Residency · Residency · Neurosurgery

Cervical Spondylotic Myelopathy

Overview

Cervical spondylotic myelopathy (CSM) is the most common cause of spinal cord dysfunction in adults over age 55. Progressive degenerative changes of the cervical spine cause narrowing of the spinal canal with compression of the spinal cord. MRI evidence of cord compression is found in up to 8% of asymptomatic individuals over 70. CSM is a clinical diagnosis requiring both cord compression on imaging and clinical signs and symptoms of myelopathy. It has an insidious onset with stepwise or gradual progression, and spontaneous improvement is rare.

Pathophysiology

Static Factors

Static contributors to canal narrowing include disc degeneration with bulging or herniation, osteophyte formation at the uncovertebral joints and facets, ligamentum flavum hypertrophy and buckling, and ossification of the posterior longitudinal ligament (OPLL), which is more common in East Asian populations. Congenital canal stenosis (anteroposterior diameter under 13 mm) predisposes to myelopathy, while a diameter under 10 mm virtually guarantees it.

Dynamic Factors

Extension narrows the canal further as the ligamentum flavum buckles inward. Flexion stretches the cord over anterior osteophytes. Repetitive microtrauma to the cord occurs with normal cervical motion, which explains why minor trauma can precipitate myelopathy in patients with pre-existing stenosis.

Cord Pathology

Chronic compression leads to ischemia, particularly in the watershed zones of the lateral columns. Demyelination occurs initially, followed by neuronal loss and gliosis. Gray matter central necrosis precedes white matter changes. On MRI, T2 signal hyperintensity may reflect edema (potentially reversible) or myelomalacia/gliosis (irreversible). T1 hypointensity indicates more advanced disease with cavitation and necrosis, and carries a poor prognosis.

Clinical Presentation

Symptoms

Gait instability and imbalance are often the earliest symptoms. Patients develop clumsy hands with difficulty performing fine motor tasks such as buttoning shirts, writing, or using chopsticks. Non-dermatomal numbness or paresthesias affect the hands or feet. Neck stiffness and pain may be minimal or absent. Urinary urgency or frequency is a late finding. Lhermitte sign (electric sensation down the spine with neck flexion) may be present.

Signs

Upper motor neuron findings include hyperreflexia, clonus at the ankle or wrist, and a positive Babinski sign. Hoffman sign (flicking the distal phalanx of the middle finger causes flexion of the thumb and index finger) is present in approximately 80% of CSM patients. The inverted radial reflex produces finger flexion instead of wrist extension when the brachioradialis is tapped. Myelopathy hand manifests as the finger escape sign (inability to keep the small and ring fingers adducted) and loss of rapid grip-release cycling (fewer than 20 times in 10 seconds is abnormal). Gait is broad-based and spastic with difficulty in tandem walking. A combination of upper and lower motor neuron signs occurs at the level of compression.

Grading Scales

The modified Japanese Orthopedic Association (mJOA) score ranges from 0-18, with mild myelopathy scored 15-17, moderate 12-14, and severe below 12. The Nurick grade (0-5) is based on ambulatory status.

Diagnostic Workup

MRI (Primary Imaging)

Sagittal and axial T1 and T2 sequences assess the number of levels compressed, severity of compression, and cord signal change. T2 hyperintensity may represent edema (reversible) or gliosis (irreversible). T1 hypointensity suggests myelomalacia and is associated with worse surgical outcomes. The "snake eye" appearance on axial T2 reflects bilateral anterior horn cell ischemia.

CT Scan

CT is best for evaluating bony anatomy, OPLL, and foraminal stenosis. CT myelography is used when MRI is contraindicated and provides excellent canal diameter measurement.

Dynamic Radiographs

Flexion-extension lateral views assess instability, and overall cervical alignment (kyphosis versus lordosis) is evaluated.

Electrodiagnostics

SSEPs and MEPs can quantify cord dysfunction. EMG may help differentiate CSM from peripheral neuropathy or ALS.

Natural History

CSM is generally progressive, and spontaneous improvement is uncommon. Approximately 20-60% of patients worsen over 3-6 years without surgery. The most common pattern is stepwise deterioration with stable periods punctuated by acute worsening. Mild myelopathy (mJOA 15-17) has the most unpredictable course. Patients with established myelopathy are at risk for acute deterioration after minor trauma such as falls or motor vehicle collisions.

Surgical Management

Indications

Surgery is recommended for moderate to severe myelopathy (mJOA below 15). For mild myelopathy (mJOA 15-17), surgery versus structured observation with serial exams is controversial, though the AOSpine CSM-NA study suggests benefit from surgery. Progressive neurological decline warrants surgery regardless of severity.

Anterior Approaches

ACDF is appropriate for 1-3 level disease and provides direct decompression of anterior pathology, though pseudarthrosis risk increases with the number of levels (up to 30% for 3-level ACDF). Anterior cervical corpectomy and fusion (ACCF) removes the vertebral body and adjacent discs to decompress multiple levels, using a strut graft with anterior plating. ACCF is well-suited for OPLL or retrovertebral pathology but carries a higher complication rate than ACDF.

