Stingers, cervical cord neurapraxia, and stenosis

Abstract

The risk of sustaining a stinger, CCN, or a more serious catastrophic injury to the cervical spine increases with increasing stenosis. The RR of a player sustaining a second stinger or CCN increases exponentially when compared with the risk of a player sustaining an initial stinger or CCN. Intravenous steroids have no role in the management of stingers or CCN. Players who remain symptomatic after a stinger, players with persistently abnormal diagnostic studies after a stinger, and any player who experiences a CCN should be excluded from further participation in contact sports.

Full text

Stingers, cervical cord neurapraxia, and stenosis
Frank P. Castro, Jr., MD
a,b,
*
a
Tulane University Health Sciences Center, 1430 Tulane Avenue SL-32, New Orleans, LA 70112, USA
b
Spine Surgery, P.S.C., 210 East Gray Street, Suite 601, Louisville, KY 40202, USA
The athletic future of a player who has sustained a neurapraxic injury to the
cervical spine is debatable. Numerous variables, such as the position played, head
position at the time of contact, equipment worn, previous history of injuries, body
morphology, and cervical anatomy, all influence the decision-making process.
Tommy Maddox of the Pittsburgh Steelers was recently faced with such an
injury. He experienced a transient episode of quadriplegia during a 2002 National
Football League (NFL) game. Tommy lowered his head during a collision with a
defensive tackler of the Tennessee Titans. By the time he arrived at the hospital
his quadriplegia had resolved.
This article reviews the relationship between cervical spinal stenosis and two
neurological injuries of the cervical spine, stingers and cervical cord neura-
praxia (CCN).
Anatomy
The sagittal diameter of the cervical (C) canal reaches adult dimensions by
about age thirteen [1]. The canal size remains constant while the bony structures
around it continue to enlarge. Vertebral body shape from C3 to C7 remains
constant descending the spinal column, but the size increases. The average
vertebral body width from C3 to C7 increases from 17 mm to 23 mm, depth
increases from 16 mm to 18 mm, and height increases from 11 mm to 13 mm [2].
Sagittal diameters remain fairly constant at 14 mm to 15 mm from C3 to C7 [3,4].
The spinal canal cross-sectional area has been reported to be narrowest at C4,
followed by C5 [5,6]. The cross-sectional area of the spinal cord at the cervical
enlargement has been reported to be largest at both C4-C5 [5,6] and C6 [7].
0278-5919/03/$ – see front matter D2003 Elsevier Inc. All rights reserved.
doi:10.1016/S0278-5919(02)00094-7
* Spine Surgery, P.S.C., 210 East Gray Street, Suite 601, Louisville, KY 40202.
E-mail address: Bozothetruth@netscape.net
Clin Sports Med 22 (2003) 483– 492

Pedicle inclination decreases from 40°in the sagittal plane at C3 to 29°degrees
at C7 [2]. Spinous process length increases from C3 to C7, allowing for the
increased torque needed to resist loads on the head. The nerve roots exit at a 45°
angle through the neural foramen, which are approximately 9 mm in height, 4 mm
in width, and 5 mm in length [8]. The exiting nerves are under some tension, as they
retract 10% to 20% of their length when cut in vivo. Nerve root pressures are
highest when the cervical spine is at 40°of extension and neutral rotation [10].
Nerve root pressures are reduced when the arm is moved from the neutral to the
abducted position [11,12]. Intraneural blood flow demonstrates measurable reduc-
tions when strain is increased 8% by stretching of the nerve. When stretching of the
nerve increases strain measurements to 15%, intraneural blood flow stops [13].
The center of rotation for C-spine flexion and extension has been reported to
be anterior to the spinal cord and spinal canal. Consequently, the spinal column
and spinal cord lengthen in flexion and shorten in extension [14]. The spinal
canal and spinal cord slide relative to one another during flexion and extension.
The ‘‘neutral point’’ at which no relative motion between the cord and vertebrae
occurs is at C5 [14].
Extension of the cervical spine results in statistically significant stenosis when
compared with the flexed or neutral positions [15,16]. From flexion to extension
the average disk bulge changes 1.16 mm, or 11% of the canal diameter. More
importantly, the ligamentum flavum undergoes volume redistribution from a
long, slender, taut structure in flexion to a thickened, fat structure in extension.
The ligamentum flavum can encroach the spinal canal by 2.7 mm, reducing the
canal diameter by 20% to 30%. Cervical neuroforamenal diameters demonstrates
a statistically significant 10% to 13% decrease when the neck is positioned in
twenty to thirty degrees of extension [9]. Neuroforaminal size is smallest at C5
and largest at C7 [9].
Cervical stenosis
Cervical stenosis, or narrowing of the cervical spinal canal, defined by its
midsagittal diameter or cross-sectional area, has been retrospectively shown to be
an important factor in the occurrence and severity of neurological injury
following cervical trauma [3,12,17]. Sagittal canal diameters were significantly
smaller in patients with spinal cord injuries as compared with normal controls
[3,12]. Football players with stenosis were reported to be at higher risk for
recurrent stingers [18,19] and CCN [20 – 22]. Complete neurological recovery has
yet to be documented in athletes with fracture-dislocation injuries when magnetic
resonance imaging (MRI) documented spinal stenosis. This 0% recovery is
markedly different from the reported 21% complete recovery rate after frac-
ture-dislocation in an athlete with normal spinal canal dimensions [20].
The mean sagittal diameter from C3 through C7 measures approximately
14 mm to 15 mm [3,4]. Canal widths above 15 mm are considered normal; widths
less than 13 mm are considered stenotic [23]. Measurements of the midsagittal
F.P. Castro, Jr. / Clin Sports Med 22 (2003) 483–492484

