1

2 N ec k Inju r i es
3
4 a,b, c d,e
5 Benjamin Oshlag, MD *, Tracy Ray, MD , Benjamin Boswell, DO Q4 Q5
Q6 Q1
6 Q2
7 KEYWORDS
8
9  Neck injuries  Cervical spine  Spinal cord injury  Spinal immobilization
 Cervical collar  Sports medicine
10
11
12 KEY POINTS
13
14  Neck injuries are relatively uncommon and usually self-limited, so that a full recovery can
15 be expected.
16  Catastrophic injury patterns for cervical spine injuries are often related to direct axial load
17 trauma with a slightly forward-flexed neck, in which the normal lordotic curve is lost.
18  Cervical spine imaging should begin with radiographs or computed tomography. When
19 indicated, MRI should be used to evaluate for ligamentous, muscle, and spinal cord
involvement.
20
 Routine cervical spine immobilization in a hard cervical collar may provide more harm than
21
benefit in neck injuries, and a more individualized approach may be more reasonable.
22
 Return to play from neck injuries varies based on severity of injury, but athletes should be
23
able to demonstrate normal strength and pain-free range of motion before they are
24 cleared for full activity.
25
26
27
28
29 INTRODUCTION/BACKGROUND
30 Spinal Cord Injury Epidemiology
31 An estimated 10,000 to 11,000 spinal cord injuries (SCIs) occur each year in the United
32 States, and approximately 10% of spinal cord injuries in the United States are related
33 directly or indirectly to athletic events.1 The spectrum of SCI ranges from minor and
34 temporary “burners” or “stingers,” to severe but nonpermanent fractures and im-
35 pingements, to permanently disabling spinal damage, and even to fatalities. Realisti- Q7
36 cally, neck injuries are relatively uncommon and usually self-limited so that a full
37 recovery can be expected.2 However, because of their potential to cause permanent
38
39
40 a
Department of Orthopedics, Columbia University Medical Center, 622 West 168th Street,
41 PH11, New York, NY 10032, USA; b Department of Emergency Medicine, Columbia University
42 Medical Center, 622 West 168th Street, PH11, New York, NY 10032, USA; c Duke University,
43 Box 3639, DUMC, Durham, NC 27710, USA; d Division of Sports Medicine, Department of Or-
44 thopaedic Surgery, Case Western Reserve University School of Medicine, University Hospitals
Cleveland, 11100 Euclid Avenue, Cleveland, OH 44106, USA; e Department of Emergency
45
Medicine, Case Western Reserve University School of Medicine, University Hospitals Cleveland,
46 11100 Euclid Avenue, Cleveland, OH 44106, USA
47 * Corresponding author.
48 E-mail address: boshlag@[Link]

Prim Care Clin Office Pract - (2019) -–-

[Link] [Link]
0095-4543/19/ª 2019 Elsevier Inc. All rights reserved.

