The brachial plexus is composed of the C5 through T1 nerve roots and is divided into roots, trunks, divisions, cords, and branches (Fig. 8.1). Usual mechanisms of injury are compression and traction. Traction injuries to the brachial plexus occur from forceful lateral flexion of the head and neck away from the side of injury. Arm position at the time of impact usually dictates the region of the plexus that is injured. If the arm is adducted, the upper roots are subjected to greater stress. If the arm is abducted, the lower roots are more susceptible to injury.

Compression injuries are usually the result of direct trauma (i.e., head and neck turned forcefully toward the side of injury) or sustained external pressure to regions overlying the plexus, such as the supraclavicular fossa. A concomitant clavicle fracture frequently occurs. Neck hyperextension and axial compression are also common in contact sports and can lead to nerve root compression and injury at the level of the neural foramina.

Acute brachial plexus injuries are usually diagnosed clinically. Motor and sensory examinations and reflexes should be documented for the upper and the lower extremities. A comprehensive vascular examination should also be performed. A thorough shoulder examination should rule out intrinsic shoulder pathology as the cause of symptoms.

Plain radiographs of the cervical spine, shoulder, and chest may be obtained. Suspicious findings include fractures of the transverse processes, clavicle, and ribs. An elevated hemidiaphragm may also be associated with cervical nerve root injury (i.e., phrenic nerve C3–C5 nerve roots). Computed tomography (CT) myelography may be used to evaluate injuries at the level of the nerve root while magnetic resonance imaging (MRI) is more useful distally in the brachial plexus. Electrodiagnostic studies can also help confirm the diagnosis. Other diagnoses that may present similarly should be considered in the differential diagnosis, such as:

Pain with range of motion or axial compression of the neck may suggest a spine fracture. Spurling maneuver can reproduce radicular pain associated with disk herniation or foraminal stenosis (Fig. 8.2). Examination of the scapula should include forward elevation and wall push-off to detect medial scapular winging from serratus anterior palsy (C5–C7 nerve roots, long thoracic nerve). Trapezius, levator scapulae, and rhomboid dysfunction (C5 nerve root, dorsal scapular nerve) can cause lateral winging.

Once cervical spine instability has been ruled out, the brachial plexus traction test can be performed, which involves controlled separation of the athlete’s head and shoulder (Fig. 8.3). It can reproduce symptoms from a
traction injury to the upper or lower trunk. Tinel sign with percussion along the supraclavicular fossa may produce electric shock–like symptoms or pain into the extremity.

Stingers have been reported to occur in up to 50% of athletes involved in contact or collision sports. After this event, the athlete experiences sudden pain, burning, and sometimes tingling that begins in the neck, radiates into the shoulder, and continues down the arm and into the hand. Symptoms do not follow a dermatomal pattern. Weakness of the supraspinatus, infraspinatus, deltoid, and biceps muscle often is noted. Symptoms normally resolve quickly (10 to 15 minutes) but on some occasions may last for an extended period of time.

Burners are can result from traction injury to the brachial plexus or compression of the cervical roots at the intervertebral foramen as described in the previous section. Direct impact to the plexus within the supraclavicular region also has been reported. Traction injuries can occur with tackling. This causes sudden lateral deviation of the head away from the affected side and simultaneous depression of the ipsilateral shoulder (Fig. 8.4). These injuries are more frequent in high
school athletes, possibly because of less developed supportive neck musculature.

Cervical root compression occurs at the level of the intervertebral foramen. The foramen is dynamically narrowed during activities that cause cervical spinal extension, compression, and rotation toward the symptomatic side. These injuries are seen more commonly in collegiate or professional athletes. Patients present with more neck pain and diminished range of motion than do patients with traction injuries. Direct trauma to the supraclavicular region at Erb point (2 to 3 cm above the clavicle posterior to the sternocleidomastoid muscle) can produce a burner with upper trunk deficits predominating. Spurling maneuver is used to evaluate compression-type injuries, whereas the brachial plexus stretch test can be used to reproduce symptoms of traction-type injuries.

