Cervical myelopathy

Cervical myelopathy (CM) is the most common cause of spinal cord dysfunction in adults aged over 50 years in Australia and worldwide. It results from progressive compression of the cervical spinal cord secondary to degenerative changes in the cervical spine, including disc herniation, osteophyte formation, ligamentum flavum hypertrophy, and ossification of the posterior longitudinal ligament (OPLL). The condition carries a significant burden of disease — an estimated 1 in 1000 Australians aged over 50 will develop symptomatic cervical myelopathy requiring clinical attention.

Australian data from the Australian Orthopaedic Association and cervical spine registries suggest that cervical myelopathy accounts for approximately 15–20% of all cervical spine presentations in tertiary referral centres. The annual surgical rate in Australia is estimated at 1.6 per 100,000, though many cases are managed conservatively. The condition disproportionately affects older adults, with the highest incidence in those aged 55–75 years, and a male predominance (male:female ratio approximately 2:1).

Degenerative cervical myelopathy (DCM) is the preferred umbrella term encompassing cervical spondylotic myelopathy (CSM) and other degenerative causes. Secondary causes — including rheumatoid arthritis (RA), ankylosing spondylitis, and inflammatory joint disease — account for a minority of cases but are important to recognise due to their distinct management pathway. In Australian rheumatology practice, CM in the context of RA (particularly atlantoaxial subluxation) is an important consideration.

Degenerative Mechanisms

The pathophysiology of cervical myelopathy is multifactorial, involving both static and dynamic components. Static compression results from structural narrowing of the spinal canal by disc herniation, spondylotic osteophytes (hard disc), hypertrophied facet joints, and thickened/buckled ligamentum flavum. Dynamic compression occurs with flexion/extension movements that further narrow the canal diameter, causing repetitive cord microtrauma.

• Disc degeneration: Loss of disc height and herniation narrows the anterior spinal canal. Disc desiccation (loss of proteoglycans) is the initiating step.
• Osteophyte formation: Uncinate processes and vertebral end-plates develop spurs (spondylosis) that encroach on the spinal canal and foramina.
• Ligamentous hypertrophy: Ligamentum flavum hypertrophy and buckling (especially at C3–4 and C4–5) compresses the cord posteriorly.
• OPLL: Ossification of the posterior longitudinal ligament is particularly prevalent in East Asian populations and can cause severe myelopathy.

Vascular and Neurological Mechanisms

Cord compression leads to ischaemia of the anterior spinal cord via compression of the anterior spinal artery and its perforators. This produces demyelination and axonal loss in the lateral corticospinal tracts (causing upper motor neuron signs in the lower limbs), the dorsal columns (causing proprioceptive loss), and the anterior horn cells (causing lower motor neuron signs in the upper limbs at the level of compression).

The pathological hallmark is central grey matter ischaemia at the level of compression. Signal change on MRI T2 (hyperintensity) represents oedema or myelomalacia and is an important prognostic marker — early oedematous change (potentially reversible) versus established myelomalacia (irreversible).

Inflammatory Causes

In rheumatoid arthritis, atlantoaxial subluxation (AAS) and vertical subluxation (cranial settling) are the principal mechanisms of cervical myelopathy. Pannus formation around the odontoid process compresses the cervicomedullary junction. Subaxial subluxation may also occur. These inflammatory mechanisms are distinct from degenerative CSM and warrant urgent rheumatology and neurosurgical review.

Typical Symptoms

Cervical myelopathy typically presents insidiously with a progressive or stepwise course. The classic triad is: (1) bilateral hand dysfunction (loss of dexterity, clumsiness); (2) gait disturbance (spastic gait, broad-based, unsteady); and (3) bladder dysfunction (urgency, frequency). Neck pain is variable — many patients have minimal or no neck pain.

• Upper limb: Clumsiness (difficulty buttoning shirts, opening jars), hand wasting and weakness (intrinsic minus hand), tingling or numbness in fingers, grip weakness
• Lower limb: Spastic gait, leg stiffness, difficulty climbing stairs, falls
• Bladder/bowel: Urinary urgency/frequency (early); retention or incontinence (late)
• Sensory: Patchy sensory disturbance, Lhermitte's sign (electric shock sensation down spine on neck flexion)

Clinical Signs

Examination reveals upper motor neuron signs below the level of compression and lower motor neuron signs at the level. Key signs include:

• Hyperreflexia: Exaggerated knee and ankle reflexes
• Hoffman's sign: Positive finger flexion reflex — pathological above C7 level
• Babinski sign: Extensor plantar response
• Clonus: Ankle clonus 3 or more beats is significant
• Inverted radial reflex: Absence of brachioradialis reflex with finger flexion
• Grip and release test: Fewer than 20 grip-and-release cycles in 10 seconds is abnormal
• Tandem gait: Impaired tandem walking indicates myelopathic gait
• Lhermitte's sign: Elicitable on neck flexion

Nurick Classification

Investigation is directed at confirming the diagnosis, determining the level and severity of cord compression, and excluding alternative or secondary causes.

