Does this patient have neck pain?
Cervical spondylotic myelopathy
The onset of cervical spondylotic myelopathy is insidious, often involving gait spasticity followed by upper extremity numbness and the loss of fine motor hand control. Symptoms vary, but may include:
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Spastic, scissoring gait abnormality has been noted by some authors to be the earliest most consistent symptom, possibly caused by dorsal column dysfunction causing proprioceptive disruption as well as diminished pain sensitivity.
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Neck, subscapular or shoulder pain with radiation to the arms.
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Sensory loss and paresthesias in arms (possibly in a dermatomal distribution).
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Upper motor neuron signs such as clonus, hyperreflexia, and hypertonia may be present in the lower extremities. Babinski sign may be present, but is not as common as clonus.
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Weakness, muscle wasting, and hyporeflexia may be found in the upper extremities, with the C5-C7 myotomes being most commonly involved.
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Bladder dysfunction, urgency, frequency, and retention may also occur.
Other clinical syndromes associated with cervical spondylosis include neck pain and cervical radiculopathy.
Cervical radiculopathy
Patients report radicular pain radiating to the upper extremities with or without neck pain. Additionally, symptoms are often reported to be insidious in onset, typically without an identifiable acute inciting event. Clinical exam must assess for sensory and motor deficits and reflex abnormalities. Abnormal reflexes will help distinguish radiculopathy from myelopathy.
Paresthesia or numbness in a nerve root distribution can occur in approximately 80% of cases, but it may also be non-localizable. C5-C6 distribution radiculopathies are the most common; however, because of dermatomal overlap, well-demarcated lesions localizable to a single root are not easily or commonly found. Subjective weakness is less common than paresthesias.
Initial symptoms of pain and paresthesia tend to be markedly more severe with disc herniation. Meanwhile, radiculopathy secondary to spondylosis and foraminal narrowing are more common and may be more gradual in onset, with slowly progressive neurological symptoms. Neck and arm pain are ubiquitous in cervical radiculopathy, although not often in clear-cut dermatomal patterns. Potential sites of pain include the chest, shoulder, scapula, and cervical spine.
Any thorough physical evaluation of radiculopathy must include an assessment for classic “danger signs”. Symptoms such as gait disturbance and bowel/bladder dysfunction may be indicative of myelopathy. Fevers, chills, sweats, unintentional weight loss, history of neoplasm, drug use, and chronic immune suppression should alert the clinical to potential infectious process or neoplastic etiology.
Although sensory symptoms such as burning and tingling may follow a dermatomal distribution, pain from radiculopathy is more frequently referred in a myotomal pattern. Sensory loss at C5, C6, C7, C8 may be found in the lateral upper arm (C5), thumb and index finger (C6), posterior forearm/third finger (C7) or fifth finger (C8).
C5, C6, C7 nerve root radiculopathy may manifest with hyporeflexia at the pronator/brachioradialis, biceps, and triceps reflexes respectively. There are no standard reflexes associated with C8 and T1 nerve roots.
If musculoskeletal shoulder pain is believed to be part of the differential, a thorough shoulder examination must be done, evaluating for asymmetry, pain on palpation, range of motion, and strength. Shoulder instability can mimic radiculopathic pain, but is found in a nondermatomal pattern.
Peripheral nerve injuries must also be considered as possible causes of pain, again not distributed in a dermatomal pattern. Brachial plexitis should also be considered in the differential diagnosis. Pain/sensory changes in multiple dermatomal distributions in the absence of neck pain and with a negative Spurling’s maneuver, raises the possibility of plexopathy and may prompt the need for neoplastic workup.
The Spurling’s test is highly specific for cervical radiculopathy but relatively insensitive ((had a sensitivity of 6/20 (30%) and a specificity of 160/172 (93%)), meaning that a negative Spurling’s does not definitely exclude diagnosis of cervical radiculopathy.
