CHAPTER SYNOPSIS:
Cervical radiculopathy is the most common presentation of cervical disc disease and usually involves mixed components of neck and arm symptoms. The most commonly clinical complaints include pain, tingling, numbness, and motor or sensory loss along the distribution of a specific nerve root. The physical examination is often the key to determining the exact pathology and, therefore, the appropriate treatment course. This chapter reviews the variable clinical presentations of cervical radiculopathy, diagnosis, and current treatment recommendations.
IMPORTANT POINTS:
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Cervical radiculopathy can be classified into two broad categories based on the pathophysiology involved:
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Compressive (most common)
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Disc herniation
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Degenerative cervical spondylosis
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Noncompression
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Infectious
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Inflammatory
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Neoplastic
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Treatment for surgical radiculopathy can be classified into operative and nonoperative treatments:
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Nonoperative treatment indicated for nonprogressive pathology may be divided into two types:
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Conservative (analgesics, oral corticosteroids, physical therapy, cervical traction)
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Epidural glucocorticoid injections
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Surgical treatment is typically based on the actual pathology causing the radiculopathy, but the most common procedures include:
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Anterior cervical discectomy and fusion
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Posterior laminoforaminotomy
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Cervical arthroplasty
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SURGICAL PEARLS:
Anterior Cervical Discectomy and Fusion
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Directly decompress the nerve root by removing disc, as well as any osteophytes or other compressing structures
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Indirectly decompress the nerve root by distracting the disc space and placing graft material in place
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Eliminate dynamic motion by fusion step, which may be an additional source of pain
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Posterior Laminoforaminotomy
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Indicated for isolated lateral disc herniation with radicular symptoms but no significant neck pain
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Localize the cervical level
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Create keyhole foraminotomy in laminae
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Expose and decompress the affected nerve root
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Cervical Arthroplasty
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Preserves motion, which is theorized to minimize disease at the adjacent spinal levels
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Expose and remove the disc as before
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Insert the arthroplasty device
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SURGICAL PITFALLS:
Anterior Cervical Discectomy and Fusion
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The anterior dissection is more difficult and risks injury to important anterior neck structures (carotid artery, trachea, esophagus, recurrent laryngeal nerve).
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Posterior Laminoforaminotomy
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Has been shown to have increased incisional pain after surgery secondary to dissection through the posterior spinal muscles.
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Cervical Arthroplasty
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Although early results show promising results, long-term data are still pending.
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VIDEO AVAILABLE:
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Cervical spine degenerative disease is a common condition in industrialized nations, and patients typically have symptoms of neck pain, referred arm pain, weakness, gait dysfunction, and/or sensory loss. A cervical radiculopathy is the most common presentation of degenerative cervical disease and is typically associated with neck pain in addition to concurrent arm pain. Although this is the most frequent presentation, numerous other potential causative factors of a cervical radiculopathy exist. Therefore, the goal of this chapter is to specifically define and delineate cervical radiculopathies, and review their causes, clinical presentation, diagnosis, and possible treatment strategies.
The term radiculopathy refers to pain, tingling, numbness, motor loss, or sensory loss arising from a nerve root. Patients with cervical spine radiculopathies have diffuse neck pain accompanied by spasms of muscles in upper torso and lancing pain radiating from the posterior neck down toward the arm. This pain characteristically worsens with neck movement, particularly lateral bending or axial loading. Paresthesia, which patients typically describe as “numbness,” is a common feature and is reported in approximately 80% of patients. Special care must be taken to accurately diagnose the condition of a cervical radiculopathy before initiating a treatment algorithm because the treatment will be determined by the underlying cause of the radiculopathy. Overall, a variety of treatments options depend on the source of the cervical radiculopathy.
ANATOMY
The cervical spine consists of seven mobile cervical vertebrae, where C1 is an osseous ring connecting the cervical spine to the cranium, and the C2-7 vertebrae are separated by intervertebral discs. These discs have a dense fibrous outer layer, annulus fibrosis that contains a more gelatinous inner layer, nucleus pulposus. The vertebral body and disc complexes form the ventral portion of the spinal canal, whereas the posterior portion of the canal is formed by the lamina and posterior spinal elements. Laterally, the spinal canal is defined by the pedicles that connect the lamina to the vertebral bodies. The central portion of this canal consists of the cervical spinal cord surrounded by cerebrospinal fluid and the dura mater. Eight cervical nerve roots arise from the rootlets off the cervical spinal cord. The cervical nerves 3 to 7 exit the spinal canal through the neuroforamina created by the boundaries of the pedicles and vertebral bodies, and are labeled in respect to the corresponding vertebral body and pedicle from which they exit. The exception is the eighth cervical nerve, which departs beneath the C7 pedicle. As these cervical nerve roots course from the spinal cord and through their respective neuroforamina, there are multiple sites of potential compression such as from circumferential osseous spondylosis, herniated disc material, and buckling of the ligament flavum. Although any cervical nerve roots may be affected by these compressible lesions, the C7 nerve root is the most commonly involved and is reported in approximately 70% of cases. The C6 nerve root is the next most commonly affected and seen in about 20% of patients.
