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Cervical Myelopathy

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Cervical Myelopathy

Comprehensive guide to cervical myelopathy - cord compression, upper motor neuron signs, Nurick classification, surgical timing, anterior vs posterior approaches, and clinical decision-making for orthopaedic exam

complete
Updated: 2024-12-17
High Yield Overview

CERVICAL MYELOPATHY - SPINAL CORD COMPRESSION

Progressive UMN Signs | Cord Compression | Surgical Decompression

50-60Peak age of symptom onset (years)
70-80%Surgery improves or halts progression
T2High signal on MRI = cord edema/gliosis
NurickGrading scale for functional impairment

NURICK CLASSIFICATION (FUNCTIONAL IMPAIRMENT)

Grade 0
PatternRoot signs only, no cord involvement
TreatmentObserve or treat radiculopathy
Grade 1
PatternCord signs, normal gait
TreatmentConsider early surgery
Grade 2
PatternMild gait abnormality, employment not affected
TreatmentSurgery recommended
Grade 3
PatternGait abnormality prevents employment
TreatmentSurgery indicated
Grade 4
PatternAble to walk only with assistance
TreatmentUrgent surgery
Grade 5
PatternChair-bound or bedridden
TreatmentUrgent surgery, guarded prognosis

Critical Must-Knows

  • Progressive disease - natural history is stepwise or gradual decline without treatment
  • MRI is gold standard - shows cord compression and T2 signal change (edema/gliosis)
  • Upper motor neuron signs - hyperreflexia, Hoffman sign, Babinski, inverted radial reflex
  • Surgery halts progression - improves or stabilizes symptoms in 70-80% of patients
  • Surgical timing matters - early intervention (Nurick 1-2) has better outcomes than late (4-5)

Examiner's Pearls

  • "
    Myelopathy = UMN signs; radiculopathy = LMN signs (important distinction)
  • "
    Lhermitte sign (neck flexion causes electric shock down spine) suggests cord compression
  • "
    Hoffman sign (flick middle finger, thumb flexes) is sensitive but not specific
  • "
    T2 hyperintensity on MRI correlates with worse prognosis and poor recovery
  • "
    AOSpine CSM studies: anterior vs posterior approaches have similar outcomes when appropriate

Clinical Imaging

Imaging Gallery

Cervical myelopathy imaging showing X-ray and MRI with cord compression and T2 signal change
Click to expand
49-year-old male with cervical myelopathy: (A) Pre-operative lateral radiograph shows atlas hypoplasia and OPLL at sub-axial region, (B) MRI T2 sagittal shows cord compression with high signal change (arrow), indicating myelomalacia. (C, D) Post-operative imaging showing decompression and improved cord signal.Credit: Chang H et al., Asian Spine J (PMC2857503) - CC-BY

Critical Cervical Myelopathy Exam Points

UMN vs LMN Distinction

Myelopathy is UMN (hyperreflexia, Hoffman, Babinski, clonus, spasticity). Radiculopathy is LMN (hyporeflexia, weakness, dermatomal sensory loss). Can coexist as myeloradiculopathy. The level of cord compression determines which nerve roots are affected (LMN at level, UMN below).

Progressive Without Surgery

Natural history is progressive decline. Stepwise deterioration (20%) or gradual decline (60%). Only 20% remain stable without treatment. Surgery halts progression in most cases, with improvement in 50-70% if operated early.

Surgical Timing Critical

Early surgery (Nurick 1-2) yields better outcomes than late surgery (Nurick 4-5). Severe myelopathy (Nurick 5, T2 hyperintensity, long symptom duration over 18 months) predicts poor recovery. Operate before irreversible cord damage occurs.

Anterior vs Posterior Choice

Anterior approach: 1-2 levels, anterior compression (disc, osteophyte). Posterior approach: multilevel (more than 3 levels), congenital stenosis, OPLL. Combined approach: severe multilevel with kyphosis. AOSpine studies show equivalent outcomes when used appropriately.

