Diagnosis and Management of Cervical Spondylosis 

Updated: Nov 09, 2018
Author: Sandeep S Rana, MD; Chief Editor: Tarakad S Ramachandran, MBBS, MBA, MPH, FAAN, FACP, FAHA, FRCP, FRCPC, FRS, LRCP, MRCP, MRCS 

Overview

Background

Cervical spondylosis is a common degenerative condition of the cervical spine. It is most likely caused by age-related changes in the intervertebral disks. Clinically, several syndromes, both overlapping and distinct, are seen. These include neck and shoulder pain, suboccipital pain and headache, radicular symptoms, and cervical spondylotic myelopathy (CSM). As disk degeneration occurs, mechanical stresses result in osteophytic bars, which form along the ventral aspect of the spinal canal.

Frequently, associated degenerative changes in the facet joints, hypertrophy of the ligamentum flavum, and ossification of the posterior longitudinal ligament occur. All can contribute to impingement on pain-sensitive structures (eg, nerves, spinal cord), thus creating various clinical syndromes. Spondylotic changes are often observed in the aging population. However, only a small percentage of patients with radiographic evidence of cervical spondylosis are symptomatic.

Treatment is usually conservative in nature; the most commonly used treatments are nonsteroidal anti-inflammatory drugs (NSAIDs), physical modalities, and lifestyle modifications. Surgery is occasionally performed. Many of the treatment modalities for cervical spondylosis have not been subjected to rigorous, controlled trials. Surgery is advocated for cervical radiculopathy in patients who have intractable pain, progressive symptoms, or weakness that fails to improve with conservative therapy. Surgical indications for cervical spondylotic myelopathy remain somewhat controversial, but most clinicians recommend operative therapy over conservative therapy for moderate-to-severe myelopathy.

A 48-year-old man presented with neck pain and pre A 48-year-old man presented with neck pain and predominantly left-sided radicular symptoms in the arm. The patient's symptoms resolved with conservative therapy. T2-weighted sagittal MRI shows ventral osteophytosis, most prominent between C4 and C7, with reduction of the ventral cerebrospinal fluid sleeve.

Pathophysiology

Cervical spondylosis is the result of disk degeneration. As disks age, they fragment, lose water, and collapse. Initially, this starts in the nucleus pulposus. This results in the central annular lamellae buckling inward while the external concentric bands of the annulus fibrosis bulge outward. This causes increased mechanical stress at the cartilaginous end plates at the vertebral body lip.

Subperiosteal bone formation occurs next, forming osteophytic bars that extend along the ventral aspect of the spinal canal and, in some cases, encroach on nervous tissue.[1, 2] These most likely stabilize adjacent vertebrae, which are hypermobile as a result of the lost disk material.[3, 4] In addition, hypertrophy of the uncinate process occurs, often encroaching on the ventrolateral portion of the intervertebral foramina.[1] Nerve root irritation also may occur as intervertebral discal proteoglycans are degraded.[5]

Ossification of the posterior longitudinal ligament, a condition often seen in certain Asian populations, can occur with cervical spondylosis. This condition can be an additional contributing source of severe anterior cord compression.[6]

Cervical spondylotic myelopathy occurs as a result of several important pathophysiological factors. These are static-mechanical, dynamic-mechanical, spinal cord ischemia, and stretch-associated injury. As ventral osteophytes develop, the cervical cord space becomes narrowed; thus, patients with congenitally narrowed spinal canals (10-13 mm) are predisposed to developing cervical spondylotic myelopathy.

Age-related hypertrophy of the ligamentum flavum and thickening of bone may result in further narrowing of the cord space.[2, 7, 8] Additionally, degenerative kyphosis and subluxation are fairly common findings that may further contribute to cord compression in patients with cervical spondylotic myelopathy.[6, 9] Dynamic factors relate to the fact that normal flexion and extension of the cord may aggravate spinal cord damage initiated by static compression of the cord. During flexion, the spinal cord lengthens, resulting in it being stretched over ventral osteophytic bars. During extension, the ligamentum flavum may buckle into the cord, pinching the cord between the ligaments and the anterior osteophytes.[7, 10]

Spinal cord ischemia also most likely plays a role in cervical spondylotic myelopathy. Histopathologic changes seen in persons with cervical spondylotic myelopathy frequently involve gray matter, with minimal white matter involvement—a pattern consistent with ischemic insult. Ischemia most likely occurs at the level of impaired microcirculation.[11]

Stretch-associated injury has recently been implicated as a pathophysiologic factor in cervical spondylotic myelopathy.[12] The narrowing of the spinal canal and abnormal motion seen with cervical spondylotic myelopathy may result in increased strain and shear forces, which can cause localized axonal injury to the cord.

Epidemiology

Frequency

Cervical spondylotic myelopathy is the most common cause of nontraumatic spastic paraparesis and quadriparesis. In one report, 23.6% of patients presenting with nontraumatic myelopathic symptoms had cervical spondylotic myelopathy.[13]

Demographics

Cervical spondylosis may affect males earlier than females, but this is not true in all studied populations.

Irvine et al defined the prevalence of cervical spondylotic myelopathy using radiographic evidence. In males, the prevalence was 13% in the third decade, increasing to nearly 100% by age 70 years. In females, the prevalence ranged from 5% in the fourth decade to 96% in women older than 70 years. Another study examined patients at autopsy. At age 60 years, half the men and one third of the women had significant disease.[14] A 1992 study noted that spondylotic changes are most common in persons older than 40 years. Eventually, greater than 70% of men and women are affected, but the radiographic changes are more severe in men than in women.[15]

 

 

Presentation

History

The various clinical syndromes seen with cervical spondylosis manifest quite differently.

Intermittent neck and shoulder pain, or cervicalgia, is the most common syndrome seen in clinical practice.[2] This can be a frustrating problem for physicians and patients because often the patient has no associated neurologic signs. When neurologic deficits are present, diagnostic imaging can often help define the cause. When they are not present, however, imaging findings are not usually helpful because the incidence of radiologic abnormalities is quite high in persons in this age group, even in asymptomatic patients.

