Stingers or "burners" are characterized by transient unilateral upper extremity pain and paresthesias resulting from a blow to the neck and shoulders. Stingers are common in American football and have been reported in up to 50% to 65% of college players (Clancy et al., 1977; Sal-lis et al., 1992). Stingers are peripheral nerve injuries and are considered a transient neurapraxia of the cervical nerve roots, usually involving the upper trunk of the brachial plexus (C5-C6). Stingers typically manifest with dysesthe-sia (burning pain) that begins in the shoulder and radiates down the arm. They often are associated with transient numbness or weakness, and all symptoms typically resolve in minutes.

Stingers can occur from a tensile or compression overload (Watkins, 1986). In most high school athletes, the mechanism of injury involves a tensile or traction injury when the involved arm and the neck are stretched in opposite directions. This occurs when the neck is forcibly flexed away while the shoulder is depressed. In college and professional athletes, who have a higher likelihood of degenerative changes of the cervical spine, a compression mechanism is more likely. This involves a pinch of the cervical nerve root within the neural foramen as the neck is forcibly extended in a posterolateral direction (Levitz et al., 1997).

Stingers are always unilateral, a distinguishing feature from spinal cord injuries, which involve symptoms in multiple limbs. Athletes are safe to return to play when symptoms have fully resolved and the athlete can demonstrate full cervical ROM and a normal neurologic examination.

Radiography and MRI should be considered in athletes with recurrent stingers to evaluate for cervical degenerative disk disease (Levitz et al., 1997). Rarely, more significant nerve injury involving axonotmesis (axon disruption) occurs, causing persistent weakness. Athletes with significant weakness 24 to 48 hours after injury may benefit from treatment with a short burst of oral corticosteroids. If weakness persists, electromyography performed 2 weeks or more after the injury will assess the distribution and degree of injury. Fortunately, most cases of axonotmesis recover within 1 year (Clancy et al., 1977).

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