Axial loading

The mechanism of injury to the cervical spine and associated anatomic risk factors that lead to serious neurologic injury have been the subject of active interest and debate within the sports medicine and spine surgery communities. Early research suggested that serious cervical spine injuries occurred from forced hyperflexion2–7,¹⁶ or hyperextension.^17–20 However, more recently axial loading has been defined as the most likely mechanism for catastrophic injury to the cervical spine during sports competition.

Axial loading occurs when a player strikes another player with the top of the head as the point of initial contact (so-called ‘spear tackling’). Axial loading places the cervical spine at a biomechanical disadvantage and makes it particularly susceptible to severe injury. Typically, most forces from a traumatic load to the cervical spine are dissipated through controlled spinal motion, the paravertebral muscles, and the intervertebral discs. When the top or crown of the helmet is used for initial contact, the neck is typically flexed approximately 30° and loses its normal cervical lordosis and ability to properly distribute force (Fig. 126.1). In this position the cervical spine assumes the characteristics of a segmented column and forces are transmitted along the longitudinal axis of the spine (Fig. 126.2).²¹

Fig. 126.1 (A) In the normal upright anatomical position, the cervical spine is slightly extended with a natural cervical lordosis. (B) When the neck is flexed to approximately 30°, the cervical spine is straightened and loses its ability to properly distribute force.

Fig. 126.2 (A) Spear-tackler’s spine involves loss of the normal cervical lordosis and an axial load. (B) The straightened cervical spine assumes the characteristics of a segmented column and forces are transmitted along the longitudinal axis of the spine, first compressing the intervertebral discs. When maximum compression is reached the spine flexes and fails (C) with potential fracture, subluxation, or dislocation (D,E).

In athletes with cervical spinal stenosis, axial loading followed by forced hyperextension or hyperflexion can cause transient or permanent sensory and motor changes. Penning¹⁹ described a ‘pincer mechanism’ with compression of the spinal cord between a vertebral body and the spinolaminar line of an adjacent vertebra. Compression of the spinal cord occurs in hyperextension when the distance between the posteroinferior margin of the superior vertebral body and the anterosuperior aspect of the spinolaminar line of the subjacent vertebra decreases (Fig. 126.3). With hyperflexion, the anterosuperior aspect of the spinolaminar line of the superior vertebra and the posterosuperior margin of the inferior vertebra approximate. Eismont et al.²⁰ also noted that hyperextension causes narrowing of the anteroposterior diameter of the spinal canal and can compress the spinal cord. Torg et al.²² described an axial load input with subsequent hyperextension and indentation of the ligamentum flavum with compression of the spinal cord. In each of these mechanisms, the anteroposterior diameter of the spinal canal decreases, resulting in compression of the spinal cord. Transient or permanent cervical cord injury can occur and usually involves a contusion of the spinal cord with temporary restriction of blood flow and a focal area of ischemia.⁸

Fig. 126.3 Hyperextension ‘pincer mechanism’ as described by Penning.¹⁹ During hyperextension, the distance between the posteroinferior aspect of the superior vertebral body and the anterosuperior aspect of the spinal laminar line of the subjacent vertebra decreases, and the cord is pinched between the two vertebral bodies.

While advances in helmet materials and equipment used in American football lead to a decrease in head injuries, it also contributed to the development of dangerous playing techniques using the top of the helmet as the initial point of contact. Torg et al.²³ compared the total number of head and neck injuries in the National Football League between 1971 and 1975 with previous work done by Schneider²⁴ analyzing injuries between 1959 and 1963. The major difference between these time periods was the type and quality of helmet worn during competition. The study found a reduction in intracranial hemorrhages of 66% and deaths due to intracranial injury of 42%. However, the study also found a 204% increase in cervical spine fractures, subluxations, and dislocations and a 116% increase in the number of cases of permanent quadriplegia. The majority of cases of permanent quadriplegia that occurred were due to direct compression when a player struck another player with the top of his helmet.

Delineation of the axial load mechanism as the major cause of catastrophic cervical spine injury in American football resulted in rule changes that caused a sustained decrease in the rate of cervical spine injuries and quadriplegia. In 1976 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. In 1976, the rate of cervical spine fracture, subluxation, and dislocation was 7.72/100 000 and 30.66/100 000 in high school and college athletes, respectively. In 1987, this had decreased to 2.31/100 000 and 10.66/100 000 serious injuries to the cervical spine in high school and college athletes, respectively.²¹ Injuries resulting in permanent quadriplegia also significantly decreased as a result of the rule changes. In 1976, the rate of quadriplegia was 2.24/100 000 and 10.66/100 000 in high school and college athletes, respectively. In 1977, only 1 year after the rule changes, these rates decreased to 1.30/100 000 and 2.66/100 000 in high school and college athletes, respectively, and have continued to remain low.²¹

In 1990 Torg and colleagues²⁵ further confirmed axial loading as the mechanism in catastrophic cervical spine injury by review of actual game films and videotapes. Analysis of films allowed an accurate determination of the mechanism of injury in 85% of cases, and axial loading was found to be the mechanism in every case.

