Treatment and Return to Play

Initial management for the athlete with an episode of CCN includes immobilization and clinical, standard radiographic, as well as advanced radiographic examination. None of the MRIs in Torg, nor Maroon’s study, that had experienced CCN demonstrated any posttraumatic cord swelling, deformity, or syrinx; however, it is important to rule out focal lesions with cord compression or instability [1, 5]. CCN must be differentiated from the more common symptoms following brachial plexus stretch injuries or radiculopathy.

The majority of patients that experience CCN will be treated non-operatively with supportive care. However, in two series, 8.5% of 142 patients underwent surgery for cord compression or spinal instability [1, 7]. Additionally, in a series of five professional athletes who underwent anterior cervical decompression and fusion for focal cord compression after an episode of CCN, all five athletes returned to their prior level of sport [5].

Return to play criteria following CCN remains controversial [15, 16]. A review of 170 articles demonstrated current research lacks prospective randomized trials regarding return to play criteria following CCN [17]. Therefore, return to play is primarily based on expert opinion, case series, and retrospective reviews. Generally agreed-upon basic requirements for returning to athletics include normal strength, painless range of motion, and vertebral stability [16].

Additionally, with the more frequent use of MR imaging, it is suggested that the players have “functional reserve ” around the cord. In MR imaging of ten athletes that experienced episodes of CCN, all subjects had stenosis between 7 and 12 mm over three levels on MRI, but only three had no functional reserve at those levels. The three athletes with no functional reserve voluntarily retired, and the other seven returned to their sport without subsequent episodes of CCN [18, 19].

A recommended relative contraindication for return to play is the presence of T2 hyperintensity on MR imaging [14, 17, 20, 21]. However, a recent study of five patients who were treated operatively concluded that if postoperatively the contact athlete is symptom-free, T2 hyperintensity may not be a contraindication to return to play [22]. However, the numbers within this study are small, and it is unknown if this study’s conclusions regarding T2 hyperintensity are reproducible in the athlete that does not undergo surgical intervention. In a study of four athletes that had one episode of CCN, MR imaging demonstrated maintained functional reserve. None of these athletes had recurrent episodes of CCN once they returned to their sport [23]. Additionally, dynamic flexion and extension cervical magnetic imaging would further evaluate for stenosis and the presence of the pincer mechanism; however, this is of limited availability.

Torg’s study of 110 adult athletes demonstrated 57% of the subjects returned to sports participation at their previous level of competition. Among this group there was no significant difference between the group that returned to play and the group that did not in regard to age, sex, sport, CCN clinical grade, or radiologic findings. However, of the athletes that returned to contact sports, 56% (N = 35) experienced a second episode of CCN with an average of 3.1 ± 4 episodes. Subjects who experienced recurrence had smaller disc-level canal diameter and had less space available for the cord diameter compared with those with no recurrence (p = 0.05). Therefore, it is important to counsel athlete’s with CCN that there is a 50% chance that it may occur again and specifically take these factors of stenosis into account during counseling.

Predictors for recurrence are different in the pediatric population. In the single case series of pediatric CCN and return to sport, Torg ratios were calculated and noted to be above 0.8 for all patients, and no instability was seen on flexion and extension radiographs. Furthermore, MR imaging was obtained for each patient and demonstrated no evidence of extraneural pathology or stenosis. Among the ten subjects with long-term follow-up in the study, each had returned to his or her sport without a subsequent episode of CCN. This leads to the conclusion that the relative hypermobility of the pediatric cervical spine is an inciting factor, rather than pre-existing stenosis [8].

Risks of return to sport can be catastrophic. Cantu reported on a case involving a high school athlete who described an episode of CCN. Radiographs demonstrated a vertebral canal space of 12 mm, consistent with spinal stenosis, and Torg ratios of 0.48 at C4 and 0.5 at C5. The athlete returned to football and during a tackle incurred a spinal cord injury with right-sided hemisensory loss and a flaccid left side. MR imaging after this tackle demonstrated a disc herniation and displacement of the spinal cord. Surgery was performed; however, the patient remained with permanent neurologic deficits [13].

