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© 2002 The Journal of Bone and Joint Surgery, Inc.
Injuries to the Cervical Spine in American Football Players
Investigation performed at MCP-Hahnemann University School
of Medicine, Philadelphia, Pennsylvania
A national registry has documented data on more than 1300 cervical spine injuries resulting from tackle football. Axial loading of the cervical spine is the primary injury mechanism, an observation with profound implications regarding implementation of preventative measures. Characteristic injury patterns involving the middle (third and fourth) cervical segment and the more favorable response to prompt reduction of these injuries are emphasized. The marked instability and grave prognosis of axial load teardrop fractures are attributed to the associated sagittal vertebral body and posterior arch fractures. Spear tackler’s spine is described and is classified as an absolute contraindication to participation in collision sports. Cervical cord neurapraxia, with or without transient quadriplegia, is neither associated with nor presages permanent neurologic sequelae. However, there is a considerable risk of recurrence, which can be predicted on the basis of canal diameter data. The concept of spinal cord resuscitation is proposed as a means of obtaining maximum neurologic recovery by reversing the secondary injury phenomenon that occurs in acute spinal cord trauma. Athletic trauma to the cervical spine resulting in injury to the spinal cord is an infrequent but potentially catastrophic event. Recognition of the problems presented by injury to the cervical spine and spinal cord led to a series of field, clinical, and basic research studies conducted over the past twenty-five years. As a result of these efforts, basic questions have been answered regarding the epidemiology, prevention, pathomechanics, pathophysiology, and histochemical responses of reversible and irreversible cervical cord injuries.
Allen et al.1 studied 165 closed indirect fractures and dislocations of the lower cervical spine, demonstrating various "spectra of injuries," and developed a classification based on the mechanism of injury as determined by the presumed attitude of the cervical spine at the time of failure and the initial dominant mode of failure. The common mechanisms were compressive flexion, vertical compression, distractive flexion, compressive extension, distractive extension, and lateral flexion. Injuries resulting in spinal cord trauma have been associated with football, water sports, gymnastics, wrestling, rugby, trampolining, and ice hockey, to name a few. Traditionally, on the basis of interpretation of post-injury radiographs, hyperflexion and hyperextension have been implicated as the primary mechanisms of cervical spine injuries. In 1973, Schneider2 reported on a series of cervical spine injuries sustained in tackle football that he attributed to striking of the head on another player’s knee, acute cervical hyperextension, tackling by grabbing the face guard, so-called clotheslining or neck-tackling, the karate blow, forced hyperflexion, and head-butting. He concluded that the most serious injuries occurred as a result of forced hyperflexion. Other authors drew similar conclusions3-5. Hyperflexion has also been reported to be the most frequent cause of serious cervical injuries in other sports6-13. Carvell et al.14 (in a study of rugby injuries), Gehweiler et al.15 (diving), Leidholt16 (football), Macnab17 (diving), McCoy et al.18 (rugby), O’Carroll et al.19 (rugby), Paley and Gillespie20 (general sports), Piggot and Gordon21 (rugby), Scher22 (rugby), Williams and McKibbin23 (rugby), and Wu and Lewis24 (wrestling) all concluded that hyperflexion was the predominant mechanism of injury to the cervical spinal cord. Hyperextension has also received attention as an additional mechanism leading to cervical spinal cord injury25-29, whereas axial loading has received little attention in the literature. While some authors, such as Kazarian30 (general sports), Kewalramani et al.31 (diving), Albrand et al.32,33 (diving), Maroon et al.34 (football), Mennen35 (diving), Rogers36 (diving), and Scher37-41 (rugby), recognized axial loading as a possible mechanism, it was not generally accepted as the predominant mechanism producing spinal cord damage.
The National Football Head and Neck Injury Registry, established in 1975, has collected data on more than 1300 cervical spine injuries42-44. The criteria for inclusion of injuries in the Registry were a need for hospitalization for more than seventy-two hours; a need for an operation; and a fracture, subluxation, or dislocation resulting in neurologic injury or death. Data on each injury were collected from the athlete, parents, and school officials as well as from radiographs and medical reports. When available, game films or videotapes of the injury were analyzed to determine the mechanism of injury. The total number of head and neck injuries from 1971 to 1975 was calculated retrospectively and compared with the data on injuries from 1959 to 1963 compiled by Schneider45 in a similar study. It was found that while both intracranial hemorrhages and deaths due to intracranial injuries had decreased by 66% and 42%, respectively, the number of cervical spine fractures, subluxations, and dislocations had increased by 204% and the number of cases of permanent cervical quadriplegia had increased by 116% (Fig. 1). The majority of the cases of permanent cervical quadriplegia that occurred between 1971 and 1975 was determined to have been due to so-called spearing, or direct compression, when the player made initial contact with the top of his helmet (Fig. 2).
