Cervical Disc Herniation

Etiology

An intervertebral disc is a cartilaginous structure composed of 3 components: an inner nucleus pulposus, an outer annulus fibrosus, and endplates that anchor the discs to adjacent vertebrae. Disc herniation occurs when all or part of the nucleus pulposus protrudes through the annulus fibrosus, and may develop acutely or gradually over time (see Image. Stages of Nucleus Pulposus Herniation). Chronic herniations occur as the intervertebral disc degenerates and dries out with age, typically causing symptoms that develop gradually and are generally less severe. In contrast, acute herniations generally are the result of trauma, resulting in the nucleus pulposus extruding through a defect in the annulus fibrosus. This injury typically results in a sudden onset of more severe symptoms compared to chronic herniations.[5]

Epidemiology

The prevalence of cervical disc herniation increases with age for both men and women and is most common in people in their third to fifth decades of life. This condition occurs more frequently in women, accounting for more than 60% of cases. The most commonly diagnosed patients, regardless of sex, are between the ages of 51 and 60.[6][7]

Pathophysiology

The pathophysiology of herniated discs is thought to be a combination of mechanical compression of the nerve by the bulging nucleus pulposus and a local increase in inflammatory cytokines. Compressive forces can result in varying degrees of microvascular damage, ranging from mild compression, which produces obstruction of venous flow and causes congestion and edema, to severe compression, which can lead to arterial ischemia.

Herniated disc material and nerve irritation may induce the production of inflammatory cytokines, which can include: interleukins 1 and 6, substance P, bradykinin, tumor necrosis factor-alpha, and prostaglandins. There may even be an additional role stretching of the nerve root plays in reproducing symptoms. The trajectory of the cervical nerve as it exits the neural foramen makes it susceptible to stretch, in addition to compression from a herniation. This arrangement could partly explain why certain patients experience pain relief from arm abduction, which presumably decreases the amount of stretch the nerve experiences.[8][9]

Herniations are more likely to occur posterolaterally, where the annulus fibrosus is thinner and lacks the structural support from the posterior longitudinal ligament. Due to the proximity of the herniation to the traversing cervical nerve root, a herniation that compresses the cervical root as it exits can result in radiculopathy in the associated dermatome.[10] Nucleus pulposus herniations manifest in several forms. A disc protrusion arises when the nucleus pulposus bulges yet remains confined within the annulus. Breaching through damaged annular fibers allows nucleus pulposus material to escape, producing a disc extrusion. Detached portions of the extruded nucleus pulposus form a sequestered fragment.

Degenerative disc disease, cervical spondylosis, and disc herniation represent interlinked stages of cervical spine degeneration.[11][12] Degenerative disc disease describes the progressive biochemical and structural deterioration of intervertebral discs, leading to dehydration, annular tears, and a loss of shock-absorbing function. This process often contributes to broader osteoarthritic changes of the cervical spine known as cervical spondylosis. Within this context, a disc herniation occurs when compromised annular fibers allow the nucleus pulposus to extend into the spinal canal or neural foramina—a focal complication rooted in the ongoing degeneration of the disc.

History and Physical

History

Cervical disc herniations most commonly occur between C5–C6 and C6–C7 vertebral bodies, causing symptoms at C6 and C7, respectively. The history of these patients should include the chief complaint, onset of symptoms, factors that alleviate and aggravate symptoms, radicular symptoms, and any past treatments. The most common subjective complaints are axial neck pain and ipsilateral arm pain or paresthesias in the associated dermatomal distribution. 

