Updated: Apr 6, 2006
Acute cervical spine injury has been associated with sports such as football, gymnastics, rugby, ice hockey, and diving. Athletes with cervical disc injury may present with neck pain, radicular pain, quadriparesis, or quadriplegia secondary to myelopathy.
Cervical disc injury includes 2 entities. The more common form involves annular tears with herniation of the nucleus pulposus (ie, soft disc herniation). The second type of disc injury is an annular tear without herniation of the nucleus pulposus (ie, internal disc disruption).
When considering the term cervical disc injury, it is important to recognize the natural history of cervical degenerative disease. It is this process that may insidiously predispose one to cervical disc injury of either an acute or chronic nature. Cervical disc injuries can be treated conservatively or by surgery, depending on the clinical presentation.
Return to play is an important but controversial issue following successful treatment of cervical disc injury. No accepted universal guidelines regarding return to play exist.
This article intends to outline the etiopathology, evaluation, and treatment of cervical disc disease. Available guidelines for return to play following cervical disc injury are also presented.
In a study of asymptomatic individuals younger than 40 years, the incidence of cervical disc herniation was 10%, the incidence of disc degeneration was 25%, and the incidence of foraminal stenosis was 4% (Boden, 1990). In a more recent study, the incidence of cervical focal disc protrusions in asymptomatic volunteers was 50% and of annular tears at one or more levels was 37% (Ernst, 2005).
Seven cervical vertebrae articulate with one another anteriorly via the interbody joint with an intervening intervertebral disc and 2 uncovertebral joints. Laterally, they articulate via the paired posterolaterally placed zygapophyseal (facet) joints.
Each cervical vertebra forms a ring with the vertebral body anteriorly, the pedicles laterally, and the laminae posteriorly. The ring is known as the spinal or neural canal. As the vertebrae stack upon one another, the connection of the spinal foramina is known as the spinal canal. Through the spinal canal runs the spinal cord, nerve roots, vessels, and meninges (membranous covering of the spinal cord and nerve roots).
The cervical spinal nerves take origin from the spinal cord as the anterior and posterior rootlets. The posterior rootlet has a segmental brain that lies on its most lateral extent at the inner portion of the intervertebral foramen. The posterior and anterior rootlets join to form a spinal nerve, which is only approximately 2 cm long and lies within the intervertebral foramen. The spinal nerve divides into a posterior and anterior ramus at the outlet of the intervertebral foramen. The spinal nerves exit the intervertebral foramen above the numbered cervical vertebrae, and the thoracic and lumbar nerves exit the intervertebral below the numbered vertebra. Consequently, the eighth cervical nerve exits between the C7 and T1 segment (White, 1991).
The symptoms related to pathology at each of the intervertebral disc segments have been well described and are not elaborated on in this article. Note that during dynamic range of motion (ROM), the intervertebral foramen, which houses the exiting cervical nerves, becomes very dynamic. In flexion, the intervertebral foramen enlarges in patency, and it decreases with extension. In rotation, the ipsilateral side becomes smaller, and the contralateral side becomes larger. The extreme changes of the foramina are magnified when motions are coupled with flexion and extension (White, 1991).
Distinctiveness of the cervical disc
The predominance of literature has addressed the lumbar spine; much of the lumbar spine literature has been extrapolated and applied to the cervical spine. Bogduk, using microdissection, systematically evaluated 59 human cadaveric intervertebral discs. The orientation, location, and attachments of each strip bundle of collagen were recorded photographically and in sketches. He concluded that the cervical annular fibrosus did not consist of concentric laminae of collagen fibers, as noted in lumbar discs. Rather, the annulus forms a crescentic mass. The primary thickness is anterior and tapers laterally toward the uncinate processes. Posterolaterally, it is essentially deficient; posteriorly, it is represented by a thin layer of paramedian vertically oriented fibers. The anterior crescentic mass is likened to an interosseus ligament more so than a ring of concentric fibers surrounding the nucleus pulposus (Mercer, 1999).
Cervical spine injury is commonly associated with axial loading with the neck in flexion. In flexion of the neck to 30°, the normal lordosis of the cervical spine is obliterated and axial loading of the head is dissipated through a straight spine (Torg, 1989). Examples of axial loading in players include a football player striking his opponent with the crown of his helmet, an ice hockey player striking his head on the board while doing a push or check, a diver striking the ground with his head after diving in shallow water, and a gymnast accidentally landing head down while performing a somersault on a trampoline.
