ﺑﺎﺯﮔﺸﺖ ﺑﻪ ﺻﻔﺤﻪ ﻗﺒﻠﯽ
خرید پکیج
تعداد آیتم قابل مشاهده باقیمانده : -12 مورد

Clinical features and diagnosis of cervical radiculopathy

Clinical features and diagnosis of cervical radiculopathy
Authors:
Milind J Kothari, DO
Kathy Chuang, MD
Section Editors:
Jeremy M Shefner, MD, PhD
Glenn A Tung, MD, FACR
Deputy Editor:
Richard P Goddeau, Jr, DO, FAHA
Literature review current through: Apr 2025. | This topic last updated: Nov 05, 2024.

INTRODUCTION — 

Cervical radiculopathy is a clinical condition caused by a pathologic process that impairs function of one or more cervical nerve roots and often leads to neck, shoulder, or arm pain, muscle weakness, and/or numbness. Cervical radiculopathy is most commonly caused by compressive lesions such as degenerative spondylosis and intervertebral disc herniation.

This topic will review the anatomy, causes, clinical features, and diagnosis of cervical radiculopathy. The treatment and prognosis of cervical radiculopathy are discussed separately. (See "Treatment and prognosis of cervical radiculopathy".)

The clinical features and management of other neurologic disorders of the cervical spine or upper extremity are discussed elsewhere.

(See "Cervical spondylotic myelopathy".)

(See "Polyradiculopathy: Spinal stenosis, infectious, carcinomatous, and inflammatory nerve root syndromes".)

(See "Overview of upper extremity peripheral nerve syndromes".)

ANATOMY OF THE CERVICAL SPINE

Spinal column and joints — The cervical spine is comprised of vertebrae separated by intervertebral discs and joints that provide support and mobility. The cervical spinal canal is formed by a column of bony rings from each vertebra and contains the spinal cord. Paired cervical nerves arise from the spinal cord and exit the spinal canal at the intervertebral foramen.

Cervical vertebrae – There are seven numbered cervical vertebrae from the skull base caudal to the first thoracic vertebra.

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).

Cervical vertebrae C2 through C7 have vertebral bodies bounded dorsally by bony vertebral arches (consisting of pedicles, articular facets, and lamina) that meet at a spinous process to form a ring and define the spinal canal. The body of the C2 vertebra gives rise to a protrusion (the odontoid process, or dens) that projects superiorly, around which the atlas rotates.

Cervical spine joints – Multiple joints connect each cervical vertebra with its adjacent bony segment (figure 2).

A pair of atlanto-occipital joints connects the superior facets of the atlas (C1) with the occipital condyles of the skull and permits flexion and extension at the skull base. The medial atlanto-axial joint connects the dens of C2 with articular facets along C1 while paired lateral atlanto-axial joints connect lateral masses of C1 and C2. The atlanto-axial joint permits head rotation and flexion.

The other five cervical vertebrae are connected by intervertebral joints (annulus fibrosis encircling intervertebral discs) along the anterior and posterior aspects of the vertebral bodies as well as specialized paired facet and uncovertebral joints along the lateral aspects of vertebrae.

Zygapophyseal (facet) joints are paired synovial joints located along the lateral mass of a vertebra that link the inferior articular processes with the adjoining superior articular processes of the vertebra below. Facet joints provide directional stability to the spinal column. The medial branches of the dorsal ramus of the exiting spinal nerve innervate the zygapophyseal joint, and these joints can be a source of pain.

Uncovertebral joints (joints of Luschka) are paired joints located along the lateral surface of vertebral bodies that connect the vertical projection (uncinate process) that contacts the vertebral body above. They provide stability and limit lateral flexion of the cervical spine. The uncovertebral joints are a frequent site of bony overgrowth.

Together, these joints permit flexion, extension, lateral flexion, and rotational movement along the cervical spine. The upper cervical spine is chiefly responsible for rotational movements of the head. The lower cervical spine is responsible for most 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 'Degenerative cervical spondylosis' below.)

Intervertebral discs – The vertebral bodies of C2 through C7 are separated by intervertebral discs, which provide spinal 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 (figure 3).

Intervertebral foramen – The intervertebral foramen, 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.

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 [1]. The canal narrows an additional 2 to 3 mm with maximal neck extension.

Cervical nerves — There are eight paired cervical nerves. C1 through C7 are numbered according to the cervical vertebral body below the level where the nerves exit at the neural foramen. As examples, the C1 nerve root exits at the foramen between the skull base and C1 vertebral body, and the C7 nerve root exits through the C6 and C7 intervertebral foramen. As there is no C8 vertebra, the C8 nerve root exits through the C7 to T1 intervertebral foramen (figure 4).

In addition, the first thoracic nerve (T1) may also be classified along with the cervical nerves as it contributes to the brachial plexus and innervation of the arm and hand along with lower cervical nerves.

Cervical nerve roots – The paired dorsal and ventral spinal nerve roots are formed from rootlets that emerge from the spinal cord (figure 5). The dorsal roots supply afferent sensory information, and the ventral roots contain efferent fibers that subserve motor function.

The dorsal root ganglia contain the cell bodies of the sensory nerve fibers that extend distally into the arm. They are located at the dorsal nerve roots, usually in the intervertebral foramen, just outside of the spinal dural layer. The dorsal root ganglia in the upper cervical spine (ie, C4 and C5) are typically located closer to the spinal cord than those in the lower cervical spine (ie, C7 and C8); however, there is variation between individuals [2].

The cell bodies of the motor nerve fibers are located in the anterior horn cells in the ventral spinal cord.

Spinal nerves – The spinal nerves arise from the fusion of the dorsal and ventral nerve roots in the intervertebral foramen. They travel only a few millimeters in length before separating into the ventral and dorsal rami.

The shorter dorsal rami travel posteriorly around the facet joints and divide into lateral motor and medial sensory branches.

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

The dorsal rami of C2 and C3 travel superiorly to form the greater occipital nerve and third occipital nerve, respectively

The dorsal rami of C4 to C7 innervate muscles and skin of the back of the neck

The longer 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 innervates the rhomboids and levator scapulae muscles

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

-The phrenic nerve arises directly from the C3, C4, and C5 ventral rami and innervates the diaphragm

PATHOPHYSIOLOGY AND ETIOLOGIES — 

A radiculopathy is a pathologic process affecting the nerve root or spinal nerve that leads to nerve ischemia and/or inflammation, resulting in impaired neural transmission. Aberrant nerve transmission can cause pain or other sensory dysfunction as well as weakness of muscles innervated by the affected nerve.