Axial loading was documented as a mechanism of catastrophic cervical spine injuries in football players in a review of game films of actual injuries44. Stop-frame kinetic analysis, a method that allows estimation of the magnitude of injury-producing forces, was performed on sixty game films and videotapes of injuries resulting in permanent quadriplegia. The orientation of the head, cervical spine, and trunk segment of each athlete was analyzed to determine the mechanism of injury. Analysis of these films allowed an accurate determination of the mechanism of injury in 85% of the cases, and axial loading was determined to be the mechanism in every instance. On the basis of these findings, it was concluded that the improved protective capabilities of modern helmets accounted for the decrease in head injuries but led to the development of playing techniques that used the top or crown of the helmet as the initial point of contact, placing the cervical spine at risk. It was postulated that execution of headfirst techniques increased the risk of neck injury by exposing the cervical spine to excessive axial load, a force to which the cervical spine appears to be particularly susceptible46-48. In the course of a contact activity, such as tackle football, the cervical spine is repeatedly exposed to potentially injurious energy inputs46. Fortunately, most energy inputs are dissipated by controlled spinal motion through the cervical paravertebral muscles and the intervertebral discs47. However, the vertebrae, intervertebral discs, and supporting ligamentous structures can be injured when contact occurs on the top or crown of the helmet with the head, neck, and trunk positioned in such a way that forces are transmitted along the vertical axis of the cervical spine. In this situation, in which the cervical spine assumes the physical characteristics of a segmented column, motion is precluded in response to axially directed impacts, and the forces are directly transmitted to the spinal structures. With the neck in a neutral position, the cervical spine is extended as a result of the normal cervical lordosis. When the neck is flexed to 30°, the cervical spine becomes straight. When a force is applied to the vertex, the energy inputs are transmitted along the longitudinal axis of the cervical spine and are no longer dissipated by the paravertebral muscles. This results in the cervical spine being compressed between the abruptly decelerated head and the force of the oncoming trunk48. When the maximum vertical compression is reached, the cervical spine fails in a flexion mode, with the occurrence of fracture, subluxation, or facet dislocation (Fig. 3).
In 1976, in response to these data, the National Collegiate Athletic Association banned "spearing," defined as intentionally striking an opponent with the crown of the helmet as well as other tackling techniques in which the helmet is used as the initial point of contact. Similar rule changes were also enacted at the high-school level42-44. As a result of these changes, the rates of fractures, subluxations, and dislocations of the cervical spine decreased dramatically between 1976 and 1987. In 1976, the rates of these injuries were 7.72/100,000 and 30.66/100,000 for high-school and college athletes, respectively; they decreased to 2.31/100,000 and 10.66/100,000, respectively, by 1987. The number of cervical spine injuries resulting in quadriplegia also consistently decreased, from a total of thirty-four cases in 1976 to five cases in 1984 and one case in 1991. In 1976, the rates of injuries causing quadriplegia were 2.24/100,000 at the high-school level and 10.66/100,000 at the college level. In 1977, one year following the rule changes, these rates decreased to 1.30/100,000 and 2.66/100,000, respectively, and, by 1984, they decreased to 0.40/100,000 and 0/100,000. With the exception of observed increases in 1989 and 1990, the yearly incidence of permanent quadriplegia has remained low (Fig. 4).