diameter can vary because of magnification factors and differences in radiographic
technique. In 1986, Torg and Pavlov proposed using the ratio of the midsagittal
diameter of the spinal canal to the vertebral body diameter to define stenosis [22].
The ratio method eliminated measurement differences caused by different target
distances, object-to-film distances, and magnification factors. Torg et al originally
measured C3 through C6 in 24 players who experienced transient quadriplegia
[22]. The averaged Torg ratio from C3 to C6 was 0.63, with the smallest individual
level ranging between 0.31 and 0.77. Only two subjects had Torgratios greater than
0.82 at two or more cervical levels. Pavlov and Torg’s original definition of
‘‘significant cervical stenosis’’ as 0.80 or less was based on a statistical sensitivity
of the relative operating characteristic curve for the average Torg value over the
entire cervical canal, not the smallest level measured [24]. The literature that has
reported a 29% to 49% incidence of collegiate and professional football players
demonstrating a ‘‘significant cervical stenosis’’ at one or more levels is therefore a
misinterpretation of Torg’s original definition [19,25,26].
Castro et al redefined the Torg ratio definition of stenosis to 0.70 or less [18].
The 0.70 represents 1.92 standard deviations below the 0.94 + 0.125 average of
3314 cervical levels reported in the literature [18,19,25,26]. The 0.70 threshold
may also be a better predictor of ‘‘functional stenosis’’ (described below), as 0.80
has been a poor predictor of functional stenosis [4,18,19,25 – 28].
Clinically, athletes experiencing an initial episode of CCN had an average
Torg ratio of 0.6845. Athletes who experienced a recurrent episode of CCN had
smaller Torg ratios than those who returned to sports without CCN recurrence
(0.65 vs. 0.72; p < 0.05) [21].
With the availability of computerized tomographic (CT) myelography and
MRI, the concept of functional stenosis has been introduced [29]. Functional
stenosis considers bony canal dimensions, cord thickness, and the cushioning
potential of the cerebral spinal fluid (CSF). The enfolding of the ligamentum
flavum or disc protrusions may be insignificant if the functional reserve is
adequate. Currently, no guidelines exist to determine adequate versus inadequate
functional stenosis.
Stingers
A ‘‘burner’’ or ‘‘stinger’’ is a transient neurological event characterized by
pain and paresthesias in a single upper extremity following a blow to the neck or
shoulder. Players may experience tingling, burning, or numbing sensations in a
circumferential rather than a dermatomal distribution [30]. Symptoms may
radiate to the hand on the affected side or may be localized to the neck. The
precipitating event usually involves the downward displacement of the shoulder
with concomitant lateral flexion of the neck towards the contralateral shoulder.
Stingers with prolonged neurological symptoms are the most common reason for
high school and collegiate football players to be referred to emergency rooms and
orthopaedic clinics for evaluation of the cervical spine [18,19].
F.P. Castro, Jr. / Clin Sports Med 22 (2003) 483–492 485