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 2 Oshlag et al

49 damage to the spinal cord and even death, neck injuries have come to represent one
50 of the most feared injuries in sports.2,3
51 Injury patterns in cervical spine injuries are seen across a wide range of sports.
52 Sports-related cervical spine injuries are most common in athletes 30 years old or
53 younger, with more than half occurring in those younger than 18.1 The most common
54 sports associated with injuries varies by region. Ice hockey injuries are more common
55 in Canada, whereas rugby injuries are more common in Europe, South Africa, and
56 Australia.2
57 Football notoriously contributes the highest numbers per year of head and neck in-
58 juries because of the high numbers of participants and the repetitive contact style of
59 play.4 Cervical spine injuries occur in roughly 10% to 15% of all football players, with
60 the highest percentages in athletes who play defensive positions.5 Although football is
61 the leading cause of cervical sprains in the United States, cycling is associated with
62 more cervical fractures in men, and horseback riding in women.1
63 Compared with female individuals, incidence of cervical spine injuries in male individ-
64 uals was 1.7 times greater for neck sprains and 3.6 times greater for fractures.1 Many
65 other sports have proportionally high risk for SCIs as well. These range from contact
66 sports like hockey, wrestling, and lacrosse to nonorganized sports like diving, surfing,
67 and skiing and high-energy sports like gymnastics, cycling, and horseback riding.1,3–5
68
69 History
70 As awareness has grown of the long-term effects of head and spine injuries in all
71 sports, there have been endeavors to protect athletes through rule changes,
72 advanced equipment, improved medical care at athletic events, new styles of coach-
73 ing, and updated practice strategies.6 In 1976, the National Collegiate Athletic Asso-
74 ciation (NCAA) banned the practice of “spearing,” a tackling technique that involves
75 lowering the head to use the crown of the helmet as the initial point of contact, in col-
76 legiate football.1,4,6 Over the following decades, the rate of cervical spine injuries fell
77 by 70%, and cases of traumatic quadriplegia in US football decreased by 82%.1,3
78 There are still many cases each year of SCI during sporting events, and tracking of
79 these injuries is largely considered to be inadequate.5,6 Experts continue to debate
80 standards for field-side medical action and return-to-play guidelines, a conflict that
81 is polarizing because of the seriousness of SCI.3 The general attitude of fear surround-
82 ing SCI in recent years has led medical professionals to use extreme caution and a
83 rule-of-thumb approach when dealing with acute neck injuries during sporting
84 events.3,5,7,8 If there is any suspicion that an athlete has an SCI, the traditional practice
85 has been to err on the side of caution and immediately immobilize the neck and spine
86 using a “boarding” technique; however, as outlined later in this article, more recent
87 studies indicate a need to possibly reconsider this approach.
88
89
90 ANATOMY OF THE CERVICAL SPINE
91 Overview
92 The cervical spine is the uppermost segment of the spinal column. It contains 7 cer-
93 vical vertebrae, C1 to C7. The spinal cord passes through the center of the cervical
94 vertebrae by way of the spinal canal, with 8 nerve roots that exit from between each
95 vertebra. Both static and dynamic stabilizers maintain the structural integrity of the
96 cervical spine, including bones, cartilage, ligaments, muscles, and tendons. They
97 form a complex infrastructure, both strong and flexible, that upholds the alignment
98 of the cervical spine, allows for a wide range of motion, and functionally dissipates
99 and absorbs the impact of external forces to the head and neck.

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100 Upper Cervical Spine: Atlas and Axis

101 The first cervical vertebra (C1) is the atlas. Unlike the normal vertebral body shape of
102 the other spinal segments, the atlas is a ringlike structure that articulates with the oc-
103 cipital bone at the base of the skull, at the atlanto-occipital joint.8 This synovial joint is
104 composed of 2 articular capsules, 2 membranes, and 2 ligaments.8 It connects the su-
105 perior articular facets of the atlas to the occipital condyles, creating a flexible structure
106 that allows for approximately 50% of all cervical flexion and extension, earning it the
107 nickname of the “yes” joint.5
108 The second cervical vertebra (C2) is the axis. The axis has a typical vertebral body,
109 but is distinguished by an upward, fingerlike projection known as the dens, or the
110 odontoid process.9 The odontoid process serves as a pivot point around which the
111 ring-shaped axis rotates. The axis articulates with the atlas at the atlantoaxial joint,
112 where the anterior arch of the atlas meets the dens.7,8 This complex joint holds C1
113 and C2 together, and is responsible for the high level of mobility and rotation in the
114 neck.8 Two alar ligaments extend from the odontoid process to the inner border of
115 the occipital condyles, restricting rotation in the joint.4 The odontoid process is also
116 attached centrally to the occipital bone at the anterior foramen magnum by the apical
117 ligament.4 Another stabilizing structure for C1 and C2 is the transverse atlantal liga-
118 ment, which, together with the superior and inferior longitudinal bands, forms a thick,
119 strong “cross bar” through the ring of the atlas, holding the dens securely against the
120 anterior arch.4,7 Lateral joint capsules contribute to the strength of the joint as well.4
121 The atlantoaxial joint accounts for approximately 50% of all cervical rotation, and
122 has been aptly called the “no” joint.5
123
124 Lower Cervical Spine
125
126 Although C1 and C2 and the joints between them make up the upper segment of the
127 cervical spine, the lower segment includes C3 through C7 and ends at T1.5,7–9 The
128 bony structure of these vertebrae is relatively consistent: oval vertebral bodies with
129 large triangular foramina through their transverse processes and a spinal canal that
130 is less spacious than it is in the upper cervical spine.4,7 C7 has a notably longer,
131 more prominent spinous process that is often used as a palpable reference for locating
132 the end of the cervical spine. The 45-degree angle of the facet joints of C3 to C7 allows
133 for cervical flexion and extension while limiting axial rotation.4 Motion in this part of the
134 neck is coupled so that axial rotation occurs with lateral bending.4,5 Both the lower
135 segment of the cervical spine as well as the upper are strengthened and supported
136 by a network of muscles, tendons, ligaments, and other structures.
137
138 Ligaments
139 Ligaments play a major role in the biomechanics of the cervical spine. The anterior lon-
140 gitudinal ligament limits hyperextension and forward movement.8,9 It extends from the
141 occipital bone and the anterior tubercle of the atlas all the way down to the sacrum,
142 blending with the outer lamellae of the intervertebral disks and attaching to the ventral
143 surface of the vertebrae as it passes between them. The posterior longitudinal liga-
144 ment prevents hyperflexion.8,9 It forms the anterior wall of the spinal canal and at-
145 taches to the dorsal surfaces of the vertebral bodies, extending from the occipital
146 bone to the coccyx. The supraspinal ligament connects the apices of the spinous pro-
147 cesses and resists spinal separation and flexion.9 Intertransverse and capsular liga-
148 ments limit lateral bending9 by connecting the transverse processes of adjacent
149 vertebrae and padding the articulate capsules that surround and cushion the vertebral
150 bones. The ligamentum flavum maintains constant disk tension, elongating with

