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Clinical features and diagnosis of cervical radiculopathy

Clinical features and diagnosis of cervical radiculopathy
Authors:
Milind J Kothari, DO
Kathy Chuang, MD
Section Editor:
Jeremy M Shefner, MD, PhD
Deputy Editor:
Richard P Goddeau, Jr, DO, FAHA
Literature review current through: Dec 2022. | This topic last updated: Oct 06, 2022.

INTRODUCTION — Cervical radiculopathy is a clinical condition due to a pathologic process affecting the nerve root that may cause neck, shoulder, or arm pain, muscle weakness, and/or sensory symptoms.

Neck pain is extremely common and may arise from a number of causes. Cervical spondylosis and disc herniation were not thought to be causes of neck and arm pain until the 1940s, when ruptured cervical discs were first recognized as a cause of radicular symptoms in the arm in the absence of myelopathy [1]. In the early 20th century, symptoms now attributed to cervical radiculopathy were often ascribed to scalenus anticus compression of the brachial plexus and were treated by surgical section of the muscle.

Compressive cervical radiculopathy is recognized to be a common source of arm pain with or without sensory and motor dysfunction.

This topic will review the anatomy, pathophysiology, epidemiology, clinical evaluation, and diagnosis of cervical radiculopathy. The treatment of cervical radiculopathy is discussed separately. (See "Treatment and prognosis of cervical radiculopathy".)

ANATOMY

Spinal column and joints — The cervical spinal column is comprised of seven vertebral bodies. The C1 vertebra (also known as the atlas) is a circular ring of bone without a body or a spinous process. The atlas connects the spine to the occipital bone of the skull superiorly, and articulates with the C2 vertebra (also known as the axis) inferiorly, without an intervening vertebral disc (figure 1).

The body of the C2 vertebra (also known as the axis) gives rise to a protrusion (the odontoid process, or dens) that projects superiorly, around which the atlas rotates.

The other five cervical vertebrae are joined by zygapophyseal (facet) joints located at the posterior portion of the vertebrae. The vertebral body also has a vertical projection called the uncinate process that makes contact with the disc and vertebral body above. The points of contact are the uncovertebral joints, or joints of Luschka, and are located along the lateral surface of the vertebral bodies.

Zygapophyseal joints are true synovial joints that link adjoining vertebral bodies and provide directional stability to the spinal column. The medial branches of the dorsal ramus of the exiting spinal nerve innervates the zygapophyseal joint, and these joints can be a source of pain.

Uncovertebral joints are anteromedial to the exiting nerve roots; they are not true synovial joints. The uncovertebral joints are a frequent site of bony overgrowth.

The vertebral bodies are separated by intervertebral discs, which provide support and mobility. The discs are composed of a gelatinous nucleus pulposus surrounded by a ring (the annulus fibrosis). The disc nucleus is approximately 90 percent water and desiccates with age, undergoing replacement with fibrous tissue. The annulus fibrosis is reinforced by the anterior longitudinal ligament and the posterior longitudinal ligament. The posterior longitudinal ligament does not extend very far laterally, making the nucleus more likely to herniate through the annulus laterally rather than in the midline.

The spinal canal is widest in the upper part of the cervical spine. At the C1 to C3 levels, the maximal anterior posterior dimension of the canal ranges from 16 to 30 mm, and at the C4 through C7 levels it ranges from 14 to 23 mm [2]. The canal narrows an additional 2 to 3 mm with maximal neck extension.

The upper cervical spine is responsible for rotational movements of the head. The lower cervical spine is responsible for flexion and extension movements of the head. Spondylotic disease most commonly occurs in the lower cervical spine, and it is unusual at high cervical levels. (See 'Cervical spondylosis' below.)

Intervertebral foramina — The intervertebral foramina, through which the spinal nerves exit, are bounded on the anteromedial margins by the uncinate processes of the lower cervical vertebral bodies extending superiorly, on the superior margins by the pedicles of the upper cervical vertebral bodies, on the posterior margins by the zygapophyseal joints, and inferiorly by the pedicles of the lower cervical vertebral bodies.