Cervical discogenic pain
Discogenic spine pain tends to be diffuse and axial, not easily demarcated into dermatomal patterns. Hallmarks distinguishing discogenic from radicular pain include: lack of sidedness (i.e. pain is not left or right sided, but rather spans bilaterally across the affected spinal level) and lack of symptoms involving the extremities. The symptoms of discogenic pain are nonspecific and multifaceted, possibly including posterior neck pain, occipital and suboccipital pain, and scapular pain.
Prior authors have noted that heavy lifting and other motions which elevate intradiscal pressure may exacerbate discogenic pain. Other exacerbating factors include coughing, sneezing, or other Valsalva type maneuvers. Sitting pain is common because driving and operating heavy machinery generate vibratory forces that can also worsen discogenic pain. Lying in recumbent or supine position lowers intradiscal pressure and may ameliorate symptoms.
On examination, the clinician will not find neurologic deficits, but rather pain limited cervical range of motion. Reflexes and strength testing should be normal.
Cervical facet disease
Dull neck pains localized to the posterior neck with reduction of ROM are common symptoms of cervical facet disease. Facet disease may also cause intermittent radiation of pain to the shoulder or mid back. Up to 88% of patients with Z-joint pain may have headaches.
Cervical facet/zygapophyseal joint (Z-joint) pain may present with loss of cervical range of motion, tenderness to palpation over the facet joints or paraspinal muscles, pain with cervical extension or rotation, and the absence of neurologic abnormalities.
Joint pain referral patterns have been mapped as follows:
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C2-C3 facets: posterior upper cervical region and head
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C3-C4 facets: posterolateral cervical region without extension into the head or shoulder
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C4-C5 facets: posterolateral middle and lower cervical region, and top of the shoulder
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C5-C6 facets: posterolateral middle and lower cervical spine and superolateral aspect of shoulder extending to spine of the scapula
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C6-C7 facets: superolateral shoulder extending to inferior border of the scapula.
What tests to perform?
Cervical spondylotic myelopathy
Imaging
Plain films may demonstrate osteophyte formation, kyphosis, or anterolisthesis or retrolisthesis.
Plain lateral X-rays can be used to assess the AP canal diameter and possible causes of cord compromise. Cervical spondylotic myelopathy is probable if the canal diameter is less than 10 mm and unlikely if the canal diameter is greater than 16 mm. A Torg ratio (canal/vertebral body width) of < 0.8 (normal is 1.0) may also suggest cervical spine stenosis. See Figure 1.
Figure 1.
Torg Ratio.

MRI is our primary tool in the assessment of cervical stenosis. MRI enables detailed bony and tissue analysis of the spinal cord, intervertebral discs, vertebral osteophytes, and ligaments. Additionally, the ability to rule out a tumor or syrinx with MRI is critical in the diagnosis of cervical stenosis.
Nonetheless, while MRI provides adequate bony anatomical imaging with the ability to assess dynamic cord signal changes, CT is better for the assessment of vertebral osteophytes and detailed bony anatomy. CT can also be a useful adjunct to assess bony canal diameter or to better delineate the bony component of a disc-osteophyte complex.
A clinician should always begin with a fat suppressed MRI image as it provides superior detection of early cord pathology in comparison to T2-weighted images. T2-weighted MRI images at the level of spinal compression may also show signal changes representative of edema, inflammation, ischemia, myelomalacia, or gliosis. In cases of clinically mild cervical myelopathy, increased signal intensity is not related to a poor outcome of conservative treatment or severity of myelopathy.
At our institution, we use fat suppressed sequencing to assess for cord edema or myelomalacia.
Cervical radiculopathy
Imaging
Imaging is typically pursued in all patients when symptoms do not resolve after 6-8 weeks of conservative treatment or sooner when there is evidence of myelopathy or weakness is discovered on initial clinical exam. Early imaging is also indicated when there is a history of cancer, or clinical signs and symptoms suggest infection. Plain film x-rays be obtained at initial evaluation for baseline assessment of cervical spine disease, particularly foraminal compromise in a patient with radiculopathy.
Although soft tissue pathology is not readily seen on plain films, important information regarding disc height loss, bony anatomical arrangement, gross spondylosis, cervical stenosis, and cervical spine alignment can be very useful in deciding next clinical steps. Plain films with flexion and extension views are important for presurgical evaluation as well and useful in assessing cervical spine translational and angulation changes.