The effects of axial loading of the cervical spine include fracture of vertebrae, cervical disc herniations, ligament rupture, facet fracture, and dislocations. The neurologic deficits are greater in athletes with congenital spinal stenosis (Torg and Corcoran, 1997).
New guidelines in athletic sports have decreased the incidence of spinal cord injury. For example, permanent cervical quadriplegia has decreased significantly in high school and college level football, secondary to changes in the rules involving tackling. The Guidelines of NCCA Football rules committee banned spear tackling in football (NCAA 1976). In 1977, The American Academy of Pediatrics published a statement banning the use of trampolines in schools because of the high incidence of quadriplegia associated with this apparatus (AAP, 1981). The Canadian Committee on the prevention of spinal injury due to hockey recommends rules against boarding and crosschecking and on education to avoid spearing and impact with boards (Tator, 1984). Similar guidelines for diving prohibit diving in water that is less shallow than twice one's height (Torg, 1989).
Disc herniation resorption
Absorption of a cervical herniated disc has been appreciated. Mochida followed the regression of cervical disc herniation by using MRI. He noted that acutely, active resorption of herniated material occurred. The MRI findings did suggest that part of the resorbed material may have consisted of hemorrhagic substance. Mochida noted that extruded material exposed to the epidural space was resorbed more quickly than subligamentous herniation probably because of increased exposure to the immune system (Mochida, 1998).
Resorption of herniated disc material should not be confused with repair. Injured or degenerative disc material does not repair itself to a significant extent. In review of intervertebral segment physiology and metabolic turnover, Nachemson drew some remarkable conclusions. He cited that diffusion of solutes can take place through the central portion of the endplates, as well as through the annulus fibrosus. There are also vascular contacts between the marrow spaces, the vertebral body, and the hyaline cartilaginous endplates. These vascular contacts are significantly less in discs that show advanced degenerative changes. He also cited that the area between the nucleus and annulus posteriorly is proportionally less than the area of the anterior margins, lending itself to possible nutrient deficiency and hastened fibrotic infiltration.
The surface area for diffusion is smaller posteriorly. Combining the relative diffusion limitations posteriorly and the mechanics of posterolateral disc herniation, it becomes rather apparent why a possible pattern of failure exists in this region (Nachemson, 1976).
Athletes with symptomatic cervical disc injuries commonly present with segmental neck pain, muscle spasm, loss of ROM, and referred pain in both radicular and nonradicular distribution. Nerve root involvement leads to radicular upper extremity pain, weakness, and sensory changes. Pain symptoms may be exacerbated with motion, lifting, and Valsalva maneuvers.
Cervical disc injuries are relatively common in athletes involved in both contact and noncontact sports. Information on cervical injuries has primarily been obtained from evaluation of football players; however, this information can be applied to athletes who play other high-risk sports. Sports associated with cervical injuries include football, rugby, ice hockey, wrestling, gymnastics, cheerleading, baseball (headfirst slides), and swimming (diving into shallow water).
Cervical Discogenic Pain Syndrome
Cervical Facet Syndrome
Cervical Radiculopathy
Cervical Spine Sprain/Strain Injuries
Physical therapy emphasizes segmental mobilization, postural training, and reconditioning.
Surgery is indicated in acute cervical disc herniation causing central cord syndrome and in cervical disc herniations refractory to conservative measures. Studies have shown that an anterior discectomy with fusion is the recommended procedure for central or anterolateral soft disc herniation, while a posterior laminotomy-foraminotomy may be considered when technical limitations for anterior access exist (eg, short thick neck) or when the patient has had prior surgery at the same level (Herkowitz, 1990).
Translaminar cervical epidural injections can decrease the inflammation secondary to acute disc herniation and help the patient to tolerate physical therapy.
This phase of rehabilitation focuses on soft tissue overload and biomechanical dysfunction. Goals of this phase are to eliminate pain, normalize spinal mechanics, and improve neuromuscular control of the injured cervical spine. Restoration of the resting muscle length and full, pain-free, cervical ROM are necessary. Strengthening exercises start in simple planes and progress to complex muscle patterns.
Surgical treatment for cervical disc herniation is needed in only a very small percentage of athletes. This includes those with any evidence of a cervical myelopathy or progressive neurologic deficits and those in whom conservative treatment has failed for a period of 3 months. Radiographically confirmed evidence of cervical disc disease should be available before performing this surgery. The common surgical procedures for cervical disc injuries include (1) anterior decompression and fusion (ADCF), (2) laminectomy, laminotomy-facetectomy, and (3) laminoplasty.