  • A large part of the problem is that the source of pain in this situation is poorly understood. This syndrome is possibly related to compression of the sinovertebral nerves and the medial branches of the dorsal rami in the cervical region.[16]

  • The neck pain experienced with cervical spondylosis is often accompanied by stiffness, with radiation into the shoulders or occiput, that may be chronic or episodic with long periods of remission.[2]

  • One third of patients with cervicalgia due to cervical spondylosis present with headache, and greater than two thirds present with unilateral or bilateral shoulder pain. A significant amount of these patients also present with arm, forearm, and/or hand pain.[16]

Another poorly understood clinical syndrome seen with cervical spondylosis is chronic suboccipital headache. Although the C1 thru C3 dermatomes are represented on the head and it would seem likely that occipitoatlantal and atlantoaxial degeneration would cause pain in these areas, no contributions to these joints occur from the dorsal rami of C1-C3. In addition, the greater occipital nerve cannot usually be compressed by bony structures. Regardless, headaches can be the dominant symptom in a patient with degenerative cervical disease. The headaches are usually suboccipital and may radiate to the base of the neck and the vertex of the skull.[16]

Perhaps more thoroughly understood than the above-discussed syndromes is radiculopathy associated with cervical spondylosis. The most commonly involved nerve roots are the sixth and seventh nerve roots, which are caused by C5-C6 or C6-C7 spondylosis, respectively. Patients usually present with pain, paresthesias or weakness, or a combination of these symptoms. The vast majority of these patients present without a history of trauma or other recalled precipitated cause. The pain is usually in the cervical region, the upper limb, shoulder, and/or interscapular region. At times, the pain may be atypical and manifest as chest pain (pseudoangina) or breast pain. Usually, the pain is more frequent in the upper limbs than in the neck, although it is frequently present in both areas.[17] Cervical radiculopathy is not usually associated with myelopathy.[2]

Cervical spondylotic myelopathy is the most common cause of nontraumatic paraparesis and tetraparesis. The process usually develops insidiously.

In the early stages, patients often present with neck stiffness. Patients also may present with stabbing pain in the preaxial or postaxial border of the arms.[10] Patients with a high compressive myelopathy (C3-C5) can present with a syndrome of "numb, clumsy hands," for which the patient describes difficulty writing, a loss of manual dexterity, nonspecific and diffuse weakness, and abnormal sensations.[2] Those patients with a lower myelopathy typically present with a syndrome of weakness, stiffness, and proprioceptive loss in the legs. These patients often exhibit signs of spasticity.

Weakness or clumsiness of the hands may be seen in conjunction with weakness in the legs. Motor loss in the hands with relative sparing of the legs, however, is a relatively rare syndrome. Symptoms are commonly asymmetric in the legs.

Loss of sphincter control and urinary incontinence are rare; some patients, however, report urinary urgency, frequency, and/or hesitancy.[2, 10]

Cervical spondylotic myelopathy significantly affects patients' quality of life. A recent study reported that greater than one third of patients with cervical spondylotic myelopathy have anxious or depressed moods related to their decreased mobility.[18]

Another syndrome that may be seen in relation to cervical spondylosis is central cord syndrome. This syndrome typically occurs when an elderly patient experiences an acute hyperextension injury with preexisting acquired stenosis due to ventral osteophytes and infolding of redundant ligamentum flavum, resulting in acute cord compression. Patients usually present with a history of a blow to the forehead. The syndrome consists of greater upper extremity weakness than lower extremity weakness, varying degrees of sensory disturbances below the lesion, and myelopathic findings such as spasticity and urinary retention.[19]

Rarely, dysphagia or airway dysfunction has been reported secondary to cervical spondylosis.[20, 21, 22, 23, 24] Dysphagia may occur when large anterior osteophytes cause mechanical compression of the esophagus or periesophageal inflammation causes motion over the osteophytes. Conservative therapy with anti-inflammatory medications and other modalities has been advocated for mild-to-moderate cases of dysphagia, while surgery has been reserved for more severe cases.[22]

Physical

Examination findings include neck pain, radicular signs, and myelopathic signs. Patients with neck pain from spondylosis often present with neck stiffness. This is a nonspecific sign, and other causes of neck pain and stiffness (eg, myofascial pain, intrinsic shoulder pathology) must be considered and excluded.

If the history is compatible with cervical radiculopathy, carefully search for signs of muscle atrophy in the supraspinatus, infraspinatus, deltoid, triceps, and first dorsal interosseus muscles.

Winging of the scapula also may be present because it can occur with C6 or C7 radiculopathy. Palpate all muscles because this may allow earlier detection of wasting than visualization can provide. If weakness is detected in either 1 myotomal distribution or 2-3 peripheral nerves, peripheral nerve injury can likely be excluded as the cause. Muscle testing is important because muscle findings have more specificity than sensory or reflex findings.

Perform a detailed sensory and reflex examination in every patient who presents with a history suggestive of cervical spondylosis. Note that radicular findings often do not adhere strictly to textbook dermatomal charts. Patients often experience more pain proximally in their limbs, while, distally, paresthesias dominate.

Look for physical evidence of other causes of radiculopathy-type symptoms (eg, tenderness lateral to the neck in the supraclavicular fossa, Tinel sign).

The neck compression test (Spurling test or sign), if positive, is useful when assessing a patient for cervical radiculopathy.

  • This test is best performed by having the patient actively extend his or her neck, laterally flex, and rotate to the side of the pain while sitting. Next, use careful compression by slight axial loading. This maneuver works by narrowing the ipsilateral neural foramina during flexion and rotation, while the initial extension causes posterior disk bulging.

  • While this maneuver has a low sensitivity for cervical radiculopathy, it has a specificity of nearly 100%. Other useful tests are the axial manual traction test and the shoulder abduction test.

In cervical spondylotic myelopathy, the most typical examination findings are suggestive of upper motor dysfunction, including hyperactive deep tendon reflexes, ankle and/or patellar clonus, spasticity (especially of the lower extremities), the Babinski sign, and the Hoffman sign.

  • The Hoffman sign is a reflex contraction of the thumb and index finger after nipping the middle finger. Although this sign is usually present with corticospinal tract dysfunction, unlike the Babinski sign, it can also be present in generalized hyperreflexic states and in neurosis. It also may be found (usually bilaterally and incomplete) in persons without cervical spondylotic myelopathy.

  • Thus, this sign is only valuable if it is associated with other upper motor neuron–related findings. The Hoffman sign is best elicited by positioning the patient's hand at rest and then stabilizing the proximal phalanx between the examiner's index and middle finger; with the examiner's thumb, the patient's distal middle finger is flicked downward. The sensitivity of this examination maneuver may be increased by examining the patient during multiple full flexions or extensions of the neck (dynamic Hoffman sign).