Radiculopathy most frequently occurs at the intervertebral foramen but in some cases may also occur more proximally in the lateral recess of the spinal canal or distally along the course of the proximal spinal nerve.

Lower cervical roots are more frequently affected by compression than higher cervical roots [3]. In a series of cases that came to surgery, C7 was the most frequently affected nerve root, accounting for approximately 70 percent of patients with cervical radiculopathy [4]. C6 root involvement was found in approximately 20 percent, while involvement of the C5, C8, and T1 levels together accounted for the remaining 10 percent.

The causes of radiculopathy can be divided into compression from spinal causes and nonstructural etiologies. Most radiculopathies arise from degenerative spinal causes of nerve root compression, most commonly cervical spondylosis or disc herniation (figure 3).

Degenerative cervical spondylosis — Spondylosis is a degenerative process of the joints of the spine and is the most common cause of compressive radiculopathy, accounting for more than 68 percent of cases in a population-based study (figure 3) [3].

Spinal sites – Cervical spondylosis can occur at intervertebral, uncovertebral, and zygapophyseal joints and may cause either radiculopathy due to impingement of nerve roots or myelopathy due to impingement on the spinal cord.

Spondylosis at the zygapophyseal and uncovertebral joints typically results in neural foraminal narrowing, compression of the nerve roots, and radicular symptoms (image 1). Less commonly spondylosis at these joints may cause myelopathy when secondary bony overgrowth impinges on the spinal cord [5].

Spondylosis at the intervertebral joints along the margins of the vertebral bodies and the posterior longitudinal ligament can cause radiculopathy but more typically results in compression of the spinal cord and myelopathy. (See "Cervical spondylotic myelopathy".)

Pathogenesis – The pathogenesis of spondylosis is not completely understood. The degenerative changes seen in spondylosis may begin 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 between the intervertebral discs, and the uncovertebral joints. Increased stress is hypothesized to lead to ligamentous hypertrophy and bony formation, which is called an osteophyte or "hard disc."

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 [1,6-8]. Microscopic examination of vertebral osteophytes supports traction as a mechanism for their formation [9]. Genetic causes may also contribute to the degree of spondylotic changes in the spine [10].

Disc herniation — Intervertebral disc herniation is a common cause of compressive radiculopathy, especially in younger patients (figure 3 and image 2 and image 3) [11]. In one large series of patients with cervical radiculopathy, disc protrusion was identified as the probable cause in 21.9 percent of patients [3].

Spinal sites – Disc herniation is most likely to result in root compression and radicular symptoms if it occurs laterally, whereas spinal cord compression and myelopathy can occur if there is herniation of a large midline disc. Cervical radiculopathy and myelopathy can coexist when a disc herniation is large. (See "Cervical spondylotic myelopathy".)

Pathogenesis – The pathogenesis of disc herniation involves a combination of pressure and degenerative changes at the intervertebral joint. The intervertebral disc is composed of a tough, ligamentous outer annulus fibrosis and a gelatinous inner nucleus pulposus. Age-related degenerative changes lead to desiccation of the nucleus pulposus, reduction of the disc height, and compression with fissures in the annulus fibrosis. This process leads to buckling of the annulus and/or prolapse of disc material through a tear in the annulus, often triggered by a physical activity that results in compression of an adjacent nerve root. Inflammation and radicular symptoms may also occur if prolapsed material presses on a nerve root.

Other causes — Less common sources of cervical radiculopathy include ischemic, traumatic, infiltrative, inflammatory, and neurodegenerative causes (table 1):

Ischemia/infarction (eg, due to diabetes mellitus) [12]

Trauma (eg, root avulsion) (image 4) [13,14]

Infectious processes (eg, herpes zoster, Lyme disease) (image 5 and image 6) [15-17]

Extrinsic compression by tumor, vascular lesion, or inflammation (eg, schwannoma, arterial dissection) (image 7) [18,19]

Infiltration by tumor or granulomatous tissue (eg, sarcoidosis) (image 8) [20]

Inflammatory conditions (eg, Guillain-Barré syndrome, paraneoplastic radiculoneuropathy or neuronopathy) [21]

Nonstructural radiculopathies tend to affect the ventral and dorsal root more diffusely than spondylosis or disc herniation and may also preferentially affect the dorsal root ganglion. In addition, some tumors and inflammatory conditions produce symptoms and signs involving multiple myotomes and dermatomes, indicating a polyradiculopathy rather than a radiculopathy from compression of a single nerve root from spondylosis or herniation. (See "Polyradiculopathy: Spinal stenosis, infectious, carcinomatous, and inflammatory nerve root syndromes".)

While cervical spine imaging studies are usually abnormal in compressive radiculopathy, they may be completely normal in some cases of nonstructural radiculopathy such as nerve root infarction from diabetes mellitus. Thus, electrodiagnostic studies may be particularly important to confirm a nondegenerative radiculopathy as a cause of symptoms [22]. (See 'Neurodiagnostic studies' below.)

EPIDEMIOLOGY — 

Cervical radiculopathy is a common cause of both acute and chronic neck pain and upper-limb motor and sensory symptoms. The prevalence ranges between 1.2 and 5.8 per 1000 people in epidemiologic studies [23]. The mean age of diagnosis of cervical radiculopathy is 48 years old [3]. Incidence rates are highest among males and middle-aged adults, ranging from 64 per 100,000 females to 107 per 100,000 males and increasing from 16 per 100,000 individuals aged 15 to 29 years old up to 203 per 100,000 individuals aged 50 to 54 years old after which it subsequently declines steeply after the age of 60 years [3].

CLINICAL MANIFESTATIONS — 

The clinical features of cervical radiculopathy may include pain, sensory symptoms, and weakness in the neck, shoulder, or arm/hand [8,24]. Specific clinical manifestations vary by cervical nerve root involvement (table 2). (See 'Radicular presentations' below.)

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 even facial pain [25,26]. 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 6). Weakness typically occurs in severe cases of cervical radiculopathy and may be reported by patients or demonstrated on examination. Examination may also show diminished or absent muscle stretch reflexes in the distribution of the involved nerve root.

Temporal features

Antecedent events – Reported antecedent events with cervical radiculopathy include physical exertion or trauma [3,26]. Playing golf, shoveling snow, and diving from a board have also been reported to be antecedent events [26,27]. However, most cases have no readily identifiable precipitant.