Anterior decompression and fusion
A herniated disc in the neck is commonly approached anteriorly. Both lateral and central discs can be removed through this approach. Other indications include progressive neurologic deficit and unremitting pain.
The results from cervical discectomy have shown an approximately 95% chance of good-to-excellent relief from the radiating arm pain (Gore, 1984). Numbness in the upper extremity generally improves. Weakness in the affected arm may require some physical therapy to maximize recovery. Three to 6 months following surgery, the patient may resume full, unrestricted activities.
Complications from this surgery are very rare. The most common complications following anterior decompression and fusion are transient sore throat, hoarseness, and difficulty swallowing. Other complications include failure of bony fusion, which occurs in 5-8% of patients. Pseudarthrosis is commonly related to the number of levels fused. When it occurs, half of the patients have no symptoms from it and nothing further is required. No correlation exists between radiologic appearance of pseudarthrosis alone and the clinical outcome. Careful considerations must be made before reoperating. For the 50% of patients who do develop neck pain as a result of the failure of fusion, additional surgery may be required to obtain a solid fusion of the disc and to alleviate the neck pain.
Permanent spinal cord injury is the most dreaded complication and occurs at a rate of 1 in 1000 (Flynn, 1982). The infection rate is less than 1 in 100. Other rare complications include recurrent injury to the laryngeal nerve, laceration of vertebral and carotid vessels, and injury to the trachea or esophagus.
Laminectomy
A cervical laminectomy is a procedure designed to resect the lamina on one or both sides to increase the axial space available for the spinal cord. The procedure is typically indicated for spinal stenosis. The indication in the context of cervical disc disease is when more than 3 levels of disc degeneration with anterior spinal cord compression are present. Single-level cervical disc herniation is ideally managed from the anterior approach. The complications of the posterior approach include instability leading to kyphosis, recalcitrant myofascial pain, and occipital headaches.
Postlaminectomy kyphosis requires revision surgery. If preexistent kyphosis is present, an anterior approach is favorable because in a patient with kyphosis, laminectomy may accelerate kyphosis. As an alternative to laminectomy, a foraminotomy can be used to remove a single-level unilateral lateral disc herniation. This involves removal of 50% of the facet joint on one side. This procedure is effective when radicular arm pain is greater than axial neck pain. Foraminotomy can also be performed anteriorly and has a success rate of 91% in relieving radicular pain (Johnson, 2000).
Laminaplasty
Kyphotic deformity is a well-known complication of laminectomy. This prompted a group of Japanese surgeons to preserve the posterior wall of the spinal canal while decompressing the spinal canal using a Z-plasty technique for the lamina. The variant of the procedure uses a hinge door for the lamina. Laminaplasty is commonly indicated for multilevel spondylotic myelopathy. Comparative studies with laminectomy have shown that patients with laminaplasty have superior functional recovery in spondylotic myelopathy (Miyazaski, 1994). The incidence of spinal cord injury with laminaplasty is approximately 10 times lower than that of laminectomy. Nerve root injury is commonly seen in about 11% of the surgeries. This complication is unique to laminaplasty, and the suggested etiology is traction on the nerve root with posterior migration of the spinal cord.
Recent advances in surgical intervention
Spinal fusion at the cervical disc produces a painless, stable spinal segment at the cost of mobility. In the field of cervical disc prostheses, research is focusing on how to maintain both stability and mobility at the spinal segment. However, only a few studies have been performed and the results have been variable. A study by Pointillart showed that a cervical disc prosthesis failed to achieve the intended mobility in 8 of 10 patients and that pain developed in the other 2 patients in whom mobility persisted (Pointillart, 2001). However, a larger more recent study with 60 patients showed clinical success rates at 6 months and 1 year after implantation of 86% and 90%, respectively (Goffi, 2003).
Other recent surgical interventions include microsurgical posterior herniotomy with en bloc laminoplasty and a minimally invasive anterior contralateral approach for the treatment of cervical disc herniation (Aydin, 2005).
The final phase of rehabilitation requires functional, nonpainful, cervical ROM and proper spinal and shoulder girdle mechanics. Sport appropriate flexibility, strength, and skills are necessary prior to return to play. Sport-specific activities should be reviewed to ensure correct techniques, especially in contact and collision sports.
Oral nonsteroidal anti-inflammatory drugs (NSAIDs) can help decrease pain and inflammation. Various oral NSAIDs can be used, and none of these holds a clear distinction as the drug of choice. The choice of NSAIDs is largely a matter of convenience (how frequently doses must be taken to achieve adequate analgesic and anti-inflammatory effects) and cost.