Pathophysiology and Classification
Although cervical radiculopathies have numerous causative factors, these can be generally divided into two broad categories: compressive or noncompressive.
Compressive Radiculopathies
Compressive radiculopathies are the most common form of cervical radiculopathy because of the inherent mobility of the spine, the anatomic relation of the osseous elements, and potential for disc herniations. The two main mechanisms for compressive cervical radiculopathies are acute disc herniation and degenerative cervical spondylosis. Herniation of disc material typically affects a younger population in that the disc is well hydrated and the central nucleus pulposus can rupture from its central location. As the disc ages, the disc material desiccates and loses hydration and material, thus limiting the potential for expulsion. When the herniated disc material protrudes, it is typically expelled onto the lateral portion of the spinal canal because of the strong centrally located posterior longitudinal ligament directing it in such a path. This results in the material causing direct pressure on the nerve root as it exits the spinal canal, in addition to the release of cytokines and chemical irritation to the nervous tissue.
Patients typically present as the result of minor trauma or after vigorous exercise with intractable pain. If the herniated disc material prolapses medially, it may compress directly on the spinal cord depending on the size of the spinal canal, as well as size of the disc herniation. Patients with an isolated central disc herniation and spinal cord compression may present with a cervical myelopathy, which is often painless, or central cord syndrome after trauma where pain and weakness predominate in the hands.
In the elderly population with aging spines, degenerative changes in the form of cervical spondylosis may produce a cervical radiculopathy. This results as a consequence of narrowing of the neuroforamina caused by presence of osteophytes or “bone spurs” that develop along the junction of the vertebrae and disc space. Because the nerve exits through the passage contained by the pedicles, degeneration of the disc material results in the loss of height between the pedicles and a constriction of the neural foramen. Concurrently, buckling of the posterior ligamentum flavum occurs because of loss of tension, as well as formation of osteophytes at the disc margins. These combined effects result in circumferential constriction of the foramen and subsequent neural compression. This global process results in spondylosis being the most common cause of cervical radiculopathy, where approximately 70% of cases are due to spondylosis and only 20% from acute disc herniations. Although these are the most common causative factors of compressive radiculopathies, other less likely causes include focal masses, neoplasms, infection, and neurogenic thoracic outlet syndrome.
Noncompressive Radiculopathies
Noncompressive radiculopathies are less common than compressive radiculopathies but should be considered in the differential of any patient with a cervical radiculopathy, particularly in the absence of compressible lesions on imaging studies. Noncompressive radiculopathies can be divided into three broad categories:
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Infectious
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Inflammatory
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Neoplastic
An additional categorization method is to subdivide by the causative agent or pathophysiology of the radiculopathy:
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Inflammation within the nerve root
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Injury of the connecting tissue or blood vessels surrounding the nerve root, or both
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Direct penetration of the foreign agent
Infections that cause noncompressive cervical radiculopathy include herpes zoster, cytomegalovirus, HIV, and Lyme disease. Herpes zoster virus and cytomegalovirus can cause cervical radiculopathy by infecting the nerve root leading to the symptoms of pain or tingling in the upper limb. Cases of radiculopathy caused by HIV have been documented; however, most radiculopathies in patients with HIV infection are due to opportunistic processes, such as cytomegalovirus. The radiculopathy associated with Lyme disease is generally an axonopathy and not caused by demyelination. Radiculopathy is due to untreated late-stage Lyme disease.
Inflammatory processes such as vasculitis, sarcoidosis, and Parsonage–Turner syndrome are known to cause noncompressive radiculopathies. Parsonage–Turner syndrome is an idiopathic inflammatory condition of the brachial plexus that appears sporadically. Patients present with severe pain for 1 to 2 weeks and then progressive weakness. It is diagnosed with an electromyographic (EMG) study; however, recovery is determined by a return to clinical strength as EMG reports have been known to be abnormal for up to 7 years after diagnosis.
Lymphoma and carcinomatous meningitis are neoplastic conditions that can cause noncompressive radiculopathies. Cases of various types of lymphoma and corresponding cervical radiculopathy, including Hodgkin lymphoma, have been documented. Noncompressive radiculopathies are more diffuse injuries than compressive radiculopathies and typically affect the dorsal root ganglion in addition to the exiting nerve root. Unfortunately, imaging studies are not particularly conclusive for noncompressive radiculopathies; therefore, special attention needs to be paid to medical history, physical evidence, and neurophysiologic data that are suggestive of infectious or inflammatory processes.