• Essential
  MRI Cervical Spine (with and without contrast)

  The investigation of choice. Evaluates cord compression, T2 hyperintensity (myelomalacia/oedema), disc disease, OPLL, and ligamentous hypertrophy. Contrast helps differentiate infection, tumour, and demyelination from degenerative disease. Medicare rebate available (Item 63562).
• Essential
  Cervical Spine X-rays (AP, lateral, oblique)

  First-line imaging. Demonstrates disc space narrowing, osteophytes, foraminal narrowing, and alignment. Flexion/extension views assess instability, particularly in RA.
• Essential
  Full Blood Count, ESR, CRP

  Baseline bloods. Elevated inflammatory markers suggest inflammatory arthropathy, infection, or malignancy as the aetiology.
• Essential
  Rheumatoid Factor and Anti-CCP Antibodies

  If RA-related cervical myelopathy is suspected (atlantoaxial subluxation). Positive in approximately 80% of RA-related CM cases.
• Recommended
  CT Cervical Spine

  Best for bony detail — OPLL, osteophyte characterisation, and surgical planning. Often complementary to MRI. CT myelogram if MRI contraindicated.
• Recommended
  Nerve Conduction Studies (NCS) and EMG

  Differentiates myelopathy from peripheral neuropathy, motor neuron disease, or Charcot-Marie-Tooth. Important when diagnosis is uncertain.
• Recommended
  Modified Japanese Orthopaedic Association (mJOA) Score

  Functional outcome measure (score 0–18). Baseline documentation is essential. Mild CM 15–17, moderate CM 12–14, severe CM below 12. Used to guide surgical decision-making.
• Recommended
  Somatosensory Evoked Potentials (SSEP)

  Electrophysiological test of dorsal column function. Useful for intraoperative monitoring and as a prognostic tool. Available at tertiary neurophysiology services.

Severity assessment uses clinical and radiological parameters to guide management decisions, particularly for surgical referral.

Radiological Severity Markers

• Torg-Pavlov ratio: Less than 0.8 predicts cord compression risk (ratio of spinal canal to vertebral body width on lateral X-ray)
• Sagittal diameter: Functional canal diameter less than 13 mm is associated with myelopathy risk; less than 10 mm is high risk
• T2 cord signal: Presence and length of T2 hyperintensity correlates with severity and prognosis; T1 hypointensity indicates myelomalacia (poor prognosis)
• Compression ratio: Axial cord area less than 60 mm squared is associated with severe myelopathy

Conservative management is appropriate for mild cervical myelopathy (mJOA 15 or above) with careful monitoring, and as temporising management pending surgical review. It is not appropriate as sole long-term management for moderate-severe CM.

Activity Modification and Physiotherapy

• Avoidance of high-risk activities: contact sports, diving, gymnastics, and axial cervical loading activities
• Supervised physiotherapy: postural training, cervical range of motion (gentle), core strengthening; avoid neck manipulation (contraindicated)
• Occupational therapy: adaptive aids for hand dysfunction, home safety assessment for falls prevention
• Cervical collar: short-term use (2–4 weeks) during acute exacerbations only; prolonged use causes muscle deconditioning

Pharmacological Management

Surgical decompression is the definitive treatment for moderate-to-severe cervical myelopathy (mJOA below 15) and for mild CM with radiological evidence of progression or significant cord compression. The AO Spine International Clinical Practice Guidelines recommend surgical treatment for moderate and severe DCM.

Surgical Approaches

Surgical Referral Criteria

• mJOA score below 15 (moderate or severe CM)
• Progressive neurological deterioration (even if mild at presentation)
• Functional limitation from myelopathy affecting daily activities or employment
• Radiological evidence of significant cord compression with T2 signal change
• RA-associated atlantoaxial subluxation with myelopathy (urgent referral)
• Acute myelopathic deterioration (emergency referral)

Acute Cervical Cord Injury and Central Cord Syndrome

Acute deterioration in a patient with known or unknown cervical myelopathy often results from relatively minor trauma (hyperextension in a spondylotic spine) or spontaneous vascular events. Central cord syndrome is the most common incomplete spinal cord injury pattern — disproportionate upper limb weakness greater than lower limb weakness, with variable sensory loss below the level.

RA Atlantoaxial Subluxation — Acute Presentation

In RA patients, sudden neurological deterioration with occipital or suboccipital pain, Lhermitte's sign, or drop attacks may indicate acute atlantoaxial instability. This is a neurosurgical emergency. Urgent MRI and immediate neurosurgical consultation is required. In the interim, immobilise with a hard cervical collar and avoid neck flexion.

Regular monitoring is essential for patients with cervical myelopathy, whether managed conservatively or post-surgically.

