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Cervical Radiculopathy
Cervical Radiculopathy Daniel Roth, DO, MBA, MS, Ai Mukai, MD, Priya Thomas, BS, Thomas H. Hudgins, MD, and Joseph T. Alleva, MD, MBA Neck pain is a common complaint in the U.S. It is estimated that 30%-50% of adults will experience neck pain in a given year.1 Neck and back pain together account for about 65% of cases of disability, although neck pain less frequently leads to disability claims.2 Interestingly, neck pain has the highest frequency in those working in hospitals and offices, while those working in industrial/service and forestry sectors have the lowest frequency of neck pain.3 Women tend to have higher rates of trauma-related neck pain and demonstrate greater spinal motions. This may be related to men having anatomically wider and longer disk facet depth than women.4 Between 1993 and 1995 cervical spine conditions consumed 696,000 bed days during 161,000 hospitalizations with an average of 4.3 days per stay. About 13,000 men were admitted more commonly with trauma and 17,000 women were admitted more commonly with degenerative conditions.5 Bovim and colleagues published a prevalence study in which 35% of the general Norwegian population reported neck pain within the past year. Approximately 14% of respondents reported neck pain lasting more than 6 months.6 In a study done in Finland, 9.5% of men and 13.5% of women reported chronic neck pain syndrome.7 In North America, the Saskatchewan Health and Back Pain Survey reported 54% of respondents experienced neck pain in the previous 6 months, of which almost 5% said pain was highly disabling.8 Risk factors that have been identified for cervical degeneration include the following: Strongly Implicated 1. 2. 3. 4.
Cigarette smoking Axial load-bearing High-risk occupation: meat carriers, dentists, professional drivers Prior lumbar radiculopathy
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Possibly Implicated 1. 2. 3. 4. 5. 6. 7. 8. 9.
Metabolic disturbance Prior cervical trauma Vibrational exposure Diet/nutritional factors Genetic factors Racial factors Gender Atherosclerosis Auto-immune factors
No Role Identified 1. Repeated turning of the neck 2. Sports 3. Sedentary occupations Several pathologies can cause pain originating from the cervical spine. Herniated nucleus pulposus (HNP) is a condition in which the central part of an intervertebral disk gets pushed out, which can cause neck pain from the inflammatory response or nerve dysfunction from the inflammation or mechanical compression of spinal nerves. Spinal stenosis is a narrowing of the spinal canal or the intervertebral foramina, which is usually a result of spondylosis or cervical degenerative disk disease (DDD). Spinal stenosis can occur from bone spurs, or osteophytes, from spondylolisthesis, or slipping of 1 vertebral body on another, or from ligamentous thickening causing compression. If the narrowing causes spinal nerve dysfunction, patients can acquire radicular symptoms. If there is cord compression, or myelopathy, bowel and bladder dysfunction, as well as motor and sensory deficits, may result. HNP and DDD and its related pathologies including stenosis are the most common cervical pathologies causing radicular symptoms. HNP accounts for about 20%-25% of cervical radiculopathies and DDD accounts for about 70%-75%.
Anatomy The cervical spine has 7 vertebrae (C1-C7) and 8 spinal nerves (C1-C8). The C1 vertebra is called the atlas and is a ring of bone, which rotates around the odontoid process of the axis, or the C2 vertebra. Between 2 vertebrae are 2 openings called the foramen, where a spinal nerve, blood vessels, and the sinuvertebral nerves pass through. The superior and inferior borders of this foramen are the pedicles, the anterior border is the 738
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intervertebral disk and vertebral bodies, and the posterior border is the facet, or zygapophyseal joint. In 1%-15% of the population, a bony arch may form converting the groove on C1 for the vertebral artery and the first cervical nerve into an arcuate foramen.1 There is also a spinal canal that is bordered by the laminae and the ligamentum flavum posteriorly and anteriorly by the vertebral bodies and intervertebral disks. The midsagittal (anteroposterior) diameter of the canal in the upper cervical spine (C1-3) is about 21 mm, whereas the lower cervical spine (C4-7) is 18 mm. The cervical spinal cord usually occupies about 40% of the cervical canal. Cervical extension decreases the canal diameter by 2-3 mm.9 The posterior longitudinal ligament stretches from the axis to the sacrum and is the anterior border of the spinal canal. It is broader in the cervical and thoracic spine compared to the lumbar spine. The ligamenta flava are ligaments between the laminae. This ligament can thicken with age and can contribute to cervical canal stenosis, which can lead to myelopathy and radicular symptoms. The occiput and the first cervical vertebra (atlas) form the atlantooccipital joint and have about 1/3 of flexion and extension and 1/2 of lateral bending of the cervical spine. The occipitovertebral ligaments connect the occiput to the atlas and permit flexion and extension of the joint. The C1-C2 joint, or the atlanto-axial joint, has no disk between them and has about 1/2 of rotational range of motion. The transverse ligament of the atlas holds the odontoid process in place and is stronger than the odontoid process itself. There is also a pair of alar ligaments on both sides of the occipital condyles, which limit rotation. Normal cervical spine has a shallow lordosis, which can be decreased or even reversed in patients with degenerative changes and increased in patients with increased thoracic kyphosis. The intervertebral disks provide support to the cervical spine while maintaining mobility. The disk is comprised of a nucleus polposus, surrounded by the annulus fibrosus. The annulus is primarily composed of type 1 collagen, while the nucleus pulposus is composed predominantly of type 2 collagen. The collagen fibers of the annulus are arranged in 15-25 layers of alternating obliquely arranged fibers, which allows for mobility and provides tensile strength. The collagen fibers attach to the vertebral bodies, the anterior and posterior longitudinal ligaments, and the vertebral endplates. The type 2 collagen, proteoglycan, and hyaluronan long chains that comprise the nucleus pulposus have negatively charged branching side chains that are very hydrophilic, which maintain that “hydration” of the disk. The vascular supply of the cervical spine originates from the vertebral DM, December 2009
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arteries and its segmental medullary arteries, which send anterior and posterior branches to the spinal cord along the ventral and dorsal roots. In the cervical spine, the anterior spinal artery can become occluded in hyperextension injuries with cervical canal stenosis and spondylosis, which can cause ischemia to the anterior 2/3 of the cord. Each cervical spinal nerve has a ventral and a dorsal spinal root. The ventral horn of the spinal cord contains alpha motor neurons, which give off efferent motor fibers in the ventral root. The dorsal root ganglion and its afferent sensory fibers travel in the dorsal root. The ventral and dorsal root combine to form a spinal nerve, which then divides into the dorsal primary ramus and the ventral primary ramus. The dorsal ramus supplies the posterior neck structures, whereas the ventral ramus supplies prevertebral and paraspinal muscles and then forms the brachial plexus, which then go on to innervate the upper limb. A myotome is a group of muscles innervated by 1 spinal nerve. A dermatome is the sensory distribution of a dorsal root.10 The myotome, dermatome, and muscle stretch reflexes can help localize the level of the cervical radiculopathy and radiculitis.
Pathology Cervical degenerative disease is a spectrum of clinical syndromes associated with neck pain and neurologic symptoms. It includes spondylotic degeneration, disk displacement with radiculopathy, and cervical spondylotic myelopathy. The first description of myelopathy was in 1838 of a patient with a spondylotic bar into the spinal canal and reducing area by 1/3. There is a consensus on nomenclature for HNP in the lumbar spine, specifically, disk bulge, protrusion, extrusion, and sequestration. Currently, there is no consensus on nomenclature for HNP in the cervical spine because there are anatomic differences in the cervical spine when compared to the lumbar spine.11 Regardless of lack of nomenclature, HNP does cause pain in the cervical spine. The disk is thought to start degenerating in the second decade with repetitive strain causing posterolateral annular tear, circumferential tears causing radial fissures, and nuclear material extrusion through these tears causing disk desiccation and nuclear degradation. HNP causes radicular pain through chemical radiculitis from proteoglycans and phospholipases released from the nucleus pulposus, which propagate an inflammatory cascade, and from direct nerve injury/compression, which can lead to nerve demyelination and neurologic symptoms. DDD can cause mechanical nerve root compression in the intervertebral foramen from decreased disk height, 740
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foraminal hypertrophy, ligamentum hypertrophy, spondylolisthesis, and periradicular fibrous tissue. In cervical disk degeneration, the nucleus pulposus desiccates and loses mechanical competence, which increases strain on the annulus, leading to tearing of the annulus and disk protrusion. The disk protrusion itself can cause root or cord impingement, which can cause various nerve dysfunction symptoms including sensory and motor changes. This disk collapse translates into excess motion in the zygapophyseal joints posteriorly and increased strain in the supporting ligaments.12 Degenerative changes affect all levels but is relatively less common above C3-C4 disk.13 Most commonly the C5-6 disk space (affect C6 nerve root) followed by C6-7 (C7 nerve root) are affected. Cervical spondylotic radiculopathy starts about 10 years after the disk starts to degenerate, and the mechanical incompetence of the motion segment leads to spondylotic degeneration of facets and uncovertebral joints.13 As the disk loses height, uncovertebral joints come into contact leading to osteophyte formation. The zygapophyseal joints override and also form osteophytes. These osteophytes are also called “hard” disk protrusions and can themselves compress nerves. Spondylotic radiculopathy patients are more likely to complain of multilevel or bilateral radicular symptoms.12,13 Cervical spondylotic myelopathy happens when degeneration of spine with osteophyte formation causes compression of the central spinal canal, affecting cord function through vascular insufficiency and direct mechanical pressure. Cervical spondylosis accounts for more than half of all cervical myelopathy cases. Compression of the spinal cord and nerve roots by herniation of nucleus pulposus in cervical region is the most common cause of spinal cord dysfunction in patients older than 55 years. Myelopathy is most common at C5-6, then C4-5, C6-7, C3-4. Five categories of spondylotic myelopathy exist, as follows: 1. Most common—transverse lesion syndrome (corticospinal and spinothalamic tracts) so upper motor neuron (UMN) weakness with gait difficulties and lower extremity spasticity 2. Motor syndrome, mostly corticospinal or anterior horn cell—rare sensory, motor weakness, and gait difficulties 3. Central cord syndrome—mostly central gray matter of cord so upper motor and sensory involvement with lower extremity sparing 4. Brown-Sequard syndrome unilateral cord lesion with ipsilateral hemiparesis from corticospinal tract involvement with contralateral pain DM, December 2009
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and temperature analgesia reported below level of lesion best prognosis for recovery 5. Brachialgia cord syndrome typically predominant upper limb pain with some associated long tract involvement—lower motor neuron flaccid weakness in upper extremities may be combined with spastic UMN lower extremity involvement.