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151 flexion and shortening with extension.9 Although they are only thinly developed in the
152 cervical spine, the membranous fibers of interspinal ligaments prevent excessive rota-
153 tion,9 as they connect adjoining spinous processes, extending from the root to the
154 apex of each process.
155
156 Muscles
157 Muscles are dynamic stabilizers that function by moving the head and neck through
158 controlled contractions. The splenius capitis and cervicis are deep muscles in the
159 back used to extend the head and neck and to laterally flex and rotate the head to
160 the same side with unilateral contraction.9 The semispinalis capitis (complexus), semi-
161 spinalis cervicis, and spinalis cervicis are muscles connected to thoracic vertebrae
162 that extend and laterally flex and rotate the head and neck toward the side opposite
163 the contraction.9 Other muscles that move the head and neck include the trapezius,
164 the sternocleidomastoid, and the anterior/middle scalenes.9
165
166 Other Stabilizers
167 In addition to the those mentioned previously, other support mechanisms include
168 intervertebral disks, zygapophyseal joint capsules, and uncovertebral joints.9 Between
169 each pair of vertebrae (except for the atlas and the axis), there are small disks made of
170 an inner gelatinous material called nucleus pulposus, encased by an outer ring called
171 the annulus fibrosis.5,8,9 These intervertebral disks act as fibrocartilaginous joints,
172 enabling slight movement between vertebrae, but they also act as cushiony ligaments,
173 holding the spine together comfortably. They play a crucial role as shock absorbers in
174 the spine.4 Zygapophyseal (facet) joint capsules are synovial joints located between
175 the articular processes of each vertebrae.5,9 In the cervical spine, they help to restrain
176 forward translation. Finally, the uncovertebral joints are not true synovial joints, but
177 arising from the posterolateral margins of the vertebral bodies in C3 to C7.9
178
179 Lordosis
180 When the cervical spine is properly aligned by all of these structures, it assumes a nat-
181 ural lordotic curve8; however, when the chin is lowered and the neck is flexed to 30 or
182 more, the normal lordotic curve flattens out and the cervical spine converts into a
183 segmented column.5,8 In this position, the extra elasticity provided by the loose
184 spacing of the vertebrae is lost.1,4 Forces applied to the top of the head are now
185 directed straight down the spinal column8 instead of dissipating correctly through
186 the network of paravertebral musculature, intervertebral disks, and the normal lordotic
187 curve of the cervical spine.5
188
189 Injury Patterns
190 Although uncommon, both fatal and severe, nonfatal brain and spine injuries can
191 occur during sports-related activities. These injuries have been noted in contact
192 sports, such as football, ice hockey, wrestling, and rugby, as well as in noncontact
193 sports like cheerleading, swimming and diving, baseball, equestrian, gymnastics,
194 pole vault, rodeo, snowboarding, and skiing. Patterns exist in brain and cervical spine
195 injuries that vary with each sport. Understanding these patterns is essential in preven-
196 tion and recognition of injuries.10
197 Hyperflexion or hyperextension of the cervical spine in an athlete with a develop-
198 mental or congenitally narrow spinal canal may cause neurologic injury by a pincer
199 mechanism.11 External forces that cause a combination of side bending and extension
200 may lead to neuroforaminal compression or stretching, leading to injury of one or mul-
201 tiple cervical nerve roots. This is the mechanism involved with the injury known as a