Cervical cord neurapraxia (CCN) or transient quadriplegia
Episodes of CCN are described in terms of the neurological deficit, duration of
symptoms, and anatomical distribution. ‘‘Paresthesia,’’ ‘‘paresis,’’ and ‘‘plegia’’
describe a continuum of neurological deficits that range from sensory involve-
ment only, to sensory involvement with motor weakness, to episodes of complete
paralysis. CNN symptoms that last fewer than 15 minutes are considered grade I
injuries. Grade II injuries last between 15 minutes and 24 hours. Grade III injuries
persist for longer than 24 hours. When all four extremities are involved, a ‘‘quad’’
pattern is noted. The anatomic pattern may also be considered ‘‘upper’’ for
episodes involving both arms and ‘‘lower’’ for episodes involving the legs. A
‘‘hemi’’ pattern involves an ipsilateral arm and leg [21].
Mechanism of injury
The exact mechanism of injury causing a stinger is still debated. Most
practitioners believe that shoulder depression with lateral flexion to the con-
tralateral side produces a traction injury to the brachial plexus [31,32]. Others
believe that stingers result from ipsilateral head rotation. When the head is turned
towards the affected side, the neuroforamen narrows and compresses the exiting
nerve root. Slipman et al demonstrated how stimulation of a single nerve root
frequently provoked symptoms outside the classic dermatomal distributions [33].
Thus, it is feasible that stingers may result from trauma to a single nerve root
[34]. Direct blunt trauma at Erb’s point has also been proposed as an etiology for
stinger experience [35]. Electromyographical studies have demonstrated abnor-
malities in the roots, cords, trunks, and peripheral nerves of players sustaining
stingers [36,37]. Clinically, long-term muscle weakness with persistent par-
esthesias may result from severe or repeated stingers [38,39].
The pincher mechanism as proposed by Penning is currently believed to
explain the mechanism of injury with CCN [40]. During extension the cervical
spine shortens (in length), the dura mater folds, the spinal cord thickens, the
ligamentum flavum buckles, and the subarachnoid space narrows [16]. These
events, alone or in combination, serve to increase pressure on and decrease blood
flow to the spinal cord. The pincher mechanism also explains the central cord
syndrome seen in elderly patients after hyperextension injuries.
Treatment
By definition, stingers are transient injuries and usually do not require formal
treatment. Many physicians administer steroids to patients with CCN in accord-
ance with the Bracken protocol [41]. It is important to understand that the
Bracken protocol is experimental [42,43]. The Food and Drug Administration has
never given approval for the use of methylprednisolone in the treatment of acute
spinal cord injuries. There have been no published reports demonstrating any
F.P. Castro, Jr. / Clin Sports Med 22 (2003) 483–492486

significant functional benefits after receiving high-dose steroids. In fact, most
publications report additional morbidity associated with high-dose steroid usage
[44]. As of the writing of this paper, there have been no reports that institution of
the Bracken protocol has altered the natural history of athletes having experi-
enced CCN. Therefore, I believe that the administration of intravenous steroids in
accordance with the Bracken protocol after CCN is contraindicated, as it may be
harmful to the athlete [43,45].
Incidence
Literature from the 1970s estimated that one or more stingers were experi-
enced by at least 50% of football players at least once during their careers
[31,32]. Rule changes and equipment improvements may have lowered the
prevalence of stingers. Castro et al reported a yearly stinger incidence of 7.7%
(23 collegiate players over 298 player-years) [18]. The prevalence of a stinger in
this study was 18% (23 of the 130 players). Although a small Torg ratio did not
place players at increased risk for experiencing their first stinger, players who
experienced multiple stingers demonstrated significantly smaller Torg ratios. The
relative risk (RR) of a player experiencing recurrent stingers was twice that of the
risk of a player experiencing an initial stinger. Similarly, Meyer et al reported a
yearly stinger incidence of 3.7% (40 collegiate players over 1064 player-years)
and a stinger experience prevalence of 15% (40 of the 266 players) [19]. Players
experiencing a stinger were three times more likely to experience a stinger
recurrence compared with the risk for experiencing an initial stinger for that
cohort (Table 1). The position played and body morphology have also been
identified as risk factors for initially sustaining a stinger independent of cervical
stenosis [18,46,47].
Torg et al estimated the CCN incidence to be 0.06% (24 of 39,377) for
collegiate football players in 1984 [28]. Five of seven athletes who returned to
contact sports experienced a second episode of CCN. Torg later reported that 35
of 62 or 56% of athletes who returned to play after having experienced CCN had
a second CCN episode [21]. Although one might think that 56% represents the
relative risk of experiencing a recurrent CCN, the RR of experiencing a recurrent
CCN is determined by dividing the incidence of recurrent CCN by the incidence
of an initial episode of CCN. Thus, the athlete who has experienced a CCN is
933 times more likely to experience a CCN recurrence than another athlete is to
experience a first CCN episode (see Table 1).
In 2001, one college player and two high school players were reported to the
Center for Catastrophic Sports Injury Research as having experienced CCN
(Table 2). If one assumes that reporting was 100% compliant, then the yearly
incidence of CCN for high school football players was 0.00013% (2 divided by
1,500,000), and the CCN incidence for collegiate level football players was
0.0013% (1 divided by 75,000). In 1999 and 2002 at least one professional
football player sustained a CCN. The yearly CCN incidence approximates
F.P. Castro, Jr. / Clin Sports Med 22 (2003) 483–492 487