Diagnosis History As with any disease entity, obtaining a thorough and detailed history is important to establish a diagnosis of cervical radiculopathy and/or stenosis. The physician should first determine the chief complaint (pain, numbness, weakness, location of symptoms). In greater than 70% of cervical radiculopathy or stenosis, pain is the primary presenting feature. A visual analog scale from 0 to 10 can be used to determine the patient’s perceived level of pain. Additionally, anatomic pain drawings can also be helpful in giving the physician a quick review of the patient’s pain pattern, which will be helpful in narrowing the differential diagnosis.14,15 Acquiring a specific timeline is also important to addressing the cause of pain. Previous episodes of similar symptoms or localized neck pain are important for the diagnosis and ultimate treatment. Symptoms suggestive of a cervical myelopathy, such as changes in gait, bowel, or bladder dysfunction, or lower extremity sensory changes or weakness should also be obtained. The examiner should ask what previous treatments have been tried, including the use of ice and/or heat and medications such as acetaminophen, aspirin, nonsteroidal anti-inflammatory medications, and steroids. Questions regarding previous medical treatment should also include physical therapy, traction, manipulation, previous injection therapy, or surgical treatments. A complete social history should include the patient’s occupation, sport and position, hobbies, and the use of nicotine and/or alcohol.15 The typical patient with cervical radiculopathy or stenosis presents with an insidious onset of neck and arm pain. The discomfort can range from a dull ache to a severe burning pain. Typically, pain is referred to the medial border of the scapula, and the patient’s chief complaint is lower neck or shoulder pain. As the condition progresses, the pain radiates to the upper or lower arm and into the hand, along the sensory distribution of the nerve root(s) that is involved. The older patient may have had previous episodes of neck pain or give a history of having spondylosis of the cervical spine that may have been previously diagnosed by another 742
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physician. It is important to recognize that acute disk herniations, and sudden narrowing of the neural foramen, may also occur in injuries involving cervical extension, lateral bending, or rotation with axial loading. These patients usually complain of increased pain with neck positions that cause foraminal narrowing including extension, lateral bending, or rotating toward the symptomatic side. Some patients report a reduction in their radicular-type symptoms by abducting their shoulder and placing their hand behind their head. This relief in symptoms is thought to occur by decreasing tension at the nerve root. Patients may complain of sensory changes along the involved nerve root dermatome, which can include tingling, numbness, or loss of sensation. Some patients may complain of motor weakness. A very small percentage of patients will present only with weakness, without significant pain or sensory complaints.16
Differential Diagnosis The differential diagnosis of neck pain is quite expansive and includes the following conditions: 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) Frozen shoulder syndromes Glenohumeral arthritis Gout (infrequently) Heart disease DM, December 2009
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Hyperabduction syndrome Intervertebral osteoarthritis Idiopathic brachial plexopathy Intrinsic neoplasia Nerve injuries Occipital neuralgia Osteomyelitis Osteoarthritis of apophyseal joints Paget’s disease Pancoast’s tumor Pharyngeal infections Postural disorders Psychogenic disorders Rheumatoid arthritis Rib-clavicle compression Rotator cuff tears and tendonitis Scalene muscle tightness Septic arthritis Spinal cord tumors Sternocleidomastoid tendinitis Subacromial bursitis Synovial cysts Tabes dorsalis Thoracic disk Thoracic outlet syndrome Tropical spastic paraparesis An important aspect of narrowing the differential diagnosis in cervical spine pain includes factors such as the length and nature of the symptoms, and whether the pain began insidiously or acutely. Establishing a working diagnosis and using the following information on physical examination and diagnostic testing will help to ascertain the appropriate diagnosis.1,14,15,17
Physical Examination Observation. The physical examination begins with observation of the patient during the history portion of the evaluation. This includes head and neck posture and movement during normal conversation. Typically, the patient exhibits a head tilt away from the side of injury and may hold his or her neck stiffly. Active range of motion is usually reduced, particularly in extension, rotation, and lateral bending, either toward or 744
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away from the affected nerve root. Increased pain with lateral bending away from the affected side can cause increased displacement of a disk herniation on a nerve root, whereas ipsilateral pain would suggest an impingement of a nerve root at the site of the neural foramen.18 The clinician should also look for asymmetries of the neck, shoulders, back, hips, and legs by inspecting the patient in the standing position from anterior, posterior, and lateral viewpoints. A patient with cervical radiculopathy and/or stenosis may have a change in the normal cervical lordosis or thoracic kyphosis.15 Palpation. On palpation, tenderness is usually noted along the cervical paraspinal muscles, usually more pronounced along the ipsilateral side of the affected nerve root. Muscle tenderness may be present along the muscles where the symptoms are referred (eg, medial scapula, proximal arm, lateral epicondyle). Associated hypertonicity or spasm on palpation in these painful muscles may occur. The areas over the bony elements of the spine should also be palpated, especially the spinous processes and articular pillars of the cervical spine. In any patient with cervical pain, the examiner needs to evaluate for segmental movement or a step-off deformity between the spinous processes.15,19 Motor. Manual muscle testing is an important aspect of determining an affected nerve root level on physical examination. Manual muscle testing is performed to detect subtle weakness in a myotomal distribution. The limb of the affected side is placed in the antigravity position; the force is applied just proximal to the next distal joint. Motor weakness is usually the last symptom seen in cervical radiculopathy or stenosis. It is very important that if any clinical weakness is noted in the affected limb, that this be compared with the unaffected side.14,19 Sensory. On sensory examination, a dermatomal decrease or loss of sensation should be noted in patients with a single nerve root radiculopathy. In addition, patients with radiculopathy may have hyperesthesia to light touch and pinprick examination.14 However, the sensory examination can be quite subjective because it requires a response by the patient. The sensory examination should be performed with both light touch and pinprick. In cases of mild radiculopathy, the pinprick examination may be the only sensory test that is positive, and this is more reliable.17 Deep Tendon Reflexes. The deep tendon reflexes, or muscle stretch reflexes, are helpful in the evaluation of patients who present with limb symptoms that are suggestive of a radiculopathy or stenosis. The examiner must position the limb properly when obtaining these reflexes, and the patient needs to be as relaxed as possible. Any grade of reflex can be normal, so it is the asymmetry of the reflexes that is most helpful. DM, December 2009
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The biceps brachii reflex is obtained by tapping the distal tendon in the antecubital fossa. This reflex occurs at the C5-C6 level. The brachioradialis reflex is another C5-C6 reflex that can be obtained by tapping the radial aspect of the wrist. The triceps reflex can be obtained by tapping the distal tendon at the posterior aspect of the elbow, with the elbow relaxed at about 90° of flexion. This tests the C7-C8 nerve roots. The pronator reflex can be helpful in differentiating C6 and C7 nerve root problems. If this reflex is abnormal in conjunction with an abnormal triceps reflex, then the level of involvement is more likely to be C7. The pronator reflex is performed by tapping the volar aspect of the distal radius with the forearm in a neutral position and the elbow flexed. This results in a stretch of the pronator teres, resulting in a reflex pronation.17,18 Upper Tract Signs. Lhermitte’s sign is performed by flexing the neck and asking the patient about symptoms of an electric shock-like sensation radiating down the spine, and in some patients, into the extremities. This sign has been found in patients with cervical cord involvement, severe cervical spondylosis, and in patients with tumor and multiple sclerosis; however, the Lhermitte’s sign should be negative in those with cervical radiculopathy.15 The Babinski’s reflex and Hoffman’s sign should also be examined. The Babinski is elicited with a stroke along the plantar aspect of the foot from a medial to lateral and posterior to anterior approach. A positive sign is an up going first toe; this points to a possible myelopathy. Hoffman’s sign is a test involving the upper extremity. With brisk, downward pressure, the examiner puts pressure across the fingertip of the third digit. If the thumb moves in the medial or adducted direction, this is a positive sign. Again, this points to a possible myelopathy or other central process. Cervical myelopathy is most commonly seen in a patient with longstanding cervical stenosis, usually in elderly people after a fall.15,17
