Guidelines The relative paucity of neurological injuries and ligamentous/ bony injuries in athletes has necessitated reliance upon small case series and expert opinion to determine return to play guidelines. In 1997, after an extensive literature review, Torg and Ramsey-Emrhein38 determined management guidelines for participation in collision activities with congenital, developmental, or post injury lesions of the cervical spine. These guidelines were developed from the best-available data compiled from more than 1200 cervical spine injuries documented by the National Football Head and Neck Injury Registry39-41 as well as clinical and anecdotal experience. Many other authors have also presented return to play criteria after cervical spine injury.7,10,12,42,43 Because the nature of many of these recommendations are not a result of large-scale randomized studies, standardized criteria for return to play have not been recognized uniformly by the medical community.4 Morganti et al44 presented radiographs and case histories of 10 athletes who had sustained neck injury to 346 physicians asking for recommendations for return to play to various levels of sports. Only 49% of respondents reported using published guidelines in decision-making.44 A higher return to level of play was recommended by physicians who were in fewer years in practice and also by physicians with a spine subspecialty interest.44 The study concluded that there was no consensus on the post injury management of many cervical spine-injured patients.44 It is important to be aware of the return to play criteria after nonoperative treatment of a stinger, CCN, ligamentous injury, or fracture. In the setting of a cervical disk herniation causing a burner or stinger, there is no contraindication to participation in contact activities following conservative treatment as long as patients have full, pain-free cervical range of motion and have a normal neurological examination.38 On the contrary, patients with CCN and documented cord compression secondary to a herniated disk are not allowed to return to play. Criteria for ligamentous cervical instability as previously described by White et al21 have been taken by Torg et al38 to represent an absolute contraindication to further participation in contact activities. After a ligamentous injury, particularly with lesser degrees or borderline displacement or rotation, the return to sports should be individualized and determined by level of performance, body habitus, and position played.38 In all cases however, patients should have pain free-range of motion and be neurologically normal. An acute fracture of either the body or posterior elements with or without ligamentous injury is an absolute contraindication to play.38 The following healed fractures in an asymptomatic patients who is neurologically normal and has full range of motion are not contraindications to play: (1) Stable vertebral body compression fracture or an end plate fracture without a sagittal component on anteroposterior xrays and without ligamentous or posterior bony structure involvement; (2) Healed spinous process fracture.38 Relative contraindications to play include patients who have a healed stable fracture involving the posterior neural ring in patients
B.W. Su and A.S. Hilibrand
204 who are asymptomatic and neurologically normal.38 Absolute contraindications to further participation in contact sports include: (1) vertebral body fracture with a sagittal component; (2) fracture of the vertebral body with or without displacement with associated posterior arch fractures and ligamentous laxity; (3) comminuted fractures of the vertebral body with displacement into the spinal canal; (4) any healed fracture of either the vertebral body or posterior components with associated pain, neurological findings, and limitation of normal cervical motion; and (5) healed displaced fractures involving the lateral masses with resulting facet incongruity.38 Return-to-play decisions after a fusion procedure for fracture, ligamentous instability, or herniated disks are controversial. Torg et al38 set out management guidelines for return to play contact sports after a cervical fusion and concluded that return to play is not contraindicated for an athlete with a single-level anterior or posterior cervical decompression and fusion as long as the patient is asymptomatic, neurologically normal, and has normal pain-free cervical spine range of motion. However, in the subset of patients who have a successful 1 level fusion but have concomitant congenital narrowing of the spinal canal, return to play is absolutely contraindicated.38 In a study of football players who underwent an ACDF for cervical disk herniations, all patients in the study were allowed to return to active play.9 Two of the players developed subsequent career-ending disk herniations, one above and the other below the fusion level, with one player requiring repeated spinal cord decompression.9 The authors concluded that neurologically intact athletes with focal cord compression caused by a single-level herniated disk may safely return to football after undergoing decompressive surgery and confirmation of fusion.9 However, there should be an understanding that there may be an increased chance of repeated herniation above or below a fused level.9 A healed 2- or 3-level cervical decompression and fusion is considered a relative contraindication to return to play.38 If the patient is allowed to return to play he/she must be asymptomatic, neurologically normal, and have pain free cervical range of motion. The relative contraindication to play was determined by the presumption of increased stresses at the levels above and below the fusion level and the propensity to develop adjacent degenerative changes. Hilibrand et al45 investigated the rate of adjacent level disease in 374 patients who underwent single or multiple-level ACDF with at least 2-year follow-up. Symptomatic adjacent segment disease occurred at a rate of 2.9%/year during the first 10 years after the operation. The levels at greatest risk were the C5/6 and C6/7 levels and when there was preexisting radiographic evidence of degeneration at the adjacent level implying that adjacent levels with these characteristics should be included in the fusion. Interestingly, the risk of new disease at an adjacent level was significantly lower after a multilevel fusion than it was following a single level fusion indicating that increasing the number of fusion levels does not increase adjacent level degeneration. Although this finding may indicate that a 2- or 3
