“Stingers” or “burners” are colloquial terms used by athletes and trainers to describe a set of symptoms that involve pain, burning, and/or tingling down an arm, occasionally accompanied by localized weakness. The symptoms typically abate within seconds or minutes, rarely persisting for days or longer. It has been estimated that a stinger will occur at least once during the career of over 50% of athletes in contact/collision sports (4,5).
There are two typical mechanisms by which stingers may occur-traction on the brachial plexus or nerve root impingement within the cervical neural foramen. The majority of high-school level injuries are of the brachial plexus type, while most at the college level and virtually all in the professional ranks result from a pinch phenomenon within the neural foramen.
The brachial plexus stinger commonly involves a forceful blow to the head from the side but also can result from head extension or shoulder depression while the head and neck are fixed. Nerve root impingement usually occurs when the athlete's head is driven toward his shoulder pad. The dorsal spinal nerve root ganglion lies close to the posterior intervertebral facet joints and is pinched when the neural foramen is compressed.
With either type of stinger the athlete experiences a shock-like sensation of pain and numbness radiating into the arm and hand. The symptoms typically are purely sensory in nature and most commonly involve the C5 and C6 dermatomes. On occasion, weakness may also be present but unless severe usually does not alter the prognosis. The most common muscles involved include the deltoid, biceps, supraspinatus, and infraspinatus.
Stingers are always unilateral and almost never involve the lower extremities. Thus, if symptoms are bilateral and/or involve the legs, then the burning hands syndrome of central spinal cord contusion with all its implications for diagnosis and treatment of spinal cord injury must be considered.
When not associated with any neck pain or limitation of neck movement, if all motor and sensory symptoms clear within seconds to minutes, the athlete may safely return to competition. This is especially true if the athlete has experienced similar symptoms in the past. If there are any residual symptoms or complaints of neck pain, return should be deferred pending further workup.
On rare occasions a stinger may result in prolonged sensory complaints or weakness that persists more than a few minutes. In such a situation magnetic resonance imaging (MRI) of the cervical spine should be considered to look for a herniated disc or other compressive pathology. If symptoms persist for more than 2 wk, then electromyography (EMG) should allow for an accurate assessment of the degree and extent of injury, whereas an EMG prior to 14 d after injury is not likely to be accurate.
Some athletes seem predisposed to a series of recurrent stingers. It has been suggested that repeated stinger injuries over many years may lead to proximal arm weakness and constant pain. Thus, if an athlete suffers two or more stingers, particularly in rapid succession, consideration can be given to the use of high shoulder pads supplemented by a soft cervical roll, which should limit lateral neck flexion and extension. Examining and or changing the athlete's blocking and tackling techniques or changing the player's position may also be helpful in preventing recurrences (12). If, despite these interventions, stingers repeatedly recur, cessation of the causative athletic activity may be necessary.
Transient bilateral motor and or sensory neurological symptoms after an athlete receives a blow to the head or whiplash neck injury suggest cervical spinal cord injury. The development of transient neurological deficit may occur in association with sports. A 1984 survey of over 500 NCAA football programs (with a total of over 39,000 players) found that the incidence of transitory paresis and paresthesias was 1.3 per 10,000 participants, and the incidence of numbness and tingling was 6.0 per 10,000 participants(18). When faced with an athlete who has suffered a transient neurological deficit, the physician must do a thorough workup to rule out bony or ligamentous injury to the spine. Plain cervical spine films with flexion and extension views are essential. A computed tomography (CT) scan and/or a polytomography may be necessary to evaluate subtle bony injuries. If no bony or ligamentous abnormalities are identified in a patient with transient neurological deficit, the physician must rule out ongoing extrinsic cord or nerve root compression or intrinsic cord abnormalities. This is most readily accomplished by an MRI. Somatosensory evoked potentials may also prove useful in documenting physiological cord dysfunction. Special concerns should be raised if any intrinsic abnormalities are seen on MRI or are documented by somatosensory evoked potentials, as this provides direct evidence of an overt, though mild, spinal cord injury and should preclude a return to sports. If no evidence of spinal cord injury is found and no bony or ligamentous problems are identified, including no spinal stenosis, then return to competition probably is safe. A second episode of transient neurological deficit should initiate another complete workup. If all of the studies remain normal, a return to competition need not be precluded; however, concerns should be raised about the recurrent nature of the problem and consideration given to limiting further athletic activity in contact or collision sports.