Strains and sprains

Soft tissue injuries to the cervical spine, such as muscle or tendon strains and ligament sprains, are probably the most common sports-related neck injuries. These injuries are typically mild and self-limiting and present with minor neck pain and without any neurologic symptoms. Indicators of a more significant spine injury include significant cervical muscle spasm, tentative active range of motion, and severe pain. Evaluation of the athlete includes active cervical spine range of motion and strength testing of the neck and upper extremities. Manual compression and axial load to the cervical spine (Spurling’s maneuver) should not cause pain or radicular symptoms and is helpful in ruling out more significant injury. The athlete can return to play when full pain-free range of motion and normal strength of the cervical spine are restored. It is important that no symptomatic athlete returns to competition. Occasionally, more significant ligamentous injury may go unrecognized but should be suspected if persistent muscle spasm and limited range of motion lasts days or weeks following the injury. In this case, flexion and extension radiographs of the cervical spine should be taken to rule out instability.

Stingers

‘Stingers’ or ‘burners’ are descriptive terms used to characterize transient unilateral upper extremity pain and paresthesias following a blow to the neck or shoulders. Because of confusion with a potentially more serious central cord injury called ‘burning hands syndrome,’²⁶ use of the term ‘stinger’ rather than ‘burner’ is encouraged. Stingers are very common and are reported in up to 50–65% of college football players.^27,28

Stingers are peripheral nerve injuries, not spinal cord injuries, and are considered a transient neurapraxia of the cervical nerve roots or upper trunk of the brachial plexus, usually involving the C5 and/or C6 distribution. Because the dorsal root ganglion is positioned within the neural foramen, symptoms may be purely sensory and in a dermatomal distribution. Stingers are characterized by burning dysesthesias that typically begin in the shoulder region and radiate unilaterally into the arm and hand. Weakness, numbness, or both are sometimes associated with the burning pain. Initially, there can be a great deal of posterior cervical tenderness because the posterior primary ramus of the nerve innervates the skin in that area and comes directly off the dorsal root ganglion.

Stingers usually result from one of two mechanisms: tensile overload or compression overload.²⁹ While either mechanism is possible in any athlete, the mechanism of injury is more likely depending on the age of the athlete. In most high school athletes, the mechanism involves a tensile or stretch injury when the involved arm and neck are stretched in opposite directions. This occurs as the neck is forcibly stretched away while the ipsilateral shoulder is depressed (Fig. 126.4). In the older college or professional athlete with a higher likelihood of degenerative changes of the cervical spine, a compressive mechanism is more likely. This involves a compression or ‘pinch’ of the cervical nerve root within the neural foramen as the neck is forcibly flexed in a posterolateral direction towards the symptomatic upper extremity (see Fig. 126.4).³⁰

Fig. 126.4 ‘Stingers’ result from either a tensile or compression load. A blow to the neck producing lateral neck flexion with ipsilateral shoulder depression causes a traction or tensile load to the cervical nerve roots and upper trunk of the brachial plexus. Forceful flexion of the neck in a posterolateral direction causes compression of the nerve roots within the neural foramen.

Stingers must be differentiated from spinal cord injuries. The key distinguishing feature is that stingers result in unilateral upper extremity impairment. Spinal cord injury results in multiple limb involvement, i.e. bilateral upper extremities or both upper and lower extremities. Stingers typically resolve in minutes. Sideline evaluation of an athlete with a stinger involves a complete neck and upper extremity neurologic examination. As the symptoms improve, the athlete will demonstrate improved cervical spine range of motion. Athletes with transient stingers are safe to return to play when symptoms have fully resolved, the athlete can demonstrate normal cervical neck range of motion, Spurling’s maneuver is negative, and neurologic and strength examinations are normal.

Recurrent stingers are more common in the presence of cervical degenerative disc disease. Levitz et al.³⁰ studied 55 athletes with recurrent stingers. The mechanism of injury was extension combined with ipsilateral compression in 83% of patients, and 70% had a positive Spurling’s sign. Eighty-seven percent of patients had evidence of disc disease by magnetic resonance imagimg (MRI), and 93% had disc disease or narrowing of the intervertebral foramina. The authors concluded that nerve root compression in the intervertebral foramina secondary to degenerative disc disease was the likely cause of recurrent or chronic stinger syndromes in collegiate and professional athletes. Athletes with more than one stinger can be placed in a protective neck collar that limits lateral neck flexion and hyperextension.