level fusion should not be a relative contraindication to play, it must be noted that the loads placed on adjacent levels are clearly greater in professional football players than the average patient. Other authors have questioned whether the forces to the fused cervical spine during competitive football lead to a predisposition of symptomatic adjacent level degeneration and reherniation.46 Athletes participating in contact sports who are allowed to return to play after an ACDF need to be closely monitored for symptomatic adjacent level disease. Patients with more than a 3-level fusion are not allowed to return to contact sports.38
References 1. Maroon JC, Bailes JE: Athletes with cervical spine injury. Spine 21: 2294-2299, 1996 2. Clarke KS: Epidemiology of athletic neck injury. Clin Sports Med 17: 83-97, 1998 3. 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 21:640-649, 1993 4. 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 2:351-356, 2002 5. Torg JS, Pavlov H, Genuario SE, et al: Neurapraxia of the cervical spinal cord with transient quadriplegia. J Bone Joint Surg 68:1354-1370, 1986 6. Boden BP, Tacchetti RL, Cantu RC, et al: Catastrophic cervical spine injuries in high school and college football players. Am J Sports Med 34:1223-1232, 2006 7. Torg JS, Corcoran TA, Thibault LE, et al: Cervical cord neurapraxia: classification, pathomechanics, morbidity, and management guidelines. J Neurosurg 87:843-850, 1997 8. Herzog RJ, Wiens JJ, Dillingham MF, et al: Normal cervical spine morphometry and cervical spinal stenosis in asymptomatic professional football players. Plain film radiography, multiplanar computed tomography, and magnetic resonance imaging. Spine 16:S178-S186, 1991 9. 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 6:356-363, 2007 10. Cantu RC: Stingers: transient quadriplegia, and cervical spinal stenosis: return to play criteria. Med Sci Sports Exerc 29:S233-S235, 1997 11. Clancy WG Jr, Brand RL, Bergfield JA: Upper trunk brachial plexus injuries in contact sports. Am J Sports Med 5:209-216, 1977 12. 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 17:127-135, 1998 13. Mundt DJ, Kelsey JL, Golden AL, et al: An epidemiologic study of sports and weight lifting as possible risk factors for herniated lumbar and cervical discs. The Northeast Collaborative Group on Low Back Pain. Am J Sports Med 21:854-860, 1993 14. Levitz CL, Reilly PJ, Torg JS: The pathomechanics of chronic, recurrent cervical nerve root neurapraxia. The chronic burner syndrome. Am J Sports Med 25:73-76, 1997 15. Meyer SA, Schulte KR, Callaghan JJ, et al: Cervical spinal stenosis and stingers in collegiate football players. Am J Sports Med 22:158-166, 1994 16. Albright JP, Moses JM, Feldick HG, et al: Nonfatal cervical spine injuries in interscholastic football. JAMA 236:1243-1245, 1976 17. Cantu RC, Mueller FO: Catastrophic spine injuries in football (197789). J Spinal Disord 3:227-231, 1990 18. Webb JK, Broughton RB, McSweeney T, et al: Hidden flexion injury of the cervical spine. J Bone Joint Surg 58:322-327, 1976 19. Kahn EA, Schneider RC: Chronic neurological sequelae of acute trauma to the spine and spinal cord. I. The significance of the acute-flexion or
Cervical disk herniations and fractures/ligamentous injuries
20.
21.
22. 23. 24.
25. 26.
27.
28.
29. 30.
31.
32.
tear-drop fracture-dislocation of the cervical spine. J Bone Joint Surg 38-A:985-997, 1956 Torg JS, Pavlov H, O’Neill MJ, et al: The axial load teardrop fracture. A biomechanical, clinical and roentgenographic analysis. Am J Sports Med 19:355-364, 1991 White AA 3rd, Johnson RM, Panjabi MM, et al: Biomechanical analysis of clinical stability in the cervical spine. Clin Orthop Relat Res 109:8596, 1975 Shannon B, Klimkiewicz JJ: Cervical burners in the athlete. Clin Sports Med 21:29-35:vi, 2002 Rihn JA, Anderson DT, Lamb K, et al: Cervical spine injuries in American football. Sports Med 39:697-708, 2009 Bush K, Hillier S: Outcome of cervical radiculopathy treated with periradicular/epidural corticosteroid injections: a prospective study with independent clinical review. Eur Spine J 5:319-325, 1996 Scherping SC Jr: Cervical disc disease in the athlete. Clin Sports Med 21:37-47:vi, 2002 Bohlman HH, Emery SE, Goodfellow DB, et al: Anterior cervical discectomy and arthrodesis for cervical radiculopathy. Long-term follow-up of one hundred and twenty-two patients. J Bone Joint Surg 75:1298-1307, 1993 Wang JC, McDonough PW, Endow KK, et al: Increased fusion rates with cervical plating for two-level anterior cervical discectomy and fusion. Spine 25:41-45, 2000 Kaiser MG, Haid RW Jr, Subach BR, et al: Anterior cervical plating enhances arthrodesis after discectomy and fusion with cortical allograft. Neurosurgery 50:229-236, 2002; discussion 36-38 Mazur JM, Stauffer ES: Unrecognized spinal instability associated with seemingly “simple” cervical compression fractures. Spine 8:687-692, 1983 Mummaneni PV, Burkus JK, Haid RW, et al: Clinical and radiographic analysis of cervical disc arthroplasty compared with allograft fusion: a randomized controlled clinical trial. J Neurosurg Spine 6:198-209, 2007 Murrey D, Janssen M, Delamarter R, et al: Results of the prospective, randomized, controlled multicenter Food and Drug Administration investigational device exemption study of the prodisc-C total disc replacement versus anterior discectomy and fusion for the treatment of 1-level symptomatic cervical disc disease. Spine J 9:275-286, 2009 Heller JG, Sasso RC, Papadopoulos SM, et al: Comparison of Bryan cervical disc arthroplasty with anterior cervical decompression and
205
33.
34.
35. 36.
37. 38.
39.
40.
41.
42.
43. 44. 45.
46.