Numerous biomechanical studies have supported the axial loading theory49. Mertz et al.50, Hodgson and Thomas51, and Sances et al.52 measured forces to the cervical spine when axial impulses were applied to helmeted cadaver head-spine-trunk specimens. The authors were able to produce fractures of the lower cervical spine when the impulse was applied to the crown of the helmet. Hodgson and Thomas determined that direct vertex impact imparted a larger force to the cervical vertebrae than did impact applied farther forward on the skull. Gosch et al.53 investigated three different injury modes (hyperflexion, hyperextension, and axial compression) in anesthetized monkeys and concluded that axial compression produced cervical spine fractures and dislocations. Maiman et al.54, Roaf55, and White and Punjabi56 demonstrated that axial loading of isolated spinal units caused vertebral body fractures in the lower cervical spine. Roaf55 subjected spinal units to forces with different directions and magnitudes and concluded that hyperflexion of the cervical spine was an anatomical impossibility. In contrast, he was able to produce almost every variety of spinal injury with a combination of compression and rotation. Bauze and Ardran57 postulated that axial loads were responsible for cervical spine dislocations as well as fractures. They demonstrated failure of the facet joints and posterior ligaments when axial loads were applied to cadaveric spines. When the caudad portion of the spine was flexed and fixed and the cephalad part was extended and free to move forward, vertical compression produced bilateral dislocation of the facet joints without fracture. If lateral tilt or axial rotation occurred as well, a unilateral dislocation was produced. The observed forces were all less than those required for osseous failure and allowed facet dislocation without associated osseous injury. Nightingale et al.58 analyzed the relationships among head motion, local deformations of the cervical spine, and injury mechanisms using a cadaver head-and-neck model impacted in an anatomically neutral position. They observed that classic concepts of flexion and extension as a mechanism of injury of the cervical spine do not apply to a vertically impacted head. They further concluded that straightening of the cervical spine before injury may be a necessary element of the compressive flexion mechanism. Analysis of data from the National Football Head and Neck Injury Registry supports the clinical and laboratory observations that the axial energy inputs to the straightened cervical spine result in compressive deformation and subsequent buckling in a flexion mode with subluxation, dislocation, fracture, or fracture-dislocation at any level or levels. Clinical entities peculiar to axial loading of the cervical spine and associated with irreversible cervical cord lesions have been described.
Injuries at the third and fourth levels of the cervical spine involving the osseous and ligamentous structures and intervertebral disc have been infrequently reported in the literature59. During the eighteen-year period from 1971 to 1988, the National Football Head and Neck Injury Registry documented 1062 injuries, twenty-five (2.4%) of which were at the third and fourth cervical levels. Four of these injuries involved acute herniation of the intervertebral disc; four, anterior subluxation of the third cervical vertebra on the fourth cervical vertebra; six, unilateral dislocation of the joint between the articular processes; seven, bilateral dislocation of the joints between the articular processes; and four, fracture of the fourth cervical vertebra. Axial loading was again the predominant injury mechanism. Injuries to the middle cervical segment are unique in that they generally do not involve fracture of the osseous elements. Prompt reduction of both unilateral and bilateral facet dislocations led to more favorable results. Two patients in whom a unilateral facet dislocation was reduced within three hours after injury and was subsequently fused anteriorly had marked neurologic recovery. The other four patients, two of whom underwent delayed open reduction and two of whom were treated with closed skeletal traction, remained quadriplegic. All four patients in whom a bilateral facet dislocation was reduced successfully with either closed or open methods had no neurologic recovery, but all four patients survived. The three patients who did not have a successful reduction died59,60.