Onset – The onset of symptoms is most frequently acute when caused by a herniated nucleus pulposus but may be more indolent when due to spondylosis.

Radicular presentations — Evaluation of symptoms and abnormal findings on neurologic examination can help identify radiculopathy and specify the affected spinal level. Clinical features associated with radiculopathies at specific spinal levels are summarized in the table (table 2) and described in greater detail below.

Of note, significant overlap in dermatomes and shared muscle innervation can make it difficult to discriminate clinically between individual radiculopathies. Similarly, single-level radiculopathies may not present with significant weakness due to shared muscle innervation. The presence of severe weakness in this setting may instead suggest polyradiculopathy, brachial plexopathy, or peripheral nerve as the cause of symptoms. (See 'Other peripheral nerve conditions' below.)

C1 to C4 radiculopathies — Radiculopathies of the upper four cervical roots may be classified together due to their rarity and shared clinical symptoms that localize to the head and neck.

C1 radiculopathy – Mild weakness of neck flexion or extension may be present with a C1 radiculopathy. The C1 nerve root does not have a sensory component, so patients do not have associated sensory loss but may report upper cervical pain associated with muscle weakness.

C2 radiculopathy – Patients may have mild weakness of neck flexion or extension but also may report posterior scalp pain, paresthesias, or sensory loss.

C3 radiculopathy – Pain and sensory loss may be present in the back of the head and upper neck as well as the ear down to the angle of the jaw (figure 7). Motor impairment may involve both neck flexion/extension as well as shoulder elevation.

C4 radiculopathy – Pain typically localizes to the mid or lower neck, and sensory loss may be present in the lower neck and shoulders, while weakness of shoulder elevation may be present.

Upper cervical spine joint dysfunction may lead to a compressive radiculopathy or can be a primary source of pain resulting in chronic headache. (See "Cervicogenic headache".)

C5 radiculopathy — C5 radiculopathy is typically associated with more proximal neck and shoulder symptoms than the more common C6 and C7 radiculopathies.

Pain and sensory symptoms – Pain typically localizes to the neck and shoulder but may also extend to the scapula. Sensory loss may be reported involving the lateral upper arm.

Weakness – Patients may report shoulder or elbow flexion weakness, and examination may identify impairment of shoulder abduction and external rotation along with impaired elbow flexion and possibly forearm supination.

Reflex loss – Diminished ipsilateral biceps and brachioradialis stretch reflexes are common in patients with C5 distribution weakness.

C6 radiculopathy — C6 radiculopathy is the second most common level reported after C7.

Pain and sensory symptoms – Pain may be reported from the ipsilateral neck distally to involve the shoulder, lateral arm, and forearm, as well as the lateral hand. Sensory loss may be reported in the lateral forearm and hand, including the thumb and index finger.

Weakness – C6 radiculopathy may produce weakness similar to motor findings of a C5 radiculopathy, including impairment of shoulder abduction and external rotation along with impaired elbow flexion and forearm pronation. However, C6 radiculopathy is more likely to produce weakness of both forearm supination and pronation.

Reflex loss – Diminished ipsilateral biceps and brachioradialis stretch reflexes are common in patients with weakness.

C7 radiculopathy — Radiculopathy at the C7 level is the most common encountered in clinical practice.

Pain and sensory symptoms – Pain may be proximal, in the neck or shoulder, and/or distally in the hand or middle finger. Sensory loss may localize to the distal hand or middle finger.

Weakness – Weakness may be identified with attempts at elbow extension, wrist extension, forearm pronation, and wrist flexion.

Reflex loss – Loss of stretch reflex at the ipsilateral triceps may be identified in patients with C7 radiculopathy.

C8 radiculopathy — C8 radiculopathy typically involves more distal and medial arm and hand symptoms than the more common C6 or C7 radiculopathies. There is no reliable muscle stretch reflex to test at the C8 level. Some patients may have ipsilateral triceps hyporeflexia. The finger flexion reflex that localizes to the C8 level is difficult to elicit and can be challenging to interpret because asymmetric findings may indicate either peripheral nerve impairment on the hypoactive side or contralateral central dysfunction on the comparatively hyperactive side.

Pain and sensory symptoms – Pain and sensory symptoms are typically reported in the medial aspect of the forearm and hand, including the fourth and fifth digits. Some patients also report proximal pain in the ipsilateral neck and shoulder as well.

Weakness – Weakness may be identified with wrist or proximal finger extension as well as distal finger flexion, extension, adduction, and abduction.

T1 radiculopathy — Radiculopathy at the first thoracic level is sometimes classified with cervical radiculopathies because the nerve roots that form the brachial plexus and innervation to the arm and hand span the C5 through T1 levels (figure 8 and figure 6). However, T1 radiculopathy due to cervical spondylotic changes or disc herniation is relatively uncommon due to the presence of the first rib which limits range of motion at this level. There is no stretch reflex to test at the T1 level.

Pain and sensory symptoms – Pain and sensory loss in the medial arm and forearm may be reported in patients with a T1 radiculopathy.

Weakness – Weakness of thumb abduction and flexion and finger abduction and adduction may be found in T1 radiculopathy.

DIAGNOSTIC EVALUATION — 

Cervical radiculopathy is a clinical diagnosis made based on compatible history and clinical findings. There is no "gold standard" test to establish or exclude the condition.

Neuroimaging and other diagnostic testing are reserved for select patients with high-risk features for suspected structural or inflammatory conditions and those with progressive or severe weakness who are at risk for permanent neurologic impairment. (See 'Diagnostic testing for selected patients' below.)

Clinical diagnosis

History — Patients frequently report a radicular pattern of pain and/or paresthesias at the onset of cervical radiculopathy. Some may report a specific activity that triggered the onset of symptoms, especially if it is due to intervertebral disc herniation.

Patients with motor involvement may report functional impairments such as an inability to perform manual tasks (eg, grasping an object, buttoning a shirt). Weakness in muscles innervated by multiple nerve roots may be mild and inapparent to the patient, identified on neurologic examination or electrodiagnostic testing only.

Patients with radicular symptoms should be assessed for associated systemic features suggestive of infectious, neoplastic, or inflammatory etiology that warrant neuroimaging. (See 'Diagnostic testing for selected patients' below.)