fusion: clinical and radiographic results of a randomized, controlled, clinical trial. Spine 34:101-107, 2009 Goffin J, Casey A, Kehr P, et al: Preliminary clinical experience with the Bryan cervical disc prosthesis. Neurosurgery 51:840-845, 2002; discussion 5-7 Goffin J, Van Calenbergh F, van Loon J, et al: Intermediate follow-up after treatment of degenerative disc disease with the Bryan cervical disc prosthesis: single-level and bi-level. Spine 28:2673-2678, 2003 Duggal N, Pickett GE, Mitsis DK, et al: Early clinical and biomechanical results following cervical arthroplasty. Neurosurg Focus 17:E9, 2004 Duggal N, Rabin D, Chamberlain RH, et al: Traumatic loading of the Bryan cervical disc prosthesis: an in vitro study. Neurosurgery 60:388392, 2007; 92-93 Jensen WK, Anderson PA, Nel L, et al: Bone ingrowth in retrieved Bryan cervical disc prostheses. Spine 30:2497-2502, 2005 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 16:501-530, 1997 Torg JS, Truex R Jr, Quedenfeld TC, et al: The National Football Head and Neck Injury Registry. Report and conclusions 1978. JAMA 241: 1477-1479, 1979 Torg JS, Vegso JJ, O’Neill MJ, et al: The epidemiologic, pathologic, biomechanical, and cinematographic analysis of football-induced cervical spine trauma. Am J Sports Med 18:50-57, 1990 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 254:3439-3443, 1985 Cantu RC, Bailes JE, Wilberger JE Jr: Guidelines for return to contact or collision sport after a cervical spine injury. Clin Sports Med 17:137146, 1998 Wilberger JE Jr: Athletic spinal cord and spine injuries. Guidelines for initial management. Clin Sports Med 17:111-120, 1998 Morganti C, Sweeney CA, Albanese SA, et al: Return to play after cervical spine injury. Spine 26:1131-1136, 2001 Hilibrand AS, Carlson GD, Palumbo MA, et al: Radiculopathy and myelopathy at segments adjacent to the site of a previous anterior cervical arthrodesis. J Bone Joint Surg 81:519-528, 1999 Fehlings MG, Farhadi HF: Cervical stenosis, spinal cord neurapraxia, and the professional athlete. J Neurosurg Spine 6:354-355, 2007; discussion 5.
A
thletic injuries to the cervical spine account for 10% of the 10,000 cervical spine injuries in the United States.1 The severity of neurological injury can range from a single episode of radiculopathy to complete quadriplegia secondary to a fracture or dislocation. Contact and collision sports, such as football, have been specifically implicated in catastrophic injuries. The incidence of complete quadriplegia among high school and college football athletes has been reported to range between 2.5 per 100,000 (reported in 1976) and 0.5 per 100,000 (reported in 1991).2 This discrepancy is at least in part the result of system-wide changes for protective equipment and rule changes, such as the banning of spear tackling, which has been implicated in causing neurological injuries in football.3 Two of the most commonly reported and studied neurological injuries in contact athletes are “stingers” and cervical cord neuropraxia (CCN). Although a herniated disk can cause either phenomenon, it is important to clearly differentiate the 2 entities on the basis of clinical presentation because they have differing pathophysiology and clinical management. CCN is a transient neurological phenomenon that presents as temporary bilateral burning paresthesias and is associated with various degrees of bilateral extremity weakness. There
*Mt. Tam Spine Center, Larkspur, CA. †The Rothman Institute, Philadelphia, PA. Address reprint requests to Alan S. Hilibrand, MD, The Rothman Institute, 925 Chestnut St, Philadelphia, PA 19107. E-mail: ahilibrand@gmail. com
198
1040-7383/$-see front matter © 2010 Elsevier Inc. All rights reserved. doi:10.1053/j.semss.2010.06.008
can be varying degrees of neurological involvement affecting 2 or 4 limbs. The duration of symptoms is typically only 10 to 15 minutes, but some patients can have residual symptoms up to 36 hours.4 The incidence in college football players is 1.3 per 100,000,5 and the mechanism of injury is thought to be hyperflexion, hyperextension, and axial compression forces.6 Torg et al7 described and classified CCN in 110 cases and found that it was not associated with permanent neurological injury, and no permanent morbidity occurred in patients who returned to contact activities. Evaluation of athletes who had CCN revealed a consistent finding of developmental narrowing of the canal, protrusion of a disk, or instability of the cervical spine.7 Torg et al5 proposed a ratio of canal to vertebral body depth of less than 0.8 as a risk factor for CCN with a sensitivity of 90%. However, Herzog et al8 found that approximately 33% of asymptomatic and 49% of all players have low Torg ratios, leading to low positive predictive values (PPV 0.2%) for determining future neuropraxic injuries and effacement of the subarachnoid space on magnetic resonance image (MRI; PPV 13%). Maroon et al9 recently examined the pathologic findings in 5 elite football players who had cervical neuropraxia. In all cases, MRI demonstrated marked focal cord compression secondary to a herniated disk and degenerative changes at a single level (Fig. 1).9 A “stinger” is descriptive of a unilateral upper extremity sensory disturbance and commonly motor weakness an athlete experiences at the time of injury. Stingers or burners are extremely common and can occur in as many as 50% of athletes involved in contact or collision sports.10,11 It occurs
Cervical disk herniations and fractures/ligamentous injuries
199
Figure 1 Five examples of focal neural compression secondary to disk disease in professional football players. (Reprinted with permission from Maroon et al.9)
because of an overload to the cervical spine and is not a result of spinal cord injury.12 Mechanisms proposed for a stinger include traction to the brachial plexus, compression to the brachial plexus from a direct blow, or compression of the nerve root within the cervical foramen from an extension injury. Mundt et al13 examined the association between participation in noncontact sports and herniated cervical intervertebral disks and found that most noncontact sports are not associated with an increased risk of herniation. The mechanism of protection was hypothesized to be secondary to improved muscular conditioning that protected the disk from stresses placed on the spine.13 On the contrary, Levitz et al14 studied 55 contact athletes with recurrent burners and found that 83% had a mechanism of injury of extension combined with ipsilateral-lateral deviation, with 70% exhibiting a positive Spurling’s sign.14 Twentynine patients (53%) had developmentally narrowed cervical canals, and 48 patients (87%) had evidence of disk disease by magnetic resonance imaging.14 They defined “disk disease” as either a disk bulge, disk protrusion, or a frank disk herniation deforming the cord. Fifty-one patients (93%) had disk disease or narrowing of the intervertebral foramina secondary to degenerative disk disease.14 The authors concluded that nerve root compression in the intervertebral foramina secondary to disk disease is a common cause in athletes with recurrent or chronic burner syndromes.14 Similarly, Meyer et al15 studied 266 football players and found that 15% reported a symptomatic stinger with most football players having an extension compression mechanisms rather than a brachial plexus stretch mechanism implying that foraminal compression led to the stinger. Although the Torg ratio was developed to examine stenosis in patients with cervical neuropraxia, Meyer et al15 evaluated the relationship of cervical stenosis in 40 football players who had stingers. The mean Torg ratio was significantly smaller for the stinger group compared with the asymptomatic group and the Torg ratio was less than 0.8 at one or more levels in