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 Neck Injuries 5

202 burner or stinger. Acceleration or deceleration forces that occur in whiplash injuries
203 commonly cause injury to the muscle, ligamentous supports, or cervical facet joints.12
204 Among all sports, football has the highest number of catastrophic brain and cervical
205 spine injuries.13 A review of 1300 cervical spine injuries from the National Football
206 Head and Neck Injury Registry has documented axial loading as the major mechanism
207 of catastrophic cervical spine injuries.14 In the normal cervical spine, the natural
208 lordosis of the vertebral arch is able to tolerate substantial force by dissipating forces
209 evenly across multiple levels. When the neck is flexed forward 30 , however, it be-
210 comes a straight segmented column that does not dissipate forces equally. Axial
211 loading with the neck in a flexed position can then result in excessive forces on the
212 vertebral bodies, leading to fractures and SCIs.15 This is referred to as “spear tack-
213 ling,” and has been banned from football, although these injuries do continue to occur.
214 Although the number of catastrophic cervical spine injuries in ice hockey is low
215 compared with other sports, the incidence per 1000 participants remains relatively
216 high.16 The typical mechanism of injury is axial loading caused by a blow to the
217 head from collision with the boards, other players, the ice, or the goal post.17 Most
218 of these injuries occur when the injured player is checked from behind, causing the
219 athlete to be thrown horizontally into the boards.18
220
221 Differential Diagnosis
222 See Table 1.
223
224 Examination
225 The physical examination of the neck with a suspected injury should focus on several
226 elements. Visual inspection should be made of the spinal curvature, evaluating for
227 ecchymosis or erythema, lacerations, and obvious deformities. The examiner should
228 palpate for deformities, step-offs, and midline or paraspinal tenderness. Active and
229 passive range of motion should be tested for flexion, extension, side bending, and
230 rotation. Strength testing should be examined manually for bilateral upper and lower
231 extremities. Sensation should be tested in all cervical dermatomes. Reflexes should
232 be tested for at C5 (biceps), C6 (brachioradialis), C6/7 (pronator), and C7 (triceps),
233
234
235 Table 1
Q15
236 Differential diagnosis
237 Cervical muscle Injury to soft tissue of the neck, specifically a muscle or tendon.
238 strain
239 Cervical ligament Injury to a ligamentous support of the cervical spine.
240 sprain
241 Cervical spine Injury to the bony structures of the cervical spine, specifically the
242 fracture vertebral body or vertebral processes.
243 Herniated disk Herniation of the intervertebral disk, causing nerve root
244 compression.
245 Transient Neuropraxia causing bilateral burning or tingling pain, loss of
246 quadriplegia strength, or loss of sensation, usually lasting <15 min but
247 potentially as long as 48 h.
248 Cervical radiculopathy Traction on the cervical nerve roots, causing unilateral shoulder/
249 (burner/stinger) arm burning or stinging.
250 Cervical cord injury Most catastrophic of spinal cord injuries, often leading to partial
paralysis, complete paralysis, or death.
251
252 Nonorthopedic causes Cardiovascular, endocrine, pulmonary, infectious.

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253 L4 (patellar), L5 (medial hamstring), and S1 (Achilles), as well as pathologic reflexes