CERVICAL SPINAL STENOSIS
Some debate exists over the definition of spinal stenosis. In the past, the anteroposterior (AP) diameter of the spinal canal measured from the posterior aspect of the vertebral body to the most anterior point on the spinal laminar line was used to determine the presence of stenosis. General consensus has been that between C3 and C7, canal heights are normal above 15 mm and spinal stenosis is present below 13 mm. Resnick believes that CT and myelography are the most sensitive diagnostic modalities in determining spinal stenosis(15). He points out that plain x-rays failed to appraise the width of the spinal cord and thus are not useful when stenosis results from ligamentous hypertrophy or disc protrusion. Ladd and Scranton state that the AP diameter of the spinal canal is “unimportant” if there is total impedance of the contrast medium (9). They argue that an enhanced myelogram is needed in the injured athlete since CT alone fails to reveal dural compression adequatley. Thus, spinal stenosis cannot be defined by bony measurements alone (3,8).“Functional” spinal stenosis, defined as the loss of the cerebrospinal fluid around the cord or in more extreme cases deformation of the spinal cord whether documented by contrast, CT, myelography, or MRI, is a more accurate measure of stenosis (3). The term“functional” is taken from the radiographic term “functional reserve” as applied to the protective cushion of CSF around the spinal cord in a nonstenotic canal.
Cervical spinal canal stenosis in the athlete may be a developmental or congenital condition or may be caused by acquired degenerative changes in the spine. It is well known that long-term sports participation predisposes the athlete to degenerative changes (2). When the minimum AP diameter of the cervical spine in the general population is compared with that of patients with cervical spondylitic myelopathy, it is clear that a substantial number of individuals have a constitutionally narrow spinal canal. The central question, however, is whether a narrow canal alone predisposes to the development of myelopathy. In sports, most attention is focused on developmental spinal stenosis as a result of dramatic cases of spinal cord injury associated with a congenitally small spinal canal in several football players. In spite of this, however, there is not abundant information concerning the risk of an asymptomatic narrow canal in an athlete. Schneider has been quoted as collecting “large series of cases of athletes who sustained an injury to the neck and who were later discovered to have stenosis of the cervical spine.” Permanent neurological deficit, quadriplegia, or death occurred in a high percentage of these athletes. However, no details are available from these series (7,16,17).
Anyone with developmental or spondylitic narrowing of the spinal canal is especially at risk for neurological injury during hyperextension(6). When the neck is hyperextended, the sagittal diameter of the spinal canal is further compromised by as much as 30% by infolding of the interlaminar ligaments. Thus, it is understood that hyperextension is the mechanism most likely to further compromise an already narrow spinal canal and lead to neurological symptoms.
While the precise percentages of increased risk of spinal cord injury in the athlete with documented spinal stenosis remain unknown, I believe this athlete should not engage in collision sports such as football. I base this opinion on three main bodies of evidence.
First, the reports in the sports medicine, neurology, orthopedic, and radiological literature suggest that cervical spinal stenosis predisposes the patient to spinal cord injury. This includes the work of Matsuura et al.(10) who found in 42 spinal cord injuries as compared with 100 controls that “the sagittal diameter of the spinal canals of the control group were significantly larger than those of the spinal cord injured group.” Esimont et al. (6) concluded that“our results provide evidence that the sattigal diameter of the spinal canal of some individuals may be inherently smaller than normal, and that this reduced size may be a predisposing risk factor for spinal cord injury.” Others who have concluded spinal stenosis predisposes to spinal cord injury include Wolfe et al. (19), Penning(14), Alexander et al. (1), Mayfield(11), Nugent (13), as well as Ladd and Scranton (9), who conclude that “patients who have stenosis of the cervical spine should be advised to discontinue participation in contact sports.”
Secondly, my views are further based on personal meetings and lengthy discussions with leading authorities in this field, such as the late Dr. Richard Schneider and Dr. Robert Watkins, and over 25 yr of personal neurosurgical experience, much of it dealing with cervical spine problems in both athletes and nonathletes.
Finally, my opinions are based on my work with the National Center for Catastrophic Sports Injury Research, where we have seen quadriplegia occur in a stenotic spinal canal after an initial episode of transient quadriplegia without fracture or dislocation. In a normal size canal, quadriplegia has not been seen without fracture/dislocation of the spine. And most importantly, we have yet to see complete neurological recovery with fracture/dislocation when spinal stenosis was documented by MRI. This 0% is compared with a 21% complete recovery rate after fracture/dislocation when the spinal canal is of normal size.
After a first stinger, especially if symptoms persist more than an hour, if there is associated neck pain or numbness or weakness in a nerve root distribution, a cervical MRI is recommended in addition to cervical spine x-rays to rule out intraspinal pathology such as a ruptured disc or lateral spinal stenosis.
As previously discussed, I do not believe an athlete with documented spinal stenosis should be playing a contact or collision sport. It is not cost-effective to screen all athletes participating in collision sports with an MRI to rule out this condition. However, if such an athlete has spinal cord symptoms after an injury, I believe an MRI should be a part of the workup. Documentation of spinal stenosis by MRI represents an absolute contraindication to further collision sports participation in my opinion.
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