Physical examination — A careful neurologic examination is performed to localize symptoms to a specific nerve root (table 2) (see 'Radicular presentations' above) as well as to identify features suggestive of alternative conditions such as cervical myelopathy or musculoskeletal mimics. (See 'Differential diagnosis' below.)

Patients with a suspected infectious cause of cervical radiculopathy also require a general examination to assess for rash (eg, vesicles) or meningismus. Similarly, patients with weakness and wasting of the shoulder girdle muscles should undergo a careful examination of the shoulder, including assessment of passive and active range of motion. (See "Evaluation of the adult with shoulder complaints".)

Neurologic examination – The pattern of numbness, weakness, and/or diminished or absent stretch reflexes can help identify dysfunction at specific nerve root levels (table 2).

Paresthesia or numbness in a root distribution occurs in 80 percent of patients with cervical radiculopathy, but it is frequently nonlocalizing. Because of the 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. Paresthesias are more common than numbness [3]. By contrast, a sharp demarcation of sensory loss is more frequently seen in peripheral nerve lesions.

Weakness may be present in muscles innervated by the affected root. However, muscle weakness must be distinguished from inadequate voluntary effort due to pain. In addition, motor findings in patients with a radiculopathy are often mild or absent in muscles that are powerful or innervated by multiple nerve roots. Weakness with atrophy suggests chronic motor impairment.

Muscle stretch reflex abnormalities can be an objective measure of focal neurologic dysfunction, including for patients with nonlocalizing sensory findings or a pain-limited motor examination [28]. Reflexes are typically reduced ipsilaterally when radiculopathy involves the C5 (biceps and brachioradialis), C6 (biceps and brachioradialis), or C7 (triceps) nerve roots. Impairment of the finger flexion reflex may occasionally be seen with some patients with a C8 radiculopathy, but there are no standard reflexes that reflect the distribution of the upper cervical or T1 nerve roots.

Provocative maneuvers – Specific clinical maneuvers may be performed as a part of the physical examination to help identify cervical radiculopathy as the source of symptoms.

Spurling maneuver – The Spurling maneuver (or neck compression test) is performed by extending and rotating the patient’s neck to the side of the pain, followed by applying downward pressure on the head (picture 1) [25]. The Spurling test is positive if limb pain or paresthesias are produced, and the test should then be stopped. Limb pain or paresthesia occurs because neck extension causes posterior disc bulging, whereas lateral flexion and rotation narrow the ipsilateral neural foramina.

Production of neck pain alone in response to the Spurling maneuver is nonspecific and constitutes a negative test.

Caution should be used in performing the Spurling maneuver; it should not 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. (See 'Cervical spondylotic myelopathy' below.)

The Spurling test has high specificity for the presence of cervical radiculopathy, but its sensitivity is low to moderate [29-31]. As an example, one study that used electrodiagnostic testing as a reference found that the Spurling maneuver had a sensitivity and specificity of 30 and 93 percent, respectively [30].

Shoulder abduction relief test – The shoulder abduction relief test is performed by asking the patient to lift the symptomatic arm above the head and rest the extended hand on the top of the head. The test is positive if the patient has an improvement in or resolution of the radicular symptoms.

A 2006 systematic review found that the shoulder abduction test demonstrated low to moderate sensitivity and moderate to high specificity [31].

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

Diagnostic testing for selected patients

Indications for testing — Neuroimaging with or without other diagnostic testing is indicated for patients with the clinical diagnosis of cervical radiculopathy who have the following features (algorithm 1):

Severe or progressive neurologic deficit, including those with myotomal weakness or those with nonmyotomal weakness (eg, bilateral or multiple spinal level involvement) and/or urinary retention suspicious for myelopathy. (See 'Cervical spondylotic myelopathy' below.)

Associated features suggestive of possible traumatic, infectious, neoplastic, or inflammatory etiology, including [28]:

Fever, chills, and/or night sweats

Unexplained weight loss

Immunosuppression (eg, concurrent chemotherapy or immunosuppressive therapy)

Antecedent trauma

Active or prior malignancy

History of inflammatory arthritis

Intravenous recreational drug use

Active anticoagulant therapy

Age ≥60 years

Symptoms that persist despite four to six weeks of conservative therapy

We typically start with neuroimaging of the cervical spine and perform neurodiagnostic studies and other testing when cervical spine imaging is nondiagnostic.

For other patients who have a clinical diagnosis of acute cervical radiculopathy and milder symptoms without features suggestive of a high-risk underlying infectious, neoplastic, or hemorrhagic mechanism, we start with conservative therapy (see "Treatment and prognosis of cervical radiculopathy", section on 'Our approach'). Acute cervical radiculopathy can be painful but is often self-limited when due to degenerative spondylosis or disc herniation, which are common causes of the condition.

Neuroimaging — For patients with a clinical diagnosis of cervical radiculopathy who have an indication for diagnostic testing, we perform neuroimaging of the cervical spine to identify a structural abnormality that correlates with clinical symptoms.

Selection of imaging modality — Multiple imaging modalities may be used to support the diagnosis of cervical radiculopathy. Magnetic resonance imaging (MRI) of the cervical spine without contrast is typically used as the initial test to identify bony and soft tissue abnormalities that may be present in patients with common compressive causes of radiculopathy. However, computed tomography (CT) is frequently the initial test in the setting of acute traumatic injury and may also be used as an alternative study for patients unable to undergo MRI.

MRI — For most patients, cervical spine MRI is the preferred study for the initial evaluation of the cervical spine [32]. Noncontrast MRI studies are used for most patients with possible compressive causes of radiculopathy (image 2). However, gadolinium-enhanced T1 sequences are required when there is a suspicion of metastatic disease, osteomyelitis, or other inflammatory conditions (image 5 and image 7). 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 fibrosis strongly and persistently enhances [33]. However, postoperative soft tissue changes seen on MRI may not be clinically relevant [7].

MRI generally provides superior imaging of soft tissue structures compared with CT myelography but may underestimate the amount of bony abnormality. Even with meticulous technique, imaging the neural foramina is difficult, and false-negative and false-positive results occur [34].

CT – CT of the cervical spine may be performed as an alternative initial imaging test for patients unable to obtain an MRI [32]. Noncontrast CT imaging is typically performed to assess for cervical radiculopathy, but contrast should be used if an inflammatory, infectious, or neoplastic condition is suspected. CT may provide detailed information about bony changes at the neural foramina, the presence of osteophytes, and narrowing of intervertebral disc space (image 1) but does not well identify nerve roots to confirm compression. CT is also commonly used in patients with a traumatic onset of symptoms to identify or exclude a vertebral fracture.