47.5% of the stinger group; players with a Torg ratio less than 0.8 had 3 times the risk of incurring stingers.15 This study agrees with that by Levitz et al,14 which indicates that there may be a relationship between central stenosis and the development of foraminal stenosis leading to “stingers” from root compression. The combination of disk disease and cervical spinal canal stenosis that leads to shortened pedicles may lead to an alteration in normal cervical spine mechanics that may make these athletes more prone to chronic burner syndromes secondary to foraminal stenosis. Because of their inherent mobility, the fifth, sixth, and seventh nerve roots are the most susceptible to injury.12 Fractures and ligamentous injuries have also been well described in collision sports. Albright et al16 examined the incidence of nonfatal neck injuries in high school football players with an injury significant enough to have caused the athlete to miss at least 1 practice or game. The incidence of radiographic evidence of neck injuries (compression fracture, abnormal motion, abnormal disk space, and neural arch fracture) was as high as 32% and was related to years of experience with a significant increase in injury after the junior high school year.16 Cantu and Mueller17 found that catastrophic football injuries resulted from either a combined fracture-dislocation (33%) or an anterior compression fracture (22%). In a study of 193 catastrophic cervical spine injuries in high school and college football players, Boden et al6 found that 95 athletes had a fracture, dislocation, or major ligamentous injury in the subaxial cervical level, 9 athletes at the C1 or C2 levels, and 7 athletes at combined upper and lower levels. The importance of recognizing injuries with subtle presentations, such as an anterior vertebral compression fracture but result in instability is outlined by Webb et al who described 7 patients who developed late vertebral deformity after flexion injuries of the cervical spine.18 All of these cases were associated with an anterior vertebral compression fracture.18 They described a radiological tetrad that suggested damage to the posterior interspinous complex of the cervical
200 spine: (1) interspinous widening, (2) vertebral subluxation, (3) vertebral compression fracture, and (4) loss of cervical lordosis.18 One important type of fracture of particular concern in athletes participating in contact sports is the teardrop fracture. In 1956, Kahn and Schneider19 described a teardrop fracture as a triangular fracture fragment at the anterior-inferior corner of a cervical vertebral body. Their description was determined solely by analysis of lateral radiographs and did not mention a sagittal body or posterior arch fracture; both subsequently recognized as important components of the fracture type.19 Torg et al20 subsequently analyzed 58 teardrop fractures included in the National Football Head and Neck Injury Registry (Fig. 2). Most of The fractures were at C5 with 2 types of teardrop fractures described; (1) an isolated fracture of the anterior-inferior corner of the vertebral body (2) an additional sagittal fracture of the vertebral body, ie, a three-part, two-plane fracture pattern through the lamina. In the absence of a fracture, it is also critical to rule out ligamentous instability of the cervical spine. In a classic 1975 biomechanical analysis by White et al,21 the stability of the cervical spine was described in relationship to the ligaments and facets. The authors defined the anterior elements to include the posterior longitudinal ligament (PLL) and all the anatomic structures anterior to it, including the intervertebral disk.21 The posterior elements included the structures posterior to the PLL (Fig. 3).21 The ligaments were transected from anterior to posterior as well as posterior to anterior and then tested biomechanically in flexion and extension.21 Displacement with all ligaments intact were very small with no horizontal displacement exceeding 2.7 mm and no angular displacement exceeding 10.7 degrees.21 On the basis of magnification of a standard cervical spine radiograph, this led to greater than 3.5 mm of horizontal displacement as evidence of instability in a clinical setting.21 This detail regarding horizontal displacement is important to emphasize particularly in the era of digital radiographs because displacement is now commonly measured with a precalibrated scale on a com-
Figure 2 Tear drop fracture which includes an anterior-inferior vertebral body fracture, sagittal fracture, and posterior arch fracture. (Reprinted with permission from Torg et al.20)
B.W. Su and A.S. Hilibrand
Figure 3 Diagram of anatomy of cervical motion segment demonstrating the anterior and posterior elements. Anterior elements include the PLL and all the anatomic structures anterior to it, including the intervertebral disk. The posterior elements included the structures posterior to the PLL. (Reprinted with permission from White et al.21)
puter monitor rather than by hand from a printed radiograph. As such, no normal adult spine free of degenerative changes should demonstrate horizontal motion of more than 2.7 mm between vertebrae on either flexion or extension.21 Because angulation is not effected by magnification, the authors set ⬎11 degrees of angulation more than either normal adjacent vertebra as unstable (Fig. 4).21 Notably, with some ligaments cut and just before complete failure, the maximum displacement recorded was 4.9 mm, and the maximum angular displacement was 15.7 degrees, indicating that only modest displacement occurs before complete and sudden failure. There was not a stepwise increase in deformation of the spine with each ligament transected but rather very small changes in displacement before complete catastrophic failure with no predictable “prefailure” phase.21 Examination of the importance of ligamentous structures led to the conclusion that if a motion segment has all of its anterior elements “plus one” additional posterior structure, or all of its posterior elements “plus one” of the additional anterior structures then the spine would be stable under physiological loads.21 If any one of the following 3 condition exists, then
Cervical disk herniations and fractures/ligamentous injuries
Figure 4 (A) On a neutral, flexion, or extension lateral x-ray, no normal adult spine should permit horizontal motion of more than 2.7 mm (3.5 mm if measured on a printed radiograph) or (B) greater than 11 degrees of angulation more than either normal adjacent vertebra. (Reprinted with permission from White et al.21)
the spine is unstable or on the brink of instability: (1) either all the anterior or all the posterior elements are destroyed; (2) more than 2.7 mm (3.5 mm on a printed radiograph) of horizontal displacement of 1 vertebra in relation to an adjacent vertebra anteriorly or posteriorly measured on a neutral, flexion, or extension radiograph; or (3) more than 11 degrees of rotational difference to that of either adjacent vertebra, measured on a neutral, flexion, or extension radiograph.21