Schneider and Kahn61 apparently were the first to define a triangular fracture fragment at the anteroinferior corner of a cervical vertebral body as a teardrop fracture. Their description was based solely on analysis of lateral radiographs. They did not describe findings on anteroposterior radiographs or mention the possibility of a sagittal vertebral body fracture or a posterior arch fracture. Schneider and Kahn did not distinguish between an isolated fracture of the anteroinferior corner and one associated with a sagittal fracture of the vertebral body. They concluded that the teardrop fracture was caused by acute flexion of the cervical spine and resulted in a severe neurologic deficit. Acute flexion and teardrop39 have been accepted as the terms describing vertebral body fractures with a fracture fragment at the anteroinferior corner. Others have described these fractures as burst or compression fractures or have used the terms flexion teardrop and burst interchangeably62,63. Inherent in the descriptive terminology of these injuries is confusion regarding the mechanism of injury. These fractures have been attributed to flexion, hyperflexion, hyperflexion with compression, axial loading, hyperextension, and a combination of hyperextension and hyperflexion. Woodford64 reported that the sagittal fracture occurs with burst fractures caused by an axial force but not with flexion teardrop fractures and stated that the two fractures can be differentiated on the basis of the mechanism of injury. Allen et al.1 observed that vertical compression fractures with an anterior fracture fragment can be differentiated from fractures at the anteroinferior corner caused by compression flexion. Lee et al.65 reported that forceful flexion produces the triangular fracture at the anteroinferior corner and strong axial load compression produces the sagittal fracture. Because of the inconsistency with regard to terminology and mechanism of injury, the neurologic sequelae of each of the fracture patterns had not been clarified. Data on fifty-five patients with fifty-eight teardrop fractures included in the National Football Head and Neck Injury Registry were analyzed66. Nine fractures were at the fourth cervical level; forty-three, at the fifth cervical level; and six, at the sixth cervical level. Axial compression was determined to be the mechanism responsible for fifty-one of the fifty-five injuries. Radiographically, patients were divided into two groups according to the fracture pattern. Six had an isolated fracture of the anteroinferior corner of the vertebral body, and the other forty-nine had, in addition, a sagittal fracture of the vertebral body; that is, they had a three-part, two-plane fracture pattern through the lamina (Fig. 5). Forty-five patients in the series were permanently quadriplegic, and ten had transient neurologic symptoms. Five of the six patients with an isolated fracture of the anteroinferior corner had no serious neurologic sequelae. One patient with fractures of the posterior elements of the subjacent vertebra was quadriplegic. Of the forty-nine patients with a documented three-part, two-plane injury, forty-four (90%) were quadriplegic.
The terms flexion teardrop, acute flexion teardrop, and burst fracture are incomplete descriptors of a comminuted fracture of the cervical vertebral body, and they inaccurately explain the mechanism of injury. The anteroinferior corner (teardrop) fracture has two patterns; it can be an isolated fracture, which is usually not associated with permanent neurologic sequelae, and it can be a three-part, two-plane fracture that includes a sagittal fracture of the vertebral body and a fracture of the posterior neural arch, which is usually associated with permanent neurologic sequelae. The mechanism of both fracture patterns is axial loading. When either type of lesion is suspected, an anteroposterior radiograph, in addition to a lateral radiograph, is essential in the initial screening process to determine the presence of a sagittal vertebral fracture or a fracture of the posterior neural arch. Computed tomography may then better define the anatomy.
Spear tackler’s spine is a clinical entity that constitutes an absolute contraindication to participation in tackle football and other collision activities that expose the cervical spine to axial energy inputs. A subset of football players were identified who demonstrated developmental narrowing of the cervical canal (a canal-vertebral body ratio of <0.8), straightening or reversal of the normal cervical lordosis, and post-traumatic radiographic abnormalities and who had been seen employing spear-tackling techniques on videotape. Fifteen patients who met these criteria were identified between 1987 and 199067. Eleven had complete neurologic recovery: four of them had a transient episode of cervical cord neurapraxia and seven had a brachial plexus root radiculopathy, all of which resolved. The other four patients had a permanent neurologic deficit: two had quadriplegia; one, incomplete hemiplegia; and one, residual long-tract signs. Three of these four patients had acute fracture-dislocation of the cervical spine. Permanent neurologic injury occurred as the result of axial loading of a persistently straightened cervical spine due to head-impact playing techniques. On the basis of these observations, it was concluded that individuals with the aforementioned characteristics of spear tackler’s spine should be precluded from participation in tackle football and other collision activities, such as rugby and ice hockey, that expose the cervical spine to axially directed energy inputs.
Neurapraxia of the cervical spinal cord with transient quadriplegia was previously described by one of us (J.S.T.)68. The prevalence of cervical cord neurapraxia has been estimated to be seven per 10,000 football participants. Usually, the athlete has an acute, transient neurologic episode of cervical spinal cord origin associated with sensory changes of burning pain, numbness, tingling, or loss of sensation with or without motor changes of weakness or complete paralysis. The episode is transient, with complete recovery usually occurring in ten to fifteen minutes but sometimes taking up to two days. Although the athlete experiences burning paresthesias in the arms, the cervical area is pain-free at the time of injury and there is complete return of motor function and a full painless range of motion of the cervical spine. In athletes with diminution of the anteroposterior diameter of the spinal canal, the cord can, on forced hyperextension or hyperflexion, be compressed, causing transient motor and sensory manifestations. The mechanics of cervical spinal cord compression have been described by Penning69 as the "pincer mechanism" (Fig. 6). With hyperextension, the posteroinferior aspect of the superior vertebral body and the anterosuperior aspect of the spinolaminar line of the subjacent vertebra approximate. With flexion, the anterosuperior aspect of the spinolaminar line of the superior vertebra and the posterosuperior aspect of the body of the subjacent vertebra approximate. In each situation, the anteroposterior diameter of the canal decreases, resulting in compression of the spinal cord and thus a transient disturbance of sensory and/or motor function.