Provocative Tests The foraminal compression test or Spurling’s test is statistically the best provocative test for confirming the diagnosis of cervical radiculopathy, when performed properly. It is performed by extending the neck and rotating the head and then applying downward pressure on the head. The test is considered positive if pain radiates into the limb ipsilateral to the side to which the head is rotated. The Spurling’s test has been found to be very specific (93%), but not sensitive (30%), in diagnosing acute radiculopathy. Therefore, it is not useful as a screening test, but it is clinically useful in helping to confirm cervical radiculopathy.20 746
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Manual cervical distraction can be used as a physical examination test. With the patient in a supine position, gentle manual distraction often greatly reduces the neck and limb symptoms in patients with radiculopathy. However, this will also relieve the symptoms of cervical facetogenic pain and cervical discogenic pain. It should be used as a tool in the physical examination but is less specific than the Spurling’s test.17,20 The upper limb tension test and shoulder abduction test are 2 other commonly used provocative tests used to reproduce clinical symptoms. In recent years, however, these tests have failed to hold up in clinical studies and have shown poor intra-rater reliability. The provocative test with the overall best reliability is the Spurling’s test.21
Imaging Plain Radiography. Radiography of the cervical spine is usually the first diagnostic test ordered in patients who present with neck and limb symptoms, and more often than not, this study is diagnostic of cervical disk disease as the cause of the radiculopathy. On the lateral view, look for disk-space narrowing, comparing the level above and below. Typically, the cervical disk spaces get larger from C2-C6, with C5-C6 being the widest disk space in normal necks, and C6-C7 slightly narrower. Besides narrowing, look for subchondral sclerosis and osteophyte formation.22 On oblique views, look for foraminal stenosis at the level of the suspected radiculopathy, comparing it with the opposite foramina, if uninvolved. For example, in a patient with pain or sensory changes along the right C6 nerve distribution, look for narrowing of the right C5-C6 neural foramina as compared with the left side.22 Lateral, anteroposterior, and oblique views should be ordered. An openmouth view should only be ordered to rule out injury to the atlanto-axial joint when significant acute trauma has occurred. Visualizing all 7 cervical vertebrae is very important. If C7 cannot be properly seen, then a “swimmer’s view” (supine oblique view, in which the patient’s arm is extended over the head) or a computed tomography (CT) scan should be obtained for better visualization of the C7 and T1 segments.22 The atlantodens interval is the distance from the posterior aspect of the anterior C1 arch and the odontoid process. This interval should be less than 3 mm in adults and less than 4 mm in children. An increase in the atlantodens interval suggests atlanto-axial instability, such as in cases of trauma or rheumatoid arthritis. Flexion and extension views can be helpful in assessing spinal mobility and stability in these patients.22,23 The clinician should be aware of the limitations of plain radiographs. Problems with both specificity and sensitivity exist. Correlations of DM, December 2009
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findings on plain radiographs and cadaver dissections have found a 67% correlation between disk-space narrowing and anatomic findings of disk degeneration. However, radiographs identified only 57% of large posterior osteophytes and only 32% of abnormalities of the apophyseal joints that were found on dissection.22 CT Scanning. CT scanning provides good visualization of bony elements and can be helpful in the assessment of acute fractures. It can also be helpful when C6 and C7 cannot be clearly seen on traditional lateral radiographic views. The accuracy of CT imaging of the cervical spine ranges from 72% to 91% in the diagnosis of disk herniation. The accuracy has approached 96% when combining CT scanning with myelography. The addition of contrast material allows for the visualization of the subarachnoid space and assessment of the spinal cord and nerve roots.24 CT scanning with myelography is thought to best assess and localize spinal cord compression and any underlying atrophy. This study can also determine the functional reserve of the spinal canal in evaluating patients with possible cervical stenosis. Because of the improved soft-tissue visualization provided by magnetic resonance imaging (MRI), CT scanning is being replaced by MRI for most cervical spine disorders.22-24 Magnetic Resonance Imaging. MRI has become the method of choice for imaging the neck to detect significant soft-tissue pathology, such as disk herniation. MRI can detect ligament and disk disruption, which cannot be demonstrated by other imaging studies. The entire spinal cord, nerve roots, and axial skeleton can be visualized. This study is usually performed in the axial and sagittal planes.23,24 MRI has been found to be quite useful in evaluating the amount of cerebrospinal fluid surrounding the cord in the evaluation of patients with cervical canal stenosis, although the T2-weighted images tend to exaggerate the degree of stenosis. The use of MRI in the evaluation of patients with possible cervical stenosis can be helpful in determining the functional reserve of the spinal canal.25 Although MRI is believed to be the imaging method of choice in the evaluation of cervical radiculopathy, abnormalities have also been found in asymptomatic subjects.22 Ten percent of subjects younger than 40 years were noted to have disk herniations in 1 study. Of subjects older than 40 years, 20% had evidence of foraminal stenosis and 8% had disk protrusion or herniation. Therefore, as with all imaging studies, the MRI findings must be used in conjunction with the patient’s history and physical examination findings.23 The Torg-Pavlov ratio is a measurement used by radiologists using 748
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plain films, by which the anteroposterior diameter of the vertebral body is measured and divided by the anteroposterior diameter of the central canal. The resultant ratio is used to define the severity of degeneration. Prasad et al performed a study comparing MRI measurements of the cervical spine to the Torg-Pavlov ratio and found that the MRI findings are statistically much more significant for determining central canal stenosis as it related to symptomatic radiculopathy or myelopathy.26
Diagnostic Testing Electromyography. Electrodiagnostic studies are important in identifying physiological abnormalities of the nerve root and in ruling out other neurologic causes for the athlete’s complaints. Electromyography (EMG) has been shown to be a useful diagnostic test in the diagnosis of radiculopathy and has correlated well with findings on myelography and surgical outcomes.27 EMG has 2 parts, as follows: (1) nerve conduction studies and (2) a needle-electrode examination. The nerve conduction studies are performed by placing surface electrodes over a muscle belly or sensory area and stimulating the nerve that supplies either the muscle or the sensory area from fixed points along the nerve. From this, the amplitude, distal latency, and conduction velocity can be measured. The amplitude reflects the number of intact axons, whereas the distal latency and conduction velocity is more of a reflection of the degree of myelination.27 The needle EMG portion of the electrodiagnostic examination involves inserting a fine-needle electrode into a muscle. Electrical activity is generated by the needle insertion into the muscle, voluntary muscle contraction, and the spontaneous firing of motor units. The activity is observed on an oscilloscope screen and quantified; an audible sound is also generated. Denervated muscle produces spontaneous electrical activity while the muscle is at rest. These potentials are called fibrillations or positive sharp waves based on their characteristic shape and sound. Changes can be also seen in the configuration of the individual motor unit, as well as an increase in the firing rate of the individual motor units.27,28 The timing of the EMG evaluation is important because positive sharp waves and fibrillation potentials first occur 18-21 days after the onset of a radiculopathy; therefore, it is best to delay this study until 3 weeks after an injury, so that it can be as precise a study as possible. The primary use of EMG is to diagnose nerve root dysfunction when the diagnosis is uncertain or to distinguish a cervical radiculopathy from other lesions, which are unclear on physical examination. Although electrodiagnostic studies are very sensitive and specific, a “normal” EMG in the face of DM, December 2009
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signs and symptoms that are consistent with a cervical radiculopathy does not exclude the diagnosis of cervical radiculopathy. Repeating the EMG several months later can also serve as a tool to assess recovery of motor units, thus nerve axons.28,29
Pharmacologic Treatment Anti-inflammatories The goal of the initial treatment of cervical radiculopathy should be to minimize pain and improve function. First-line agents used are typically the anti-inflammatories. The rationale is to counteract the neurotoxic/ proinflammatory chemicals present during cervical radiculopathy. The presence of phospholipase,2 nitric oxide, prostaglandin E2, and interleukin-6 have all been established in both herniated and degenerated disks.30,31 It is thought that these agents contribute to pain by irritating nerves, altering conduction, and in some cases, causing axonal damage. Nerves affected would be those found in the outer annulus, as well as adjacent spinal nerves.