0.003%. Even though the compliance rate of injury reporting is probably
significantly less than 100%, it appears that the risk of CCN increases exponen-
tially from the high school to the professional level. This observation may be
related to several factors. The Torg ratio decreases with skeletal growth [1].
Professional athletes have larger masses and are capable of generating greater
velocities prior to contact; thus, the potential kinetic energy of a collision (one-
half the mass times the velocity squared) is greater. Expectations also play a
significant role in the occurrence of cervical spine injuries. Offensive players
usually have the greatest ability to determine the extent of a collision because
they have the option to change directions at the last second, whereas defensive
players must try to anticipate what the other player is going to do. The
unexpected collision may leave a player vulnerable to injury. An analogous
situation is that of central cord syndrome in the elderly, in which the unexpected
nature of the fall rather than the velocity of impact seems to affect the injury.
Table 1
The relative risk of experiencing a stinger or CCN
N Denominator Incidence RR
Stinger
Initial 63 396 16% 5% players/year
Recurrent 26 63 41% 2.6 *
CCN
(1984) 24 39,377 0.06%
Recurrent 35 62 56% 933 **
Permanent neurological injury
after having experienced a
CCN episode***
162
Risk for permanent neurological
injury after initial CCN experience
compared to risk for permanent
neurological injury without
previous CCN
3225***
Adapted from Cantu RC. Sports medicine aspects of cervical spinal stenosis. Exerc Sport Rev
1995;23:399 – 409.
* Risk for stinger recurrence compared to risk for initial stinger experience based on combined
data of Castro et al [18], and Meyer et al [19] papers
** RR for CCN recurrence compared to risk for initial experience of CCN experience based on
paper by Torg et al [21]
*** See text for calculation
Table 2
The 2001 cervical spine injury list
High school College Professional
Incomplete neurological recovery 6 0 0
CCN 2 1 0
C-spine Fracture 3 2 0
F.P. Castro, Jr. / Clin Sports Med 22 (2003) 483–492488

Similarly, if one analyzed the total number of CCN cases in the literature and
applied realistic denominators, similar conclusions would be made. Torg et al
reported 28 cases of CCN in professional athletes, 49 collegiate cases, 29 high
school cases, and 4 recreational cases [41]. The denominator for an equal
comparison would be player-years. The Center for Catastrophic Sports Injury
Research estimated that there are approximately 35,000 professional and semi-
professional football players, 75,000 college athletes, and 1,500,000 high school
football players [48]. The difference in the denominator applied to determine
player-years grows geometrically with each year. For example, let us assume that
the 110 cases above were collected over a 10-year interval. The respective
denominators would be: 350,000 player-years at the professional level, 750,000
player-years at the college level, and 15,000,000 player-years at the high school
level. The estimated incidences would be 80 cases for every 100,000 professional
player-years, 6 cases for every 100,000 collegiate player-years, and 2 cases for
every 100,000 high school player-years.
Cantu reported one case of quadriplegia in an athlete who experienced CCN;
however, the year in which the athlete experienced the catastrophic injury was not
reported in the article [29]. For the sake of argument, let us assume that the CCN
injury occurred in 1995 and that the quadriplegic injury occurred before the 2000
season. This time period was arbitrarily chosen to maximize the number of
catastrophic cervical spine injuries that occurred each year [15]. To make the
estimate even more conservative, we will assume that all 62 players reported by
Torg et al played all 5 years [21]. The estimated RR for a player having already
experienced a CCN and subsequently having a catastrophic neck injury would
then be 3225 ([1/62], [9/1,800,000]) if the injury occurred in 1995. If the injury
occurred in 1999, the RR would equal 645.
Eighty-six football players were reported to experience incomplete neuro-
logical recovery after a cervical cord injuries between 1990 and 2001. Seventy-
one of these injuries occurred in high school players, 11 in college players, and 4
in professional players [48]. Using the player-years denominator, one sees that
the incidence for incomplete neurological recovery is 0.4 high school players per
100,000 player-years, the risk for incomplete recovery for collegiate athletes is
1.2 players per 100,000 player-years, and the incidence in professional players is
1 player per 100,000 player-years.
Return to play
When the risks outweigh the benefits, players should not be allowed to return
to contact sports. Isolated stingers are considered benign injuries. With the
appropriate rest, diagnostic studies, and rehabilitation, players may return to play
[49]. Players with residual muscle weakness, cervical anomalies, or abnormal
electromyographic studies should be excluded from contact sports.
Return to play after CCN is highly controversial. Although guidelines for
return to play after CCN have been published [20,22], many physicians exclude
F.P. Castro, Jr. / Clin Sports Med 22 (2003) 483–492 489

