Philadelphia Orthopaedic Society October 8, 2007 Vice Chairman, Department of Orthopaedic Surgery Associate Director, Center for Spine Health, Neurological Institute Cleveland Clinic Cervical cord neurapraxia. Injury to the cervical spine may either be permanent or transient. In 1986 Torg and colleagues described a clinical entity known as transient neurapraxia of the cervical spinal cord, also known as cervical cord neurapraxia (CCN), which resulted from sudden cervical cord compression from a football collision 1. Clinical features of this condition include sensory, motor or combined neurological findings and may occur in one or more extremities. Sensory symptoms include burning pain, numbness, tingling or loss of sensation. Motor findings range from weakness to complete paralysis. Signs and symptoms of CCN typically resolve within ten to fifteen minutes, but may last up to 48 hours. In a survey of nearly 40,000 NCAA football players from the 1984 collegiate football season, the authors identified 5 players with transient quadriplegia and paresthesias (incidence of 1.3 per 10,000 participants) and another 24 players with only transient paresthesias in the upper extremities, lower extremities, or both (incidence of 6.0 per 10,000 participants) 1. The overall incidence of CCN (sensory symptoms, motor findings or both) was therefore 7.3 per 10,000 participants. Based upon the observation that no player with CCN subsequently sustained a permanent injury, and that no player with permanent spinal injury recalled having had a preexisting episode of CCN, the authors concluded that a player with an episode of CCN, regardless of whether or not there were associated motor findings, was not predisposed to permanent neurological injury. It was recommended, however, that athletes with CCN having demonstrable instability or degenerative changes should be precluded from playing contact sports. The risk of a recurrent episode of cervical cord neurapraxia was examined in a subsequent study by the same authors 2. Fifty-six percent of athletes returning to contact sports, including 62% of players returning to football, experienced a recurrent episode of CCN. Increased risk of recurrence was associated with a smaller canal diameter, resulting in less space available for the spinal cord. A key conclusion of this article was that there was no observed correlation between the severity of injury and the degree of narrowing, provided that there was no cervical instability present. The potential long-term effects of recurrent episodes of CCN were not addressed in this study. Although Torg felt that there was no causal relationship between transient cervical cord neurapraxia and permanent paralysis and thus felt that the two events were unrelated, not all authors share this opinion. In addition, there is controversy regarding the potential significance of mild spinal canal stenosis without instability in a player with a single episode of transient CCN. Based upon data collected from the National Center for Catastrophic Sports Injury Research, Cantu, and colleagues reported a case of quadriplegia following an episode of CCN in a player with a stenotic spinal canal who had no evidence of fracture or dislocation 3. They believed that this would not occur in a normal sized canal, unless there was an associated fracture, dislocation or other evidence of instability. Therefore, the presence of cervical canal stenosis was thought to pose a risk for permanent spinal cord injury in the event of transient instability, and the presence of a large diameter canal is "protective" against permanent injury. The return-to-play decision is based on many factors. These include the nature of the injury, the clinical and radiographic findings, the sport and position, the level of competition (for example, high school versus collegiate or professional) and other factors. The role of the physician is to determine if there is any structural problem within the cervical spine that would place the athlete at greater than normal risk for a permanent spinal cord injury. The evaluation begins with a thorough neurological exam. Residual neurological deficit is a contraindication to return to athletic competition. A complete radiographic series of the cervical spine must be performed which includes anteroposterior (AP), neutral lateral, flexion-extension lateral, obliques and odontoid views. Magnetic resonance imaging (MRI) is the initial imaging modality of choice to evaluate the spinal cord and nerve roots. If there is any question about the quality of the study or the ability to visualize potential pathology, a myelogram and computed tomogram (myelo/CT) should be obtained. Other diagnostic tests such as electromyography (EMG) and nerve conduction studies (NCS) can be obtained if needed. Although some authors have emphasized the greater importance of spinal stability over actual spinal canal diameter in determining the potential for permanent spinal cord injury, it is obvious that a narrowed canal cannot protect against the possibility of instability. Therefore, instability in the presence of a narrowed canal portends a more serious prognosis for potential permanent spinal cord injury than does instability with a normal or large canal. Cantu, and colleagues described functional spinal stenosis and defined this as loss of the protective cerebrospinal fluid (CSF) cushion around the spinal cord or actual cord deformation 4. Functional stenosis can be seen on MRI as a loss of the white cerebrospinal fluid (CSF) "cushion" around the spinal cord on the T2 sagittal and axial images. It is intuitive that an individual with CCN and functional stenosis has the potential for permanent injury if he/she were to sustain an episode of transient instability that resulted in a critical degree of canal narrowing. It seems logical that athletes with functional stenosis should avoid contact and collision activities that could predispose them to such instability. A synopsis and modification of several authors' return to play criteria is summarized in Tables 1, 2 and 3. The most controversial scenario is whether or not to clear an asymptomatic player having a single episode of CCN, mild stenosis and no objective evidence of instability. (Player must be asymptomatic with normal neurological exam and normal motion) Healed fracture with normal alignment Asymptomatic clay shoveler's (C7 spinous process) fracture Asymptomatic cervical disc herniation Single level sub-axial fusion (congenital or post-surgical) Spina bifida occulta Single episode of prior CCN with normal radiographs/MRI and normal spinal canal Spinal canal/vertebral body ratio < 0.8 and asymptomatic Single episode of CCN with mild stenosis and no instability 2 episodes of CCN and normal MRI and x-rays 2 level sub-axial cervical fusion More than 2 episodes of CCN Spinal cord changes (myelomalacia) by MRI Presence of cervical myelopathy Persistent neurological deficit following spine injury Multilevel congenital fusion or > 2 level surgical fusion or cervical laminectomy C1-2 abnormalities: C1-2 instability or C1-2 fusion or rotatory fixation Occiput-C1 abnormalities: occiput-C1 assimilation (fusion) or Arnold-Chiari malformation Unhealed fracture (except spinous process fracture) or ligamentous instability Kyphotic deformity Symptomatic cervical disc herniation Spear tackler's spine: canal stenosis + degenerative changes + reversal of lordosis + history of spearing techniques (Tables 1, 2, 3 adapted from Bell GR. Cervical Neurapraxia and Return to Play. Contemporary Spine Surgery 2003; 4(8): 57-64) 1. Torg JS, Pavlov H, Genuario S, et al: Neurapraxia of the Cervical Spinal Cord with Transient Quadriplegia. J. Bone and Joint Surgery 68-A (9):1354-1370, 1986 |