CT myelography — CT myelography is an alternative for patients who are not able to undergo MRI or for patients with metallic implants that cause imaging distortion with MRI. Some authors also consider it the imaging study of choice for some patients without metallic implants, such as those in the postoperative setting following cervical spine surgery [7].

CT myelography may be superior to MRI in distinguishing osteophytes from soft tissue material and to identify ventral and dorsal nerve roots (image 3) [35,36]. However, some studies suggest that CT myelography may be inadequate to assess developing osteophytes [35,37]. In addition, CT myelography requires the use of contrast and exposes patients to radiation, unlike MRI.

Plain radiographs — Plain radiographs of the cervical spine are rarely diagnostic in the setting of cervical radiculopathy, except for patients following a trauma [1]. Nerve roots, disc herniation, and other soft tissues of the cervical spine are not well visualized by plain radiographs.

Selected patients with a suspicion of cervical radiculopathy due to spondylolisthesis may warrant cervical spine radiographs obtained with flexion and extension views to identify vertebral subluxation. 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.

Limitations of imaging — Imaging studies of the cervical spine can support the diagnosis of compressive radiculopathy in the proper clinical setting of symptoms or signs suggesting radiculopathy [38]. However, imaging findings alone do not establish the diagnosis of cervical radiculopathy because abnormal findings may represent false-positive or clinically irrelevant results in some cases, and normal findings may represent false-negative results in other cases [39-41].

Asymptomatic abnormalities – Abnormal spinal imaging findings must be correlated with clinical findings because of the high prevalence of asymptomatic degenerative changes in the cervical spine. In a case series of 100 patients who were referred for 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 years and older [39].

Mislocalized lesion – In rare patients with cervical radiculopathy, the clinical findings localized by neurologic examination and correlated with neurodiagnostic studies have been found to be caused by nerve root or spinal cord lesions at other levels. In a retrospective study of 31 patients with C8 radiculopathy on examination who had imaging with MRI or CT myelography, C8 root compression at C7/T1 (the expected level) was observed in only 16 percent [41]. 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 hypothesized that upper cervical cord compression may result in a vasculopathy that leads to degeneration of anterior horn cells mimicking a C8 radiculopathy, while the intramedullary cervical cord lesions may have preferentially involved C8 motor neurons. Alternative explanations include an anatomic variant of a "prefixed" brachial plexus, which results in the shifting of cervical innervation rostrally by one level [42-44]. Similarly, a T1 root lesion may mimic a C8 radiculopathy in the setting of a "postfixed" brachial plexus, in which the cervical innervation is shifted caudally by one level.

Nonstructural etiologies – Neuroimaging is performed to support the diagnosis of compressive causes of cervical radiculopathy. However, imaging may be completely normal in some causes of nondegenerative radiculopathy, such as nerve root infarction or inflammatory conditions such as Guillain-Barré syndrome.

Neurodiagnostic studies — We perform neurodiagnostic testing for patients with suspected cervical radiculopathy who have an indication for diagnostic testing when neuroimaging is nondiagnostic or when the relation between symptoms and abnormal imaging results is uncertain.

The clinical diagnosis of radiculopathy may be confirmed by neurodiagnostic studies. Upper extremity electrodiagnostic studies consist 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 may support the clinical diagnosis of cervical radiculopathy in some patients with motor impairment. Compound motor action potentials may be reduced in nerve root lesions due to axonal loss. In addition, NCS may be useful to exclude other causes of symptoms such as entrapment neuropathies (eg, carpal tunnel syndrome) as the source of symptoms or to identify when radiculopathy and an entrapment neuropathy coexist.

However, 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 many cases of cervical radiculopathy [22]. In addition, compound motor action potentials are not reduced in lesions due to demyelination alone. Even some chronic axonal lesions may be difficult to detect with NCS due to reinnervation, which often maintains the amplitude of the compound motor action potential within the normal range.

Electromyography – Needle EMG may help confirm the diagnosis of a radiculopathy by showing a myotomal pattern of abnormalities. A myotome is a group of muscles innervated by a given nerve root. Peripheral nerve impairment such as from a radiculopathy causes abnormal muscle activity that can be detected with EMG. Within the affected myotome, 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. Fibrillations are seen earliest 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 [45].

Needle EMG also reveals the presence of reinnervation after axon loss. Over the course of several months, new branches from adjacent nerve fibers grow to innervate 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 in 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 nonstructural radiculopathies.

Neurodiagnostic testing is typically delayed until symptoms have persisted for three weeks or longer; a false negative result may be obtained if the studies are performed earlier.

Laboratory testing and cerebrospinal fluid analysis — Laboratory testing and/or lumbar puncture for cerebrospinal fluid (CSF) analysis are typically performed to identify an infectious, inflammatory, or neoplastic cause of cervical radiculopathy when the etiology remains uncertain despite neuroimaging and neurodiagnostic studies.

Infectious and systemic causes of radiculopathy include Lyme disease, herpes zoster infection, and sarcoidosis, amongst others. (See "Clinical manifestations of Lyme disease in adults" and "Epidemiology, clinical manifestations, and diagnosis of herpes zoster" and "Neurologic sarcoidosis".)

DIFFERENTIAL DIAGNOSIS — 

The differential diagnosis of cervical radiculopathy includes both central nervous system conditions of the cervical spine and brain and peripheral nerve conditions of the upper extremities, as well as nonneurologic conditions that produce pain, numbness, and/or weakness in the neck/shoulder/arm. Specific clinical features that help localize symptoms and the presence of associated features may help identify these alternative causes of symptoms.

Cervical spondylotic myelopathy — Patients with compressive cervical cord myelopathy (image 9) may present with neck pain along with radicular symptoms at the level of compression similar to patients with cervical radiculopathy. However, neurologic symptoms extend beyond a radicular distribution including bilateral motor and/or sensory symptoms. Sensory signs may 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. In addition, specific myelopathic features may include:

Increased muscle tone and spasticity caudal to the level of the spinal dysfunction

Hyperactive muscle stretch reflexes

Presence of pathologic reflexes (eg, Babinski and Hoffman signs) and clonus

Bladder dysfunction

The Lhermitte phenomenon, a shock-like paresthesia occurring with neck flexion, may also be present if there is compression of the cervical cord by a midline disc herniation or spondylosis.