Quick Decision Guide - Surgical Approach Selection

ScenarioCompression PatternApproachKey Pearl
Single level C5-6 disc herniationAnterior compressionACDF (anterior cervical discectomy fusion)Gold standard for 1-2 level anterior pathology
Multilevel stenosis (C3-7), lordotic spineCircumferential compressionLaminoplasty or laminectomy + fusionPosterior approach preserves motion with laminoplasty
Severe OPLL (more than 60% canal), ossifiedAnterior compression, multilevelPosterior laminoplasty (avoid anterior if OPLL thick)Anterior approach risks CSF leak with OPLL removal
Multilevel stenosis with kyphosisCircumferential, deformityCombined anterior + posterior or PCF aloneCorrect deformity to prevent progression
Mnemonic

HOFFMANClinical Signs of Cervical Myelopathy

H
Hoffman sign
Flick middle finger DIP, thumb and index flex (UMN sign)
O
Opposite reflexes
Inverted radial reflex (finger flexion on brachioradialis tap)
F
Finger escape sign
Ulnar drift of ring and little finger when extended (intrinsic weakness)
F
Functional impairment
Gait disturbance, hand clumsiness (buttoning, writing)
M
Motor UMN signs
Hyperreflexia, spasticity, weakness
A
Altered sensation
Numb clumsy hands, loss of proprioception, sensory level
N
Neurogenic bladder
Urgency, frequency, retention (advanced disease)

Memory Hook:HOFFMAN is the classic myelopathy sign - remember it encompasses all UMN features of cord compression!

Mnemonic

GRADESNurick Grading Scale for Myelopathy Severity

G
Grade 0: radiculopathy only
No cord signs, root symptoms only
R
Grade 1: cord signs, normal gait
Reflex changes but walks normally
A
Grade 2: abnormal gait, works
Mild gait issues, employment not affected
D
Grade 3: difficulty with employment
Gait prevents full-time work
E
Grade 4: assistance to walk
Requires cane or walker
S
Grade 5: severe disability
Chair-bound or bedridden

Memory Hook:GRADES 0 to 5: remember the Nurick scale progresses from no cord signs to complete disability!

Mnemonic

SIGNALMRI Findings in Cervical Myelopathy

S
Stenosis
Canal narrowing (normal more than 13mm, stenotic less than 10mm AP diameter)
I
Indentation of cord
Cord compression and deformity at affected levels
G
Gliosis or edema
T2 hyperintensity within cord (poor prognostic sign)
N
Nerve root compression
May coexist as myeloradiculopathy
A
Atrophy of cord
Cord thinning, 'snake-eye' appearance on axial T2 (severe)
L
Loss of CSF space
Obliteration of anterior and posterior CSF around cord

Memory Hook:SIGNAL changes on T2 MRI tell the story of cord compression and predict surgical outcome!

Mnemonic

OPERATEIndications for Surgery in Cervical Myelopathy

O
Objective UMN signs
Hyperreflexia, Hoffman, Babinski, clonus present
P
Progressive symptoms
Worsening over months, not static or radiculopathy alone
E
Early intervention better
Nurick 1-2 have better outcomes than 4-5
R
Radiological compression
MRI shows cord compression and signal change
A
Ability to walk affected
Gait disturbance (Nurick grade 2 or more) is clear indication
T
Timing is critical
Do not delay - natural history is progressive decline
E
Elderly can benefit
Age alone not a contraindication if healthy

Memory Hook:OPERATE criteria guide surgical decision-making - do not wait for severe disability before intervening!

Mnemonic

Handy Legs Walk BadlyProgression of Myelopathy Symptoms

H
Handy
Hand clumsiness is often the first symptom
L
Legs
Lower limb weakness follows
W
Walk
Gait disturbance develops
B
Badly
Bladder symptoms indicate severe disease

Memory Hook:Myelopathy progresses from hands to legs to gait to bladder!

Mnemonic

Canal is Half the BodyStenosis Measurement (Pavlov Ratio)

C
Canal
Measure AP diameter of spinal canal
H
Half
Ratio less than 0.8 indicates stenosis
B
Body
Divide by vertebral body AP diameter

Memory Hook:Pavlov ratio = Canal / Body. Less than 0.8 = stenosis, less than 1.0 = borderline!

Mnemonic

VITAMINSDifferential Diagnosis of Myelopathy

V
Vascular
Anterior spinal artery syndrome, AVM
I
Infectious
Epidural abscess, transverse myelitis
T
Trauma
Cord injury, SCIWORA
A
Autoimmune
MS, neuromyelitis optica
M
Metabolic
B12 deficiency, copper deficiency
I
Idiopathic
Syringomyelia
N
Neoplastic
Intramedullary tumor, metastasis
S
Spondylotic
Degenerative cervical myelopathy (most common)

Memory Hook:Rule out VITAMINS before diagnosing spondylotic myelopathy!