254 with the Hoffman and Babinski reflex tests. Special tests such as the Spurling and
255 Lhermitte should be performed as well.12
256 In the setting of acute trauma, a physician and/or certified athletic trainer with skills
257 in the acute management of cervical spine injuries should evaluate and treat the pa-
258 tient. Focus should be placed on cervical stabilization. Although the lead rescuer is
259 maintaining stability, another rescuer should make a primary assessment of airway,
260 breathing, and circulation. If no further emergencies require immediate action, then
261 secondary assessment may proceed. The second rescuer should palpate for normal
262 curvature, deformities, lacerations, step-offs, and tenderness to bone or soft tissue.
263 The second rescuer also should perform a neurologic examination of the athlete.
264 This should be composed of motor and sensation testing, as well as a mental status
265 assessment. If an athlete is unconscious or if assessment is limited, a cervical cord
266 injury should be assumed.
267
268 Imaging
269 Many studies have helped determine whether or not to perform imaging. The National
270 Emergency X-Radiography Utilization Study (NEXUS) criteria and Canadian Cervical
271 Spine Rule (CCR) have been established to guide use of cervical spine radiography
272 in patients with trauma. For alert patients with trauma, the CCR is superior
273 to the NEXUS with respect of sensitivity and specificity for cervical spine injury
274 (Figs. 1 and 2).19,20 Q8
275 If imaging is indicated, plain radiographs are an appropriate initial study to evaluate
276 for bony anatomy and instability. Radiographs should include anteroposterior, lateral,
277 and open-mouth (Odontoid) views. Flexion and extension views may be ordered to
278 evaluate for abnormal segmental motion, ligamentous laxity, or atlantoaxial instability.
279 The Torg-Pavlov ratio compares the diameter of the spinal canal to that of the vertebral
280 body, and can be measured in the lateral view. A ratio of less than 0.8 is used to predict
281 cervical stenosis, although its use is controversial and generally of historical signifi-
282 cance only.
283
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303 Fig. 1. Canadian cervical spine rule. Q13 Q14

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Fig. 2. National Emergency X-Radiography Utilization Study C-spine criteria.
331
332
333 Computed tomography (CT) imaging is useful to evaluate for clinically suspected
334 fracture or bony pathology when radiographs are negative or equivocal. CT imaging
335 is superior to radiographs in detecting both clinically significant and insignificant cer-
336 vical spine injuries, and is recommended as the imaging modality of choice in chil-
337 dren.21 CT allows for better visualization of bony detail. For patients with neurologic
338 symptoms who are unable to undergo MRI, CT myelogram is a useful tool to evaluate
339 for spinal stenosis or neural compression.
340 MRI is a useful imaging tool to evaluate for soft tissue injury, ligamentous disruption,
341 or disk herniation. MRI is also used to evaluate for SCIs, such as cord compression,
342 cord disruption, cord contusions, or nerve root impingement. MRI is also useful for
343 cervical canal measurements and functional reserve, the protective cushioning of ce-
344 rebrospinal fluid around the spinal cord.12 MRI has been found to identify additional
345 injuries in 23.6% of patients with a normal CT, although the clinical significance of
346 these abnormal findings is uncertain in the setting of patients without neurologic
347 abnormalities.22
348
349 Other testing
350 In patients with persistent motor or sensory abnormalities after a cervical
351 spine injury, an electromyogram and Nerve Conduction Study can be a useful
352 diagnostic test. This is performed in the outpatient clinic setting. It can be used
353 to differentiate whether a lesion is at the nerve root, brachial plexus, or peripheral
354 nerve.