Magnetic resonance imaging (MRI) is the first-line approach. Though some literature suggests that T2 weighted images are better for assessing the neural foramina, this is not agreed upon by all radiologist. What is most important in imaging is to obtain thin slices that are perpendicular to the disc space.
Fat suppressed sequences are very sensitive for minor cord and root inflammation and are capable of detecting bony inflammation of the facet joints possibly implicated in the development of cervical radiculopathy.
Gadolinium-enhanced T1 sequences are used to rule out osteomyelitis, metastatic neoplastic processes, and systematic inflammatory processes.
Although CT is better at detecting osteophytic changes of the spine, MRI remains the preferred less invasive test of choice. Clinically, CT may be useful if MRI reveals cord compromise and it is unclear whether etiology is soft tissue or disc osteophyte. CT is also the default option if the patient has a pacemaker and it can be helpful to add myelography to better assess the anatomy.
EMG can be used to confirm cervical radiculopathy in those cases where imaging (MRI) does not correlate well with clinical examination. If such a mismatch exists, EMG may be used to assess for myotomal denervation after approximately 3-6 weeks since onset of injury. EMG will also be useful in a patient who has suspected plexus injury and weakness in limbs that are not confirmed by or do not match up with MRI, or if there is peripheral entrapment or concomitant nerve compression like carpal tunnel syndrome.
Cervical discogenic pain
Imaging
Cervical spine plain films are commonly used in initial evaluation of cervical disc disease. Important information regarding disc height loss and degeneration, bony anatomical alignment, gross spondylosis with foraminal narrowing, small cervical canal diameter can be very useful in deciding next clinical steps. Plain films with flexion and extension views are important to assess for increased mobility at a segment. Flexion and extension views are not typically done on initial evaluation in nontraumatic cases unless the patient is not recovering. Evaluation of the dens with C1-C2 open mouth films may be indicated in patients over 65 years of age who may be more susceptible to disease at that level.
MRI is a reliable first line test for the evaluation of cervical disc disease (i.e., disc herniation). MRI is very good at distinguishing disc herniation from osteophytic compression (foraminal encroachment), but some clinicians may use CT as an adjunct if MR image quality is not optimal. A high intensity zone in the annulus may be seen on T2-weighted MRI images in discogenic disease; however radial fissures of the annulus are most easily seen on a post discogram CT scan.
Disc desiccation, loss of disc height, annular fissure, osteophytes, and reactive end plate changes are the general radiological markers of disc degeneration seen on MRI.
Although CT discography is useful in implicating specific disc levels in discogenic pain, it is rarely if ever done due to its invasiveness. Additionally discography is sensitive but not specific to discogenic pain.
Cervical facet disease
Imaging
Initial radiographs should be AP, lateral and oblique views of the cervical spine, to assess joint space, foraminal narrowing, facet arthropathy. For older patients, it is worthwhile to get open mouth imaging to assess for C1-C2 cervical spine instability.
While subluxation is detectable by plain films, CT is more sensitive in detecting joint fracture.
MRI is the next step in imaging and is especially helpful when fat suppressed images are performed to suppress fat signal to optimize sensitivity in detecting bony facet inflammation.
How should patients with neck pain be managed?
Cervical spondylotic myelopathy
The mainstay of conservative management is reduction of vigorous neck range of motion, restriction of heavy lifting, and postural education. Cervical traction is contraindicated in cervical spondylotic myelopathy.
Patients with good outcomes on conservative treatment tend to be of older age and have normal central motor conduction times on nerve conduction studies (a measure for studying central motor pathways calculated by determining the difference between the latency of motor-evoked potentials and peripheral conduction time).
Patients with good outcomes in surgically treated groups tend to have had more severe clinical neurological deficits. Synthesizing these trends, a study suggest that patients should be treated conservatively if they have a spinal transverse area larger than 70 mm2 on MRI, are of older age, and have normal CMCT (Kadanka et al, 2004).