Nerve roots and dorsal root ganglia — The dorsal and ventral spinal nerve roots are formed from rootlets that emerge from the spinal cord. The dorsal roots supply afferent sensory information, and the ventral roots contain efferent fibers that subserve motor function.

The dorsal root ganglia are located on the dorsal nerve roots, usually in the intervertebral foramen, just outside of the spinal dural layer. The dorsal root ganglia contain the cell bodies of the sensory nerve fibers that extend distally into the arm. The cell bodies of the motor nerve fibers are located in the anterior horn cells in the ventral spinal cord.

There is a tendency for the dorsal root ganglia in the upper cervical spine (ie, C4 and C5) to be located closer to the spinal cord than in the lower cervical spine (ie, C7 and C8); however, there is also individual variation [3].

The dorsal and ventral roots fuse to form the spinal nerve in the intervertebral foramen. (See 'Intervertebral foramina' above.)

The spinal nerve is only a few millimeters in length and separates into the ventral and dorsal rami. The dorsal rami travel posteriorly around the interpeduncular joints and divide into lateral motor and medial sensory branches that supply the muscles and skin of the back of the neck.

The dorsal ramus of C1 innervates the deep muscles of the neck and does not have a sensory distribution

The dorsal ramus of C2 travels superiorly to form the greater occipital nerve

The ventral rami continue laterally over the transverse processes, passing immediately behind the vertebral arteries and between the scalene muscles.

The ventral rami arising from the spinal nerves C1 to C4 form the cervical plexus

The ventral rami arising from spinal nerves C5 to T1 form the brachial plexus

There are a few muscles innervated directly by the ventral rami proximal to the brachial plexus:

The dorsal scapular nerve arises directly from the ventral C5 ramus and supplies the rhomboids and levator scapulae muscles

The long thoracic nerve arises directly from the C5, C6, and C7 ventral rami and supplies the serratus anterior muscle

The cervical nerve roots exit through the intervertebral foramen above the corresponding vertebral body. As an example, the C7 nerve root exits through the C6 and C7 intervertebral foramen.

It is important to remember that there are seven cervical vertebrae, but eight cervical nerve roots. As there is no C8 vertebra, the C8 nerve root exits through the C7 to T1 intervertebral foramen.

PATHOPHYSIOLOGY — A radiculopathy is a pathologic process affecting the nerve root. The causes of radiculopathy can be divided into compressive and nondegenerative etiologies. The majority of radiculopathies arise from nerve root compression (figure 2). The two predominant mechanisms of compressive cervical radiculopathy are cervical spondylosis and disc herniation. (See 'Cervical spondylosis' below and 'Disc herniation' below.)

Although compressive radiculopathy is by far more common, the possibility of a nondegenerative disorder should always be considered. (See 'Nondegenerative causes' below.)

Cervical spondylosis — "Spondylosis" is the Greek word for "vertebra," and it is a general term for nonspecific, degenerative changes of the spine. Often, cervical spondylosis is a cause of cervical canal stenosis, but the two terms are not interchangeable.

Although the causes of spondylosis have not been well defined, aging is clearly an important factor. Degenerative changes occur in the vertebral discs, the zygapophyseal and uncovertebral joints, and the vertebral bodies (figure 2). Gradually, there is bone formation in these areas, which is called osteophyte or "hard disc."

Bony growth at the zygapophyseal and uncovertebral joints typically results in neural foraminal narrowing, compression of the nerve roots, and radicular symptoms.

Degenerative changes along the margins of the vertebral bodies and the posterior longitudinal ligament typically result in compression of the spinal cord and myelopathy. A congenitally narrow cervical canal is a risk factor for the development of spondylotic cervical myelopathy [4].