Nonsteroidal Anti-inflammatory Drugs The most commonly used class of medication is the nonsteroid anti-inflammatory agents. Despite their prolific use, there are no convincing studies for their use in this clinical scenario. One could extrapolate benefit here from some low back studies that have been done.32 Nonsteroidal anti-inflammatory drugs (NSAIDs) reversibly inhibit the enzyme cyclooxygenase (in the cyclooxygenase pathways). This in turn prevents the formation of pro-inflammagens, prostaglandin, and thromboxane. There are several advantages to these medications. First, they are readily available and, when used regularly, have both anti-inflammatory and pain-relieving properties. There are known disadvantages as well. Older NSAIDs affect both parts of the cyclo-oxygenase pathway of COX-1 and COX-2. The COX-1 pathway is responsible for maintaining normal gastrointestinal, renal, and platelet functions. The COX-2 pathway modulates the inflammatory response. With this in mind, the regular usage of a nonspecific inhibited COX should be monitored accordingly for potential toxicity. Gastrointestinal symptoms occur in 15%-20% taking NSAIDs on an ongoing basis; 2%-4% can develop ulcers and 1%-2% can perforate.33 Gastric toxicity increases in those with a history of peptic ulcer disease; those using high-dose or prolonged NSAID; those with co-administration of blood thinning agents or other anti-inflamma750
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tories; those with increased age; and those who smoke or drink alcohol. Proton pump inhibitors or a prostaglandin analogue can offer a protective effect when given concomitantly. COX-2-selective NSAIDs, by contrast, appear to have better gastrointestinal tolerability and no platelet inhibition. They provide comparable analgesic and anti-inflammatory properties. Renal adverse effects, such as sodium/water retention, edema, acute renal failure, and hypertension, can occur in both the older and the newer agents.34 It is also not clear as to the relationship between the increase of cardiovascular events and the COX-2 class of medication. Using these medications should be done cautiously and/or on a limited base for patients with cervical radiculopathy and the above comorbidity.
Oral Steroids As opposed to the NSAIDs, glucocorticoids have no true analgesic property but are potent anti-inflammatories. Generally, they are used for cervical radiculopathy when the NSAIDs have failed or in some severe cases as an initial treatment. They are phospholipase 2 inhibitors but also reduce cell mobilization and vascular permeability. Although side effects of oral steroids are well documented and numerous, a rapid taper (ie, Medrol pack) administration is generally well tolerated in those patients where there are no contraindications. In this review, there has been no convincing evidence showing avascular necrosis with an isolated, rapid steroid taper.
Opioids Opioids are a reasonable choice of medication for pain control during the acute and subacute stages. This is particularly true when pain is severe and/or the anti-inflammatories are not providing satisfactory pain control. The ultimate goal is to control pain so patients can start returning to normal function and participate optimally in their rehabilitation.
Neuropathics Included in this class would be the antidepressants and anticonvulsant agents. To date there are no convincing studies on the use of these agents in cervical radiculopathy. The mechanism of action for the antidepressant is thought to come from their inhibitory effect on seratonin and norepinephrine uptake, as well as potential substance P reduction.35 The mechanism of action for anticonvulsant medication is even less understood. Medications such as pregabalin have been approved for use in diabetic peripheral neuropathy and post herpetic neuralgia. They therefore have “implied” benefit for cervical radiculopathy and are DM, December 2009
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therefore commonly used off-label. These medications are generally well tolerated when started at a low dose and titrated slowly. Generally, they have few drug interactions and patient contraindications.
Cervical Epidural Steroid Injections There are 2 approaches in this regard, transforaminal and translaminar. The mechanism of action of this therapeutic modality is thought to be the same as its oral counterpart. More specifically it functions to suppress elements of the inflammatory cascade.36 There are 3 presumed benefits if one compares cervical epidural steroid injections to oral steroids: the ability to use a lower dose of steroid, the ability to be directly administered to the area of pathology, and the capability of avoiding some of the systemic effects. The exact success rate of cervical epidural steroid injections is difficult to decipher because of varying study designs as well as techniques used. It is generally accepted to hover around 60%, which is successful at providing long-term relief of pain and improved function.19 There are no conclusive studies comparing the efficacy of transforminal vs interlaminar approach. However, there is, as of late, an expanding amount of literature pointing to the potential serious neurologic sequelae after the cervical transforaminal approach. The mechanism of injury is thought to be either embolic (from particulate matter of the steroid), vasospastic, or thrombotic. All are thought to be caused by inadvertent intra-arterial injection during the procedure. Damage may ensue because of infarct to the spinal cord, midbrain, pons, cerebellum, and temporal and occipital lobes.37 An interlaminar technique, under fluoroscopy, using a low particulate steroid is likely a relatively safe and effective approach.37,38
Rehabilitation Once the acute pain has been managed, a course of rehabilitation is indicated for several reasons. The first is to restore function in a patient who has an inevitable lost in range of motion and has become reconditioned. Second, it would be to help further improve any residual discomfort. Finally, it would be to put into place preventative measures with a goal to avoid recurrence. Because rehabilitation approaches vary and are typically used in conjunction with other modes of treatment (pharmacopia, injections, relative rest, etc), there are no conclusive outcome studies. However, there are numerous studies that demonstrate its successful role when utilized as an adjunct.39-41 A typical approach will likely involve aspects of flexibility strengthening and functional reconditioning. Flexibility will often times address 752
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muscles with a tendency toward tightness (ie, scalenes, trapezius, pectoralis), while strengthening will likely address those muscle with a tendency for relative weakness. These are sometimes referred to as the scapular stabilizers. Strengthening this group of muscles (rhomboids, midtrapezius, etc) will provide support to the cervical spine and attempt to restore appropriate posture. Therapists will also incorporate various mobilization techniques to restore range of motion and reduce pain. For the management of chronic neck pain, specific neck exercises that include active activation of the deep neck muscle and dynamic strengthening can significantly improve disability scores.42 Strength and fitness training may be advised for patients with chronic neck pain, but strength training is much more effective than stretching and aerobic exercising alone.43-45 Passive modalities include the application of heat, electrical stimulation, massage, myofascial release, and traction. Passive modalities are often used to decrease level of pain and inflammation and to facilitate participation in an active rehabilitation program that often involves stretching and strengthening. Active treatment refers to therapeutic exercises that are aimed at improving patient’s strength, endurance, flexibility, posture, and body mechanics. An early, active strategy is recognized to improve functions, increase activity, and prevent chronicity.42 No one modality (see below), in isolation or combination, has been shown to improve recovery from cervical radiculopathy: ● ● ● ● ● ●
Massage/manipulation Cervical traction Ice Heat Electrical stimulation Diathermy
In these authors’ view, they are useful, short-term adjuncts to reduce pain to allow patients to carry out their rehabilitation. Surgical consultation is warranted when there are signs of progressive neurologic decline, more specifically strength. It is also warranted when there are myelopathic signs on physical examination and/or imaging (ie, myelomalacia and cord compression on MRI).
REFERENCES 1.
Clark CR, Benzel EC, Currier BL, et al. The Cervical Spine, 4th ed. The Cervical Spine Research Society Editorial Committee. Philadelphia, PA: Lippincott Williams & Wilkins 2005.
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16. 17. 18. 19. 20. 21.