Overall, surgery is more suitable for patients with worse neurological status and decreased transverse area of spinal cord.
In another study, surgical treatment did not show any better outcome results than conservative treatment in patients with no or very gradual neurological involvement. Conservative treatment should be carried out intensively while the disease process is still of relatively short duration as it is likely not as effective in disease of long duration.
Overall, symptoms of minimal neurological compromise without gait disturbance or pathologic reflexes may be pursued conservatively, but patients with clinical myelopathy and radiological spinal cord compression warrant surgical intervention.
Follow-up should occur at 6 months from initial diagnosis at which repeat MRI should be performed to assess for additional radiologic advancement and cord signal changes. Subsequently, yearly follow up is appropriate for symptomatic monitoring.
Urgent decompression is warranted for patients with evidence of severe myelopathy and progressive neurological deterioration on follow-up.
Cases in which there is a high concern for increased cervical spine segmental motion may warrant temporary bracing and should be referred sooner for surgical evaluation. Stability is assessed with flexion and extension x-rays. Angulation of greater than 10 degrees and translation of greater than 3mm is cause for concern at the stenotic level.
Cervical radiculopathy
In the absence of motor deficits and myelopathy, patients with pain and paresthesias from radiculopathy are treated conservatively with physical therapy to begin neuromotor reeducation to improve spine strength and stability. Neuroimaging with MRI is pursued in patients with clinical evidence of motor weakness.
The following approach for initial treatment is often used in our clinic:
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A short 2 week course of oral anti-inflammatories with a brief period of relative rest (no more than 2 days) followed by physical therapy.
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If there is no improvement after therapy and NSAIDS, we will extend the medication another 2 weeks.
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In cases in which foraminal compromise is suspected, cervical traction may be considered (but is not indicated in cases in which paracentral disc herniation is suspected).
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Although others have suggested the use of a cervical collar, we recommend use of a cervical collar only overnight. This allows relaxation of neck paraspinal musculature and prevents awkward neck positioning during sleep.
Conservative therapy is appropriate for patients with cervical radiculopathy who have radicular pain, paresthesia, numbness, motor weakness, and sensory loss in the absence of myelopathy. Reports indicate that 80 % of patients treated conservatively experience excellent recovery with resolution of pain and motor/sensory deficits.
Rarely, cyclobenzaprine or diazepam may be used to relieve painful muscle spasms. This treatment regimen may be most useful in helping alleviate pain to ease participation in therapy and enabling patients to sleep at night.
We re-evaluate our patients in 4-8 weeks to assess response to conservative treatment and proceed to radiography as described above if there is no clinical improvement or if symptoms worsen. At this point, a tapering methylprednisolone dose pack may also be considered (but only after proper imaging has been done to rule out infectious processes, if clinically suspected).
After another 4-8 weeks of therapy, we may consider epidural glucocorticoid injections. Transforaminal or interlaminar epidural glucocorticoid injections can provide symptomatic relief for 6 months or longer in up to 60% of patients.
Nonparticulate glucocorticoid (i.e., dexamethasone) can reduce the risk of ischemic complications related to epidural steroid injections.
Cervical discogenic pain
A multifaceted, comprehensive rehabilitation program is the mainstay of conservative treatment for cervical discogenic pain and should focus on cervical spine strengthening, stabilization, stretching, and range of motion. Neuromuscular reeducation is critical in developing compensatory postural changes. Stretching must be coupled with strengthening to maintain gains made through therapy.
NSAIDs may be used to control pain and inflammation which may ease participation in therapy. Additionally, tricyclic antidepressants may assist in pain control and sleep regulation. Opiates should be used sparingly. In some cases, nighttime use of a soft cervical collar may help alleviate pain. Limited nighttime use of cervical collar is recommended so as to prevent loss of range of motion and strength, which can occur with chronic daytime use.
Modalities such as ice, heat, and TENS therapy are used in practice but have not been proven to be effective in randomized controlled trials.
Surgery is not indicated in cases of central disc herniation without evidence of myelopathy or progressive neurological decline (i.e. bowel/bladder dysfunction, motor weakness, persistent pain). The best candidates for surgery are patients with motor weakness, worsening myelopathy, recalcitrant radicular pain, and mechanical instability of the cervical spine.