Overview and Epidemiology

Clinical Significance

Cervical myelopathy is the most common cause of spinal cord dysfunction in adults over 55 years. It results from chronic compression of the cervical spinal cord, most commonly due to degenerative changes (spondylosis, disc herniation, ligamentum flavum hypertrophy, OPLL). The natural history without surgery is progressive neurological decline in 80% of cases. Early surgical decompression halts progression and improves outcomes in 70-80% of patients.

Demographics

  • Peak age 50-60 years (degenerative), younger with trauma or congenital stenosis
  • Men more than women (2:1 ratio) due to higher rates of cervical spondylosis
  • Most common levels: C5-6 and C6-7 (maximum motion and degeneration)
  • Risk factors: congenital stenosis (canal less than 13mm AP), occupation (repetitive neck flexion/extension)

Clinical Impact

  • Progressive disability: 60% gradual decline, 20% stepwise deterioration, 20% stable
  • Functional impairment: gait disturbance, hand clumsiness (buttoning, writing), falls
  • Surgical outcomes: 50-70% improve, 20-30% stabilize, 5-10% worsen despite surgery
  • Predictors of poor recovery: severe myelopathy (Nurick 4-5), T2 hyperintensity, long symptom duration (more than 18 months)

Pathophysiology and Anatomy

Understanding Cord Compression Mechanisms

The cervical spinal cord occupies approximately 60-70% of the spinal canal cross-sectional area. Normal AP canal diameter is 14-17mm. When the canal narrows to less than 13mm (relative stenosis) or less than 10mm (absolute stenosis), the cord is at risk of compression. Compression can be static (anatomical narrowing) or dynamic (worsened with neck flexion/extension). The pathophysiology involves:

  1. Direct mechanical compression - squeezing of cord parenchyma
  2. Ischemia - compression of anterior spinal artery or intramedullary vessels
  3. Chronic repetitive trauma - microtrauma with neck motion leading to gliosis and myelomalacia
OPLL causing severe cervical cord compression on MRI
Click to expand
Ossified Posterior Longitudinal Ligament (OPLL) causing pronounced spinal cord compression. Sagittal T2 MRI (left) shows multilevel OPLL with severe canal stenosis; axial T2 (right) demonstrates marked cord compression with effacement of CSF space - classic OPLL appearance requiring posterior laminoplasty.Credit: Murayama K et al., Medicine (Baltimore) (PMC4616720) - CC-BY

Causes of Cervical Cord Compression

CauseMechanismTypical AgeTreatment Approach
Cervical spondylosisDegenerative: disc bulging, osteophytes, facet hypertrophyMore than 50 yearsAnterior (1-2 levels) or posterior (multilevel)
OPLL (ossification of PLL)Heterotopic ossification of posterior longitudinal ligamentEast Asian, more than 50 yearsPosterior laminoplasty preferred (avoid anterior CSF leak risk)
Congenital stenosisDevelopmental narrow canal (Pavlov ratio less than 0.8)Younger age, traumaPosterior decompression if symptomatic
Disc herniation (acute)Posterior disc extrusion compressing cord40-60 yearsAnterior discectomy and fusion
Ligamentum flavum hypertrophyPosterior compression from ligament thickeningElderlyPosterior laminectomy or laminoplasty

Cord Anatomy and Vulnerability

The cervical cord is most vulnerable at C5-6 and C6-7 due to maximal motion and narrowest canal diameter at these levels. The cord's blood supply is watershed between anterior spinal artery (80% of cord) and posterior spinal arteries (20%). Compression can cause ischemia and infarction, leading to irreversible damage.

Biomechanics of Dynamic Compression

Flexion narrows the canal anteriorly (ligamentum flavum buckles posteriorly). Extension narrows posteriorly (disc and osteophytes protrude anteriorly). This pincer effect causes repetitive microtrauma with daily activities, explaining the progressive nature of myelopathy.