Posterior Approaches

Cervical laminectomy with lateral mass fusion is appropriate for multilevel (more than 3 levels) compression and requires preserved or correctable lordosis. Lateral mass screw fixation eliminates the risk of post-laminectomy kyphosis but results in loss of motion and potential adjacent segment disease.

Cervical laminoplasty (open-door Hirabayashi or French-door technique) preserves motion without requiring fusion and enlarges the canal posteriorly. It is ideal for multilevel compression (C3-C6 or C3-C7) with preserved lordosis. It is contraindicated with significant kyphosis (the cord will not drift posteriorly) or instability. Advantages include motion preservation and avoidance of fusion-related complications. Disadvantages include axial neck pain (30-60%), C5 palsy (5-10%), and limited kyphosis correction.

Approach Selection

An anterior approach is preferred for 1-2 levels of compression, kyphotic alignment, or predominantly anterior pathology (disc herniation, OPLL). A posterior approach is preferred for 3 or more levels of compression, lordotic alignment, predominantly posterior compression (ligamentum flavum hypertrophy), or congenital stenosis. Combined anterior-posterior approaches are considered for severe multilevel stenosis with kyphosis or after corpectomy spanning 3 or more levels where posterior fixation adds stability.

Outcomes

Surgical decompression halts progression in over 95% of cases. Neurological improvement occurs in 60-80% of patients. Preoperative severity is the strongest predictor, with more severe myelopathy yielding less recovery. Duration of symptoms correlates inversely with recovery, favoring earlier surgery. AOSpine CSM studies confirm that surgery is more effective than conservative management for moderate-to-severe CSM.

Complications

C5 palsy occurs in 2-10% of cases and likely results from nerve root tethering after posterior cord shift. Other complications include CSF leak (posterior approaches), adjacent segment disease (fused segments), dysphagia (anterior approaches), wound infection, hematoma, and hardware failure.

<image>Sagittal T2-weighted MRI of the cervical spine demonstrating multilevel cervical spondylotic myelopathy with disc-osteophyte complexes at C3-C4, C4-C5, and C5-C6 causing ventral cord compression, with focal T2 hyperintensity (myelopathy signal) within the spinal cord at the C4-C5 level</image>

<image>Axial CT scan of the cervical spine at C5 level showing ossification of the posterior longitudinal ligament (OPLL) with significant canal narrowing, demonstrating the dense ossified mass posterior to the vertebral body extending across the canal</image>

<image>Intraoperative photograph of an open-door cervical laminoplasty (Hirabayashi technique) showing the lamina hinged open on one side and held open with miniplate and screws, exposing the expanded posterior spinal canal with the dura visible beneath</image>

<image>Lateral cervical spine radiograph following C3-C7 laminectomy with lateral mass screw-rod fixation, showing restoration of cervical lordosis and instrumentation spanning the decompressed levels</image>

Clinical Pearls

CSM is a clinical diagnosis; asymptomatic cord compression on MRI alone does not mandate surgery but warrants close follow-up. Hoffman sign, clonus, and gait abnormalities should always be assessed in any patient presenting with cervical complaints. T1 hypointensity on MRI (myelomalacia) is the strongest negative prognostic indicator; these patients still benefit from surgery to prevent further decline, but recovery is limited. Laminoplasty and laminectomy-fusion require lordotic alignment to allow posterior cord drift; posterior decompression alone should not be performed in kyphotic patients. C5 palsy is a postoperative complication of both anterior and posterior approaches; prophylactic C4-C5 foraminotomy may reduce the risk. Patients with CSM should be counseled to avoid high-risk activities (contact sports, trampolines) and appropriate cervical precautions should be taken during intubation. The myelopathy hand (finger escape sign) is highly specific for cervical cord compression and is a useful bedside test.

References

• Fehlings MG, et al. "Efficacy and Safety of Surgical Decompression in Patients with Cervical Spondylotic Myelopathy: Results of the AOSpine North America Prospective Multi-Center Study." J Bone Joint Surg Am. 2013;95(18):1651-1658.
• Karadimas SK, et al. "Pathophysiology and Natural History of Cervical Spondylotic Myelopathy." Spine. 2013;38(22 Suppl 1):S21-36.
• Hirabayashi K, et al. "Operative Results and Postoperative Progression of Ossification Among Patients with OPLL." Spine. 1981;6(4):354-364.
• Lau D, et al. "Laminoplasty versus Laminectomy with Posterior Spinal Fusion for Multilevel Cervical Spondylotic Myelopathy." Spine. 2017;42(15):E911-E917.
• Nouri A, et al. "Degenerative Cervical Myelopathy: Epidemiology, Genetics, and Pathogenesis." Spine. 2015;40(12):E675-E693.

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