Cervical facet disease
Overall, the key to rehabilitation is postural reeducation, strengthening, and developing compensatory neuromuscular dynamics. Functional strengthening of the scapula, postural reeducation, and cervical stabilization are the pillars to rehabilitation. Studies have shown that cervical stabilization therapy can reduce pain, improve function, and prevent recurrent injury.
Cryotherapy causes local vasoconstriction and reduction in the release of inflammatory mediators, making it a potentially useful modality for symptomatic control of cervical facet pain.
As an adjunct to physical therapy, we often recommend a soft cervical collar to wear at night with the velcro in the front. This is particularly helpful for patients who experience night pain and/or morning stiffness.
Patients who do not respond to a physical therapy and 2 weeks of NSAID therapy may benefit from a second 2 week course of NSAIDs. In rare cases, a 1 week course of tapering methylprednisolone dose pack can help if the patient has been successful in obtaining better cervical spine motion through therapy but has persistent pain. If after 12 weeks, symptoms remain refractory or worsen, corticosteroid injection of the facet joints may be considered. Medial branch blocks to confirm the diagnosis of facet mediated pain, followed by radiofrequency ablation of the medial branches that supply the facet joints are another alternative option that may provide over 12 months of neck pain relief in 58-74% of patients.
Narcotic pain medications may be needed for moderate to severe pain, but can limit recovery. We have found tramadol to be more helpful and less likely to promote dependence than narcotic medications and has equal efficacy in our patients.
Muscle relaxing benzodiazepines may be helpful in muscle spasm relief. We suggest they be taken at night.
Cervical fusion is only in order when a patient fails conservative treatment. A study has noted that cervical fusion for facet arthropathy is unfavorable when compared to that for radiculopathy (Williams et al, 1968). In multiple years of practice, our institution has not referred a single patient with facet arthropathy for cervical fusion.
What happens to patients with neck pain?
Cervical spondylotic myelopathy
Cervical spondylotic myelopathy is the most common cause of myelopathy in adults over 55 years, capable of causing worsening pain. It may manifest as a slow, stepwise decline or there may be a long period of quiescence. Long periods of severe stenosis are associated with demyelination and may result in necrosis of both gray and white matter. With severe and/or long lasting symptoms, the likelihood of improvement with nonoperative measures is low.
Objectively measurable deterioration is rarely seen acutely in patients younger than 75. Patients with cervical stenosis without myelopathy who have abnormal electromyography findings or clinical radiculopathy may develop symptomatic cervical spondylotic myelopathy.
The levels most likely to be involved by degenerative changes are C5-6, C6-7 and C4-5, in that order. Some studies have suggested that soft tissue injuries which result in severe initial pain are positively correlated with poor long term outcome.
Spinal canals that are congenitally or developmentally narrow can be further compromised with the development of degenerative disc osteophyte complexes, protrusion of disc material, hypertrophy of the ligamentum flavum, and ossification of the posterior longitudinal ligament.
Compression of the spinal cord may be accompanied by ischemic changes. Anatomically, the anterior spinal artery is susceptible to compression from disc herniation, osteophytes, and ossification of the posterior longitudinal ligament, while the segmental branches may be compromised by osteophytic narrowing of the intervertebral foramina.
Cervical spondylosis/arthritis is capable of injuring spinal nerve roots as well as the cord and anterior horn cells in the spinal cord gray matter, causing lower motor neuron deficits. As stated above, the C5-6, C6-7 segments are most frequently involved, leading to the presence of lower motor neuron signs (hyporeflexia, fasciculations, atrophy, weakness) in the C6 or C7 myotomes.
Importantly, the above findings of hyperreflexia, clonus, and spasticity are found in the presence of upper motor neuron signs globally.
Cervical radiculopathy
By definition, a radiculopathy is a disease of the nerve root, most often resulting from paracentral disc herniation or foraminal narrowing and impingement. Foraminal impingement ranks as the most prevalent etiology of radiculopathy, with as many as 75% of cases resulting from decreased disc height and spinal degenerative disease of the uncovertebral joint and Z-joint.