The pathophysiology of spondylosis is not completely understood. One widely cited theory states that the sequence of degenerative changes seen in spondylosis begins with desiccation of the vertebral disc, which is estimated to be 90 percent water in early adult life, but only 69 percent water by the eighth decade of life. As the disc loses water content, the height of the disc decreases and the annulus fibrosis is weakened.

These changes lead to increased stress at the zygapophyseal joints, the vertebral end plates, and the uncovertebral joints. Increased stress is hypothesized to lead to osseous and ligamentous hypertrophy and osteophyte formation. Evidence supporting the role of mechanical stress in spondylosis comes from the observation that spinal degenerative processes, such as osteophyte formation, are most common in the relatively mobile cervical and lumbar regions of the spine and are not prominent in the relatively rigid thoracic spine [2,4-6]. Microscopic examination of vertebral osteophytes supports traction as a mechanism for their formation [7]. Genetic causes may contribute to the degree of spondylitic changes in the spine [8].

Disc herniation — Disc herniation is another common cause of compressive radiculopathy (figure 2). The intervertebral disc is composed of a tough, ligamentous outer annulus and a gelatinous inner nucleus pulposus. The combination of intervertebral pressure and degeneration of the ligamentous fibers can lead to a tear in the annulus, allowing the nucleus pulposus to prolapse through the annulus. Inflammation and radicular symptoms may ensue if the prolapsed material presses on a nerve root.

Disc herniation is most likely to result in root compression and radicular symptoms if it occurs laterally, whereas spinal cord compression and clinical myelopathy can occur if there is herniation of a large midline disc.

In one large series of patients with cervical radiculopathy, disc protrusion was identified as the probable cause in 21.9 percent of patients [9].

Nondegenerative causes — Some causes of nondegenerative radiculopathy include infectious processes (especially herpes zoster and Lyme disease), nerve root infarction, root avulsion, infiltration by tumor, infiltration by granulomatous tissue, demyelination, and inflammatory and neurodegenerative conditions (table 1).

In general, nondegenerative radiculopathies tend to affect the ventral and dorsal root more diffusely than compressive etiologies. In contrast to most compressive types, nondegenerative radiculopathies may also affect the dorsal root ganglion. The deficit associated with nondegenerative radiculopathy may span multiple myotomes and dermatomes, leading to motor and sensory deficits that are more complete than are typical for a compressive radiculopathy.

While cervical spine imaging studies are usually abnormal in compressive radiculopathy, they may be completely normal in nondegenerative radiculopathy. Thus, electrodiagnostic studies may be particularly important to confirm a nondegenerative radiculopathy [10]. (See 'Imaging studies' below and 'Electrodiagnostic studies' below.)

EPIDEMIOLOGY — Cervical radiculopathy is a common cause of both acute and chronic neck pain and upper-limb motor and sensory symptoms. One of the largest epidemiologic studies of cervical radiculopathy was a retrospective population-based review of 561 patients (332 males and 229 females) with cervical radiculopathy seen from 1976 to 1990 in Rochester, Minnesota [9]. All patients with complaints of neck pain were screened, and clinical criteria using symptoms, signs, and diagnostic testing were used to retrospectively make the diagnosis of definite, probable, or possible cervical radiculopathy. A total of 561 cases (332 males and 229 females) with cervical radiculopathy were identified.

The following observations were reported [9]:

The mean age at diagnosis was 47.9 years (range 13 to 91 years)

Average annual incidence rates per 100,000 people for males and females were 107.3 and 63.5, respectively; the male-to-female ratio was 1.7:1

Age-specific incidence rates per 100,000 people were highest for the 50- to 54-year age group, 245.1 in males and 164.5 in females, and declined steeply after the age of 60 years.

A 2020 systematic review similarly reported an incidence of 0.832 and 1.79 per 1000 person-years and prevalence between 1.21 and 5.8 per 1000 people [11].