Management In football players with radiological abnormalities, at the time of injury, approximately 1 of 3 players experience more than
201 neck pain.16 This often includes upper extremity weakness and numbness, headaches, or transient visual disturbances.16 Management of players with stingers, CCN, and fractures or ligamentous injury always begins with a detailed assessment on the sideline with particular attention to mechanism of injury, distribution and duration of symptoms, evaluation of cervical range of motion within pain tolerance, palpation for muscle spasm, localized bony tenderness, and a detailed neurological examination. Interestingly, in a series of athletes with cervical spine injuries presented by Albright et al,16 a licensed physician examined only 55% of injured players, while another 11% were seen by a chiropractor. The management of a “stinger” has been well described by several authors.12,22,23 The duration of pain can vary from seconds to hours, rarely persisting longer than several days, although specific myotomal weakness can persist even longer. Athletes should not return to play in the same game if there is loss of cervical range of motion or persistent pain and weakness. If weakness persists for more than 2 weeks or worsens over the first few days, electromyography is reasonable as early as 7 days after the onset of symptoms. Imaging studies should include flexion and extension views for evaluation of any fractures or instability. Central stenosis as measured by the Torg ratio in the setting of a “stinger” may prompt obtaining an MRI, which is useful for evaluating the presence of central stenosis, foraminal stenosis, and any cord compromise. Some authors have advocated that an acute disk herniation be ruled out before return to play if significant pain and weakness occurs in the setting of a stinger.12 In a series of professional football players presented by Maroon et al,9 a linebacker experienced 8 to 9 episodes of upper-extremity paraesthesia that resolved and were thought to be stingers. A subsequent MRI demonstrated marked cord compression from a disk herniation.9 If an MRI does not demonstrate significant central or foraminal stenosis, the patient with a resolved stinger should focus on neck strengthening and stretching in a comprehensive program that is aggressive but does not cause further injury to the patient.22,23 By contrast, if an MRI demonstrates significant stenosis secondary to a disk herniation, the patient should be managed more cautiously and largely as any nonathlete patient who presents with a first-time disk herniation. If foraminal stenosis is present and correlates to the patient’s clinical symptoms/examination, it is our preference to begin with a selective nerve root injection at the affected level followed by range of motion and strengthening exercises. Bush and Hillier24 reported clinical success and avoidance of surgery using selective cervical nerve root injections. If symptoms persist after 6 weeks of nonoperative treatment, the patient is offered surgical intervention. The management of a player with CCN includes immediate removal from sporting that particular event.4 A complete neurological and radiographic examination should be performed on a timely basis. If the patient complains of neck stiffness and constant neck pain, the patient has a fracture unless proven otherwise. Following stabilization, the patient should be taken to a medical facility and undergo appropriate imaging studies, including X-ray, computed tomography
202 (CT), and MRI for evaluation of fracture, ligamentous injury, or a disk herniation. It is critical to be able to see the C7/T1 junction which often requires a CT scan. In the absence of a fracture or ligamentous injury leading to instability or a persistent neurological deficit, surgical intervention is not indicated in patients who have focal cord compression secondary to a herniated disk. A central disk herniation should be treated similarly to the nonathlete with conservative care. However, if a player desires to return to play, surgical treatment should be considered, as focal spinal cord compression from a disk herniation is a contraindication to play. Surgery for a herniated disk can be approached from an anterior or posterior approach. A posterior laminoforaminotomy is limited to a smaller cohort of patients as it requires the disk herniation to be lateral to the boundary of the spinal cord. A posterior approach would only be suitable for a patient with a herniated disk leading to foraminal stenosis and recurrent stingers. Plain radiographs must also demonstrate no disk narrowing, osteophyte formation, or motion of flexion extension films. One potential advantage is that a laminoforaminotomy may allow a faster return to play because a fusion procedure is not performed. As such, some authors have suggested expanding the indications for a posterior procedure in this subset of patients.25 Our procedure of choice in an athlete with a herniated disk is an anterior cervical diskectomy and fusion (ACDF) with allograft. In long-term studies, an ACDF has been shown to result in relief of radicular pain in approximately 90% of patients with an equally high fusion rate.26 One benefit of anterior surgery in this setting is the avoidance of any muscle dissection, which is required with any posterior procedure. It is our preference to use plate fixation for all ACDFs, particularly in athletes who have an increased biomechanical demand on the construct and to minimize postoperative immoblilization. Plating has been shown to increase fusion rates, particularly for 2 or more level ACDFs with Wang et al27 reporting an increase in fusion rates from 75% to 100%. When allograft is used, plating significantly increases fusion rates in both 1 and 2 level ACDF.28 Use of a cervical disk replacement (CDR) in an athlete with a cervical disk herniation is discussed later in this manuscript. In all athletes with persistent neck pain, it is imperative to rule out a fracture or ligamentous injury with a CT or MRI scan. Mazur and Stauffer29 reported on 27 patients who had seemingly stable compression cervical vertebral fractures. Although most patients healed without problems, 6 patients demonstrated persistent progressive postinjury instability related to posterior ligament rupture.29 As muscle spasm diminished, the patients could be given a more reliable flexion-extension radiographic examination, unmasking the hidden posterior instability.29 Close follow-up of patients with simple compression fractures of the cervical spine is mandatory.29 In the series of teardrop fractures described by Torg et al,20 45 patients in the series were permanently quadriplegic, and 10 had transient neurologic symptoms.20 All but 1 patient with an isolated corner fracture had no serious neurologic injury. Of the 49 patients with a documented 3-part, 2-plane injury, 44 (90%) were quadriplegic.20 It is therefore critical to study
B.W. Su and A.S. Hilibrand advanced imaging, ie, CT scan to determine whether the injury is an isolated corner fracture or a 2-plane fracture that includes a sagittal split of the vertebral body and a fracture of the posterior neural arch, which is usually associated with neurologic sequelae.20 The treatment of fractures and dislocations in athletes is similar to that for nonathletic cervical spine trauma. Patients with fractures, dislocation, or ligamentous injuries in the setting of a spinal cord injury should be decompressed and stabilized as soon as possible.