Conservative treatment for cervical radiculopathy yields very good results. More than 80% of patients will show recovery without surgical intervention.
Nerve-root compression alone does not necessitate pain unless the dorsal-root ganglion is also compressed. Hypoxia of the nerve root and dorsal ganglion exacerbate the impact of nerve root compression.
Inflammatory mediators such as prostaglandin E2, interleukin-6, and nitric oxide have been shown to be released by herniated cervical intervertebral disks. Resolution of painful symptoms has been shown to correlate with improvement of disc herniation on radiographic follow-up.
Prior studies have shown that although surgical treatment yields more significant reduction in pain than physical therapy, at 1 year there is no difference in outcome between the two treatment groups.
Cervical discogenic pain
Cervical spine disease may account for as much as 36% of all spinal intervertebral disc disease. Herniated nucleus pulposus, degenerative disc disease, and internal disc disruption are the general subtypes of cervical disc dysfunction.
Disc herniation is characterized by encroachment of the intradiscal material and the annulus fibrosus past the posterior aspect of the vertebral body. Based on degree of herniation, a disc can be described as bulging, protruding, extruded, or sequestered. Degenerative disc disease is characterized by gradual loss of disc height, nucleus pulposus degeneration, and progressive annular tears. Lastly, intradiscal disease is characterized as disruption self-limited to the internal matrix of the annulus itself.
Several authors have described the progression of degenerative disc disease. Circumferential tears form in the posterolateral annulus after repetitive use and may evolve to coalesce into radial tears, which in turn can become radial fissures. Subsequently, loss of disc height can occur due to tears through the disc causing annular fissure.
Annular fissuring within the disc without external disc deformation is the definition of intradiscal degeneration and may result from trauma-related nuclear degradation, cervical flexion/rotation-induced annular injury, or whiplash. Because the periphery of the annulus is innervated, the disc can be a major cause of pain.
Cervical facet disease
The prognosis for patients with cervical facet joint pain is generally good and most pain and radicular symptoms caused by encroachment upon the foramen or nerve root by cervical facet arthropathy and osteophytic changes often completely resolve with physical therapy.
How to utilize team care?
Cervical spondylotic myelopathy
Specialty consultations
Orthopedics/Neurosurgery consultation should take place as soon as possible in setting of acute deterioration and progressive neurological decline. Typically, a patient with spondylosis and cord signal changes should be evaluated by a surgeon even if conservative measures are initially chosen.
Therapists (physical and occupational)
The cornerstone of conservative therapy is to improve balance and ADLs as well as gait stability and mechanics. If surgery is indicated and the patient is at high risk for further injury, immobilize the cervical spine with a collar or brace that holds the head in a neutral or slightly flexed position. Manipulation and traction are contraindicated because of the potential for aggravation of neurological injury.
Cervical radiculopathy
Surgery should be recommended for patients with persistent, progressive disabling symptoms with worsening neurological deficits or evidence of severe myelopathy.
Cervical discogenic pain
Orthopedic or neurosurgical spine consultation is warranted in the setting of acute deterioration, failure of non-operative care and progressive neurological decline.
Cervical facet disease
Orthopedics/Neurosurgery consultation should take place in setting of acute deterioration and/or progressive neurological decline.
Are there clinical practice guidelines to inform decision making?
Cervical spondylotic myelopathy
No.
Cervical radiculopathy
No.
Cervical discogenic pain
No.
Cervical facet disease
No.
Other considerations
Cervical spondylotic myelopathy
ICD-10 codes
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M47.12
Cervical radiculopathy
ICD-10 codes
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M54.12
Cervical discogenic pain
ICD-10 codes
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M50.30 – Other cervical disc degeneration, unspecified cervical region
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M50.31 – Other cervical disc degeneration, high cervical region
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M50.32 – Other cervical disc degeneration, mid-cervical region
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M50.90 – Cervical disc disorder, unspecified
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M50.20 – Other cervical disc displacement, unspecified cervical region
Cervical facet disease
ICD-10 codes
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M47.812 – spondylosis without myelopathy or radiculopathy, cervical region
What is the evidence?