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Weinstein JN. Neck and back pain. In: Physical Medicine and Rehabilitation State of Art Review. Philadelphia, PA: Hanley & Belfus, 1990. p. 201-14. Hogg-Johnson S, van der Velde G, Carroll LJ, et al. The burden and determinants of neck pain in the general population: Results of the bone and joint decade 2000-2010 task force on neck pain and its associated disorders. Spine 2008;33:S39-51 (suppl). Stemper BD, Yoganandan N, Pintar FA, et al. Anatomical gender differences in cervical vertebrae of size-matched volunteers. Spine 2008;33:E44-9. Praemer A, Furner S, Rice DP. Musculoskeletal Conditions in the United States. Rosemont, IL: American Academy of Orthopedic Surgeons, 1999. p. 27-70. Bovim G, Schrader H, Sand T. Neck pain in the general population. Spine 1994;19:1307-9. Makela M, Heliovaara M, Sievers K, et al. Prevalence, determinants and consequences of chronic neck pain in Finland. Am J Epidemiol 1991;134:1356-67. Cote P, Cassidy J, Carroll L. The factors associated with neck pain and its related disability in the Saskatchewan population. Spine 2000;25:1109-17. Devereaux MW. Anatomy and examination of the spine. Neurol Clin 2007; 25:331-51. Levin KH, Covington EC, Devereaux MW, et al. Neck and low back pain. New York, NY: Continuum, 2001. Murtagh FR. The importance of being earnest—About disk nomenclature. AJNR Am J Neuroradiol 2007;28:1-2. Lestini WF, Wiesel SW. The pathogenesis of cervical spondylosis. Clin Orthop Relat Res 1989;239:69-93. Montgomery DM, Brower RS. Cervical spondylotic myelopathy. Clinical syndrome and natural history. Orthop Clin North Am 1992;23:487-93. Rhee J, Yoon T, Riew K. Cervical radiculopathy. J Am Acad Orthop Surg 2007;15:486-94. Rao R, Currier BL, Albert TJ, et al. Degenerative cervical spondylosis: Clinical syndromes, pathogenesis, and management. J Bone Joint Surg 2007;89: 1360-78. Polston D. Cervical radiculopathy. Neurol Clin 2007;25:373-85. Wainner R, Gill H. Diagnosis and nonoperative management of cervical radiculopathy. J Orthop Sports Phys Ther 2000;30:728-44. Dvorak J. Epidemiology, physical examination, and neurodiagnostics. Spine 1998;23:2663-72. Carette S, Fehlings M. Clinical Practice. Cervical radiculopathy. N Engl J Med 2005;353:392-9. Tong H, Haig A, Yamakawa K. The Spurling’s test and cervical radiculopathy. Spine 2002;27:156-9. Rubinstein S, Pool JJ, van Tulder MW, et al. A systematic review of the diagnostic accuracy of provocative tests of the neck for diagnosing cervical radiculopathy. Eur Spine J 2007;16:307-19. Kaiser J, Holland B. Imaging of the cervical spine. Spine 1998;15:2701-12. Yue W, Tan SB, Tan MH, et al. The Torg-Pavlov ratio in cervical spondylotic myelopathy: A comparative study between patients with cervical spondylotic myelopathy and a nonsponylotic, nonmyelopathic population. Spine 2001;26: 1760-4. Stafira J, Sonnad JR, Yuh WT, et al. Qualitative assessment of cervical spinal DM, December 2009
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stenosis: Observer variability on CT and MR images. AJNR Am J Neuroradiol 2003;24:766-9. Golash A, Birchall D, Laitt RD, et al. Significance of CSF measurements in cervical spondylitic myelopathy. Br J Neurosurg 2001;15:17-21. Prasad S, O’Malley M, Caplan M, et al. MRI measurements of the cervical spine and their correlation to Pavlov’s ratio. Spine 2003;28:1263-8. Silver J. Easy EMG. Philadelphia, PA: Lippincott Williams and Wilkins, 2005. Dillingham T, Laudy TD, Andary M, et al. Identification of cervical radiculopathies: Optimizing the electromyographic screen. Am J Phys Med Rehabil 2001;80: 84-91. Tsao B. The electrodiagnosis of cervical and lumbosacral radiculopathy. Neurol Clin 2007;25:473-94. Saal JS, Franson RC, Dobrow R, et al. High levels of inflammatory phospholipase A2 activity in lumbar disc herniations. Spine 1990;15:674-8. Kang JD, Georgeslcu HI, McIntyre-Larkin L, et al. Herniated cervical intervertebral discs spontaneously produce matrix metalloproteinases, nitric oxide, interleukin-6, and prostaglandin E2. Spine 1995;20:2373-8. Koes BW, Scholten RJ, Mens JM, et al. Efficacy of non-steroidal anti-inflammatory drugs for low back pain: A systematic review of randomized clinical trails. Ann Rheum Dis 1997;56:214-23. Singh G, Ramey GR, Morfeld D, et al. Gastrointestinal tract complications of nonsteroidal anti-inflammatory drug treatment in rheumatoid arthritis. A prospective observational cohort study. Arch Intern Med 1996;156:1530-6. FitzGerald GA, Patrono C. The coxibs, selective inhibitors of cyclooxygenase-2. N Engl J Med 2001;345:433-42. Ward N. Tricyclic antidepressants for chronic low back pain: Mechanisms of action and predictors of response. Spine 1986;11:661-5. Korovessis PG. The role of steroids and their effects on phospholipase A2. Spine 2000;25:2004-5. Abbasi A, Malhotra G, Malanga G, et al. Complications of interlaminar cervical epidural steroid injections: A review of the literature. Spine 2007;32: 2144-51. Dreyfuss P, Baker R, Bogduk N. Comparative effectiveness of cervical transforaminal injections with particulate and nonparticulate corticosteroid preparations for cervical radicular pain. Am Acad Pain Med 2006;7:237-42. Heckmann JC, Lang CJ, Zobelein I, et al. Herniated cervical intervertebral discs with radiculopathy: An outcome study of conservatively or surgically treated patients. J Spinal Disord 1999;12:396-401. Saal JS, Saal JA, Yurth EF. Nonoperative management of herniated cervical intervertebral disc with radiculopathy. Spine 1996;21:1877-83. Sampath P, Bendebba M, Davis JD, et al. Outcome in patients with cervical radiculopathy: Prospective, multicenter study with independent clinical review. Spine 1999;24:591-7. Chiu TT, Lam TH, Hedley AJ. A randomized controlled trail on the efficacy of exercise for patients with chronic neck pain. Spine 2005;30:E1-7. Dreyer SJ, Boden SD. Nonoperative treatment of neck and arm pain. Spine 1998;23:2746-54.
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Rosenfeld M, Seferiadis A, Carlsson J, et al. Active intervention in patients whiplash-associated disorders improves long-term prognosis: A randomized controlled clinical trial. Spine 2003;28:2491-8. Ylinen J, Takala EP, Nykanen M, et al. Active neck muscle training in the treatment of chronic neck pain in women: A randomized controlled trial. J Am Med Assoc 2003;289:2509-16.
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Cigarette smoking Axial load-bearing High-risk occupation: meat carriers, dentists, professional drivers Prior lumbar radiculopathy
Dis Mon 2009;55:737-756 0011-5029/2009 $36.00 ⫹ 0 doi:10.1016/j.disamonth.2009.06.004 DM, December 2009
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Possibly Implicated 1. 2. 3. 4. 5. 6. 7. 8. 9.
Metabolic disturbance Prior cervical trauma Vibrational exposure Diet/nutritional factors Genetic factors Racial factors Gender Atherosclerosis Auto-immune factors
No Role Identified 1. Repeated turning of the neck 2. Sports 3. Sedentary occupations Several pathologies can cause pain originating from the cervical spine. Herniated nucleus pulposus (HNP) is a condition in which the central part of an intervertebral disk gets pushed out, which can cause neck pain from the inflammatory response or nerve dysfunction from the inflammation or mechanical compression of spinal nerves. Spinal stenosis is a narrowing of the spinal canal or the intervertebral foramina, which is usually a result of spondylosis or cervical degenerative disk disease (DDD). Spinal stenosis can occur from bone spurs, or osteophytes, from spondylolisthesis, or slipping of 1 vertebral body on another, or from ligamentous thickening causing compression. If the narrowing causes spinal nerve dysfunction, patients can acquire radicular symptoms. If there is cord compression, or myelopathy, bowel and bladder dysfunction, as well as motor and sensory deficits, may result. HNP and DDD and its related pathologies including stenosis are the most common cervical pathologies causing radicular symptoms. HNP accounts for about 20%-25% of cervical radiculopathies and DDD accounts for about 70%-75%.
Anatomy The cervical spine has 7 vertebrae (C1-C7) and 8 spinal nerves (C1-C8). The C1 vertebra is called the atlas and is a ring of bone, which rotates around the odontoid process of the axis, or the C2 vertebra. Between 2 vertebrae are 2 openings called the foramen, where a spinal nerve, blood vessels, and the sinuvertebral nerves pass through. The superior and inferior borders of this foramen are the pedicles, the anterior border is the 738
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intervertebral disk and vertebral bodies, and the posterior border is the facet, or zygapophyseal joint. In 1%-15% of the population, a bony arch may form converting the groove on C1 for the vertebral artery and the first cervical nerve into an arcuate foramen.1 There is also a spinal canal that is bordered by the laminae and the ligamentum flavum posteriorly and anteriorly by the vertebral bodies and intervertebral disks. The midsagittal (anteroposterior) diameter of the canal in the upper cervical spine (C1-3) is about 21 mm, whereas the lower cervical spine (C4-7) is 18 mm. The cervical spinal cord usually occupies about 40% of the cervical canal. Cervical extension decreases the canal diameter by 2-3 mm.9 The posterior longitudinal ligament stretches from the axis to the sacrum and is the anterior border of the spinal canal. It is broader in the cervical and thoracic spine compared to the lumbar spine. The ligamenta flava are ligaments between the laminae. This ligament can thicken with age and can contribute to cervical canal stenosis, which can lead to myelopathy and radicular symptoms. The occiput and the first cervical vertebra (atlas) form the atlantooccipital joint and have about 1/3 of flexion and extension and 1/2 of lateral bending of the cervical spine. The occipitovertebral ligaments connect the occiput to the atlas and permit flexion and extension of the joint. The C1-C2 joint, or the atlanto-axial joint, has no disk between them and has about 1/2 of rotational range of motion. The transverse ligament of the atlas holds the odontoid process in place and is stronger than the odontoid process itself. There is also a pair of alar ligaments on both sides of the occipital condyles, which limit rotation. Normal cervical spine has a shallow lordosis, which can be decreased or even reversed in patients with degenerative changes and increased in patients with increased thoracic kyphosis. The intervertebral disks provide support to the cervical spine while maintaining mobility. The disk is comprised of a nucleus polposus, surrounded by the annulus fibrosus. The annulus is primarily composed of type 1 collagen, while the nucleus pulposus is composed predominantly of type 2 collagen. The collagen fibers of the annulus are arranged in 15-25 layers of alternating obliquely arranged fibers, which allows for mobility and provides tensile strength. The collagen fibers attach to the vertebral bodies, the anterior and posterior longitudinal ligaments, and the vertebral endplates. The type 2 collagen, proteoglycan, and hyaluronan long chains that comprise the nucleus pulposus have negatively charged branching side chains that are very hydrophilic, which maintain that “hydration” of the disk. The vascular supply of the cervical spine originates from the vertebral DM, December 2009
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arteries and its segmental medullary arteries, which send anterior and posterior branches to the spinal cord along the ventral and dorsal roots. In the cervical spine, the anterior spinal artery can become occluded in hyperextension injuries with cervical canal stenosis and spondylosis, which can cause ischemia to the anterior 2/3 of the cord. Each cervical spinal nerve has a ventral and a dorsal spinal root. The ventral horn of the spinal cord contains alpha motor neurons, which give off efferent motor fibers in the ventral root. The dorsal root ganglion and its afferent sensory fibers travel in the dorsal root. The ventral and dorsal root combine to form a spinal nerve, which then divides into the dorsal primary ramus and the ventral primary ramus. The dorsal ramus supplies the posterior neck structures, whereas the ventral ramus supplies prevertebral and paraspinal muscles and then forms the brachial plexus, which then go on to innervate the upper limb. A myotome is a group of muscles innervated by 1 spinal nerve. A dermatome is the sensory distribution of a dorsal root.10 The myotome, dermatome, and muscle stretch reflexes can help localize the level of the cervical radiculopathy and radiculitis.