Cervical Disk Replacement in Athletes CDR has been gaining popularity as an alternate to an ACDF for treatment of radiculopathy or myelopathy secondary to a herniated disk at a single level. The advantage of motion preserving technology, such as the CDR, is a possible longterm reduction in rates of adjacent level degeneration. This is particularly interesting in the setting of athletes because Maroon et al9 have demonstrated an increased chance of repeated herniation above or below a fused level after an ACDF. There are no clinical studies related to the outcomes of CDR specifically in athletes. However, it is important to consider that athletes withstand greater loads to the cervical spine, making the biomechanical stability and ingrowth of a specific CDR device a particularly important consideration. As of 2009, the Food and Drug Administration-approved CDRs, which had a minimum of 2 year follow-up, included the Prestige ST (Medtronic Sofamor Danek, Memphis, TN), Bryan (Medtronic Sofamor Danek, Memphis, TN), and Prodisk-C (Synthes Spine, Paoli, PA). The current Food and Drug Administration indication for CDR is the treatment of radiculopathy and/or myelopathy due to neural compression caused by a disk herniation or spondylotic changes at a single level between C3-7 which has been refractory to at least 6 weeks of nonoperative treatment. When the Prestige ST CDR was compared with an ACDF, there were no differences in any functional outcome measure at 2 years.30 Similarly, Murrey et al31 reported on a randomized controlled trial comparing the Prodisk-C CDR to a single-level ACDF and found that at 1 and 2 years, there were no differences in any outcomes between the 2 groups. Heller et al32 reported on the 2-year outcomes of the Bryan CDR and found significant improvements in SF-36 mental component score, physical component score, and arm pain scores at 1 year follow-up in favor of the CDR, but these differences were not maintained at 2 years. However, the CDR group did have statistically lower Neck Disability Index and neck pain scores, that is, 16 versus 19 for Neck Disability Index and 23 versus 30 for neck pain at 2 years.32 Other studies of the Bryan CDR have demonstrated similar improvements in functional outcomes to the U.S. Investigational Device Exemption studies.33-35 In summary, the clinical improvement after CDR at 2-year follow-up seems to be similar to an ACDF. However, it is important to point out that there are no published outcomes with longer than 2-year follow-up after CDR. In addition, it appears that there is
Cervical disk herniations and fractures/ligamentous injuries preservation of range of motion with CDR, as Murrey et al31 have reported that at 2 years, 84% of the Prodisk C CDR group had 4° or greater of motion on flexion/extension radiographs. If the surgeon is considering a CDR, it is critical to follow the strict guidelines for exclusion that have been described in the published Investigational Device Exemption studies. Exclusion criteria are typically: Instability based on flexion/extension x-rays, including translation greater than 3 mm,31 greater than 11 degrees of rotational difference to that of either adjacent level,31 a fused level adjacent to the level treated,31 severe facet joint disease or degeneration,31 spondylosis evidenced by bridging osteophytes,31 reduction of motion at the index segment,32 loss of disk height greater than 50%,31 absence of motion (⬍2°), cervical kyphosis,32 or osteoporosis.31 The axial load placed on the cervical spine during contact sports is larger than the general population. This is an important consideration if an athlete is going to return to contact sports following a CDR. Duggal et al36 analyzed the strength of the normal cervical spine versus the strength after a single level Bryan CDR in a cadaveric model. A pure moment was applied to induce flexion, extension, or axial rotation until the segment failed. The prosthesis provided 63%, 45%, and 69% of the strength of a normal spine during flexion, extension, and rotation, respectively. There were no cases of prosthesis expulsion. This study does not evaluate the strength of a CDR after ingrowth of the implant, which presumably increases the strength profile on the basis of the extent of ingrowth. Jensen et al37 studied end plate ingrowth in retrieved Bryan CDR from 2 humans who had removal of the CDR and revision for failure. Bony ingrowth was quantified at a mean of 30% with no differences between peripheral, intermediate, or central locations. The degree of ingrowth was similar to that for the femoral component of total hip replacements from human retrieval studies (range, 16%-35%). The same study implanted the Bryan CDR in 2 primates and reported a range of 10% to 50% of bony ingrowth at 3 months post operatively at the bone/metal interface.37 On the basis of limited animal and human studies on CDR, it is reasonable to assume that most bone ingrowth occurs in the first 3 months after implantation and that if a patient received a CDR, athletic activities should be limited for the first 3 months. As such, a CDR in an athlete would preclude return to sport sooner than 3 months. On the basis of the uncertain strength profile after a CDR, if an athlete with a cervical disk herniation wishes to return to collision sports, our opinion is that he/she should undergo ACDF. It is logical that a fusion procedure is inherently more stable than a motion sparing procedure. However, an athlete who does not wish to return to contact sports may be an ideal candidate for a CDR because such individuals are younger active patients without posterior facet arthrosis who have a greater potential to benefit over time from a potential decreased risk of adjacent level degeneration.