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355 Acute management

356 Traditional management of suspected neck injuries has typically focused on immo-
357 bilization, taking the approach of prioritizing precautions to prevent any potential
358 cervical spine movement, to minimize the chance of neurologic injury. This protocol
359 generally involves the routine use of manual in-line stabilization, a rigid cervical col-
360 lar, and often a rigid backboard/spineboard as well, in all suspected head and neck
361 injuries, regardless of patient condition. Although this approach initially appears to
362 provide the safest framework, in practice research suggests it may be causing
363 more harm than good, and a more flexible protocol may lead to better overall
364 outcomes.23–27
365 In general, patients with suspected neck injuries can be thought of as falling
366 into 1 of 4 categories: uninjured or minor injury, stable cervical spine fractures,
367 unstable cervical spine fractures with completed neurologic deficits, and unstable
368 cervical spine fractures without or with incomplete neurologic deficits. An
369 overwhelming majority of patients (96%) fall into the first category, whereas stable
370 fractures make up approximately 3% of the total. Fewer than 1%, then, have unsta-
371 ble fractures that may potentially benefit from immobilization.28,29 Even among pa-
372 tients who have unstable fractures, neurologic deficits are rare, and most of those
373 happen immediately at the time of injury.28 Deficits that develop only later are
374 extremely rare, with 1 review finding only 41 such case reports in the literature.
375 Of those, 30 had no identifiable trigger, and only 1 developed deficits after the
376 removal of a cervical collar. In multiple cases, neurologic deficits actually devel-
377 oped after the application of a cervical collar, which can be especially dangerous
378 in patients with preexisting cervical spine abnormalities, such as ankylosing
379 spondylitis.30–33
380 Most patients, then, cannot benefit from the routine application of a cervical collar,
381 and only stand to suffer harm from its use. Research has indeed shown that cervical
382 collars lead to a number of complications, including long-term pain after use,
383 increased intracranial pressure and decreased venous return, increased aspiration
384 risk, pressure ulcers, decreased respiratory ability (as demonstrated by a 15%
385 decreased in forced expiratory volume in 1 second with use of both a collar and back-
386 board), increased intubation time, delays in treatment, and increased cost in materials
387 and extra downstream testing to “clear” the collar.34–36
388 Cervical spine immobilization is also likely the wrong goal as an approach as well. A
389 correctly fitted cervical collar will allow 30 of flexion/extension, 16 of lateral bending,
390 and 27 of rotation, and cadaveric studies have shown that they do not reduce c-spine
391 movement in cadavers with unstable fractures.37 Even internal fixation does not elim-
392 inate all movement, and the goal of acute management should aim at spinal motion
393 restriction rather than full immobilization. Cervical spine injuries typically require
394 more than 2000 to 6000 N of force, whereas a 4-kg head left hanging free to gravity
395 will generate only 40 N. In addition, awake patients with injuries will typically protect
396 their necks spontaneously, and it is unlikely that small, low-speed movements are
397 enough to cause additional injury.38,39 In fact, studies have shown that nonimmobi-
398 lized patients do not have worse neurologic outcomes than those who were
399 immobilized.28
400 A more commonsense, individualized approach has been proposed, aimed at
401 limiting spinal motion and protecting the patient in transport without attempts at full
402 immobilization. This approach calls for special attention and a more conservative
403 management plan for patients with altered mental status or existing neurologic symp-
404 toms, but would allow for awake, alert patients with no neurologic deficits to be trans-
405 ported in a position of comfort (Table 2).23–25,27 Q9

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406 Table 2
407 Spinal immobilization Q16

408
Neuro Altered
409
No Neck Pain or Signs or Mental
410 Tenderness Neck Pain or Tenderness Symptoms Status
411
Ambulatory Position of comfort Gurney position of comfort Full Position of
412 with/without support comfort
413 Nonambulatory Position of comfort Gurney supine position of Full Full
414 comfort with extrication
415 support
416
417
418 Treatment
419 Treatment of acute neck injuries will vary based on the severity of the underlying injury.
420 Soft tissue and peripheral nerve injuries such as stingers are generally self-limiting. For
421 these injuries, rest, ice, nonsteroidal anti-inflammatories, and targeted physical ther-
422 apy can help with recovery. A soft cervical collar has not been shown to provide
423 any benefit, and may actually lead to stiffness and delayed recovery. Fractures should
424 be referred to an orthopedic or neurosurgical spine specialist for definitive treatment.
425
426 Return to play
427 Return to play should focus on the safety of the athlete and his or her ability
428 to avoid further injury. The severity of the injury will generally guide the timeline
429 for full return. Soft tissue and muscle injuries are generally self-limiting, and most
430 athletes will be allowed to return as tolerated. With minor neurologic injuries,
431 such as stingers, athletes must be able to demonstrate full strength and range of
432 motion of their neck and any other affected body part before being allowed to re-
433 turn to play. They must have a completely normal neurologic examination, and not
434 have had bilateral symptoms, which would raise suspicion for a potential spinal
435 cord injury.40
436 Some fractures, such as spinous process or unilateral laminar fractures, do not
437 cause instability and may require no treatment or only brief immobilization, and the
438 athlete can be safely returned to play after healing. Other fractures carry higher risks
439 with return to sport, however, and decisions should be made in conjunction with a
440 spine surgeon.40
441 Return to play after transient quadriparesis and is controversial, and should be care-
442 fully considered on a case-by-case basis. Athletes may be able to return after an initial
443 brief episode, once they regain full strength and function, but multiple or prolonged
444 (>24 hours) episodes should prompt consideration of disqualification. Any athlete
445 with a permanent neurologic injury should be prohibited from further competition in
446 regular contact sports; however, there are some lower intensity or noncontact sports,
447 as well as sports designed for those with disabilities, in which they may participate
448 safely.40
449
450 DISCLOSURE
451
The authors have nothing to disclose. Q10
452
453
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454
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