Symptom patterns can also categorize cervical disc herniations:

• Axial neck pain: Pain centered in the cervical spine that typically worsens with movement or mechanical stress, such as lifting or prolonged posture.
• Radiculopathy: Radiating arm pain, sensory changes, or motor weakness along 1 or more dermatomes as herniated material compresses a nerve root.[13]
• Myelopathy: This includes spinal cord involvement producing gait disturbance, hand clumsiness, hyperreflexia, or spasticity.[14]

Any single pattern may occur, but patients frequently exhibit overlapping features, eg, neck pain accompanied by radicular symptoms, or radiculopathy evolving into myelopathy as cord compression progresses. Recognizing these symptom constellations clarifies diagnosis and informs the urgency of imaging, nonoperative trials, and the need for timely surgical decompression. As part of evaluating neck pain, it is essential to identify certain red flags indicative of underlying inflammatory conditions, malignancy, or infection.[15] These include: 

• Fever, chills
• Night sweats
• Unexplained weight loss
• History of inflammatory arthritis, malignancy, systemic infection, tuberculosis, HIV, immunosuppression, or drug use
• Unrelenting pain
• Point tenderness over a vertebral body
• Cervical lymphadenopathy

Physical Examination

The clinician should assess the patient’s range of motion, which can indicate the severity of pain and degeneration. A thorough neurological examination is necessary to evaluate sensory disturbances, motor weakness, and deep tendon reflex abnormalities. Careful attention should also focus on any sign of spinal cord dysfunction (see Image. Nucleus Pulposus Herniation, Tables). These include the following:

• C1 and C2: Disc herniations do not affect the occiput–C1 and C1–2 levels (ie, intervertebral discs are absent at these articulations)
• C3, C4: Vague neck, trapezial tenderness, and muscle spasms
• C5: Neck, shoulder, and scapula pain; lateral arm paresthesia; primary movements affected include shoulder abduction and elbow flexion; diminished biceps reflex
  • This may also show weakness with shoulder flexion, external rotation, and forearm supination. 
• C6: Neck, shoulder, and scapula pain; paresthesia of the lateral forearm, lateral hand, and lateral 2 digits; primary movements affected include elbow flexion and wrist extension
  • This may also show weakness in shoulder abduction, external rotation, forearm supination, and pronation—diminished brachioradialis reflex. 
• C7: Neck and shoulder pain, paresthesia of the posterior forearm and third digit, diminished triceps reflex.
  • The primary movements affected include elbow extension and wrist flexion. 
• C8: Neck and shoulder pain; paresthesia of the medial forearm, medial hand, and medial 2 digits; weakness during finger flexion, handgrip, and thumb extension
• T1: Neck and shoulder pain, paresthesia of the medial forearm, weakness of finger abduction and adduction [10]

Provocative tests include the Spurling test, Hoffman test, and Lhermitte sign. The Spurling test can aid in diagnosing acute radiculopathy and is performed by maximally extending the neck and rotating towards the involved side while compressing the head to load the cervical spine axially. This narrows the neuroforamen and may reproduce symptoms consistent with radiculopathy. The Hoffman test and Lhermitte sign can be used to assess for the presence of spinal cord compression and myelopathy. The Hoffmann sign is elicited by holding the third finger and briskly flicking the distal phalanx downward; a positive sign results when there is flexion and adduction of the thumb. The Lhermitte sign is performed by flexing the patient’s neck, which may result in an electrical sensation traveling down the spine and into the extremities.[8][16]

Myelopathy

Degenerative cervical myelopathy manifests with a wide range of symptoms. Common complaints include hand tingling, numbness, clumsiness, weakness, and gait instability.[17] Less typical manifestations represent roughly 40% of cases. A sensation of heavy legs is the only early finding linked to a quicker diagnosis.[18] Physical signs can be subtle. The Tromner sign and overall hyperreflexia offer the greatest sensitivity, whereas Babinski, Tromner, clonus, and the inverted supinator sign show high specificity. Upper motor neuron signs may be absent, so clinicians must integrate the complete symptom profile with imaging studies to establish the diagnosis.[19]

Evaluation

Most cases of acute disc herniation resolve within the first 4 weeks without intervention. Imaging is generally not recommended during this period, as it typically does not alter management. However, imaging should be considered when there is clinical suspicion of serious underlying pathology or evidence of neurologic compromise. Additionally, patients who fail to respond to conservative treatment after 4 to 6 weeks warrant further evaluation.[20] Patients who exhibit red flag symptoms listed above may warrant evaluation with lab markers.