Recommended absolute contraindications for return to play are a single event with evidence of cord injury, multiple neurapraxic events, ligamentous instability, or neuropraxic symptoms lasting greater than 36 h [6]. Additional factors to consider for return to play are the specific sport, likelihood of contact, mechanism of contract, length of future career, and anatomic features specific to the athlete; as a single episode of CCN does not substantially increase the risk of permanent spinal cord injury, there remains a small but nevertheless present risk of permanent spinal cord injury [19].

Summary

Cervical cord neurapraxia is a transient neurological deficit resulting from trauma to the cervical spine. The majority of symptoms resolve in adults within 15 min and, however, may last much longer in children. The association of cervical cord neurapraxia with cervical stenosis has been shown in many series in adults but has not been well demonstrated in children.

Our recommendations include initial management consisting of immobilization and clinical and standard and advanced radiographic examination. We believe that absolute contraindications to return to play include instability or focal cord compression that cannot be resolved with surgical intervention as well as any residual weakness in a major motor group, imbalance, loss of dexterity, or other cord-related neurologic deficits.

Return to play criteria is greatly based on expert opinion and retrospective case reviews. The literature is without any large series that would allow for recommendations based upon meaningful and accurate epidemiological results. Adults that do return to their sport have at least a 50% risk of recurrence, whereas the risk of recurrence in children has not yet been established.

Expert Opinion

The treatment of CCN remains controversial, as there is no definitive Class I data and, with the difficulties of performing a randomized controlled study, there may never be one. Therefore, only expert opinions and small case series exist to guide the treatment.

Most players who experience transient quadriplegia will not become permanently quadriplegic and most who become permanently quadriplegic have never experienced transient quadriplegia. This was consistent with Torg’s finding that, of the 117 players who became permanently quadriplegic, none had a history of transient quadriplegia in the past [7]. This is used as evidence that transient quadriplegia does not predict permanent quadriplegia and therefore, in the absence of repeated or prolonged episodes, CCN should not preclude a return to play.

The problem with this reasoning is that the number of players who become quadriplegic is small. The lack of a prior history in such a small population may not be an accurate indicator of the actual risk of CCN being a risk factor for permanent quadriplegia . This may be analogous to concluding that myelopathy is not a risk factor for quadriplegia after evaluating 117 patients with quadriplegia who never had symptoms of myelopathy. It is well-recognized that myelopathy can progress on to quadriplegia and that myelopathy is indeed a risk factor for quadriplegia, even though the vast majority of quadriplegic patients in the USA never had myelopathy. This is because, in a country like the USA, it would be rare for someone to progress on to quadriplegia without getting proper care. However, in third-world countries where access to medical care is often unavailable, it is not uncommon to see patients present with quadriplegia due to spondylotic cord compression in the absence of significant trauma.

Similarly, professional athletes who either have a prolonged episode of CCN or repeated episodes are likely to be diagnosed with stenosis and be advised to quit or become so frightened that they will voluntarily quit playing. The evidence for this is in Torg’s series of 110 players with CCN, 43% of whom gave up the game following their initial episode [7]. It is reasonable to suspect that the 43% who quit had the worst or the most prolonged episode(s) of CCN and may have been the ones at greatest risk for permanent quadriplegia due to their anatomy. By quitting, they may have eliminated the players most at risk for permanent quadriplegia, biasing the results of Torg’s study on the 117 players [1]. Unfortunately, there is no data on the risk of permanent quadriplegia following a single or multiple episodes of CCN. In Torg’s series, only 35 had recurrent episodes, and none ended up a permanent quadriplegic . If the risk of quadriplegia is one out of 36 in such a group, a sample size of 35 could easily have missed the one quadriplegic. Most nonprofessional athletes would choose to avoid an activity that is associated with a risk of permanent quadriplegia as low as 1 in 36 or even 1 in 100. In fact, we would most likely recommend surgery to any patient with condition that poses a 1% risk of quadriplegia, since the risk of surgery causing quadriplegia is lower than that.

Twenty years ago, concussions were considered inconsequential, and team doctors routinely cleared patients for play following a brief time out. We now recognize the serious consequences of repetitive trauma to the brain, with injury to the microvasculature and neural tissue. But we still do not know the consequences of similar trauma to the spinal cord. It is not difficult to imagine that similar micro-damage may occur with repetitive trauma to the spine.