Although the specific presentation of cervical myelopathy varies by spinal level and severity of compression, symptoms often begin with an insidious onset of gait disturbance. The examination usually reveals other myelopathic features. (See "Cervical spondylotic myelopathy".)

Other peripheral nerve conditions — Peripheral nerve impairment is typically distinguished from more proximal radiculopathy by identifying symptoms or signs beyond a radicular distribution.

Brachial plexopathy – A brachial plexus lesion typically consists of patchy or widespread upper extremity sensory and motor symptoms and is rarely mistaken for a cervical radiculopathy but may present in a seemingly "radicular" manner 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. A dermatomal pattern of sensory symptoms may also help distinguish radiculopathy from more distal brachial plexus lesions (figure 9). (See "Brachial plexus syndromes".)

Upper extremity mononeuropathy – Mononeuropathies of the median, ulnar, or, less commonly, other upper extremity nerves are typically distinguished from radiculopathies by identifying a peripheral nerve distribution to symptoms or signs (figure 10 and figure 11). However, pseudoradicular sensory symptoms in some patients with an entrapped nerve may make it somewhat difficult to identify a mononeuropathy as the cause of symptoms. As examples, isolated median neuropathy at the wrist (ie, carpal tunnel syndrome) may produce pain in the hand that also radiates into the forearm and the arm, while an ulnar neuropathy at the elbow may be associated with pain in the forearm as well as the upper arm. The distribution of motor symptoms and/or electrodiagnostic testing may be used to discriminate in these cases. (See "Carpal tunnel syndrome: Clinical manifestations and diagnosis" and "Ulnar neuropathy at the elbow and wrist".)

In addition, neck pain or symptoms that worsen with neck movement are important indicators that the likely diagnosis is not a more peripheral nerve condition such as a plexopathy or entrapment neuropathy.

Musculoskeletal conditions of the neck or shoulder — Orthopedic conditions of the cervical spine that do not involve nerve root compression can cause neck pain similar to symptoms in cervical radiculopathy [46]. These spinal problems occur when pain arises directly from the zygapophyseal or uncovertebral joints, or other cervical spinal structures. Weakness may be apparent when pain leads to inadequate effort on clinical examination, but the pattern is not usually radicular. Electrodiagnostic testing may be performed in some cases to exclude nerve pathology as a cause of symptoms.

These spinal conditions include:

Cervical muscle strain

Cervical discogenic pain

Facet or uncovertebral osteoarthritis

Diffuse skeletal hyperostosis

Symptomatic cervical spondylosis

Cervicogenic headache

The specific clinical features and diagnosis of these conditions are discussed separately. (See "Evaluation of the adult patient with neck pain" and "Cervicogenic headache".)

Orthopedic conditions of the shoulder may also mimic cervical radiculopathy by producing localized pain or associated weakness and sensory disturbance in the shoulder and/or arm [46]. Careful evaluation may distinguish these conditions from a radiculopathy by identifying symptoms and signs that do not conform to a radicular distribution. Imaging of the shoulder may also help identify these conditions as the cause of symptoms. These conditions include:

Rotator cuff tear (see "Presentation and diagnosis of rotator cuff tears")

Adhesive capsulitis (see "Frozen shoulder (adhesive capsulitis)")

Thoracic outlet syndrome (see "Overview of thoracic outlet syndromes")

Biceps tendinopathy (see "Biceps tendinopathy and tendon rupture")

Glenohumeral osteoarthritis (see "Evaluation of the adult with shoulder complaints", section on 'Glenohumeral osteoarthritis')

Of note, patients with orthopedic conditions of the spine or shoulder may have coexisting cervical radiculopathy [47].

Other conditions

Meningitis – Some patients with subacute or chronic meningitis may present with symptoms suggestive of a cervical radiculopathy due to focal inflammation or demyelination at the nerve root. However, most patients with meningitis have bilateral or multilevel symptoms due to more widespread inflammation than with patients who have other infectious causes of cervical radiculopathy. Such patients also typically have systemic symptoms including fever and meningismus. CSF findings in meningitis typically include an elevated protein concentration and leukocytosis. CSF culture may help identify the infectious agent. (See "Cerebrospinal fluid: Physiology, composition, and findings in disease states", section on 'Central nervous system infection'.)

Rheumatologic conditions – Patients with polymyalgia rheumatica, rheumatoid arthritis, fibromyalgia, or other rheumatologic conditions may present with neck and shoulder/arm pain but typically also note bilateral symptoms and pain in other areas along with additional systemic symptoms such as fatigue, unintentional weight loss, and fevers. (See "Clinical manifestations and diagnosis of polymyalgia rheumatica" and "Clinical manifestations of rheumatoid arthritis" and "Fibromyalgia: Clinical manifestations and diagnosis in adults".)

Vertebral artery dissection – Vertebral artery dissection typically produces unilateral neck and head pain and may cause sensory or motor symptoms in the arm due to associated brainstem ischemia. The presence of a Horner syndrome and/or nonradicular pattern to motor or sensory loss can help discriminate dissection with stroke from radiculopathy. Brain neuroimaging is performed to identify or exclude stroke in patients with suspected symptoms. (See "Cerebral and cervical artery dissection: Clinical features and diagnosis".)

In rare instances, a vertebral dissection may cause a radiculopathy when an intramural hematoma or inflammation within the cervical segment of the artery compresses the adjacent cervical nerve root [18,48].

Stroke and other cerebral lesions – Cerebral lesions such as stroke or tumors may rarely cause pseudoradicular symptoms such as isolated hand weakness and/or numbness [49-52]. Onset is typically sudden and pain does not usually accompany neurologic deficits due to small cortical strokes, unlike symptoms in cervical radiculopathy. Brain neuroimaging is performed for patients with suspected stroke or neoplasm. (See "Neuroimaging of acute stroke".)

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 spine is comprised of cervical vertebrae which are separated by intervertebral discs and cervical spine joints (figure 2) that provide support and mobility. The cervical spinal canal is formed by a column of bony rings from each vertebra and contains the spinal cord. Eight paired cervical nerves arise from the spinal cord (figure 5) and exit the spinal canal at the intervertebral foramen below the level of the adjacent vertebral body (figure 4). (See 'Anatomy of the cervical spine' above.)

Causes – Most radiculopathies arise from degenerative spinal causes of nerve root compression, most commonly cervical spondylosis or disc herniation (figure 3). 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 and etiologies' above.)