Pathology Cervical degenerative disease is a spectrum of clinical syndromes associated with neck pain and neurologic symptoms. It includes spondylotic degeneration, disk displacement with radiculopathy, and cervical spondylotic myelopathy. The first description of myelopathy was in 1838 of a patient with a spondylotic bar into the spinal canal and reducing area by 1/3. There is a consensus on nomenclature for HNP in the lumbar spine, specifically, disk bulge, protrusion, extrusion, and sequestration. Currently, there is no consensus on nomenclature for HNP in the cervical spine because there are anatomic differences in the cervical spine when compared to the lumbar spine.11 Regardless of lack of nomenclature, HNP does cause pain in the cervical spine. The disk is thought to start degenerating in the second decade with repetitive strain causing posterolateral annular tear, circumferential tears causing radial fissures, and nuclear material extrusion through these tears causing disk desiccation and nuclear degradation. HNP causes radicular pain through chemical radiculitis from proteoglycans and phospholipases released from the nucleus pulposus, which propagate an inflammatory cascade, and from direct nerve injury/compression, which can lead to nerve demyelination and neurologic symptoms. DDD can cause mechanical nerve root compression in the intervertebral foramen from decreased disk height, 740
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foraminal hypertrophy, ligamentum hypertrophy, spondylolisthesis, and periradicular fibrous tissue. In cervical disk degeneration, the nucleus pulposus desiccates and loses mechanical competence, which increases strain on the annulus, leading to tearing of the annulus and disk protrusion. The disk protrusion itself can cause root or cord impingement, which can cause various nerve dysfunction symptoms including sensory and motor changes. This disk collapse translates into excess motion in the zygapophyseal joints posteriorly and increased strain in the supporting ligaments.12 Degenerative changes affect all levels but is relatively less common above C3-C4 disk.13 Most commonly the C5-6 disk space (affect C6 nerve root) followed by C6-7 (C7 nerve root) are affected. Cervical spondylotic radiculopathy starts about 10 years after the disk starts to degenerate, and the mechanical incompetence of the motion segment leads to spondylotic degeneration of facets and uncovertebral joints.13 As the disk loses height, uncovertebral joints come into contact leading to osteophyte formation. The zygapophyseal joints override and also form osteophytes. These osteophytes are also called “hard” disk protrusions and can themselves compress nerves. Spondylotic radiculopathy patients are more likely to complain of multilevel or bilateral radicular symptoms.12,13 Cervical spondylotic myelopathy happens when degeneration of spine with osteophyte formation causes compression of the central spinal canal, affecting cord function through vascular insufficiency and direct mechanical pressure. Cervical spondylosis accounts for more than half of all cervical myelopathy cases. Compression of the spinal cord and nerve roots by herniation of nucleus pulposus in cervical region is the most common cause of spinal cord dysfunction in patients older than 55 years. Myelopathy is most common at C5-6, then C4-5, C6-7, C3-4. Five categories of spondylotic myelopathy exist, as follows: 1. Most common—transverse lesion syndrome (corticospinal and spinothalamic tracts) so upper motor neuron (UMN) weakness with gait difficulties and lower extremity spasticity 2. Motor syndrome, mostly corticospinal or anterior horn cell—rare sensory, motor weakness, and gait difficulties 3. Central cord syndrome—mostly central gray matter of cord so upper motor and sensory involvement with lower extremity sparing 4. Brown-Sequard syndrome unilateral cord lesion with ipsilateral hemiparesis from corticospinal tract involvement with contralateral pain DM, December 2009
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and temperature analgesia reported below level of lesion best prognosis for recovery 5. Brachialgia cord syndrome typically predominant upper limb pain with some associated long tract involvement—lower motor neuron flaccid weakness in upper extremities may be combined with spastic UMN lower extremity involvement.
Diagnosis History As with any disease entity, obtaining a thorough and detailed history is important to establish a diagnosis of cervical radiculopathy and/or stenosis. The physician should first determine the chief complaint (pain, numbness, weakness, location of symptoms). In greater than 70% of cervical radiculopathy or stenosis, pain is the primary presenting feature. A visual analog scale from 0 to 10 can be used to determine the patient’s perceived level of pain. Additionally, anatomic pain drawings can also be helpful in giving the physician a quick review of the patient’s pain pattern, which will be helpful in narrowing the differential diagnosis.14,15 Acquiring a specific timeline is also important to addressing the cause of pain. Previous episodes of similar symptoms or localized neck pain are important for the diagnosis and ultimate treatment. Symptoms suggestive of a cervical myelopathy, such as changes in gait, bowel, or bladder dysfunction, or lower extremity sensory changes or weakness should also be obtained. The examiner should ask what previous treatments have been tried, including the use of ice and/or heat and medications such as acetaminophen, aspirin, nonsteroidal anti-inflammatory medications, and steroids. Questions regarding previous medical treatment should also include physical therapy, traction, manipulation, previous injection therapy, or surgical treatments. A complete social history should include the patient’s occupation, sport and position, hobbies, and the use of nicotine and/or alcohol.15 The typical patient with cervical radiculopathy or stenosis presents with an insidious onset of neck and arm pain. The discomfort can range from a dull ache to a severe burning pain. Typically, pain is referred to the medial border of the scapula, and the patient’s chief complaint is lower neck or shoulder pain. As the condition progresses, the pain radiates to the upper or lower arm and into the hand, along the sensory distribution of the nerve root(s) that is involved. The older patient may have had previous episodes of neck pain or give a history of having spondylosis of the cervical spine that may have been previously diagnosed by another 742
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physician. It is important to recognize that acute disk herniations, and sudden narrowing of the neural foramen, may also occur in injuries involving cervical extension, lateral bending, or rotation with axial loading. These patients usually complain of increased pain with neck positions that cause foraminal narrowing including extension, lateral bending, or rotating toward the symptomatic side. Some patients report a reduction in their radicular-type symptoms by abducting their shoulder and placing their hand behind their head. This relief in symptoms is thought to occur by decreasing tension at the nerve root. Patients may complain of sensory changes along the involved nerve root dermatome, which can include tingling, numbness, or loss of sensation. Some patients may complain of motor weakness. A very small percentage of patients will present only with weakness, without significant pain or sensory complaints.16
Differential Diagnosis The differential diagnosis of neck pain is quite expansive and includes the following conditions: 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) Frozen shoulder syndromes Glenohumeral arthritis Gout (infrequently) Heart disease DM, December 2009
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Hyperabduction syndrome Intervertebral osteoarthritis Idiopathic brachial plexopathy Intrinsic neoplasia Nerve injuries Occipital neuralgia Osteomyelitis Osteoarthritis of apophyseal joints Paget’s disease Pancoast’s tumor Pharyngeal infections Postural disorders Psychogenic disorders Rheumatoid arthritis Rib-clavicle compression Rotator cuff tears and tendonitis Scalene muscle tightness Septic arthritis Spinal cord tumors Sternocleidomastoid tendinitis Subacromial bursitis Synovial cysts Tabes dorsalis Thoracic disk Thoracic outlet syndrome Tropical spastic paraparesis An important aspect of narrowing the differential diagnosis in cervical spine pain includes factors such as the length and nature of the symptoms, and whether the pain began insidiously or acutely. Establishing a working diagnosis and using the following information on physical examination and diagnostic testing will help to ascertain the appropriate diagnosis.1,14,15,17
Physical Examination Observation. The physical examination begins with observation of the patient during the history portion of the evaluation. This includes head and neck posture and movement during normal conversation. Typically, the patient exhibits a head tilt away from the side of injury and may hold his or her neck stiffly. Active range of motion is usually reduced, particularly in extension, rotation, and lateral bending, either toward or 744
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away from the affected nerve root. Increased pain with lateral bending away from the affected side can cause increased displacement of a disk herniation on a nerve root, whereas ipsilateral pain would suggest an impingement of a nerve root at the site of the neural foramen.18 The clinician should also look for asymmetries of the neck, shoulders, back, hips, and legs by inspecting the patient in the standing position from anterior, posterior, and lateral viewpoints. A patient with cervical radiculopathy and/or stenosis may have a change in the normal cervical lordosis or thoracic kyphosis.15 Palpation. On palpation, tenderness is usually noted along the cervical paraspinal muscles, usually more pronounced along the ipsilateral side of the affected nerve root. Muscle tenderness may be present along the muscles where the symptoms are referred (eg, medial scapula, proximal arm, lateral epicondyle). Associated hypertonicity or spasm on palpation in these painful muscles may occur. The areas over the bony elements of the spine should also be palpated, especially the spinous processes and articular pillars of the cervical spine. In any patient with cervical pain, the examiner needs to evaluate for segmental movement or a step-off deformity between the spinous processes.15,19 Motor. Manual muscle testing is an important aspect of determining an affected nerve root level on physical examination. Manual muscle testing is performed to detect subtle weakness in a myotomal distribution. The limb of the affected side is placed in the antigravity position; the force is applied just proximal to the next distal joint. Motor weakness is usually the last symptom seen in cervical radiculopathy or stenosis. It is very important that if any clinical weakness is noted in the affected limb, that this be compared with the unaffected side.14,19 Sensory. On sensory examination, a dermatomal decrease or loss of sensation should be noted in patients with a single nerve root radiculopathy. In addition, patients with radiculopathy may have hyperesthesia to light touch and pinprick examination.14 However, the sensory examination can be quite subjective because it requires a response by the patient. The sensory examination should be performed with both light touch and pinprick. In cases of mild radiculopathy, the pinprick examination may be the only sensory test that is positive, and this is more reliable.17 Deep Tendon Reflexes. The deep tendon reflexes, or muscle stretch reflexes, are helpful in the evaluation of patients who present with limb symptoms that are suggestive of a radiculopathy or stenosis. The examiner must position the limb properly when obtaining these reflexes, and the patient needs to be as relaxed as possible. Any grade of reflex can be normal, so it is the asymmetry of the reflexes that is most helpful. DM, December 2009
