Abstract

A “stinger,” otherwise known as a “burner,” is a transient, reversible peripheral nerve injury of the upper limb caused by injury to the cervical spine and shoulder. This injury usually occurs during participation in contact sports [1-3]. Stingers are considered to be underreported by athletes and are most common in American-style football, hockey, gymnastics, and wrestling [4]. In a study of collegiate American-style football players, Levitz et al [5] reported that stingers occur in 50%-65% of these athletes during the course of their career; they also reported high rates of recurrence. Mechanisms of injury include traction, compression, and direct blows [4,6-9]. Traction injuries result from ipsilateral shoulder depression and contralateral neck flexion, effectively resulting in traction on the nerve root and/or brachial plexus. At the high school level, football players are more likely to have traction injuries. Conversely, compression injuries are more likely sustained at the collegiate and professional levels [10]. Compression injuries of the nerve root stem from a combination of forced hyperextension with ipsilateral rotation and lateral flexion leading to transient neuroforaminal narrowing. Finally, a direct blow to the supraclavicular region (Erb point), where the brachial plexus is most superficial, can result in direct trauma to the plexus. Most stingers, according to the Seddon classification scheme, are characterized as firstor second-degree peripheral nerve injuries, which refer to neurapraxia (demyelination) or axonotmesis (axonal loss), respectively. A third-degree injury, or neurotmesis (complete nerve transection), is not considered within the spectrum of this disorder [11,12]. Because tackling and blocking are the two most common mechanisms of stingers, defensive backs and offensive linemen are most susceptible [10]. Symptoms appear immediately after contact [1] and generally affect the upper trunk of the brachial plexus or C5/C6 erve roots [6-8,13-15]. The primary symptom is burning pain referring to the upper limb, hich may be accompanied by weakness, numbness, and paresthesias [1,16]. Symptoms typically do not last more than 24 hours [2]. A wide range of clinical courses have been described after a stinger injury, ranging from full recovery in seconds or hours to the development of a chronic syndrome [1,5]. The distribution of weakness is dependent on the source of the nerve injury, but whether it is the root (C5 or C6) or upper trunk of the brachial plexus, the most common pattern of muscle weakness involves the deltoid, supraspinatus, and/or infraspinatus for several weeks after the injury [17]. Conflicting views exist regarding the location of the neurological lesion [13]. Some authors who included an electrodiagnostic evaluation in their studies reported a greater incidence of brachial plexus involvement [8,14,15,18]. However, Slipman et al [19] demonstrated that diagnostic cervical selective nerve root blocks frequently provoke symptoms outside the classic dermatomal distribution in nonathletes. Thus it is plausible that injury to a single nerve root can produce a more circumferential pattern of symptoms in the upper limb [20]. Several factors suggest that most stingers are caused by cervical nerve root injury [5,21]. It has been shown that there is a statistically significant 10%-13% decrease in neuroforaminal diameter when the neck is positioned in 20°-30° of extension, as is common during a stinger injury [22]. Anatomically, the cervical nerve roots appear to be more vulnerable to injury than the brachial plexus because of their orientation and

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