Lower cervical roots, particularly C7, are more frequently affected by compression than higher cervical roots. In a series of cases that came to surgery, the following observations were made [12]:

C7 was the most frequently affected nerve root, accounting for approximately 70 percent of patients with cervical radiculopathy

C6 root involvement was found in approximately 20 percent

Involvement of the C5, C8, and T1 levels together accounted for the remaining 10 percent

CLINICAL FEATURES — The clinical manifestations of cervical radiculopathy may include neck, shoulder, or arm pain; muscle weakness; sensory symptoms; or diminished deep tendon reflexes, either alone or in combination [6,13]. The clinical features vary by cervical nerve root involvement (table 2).

Onset of symptoms is most frequently acute when caused by a herniated nucleus pulposus but may be more indolent when due to spondylosis. Pain in the neck or arm occurs in nearly all patients with cervical radiculopathy, but it is usually not of localizing value. Pain may be in the cervical region, the upper limb, the shoulder, or the interscapular region. The pain may be atypical and present as chest pain (pseudo-angina), breast pain, or facial pain [14]. Sensory loss in radiculopathy is frequently mild or absent; this seeming paradox is explained by the extensive overlap of dermatomes, although this overlap is not depicted in illustrations of dermatomes (figure 3).

Danger signs — A number of findings may point to cervical myelopathy or suggest noncompressive etiologies for cervical radiculopathy:

Lhermitte phenomenon, a shock-like paresthesia occurring with neck flexion, may be present if there is compression of the cervical cord by a midline disc herniation or spondylosis, but it may also suggest intramedullary pathology, such as a multiple sclerosis plaque.

Although there is no specific presentation of cervical myelopathy, symptoms often begin with an insidious onset of gait disturbance. Other common symptoms include sensory loss, and weakness and muscle atrophy in the hands, along with neck and arm pain. Bowel and bladder incontinence can be seen with cervical myelopathy. The examination usually reveals other myelopathic features. (See "Cervical spondylotic myelopathy", section on 'Clinical presentation'.)

A history of fever, chills, unexplained weight loss, immunosuppression, cancer, or intravenous drug use should raise suspicion for tumor or infection as the cause of the radiculopathy [15].

Rapidly progressive weakness or other symptoms warrant urgent imaging and evaluation for nondegenerative causes.

Antecedent events — Reported antecedent events with cervical radiculopathy have included physical exertion or trauma immediately preceding symptom onset [9,14]. Playing golf, shoveling snow, and diving from a board have also been reported to be antecedent events [14,16]. However, most cases have no readily identifiable precipitant.

EXAMINATION — One major aim of the neurologic examination in patients with suspected cervical radiculopathy is to look for evidence of weakness and sensory disturbance in myotomal and dermatomal patterns. Another major goal is to look for signs of superimposed spinal cord dysfunction (ie, myelopathy), since cervical spondylosis may cause spinal cord compression as well as nerve root compression.

Typical clinical findings of solitary root lesions are summarized in the table (table 2). Paresthesia or numbness in a root distribution occurs in 80 percent of patients, but it also is frequently nonlocalizing. Because of extensive overlap of dermatomes, it is unusual to have well-demarcated, dense sensory loss in lesions of a single root, even if the radiculopathy is severe. Subjective weakness is less common than paresthesias [9]. By contrast, a sharp demarcation of sensory loss is frequently seen in peripheral nerve lesions, and this finding may be a helpful distinguishing feature.

In the presence of pain, it can be difficult to perform an accurate motor examination. In such cases, the reflex examination is a more objective test of nerve root function. Reflexes are typically reduced when radiculopathy involves the C5 (biceps and brachioradialis), C6 (biceps and brachioradialis), or C7 (triceps) nerve roots (table 2), but there are no standard reflexes that reflect the distribution of the C8 and T1 nerve roots.