Cervical spondylotic myelopathy
Matz, PG. “The natural history of cervical spondylotic myelopathy”. J Neurosurg Spine. vol. 11. 2009 Aug. pp. 104-11.
McCormick, WE, Steinmetz, MP, Benzel, EC. “Cervical spondylotic myelopathy: make the difficult diagnosis, then refer for surgery”. Cleve Clin J Med. vol. 70. 2003 Oct. pp. 899-904.
Emery, SE. “Cervical spondylotic myelopathy: diagnosis and treatment”. J Am Acad Orthop Surg. vol. 9. 2001 Nov-Dec. pp. 376-88.
Kadanka, Z, Mares, M, Bednarík, J, Smrcka, V, Krbec, M, Chaloupka, R, Dusek, L. “Predictive factors for mild forms of spondylotic cervical myelopathy treated conservatively or surgically”. Eur J Neurol.. vol. 12. 2005. pp. 16
Rao, SC, Fehlings, MG. “The optimal radiologic method for assessing spinal canal compromise and cord compression in patients with cervical spinal cord injur. Part I: An evidence-based analysis of the published literature”. Spine (Phila Pa 1976). vol. 24. 1999 Mar 15. pp. 598-604.
Torg, JS, Pavlov, H, Genuario, SE. “Neurapraxia of the cervical spinal cord with transient quadriplegia”. J Bone Joint Surg Am. vol. 68. Dec 1986. pp. 1354-70.
Gross, JD, Benzel, EC, Camins, MB. “Dorsal surgical approach for cervical spondylotic myelopathy”. Techniques in Neurosurgery. 1999. pp. 162-176.
Mehalic, TF, Pezzuti, RT, Applebaum, BI. “Magnetic resonance imaging and cervical spondylotic myelopathy”. Neurosurgery. vol. 26. 1990. pp. 217-227.
Matsumoto, M, Toyama, Y, Ishikawa, M, Chiba, K, Suzuki, N, Fujimura, Y. “Increased signal intensity of the spinal cord on magnetic resonance images in cervical compressive myelopath. Does it predict the outcome of conservative treatment”. Spine (Phila Pa 1976).. vol. 25. 2000. pp. 677
Yoshimatsu, H, Nagata, K, Goto, H, Sonoda, K, Ando, N, Imoto, H, Mashima, T, Takamiya, Y. “Conservative treatment for cervical spondylotic myelopathy. Prediction of treatment effects by multivariate analysis”. Spine J. vol. 1. 2001 Jul-Aug. pp. 269-73.
Mazanec, D, Reddy, A. “Neurosurgery”. Medical management of cervical spondylosis. vol. 60. 2007 Jan. pp. S43-50.
Samii, A, Luciano, CA, Dambrosia, JM, Hallett, M. “Central motor conduction time: reproducibility and discomfort of different methods”. Muscle Nerve. vol. 21. 1998 Nov. pp. 1445-50.
Samii, A, Luciano, CA, Dambrosia, JM, Hallett, M. “Muscle Nerve”. Central motor conduction time: reproducibility and discomfort of different methods. vol. 21. 1998 Nov. pp. 1445-50.
Kadanka, Z, Bednarík, J, Vohánka, S, Vlach, O, Stejskal, L, Chaloupka, R. “Conservative treatment versus surgery in spondylotic cervical myelopathy: a prospective randomised study”. Eur Spine J. vol. 9. 2000. pp. 538
Watkinson, A, Gargan, MF, Bannister, GC. “Prognostic factors in soft tissue injuries of the cervical spine”. Injury. vol. 22. 1991. pp. 307-9.
Gore, DR, Sepic, SB, Gardner, GM. “Neck pain: a long term follow-up of 205 patients”. Spine. vol. 12. 1987. pp. 1-5.
Fang, D. “Cervical Spondylotic Myelopathy J Hong Kong Med Assoc”. vol. 46. 1994 Sept. pp. 173-174.