Another occasionally useful test is the pectoralis muscle reflex.

  • This is elicited by tapping the pectoralis tendon in the deltopectoral groove, which causes adduction and internal rotation of the shoulder if hyperactivity is present. A positive result suggests compression in the upper cervical spine (C2-C4).

  • If the patient exhibits diffuse hyperreflexia, then the jaw jerk may distinguish an upper cervical cord compression from lesions that are above the foramen magnum.

In patients with cervical spondylotic myelopathy, weakness is most commonly seen in the triceps and/or hand intrinsic muscles, where upper extremity symptoms typically begin. Wasting of the intrinsic hand musculature is also a typical finding.

  • A thorough examination of patients' hands should be performed. By having the patient make a fist and release it 20 times in 10 seconds, impairment or clumsiness may be observed that may suggest cervical spondylotic myelopathy.

  • The finger escape sign may also be present. To assess this, the patient holds his or her fingers extended and adducted. If the ulnar digits drift into abduction and flexion within 30-60 seconds, cervical spondylotic myelopathy may be present.

A classic finding with examination of the lower extremities is proximal motor weakness, most commonly in the iliopsoas, followed by the quadriceps femoris; distal weakness is a less common finding. The finding of lower extremity weakness and lower extremity upper motor neuron signs but absent upper extremity symptoms and signs should trigger a workup for thoracic cord pathology.

Examine gait during any neurologic examination whenever possible. Patients with cervical spondylotic myelopathy typically exhibit a stiff or spastic gait, especially later in the course of their disease.

Another helpful sign is the Lhermitte sign.

  • This consists of electric shock–like sensations that run down the center of the patient's back and shoot into the limbs during flexion of the neck.

  • This sign is not specific for cervical spondylotic myelopathy and classically is attributed to posterior column dysfunction. Other causes of the Lhermitte sign include multiple sclerosis, tumors, and other compressive pathology.

Sensory abnormalities in cervical spondylotic myelopathy have a variable pattern upon examination.

  • Loss of vibratory sense or proprioception in the extremities can occur, particularly in the feet. Spinothalamic sensory loss may be asymmetric.

  • Diabetes mellitus or other metabolic causes of peripheral neuropathy can confound the sensory examination. Perform a complete motor examination. Wasting of the intrinsic hand musculature is a classic finding in persons with cervical spondylotic myelopathy.

Causes

In addition to age and possibly sex, several risk factors have been proposed for cervical spondylosis.

Repeated occupational trauma (eg, carrying axial loads, professional dancing, gymnastics) may contribute. The role of occupational trauma is controversial, especially in terms of worker's compensation claims and other related medicolegal clauses.

Familial cases have been reported; a genetic cause is possible.

Smoking also may be a risk factor.

Conditions that contribute to segmental instability and excessive segmental motion (eg, congenitally fused spine, cerebral palsy, Down syndrome) may be risk factors for spondylotic disease. Cervical spondylotic myelopathy may be responsible for functional declines in patients with athetoid cerebral palsy.

 

DDx

Diagnostic Considerations

Acromioclavicular pathology

Acute posterior cervical strain

Adhesive capsulitis

Aortic disease

Arachnoiditis

Arteriovenous malformation

Back pain

Bicipital tendonitis - Rotator cuff tears, lateral epicondylitis

Brainstem syndromes

Calcareous tendonitis

Cervical disk syndromes

Cervical lymphadenitis

Cervical rib

Congenital spinal lesion

Diskitis

Double crush syndrome

Epidural abscess

Extrinsic neoplasia (usually metastatic)

Fibrositis syndromes

Frozen shoulder syndromes

Gallbladder disease

Glenohumeral arthritis

Gout (infrequently)

Heart disease

Hyperabduction syndrome

Intervertebral osteoarthritis

Idiopathic brachial plexopathy (neuralgic amyotrophy)

Intrinsic neoplasia

Lung disease

Meningitis

Musculoligamentous injuries to the neck and shoulder

Neoplasms

Neoplasms of the shoulder

Nerve injuries

Occipital neuralgia

Osteomyelitis

Osteoarthritis of apophyseal joints

Paget disease

Pancoast tumor

Pancreatic disease

Peptic ulcer disease

Pharyngeal infections

Posttraumatic facet fracture with narrowing of the foramen

Postural disorders

Psychogenic disorders

Rheumatic fever (infrequently)

Rheumatoid arthritis

Rib-clavicle compression

Rotator cuff tears and tendonitis

Scalene muscle

Septic arthritis

Spinal cord tumors

Sternocleidomastoid tendinitis

Subacromial bursitis

Synovial cysts

Tabes dorsalis

Thoracic disk

Thoracic outlet syndrome

Tropical spastic paraparesis

Differential Diagnoses

 

Workup

Laboratory Studies

Cyanocobalamin (vitamin B-12) levels and a serum rapid plasma reagin may help distinguish metabolic and infectious causes of myelopathy from cervical spondylotic myelopathy. Metabolic and infectious conditions may coexist with cervical spondylosis, and, thus, an abnormal laboratory profile does not exclude cervical spondylotic myelopathy.

Imaging Studies

Although plain films of the cervical spine are the least costly and most widely available imaging modality, the imaging study of choice is MRI.

Although a narrow spinal canal with a sagittal diameter of 10-13 mm (as visualized on a plain radiograph) has been associated with a higher incidence of neurologic deficit and cervical spondylotic myelopathy, this measurement has become less important with the widespread availability of MRI. MRI allows direct visualization of neural structures and allows a more accurate estimation of the cord space.

Plain radiography can help assess the contribution of spinal alignment and degenerative spondylolisthesis to canal stenosis.

MRI is a noninvasive and radiation-free procedure that provides excellent imaging of the spinal cord and subarachnoid space and is a sensitive method for determining involvement of these by extradural pathology. MRI allows multiplanar imaging, excellent imaging of the neural elements, and increased accuracy in diagnosing intrinsic cord disease. It may detect pathology in the asymptomatic patient, or the pathology may be unrelated to the symptoms. In one report, 57% of patients who were older than 64 years had disk bulging and 26% of patients in this age group had evidence of cord compression on MRIs.[25] Some spondylotic changes (eg, small lateral osteophytes, midbody calcific densities) may be overlooked by MRI.