Pertinent lab values in the assessment of cervical disc herniation include:

• Erythrocyte sedimentation rate and C-reactive protein: These are inflammatory markers that should be obtained if a chronic inflammatory condition is suspected, such as rheumatoid arthritis, polymyalgia rheumatica, or seronegative spondyloarthropathy. These can also be beneficial if an infectious etiology is suspected.
• Complete blood count with differential: This is useful when infection or malignancy is suspected.

X-rays are the first test typically performed and are very accessible at most clinics and outpatient offices. Three views (anteroposterior, lateral, and oblique) help assess the overall alignment of the spine as well as the presence of any degenerative or spondylotic changes. These can be further supplemented with lateral flexion and extension views to assess for the presence of instability. If imaging demonstrates an acute fracture, further investigation is required using a computed tomography scan or magnetic resonance imaging (MRI). If there is a concern about atlantoaxial instability, the open-mouth (odontoid) view may assist in diagnosis.

A computed tomography scan is the most sensitive for examining the bony structures of the spine. This imaging can also reveal calcified herniated discs or any insidious process that may lead to bony loss or destruction. In patients who are unable to undergo or are otherwise ineligible for an MRI, computed tomography myelography can be used as an alternative to visualize a herniated disc. MRI is the preferred imaging modality and the most sensitive study for visualizing a herniated disc, as it has the greatest ability to demonstrate soft-tissue structures and the nerve as it exits the foramen (see Images. Cervical Spondylosis, Magnetic Resonance Image; Disc Herniations at C3–4 and C4–5, Magnetic Resonance Image; C5–6 Central Disc Herniation, Magnetic Resonance Image).

A recent attempt to classify the location and size of disc herniations introduced the foramen facet spinal system, which categorizes cervical disc herniations seen on MRI by their posterior depth and mediolateral location (see Image. Foramen Facet Spinal Disc Herniations, Magnetic Resonance Image). A posterior foraminal line and a line through the midpoint of the facet joint serve as fixed reference landmarks. Grade 1 lesions remain anterior to the foraminal line, grade 2 lesions reach the articular midline, and grade 3 lesions extend beyond. Location code A denotes central compression, B denotes paracentral compression, and C denotes foraminal compression, with AB used when central and paracentral contact are equal, yielding 7 distinct classes.[21] Electrodiagnostic testing, including electromyography and nerve conduction studies, may be useful for patients with inconclusive symptoms or imaging results, and can help differentiate cervical pathology from peripheral mononeuropathy. The sensitivity of detecting cervical radiculopathy with electrodiagnostic testing ranges from 50% to 71%.[22]

Treatment / Management

Conservative Treatment

Acute cervical radiculopathies secondary to a herniated disc are typically managed with nonsurgical treatments, as 75% to 90% of patients improve. Modalities that can be used include:

• Collar immobilization: During the acute inflammatory period, approximately 1 week of collar immobilization may benefit patients with acute neck pain.
• Traction: This may be beneficial in reducing the radicular symptoms associated with disc herniations. Theoretically, traction would widen the neuroforamen and relieve the stress placed on the affected nerve, which, in turn, would improve symptoms. This therapy involves placing approximately 8 to 12 lbs of traction at an angle of approximately 24° of neck flexion for 15 to 20 minutes.
• Pharmacotherapy: There is no evidence to demonstrate the efficacy of nonsteroidal anti-inflammatory drugs in treating cervical radiculopathy. However, they are commonly used and can be beneficial for some patients. 
  • The analgesic effect does not differ between COX-1 and COX-2 inhibitors; however, COX-2 inhibitors may be associated with decreased gastrointestinal toxicity.
  • Clinicians can consider steroidal anti-inflammatory medications, typically prednisone, in severe acute pain for a short period. A typical regimen involves a prepackaged, tapered dose of Methylprednisolone that decreases from 24 mg to 0 mg over 7 days.
  • Opioid medications are generally avoided due to a lack of supporting evidence and a higher risk of side effects.
  • When muscle spasms are severe, a short course of muscle relaxants, such as cyclobenzaprine at 5 mg, taken orally 3 times daily, may be considered.
  • Antidepressants like amitriptyline and anticonvulsants such as gabapentin and pregabalin are sometimes used to manage neuropathic pain and can offer moderate pain relief.
• Physical therapy: These treatments are commonly prescribed following a brief period of rest and immobilization. They include a range of motion exercises, strengthening exercises, ice, heat, ultrasound, and electrical stimulation therapy. Although frequently used, there is no evidence to show that they are more effective than a placebo. However, since they have not been shown to cause harm and may offer some benefit, their use is recommended when myelopathy is not present.
• Cervical manipulation: There is limited evidence suggesting that cervical manipulation may provide short-term benefits for neck pain and cervicogenic headaches. Complications from manipulation are rare and can include worsening radiculopathy, myelopathy, spinal cord injury, and vertebral artery injury.[5][8][23] 

Interventional Treatments

Perineural injections (translaminar and transforaminal epidurals, selective nerve root blocks) are an option when MRI confirms pathology. These procedures should take place under radiologic guidance.[23] Over the past few years, neuromodulation techniques have been widely used to manage radicular pain secondary to disc herniations.[24] These neuromodulatory techniques primarily consist of a spinal cord stimulation device and an intrathecal pain pump.[25][26] These devices provide minimally invasive and efficacious treatment options for patients who are not candidates for surgical intervention.(A1)

Surgical Treatment

Indications for surgical intervention include severe or progressive neurological compromise and significant pain that is refractory to nonoperative measures. Several techniques are described based on pathology. The gold standard remains the anterior cervical discectomy with fusion, as it allows for the removal of the pathology and prevents recurrent neural compression by performing a fusion (see Figure. Zero Profile Implant, Cervical Disc Prolapse Radiograph). A posterior laminoforaminotomy can be a consideration in patients with lateral herniations. Total disc replacement is a relatively new treatment option, although its specific indications are still debated.[8]

Differential Diagnosis

Accurate diagnosis requires a structured differential because many disorders replicate the pain or neurologic deficits of cervical disc herniation. Differential diagnoses include: 

• Brachial plexus injury
• Degenerative cervical spondylosis
• Muscle strain
• Parsonage-Turner syndrome
• Peripheral nerve entrapment
• Tendinopathies of the shoulder

Prognosis

Pain, restricted motion, and radiculopathy resulting from a herniated disc typically subside on their own within 6 weeks in most patients, due to enzymatic resorption or phagocytosis of the extruded disc material. There may also be a change in the hydration of the extruded material or a decrease in the local edema, resulting in pain reduction and restoration of function. In approximately one-third of patients, symptoms persist despite nonoperative intervention. If symptoms persist beyond 6 weeks, the likelihood of improvement without surgical intervention decreases.[23][27]

Complications

Without intervention, cervical disc herniation, causing compression of neural structures, can cause irreversible neurological impairment. Complications from steroid injections are typically mild and occur in 3% to 35% of cases. Other, more serious complications can include:

• Nerve injury
• Infection
• Epidural hematoma
• Epidural abscess
• Spinal cord infarction [5][28] 

Complications from surgical intervention include:

• Infection
• Recurrent laryngeal, superior laryngeal, and hypoglossal nerve injuries
• Esophageal injury
• Vertebral and carotid injuries
• Dysphagia
• Horner syndrome
• Pseudoarthrosis
• Adjacent segment degeneration [29] 

Anterior cervical discectomy with fusion is a widely performed procedure to treat disc herniations. According to a meta-analysis, the overall morbidity rate is about 16%, with a mortality rate of 0.1%. The most frequent complication is prevertebral or neck swelling, occurring in 11.3% of cases, followed by pseudarthrosis at 10% and dysphagia at 9.5% occurrence.[30]