Pavlov et al.70 devised an objective measurement to determine which athletes had a decreased anteroposterior diameter of the spinal canal (Fig. 7). The standard measurement of the spinal canal is compared with the anteroposterior width of the vertebral body at the midpoint on the lateral radiograph. This ratio method of determining narrowing of the cervical spinal canal is independent of magnification factors caused by differences in target distance, object-to-film distance, or body type because the sagittal diameter of the spinal canal and that of the vertebral body are in the same anatomical plane and are similarly affected by magnification. There is normally a one-to-one relationship between the sagittal diameter of the spinal canal and that of the vertebral body, regardless of gender or age. A spinal canal-vertebral body ratio of £0.80 was recorded at one or more levels in all patients who experienced cervical cord neurapraxia70.
Herzog et al.71, who studied a cohort of professional football players, pointed out that although the canal-vertebral body ratio has a high sensitivity for detecting cervical spinal stenosis, it has a poor positive predictive value. This was particularly true in this group consisting of football players because their large vertebral bodies increased the denominator of the equation, thus lowering the ratio and indicating stenosis in individuals with minimal absolute narrowing of the spinal canal. Subsequent to the description of cervical cord neurapraxia, questions regarding both the relationship between the sagittal diameter of the cervical spinal canal and injury as well as the reliability of the canal-vertebral body ratio as an indicator of stenosis arose. Eismont et al.72 studied the relationship between sagittal canal diameter and neurologic injury in a cohort of ninety-eight patients who had sustained traumatic cervical fracture-dislocation. Forty-five patients had no neurologic deficit, thirty-nine had incomplete quadriplegia, and fourteen had complete quadriplegia. It was observed that a small-diameter canal correlated with neurologic injury whereas a large-diameter canal offered protection against neurologic injury. Also, there was a tendency for patients with an incomplete lesion and a large canal to have more recovery than those with a small canal. The authors concluded "the importance of the study is to prevent spinal cord injury by appropriate counseling." Matsuura et al.73 subsequently compared computerized tomographic parameters in the cervical spine of cord-injured patients with those in normal controls. They concluded that the intrinsic dimensions of the cervical spinal canal may contribute a predisposition to cord injury and that this predisposition is not a manifestation of available space but rather of the shape of the canal. The smaller the ratio of the sagittal to the transverse canal diameter, the greater the predisposition to cord injury. Kang et al.74 evaluated lateral radiographs of the cervical spine of 288 patients with an acute subaxial fracture or dislocation. Of these patients, eighty-three had a complete injury of the spinal cord, ninety-two had an incomplete injury of the spinal cord, thirty had an isolated nerve root injury, and eighty-three had no neurologic deficit. The authors measured the space available for the cord at the level of the injury, the sagittal diameter of the spinal canal at the uninjured levels, and the ratio described by Pavlov et al.70 at the uninjured levels. They found that the severity of the injury was associated with the space available for the cord after the injury and that patients who had a permanent injury had had a narrower sagittal canal diameter before the injury. One of us (J.S.T.) and colleagues75 performed an epidemiologic study to address the issues of canal size and cord injury. Evaluation of forty-five athletes who had had an episode of transient neurapraxia of the cervical spinal cord revealed the consistent finding of developmental narrowing of the cervical spinal canal. The purpose of the study, which involved various cohorts of football players as well as a large control group, was to determine the relationship, if any, between a developmentally narrowed cervical spinal canal and reversible and irreversible injury of the cervical spinal cord. Cohort 1 comprised 227 college football players who were asymptomatic and had no known history of transient neurapraxia of the cervical spinal cord. Cohort 2 consisted of ninety-seven professional football players who also were asymptomatic and had no known history of transient neurapraxia of the cervical spinal cord. Cohort 3 was a group of forty-five high-school, college, and professional football players who had had at least one episode of transient neurapraxia of the cervical spinal cord. Cohort 4 comprised seventy-seven individuals who were permanently quadriplegic as a result of an injury sustained while they played high-school or college football. Cohort 5 consisted of a control group of 105 male non-athletes who had no history of a major injury of the cervical spine, an episode of transient neurapraxia, or neurologic symptoms. The mean and standard deviation of the diameter of the spinal canal, the diameter of the vertebral body, and the