Clinical manifestations – The clinical features of cervical radiculopathy may include pain, sensory symptoms (figure 6), and weakness in the neck, shoulder, or arm/hand. Specific clinical manifestations vary by cervical nerve root involvement (table 2). (See 'Clinical manifestations' above.)

Clinical diagnosis – Cervical radiculopathy is a clinical diagnosis based on compatible history and clinical findings. Patients frequently report a radicular pattern of pain and/or paresthesias at the onset of cervical radiculopathy. Physical examination may reveal a pattern of numbness, weakness, and/or stretch reflex changes that correspond to specific nerve root levels (table 2). Specialized clinical maneuvers such as the Spurling test (picture 1) and the shoulder abduction relief test may also be performed to help identify cervical radiculopathy as the source of symptoms. (See 'Diagnostic evaluation' above.)

Indications for diagnostic testing – Neuroimaging with or without other diagnostic testing is indicated for patients with the clinical diagnosis of cervical radiculopathy who have the following features (algorithm 1):

Severe or progressive neurologic deficit, including those with myotomal weakness or those with nonmyotomal weakness (eg, bilateral or multiple spinal level involvement) and/or urinary retention suspicious for myelopathy

Associated features suggestive of possible traumatic infectious, neoplastic, or inflammatory etiology, including:

-Fever, chills, and/or night sweats

-Unexplained weight loss

-Immunosuppression (eg, concurrent chemotherapy or immunosuppressive therapy)

-Antecedent trauma

-Active or prior malignancy

-History of inflammatory arthritis

-Intravenous recreational drug use

-Active anticoagulant therapy

-Age ≥60 years

Symptoms that persist despite four to six weeks of conservative therapy

For other patients who have a clinical diagnosis of acute cervical radiculopathy and milder symptoms without features suggestive of a high-risk mechanism, we start with conservative therapy (see "Treatment and prognosis of cervical radiculopathy", section on 'Our approach'). Acute cervical radiculopathy can be painful but is often self-limited when due to degenerative spondylosis or disc herniation, which are common causes of the condition.

Neuroimaging – For patients with a clinical diagnosis of cervical radiculopathy who have an indication for diagnostic testing, we perform neuroimaging of the cervical spine to identify a structural abnormality to correlate with clinical symptoms. MRI of the cervical spine without contrast is the preferred initial test to identify bony and soft tissue abnormalities found in common compressive causes of radiculopathy (image 2), whereas contrast is used in suspected inflammatory, infectious, or neoplastic causes (image 5 and image 7). CT may be used as an alternative to MRI. (See 'Neuroimaging' above.)

Neurodiagnostic testing – For patients who have an indication for diagnostic testing, we perform neurodiagnostic testing at least three weeks after symptom onset to confirm the diagnosis of cervical radiculopathy when neuroimaging is nondiagnostic or when the relation between symptoms and abnormal imaging results is uncertain. (See 'Neurodiagnostic studies' above.)

Differential diagnosis – The differential diagnosis of cervical radiculopathy includes both central nervous system conditions of the cervical spine and brain and peripheral nerve conditions of the upper extremities, as well as nonneurologic conditions that produce pain, numbness, and/or weakness in the neck/shoulder/arm. Specific clinical features that help localize symptoms and the presence of associated features may help identify these alternative causes of symptoms. (See 'Differential diagnosis' above.)