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The biceps brachii reflex is obtained by tapping the distal tendon in the antecubital fossa. This reflex occurs at the C5-C6 level. The brachioradialis reflex is another C5-C6 reflex that can be obtained by tapping the radial aspect of the wrist. The triceps reflex can be obtained by tapping the distal tendon at the posterior aspect of the elbow, with the elbow relaxed at about 90° of flexion. This tests the C7-C8 nerve roots. The pronator reflex can be helpful in differentiating C6 and C7 nerve root problems. If this reflex is abnormal in conjunction with an abnormal triceps reflex, then the level of involvement is more likely to be C7. The pronator reflex is performed by tapping the volar aspect of the distal radius with the forearm in a neutral position and the elbow flexed. This results in a stretch of the pronator teres, resulting in a reflex pronation.17,18 Upper Tract Signs. Lhermitte’s sign is performed by flexing the neck and asking the patient about symptoms of an electric shock-like sensation radiating down the spine, and in some patients, into the extremities. This sign has been found in patients with cervical cord involvement, severe cervical spondylosis, and in patients with tumor and multiple sclerosis; however, the Lhermitte’s sign should be negative in those with cervical radiculopathy.15 The Babinski’s reflex and Hoffman’s sign should also be examined. The Babinski is elicited with a stroke along the plantar aspect of the foot from a medial to lateral and posterior to anterior approach. A positive sign is an up going first toe; this points to a possible myelopathy. Hoffman’s sign is a test involving the upper extremity. With brisk, downward pressure, the examiner puts pressure across the fingertip of the third digit. If the thumb moves in the medial or adducted direction, this is a positive sign. Again, this points to a possible myelopathy or other central process. Cervical myelopathy is most commonly seen in a patient with longstanding cervical stenosis, usually in elderly people after a fall.15,17
Provocative Tests The foraminal compression test or Spurling’s test is statistically the best provocative test for confirming the diagnosis of cervical radiculopathy, when performed properly. It is performed by extending the neck and rotating the head and then applying downward pressure on the head. The test is considered positive if pain radiates into the limb ipsilateral to the side to which the head is rotated. The Spurling’s test has been found to be very specific (93%), but not sensitive (30%), in diagnosing acute radiculopathy. Therefore, it is not useful as a screening test, but it is clinically useful in helping to confirm cervical radiculopathy.20 746
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Manual cervical distraction can be used as a physical examination test. With the patient in a supine position, gentle manual distraction often greatly reduces the neck and limb symptoms in patients with radiculopathy. However, this will also relieve the symptoms of cervical facetogenic pain and cervical discogenic pain. It should be used as a tool in the physical examination but is less specific than the Spurling’s test.17,20 The upper limb tension test and shoulder abduction test are 2 other commonly used provocative tests used to reproduce clinical symptoms. In recent years, however, these tests have failed to hold up in clinical studies and have shown poor intra-rater reliability. The provocative test with the overall best reliability is the Spurling’s test.21
Imaging Plain Radiography. Radiography of the cervical spine is usually the first diagnostic test ordered in patients who present with neck and limb symptoms, and more often than not, this study is diagnostic of cervical disk disease as the cause of the radiculopathy. On the lateral view, look for disk-space narrowing, comparing the level above and below. Typically, the cervical disk spaces get larger from C2-C6, with C5-C6 being the widest disk space in normal necks, and C6-C7 slightly narrower. Besides narrowing, look for subchondral sclerosis and osteophyte formation.22 On oblique views, look for foraminal stenosis at the level of the suspected radiculopathy, comparing it with the opposite foramina, if uninvolved. For example, in a patient with pain or sensory changes along the right C6 nerve distribution, look for narrowing of the right C5-C6 neural foramina as compared with the left side.22 Lateral, anteroposterior, and oblique views should be ordered. An openmouth view should only be ordered to rule out injury to the atlanto-axial joint when significant acute trauma has occurred. Visualizing all 7 cervical vertebrae is very important. If C7 cannot be properly seen, then a “swimmer’s view” (supine oblique view, in which the patient’s arm is extended over the head) or a computed tomography (CT) scan should be obtained for better visualization of the C7 and T1 segments.22 The atlantodens interval is the distance from the posterior aspect of the anterior C1 arch and the odontoid process. This interval should be less than 3 mm in adults and less than 4 mm in children. An increase in the atlantodens interval suggests atlanto-axial instability, such as in cases of trauma or rheumatoid arthritis. Flexion and extension views can be helpful in assessing spinal mobility and stability in these patients.22,23 The clinician should be aware of the limitations of plain radiographs. Problems with both specificity and sensitivity exist. Correlations of DM, December 2009
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findings on plain radiographs and cadaver dissections have found a 67% correlation between disk-space narrowing and anatomic findings of disk degeneration. However, radiographs identified only 57% of large posterior osteophytes and only 32% of abnormalities of the apophyseal joints that were found on dissection.22 CT Scanning. CT scanning provides good visualization of bony elements and can be helpful in the assessment of acute fractures. It can also be helpful when C6 and C7 cannot be clearly seen on traditional lateral radiographic views. The accuracy of CT imaging of the cervical spine ranges from 72% to 91% in the diagnosis of disk herniation. The accuracy has approached 96% when combining CT scanning with myelography. The addition of contrast material allows for the visualization of the subarachnoid space and assessment of the spinal cord and nerve roots.24 CT scanning with myelography is thought to best assess and localize spinal cord compression and any underlying atrophy. This study can also determine the functional reserve of the spinal canal in evaluating patients with possible cervical stenosis. Because of the improved soft-tissue visualization provided by magnetic resonance imaging (MRI), CT scanning is being replaced by MRI for most cervical spine disorders.22-24 Magnetic Resonance Imaging. MRI has become the method of choice for imaging the neck to detect significant soft-tissue pathology, such as disk herniation. MRI can detect ligament and disk disruption, which cannot be demonstrated by other imaging studies. The entire spinal cord, nerve roots, and axial skeleton can be visualized. This study is usually performed in the axial and sagittal planes.23,24 MRI has been found to be quite useful in evaluating the amount of cerebrospinal fluid surrounding the cord in the evaluation of patients with cervical canal stenosis, although the T2-weighted images tend to exaggerate the degree of stenosis. The use of MRI in the evaluation of patients with possible cervical stenosis can be helpful in determining the functional reserve of the spinal canal.25 Although MRI is believed to be the imaging method of choice in the evaluation of cervical radiculopathy, abnormalities have also been found in asymptomatic subjects.22 Ten percent of subjects younger than 40 years were noted to have disk herniations in 1 study. Of subjects older than 40 years, 20% had evidence of foraminal stenosis and 8% had disk protrusion or herniation. Therefore, as with all imaging studies, the MRI findings must be used in conjunction with the patient’s history and physical examination findings.23 The Torg-Pavlov ratio is a measurement used by radiologists using 748
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plain films, by which the anteroposterior diameter of the vertebral body is measured and divided by the anteroposterior diameter of the central canal. The resultant ratio is used to define the severity of degeneration. Prasad et al performed a study comparing MRI measurements of the cervical spine to the Torg-Pavlov ratio and found that the MRI findings are statistically much more significant for determining central canal stenosis as it related to symptomatic radiculopathy or myelopathy.26
Diagnostic Testing Electromyography. Electrodiagnostic studies are important in identifying physiological abnormalities of the nerve root and in ruling out other neurologic causes for the athlete’s complaints. Electromyography (EMG) has been shown to be a useful diagnostic test in the diagnosis of radiculopathy and has correlated well with findings on myelography and surgical outcomes.27 EMG has 2 parts, as follows: (1) nerve conduction studies and (2) a needle-electrode examination. The nerve conduction studies are performed by placing surface electrodes over a muscle belly or sensory area and stimulating the nerve that supplies either the muscle or the sensory area from fixed points along the nerve. From this, the amplitude, distal latency, and conduction velocity can be measured. The amplitude reflects the number of intact axons, whereas the distal latency and conduction velocity is more of a reflection of the degree of myelination.27 The needle EMG portion of the electrodiagnostic examination involves inserting a fine-needle electrode into a muscle. Electrical activity is generated by the needle insertion into the muscle, voluntary muscle contraction, and the spontaneous firing of motor units. The activity is observed on an oscilloscope screen and quantified; an audible sound is also generated. Denervated muscle produces spontaneous electrical activity while the muscle is at rest. These potentials are called fibrillations or positive sharp waves based on their characteristic shape and sound. Changes can be also seen in the configuration of the individual motor unit, as well as an increase in the firing rate of the individual motor units.27,28 The timing of the EMG evaluation is important because positive sharp waves and fibrillation potentials first occur 18-21 days after the onset of a radiculopathy; therefore, it is best to delay this study until 3 weeks after an injury, so that it can be as precise a study as possible. The primary use of EMG is to diagnose nerve root dysfunction when the diagnosis is uncertain or to distinguish a cervical radiculopathy from other lesions, which are unclear on physical examination. Although electrodiagnostic studies are very sensitive and specific, a “normal” EMG in the face of DM, December 2009
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signs and symptoms that are consistent with a cervical radiculopathy does not exclude the diagnosis of cervical radiculopathy. Repeating the EMG several months later can also serve as a tool to assess recovery of motor units, thus nerve axons.28,29
Pharmacologic Treatment Anti-inflammatories The goal of the initial treatment of cervical radiculopathy should be to minimize pain and improve function. First-line agents used are typically the anti-inflammatories. The rationale is to counteract the neurotoxic/ proinflammatory chemicals present during cervical radiculopathy. The presence of phospholipase,2 nitric oxide, prostaglandin E2, and interleukin-6 have all been established in both herniated and degenerated disks.30,31 It is thought that these agents contribute to pain by irritating nerves, altering conduction, and in some cases, causing axonal damage. Nerves affected would be those found in the outer annulus, as well as adjacent spinal nerves.