Have analgesic, anti-inflammatory, and antipyretic activities. Their mechanism of action is not known, but they may inhibit cyclo-oxygenase activity and prostaglandin synthesis. Other mechanisms may exist as well, such as inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell membrane functions.
For arthritis. Inhibits primarily COX-2. COX-2 is considered an inducible isoenzyme, induced by pain and inflammatory stimuli. Inhibition of COX-1 may contribute to NSAID GI toxicity. At therapeutic concentrations, COX-1 isoenzyme is not inhibited; thus, GI toxicity may be decreased. Seek lowest dose of celecoxib for each patient.
200 mg/d PO qd; alternatively, 100 mg PO bid
Not established
NSAIDs may increase retention of sodium and fluid and may raise blood pressure with ACE inhibitors and diuretics; NSAIDs may especially increase risk of bleeding (eg, gastrointestinal) among individuals who drink alcohol or who are already taking aspirin, corticosteroids, heparin, and warfarin; to minimize risks of adverse effects, patients should avoid taking multiple NSAIDs concurrently; special caution is needed in any patient on anticoagulants or systemic corticosteroids, as well as in any patient with a bleeding disorder or significant alcohol use; coadministration with fluconazole may cause increase in celecoxib plasma concentrations because of inhibition of celecoxib metabolism; coadministration of celecoxib with rifampin may decrease celecoxib plasma concentrations
Documented hypersensitivity; hypersensitivity to ibuprofen or other NSAIDs; aspirin/NSAID-induced asthma
B - Usually safe but benefits must outweigh the risks.
Caution with any history of GI bleed, hypertension, or CHF; caution in elderly patients; most NSAIDs are considered Class D (unsafe) during third trimester of pregnancy; avoid use during third trimester of pregnancy due to potential risk of effecting closure of the ductus arteriosus; may cause fluid retention and peripheral edema; caution in compromised cardiac function, hypertension, and conditions predisposing to fluid retention; severe heart failure and hyponatremia may occur because celecoxib may deteriorate circulatory hemodynamics; NSAIDs may mask usual signs of infection; caution in the presence of existing controlled infections; evaluate symptoms and signs suggesting liver dysfunction
DOC for patients with mild to moderate pain. Inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.
200-400 mg PO q4-6h while symptoms persist; not to exceed 3.2 g/d
<6 months: Not established
6 months to 12 years: 4-10 mg/kg/dose PO tid/qid
>12 years: Administer as in adults
Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Documented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency; high risk of bleeding
B - Usually safe but benefits must outweigh the risks.
Category D in third trimester of pregnancy; caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in anticoagulation abnormalities or during anticoagulant therapy
For relief of mild to moderate pain and inflammation. Small dosages initially are indicated in small and elderly patients and in those with renal or liver disease. Doses over 75 mg do not increase therapeutic effects. Administer high doses with caution, and closely observe patient for response.
25-50 mg PO q6-8h prn; not to exceed 300 mg/d
<3 months: Not established
3 months to 12 years: 0.1-1 mg/kg PO q6-8h
>12 years: Administer as in adults
Coadministration with aspirin increases risk of inducing serious NSAID-related side effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Documented hypersensitivity
B - Usually safe but benefits must outweigh the risks.
Category D in third trimester of pregnancy; caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in coagulation abnormalities or during anticoagulant therapy
For relief of mild to moderate pain. Inhibits inflammatory reactions and pain by decreasing activity of cyclo-oxygenase, which results in a decrease of prostaglandin synthesis.
500 mg PO followed by 250 mg q6-8h; not to exceed 1.25 g/d
<2 years: Not established
>2 years: 2.5 mg/kg/dose PO; not to exceed 10 mg/kg/d
Coadministration with aspirin increases risk of inducing serious NSAID-related side effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Documented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency
B - Usually safe but benefits must outweigh the risks.
Category D in third trimester of pregnancy; acute renal insufficiency, interstitial nephritis, hyperkalemia, hyponatremia, and renal papillary necrosis may occur; patients with preexisting renal disease or compromised renal perfusion risk acute renal failure; leukopenia occurs rarely, is transient, and usually returns to normal during therapy; persistent leukopenia, granulocytopenia, or thrombocytopenia warrants further evaluation and may require discontinuation of drug
Guidelines for return to play following cervical spine injuries have been published by several authors with little consensus.
Torg et al have published guidelines for return to play following cervical spine injuries (Torg and Ramsey-Emrhein, 1997). The following is described in the context of cervical disc injury.