Central cervical canal and foraminal stenosis are reported as risk factors for recurrent burners. Logically, this association has been described for compression-type and extension-type injuries but not traction mechanisms. One episode of a burner or stinger significantly increases an athlete’s chance of experiencing future episodes. Athletes with a history of recurrent burners and associated degenerative disk disease or congenital stenosis should consider abstaining from participation in contact sports.

The physician must determine whether symptoms are from cervical cord or root pathology. This important distinction often is made on the playing field. By definition, burners present with unilateral arm symptoms. Athletes who present with bilateral upper or any lower extremity symptoms are more likely to have had a spinal cord injury, such as transient neuropraxia. Focal neck
tenderness or severe pain with motion should raise suspicion for a fracture or ligamentous injury to the cervical spine. In these cases, the spine should be immobilized using a collar and backboard and the patient should be transported to a hospital for immediate imaging.

Burners/Stingers are usually self-limited syndromes that do not cause permanent sequelae. Even with this favorable natural history, certain restrictions should be placed on athletes after sustaining these injuries to prevent more severe problems in the future. Athletes must fulfill particular criteria before they can return to play (Table 8.1).

If symptoms have not resolved by 3 weeks, it is reasonable to obtain an EMG. This test can help define the specific nerve root involved and determine the degree of injury. Results of this test may lag behind an athlete’s recovery. Players who demonstrate clinical weakness and moderate fibrillation potentials on EMG are withdrawn from play. In following, such athletes should rest the involved extremity until symptoms improve. At that time, physical therapy can begin and be advanced as tolerated. Athletes also should be started on year-round trapezial strengthening programs. Theoretically, strengthening the neck musculature may increase the shock-absorbing capacity of the cervical spine.

Athletes who are prone to burners can use special equipment to help prevent injuries. Commonly used devices are thicker shoulder pads, neck rolls, springs, and the “cowboy collar” (Fig. 8.5). The devices must fit correctly and be used with properly fitting shoulder pads to be effective. Educating participants about proper athletic technique is also important. Proper tackling and blocking techniques, with avoidance of spearing, should
be taught to young football players as they are learning the sport.

Cervical spine injuries constitute a large percentage of spinal injuries in sports. Injuries range from cervical sprains to catastrophic complete spinal cord injuries (SCIs). An estimated 10% to 15% of football players experience an injury to the cervical spine. The overall incidence of SCI in the high school and college populations is around 1 in 100,000. Most are incomplete, with preservation of varying degrees of neurologic function.

Cervical spine injuries may occur by hyperflexion, hyperextension, rotation, axial load, and shear forces. A review by Torg et al. of the data compiled by the National Football Head and Neck Injury Registry showed that axial loading of a slightly flexed head and neck is the most frequent contributing mechanism of injury. The slightly flexed posture reverses normal lordosis, potentiating axial load transmission down the straightened cervical spine. Pre-existing spinal stenosis predisposes to SCI from these mechanisms. Athletes can sustain cord injury despite the absence of bone or ligamentous disruption. This phenomenon has been described by Penning. When the cervical spine is in hyperextension, the cord can be compressed between the posteroinferior margin of the superior vertebrae and the anterosuperior lamina of the subjacent vertebra. Infolding of the posterior longitudinal ligament and the ligamentum flavum contributes to central canal narrowing. This transient compression can occur with energies not great enough to cause discoligamentous or bone disruption. SCI can occur without an “unstable” spinal injury. Some athletes experience multiple symptomatic episodes.

Contact sports, such as football, rugby, and wrestling, place patients at high risk for injury. Most cervical spine injuries in football players result from hyperflexion, but other mechanisms, including hyperextension, rotation, and lateral bending, have been reported. Gymnasts may sustain injuries after “missed” maneuvers that result in an uncontrolled fall. Wrestlers commonly exhibit neck hyperflexion, but also may endure rotational and horizontal shearing forces that place great stresses on the intervertebral disks, facet joints, and spinal ligaments. SCI has also been documented in noncontact sports, such as diving and surfing. These events usually result from the individual striking his or her head on the bottom of the pool or body of water, causing neck hyperflexion.