Motor signs of myelopathy below the level of spinal cord involvement include upper motor neuron type weakness, increased reflexes and tone, clonus, and Babinski and Hoffman signs. Lower motor neuron type weakness may occur at the level of spinal cord compression. Sensory signs include decreased pinprick sensation below the level of spinal cord involvement, loss of position or vibration sensation in the lower extremities, and sensory ataxic gait. These examination findings may be subtle if spinal cord compression is mild. (See "Cervical spondylotic myelopathy", section on 'Clinical presentation'.)

When the differential diagnosis includes non-neurogenic shoulder weakness and wasting, a careful examination of the shoulder, including assessment of passive and active range of motion, is important. (See "Evaluation of the adult with shoulder complaints".)

Spurling maneuver — Spurling maneuver (the neck compression test) is performed by extending and rotating the neck to the side of the pain, followed by applying downward pressure on the head [1]. This maneuver may cause limb pain or paresthesia because neck extension causes posterior disc bulging, whereas lateral flexion and rotation narrow the ipsilateral neural foramina.

The Spurling test is positive if limb pain or paresthesias are produced, and the test should then be stopped. Production of neck pain alone in response to the Spurling maneuver is nonspecific and constitutes a negative test.

The Spurling test has high specificity for the presence of cervical radiculopathy, but its sensitivity is low to moderate [17-19]. As an example, one study that used electrodiagnostic testing as a reference found that Spurling maneuver had a sensitivity and specificity of 30 and 93 percent, respectively [18]. Thus, a positive Spurling test is helpful for supporting the diagnosis of cervical radiculopathy, but a negative test does not rule out radicular pathology.

Caution should be used in performing Spurling maneuver; it should never be performed in patients who may have instability of the cervical spine, such as those with recent severe trauma, rheumatoid arthritis, cervical malformations, or metastatic disease, since it may cause further injury to the spine. In addition, it should not be performed when associated cervical myelopathy is suspected.

Shoulder abduction relief test — With the shoulder abduction relief test, the patient is asked to lift the symptomatic arm above the head, resting the hand on the top of the head. The test is positive if the patient has a decrease or disappearance of the radicular symptoms with this maneuver.

A 2006 systematic review found that the shoulder abduction test demonstrated low to moderate sensitivity and moderate to high specificity [19].

In some patients, the shoulder abduction relief test may also be helpful as a therapeutic maneuver for relief of their pain. (See "Treatment and prognosis of cervical radiculopathy", section on 'Nonsurgical therapy'.)

DIAGNOSTIC EVALUATION — Cervical radiculopathy is a clinical, and to some extent subjective, diagnosis made on the basis of the history and clinical findings. There is no "gold standard" test to establish or exclude the disease. Typical clinical findings of solitary root lesions are summarized in the table (table 2).

Although compressive radiculopathy is by far more common than nondegenerative radiculopathy, the possibility of a nondegenerative disorder should always be considered if the diagnosis is radiculopathy. (See 'Pathophysiology' above.)

Neuroimaging and electrodiagnostic testing are indicated for most patients in the following situations (algorithm 1):

When significant neurologic deficit is present, including myotomal weakness or myelopathy

When there is increased risk of or suspicion for an atypical underlying (nondegenerative) cause, including a neoplastic, infectious, or inflammatory etiology

When there are persistent symptoms that do not resolve with four to six weeks of conservative therapy

Patients without these indicators (ie, those with little or no motor deficit and a low risk of nondegenerative etiologies) do not require immediate testing (algorithm 1).

Imaging studies — Because of the high prevalence of asymptomatic degenerative changes in the cervical spine, an imaging evaluation revealing evidence of degenerative changes or disc herniation can only support the diagnosis of a cervical radiculopathy and cannot by itself establish a diagnosis [20,21]. The problem is illustrated by the results from a case series of 100 patients who were referred for magnetic resonance imaging (MRI) of the larynx and were without symptoms referable to the cervical spine; disc protrusion was found in 5 (20 percent) of 25 patients who were 45 to 54 years old, and 24 (57 percent) of 42 patients 65 and older [20].