Nonsteroidal Anti-inflammatory Drugs The most commonly used class of medication is the nonsteroid anti-inflammatory agents. Despite their prolific use, there are no convincing studies for their use in this clinical scenario. One could extrapolate benefit here from some low back studies that have been done.32 Nonsteroidal anti-inflammatory drugs (NSAIDs) reversibly inhibit the enzyme cyclooxygenase (in the cyclooxygenase pathways). This in turn prevents the formation of pro-inflammagens, prostaglandin, and thromboxane. There are several advantages to these medications. First, they are readily available and, when used regularly, have both anti-inflammatory and pain-relieving properties. There are known disadvantages as well. Older NSAIDs affect both parts of the cyclo-oxygenase pathway of COX-1 and COX-2. The COX-1 pathway is responsible for maintaining normal gastrointestinal, renal, and platelet functions. The COX-2 pathway modulates the inflammatory response. With this in mind, the regular usage of a nonspecific inhibited COX should be monitored accordingly for potential toxicity. Gastrointestinal symptoms occur in 15%-20% taking NSAIDs on an ongoing basis; 2%-4% can develop ulcers and 1%-2% can perforate.33 Gastric toxicity increases in those with a history of peptic ulcer disease; those using high-dose or prolonged NSAID; those with co-administration of blood thinning agents or other anti-inflamma750
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tories; those with increased age; and those who smoke or drink alcohol. Proton pump inhibitors or a prostaglandin analogue can offer a protective effect when given concomitantly. COX-2-selective NSAIDs, by contrast, appear to have better gastrointestinal tolerability and no platelet inhibition. They provide comparable analgesic and anti-inflammatory properties. Renal adverse effects, such as sodium/water retention, edema, acute renal failure, and hypertension, can occur in both the older and the newer agents.34 It is also not clear as to the relationship between the increase of cardiovascular events and the COX-2 class of medication. Using these medications should be done cautiously and/or on a limited base for patients with cervical radiculopathy and the above comorbidity.
Oral Steroids As opposed to the NSAIDs, glucocorticoids have no true analgesic property but are potent anti-inflammatories. Generally, they are used for cervical radiculopathy when the NSAIDs have failed or in some severe cases as an initial treatment. They are phospholipase 2 inhibitors but also reduce cell mobilization and vascular permeability. Although side effects of oral steroids are well documented and numerous, a rapid taper (ie, Medrol pack) administration is generally well tolerated in those patients where there are no contraindications. In this review, there has been no convincing evidence showing avascular necrosis with an isolated, rapid steroid taper.
Opioids Opioids are a reasonable choice of medication for pain control during the acute and subacute stages. This is particularly true when pain is severe and/or the anti-inflammatories are not providing satisfactory pain control. The ultimate goal is to control pain so patients can start returning to normal function and participate optimally in their rehabilitation.
Neuropathics Included in this class would be the antidepressants and anticonvulsant agents. To date there are no convincing studies on the use of these agents in cervical radiculopathy. The mechanism of action for the antidepressant is thought to come from their inhibitory effect on seratonin and norepinephrine uptake, as well as potential substance P reduction.35 The mechanism of action for anticonvulsant medication is even less understood. Medications such as pregabalin have been approved for use in diabetic peripheral neuropathy and post herpetic neuralgia. They therefore have “implied” benefit for cervical radiculopathy and are DM, December 2009
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therefore commonly used off-label. These medications are generally well tolerated when started at a low dose and titrated slowly. Generally, they have few drug interactions and patient contraindications.
Cervical Epidural Steroid Injections There are 2 approaches in this regard, transforaminal and translaminar. The mechanism of action of this therapeutic modality is thought to be the same as its oral counterpart. More specifically it functions to suppress elements of the inflammatory cascade.36 There are 3 presumed benefits if one compares cervical epidural steroid injections to oral steroids: the ability to use a lower dose of steroid, the ability to be directly administered to the area of pathology, and the capability of avoiding some of the systemic effects. The exact success rate of cervical epidural steroid injections is difficult to decipher because of varying study designs as well as techniques used. It is generally accepted to hover around 60%, which is successful at providing long-term relief of pain and improved function.19 There are no conclusive studies comparing the efficacy of transforminal vs interlaminar approach. However, there is, as of late, an expanding amount of literature pointing to the potential serious neurologic sequelae after the cervical transforaminal approach. The mechanism of injury is thought to be either embolic (from particulate matter of the steroid), vasospastic, or thrombotic. All are thought to be caused by inadvertent intra-arterial injection during the procedure. Damage may ensue because of infarct to the spinal cord, midbrain, pons, cerebellum, and temporal and occipital lobes.37 An interlaminar technique, under fluoroscopy, using a low particulate steroid is likely a relatively safe and effective approach.37,38
Rehabilitation Once the acute pain has been managed, a course of rehabilitation is indicated for several reasons. The first is to restore function in a patient who has an inevitable lost in range of motion and has become reconditioned. Second, it would be to help further improve any residual discomfort. Finally, it would be to put into place preventative measures with a goal to avoid recurrence. Because rehabilitation approaches vary and are typically used in conjunction with other modes of treatment (pharmacopia, injections, relative rest, etc), there are no conclusive outcome studies. However, there are numerous studies that demonstrate its successful role when utilized as an adjunct.39-41 A typical approach will likely involve aspects of flexibility strengthening and functional reconditioning. Flexibility will often times address 752
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muscles with a tendency toward tightness (ie, scalenes, trapezius, pectoralis), while strengthening will likely address those muscle with a tendency for relative weakness. These are sometimes referred to as the scapular stabilizers. Strengthening this group of muscles (rhomboids, midtrapezius, etc) will provide support to the cervical spine and attempt to restore appropriate posture. Therapists will also incorporate various mobilization techniques to restore range of motion and reduce pain. For the management of chronic neck pain, specific neck exercises that include active activation of the deep neck muscle and dynamic strengthening can significantly improve disability scores.42 Strength and fitness training may be advised for patients with chronic neck pain, but strength training is much more effective than stretching and aerobic exercising alone.43-45 Passive modalities include the application of heat, electrical stimulation, massage, myofascial release, and traction. Passive modalities are often used to decrease level of pain and inflammation and to facilitate participation in an active rehabilitation program that often involves stretching and strengthening. Active treatment refers to therapeutic exercises that are aimed at improving patient’s strength, endurance, flexibility, posture, and body mechanics. An early, active strategy is recognized to improve functions, increase activity, and prevent chronicity.42 No one modality (see below), in isolation or combination, has been shown to improve recovery from cervical radiculopathy: ● ● ● ● ● ●
Massage/manipulation Cervical traction Ice Heat Electrical stimulation Diathermy
In these authors’ view, they are useful, short-term adjuncts to reduce pain to allow patients to carry out their rehabilitation. Surgical consultation is warranted when there are signs of progressive neurologic decline, more specifically strength. It is also warranted when there are myelopathic signs on physical examination and/or imaging (ie, myelomalacia and cord compression on MRI).
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