203
Return-to-Play Guidelines The relative paucity of neurological injuries and ligamentous/ bony injuries in athletes has necessitated reliance upon small case series and expert opinion to determine return to play guidelines. In 1997, after an extensive literature review, Torg and Ramsey-Emrhein38 determined management guidelines for participation in collision activities with congenital, developmental, or post injury lesions of the cervical spine. These guidelines were developed from the best-available data compiled from more than 1200 cervical spine injuries documented by the National Football Head and Neck Injury Registry39-41 as well as clinical and anecdotal experience. Many other authors have also presented return to play criteria after cervical spine injury.7,10,12,42,43 Because the nature of many of these recommendations are not a result of large-scale randomized studies, standardized criteria for return to play have not been recognized uniformly by the medical community.4 Morganti et al44 presented radiographs and case histories of 10 athletes who had sustained neck injury to 346 physicians asking for recommendations for return to play to various levels of sports. Only 49% of respondents reported using published guidelines in decision-making.44 A higher return to level of play was recommended by physicians who were in fewer years in practice and also by physicians with a spine subspecialty interest.44 The study concluded that there was no consensus on the post injury management of many cervical spine-injured patients.44 It is important to be aware of the return to play criteria after nonoperative treatment of a stinger, CCN, ligamentous injury, or fracture. In the setting of a cervical disk herniation causing a burner or stinger, there is no contraindication to participation in contact activities following conservative treatment as long as patients have full, pain-free cervical range of motion and have a normal neurological examination.38 On the contrary, patients with CCN and documented cord compression secondary to a herniated disk are not allowed to return to play. Criteria for ligamentous cervical instability as previously described by White et al21 have been taken by Torg et al38 to represent an absolute contraindication to further participation in contact activities. After a ligamentous injury, particularly with lesser degrees or borderline displacement or rotation, the return to sports should be individualized and determined by level of performance, body habitus, and position played.38 In all cases however, patients should have pain free-range of motion and be neurologically normal. An acute fracture of either the body or posterior elements with or without ligamentous injury is an absolute contraindication to play.38 The following healed fractures in an asymptomatic patients who is neurologically normal and has full range of motion are not contraindications to play: (1) Stable vertebral body compression fracture or an end plate fracture without a sagittal component on anteroposterior xrays and without ligamentous or posterior bony structure involvement; (2) Healed spinous process fracture.38 Relative contraindications to play include patients who have a healed stable fracture involving the posterior neural ring in patients
B.W. Su and A.S. Hilibrand
204 who are asymptomatic and neurologically normal.38 Absolute contraindications to further participation in contact sports include: (1) vertebral body fracture with a sagittal component; (2) fracture of the vertebral body with or without displacement with associated posterior arch fractures and ligamentous laxity; (3) comminuted fractures of the vertebral body with displacement into the spinal canal; (4) any healed fracture of either the vertebral body or posterior components with associated pain, neurological findings, and limitation of normal cervical motion; and (5) healed displaced fractures involving the lateral masses with resulting facet incongruity.38 Return-to-play decisions after a fusion procedure for fracture, ligamentous instability, or herniated disks are controversial. Torg et al38 set out management guidelines for return to play contact sports after a cervical fusion and concluded that return to play is not contraindicated for an athlete with a single-level anterior or posterior cervical decompression and fusion as long as the patient is asymptomatic, neurologically normal, and has normal pain-free cervical spine range of motion. However, in the subset of patients who have a successful 1 level fusion but have concomitant congenital narrowing of the spinal canal, return to play is absolutely contraindicated.38 In a study of football players who underwent an ACDF for cervical disk herniations, all patients in the study were allowed to return to active play.9 Two of the players developed subsequent career-ending disk herniations, one above and the other below the fusion level, with one player requiring repeated spinal cord decompression.9 The authors concluded that neurologically intact athletes with focal cord compression caused by a single-level herniated disk may safely return to football after undergoing decompressive surgery and confirmation of fusion.9 However, there should be an understanding that there may be an increased chance of repeated herniation above or below a fused level.9 A healed 2- or 3-level cervical decompression and fusion is considered a relative contraindication to return to play.38 If the patient is allowed to return to play he/she must be asymptomatic, neurologically normal, and have pain free cervical range of motion. The relative contraindication to play was determined by the presumption of increased stresses at the levels above and below the fusion level and the propensity to develop adjacent degenerative changes. Hilibrand et al45 investigated the rate of adjacent level disease in 374 patients who underwent single or multiple-level ACDF with at least 2-year follow-up. Symptomatic adjacent segment disease occurred at a rate of 2.9%/year during the first 10 years after the operation. The levels at greatest risk were the C5/6 and C6/7 levels and when there was preexisting radiographic evidence of degeneration at the adjacent level implying that adjacent levels with these characteristics should be included in the fusion. Interestingly, the risk of new disease at an adjacent level was significantly lower after a multilevel fusion than it was following a single level fusion indicating that increasing the number of fusion levels does not increase adjacent level degeneration. Although this finding may indicate that a 2- or 3
level fusion should not be a relative contraindication to play, it must be noted that the loads placed on adjacent levels are clearly greater in professional football players than the average patient. Other authors have questioned whether the forces to the fused cervical spine during competitive football lead to a predisposition of symptomatic adjacent level degeneration and reherniation.46 Athletes participating in contact sports who are allowed to return to play after an ACDF need to be closely monitored for symptomatic adjacent level disease. Patients with more than a 3-level fusion are not allowed to return to contact sports.38
References 1. Maroon JC, Bailes JE: Athletes with cervical spine injury. Spine 21: 2294-2299, 1996 2. Clarke KS: Epidemiology of athletic neck injury. Clin Sports Med 17: 83-97, 1998 3. 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 21:640-649, 1993 4. 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 2:351-356, 2002 5. Torg JS, Pavlov H, Genuario SE, et al: Neurapraxia of the cervical spinal cord with transient quadriplegia. J Bone Joint Surg 68:1354-1370, 1986 6. Boden BP, Tacchetti RL, Cantu RC, et al: Catastrophic cervical spine injuries in high school and college football players. Am J Sports Med 34:1223-1232, 2006 7. Torg JS, Corcoran TA, Thibault LE, et al: Cervical cord neurapraxia: classification, pathomechanics, morbidity, and management guidelines. J Neurosurg 87:843-850, 1997 8. Herzog RJ, Wiens JJ, Dillingham MF, et al: Normal cervical spine morphometry and cervical spinal stenosis in asymptomatic professional football players. Plain film radiography, multiplanar computed tomography, and magnetic resonance imaging. Spine 16:S178-S186, 1991 9. 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 6:356-363, 2007 10. Cantu RC: Stingers: transient quadriplegia, and cervical spinal stenosis: return to play criteria. Med Sci Sports Exerc 29:S233-S235, 1997 11. Clancy WG Jr, Brand RL, Bergfield JA: Upper trunk brachial plexus injuries in contact sports. Am J Sports Med 5:209-216, 1977 12. 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 17:127-135, 1998 13. Mundt DJ, Kelsey JL, Golden AL, et al: An epidemiologic study of sports and weight lifting as possible risk factors for herniated lumbar and cervical discs. The Northeast Collaborative Group on Low Back Pain. Am J Sports Med 21:854-860, 1993 14. Levitz CL, Reilly PJ, Torg JS: The pathomechanics of chronic, recurrent cervical nerve root neurapraxia. The chronic burner syndrome. Am J Sports Med 25:73-76, 1997 15. Meyer SA, Schulte KR, Callaghan JJ, et al: Cervical spinal stenosis and stingers in collegiate football players. Am J Sports Med 22:158-166, 1994 16. Albright JP, Moses JM, Feldick HG, et al: Nonfatal cervical spine injuries in interscholastic football. JAMA 236:1243-1245, 1976 17. Cantu RC, Mueller FO: Catastrophic spine injuries in football (197789). J Spinal Disord 3:227-231, 1990 18. Webb JK, Broughton RB, McSweeney T, et al: Hidden flexion injury of the cervical spine. J Bone Joint Surg 58:322-327, 1976 19. Kahn EA, Schneider RC: Chronic neurological sequelae of acute trauma to the spine and spinal cord. I. The significance of the acute-flexion or
Cervical disk herniations and fractures/ligamentous injuries
20.