Injury prevention is accomplished best through good coaching, adequate preparticipation training, and implementation of proper techniques of sport-specific activity and appropriate safety measures. Studies imply that protective gear may not aid in injury prevention. Instruction and regulations that help educate players about how to avoid an axial loaded straight to the spine may have the greatest impact on cervical injury prevention. A recent review emphasizes these points by recommending that athletes avoid spear tackling, diving in unknown or shallow water, diving while intoxicated, checking from behind in hockey, or using a trampoline without spotting equipment (Morganti, 2003).
Prognosis is generally excellent for the individual with degenerative disc changes. This condition is usually asymptomatic, unless the individual has received trauma to a degenerative segment. As long as the individual maintains a good neck hygiene program emphasizing mechanical balance and conditioning, he or she generally returns to an asymptomatic state.
For excellent patient education resources, visit eMedicine's Back, Ribs, Neck, and Head Center. Also, see eMedicine's patient education articles Shoulder and Neck Pain and Neck Strain.
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acute cervical spine injury, annular tear with herniation of the nucleus pulposus, annular tear without herniation of the nucleus pulposus, cervical degenerative disease
Robert E Windsor, MD, FAAPMR, FAAEM, FAAPM, President and Director, Georgia Pain Physicians, PC; Clinical Associate Professor, Department of Physical Medicine and Rehabilitation, Emory University School of Medicine
Robert E Windsor, MD, FAAPMR, FAAEM, FAAPM is a member of the following medical societies: American Academy of Pain Medicine, American Academy of Physical Medicine and Rehabilitation, American College of Sports Medicine, American Medical Association, International Association for the Study of Pain, Physiatric Association of Spine, Sports and Occupational Rehabilitation, and Texas Medical Association
Disclosure: Nothing to disclose.
Ricardo A Nieves, MD, President, Colorado Spine, Pain and Sports Medicine, PC
Ricardo A Nieves, MD is a member of the following medical societies: American Academy of Disability Evaluating Physicians, American Academy of Pain Medicine, American Academy of Physical Medicine and Rehabilitation, and American Association of Neuromuscular and Electrodiagnostic Medicine
Disclosure: Nothing to disclose.
Kevin P Sullivan, MD, Consulting Staff, The Boston Spine Group
Kevin P Sullivan, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, International Spine Intervention Society, and North American Spine Society
Disclosure: BioAssets Development Corp Consulting fee Consulting
Samuel Punnamoottil Thampi, MD, Consulting Staff, Departments of Anesthesiology and Physical Medicine and Rehabilitation, Franklin Hospital Medical Center, North Shore-Long Island Jewish Health System
Samuel Punnamoottil Thampi, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation and North American Spine Society
Disclosure: Nothing to disclose.
Frank J King, MD, Clinical Instructor, Department of Physical Medicine and Rehabilitation, Georgia Pain Physicians/Emory School of Medicine
Frank J King, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Medical Association, and Association of Academic Physiatrists
Disclosure: Nothing to disclose.
Erik D Hiester, DO, Fellow in Interventional Pain Management, Emory Medical School/Georgia Pain Physicians
Erik D Hiester, DO is a member of the following medical societies: American Academy of Family Physicians, American Medical Association, American Osteopathic Association, and American Pain Society
Disclosure: Nothing to disclose.
Janos P Ertl, MD, Assistant Professor, Department of Orthopedic Surgery, Indiana University School of Medicine; Chief of Orthopedic Surgery, Wishard Hospital
Janos P Ertl, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Orthopaedic Association, Hungarian Medical Association of America, and Sierra Sacramento Valley Medical Society
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment
Henry T Goitz, MD, Fellowship Director, Sports Medicine, Department of Orthopedic Surgery, Henry Ford Hospital
Henry T Goitz, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons and American Orthopaedic Society for Sports Medicine
Disclosure: Nothing to disclose.
Jon B Whitehurst, MD, Clinical Instructor of Surgery, University of Illinois College of Medicine; Partner and Executive Board Member, Rockford Orthopedic Associates; Orthopedic Chairman, Rockford Memorial Hospital
Jon B Whitehurst, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Orthopaedic Society for Sports Medicine, and Arthroscopy Association of North America
Disclosure: Nothing to disclose.
Sherwin SW Ho, MD, Associate Professor, Department of Surgery, Section of Orthopedic Surgery and Rehabilitation Medicine, University of Chicago
Sherwin SW Ho, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Orthopaedic Society for Sports Medicine, and Arthroscopy Association of North America
Disclosure: Nothing to disclose.