In the proper clinical setting of symptoms or signs suggesting radiculopathy, imaging studies of the cervical spine can confirm the diagnosis of compressive radiculopathy [22]. By contrast, imaging may be completely normal in nondegenerative radiculopathy. Imaging with contrast should be performed if a nondegenerative radiculopathy is suspected.

In some patients with cervical radiculopathy, particularly those with C8 radiculopathy, the clinical and electrodiagnostic findings may be caused by nerve root or spinal cord lesions at other levels, as suggested by a retrospective study of 31 patients with isolated C8 radiculopathy who had imaging with MRI or computed tomography (CT) myelography [23]. C8 root compression at C7/T1 (the expected level) was observed in only 16 percent. Other imaging findings included cervical cord compression at or above the C6/C7 level in 23 percent, C7 root compression in 16 percent, intramedullary cervical cord lesions (syringomyelia or enhancing mass) in 13 percent, T1 root compression in 3 percent, and mild or nonspecific findings in 29 percent. Although the precise explanation for the noncorrelative neuroimaging lesions is speculative, the authors considered that upper cervical cord compression may result in a vasculopathy that results in degeneration of anterior horn cells mimicking a C8 radiculopathy, while the intramedullary cervical cord lesions may have preferentially involved C8 motor neurons.

The proposed explanation for C7 root lesions mimicking a C8 radiculopathy invokes the anatomic variant of a "prefixed" brachial plexus, which results in shifting of cervical innervation rostrally by one level [24-26]. Similarly, the explanation for a T1 root lesion mimicking a C8 radiculopathy invokes the anatomic variant of a "postfixed" brachial plexus, in which the cervical innervation is shifted caudally by one level.

MRI — MRI is currently the study of choice in most patients for the initial neuroimaging evaluation of the cervical spine, unless there is a contraindication. MRI generally provides superior imaging of soft tissue structures compared with CT myelography, but less information about bony structures. In addition, MRI may underestimate the amount of bony abnormality.

Gadolinium-enhanced T1 sequences are usually not necessary, but they are mandatory when there is a suspicion of metastatic disease, osteomyelitis, or other inflammatory conditions.

Even with meticulous technique, imaging the neural foramina is difficult, and false-negative and false-positive results occur [27].

CT myelography — CT myelography has been the traditional "gold standard" for the diagnosis of foraminal compression and is also useful for patients with metallic implants that cause distortion of MRI (see 'Issues related to prior surgery' below). CT myelography remains superior to MRI in the distinction of osteophyte from soft tissue material [28,29]. However, some studies suggest that CT myelography may be inadequate to assess developing osteophytes [28,30].

Plain radiographs — Plain radiographs of the cervical spine are rarely diagnostic in the setting of nontraumatic cervical radiculopathy, mainly because radicular symptoms are usually due to impingement of a nerve root by soft tissue, and soft tissue is not well visualized by plain radiographs. Thus, cervical plain films are usually not indicated in the absence of trauma [2].

Cervical plain films remain very important in the management of cervical trauma. In addition, plain films obtained with flexion and extension views of the cervical spine are useful for detecting the subluxation of one vertebral body over another, a condition known as spondylolisthesis. Other routine imaging modalities, such as CT myelography and MRI, image the spine in a neutral position and therefore are not ideal for the detection of spondylolisthesis.

For these reasons, flexion and extension plain films are helpful if myelopathy is present and are part of the routine presurgical evaluation of spinal stability [5].

Issues related to prior surgery — The imaging of patients with a history of cervical spine surgery differs from patients who have never undergone surgery. In patients with metallic implants, CT myelography is generally the procedure of choice, since MRI sequences will be prone to excessive distortion by metallic susceptibility artifacts. CT myelography is also considered by some authors to be the imaging study of choice even for postoperative patients without metallic implants [5]; however, many initially use MRI.