further participation after CCN. Even in the description of spear tackler’s spine
[50], the key element is the technique used to tackle. Based on the above
statistical arguments, I recommend no further participation in contact sports after
CCN experience. Variables such as stenosis, position played, and body morpho-
logy may increase the risk of CCN several-fold, but a positive history of CCN
increases the risk for CCN recurrence 993-fold. Risk of a quadriplegic injury after
a CCN may be 3225 times greater than the risk of having a catastrophic neck
injury without a previous neck injury.
Torg has stated that young patients who have had an episode of CCN, with or
without transient quadriplegia, were not predisposed to permanent neurological
injury [22,28]. This position was valid until someone who had a CCN episode
later experienced a quadriplegic injury, as has now been reported [29]. The RR of
sustaining a catastrophic injury decreases from 3325 in the first year to 645 in the
fifth year. More important, no long-term follow-up studies on athletes after CCN
exist. Studies have shown that patients with a Torg ratio of 0.72 were statistically
more likely to suffer from spondylotic myelopathy compared with normal
controls with a Torg ratio of 0.95 [52]. The male predominance of cervical
spondylotic myelopathy has also been attributed to smaller canal-to-vertebral
body ratios [51]. Trauma in addition to an already stenotic spine may accelerate
the spondylotic condition.
Summary
The risk of sustaining a stinger, CCN, or a more serious catastrophic injury to
the cervical spine increases with increasing stenosis. The RR of a player
sustaining a second stinger or CCN increases exponentially when compared
with the risk of a player sustaining an initial stinger or CCN. Intravenous steroids
have no role in the management of stingers or CCN. Players who remain
symptomatic after a stinger, players with persistently abnormal diagnostic studies
after a stinger, and any player who experiences a CCN should be excluded from
further participation in contact sports.
References
[1] Wang JC, Nuccion SL, Feighan JE, et al. Growth and development of the pediatric cervical spine
documented radiographically. J Bone Joint Surg 2001;83-A:1212 – 8.
[2] Panjabi MM, Duranceau J, Goel V, et al. Cervical human vertebrae. Quantitative three-dimen-
sional anatomy of the middle and lower regions. Spine 1993;16:861 – 74.
[3] Matsuura P, Waters RL, Adkins RH, et al. Comparison of computerized tomography parameters
of the cervical spine in normal control subjects and spinal-injured patients. J Bone Joint Surg
1989;71-A:183 – 8.
[4] Moskovich R, Shott S, Zhang ZH. Does the cervical canal to body ratio predict spinal stenosis?
Bull Hosp Joint Dis 1996;55(2):61– 71.
[5] Inoue H, Ohmori K, Takatsu T, et al. Morphological analysis of the cervical spinal canal, dural
F.P. Castro, Jr. / Clin Sports Med 22 (2003) 483–492490