Overall, the advantages of MRI significantly outweigh its deficiencies, and thus it has become the standard diagnostic study for spondylotic disease. It has been demonstrated to be an accurate imaging modality in several studies. When surgical results were used as the criterion standard, agreement with MRI findings was found in 74% of cases, agreement with CT myelography in 84% of cases, and with myelography in 67% of cases. In one study, MRI was demonstrated to be 90% sensitive for the diagnosis of cervical stenosis, while CT myelography and CT scanning were 100% sensitive.[26]

Plain films of the cervical spine are an inexpensive way of assessing spondylotic disease in symptomatic patients. Cervical spine films can demonstrate disk-space narrowing, osteophytosis, loss of cervical lordosis, uncovertebral joint hypertrophy, apophyseal joint osteoarthritis, and vertebral canal diameter. The nearly universal presence of spondylotic radiographic changes in elderly patients (and the similar appearance of a cervical spine film in a symptomatic patient and an asymptomatic patient) allows the classification of an individual patient as having mild, moderate, or severe spondylotic changes.

CT scanning is another important imaging modality. Superior to MRI in its definition of bony anatomy, CT scanning better defines the neural foramina. CT scanning is often used to complement MRI and to provide additional bony detail to characterize a lesion responsible for neural encroachment.

Myelography is also useful for demonstrating nerve root lesions. Myelography demonstrates nerve root take off very well.[27] It is particularly useful in patients under going reoperation.

Some authors, however, report that CT myelography has a lower rate of false-positive results compared with conventional myelography. Some researchers have concluded that CT myelography provides additional data only when myelography results are positive—negative myelography findings followed by CT scanning in the case of suspected spondylosis is unlikely to show any clinically useful findings.[28]

Recently, dynamic CT myelography has been reported as useful in the surgical planning for patients with cervical spondylotic myelopathy, in some cases altering the surgeon's approach on the basis of dynamic findings.[29] Nevertheless, the exact role for dynamic imaging such as dynamic CT myelography and dynamic MRI remains to be determined.

Diffusion tensor imaging (DTI), a developed magnetic resonance technique, can aid in detecting intramedullary lesions. One study found that when DTI is performed along 6 noncollinear directions with single-shot spin echoplanar imaging (EPI) sequence, it clearly revealed the intramedullary microstructure and more lesions than conventional MRI.[30]

Other Tests

Electrodiagnostic studies are useful in many patients.

  • Electromyography (EMG) can help diagnose cervical radiculopathy and, occasionally, identify cervical spondylotic myelopathy.

  • EMG is useful in the study of radiculopathy because it demonstrates a close correlation with neuroimaging and operative findings.

  • It also provides an anatomic distribution of abnormalities, thus facilitating the differential of cervical radiculopathy from other similar causes of radicular symptoms.

  • EMG can help determine how long a lesion has been present. When using modern imaging techniques such as MRI, EMG can help clarify whether a lesion observed on imaging is the cause of nerve root pathology.

  • In a patient with cervical spondylotic myelopathy, EMG can exclude specific syndromes of peripheral neuropathy rather than confirm cervical spondylotic myelopathy.

Somatosensory evoked potentials and cortical motor evoked potentials also may help evaluate spinal cord dysfunction, especially in timing intervention for the asymptomatic or minimally symptomatic patient with early cervical spondylotic myelopathy.

Histologic Findings

Histologic findings associated with cervical spondylotic myelopathy are greatest at the site of maximal compression. Changes in the gray matter range from consistent motor-neuron loss and ischemic changes in surviving neurons to necrosis and cavitation. Frequently, involvement of white matter is minimal, although it varies in degree. White matter changes, when they occur, are generally seen in the ventral inner portion of the dorsal column or in the lateral columns bordering the gray matter, with the anterior columns being only slightly damaged. Nongliotic necrosis is frequently described. Wallerian degeneration of posterior columns cephalad to the site of compression and of corticospinal tracts caudal to site of compression is frequent. Widespread proliferation of small, thickened, and hyalinized intermedullary blood vessels is frequently reported.

Many of these findings are similar to a pathological model of vascular occlusion. Extensive infarction of gray and white matter is associated with anteroposterior compression ratios of less than 20%.[11, 7] Based on a cadaveric study, the critical degree of anteroposterior compression necessary to induce histopathologic changes in the spinal cord has been suggested to be 30%.[31]

 

Treatment

Medical Care

A brief discussion of the natural history of symptomatic cervical spondylosis is necessary before discussing therapeutic intervention.

Cervical radiculopathy usually resolves without intervention. The long-term prognosis in cervical spondylotic myelopathy is less clear. Some patients experience a progressive decline, while most have long periods of stability of symptoms with intermittent exacerbations.

One study noted that 79% of patients with neck pain and/or referred pain syndromes and cervical spondylosis improved or became asymptomatic by the 15-year follow-up point.[32] Medical treatments for cervical spondylosis include neck immobilization, pharmacologic treatments, lifestyle modifications, and physical modalities (eg, traction, manipulation, exercises). No carefully controlled trials have compared these modalities; therefore, these therapies are often initiated based on a clinician's preference or specialty. Comparing the efficacy of these treatments against no treatment is difficult.

Neck immobilization (with a soft collar, Philadelphia collar, rigid orthoses, Minerva jacket, or a molded cervical pillow for support) is a common, nonoperative treatment for neck pain and/or suboccipital pain syndromes caused by spondylosis and cervical radiculopathy.

  • Despite widespread use, soft collars are largely believed to work by placebo effect because they do not appreciably limit motion of the cervical spine. They have not been demonstrated to change long-term outcomes. If worn properly, a soft collar maintains relative flexion. The collar should be worn as long as possible during the day. However, patient comfort is key.

  • As symptoms improve, the collar can be worn only during strenuous activity. Eventually, it can be discontinued. More rigid collars and devices may better limit motion of the cervical spine, but they may reduce muscle tone and cause neck stiffness from disuse. Implement a daily cervical exercise program to limit loss of muscle tone.

Pharmacologic treatment includes several options.

  • NSAIDs are the mainstay of pharmacologic treatment. They are effective in reducing the biologic effects of inflammation and pain. Their use should be monitored for adverse effects such as gastropathy, renal toxicity, hypertension, liver abnormalities, and bleeding. Selective inhibitors of cyclooxygenase-2 (COX-2) such as celecoxib can lower the risk of gastrointestinal toxicity, but recent studies have raised concerns of the association of this class of drugs with higher cardiovascular events, particularly at higher doses.