Classification Systems

Nurick Scale - Functional Impairment (Most Commonly Used)

GradeClinical PresentationGaitSurgical Indication
0Root signs only, no cord signsNormalTreat radiculopathy, observe for myelopathy
1Cord signs present, no gait difficultyNormalConsider early surgery (controversial)
2Mild gait difficulty, employment possibleAbnormal but independentSurgery recommended
3Gait difficulty prevents employmentAbnormal, independent in ADLsSurgery indicated
4Unable to walk without assistanceRequires aid (cane/walker)Urgent surgery
5Chair-bound or bedriddenNon-ambulatoryUrgent surgery, poor recovery expected

Nurick Scale Application

The Nurick scale is functional and focuses on gait and employment. It is the most widely used grading system for myelopathy severity and correlates with surgical outcomes. Grades 2-3 are clear surgical indications. Grade 1 is controversial - some advocate early surgery, others observe. Grades 4-5 have poorer outcomes but surgery still halts progression.

Modified Japanese Orthopaedic Association (mJOA) Score

mJOA Scoring (Total 18 Points)

The mJOA is a comprehensive 18-point scale assessing:

  • Motor function (upper and lower extremity): 0-5 points each
  • Sensory function (upper extremity, lower extremity, trunk): 0-2 points each
  • Sphincter function: 0-3 points

Interpretation:

  • 18 points: Normal
  • 12-17: Mild myelopathy
  • 8-11: Moderate myelopathy
  • 0-7: Severe myelopathy

Recovery rate is calculated as: (postop mJOA - preop mJOA) / (18 - preop mJOA) × 100%. A recovery rate more than 50% is considered good.

Advantages of mJOA

  • Comprehensive assessment of all neurological domains
  • Quantitative - allows calculation of recovery rate
  • Widely used in clinical trials (AOSpine CSM studies)
  • Sensitive to subtle changes in function

Disadvantages of mJOA

  • Complex - requires detailed assessment
  • Time-consuming compared to Nurick
  • Inter-observer variability can be high
  • Not intuitive - difficult to remember in exams

Anatomic Classification - Level and Compression Type

Compression Pattern and Surgical Approach

PatternDescriptionApproachRationale
Single level anteriorDisc herniation or osteophyte at one levelACDFDirect access to pathology, fusion stabilizes
Two-level anteriorDisc and osteophyte at 2 adjacent levelsACDF or arthroplastyACDF gold standard, arthroplasty preserves motion
Multilevel anterior (more than 3 levels)Spondylosis C3-7 with anterior compressionPosterior laminoplastyAvoid long anterior construct, preserve motion
Circumferential compressionAnterior (disc/osteophyte) and posterior (ligamentum flavum)Posterior laminoplasty or combinedPosterior decompresses both directions via cord drift
Congenital stenosis + acquiredNarrow canal plus superimposed spondylosisPosterior laminoplastyExpands canal, allows cord to drift posteriorly
Kyphotic deformity + compressionLoss of lordosis or kyphosis with stenosisCombined or posterior alone with fusionMust correct alignment to decompress and prevent recurrence

Clinical Assessment

History Red Flags

  • Progressive symptoms: worsening over weeks to months (not acute unless trauma)
  • Hand clumsiness: difficulty with fine motor tasks (buttoning, writing, picking up coins)
  • Gait disturbance: wide-based gait, unsteadiness, frequent falls
  • Neurogenic bladder: urgency, frequency, hesitancy (advanced disease)
  • Lhermitte sign: electric shock sensation down spine with neck flexion
  • Pain is NOT a prominent feature (unlike radiculopathy) - if severe neck/arm pain, think radiculopathy or mixed picture

Examination Essentials

  • Upper motor neuron signs: hyperreflexia, Hoffman sign, Babinski sign, clonus (ankle/patella)
  • Inverted radial reflex: tap brachioradialis, finger flexion occurs instead of forearm flexion (C5-6 level lesion)
  • Gait assessment: tandem gait (balance), heel-toe walk, Romberg sign (posterior column dysfunction)
  • Hand coordination: rapid alternating movements, finger tapping (assess speed and coordination)
  • Sensory level: may have dermatomal level or glove-and-stocking neuropathy pattern
  • Grip and release test: inability to rapidly open/close fist 20 times in 10 seconds suggests myelopathy

Beware Occult Myelopathy Masquerading as Peripheral Neuropathy

Elderly patients with diabetes or alcohol use may have superimposed myelopathy that is missed because their hand numbness is attributed to peripheral neuropathy. Key distinguishing features:

  • Myelopathy: UMN signs (hyperreflexia, Hoffman, Babinski), gait disturbance, MRI shows cord compression
  • Peripheral neuropathy: LMN signs (hyporeflexia), stocking-glove distribution, nerve conduction studies abnormal, MRI normal

Clinical pearl: If a patient with "peripheral neuropathy" has brisk reflexes and Hoffman sign, obtain a cervical spine MRI to rule out myelopathy!