21.
22. 23. 24.
25. 26.
27.
28.
29. 30.
31.
32.
tear-drop fracture-dislocation of the cervical spine. J Bone Joint Surg 38-A:985-997, 1956 Torg JS, Pavlov H, O’Neill MJ, et al: The axial load teardrop fracture. A biomechanical, clinical and roentgenographic analysis. Am J Sports Med 19:355-364, 1991 White AA 3rd, Johnson RM, Panjabi MM, et al: Biomechanical analysis of clinical stability in the cervical spine. Clin Orthop Relat Res 109:8596, 1975 Shannon B, Klimkiewicz JJ: Cervical burners in the athlete. Clin Sports Med 21:29-35:vi, 2002 Rihn JA, Anderson DT, Lamb K, et al: Cervical spine injuries in American football. Sports Med 39:697-708, 2009 Bush K, Hillier S: Outcome of cervical radiculopathy treated with periradicular/epidural corticosteroid injections: a prospective study with independent clinical review. Eur Spine J 5:319-325, 1996 Scherping SC Jr: Cervical disc disease in the athlete. Clin Sports Med 21:37-47:vi, 2002 Bohlman HH, Emery SE, Goodfellow DB, et al: Anterior cervical discectomy and arthrodesis for cervical radiculopathy. Long-term follow-up of one hundred and twenty-two patients. J Bone Joint Surg 75:1298-1307, 1993 Wang JC, McDonough PW, Endow KK, et al: Increased fusion rates with cervical plating for two-level anterior cervical discectomy and fusion. Spine 25:41-45, 2000 Kaiser MG, Haid RW Jr, Subach BR, et al: Anterior cervical plating enhances arthrodesis after discectomy and fusion with cortical allograft. Neurosurgery 50:229-236, 2002; discussion 36-38 Mazur JM, Stauffer ES: Unrecognized spinal instability associated with seemingly “simple” cervical compression fractures. Spine 8:687-692, 1983 Mummaneni PV, Burkus JK, Haid RW, et al: Clinical and radiographic analysis of cervical disc arthroplasty compared with allograft fusion: a randomized controlled clinical trial. J Neurosurg Spine 6:198-209, 2007 Murrey D, Janssen M, Delamarter R, et al: Results of the prospective, randomized, controlled multicenter Food and Drug Administration investigational device exemption study of the prodisc-C total disc replacement versus anterior discectomy and fusion for the treatment of 1-level symptomatic cervical disc disease. Spine J 9:275-286, 2009 Heller JG, Sasso RC, Papadopoulos SM, et al: Comparison of Bryan cervical disc arthroplasty with anterior cervical decompression and
205
33.
34.
35. 36.
37. 38.
39.
40.
41.
42.
43. 44. 45.
46.
fusion: clinical and radiographic results of a randomized, controlled, clinical trial. Spine 34:101-107, 2009 Goffin J, Casey A, Kehr P, et al: Preliminary clinical experience with the Bryan cervical disc prosthesis. Neurosurgery 51:840-845, 2002; discussion 5-7 Goffin J, Van Calenbergh F, van Loon J, et al: Intermediate follow-up after treatment of degenerative disc disease with the Bryan cervical disc prosthesis: single-level and bi-level. Spine 28:2673-2678, 2003 Duggal N, Pickett GE, Mitsis DK, et al: Early clinical and biomechanical results following cervical arthroplasty. Neurosurg Focus 17:E9, 2004 Duggal N, Rabin D, Chamberlain RH, et al: Traumatic loading of the Bryan cervical disc prosthesis: an in vitro study. Neurosurgery 60:388392, 2007; 92-93 Jensen WK, Anderson PA, Nel L, et al: Bone ingrowth in retrieved Bryan cervical disc prostheses. Spine 30:2497-2502, 2005 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 16:501-530, 1997 Torg JS, Truex R Jr, Quedenfeld TC, et al: The National Football Head and Neck Injury Registry. Report and conclusions 1978. JAMA 241: 1477-1479, 1979 Torg JS, Vegso JJ, O’Neill MJ, et al: The epidemiologic, pathologic, biomechanical, and cinematographic analysis of football-induced cervical spine trauma. Am J Sports Med 18:50-57, 1990 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 254:3439-3443, 1985 Cantu RC, Bailes JE, Wilberger JE Jr: Guidelines for return to contact or collision sport after a cervical spine injury. Clin Sports Med 17:137146, 1998 Wilberger JE Jr: Athletic spinal cord and spine injuries. Guidelines for initial management. Clin Sports Med 17:111-120, 1998 Morganti C, Sweeney CA, Albanese SA, et al: Return to play after cervical spine injury. Spine 26:1131-1136, 2001 Hilibrand AS, Carlson GD, Palumbo MA, et al: Radiculopathy and myelopathy at segments adjacent to the site of a previous anterior cervical arthrodesis. J Bone Joint Surg 81:519-528, 1999 Fehlings MG, Farhadi HF: Cervical stenosis, spinal cord neurapraxia, and the professional athlete. J Neurosurg Spine 6:354-355, 2007; discussion 5.