tube and spinal cord in normal individuals using CT myelography. Neuroradiology 1996;
38(2):148 – 51.
[6] Okada Y, Ikata T, Katoh S, et al. Morphologic analysis of the cervical spinal cord, dural tube and
spinal canal by magnetic resonance imaging in normal adults and patients with cervical spon-
dylotic myelopathy. Spine 1994;19:2331 – 5.
[7] Kameyama T, Hashizume Y, Ando T, et al. Morphometry of the normal cadaveric spinal cord.
Spine 1994;19:2077 – 81.
[8] Czervionke LF, Daniels DL, Ho PSP, et al. Cervical neural foramina: correlative anatomic and
MR imaging study. Neuroradiology 1988;169:753 – 9.
[9] Yoo JU, Zou D, Edwards WT, et al. Effect of cervical spine motion on the neuroforaminal
dimensions of human cervical spine. Spine 1992;17(10):1131 – 6.
[10] Farmer JC, Wiseneski RJ. Cervical spine nerve root compression: an analysis of neuroforaminal
pressures with varying head and arm positions. Spine 1994;19(16):1850 – 5.
[11] Beatty RM, Fowler FD, Hanson EJ. The abducted arm as a sign of ruptured cervical disk.
Neurosurgery 1987;21:731– 2.
[12] Eismont FJ, Clifford S, Goldberg M, et al. Cervical sagital spinal canal size in spine injury. Spine
1984;9(7):663 – 6.
[13] Lundborg G, Rydevik B. Effects of stretching the tibial nerve of the rabbit: a preliminary study of
the intraneural circulation and the barrier function of the perineurium. J Bone Joint Surg
1973;55-B:390 – 401.
[14] Reid JD. Effects of flexion-extension movements of the head and spine upon the spinal cord and
nerve roots. J Neurol Neurosurg Psychiat 1960;23:214 – 21.
[15] Chen IH, Vasavada A, Panjabi MM. Kinematics of the cervical spine canal: changes with sagital
plane loads. J Spinal Disord 1994;7(2):93– 101.
[16] Muhle C, Weinert D, Falliner A, et al. Dynamic changes of the spinal canal in patients with
cervical spondylosis at flexion and extension using magnetic resonance imaging. Invest Radiol
1998;33(8):444 – 9.
[17] Moiel RH, Raso E, Waltz TA. Central cord syndrome resulting from congenital narrowness of
the cervical spinal canal. J Trauma 1970;10:502– 10.
[18] Castro FP, Ricciardi J, Brunet ME, et al. Stingers, the Torg ratio, and the cervical spine. Am J
Sports Med 1997;25(5):603 – 8.
[19] Meyer SA, Schulte KR, Callaghan JJ, et al. Cervical spinal stenosis and stingers in collegiate
football players. Am J Sports Med 1994;22(2):158 – 66.
[20] Cantu RC. Stingers, transient quadriplegia, and cervical spinal stenosis: return to play criteria.
Med Sci Sports Exerc 1997;29(Suppl 7):S233– 5.
[21] Torg JS, Corcoran TA, Thibault LE, et al. Cervical cord neurapraxia: classification, patho-
mechanics, morbidity, and management guidelines. J Neurosurg 1997;87(6):843 – 50.
[22] Torg JS, Pavlov H, Genuario SE, Sennett B, Wisneski RJ, Robie BH, et al. Neurapraxia of the
cervical spinal cord with transient quadriplegia. J Bone Joint Surg 1986;68-A:1354 – 70.
[23] Alexander MM, Davis CH, Field CH. Hyperextension injuries of the cervical spine. Arch Neurol
Psychiatr 1958;79:146 – 50.
[24] Pavlov H, Torg JS, Robie B, et al. Cervical spinal stenosis: determination with vertebral body
ratio method. Radiology 1987;164:771– 5.
[25] Herzog RJ, Wiens JJ, Dillingham MF, et al. Normal cervical spine morphometry and cervical
spine stenosis in asymptomatic professional football players. Spine 1991;16(Suppl 6):
S178 – 86.
[26] Odor JM, Watkins RG, Dillin WH, et al. Incidence of cervical spinal stenosis in professional and
rookie football players. Am J Sports Med 1990;18:507– 9.
[27] Cantu RC. Sports medicine aspects of cervical spinal stenosis. Exerc Sport Sci Rev 1995;
23:399 – 409.
[28] Torg JS, Naranja RJ, Palov H, et al. The relationship of developmental narrowing of the cervical
spinal canal to reversible and irreversible injury of the cervical spinal cord in football players.
J Bone Joint Surg Am 1996;78-A:1308 – 14.
F.P. Castro, Jr. / Clin Sports Med 22 (2003) 483–492 491