ACKNOWLEDGMENT — 

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

  1. Levin K. Cervical Radiculopathies. In: Neuromuscular disorders in clinical practice, Katirji M, Kaminski H, Preston D, et al. (Eds), Butterworth-Heinemann, Boston 2001. p.836.
  2. Yabuki S, Kikuchi S. Positions of dorsal root ganglia in the cervical spine. An anatomic and clinical study. Spine (Phila Pa 1976) 1996; 21:1513.
  3. Radhakrishnan K, Litchy WJ, O'Fallon WM, Kurland LT. Epidemiology of cervical radiculopathy. A population-based study from Rochester, Minnesota, 1976 through 1990. Brain 1994; 117 ( Pt 2):325.
  4. YOSS RE, CORBIN KB, MACCARTY CS, LOVE JG. Significance of symptoms and signs in localization of involved root in cervical disk protrusion. Neurology 1957; 7:673.
  5. ElFiky T, Bessada B, Stienen MN, et al. Endplate and Facet Joint Changes in Cervical Spondylotic Myelopathy. World Neurosurg 2023; 175:e361.
  6. Lestini WF, Wiesel SW. The pathogenesis of cervical spondylosis. Clin Orthop Relat Res 1989; :69.
  7. Storm PB, Chou D, Tamargo RJ. Surgical management of cervical and lumbosacral radiculopathies: indications and outcomes. Phys Med Rehabil Clin N Am 2002; 13:735.
  8. Theodore N. Degenerative Cervical Spondylosis. N Engl J Med 2020; 383:159.
  9. Rothschild B, Biehler-Gomez L. Osteophytes: The product of convergent evolution. Anat Rec (Hoboken) 2022; 305:2113.
  10. Karadimas SK, Erwin WM, Ely CG, et al. Pathophysiology and natural history of cervical spondylotic myelopathy. Spine (Phila Pa 1976) 2013; 38:S21.
  11. Polston DW. Cervical radiculopathy. Neurol Clin 2007; 25:373.
  12. Mashauri HL, Makunga FJ, Luhwago EC, et al. Is it myocardial infarction? A case report of C7 cervical radiculopathy with cervical angina. SAGE Open Med Case Rep 2024; 12:2050313X231223434.
  13. Newman WC, Tempel ZJ, Tyler-Kabara EC. Posttraumatic Cervical Nerve Root Avulsion with Epidural Hematoma. World Neurosurg 2015; 84:1177.e9.
  14. Nayman A, Altan E, Koplay M, Kıvrak AS. Post-traumatic cervical nerve root avulsion: direct and indirect magnetic resonance myelography findings. Spine J 2015; 15:2103.
  15. Gumina S, Candela V, Passaretti D, Villani C. Shoulder pain due to cervical radiculopathy: an underestimated long-term complication of herpes zoster virus reactivation? Int Orthop 2018; 42:157.
  16. Nomura H, Nomura S. Simultaneous herpes zoster rash in the upper extremity and interscapular region that resembles innervation zone of the dorsal ramus of the cervical nerve root: a case report. AME Case Rep 2021; 5:25.
  17. Halperin JJ. Neuroborreliosis. J Neurol 2017; 264:1292.
  18. Bucak B, Essibayi MA, Holmes CR, et al. Cervical radiculopathy secondary to vertebral artery dissection: clinical features and outcomes. Neurol Res 2024; 46:339.
  19. Komatsu K, Toda H, Matsumoto S. Sudden-onset C8 Radiculopathy due to a Plexiform Schwannoma of the Cervical Nerve Root. Intern Med 2018; 57:3317.
  20. Tipper GA, Fareedi S, Harrison K, Tamam A. Neurosarcoidosis mimicking acute cervical disc prolapse. Br J Neurosurg 2011; 25:759.
  21. Siddiqi M, Sardar S, Alhatou MI. A young man with Guillain-Barré syndrome, with a stroke-like presentation and physical findings suggestive of cervical myelopathy. Qatar Med J 2023; 2023:16.
  22. Preston D, Shapiro B. Radiculopathy. In: Electromyography and Neuromuscular Disorders, Butterworth-Heinemann, Boston 2005. p.459.
  23. Mansfield M, Smith T, Spahr N, Thacker M. Cervical spine radiculopathy epidemiology: A systematic review. Musculoskeletal Care 2020; 18:555.
  24. Iyer S, Kim HJ. Cervical radiculopathy. Curr Rev Musculoskelet Med 2016; 9:272.
  25. Semmes R, Murphey M. The syndrome of unilateral rupture of the sixth cervical intervertebral disk with compression of the seventh cervical nerve root. A report of four cases with symptoms simulating coronary disease. JAMA 1943; 121:1209.
  26. Ellenberg MR, Honet JC, Treanor WJ. Cervical radiculopathy. Arch Phys Med Rehabil 1994; 75:342.
  27. Kelsey JL, Githens PB, Walter SD, et al. An epidemiological study of acute prolapsed cervical intervertebral disc. J Bone Joint Surg Am 1984; 66:907.
  28. Carette S, Fehlings MG. Clinical practice. Cervical radiculopathy. N Engl J Med 2005; 353:392.
  29. Viikari-Juntura E, Porras M, Laasonen EM. Validity of clinical tests in the diagnosis of root compression in cervical disc disease. Spine (Phila Pa 1976) 1989; 14:253.
  30. Tong HC, Haig AJ, Yamakawa K. The Spurling test and cervical radiculopathy. Spine (Phila Pa 1976) 2002; 27:156.
  31. Rubinstein SM, 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.
  32. Bono CM, Ghiselli G, Gilbert TJ, et al. An evidence-based clinical guideline for the diagnosis and treatment of cervical radiculopathy from degenerative disorders. Spine J 2011; 11:64.
  33. Ross JS, Robertson JT, Frederickson RC, et al. Association between peridural scar and recurrent radicular pain after lumbar discectomy: magnetic resonance evaluation. ADCON-L European Study Group. Neurosurgery 1996; 38:855.
  34. Kuijper B, Tans JT, van der Kallen BF, et al. Root compression on MRI compared with clinical findings in patients with recent onset cervical radiculopathy. J Neurol Neurosurg Psychiatry 2011; 82:561.
  35. Bartlett RJ, Hill CR, Gardiner E. A comparison of T2 and gadolinium enhanced MRI with CT myelography in cervical radiculopathy. Br J Radiol 1998; 71:11.
  36. Modic MT, Masaryk TJ, Mulopulos GP, et al. Cervical radiculopathy: prospective evaluation with surface coil MR imaging, CT with metrizamide, and metrizamide myelography. Radiology 1986; 161:753.
  37. Houser OW, Onofrio BM, Miller GM, et al. Cervical neural foraminal canal stenosis: computerized tomographic myelography diagnosis. J Neurosurg 1993; 79:84.
  38. Nardin RA, Patel MR, Gudas TF, et al. Electromyography and magnetic resonance imaging in the evaluation of radiculopathy. Muscle Nerve 1999; 22:151.
  39. Teresi LM, Lufkin RB, Reicher MA, et al. Asymptomatic degenerative disk disease and spondylosis of the cervical spine: MR imaging. Radiology 1987; 164:83.
  40. Boden SD, McCowin PR, Davis DO, et al. Abnormal magnetic-resonance scans of the cervical spine in asymptomatic subjects. A prospective investigation. J Bone Joint Surg Am 1990; 72:1178.
  41. Hehir MK, Figueroa JJ, Zynda-Weiss AM, et al. Unexpected neuroimaging abnormalities in patients with apparent C8 radiculopathy: broadening the clinical spectrum. Muscle Nerve 2012; 45:859.
  42. Lee HY, Chung IH, Sir WS, et al. Variations of the ventral rami of the brachial plexus. J Korean Med Sci 1992; 7:19.
  43. Uysal II, Seker M, Karabulut AK, et al. Brachial plexus variations in human fetuses. Neurosurgery 2003; 53:676.
  44. Matejcik V. Variations of nerve roots of the brachial plexus. Bratisl Lek Listy 2005; 106:34.
  45. Gough JG, Koepke GH. Electromyographic determination of motor root levels in erector spinae muscles. Arch Phys Med Rehabil 1966; 47:9.
  46. Chiou-Tan FY. Musculoskeletal mimics of cervical radiculopathy. Muscle Nerve 2022; 66:6.
  47. Katsuura Y, Bruce J, Taylor S, et al. Overlapping, Masquerading, and Causative Cervical Spine and Shoulder Pathology: A Systematic Review. Global Spine J 2020; 10:195.
  48. Quinn C, Salameh J. Vertebral artery dissection causing an acute C5 radiculopathy. Neurology 2013; 81:1101.
  49. Goldstein LB. Sacral pseudoradiculopathy due to centrum semiovale stroke. J Stroke Cerebrovasc Dis 1996; 6:41.
  50. Phan TG, Evans BA, Huston J. Pseudoulnar palsy from a small infarct of the precentral knob. Neurology 2000; 54:2185.
  51. Brook I, Sirdar B, Stemer A. Cervical Radiculopathy Presenting as Ischemic Stroke After Carotid Artery Stent Placement. J Med Cases 2023; 14:387.
  52. Clar SA, Cianca JC. Intracranial tumor masquerading as cervical radiculopathy: a case study. Arch Phys Med Rehabil 1998; 79:1301.
Topic 5271 Version 26.0

References