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Cervical Spondylosis, Diagnosis and Management

Author: Sandeep S Rana, MD, Clinical Associate Professor of Neurology, Drexel University College of Medicine
Contributor Information and Disclosures

Updated: Aug 14, 2009

Introduction

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 pr...

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.

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A 48-year-old man presented with neck pain and pr...

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.

Frequency

International

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

Mortality/Morbidity

See Background, Pathophysiology, and History.

Race

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

Sex

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

Age

See Sex.

Clinical

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.

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References
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Further Reading

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Keywords

cervical spondylosis, cervical spondylosis treatment, cervical degenerative joint disease, cervical spine, cervical degenerative disk disease, cervical osteoarthritis, cervical spondylotic myelopathy, CSM, disk degeneration, degenerative cervical disease, osteophytic bars, cervical radiculopathy, neck pain, shoulder pain, cervicalgia, chronic suboccipital headache, paresthesias, pseudoangina, breast pain, nontraumatic paraparesis, nontraumatic tetraparesis, numbness, clumsy hands, loss of manual dexterity, difficulty with writing, central cord syndrome, Tinel sign, Spurling sign, Babinski sign, Hoffman sign, pectoralis muscle reflex, spastic gait, Lhermitte sign

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Contributor Information and Disclosures

Author

Sandeep S Rana, MD, Clinical Associate Professor of Neurology, Drexel University College of Medicine
Sandeep S Rana, MD is a member of the following medical societies: American Academy of Neurology, American Society of Neuroimaging, and Pennsylvania Medical Society
Disclosure: Nothing to disclose.

Medical Editor

William J Nowack, MD, Associate Professor, Epilepsy Center, Department of Neurology, University of Kansas Medical Center
William J Nowack, MD is a member of the following medical societies: American Academy of Neurology, American Clinical Neurophysiology Society, American Epilepsy Society, American Medical Electroencephalographic Association, American Medical Informatics Association, and Biomedical Engineering Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

James H Halsey, MD, Professor, Department of Neurology, University of Alabama Medical Center
James H Halsey, MD is a member of the following medical societies: American Academy of Neurology, American Heart Association, American Medical Association, American Neurological Association, American Society of Neuroimaging, Medical Association of the State of Alabama, New York Academy of Sciences, Pan American Medical Association, Sigma Xi, Society for Neuroscience, and Southern Medical Association
Disclosure: Nothing to disclose.

CME Editor

Selim R Benbadis, MD, Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, University of South Florida School of Medicine, Tampa General Hospital
Selim R Benbadis, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society, and American Medical Association
Disclosure: UCB Pharma Honoraria Speaking, consulting; Lundbeck Honoraria Speaking, consulting; Cyberonics Honoraria Speaking, consulting; Glaxo Smith Kline Honoraria Speaking, consulting; Ortho McNeil Honoraria Speaking, consulting; Pfizer Honoraria Speaking, consulting; Sleepmed/DigiTrace  Speaking, consulting

Chief Editor

Howard A Crystal, MD, Professor, Departments of Neurology and Pathology, State University of New York Downstate; Consulting Staff, Department of Neurology, University Hospital and Kings County Hospital Center
Howard A Crystal, MD is a member of the following medical societies: American Academy of Neurology and American Neurological Association
Disclosure: Medivations Honoraria Consulting

 
 
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