Elderly Patients (over 75 years)

• Higher perioperative risk — frailty assessment (Clinical Frailty Scale) recommended before elective surgery
• Falls risk is significantly elevated in older adults with myelopathic gait — urgent falls prevention strategies including home assessment and walking aids
• Osteoporosis assessment (DXA scan) if fusion planned — low BMD affects fusion rates and hardware stability
• Post-operative delirium is common — preoperative cognitive assessment and delirium prevention protocols are essential
• Functional recovery is slower but still achievable — surgical intervention should not be denied on the basis of age alone

Rheumatoid Arthritis

• Atlantoaxial subluxation (AAS) is the most dangerous cervical complication of RA — atlantodens interval above 3.5 mm in adults requires investigation
• All RA patients with neck pain, occipital headache, or neurological symptoms require cervical spine X-rays with flexion/extension views and MRI
• Perioperative cervical spine precautions for ALL RA patients undergoing general anaesthesia — even asymptomatic patients may have significant instability
• DMARDs (particularly biologics — TNF inhibitors, IL-6 inhibitors) reduce the risk of cervical complications in RA by controlling synovial inflammation and pannus formation
• Anti-CCP positive, high disease activity RA represents the highest risk for cervical involvement — annual cervical X-ray monitoring is recommended

Pregnancy

• Cervical myelopathy during pregnancy is rare but serious — avoid MRI contrast (gadolinium) in first trimester unless absolutely essential
• Conservative management is preferred during pregnancy; surgical intervention reserved for rapidly progressive neurological deterioration
• Epidural anaesthesia for labour may be challenging in significant cervical disease — anaesthetic review is mandatory
• NSAIDs are contraindicated in the third trimester; paracetamol is safe throughout pregnancy

Ankylosing Spondylitis and Spondyloarthropathy

• Bamboo spine with spinal rigidity — any cervical fracture (even undisplaced) can cause catastrophic cord injury due to the rigid spinal column acting as a long bone
• Low-energy trauma in a patient with AS can cause serious cord injury — haintain a high index of suspicion and a low threshold for imaging
• Atlantoaxial involvement occurs in approximately 10% of AS cases — similar management principles to RA apply

Appropriate stewardship in cervical myelopathy management avoids over-investigation, unnecessary surgical intervention in mild stable disease, and inappropriate pharmacological management.

Avoiding Harm

• No cervical manipulation: Chiropractic or physiotherapy neck manipulation is absolutely contraindicated in cervical myelopathy — risk of acute cord injury. Advise patients explicitly and document.
• Avoid prolonged collar use: Cervical collar beyond 4 weeks causes muscle atrophy and worsens functional outcomes. Short-term use only for acute exacerbations.
• Opioid stewardship: Opioids mask neurological progression and contribute to falls risk. Not recommended for long-term CM management.
• Injection therapy: Cervical epidural steroid injections may provide temporary radicular pain relief but do not treat myelopathy and should not delay surgical referral. Transforaminal cervical epidurals carry risk of cord infarction and should be avoided.
• Watchful waiting in mild CM: Appropriate for mJOA 15 or above with stable examination and no significant radiological compression. Must be accompanied by a structured monitoring protocol and patient education about progression symptoms requiring urgent review.

Appropriate Imaging Stewardship

• Do not repeat MRI within 12 months if clinically stable (unless new neurological symptoms emerge)
• CT scan adds information in surgical planning and for OPLL but should not replace MRI as the first-line investigation
• PET scans and bone scans are not routinely indicated in degenerative CM (indicated only if malignancy is suspected)

GP Follow-Up Protocol

The GP plays a central role in long-term management, particularly for conservatively managed patients and post-surgical monitoring after discharge from specialist care.

• Conservative management: Review every 3–6 months with formal mJOA and Nurick assessment. Any progression or new symptoms triggers urgent re-referral to neurosurgery or orthopaedic spine.
• Post-surgical (year 1): Monthly review for wound, pain, and neurological recovery monitoring. Facilitate physiotherapy and occupational therapy. Communicate with neurosurgeon if recovery is inadequate.
• Post-surgical (beyond year 1): Annual review. Monitor for adjacent segment disease (new radicular symptoms, neck pain). Annual cervical X-ray in RA patients.
• RA patients: Ensure ongoing appropriate DMARD therapy. Annual cervical X-ray with flexion/extension views if any new cervical symptoms. Refer to rheumatology if RA is poorly controlled.

Patient Education

• Patients must understand the nature of cervical myelopathy and its potential for progression — report new symptoms promptly
• Avoidance of high-risk activities: contact sports, diving, axial loading, extreme neck movements
• Warning signs requiring immediate emergency assessment: acute onset of weakness, loss of bladder or bowel control, sudden gait deterioration, Lhermitte's sign
• Falls prevention: appropriate footwear, home modifications, night lighting, walking aids if required

Prevention of Secondary Causes

• Optimal management of RA and other inflammatory arthropathies with DMARDs reduces the risk of cervical instability and secondary CM
• Osteoporosis management (calcium, vitamin D, bisphosphonates where indicated) to reduce vertebral fracture risk in an already compromised cervical spine
• Smoking cessation — smoking accelerates disc degeneration and is associated with accelerated cervical spondylosis
• Weight management — obesity increases axial loading and accelerates disc degeneration

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