  • Patients who experience more chronic pain symptoms may benefit from tricyclic antidepressants (TCAs). Common side effects include dry mouth, sedation, urinary retention, constipation, and cardiac conduction blocks.

  • Muscle relaxants such as carisoprodol and cyclobenzaprine may also be beneficial in patients with a spasm in the neck muscles (which can be related to spondylotic changes).

  • Opioids could be considered in patients who have moderate-to-severe pain due to significant structural spondylosis, whose who are poor surgical candidates, and those who have failed nonopioid agents. For patients who are at risk for NSAID toxicity, particularly the geriatric population, opioids are reasonable alternatives.[33] However, opioids should be avoided if there is history of substance abuse or mood disorder.

  • Steroid use is controversial. In some patients with severe radiculopathy, a high-dose oral steroid taper may rapidly reduce pain and shorten the course of symptoms. Some patients with progressive cervical spondylotic myelopathy also may benefit. Epidural steroid injections may help patients with radicular symptoms. Patients who present within 8 hours of an acute central cord injury (which can be caused partly by ventral osteophytes) may benefit from high doses of methylprednisolone.

  • No placebo controlled trials have studied gabapentin in cervical spondylosis, but based on its efficacy in controlling neuropathic pain, it is often being used off label for chronic pain associated with cervical spondylosis.

Lifestyle modifications (eg, neck schools, instruction in body mechanics, relaxation techniques, postural awareness, ergonomics and/or workplace modifications) may alleviate symptoms.

  • Neck school is a form of small group therapy that provides techniques to patients who are willing to actively work toward recovery. It may be of limited clinical value.

  • Instruction in body mechanics focuses on low-load concepts. These include avoiding forward bending and rotation of the neck, avoiding prolonged extension of the neck, avoiding prolonged sitting or standing, and selecting the proper chair.

  • Workplace modifications and ergonomics serve to reduce strenuous neck positions during work and leisure.

Physical modalities are among the oldest treatments used for spine-related disorders.

Cervical mechanical traction, commonly used for cervical radiculopathy, in addition to cervical joint distraction, may loosen adhesions within the dural sleeves, reduce compression and irritation of discs, and improve circulation within the epidural space.

  • Studies regarding its efficacy are conflicting, with intermittent traction probably being more effective than static traction. Initially, a weight of 10 lb is recommended, eventually increasing to 20 lb as tolerated.

  • It can be used at home 2-3 times daily for 15 minutes at a time. It is contraindicated in patients who have myelopathy, a positive Lhermitte sign, or rheumatoid arthritis with atlantoaxial subluxation. A retrospective study found that cervical traction provided symptomatic relief in 81% of the patients with mild-to-moderately severe cervical spondylosis syndromes.[34]

Manipulation, most commonly practiced by chiropractors and osteopathic physicians, was described as early as 4000 years ago. It remains a popular treatment for back pain.

  • Techniques vary and include low-velocity, high-amplitude manipulation; high-velocity, low-amplitude manipulation (eg, thrusting or impulse manipulation); and nonthrusting maneuvers. Studies have reported conflicting results, and few well-controlled studies specifically concerning the treatment of cervical spondylosis symptoms have been published.

  • Contraindications to cervical manipulation include vertebral fractures, dislocations, infections, malignancy, spondylolisthesis, myelopathy, various rheumatologic and connective-tissue disorders, and the presence of objective signs of nerve root compromise. The most feared complication of cervical manipulation, vertebrobasilar artery dissection, is rare and almost impossible to predict despite multiple proposed risk factors.

Exercises designed for cervical pain include isometric neck strengthening routines, neck and shoulder stretching and flexibility exercises, back strengthening exercises, and aerobic exercises. Controlled trials regarding the efficacy of these routines are lacking.

Other commonly used modalities for pain include heat, cold, acupuncture, massage, trigger-point injection, transcutaneous electrical nerve stimulation, and low-power cold laser. Most of the passive modalities used for degenerative disease of the cervical spine are performed by physical therapists and are most efficacious in combination.

Surgical Care

Surgical care for cervical spondylosis involves anatomic correction of the degenerative pathologic entities that compress a nerve root or the spinal cord.

Indications for surgery include intractable pain, progressive neurologic deficits, and documented compression of nerve roots or of the spinal cord that leads to progressive symptoms. Surgery has not been proven to help neck pain and/or suboccipital pain. Several approaches to the cervical spine have been proposed. The approach selected is determined based on the type and location of pathology and the surgeon's preference.

Cervical radiculopathy traditionally has been approached either via the anterior approach, which was first described by Robinson and Smith in 1955, or the posterolateral approach, during which a "keyhole" foraminotomy is performed.

The anterior approach allows excellent access to midline disease and visualization of pathology without manipulation of neural elements. Robinson and Smith proposed that the anterior approach coupled with fusion using an iliac crest bone graft (autograft) arrests progressive spondylotic spurring, causes existing osteophytes to eventually regress as a result of spinal stability promoted by fusion, decompresses and enlarges the neural foramen and spinal canal by the distraction of the disk space, and minimizes surgical manipulation of the contents of the spinal canal, thereby minimizing complications.

More recently, use of allografts, which could be in form of bone graft obtained from cadavers, or ventral cervical plating have become more popular as they eliminate morbidity of harvesting the graft.[35] Success of fusion is higher with autografts due to the presence of endogenous morphogenetic proteins that are present in the harvested bones and help with osteoinduction. Research is being performed on the use of recombinant human morphogenetic proteins to improve success of fusion with allografts.[36]

When performed with fusion, anterior cervical diskectomy (ACD) yields good-to-excellent results in almost 90% of patients when no other level of spondylosis is present. When adjacent levels of spondylosis were demonstrated, only 60% of patients had good-to-excellent results.

ACD without fusion has been used based on the nonexistent correlation between successful fusion and clinical outcome and the significant incidence of pseudoarthrosis following ACD and fusion (10-20%). The advantage of this procedure is the lack of bone graft–related complications and decreased manipulation and dissection of the cervical tissues. Patients who do not undergo fusion often report a shorter postoperative hospital stay and an earlier return to daily activities.