[29] Cantu RC. Cervical spine injuries in the athlete. Semin Neurol 2000;20(2):173– 8.
[30] Hershman EB. Brachial plexus injuries. Clin Sports Med 1990;9(2):311– 29.
[31] Clancy WG, Brand RL, Bergfeld JA. Upper trunk brachial plexus injuries in contact sports. Am J
Sports Med 1977;5:209 – 16.
[32] Robertson Jr WC, Eichman PL, Clancy Jr WG. Upper trunk brachial plexopathy in football
players. JAMA 1979;241:1480– 2.
[33] Slipman CW, Plastaras CT, Palmitier RA, et al. Symptom provacation of fluoroscopically guided
cervical nerve root stimulation: are dynatomal maps identical to dermatomal maps? Spine 1998;
23(20):2235 – 42.
[34] Kelly JD, Aliquo D, Sitler MR, et al. Association of burners with cervical canal and foraminal
stenosis. Am J Sports Med 2000;28(2):214 – 7.
[35] Markey KL, Di Benedetto M, Curl WW. Upper trunk brachial plexopathy: the stinger syndrome.
Am J Sports Med 1993;21(5):650– 5.
[36] Poindexter DP, Johnson EW. Football shoulder and neck injuries: a study of the ‘‘stinger’’. Arch
Phys Med Rehabil 1984;65:601 – 2.
[37] Wilbourn AJ, Hershman EB, Bergfeld J. Brachial plexopathies in athletes, the EMG findings.
Muscle Nerve 1986;9:254.
[38] Bergfeld JA, Hershman EB, Wilbourn AJ. Brachial plexus injury in sports: a five-year follow-up.
Orthop Trans 1988;12:743 – 4.
[39] Speer KP, Bassett III FH. The prolonged burner syndrome. Am J Sports Med 1990;18(6):591 – 4.
[40] Penning L. Some aspects of plain radiography of the cervical spine in chronic myelopathy.
Neurology 1962;12:513 – 9.
[41] Bracken MB, Shepard MJ, Holford TR, et al. Administration of Methylprednisilone for 24 or
48 hours or Trilazad for 48 hours in the treatment of acute spinal cord injury. Results of the Third
National Acute Spinal Cord Injury Study. JAMA 1997;277:1597 – 604.
[42] Coleman WP, Benzel E, Cahill DW, et al. A critical appraisal of the reporting of the national
acute spinal cord injury studies (II and III) of Methylprednisolone in acute spinal cord injury.
J Spinal Disord 2000;13(3):185 – 99.
[43] Hurlbert RJ. The role of steroids in acute spinal cord injury: an evidence-based analysis. Spine
2001;26(Suppl 24):S39 – 46.
[44] Matsumoto T, Tetsuya T, Kawakami M, et al. Early complications of high-dose methylpredni-
solone sodium succinate treatment in the follow-up of acute cervical spinal cord injury. Spine
2001;26(4):426 – 30.
[45] Hulbert RJ. Methylprednisilone for acute spinal injury: an inappropriate standard of care.
J Neurosurg 2000;93:1– 7.
[46] Torg JS. Epidemiology, pathomechanics, and prevention of football-induced cervical spinal cord
trauma. Exerc Sports Sci Rev 1992;20:321– 38.
[47] Torg JS. Cervical spinal stenosis with cord neurapraxia and transient quadriplegia. Am J Sports
Med 1995;20(6):429 – 34.
[48] Mueller FO, Cantu RC. National Center for Catastrophic Sport Injury Research. Available at
www.unc.edu/depts/nccsi <http://www.unc.edu/depts/nccsi>. Accessed May 21, 2003.
[49] Weinstein SM. Assessment and rehabilitation of the athlete with a ‘‘stinger’’. Clin Sports Med
1998;17(1):127 – 35.
[50] Torg JS, Sennett B, Pavlov H, et al. Spear tackler’s spine. Am J Sports Med 1993;21(5):640– 9.
[51] Hukuda S, Kojima Y. Sex discrepancy in the canal/body ratio of cervical spine implicating the
prevalence of cervical myelopathy in men. Spine 2002;27(3):250 – 3.
[52] Yue WM, Tan SB, Tan MH, et al. The Torg-Pavlov ratio in cervical spondylotic myelopathy:
a comparative study between patients with cervical spondylotic myelopathy and a nonspondyl-
otic, nonmyelopathic population. Spine 2001;26(16):1760 – 4.
F.P. Castro, Jr. / Clin Sports Med 22 (2003) 483–492492