Gadolinium-enhanced, T1-weighted, fat-saturation MRI sequences are useful to assess for epidural scar in the setting of previous cervical spine surgery, as epidural scar strongly and persistently enhances [31]. On the other hand, postoperative soft tissue changes seen on MRI may not be clinically relevant [5].

Electrodiagnostic studies — The diagnosis of radiculopathy is usually supported by a neurodiagnostic study. An upper extremity electrodiagnostic study consists of nerve conduction studies (NCS) and a needle electromyography (EMG) examination of the muscles of the upper arm and neck. The two parts of the examination must be performed together.

Nerve conduction study – NCS alone are not sensitive for radiculopathy, in part because sensory nerve action potentials are normal when the lesion is proximal to the dorsal root ganglion, as it is in radiculopathy [10]. While compound motor action potentials may be reduced in nerve root lesions due to axonal loss, they are not reduced in lesions due to demyelination alone. In addition, chronic axonal lesions are associated with significant reinnervation, which often maintains the amplitude of the compound motor action potential within the normal range.

In patients with suspected radiculopathy, NCS are most useful to exclude entrapment neuropathies, such as carpal tunnel syndrome, as the source of symptoms.

Electromyography – Needle EMG may show a myotomal pattern of abnormalities. A myotome is the group of muscles innervated by a given nerve root. Within the affected myotome, needle EMG may provide information regarding both ongoing axon loss and compensatory reinnervation.

Fibrillation potentials, or spontaneous single muscle fiber action potentials, may be recorded if axon loss is subacute or ongoing. Fibrillation potentials develop two to three weeks after axonal injury and persist as long as muscle fibers remain denervated. Thus, their presence indicates either a recent event or ongoing axon loss. Due to the time between injury and the development of fibrillation potentials, needle EMG is often delayed until symptoms have persisted for three weeks or longer.

In a subacute lesion, fibrillations are seen first in paraspinal muscles and later in arm muscles. However, because of extensive root overlap in paraspinal muscles, fibrillation potentials noted in a specific spinal region do not closely predict the level of root injury [32].

Needle EMG also reveals the presence of reinnervation after axon loss. Over the course of several months, new branches from adjacent nerve fibers grow in to supply muscle fibers that have lost their nerve supply. Reinnervated motor units on needle EMG become longer and larger than normal. This pattern of abnormality suggests radiculopathy when seen in a myotomal pattern.

Mild cervical radiculopathies affecting only the sensory root proximal to the dorsal root ganglion may have normal EMG studies.

Electrodiagnostic studies may be confusing if the dorsal root ganglion is involved by the pathologic process. Dorsal root ganglion involvement may lower sensory amplitudes, and this could falsely suggest that the lesion is in the brachial plexus. This situation is more likely to arise in nondegenerative radiculopathies.

DIFFERENTIAL DIAGNOSIS — Radiating pain and paresthesias in the upper limb have a differential diagnosis that includes entrapment neuropathy of the median, ulnar, or, less commonly, other upper extremity nerves. An entrapped nerve may cause referred pain and paresthesias, such that a patient with isolated median neuropathy at the wrist (ie, carpal tunnel syndrome) may have pain radiating into the forearm and the arm. Similarly, an ulnar neuropathy at the elbow may be associated with pain in the arm and forearm. (See "Carpal tunnel syndrome: Clinical manifestations and diagnosis" and "Ulnar neuropathy at the elbow and wrist".)

Pain in the neck or symptoms that worsen with neck movement are important indicators that the likely diagnosis is not entrapment neuropathy. A brachial plexus lesion is rarely mistaken for a compressive radiculopathy but may present in a seemingly "radicular" manner, particularly if a trunk of the plexus is affected. As an example, the upper trunk of the brachial plexus has contributions only from the C5 and C6 nerve roots, so an upper trunk injury will mimic radiculopathy of the C5 and C6 nerve roots. (See "Brachial plexus syndromes".)