ratio of the diameter of the spinal canal to that of the vertebral body were determined at the third through sixth cervical levels on the lateral radiographs of each cohort. In addition, the sensitivity, specificity, and positive predictive value of a ratio of the diameter of the spinal canal to that of the vertebral body of £0.8 was evaluated. The findings of this study demonstrated that a ratio of £0.8 had a high sensitivity (93%) for the detection of transient neurapraxia. The findings also supported the concept that the symptoms result from a transient reversible deformation of the spinal cord in a developmentally narrowed osseous canal. None of the seventy-seven quadriplegic individuals (Cohort 4) had had an episode of transient neurapraxia of the spinal cord before the catastrophic injury. Also, none of the forty-five high-school, college, and professional players who had had an episode of transient neurapraxia (Cohort 3) became quadriplegic. These data, in combination with the absence of developmental narrowing of the cervical spinal canal in the quadriplegic group (Cohort 4), provided evidence that the occurrence of transient neurapraxia of the cord and an injury associated with quadriplegia are unrelated (Fig. 8). It was concluded that developmental narrowing of the cervical spinal canal in the absence of instability is neither a harbinger of nor a predisposing factor for permanent neurologic injury. The major factor in the occurrence of cervical quadriplegia in football is a playing technique in which the head is used as the primary point of contact, with an axial energy input to, and subsequent failure of, the cervical spine.
These findings demonstrated the high sensitivity, low specificity, and low positive predictive value of the canal-vertebral body ratio for predicting cervical cord neurapraxia. Thus, it cannot be used as a screening mechanism to determine the suitability of an individual for participation in contact sports. On the basis of available data, it appears that developmental narrowing of the cervical spinal canal without associated instability does not predispose an individual to permanent neurologic injury. Although it is a controversial issue, about which many spine surgeons disagree, we believe that cervical cord neurapraxia should not preclude an athlete from participation in contact sports75. More recently, a group of 110 patients with cervical cord neurapraxia were studied by one of us (J.S.T.) and colleagues76. In this report, a system for classification of cervical cord neurapraxia is presented, and clinical findings, radiographic findings, and magnetic resonance imaging data obtained with use of a new computerized measurement technique are analyzed. Cervical cord neurapraxia was classified according to the type of neurologic deficit. The term plegia is used for episodes with complete paralysis; paresis, for episodes with motor weakness; and paresthesia, for episodes that involved only sensory changes without motor involvement. The grade of the cervical cord neurapraxia was determined by the length of time that the neurologic symptoms had persisted: grade I indicated less than fifteen minutes; grade II, more than fifteen minutes but less than twenty-four hours; and grade III, more than twenty-four hours. The pattern of the cervical cord neurapraxia was defined by the anatomic distribution of the neurologic symptoms. The term quad was used for episodes that involved all four extremities; upper, for episodes involving both upper extremities; lower, for episodes involving both lower extremities; and hemi, for episodes involving an ipsilateral upper and lower extremity. The type of cervical cord neurapraxia was plegia in forty-four patients (40%), paresis in twenty-eight (25%), and paresthesia in thirty-eight (35%). The cervical cord neurapraxia was grade I in eighty-one patients (74%), grade II in seventeen (15%), and grade III in twelve (11%). The pattern was quad in eighty-eight patients (80%), upper in seventeen (15%), lower in two (2%), and hemi in three (3%). Of the 110 subjects in this study, 109 had complete recovery without neurologic sequelae. One patient had a residual hemiplegia secondary to operative intervention. To analyze the relationship of the spinal cord to the spinal canal, a computerized system was developed to analyze the magnetic resonance images. This system consisted of a personal computer and a color scanner with a transparency adapter. The midsagittal T1 and T2-weighted images were digitized on the scanner and then uploaded with use of an imaging software package. A graphics digitizer pad with a resolution of 0.01 mm was used to make the following measurements at the third to the seventh cervical levels. The disc-level canal diameter was measured as the shortest distance between the intervertebral disc and the osseous posterior elements to quantify spondylotic narrowing. The transverse cord diameter was determined, and the space available for the cord was calculated by subtracting the cord diameter from the disc-level canal diameter. Plots were constructed, with use of logistic regression analysis, of the percentage risk of recurrence versus the disc-level canal diameter (Fig. 9-A) and the spinal canal-vertebral body ratio (Fig. 9-B).