Cervical radiculopathy
Radhakrishnan, K, Litchy, WJ, O’Fallon, WM, Kurland, LT. “Epidemiology of cervical radiculopath. A population-based study from Rochester, Minnesota, 1976 through 1990”. Brain.. vol. 117 . 1994. pp. 325
Ellenberg, MR, Honet, JC, Treanor, WJ. “Cervical radiculopathy”. Arch Phys Med Rehabil.. vol. 75. 1994. pp. 342
Carette, S, Fehlings, MG. “Clinical practice. Cervical radiculopathy”. N Engl J Med.. vol. 353. 2005. pp. 392
Tong, HC, Haig, AJ, Yamakawa, K. “The Spurling test and cervical radiculopath”. Spine (Phila Pa 1976).. vol. 27. 2002. pp. 156
Yousem, DM, Atlas, SW, Goldberg, HI, Grossman, RI. “Degenerative narrowing of the cervical spine neural foramina: evaluation with high-resolution 3DFT gradient-echo MR imaging”. AJNR Am J Neuroradiol.. vol. 12. 1991. pp. 229
Bartlett, RJ, Hill, CR, Gardiner, E. “A comparison of T2 and gadolinium enhanced MRI with CT myelography in cervical radiculopathy”. Br J Radiol.. vol. 71. 1998. pp. 11
Modic, MT, Masaryk, TJ, Mulopulos, GP, Bundschuh, C, Han, JS, Bohlman, H. “Cervical radiculopathy: prospective evaluation with surface coil MR imaging, CT with metrizamide, and metrizamide myelography”. Radiology.. vol. 161. 1986. pp. 753
Honet, JC, Puri, K. “Cervical radiculitis: treatment and results in 82 patients”. Arch Phys Med Rehabil.. vol. 57. 1976. pp. 12
Mazanec, D, Reddy, A. “Medical management of cervical spondylosis”. Neurosurgery. vol. 60. 2007 Jan. pp. S43-50.
Aker, PD, Gross, AR, Goldsmith, CH, Peloso, P. “Conservative management of mechanical neck pain: A systematic overview and meta-analysis”. BMJ. vol. 313. 1996. pp. 1291-1296.
Slipman, CW, Lipetz, JS, Jackson, HB, Rogers, DP, Vresilovic, EJ. “Therapeutic selective nerve root block in the nonsurgical treatment of a traumatic cervical spondylotic radicular pain: a retrospective analysis with independent clinical review”. Arch Phys Med Rehabil. vol. 81. 2000. pp. 741-6.
Dreyfuss, P, Baker, R, Bogduk, N. “Comparative effectiveness of cervical transforaminal injections with particulate and nonparticulate corticosteroid preparations for cervical radicular pain”. Pain Med. May-Jun. vol. 7. 2006. pp. 237-42.
Shelerud, RA, Paynter, KS. “Rarer causes of radiculopathy: spinal tumors, infections, and other unusual causes”. Phys Med Rehabil Clin N Am. vol. 13. 2002. pp. 645-96.
Howe, JF, Loeser, JD, Calvin, WH. “Mechanosensitivity of dorsal root ganglia and chronically injured axons: a physiological basis for the radicular pain of nerve root compression”. Pain. vol. 3. 1977. pp. 25-41.
Sugawara, O, Atsuta, Y, Iwahara, T, Muramoto, T, Watakabe, M, Takemitsu, Y. “The effects of mechanical compression and hypoxia on nerve root and dorsal root ganglia: an analysis of ectopic firing using an in vitro model”. Spine. vol. 21. 1996. pp. 2089-94.
Maigne, JY, Deligne, L. “Computed tomographic follow-up study of 21 cases of nonoperatively treated cervical intervertebral soft disc herniation”. Spine. vol. 19. 1994. pp. 189-91.
Bush, K, Chaudhuri, R, Hillier, S, Penny, J. “The pathomorphologic changes that accompany the resolution of cervical radiculopathy: a prospective study with repeat magnetic resonance imaging”. Spine. vol. 22. 1997. pp. 183-6.
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Cervical discogenic pain
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