Rarely, more significant nerve injury and axonotmesis occurs causing chronic symptoms. Patients usually demonstrate persistent weakness in the distribution of the upper trunk of the brachial plexus, and muscle atrophy may be present in severe cases. Electromyography will assess the distribution and degree of injury and should be performed if symptoms have lasted more than 3 weeks. Most cases of axonotmesis have a high likelihood of recovering within 1 year.²⁷

Cervical cord neurapraxia and transient quadriplegia

Injury to the spinal cord can be complete or be neurapraxic – a reversible injury with motor and sensory function returning within 24–48 hours. Neurapraxia of the cervical spinal cord is characterized by an acute, transient sensory and/or motor change to more than one extremity. Symptoms include burning pain, numbness, tingling and loss of sensation with or without motor changes of paresis or complete paralysis.³¹ Several other terms have been used to describe cervical cord neurapraxia and have been used interchangeably, including ‘transient quadriplegia,’³¹ ‘central cervical spinal cord syndrome,’³² and ‘spinal cord concussion.’³³

The most typical pattern of incomplete spinal cord injury is the central cord syndrome. This involves weakness of the upper extremities in excess of lower extremity findings secondary to the lamination of the corticospinal tracts and selective damage to fibers serving arm and hand function. ‘Burning hands syndrome’ described by Maroon²⁶ is characterized by burning dysesthesias of the hands and associated weakness of the upper extremities and is a variant of central cord syndrome. Transient quadriplegia is a temporary paralysis characterized by loss of motor function, with or without sensory disturbances.³¹

Episodes of cervical cord neurapraxia are transient by definition and complete recovery usually occurs in 10–15 minutes, although in some patients gradual resolution occurs over 1–2 days. Except for burning paresthesia, the athlete does not experience neck pain, and there is complete return of motor function and full, pain-free range of motion of the cervical spine. Torg et al.³⁴ studied 110 patients with transient cervical cord neurapraxia and found that 40% presented with plegia (complete motor weakness), 25% with paresis (incomplete motor weakness), and 35% with only paresthesia and sensory symptoms. The neurapraxia resolved in 74% of patients within 15 minutes and lasted more than 24 hours in 11% of patients. Eighty percent of patients had symptoms in all 4 extremities, 15% in the upper extremities only, 2% in lower extremities only, and 3% with symptoms in the ipsilateral upper and lower extremities. Of 110 patients, 109 had a complete neurologic recovery, with one patient having a residual hemiplegia following operative intervention. For those athletes who did return to football, the recurrence rate for transient cervical cord neurapraxia was 56% with no athlete experiencing permanent neurologic injury, although the follow-up period was only 3 years and some athletes chose to retire from collision sports.

Cervical spinal stenosis

Cervical spinal stenosis is an important factor in the occurrence of cervical cord neurapraxia and the severity of neurologic injury following cervical spine trauma. Cervical spinal stenosis is a congenital or developmental narrowing of the cervical spinal canal defined by the midsagittal diameter or cross-sectional area. A diminished anteroposterior diameter of the spinal canal can be caused by congenital narrowing of the spinal canal, developmental spinal stenosis from degenerative changes, cervical instability, or intervertebral disc protrusion.

The method to best determine spinal stenosis in an athlete has been the subject of considerable debate. Early definitions used the absolute anteroposterior canal diameter to detect spinal stenosis – measured from the posterior aspect of the vertebral body to the most anterior point on the spinolaminar line. In general, a canal was considered normal if the diameter between C3 and C7 was >15 mm, and spinal stenosis was present if the diameter was <12 mm.³⁵

Torg et al.³¹ and Pavlov et al.³⁶ described a measurement to detect spinal stenosis using a spinal canal to vertebral body ratio (known as the ‘Torg ratio’). The ratio uses the anteroposterior diameter of the spinal canal and the anteroposterior width of the midpoint of the vertebral body (Fig. 126.5). The measurements are made at the level of the third through the sixth vertebral body on a routine lateral radiograph of the cervical spine. The ratio method eliminates error caused by magnification factors or differences in target-to-film distances. A spinal canal-vertebral body ratio of <0.8 indicates significant spinal stenosis. In Torg’s study,³¹ a ratio of <0.8 was recorded at one or more levels in 24 athletes with cervical cord neurapraxia, compared to a ratio of 1.0 or more in 49 age-matched controls with no neurologic complaints.

Fig. 126.5

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