Although it is controversial, we do not believe that individuals who experience uncomplicated cervical cord neurapraxia are at risk of incurring permanent neurologic sequelae. Rather, the problem is subsequent recurrence of transient episodes. The average rate of recurrence for players who returned to football was 56%76. The risk of recurrence is correlated with the pathoanatomyæ i.e., the smaller the canal, the greater the riskæand is clearly predictable. Our guidelines for managing athletes with developmental narrowing of the cervical spine associated with cervical cord neurapraxia are listed in Table I. We define a relative contraindication as a recommendation that an individual return to play based on less-than-unequivocal substantiated data regarding risk, as documented in the literature or by anecdotal experiences.
In 1964, Richard Schneider, MD, Professor and Chairman of the Department of Neurosurgery at the University of Michigan, who pioneered documentation and analysis of intracranial and spine injuries occurring in tackle football, stated that "there is probably no better experimental and research laboratory for human trauma in the world than the football fields of our nation."45 The more recent clinical studies discussed in the present report clearly support Schneider’s observation. Delineation of the axial load mechanism has resulted in the implementation of preventative measures in the form of rule changes that resulted in a sustained decrease in the rate of cervical spine injuries, particularly those resulting in quadriplegia42-44. A clear understanding of the pathomechanics of cervical spine injury combined with a description of specific injury patterns has aided in the initial attempts to establish criteria for return to activity77,78. Also of note are attempts to correlate both the laboratory and the clinical observations with the presumed pathophysiology of cervical cord trauma. Specifically, athletic injuries to the cervical spine have resulted in reversible, incompletely reversible, and irreversible neurologic deficits58,59,66,70,78. A recent study of an in vitro neuronal injury model correlated the degree of axonal deformation with reversible aberrations of cell membrane permeability and increases in intracellular calcium concentrations adversely affecting cell function79. It was proposed that this laboratory finding might, in part, explain the reversible nature of cervical cord neurapraxia. Delamarter et al.80 demonstrated the effect of timing of decompression of the spinal cord and the residual neurologic sequelae in a dog model. Specifically, when 50% of the diameter of the spinal cord had been compressed for six hours or longer, there was no neurologic recovery and there was progressive necrosis of the spinal cord. These findings explain the increased neurologic recovery after the prompt reduction of third and fourth cervical lesions reported in the literature as well as in anecdotal examples from the ranks of professional and intercollegiate athletes brought to the attention of the senior author (J.S.T.)59,60. The literature also supports the concept that acute spinal cord injury with concomitant subluxation and dislocation should be reduced promptly81-85. In addition, we propose that the pathophysiology of lesions resulting in irreversible neurologic sequelae following injury to the cervical cord is similar to that occurring in closed head injuries. Specifically, it is not the primary brain injury but rather the secondary injury phenomena, cerebral hypoxia and ischemia due to brain swelling, that is the greater problem. It has been well established in the neurosurgery literature that the release of excitotoxic substances, cell membrane depolarization, a rise in intracellular calcium concentration, and increased intracellular hydrostatic pressure result in increased neuronal pressure and rupture79. It is proposed that, with regard to permanent neurologic sequelae, the same phenomena occur in acute spinal cord trauma. It is the secondary injury to the cord caused by edema, hypoxia, and aberration of cell membrane potential that is largely responsible for the resultant neurologic deficit. The concept of spinal cord resuscitation, admittedly based in part on clinical observations lacking scientific format, has been proposed as an attempt to reverse the secondary injury phenomena and obtain maximum neurologic recovery. Such measures include support of both respiratory and hemodynamic function to facilitate spinal cord perfusion, prompt relief of cord deformation through realignment, intravenous administration of corticosteroids as recommended by Bracken et al.86, and early spinal stabilization.
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Introduction
Mechanisms of Injury 
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