ACD without fusion almost inevitably is followed by disk-space collapse. This procedure does not accomplish disk-space distraction and does not mechanically open the neural foramina. It does not promote stabilization of the motion segment to promote resorption of osteophytes. As a result, most surgeons choose ACD with fusion for patients with cervical radiculopathy when taking an anterior surgical approach. Instability of the cervical spine is rarely reported following ACD with or without fusion, but the incidence of postoperative neck pain is higher without fusion.

The posterolateral approach to cervical radiculopathy has similar results to the anterior approach when used for the proper indications. This approach is associated with greater initial postoperative discomfort but avoids the possibility of graft dislodgment and damage to neck structures. It is best used for nerve root decompression, when the pathologic entity is a lateral spondylotic spur or soft disk. In this approach, a keyhole foraminotomy is made by removing the medial third of the facet joint and the most lateral aspects of the lamina at the involved level and side. The underlying lateral aspect of the ligamentum flavum is then removed to visualize the nerve root. The nerve root is unroofed posteriorly, superiorly, and inferiorly so that it lies free and without tension.

The impact of facetectomies on the stability of the cervical spine has been questioned. Bilateral 50% facetectomies have been demonstrated to expose the nerve by 3-5 mm without a notable effect on stability. Bilateral facetectomies of 70% reduced the ability of the spine to withstand stresses, while increasing the exposure of the nerve root. In all likelihood, maintenance of the interspinous and most of the interlaminar ligaments is important for preserving stability in patients undergoing foraminotomy.

Surgical intervention for cervical spondylotic myelopathy is controversial.

In 1992, a thorough review of the literature pertaining to surgery for cervical spondylotic myelopathy concluded that the chances for improvement after surgery for cervical spondylotic myelopathy were approximately 50%. The conclusion was that large multicenter trials are needed to determine the benefit of surgery and to establish criteria for the operation/approach of operation. Also noted was that diagnostic errors still occur, namely with amyotrophic lateral sclerosis and multiple sclerosis.[37]

Risks of surgery are another concern. The older literature reviewed by Rowland has been criticized because of uncertainty as to whether nonspondylotic causes of myelopathy were excluded prior to surgery. With current early intervention strategies tailored to the pathophysiology of myelopathy, final outcomes clearly exceed expectant outcomes. Rowland noted in his proposed trial guidelines that patients with rapid progression of myelopathy may be allowed access to surgery without a trial of conservative therapy.

In the United States, cervical immobilization with a collar or brace is the most commonly used therapy for cervical spondylotic myelopathy. Studies demonstrate conflicting results regarding efficacy of this treatment.

Researchers have reported that symptomatic patients may deteriorate neurologically during bracing; thus, surgery is usually recommended in patients with moderate-to-severe disability or frank myelopathy. Because of the possible progressive character of cervical spondylotic myelopathy, some advocate a more aggressive approach to the disease to strive for improved outcomes.

The natural history of cervical spondylotic myelopathy is highly variable. The older literature notes the natural course of cervical spondylotic myelopathy to be that of progressive disability and deterioration in neurologic function. Nurick, however, noted that a period of initial deterioration occurs, followed by a clinical plateau that lasts for several years, during which disability does not worsen for those with mild cervical spondylotic myelopathy. He noted that older patients deteriorate more frequently and, thus, advocates surgery for those older than 60 years and for those with progressive decline in neurologic function.[38]

Another factor that must be taken into consideration is that patients with cervical spondylotic myelopathy may be at risk for significant spinal cord injury, even with minor trauma. This argument, in addition to improved surgical outcomes in those with decreased duration of symptoms, has been used as an argument supporting surgery.

Nevertheless, a Cochrane review found the natural course of cervical spondylotic myelopathy to be highly variable for patients with mild-to-moderate symptoms, in whom the review noted the disease to often remain static and symptoms to occasionally improve.[39] Similarly, for mild-to-moderate cervical spondylotic myelopathy, a 3-year prospective randomized trial found no significant difference between patients who were treated surgically and those who were treated conservatively.[40]

Excellent results have been demonstrated for patients undergoing surgical intervention. One prospective trial of 503 patients undergoing conservative management for cervical spondylotic myelopathy versus surgery reported that patients treated surgically had better outcomes than those treated medically and that medical treatment did not significantly alter neurologic outcomes.[41]

Accurately prognosticating the course of disability for any given individual with cervical spondylotic myelopathy is difficult. Once moderate signs and symptoms develop, however, surgical intervention is likely to be beneficial over further medical treatment.

The primary goal of surgery for cervical spondylotic myelopathy is decompression of the spinal cord.[42] Traditionally, for cervical laminectomy, a posterior approach has been the treatment of choice. During the previous 20 years, laminectomy has increasingly been recognized as not appropriate for all patients. Neurologic deterioration, which has been reported after laminectomy, has been attributed to the development of spinal instability and kyphotic deformities. Laminectomy also is unable to address ventral osteophytic overgrowth via a posterior approach. Through an anterior cervical approach, one can directly remove osteophytes, disk material, and even vertebral bodies, if necessary, to decompress the cord. With interposition of bone grafts and, in some instances, cervical plates (ie, instrumentation), neck instability can be prevented.

The sagittal alignment of the cervical spine is important in choosing an approach for decompressing the cervical cord in cervical spondylotic myelopathy.

Preoperative lordotic alignment of the cervical spine is necessary in order to maintain maximal benefit from posterior decompression. This is because of both the direct decompression of the cord achieved by surgical removal of compressive elements (eg, ligamentum flavum, bone) and the indirect decompression achieved ventrally by posterior drift of the spinal cord.

Fixed local or global kyphosis, therefore, may be a relative contraindication for posterior decompression.[43] In the case of kyphosis, general insufficiency of the anterior column is caused by degenerative changes in diskoligamentous structures, leading to neutralization or inversion of the physiologic cervical lordosis. Because of kyphosis, the cord shifts forward and is compressed by anterior osteophytes.

In cases of combined anterior compression and posterior bulging of the ligamentum flavum causing narrowing of the vertebral canal, a combined anteroposterior approach may be recommended.

The posterior approach (often advocated by Japanese surgeons) is also accepted as a standard decompression procedure in patients who have more than 3 segments of stenotic changes. The anterior approach involves an extensive resection.