Orthopedic problems that do not involve nerve root compression must be considered when evaluating a patient with neck pain. These problems include pain arising directly from the zygapophyseal or uncovertebral joints, as well as other orthopedic problems of the neck. In addition, shoulder impingement and rotator cuff tears may also present with neck pain, and shoulder pathology may coexist with cervical radiculopathy [33]. (See "Evaluation of the adult with shoulder complaints", section on 'Etiology'.)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Upper spine and neck disorders" and "Society guideline links: Radiculopathy".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Basics topics (see "Patient education: Neck pain (The Basics)")

Beyond the Basics topics (see "Patient education: Neck pain (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

Anatomy – The cervical spinal column is comprised of seven vertebral bodies. The vertebral bodies are separated by intervertebral discs, which provide support and mobility. The dorsal and ventral spinal nerve roots emerge from the spinal cord and travel through the intervertebral foramina. There are seven cervical vertebrae but eight cervical nerve roots. As there is no C8 vertebra, the C8 nerve root exits through the C7 to T1 intervertebral foramen. (See 'Anatomy' above.)

Pathophysiology – A radiculopathy is a pathologic process affecting the nerve root with clinical manifestations that may include pain, motor and sensory symptoms, and reflex change. Most radiculopathies arise from nerve root compression due to cervical spondylosis or disc herniation (figure 2). Less common nondegenerative causes of radiculopathy include infection (especially herpes zoster and Lyme disease), nerve root infarction, infiltration by tumor, infiltration by granulomatous tissue, root avulsion, inflammation, and neurodegenerative causes (table 1). (See 'Pathophysiology' above.)

Clinical manifestations – The clinical manifestations of cervical radiculopathy may include neck, shoulder, or arm pain or upper extremity muscle weakness, sensory symptoms (figure 3), or diminished deep tendon reflexes, either alone or in combination (table 2). (See 'Clinical features' above.)

Physical examination – In patients with suspected cervical radiculopathy, a major goal of the neurologic evaluation is to look for weakness and sensory disturbance in myotomal and dermatomal patterns. Typical clinical findings of solitary root lesions are summarized in the table (table 2). The Spurling maneuver (the neck compression test) and the shoulder abduction relief test have high specificity but poor sensitivity for cervical radiculopathy. (See 'Examination' above.)

Diagnosis and evaluation – Cervical radiculopathy is a clinical diagnosis made on the basis of the history and clinical findings. Immediate diagnostic testing is not necessary for patients with suspected radiculopathy who have little or no motor deficit and are not at increased risk of having an underlying neoplastic, infectious, or inflammatory etiology (algorithm 1). (See 'Diagnostic evaluation' above.)

Neuroimaging and electrodiagnostic testing are indicated when significant neurologic findings or localizing symptoms are present, including myotomal weakness or myelopathy, or when there are persistent radicular symptoms that do not resolve with conservative therapy. (See 'Diagnostic evaluation' above.)

Imaging – MRI is currently the study of choice in most patients for the initial neuroimaging evaluation of the cervical spine. CT myelography is the traditional "gold standard" for the diagnosis of foraminal compression and remains superior to MRI in the distinction of osteophyte from soft tissue material. Flexion and extension plain films are important in the setting of trauma and/or myelopathy and are helpful to evaluate for possible spondylolisthesis. (See 'Imaging studies' above.)

Electrodiagnostic studies – The diagnosis of radiculopathy is usually supported by electrodiagnostic studies including needle electromyography. Nerve conduction studies alone are not sensitive for radiculopathy. The sensitivity of electrodiagnostic studies is reduced if symptoms have been present for less than three weeks. (See 'Electrodiagnostic studies' above.)

Differential diagnosis – The differential diagnosis of radiating pain and paresthesias includes cervical radiculopathy, orthopedic problems of the neck or shoulder, entrapment neuropathy, and brachial plexopathy. (See 'Differential diagnosis' above.)

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Jenice Robinson, MD, who contributed to earlier versions of this topic review.

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