Laminoplasty (a modern approach) and its variants preserve the lamina to avoid excessive scar formation and to reduce the incidence of postlaminectomy kyphosis. Excellent laminoplasty results have been reported for the treatment of multilevel cervical spondylotic myelopathy.[44] Additionally, long-term results with laminoplasty have been reported with fewer late complications then laminectomy.[45] Nevertheless, some authorities advocate laminectomy.[2, 46] Laminectomy combined with lateral mass fusion may yield excellent results without progression to spinal instability or kyphosis.[47, 48, 49]

The anterior approach is advocated for cervical spondylotic myelopathy when identifiable anterior compression or kyphotic deformity is present. This approach is more frequently used in the United States because ventral compression is more common. Myelopathy due to osteophytes confined to 1-2 levels is treated using ACD and fusion with removal of the osteophytes. In severe cases, extensive decompression is performed using multilevel vertebrectomies (corpectomy) and reconstruction with bone graft and instrumentation. Recent series have reported clinical improvement rates ranging from 80-94%.[50, 51] Neither the anterior nor posterior approach has been demonstrated superior to the other, provided the appropriate procedure is performed for the proper clinical indication.[2, 52, 46]

Minimally invasive surgical techniques are being developed for management of cervical spondylosis causing foraminal or central canal stenosis manifesting as radiculopathy, myelopathy or both. In these cases, dorsal laminoforaminotomy can be performed with minimally invasive techniques using microendoscope and tubular retractor system. Typically, these cases are performed with electromyographic and somatosensory evoked potential monitoring. The goal of these techniques is to minimize injury to surrounding tissue, which leads to better outcomes with less pain.[53]

Artificial cervical disks were approved by the US Food and Drug Administration (FDA) in 2007 and are now being offered as an alternative to spinal fusion in some selected patients. Replacement with an artificial disk can potentially preserve natural neck motion and thereby reduce stress and prevent degeneration of adjoining cervical disks. A study comparing artificial cervical disk replacement with cervical fusion concluded that patients who had undergone artificial cervical disk replacement had faster recovery than their counterparts.[54] Currently, artificial cervical disk replacement is only offered for 1 level disk disease. Artificial disk replacement at 2 level disease is being performed in Europe but is considered investigational in the United States.

Of note, the number of geriatric patients seeking surgical treatment for cervical spondylotic myelopathy is steadily increasing. One study demonstrated that corrective surgical techniques could be performed in patients older than 70 years, with acceptable risk of morbidity and reasonable expectation for clinical improvement.[55]

 

Medication

Medication Summary

The goal of pharmacotherapy is to reduce pain and inflammation.

Nonsteroidal anti-inflammatory drugs

Class Summary

Used most commonly for the relief of mild to moderate pain. Although the effects of NSAIDs in the treatment of pain tend to be patient specific, ibuprofen is usually the DOC for initial therapy. Other options include naproxen and diclofenac.

Ibuprofen (Motrin, Advil, Haltran, Nuprin)

Inhibits inflammatory reactions and pain by decreasing activity of COX, which results in prostaglandin synthesis.

Naproxen (Aleve, Anaprox, Naprelan, Naprosyn)

Relieves mild to moderate pain; inhibits inflammatory reactions and pain, probably by decreasing activity of COX, which results in decreased prostaglandin synthesis.

Diclofenac (Voltaren)

Has analgesic, antipyretic, and anti-inflammatory activity; inhibits inflammatory reactions and pain, probably by decreasing activity of COX, which results in prostaglandin synthesis.

Corticosteroids

Class Summary

Used for potent anti-inflammatory activity and relieve inflammation associated with cervical radiculopathy.

Prednisone (Sterapred)

Decreases inflammation by suppressing migration of PMN leukocytes and reversing increased capillary permeability.

Methylprednisolone (Adlone, Medrol, Solu-Medrol, Depo-Medrol, Depopred)

Decreases inflammation by suppressing migration of PMN leukocytes and reversing increased capillary permeability.

Tricyclic antidepressants

Class Summary

A complex group of drugs that has central and peripheral anticholinergic effects and sedative effects. They block the active reuptake of norepinephrine and serotonin.

Amitriptyline (Elavil)

Increases synaptic concentration of serotonin and/or norepinephrine in CNS by inhibiting their reuptake at presynaptic neuronal membrane; useful as an analgesic for certain chronic and neuropathic pain.

Nortriptyline (Aventyl hydrochloride, Pamelor)

Effective in treatment of chronic pain; by inhibiting reuptake of serotonin and/or norepinephrine at the presynaptic neuronal membrane, it increases their synaptic concentration; additional pharmacodynamic effects (eg, desensitization of adenyl cyclase, down-regulation of beta-adrenergic receptors and serotonin receptors) appear to be involved.

Cyclooxygenase 2 inhibitors

Class Summary

Although increased cost can be a negative factor, incidence of costly and potentially fatal GI bleeding is clearly less with COX-2 inhibitors than with traditional NSAIDs. Ongoing analysis of cost avoidance of GI bleeding will further define populations that most benefit from COX-2 inhibitors.

Celecoxib (Celebrex)

Inhibits primarily COX-2, which is considered an inducible isoenzyme induced during 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 for each patient.

Muscle relaxants

Class Summary

Reduce associated cervical muscle spasm.

Carisoprodol (Soma)

Short-acting medication that may have depressant effects at spinal cord level.

Cyclobenzaprine (Flexeril)

Skeletal muscle relaxant that acts centrally and reduces motor activity of tonic somatic origins, influencing both alpha and gamma motor neurons; structurally related to TCAs and thus carries some of same liabilities.

Opiates

Class Summary

For use in short-term management of acute pain.

Hydrocodone and acetaminophen (Vicodin, Lortab, Norcet, Margesic, Lorcet-HD)

Drug combination indicated for moderately severe to severe pain.

Oxycodone and acetaminophen (Percocet, Roxicet, Roxilox, Tylox)

Drug combination indicated for relief of moderately severe to severe pain.

 

Questions & Answers

Overview

What is cervical spondylosis?

What are the degenerative changes that occur in response to cervical spondylosis?

What are the treatment options for cervical spondylosis?

What is the pathophysiology of cervical spondylosis?

What is the role of ossification of the posterior longitudinal ligament in the pathophysiology of cervical spondylosis?

What is the pathophysiology of cervical spondylotic myelopathy in spondylosis?

What causes cord compression in patients with cervical spondylotic myelopathy?

What is the role of spinal cord ischemia in the pathophysiology of cervical spondylosis?

How does stretch-associated injury contribute to the pathophysiology of cervical spondylosis?

What is the frequency of cervical spondylosis?

What is the prevalence of cervical spondylosis?

Presentation

What are the manifestations of the clinical syndromes seen with cervical spondylosis?

What is the most common syndrome of cervical spondylosis?

What are the signs and symptoms of cervicalgia in cervical spondylosis?

How is headache characterized in cervical spondylosis?

What are the signs and symptoms of radiculopathy in cervical spondylosis?

What causes paraparesis and tetraparesis in cervical spondylosis?

What are the early symptoms of cervical spondylosis?

What are the manifestations of muscle weakness in cervical spondylosis?

What are the urologic symptoms cervical spondylosis?

How does cervical spondylosis affect quality of life?

What are the signs and symptoms of central cord syndrome in cervical spondylosis?

How is dysphagia managed in cervical spondylosis?

Which physical findings are characteristic of cervical spondylosis?

What is the significance of winging of the scapula in cervical spondylosis?

What is included in the physical exam for cervical spondylosis?

What is the role of the neck compression test in the evaluation of cervical spondylosis?

What are the most typical exam findings of cervical spondylosis?

What is the role of the pectoralis muscle reflex test in the evaluation of cervical spondylosis?

How are the triceps and/or hand intrinsic muscles examined in the evaluation of cervical spondylosis?

Which lower extremity findings suggest cervical spondylosis?

What is the significance of gait in the evaluation of cervical spondylosis?

What is the role of the Lhermitte sign in the evaluation of cervical spondylosis?

Which sensory abnormalities are characteristic of cervical spondylosis?

What are the risk factors for cervical spondylosis?

DDX

Which conditions should be included in the differential diagnoses of cervical spondylosis?

What are the differential diagnoses for Diagnosis and Management of Cervical Spondylosis?

Workup

What is the role of lab findings in the workup of cervical spondylosis?

What is the imaging study of choice for the diagnosis of cervical spondylosis?

What are the benefits of MRI in the workup of cervical spondylosis?

What is the role of plain radiography in the workup of cervical spondylosis?

What is the role of MRI in the workup of cervical spondylosis?

What is the sensitivity of MRI in the diagnosis of cervical spondylosis?

What are the benefits of plain films in the workup of cervical spondylosis?

What are the benefits of CT scanning in the workup of cervical spondylosis?

What are the benefits of myelography in the workup of cervical spondylosis?

How is diffusion tensor imaging (DTI) used in the workup of cervical spondylosis?

What is the role of electrodiagnostic studies in the workup of cervical spondylosis?

What is the role of somatosensory and cortical motor evoked potentials in the workup of cervical spondylosis?

Which histologic findings are characteristic of cervical spondylosis?

Which histologic finding is associated with anteroposterior compression in cervical spondylosis?

Treatment

What should be discussed prior to selection of therapeutic intervention of cervical spondylosis?

What is the long-term prognosis of cervical spondylosis?

What are the medical treatment options for cervical spondylosis?

What is the role of neck immobilization in the treatment of cervical spondylosis?

What is the role of medications in the treatment of cervical spondylosis?

What is the role of lifestyle modifications in the treatment of cervical spondylosis?

When are physical modalities used for the treatment of cervical spondylosis?

What is the role of cervical mechanical traction in the treatment of cervical spondylosis?

What is the role of cervical manipulations in the treatment of cervical spondylosis?

Which exercises are designed to treat pain in cervical spondylosis?

What are the options for pain management in cervical spondylosis?

What is the goal of surgical care for cervical spondylosis?

What are the indications for surgery in cervical spondylosis?

What are the surgical approaches for cervical radiculopathy in spondylosis?

What is the role of allografts in the surgical treatment of cervical spondylosis?

What is the efficacy of anterior cervical diskectomy (ACD) for cervical spondylosis?

What is the role of anterior cervical diskectomy (ACD) without fusion in the surgical treatment of cervical spondylosis?

What are the benefits of the posterolateral approach to cervical radiculopathy for cervical spondylosis?

What is the role of facetectomies in the surgical treatment of cervical spondylosis?

What is the efficacy of surgical intervention for cervical spondylotic myelopathy in spondylosis?

What are the risks of surgery for cervical spondylotic myelopathy?

What is the most commonly used therapy for cervical spondylotic myelopathy in the US?

When is surgery indicated in the treatment of cervical spondylotic myelopathy?

What is the natural history of cervical spondylotic myelopathy?

How do surgical and medical treatment outcomes for cervical spondylotic myelopathy compare?

When should surgery be considered in the treatment of cervical spondylotic myelopathy?

What is the primary goal of surgery for cervical spondylotic myelopathy?

How does sagittal alignment of the cervical spine affect treatment selection in cervical spondylosis?

What is the role of lordotic alignment of the cervical spine in the treatment of cervical spondylosis?

What are contraindications for posterior decompression in cervical spondylosis?

When is a combined anteroposterior surgical approach indicated in the treatment of cervical spondylosis?

Which surgical approach is recommended for more than 3 segments of stenotic changes in cervical spondylosis?

What is the role of laminoplasty in the treatment of cervical spondylosis?

When is the anterior surgical approach indicated for cervical spondylotic myelopathy?

What is the role of minimally invasive surgical techniques in the treatment of cervical spondylosis?

What is the role of artificial cervical disks in the treatment of cervical spondylosis?

How safe is surgery for cervical spondylotic myelopathy in geriatric patients?

Medications

What is the goal of drug treatment for cervical spondylosis?

Which medications in the drug class Opiates are used in the treatment of Diagnosis and Management of Cervical Spondylosis?

Which medications in the drug class Muscle relaxants are used in the treatment of Diagnosis and Management of Cervical Spondylosis?

Which medications in the drug class Cyclooxygenase 2 inhibitors are used in the treatment of Diagnosis and Management of Cervical Spondylosis?

Which medications in the drug class Tricyclic antidepressants are used in the treatment of Diagnosis and Management of Cervical Spondylosis?

Which medications in the drug class Corticosteroids are used in the treatment of Diagnosis and Management of Cervical Spondylosis?

Which medications in the drug class Nonsteroidal anti-inflammatory drugs are used in the treatment of Diagnosis and Management of Cervical Spondylosis?