Clinical Signs: Myelopathy vs Radiculopathy

FeatureMyelopathy (UMN)Radiculopathy (LMN)Mixed (Myeloradiculopathy)
ReflexesHyperreflexia, clonusHyporeflexia or absentHyperreflexia below level, hyporeflexia at level
Hoffman signPositive (flick middle finger, thumb flexes)NegativePositive (indicates cord involvement)
Babinski signPositive (upgoing toe)Negative (downgoing toe)Positive (UMN tract involvement)
Sensory patternSensory level, proprioception loss, gait ataxiaDermatomal numbnessBoth patterns present
PainMinimal or absent (dull neck ache)Severe radicular pain (shooting down arm)Radicular pain plus myelopathy signs
GaitWide-based, ataxic, spasticNormalAbnormal gait
Treatment urgencyUrgent if progressiveElective (most resolve non-operatively)Urgent (myelopathy component dictates)

Investigations

Multimodal imaging workup for cervical myelopathy showing X-ray, 3D CT, and MRI
Click to expand
Comprehensive imaging workup in a 79-year-old with cervical myelopathy: (A) Lateral X-ray shows narrowing of atlas ring; (B) 3D CT reconstruction confirms bony anatomy; (C) MRI sagittal shows cord compression; (D, E) Follow-up imaging demonstrating the complete diagnostic workup from plain films to advanced cross-sectional imaging.Credit: Chang H et al., Asian Spine J (PMC2857503) - CC-BY

Diagnostic Imaging Protocol

First LineCervical Spine X-rays (AP, Lateral, Flexion/Extension)

Purpose: Assess alignment, instability, bony pathology

  • Lateral: Measure Pavlov ratio (canal diameter / vertebral body diameter). Normal more than 1.0, stenotic less than 0.8
  • Flexion/Extension: Assess for dynamic instability (more than 3mm subluxation or more than 11 degrees angulation)
  • AP: Look for degenerative changes, osteophytes
  • Limitations: Cannot visualize cord, disc, or soft tissue compression
Gold StandardMRI Cervical Spine (T1 and T2, Sagittal and Axial)

Purpose: Visualize cord compression, cord signal changes, disc pathology

  • T2 sagittal: Shows cord compression, canal stenosis, disc bulging
  • T2 axial: Shows cord deformity and T2 hyperintensity (edema/gliosis - poor prognostic sign)
  • T1 sagittal: Shows T1 hypointensity (myelomalacia - severe chronic compression)
  • Interpretation: Cord compression + T2 signal change + clinical myelopathy = surgical indication
AdjunctCT Cervical Spine

Purpose: Bony detail, OPLL assessment, preoperative planning

  • When indicated: OPLL suspected (assess ossification thickness), preoperative planning for screw trajectories
  • CT myelogram: If MRI contraindicated (pacemaker, claustrophobia), shows cord compression but not intrinsic signal
FunctionalFlexion/Extension MRI (Dynamic MRI)

Purpose: Assess dynamic compression not visible on neutral MRI

  • Rationale: Some patients have cord compression only in flexion or extension
  • Limitations: Not widely available, increased cost
ElectrophysiologySomatosensory Evoked Potentials (SSEP)

Purpose: Assess cord function, intraoperative monitoring

  • Preoperative: Can confirm diagnosis if MRI equivocal (prolonged latency or reduced amplitude)
  • Intraoperative: Monitor cord function during decompression (more than 50% amplitude drop = cord ischemia risk)

MRI Signal Changes - Prognostic Significance

T2 hyperintensity (bright signal on T2 within the cord) indicates:

  • Edema (early, reversible) or gliosis/myelomalacia (late, irreversible)
  • Prognostic marker: T2 hyperintensity predicts poorer surgical outcomes
  • Snake-eye sign: Bilateral symmetric T2 hyperintensity on axial MRI at grey matter, suggests severe chronic compression and very poor prognosis

T1 hypointensity (dark signal on T1) indicates:

  • Myelomalacia (cord necrosis) - irreversible damage
  • Very poor prognosis for neurological recovery

Clinical correlation: Severity of T2 changes correlates with Nurick grade and recovery potential. Early surgery (before T2 changes develop) yields best outcomes.

Management Algorithm

📊 Management Algorithm
cervical myelopathy management algorithm
Click to expand
Management algorithm for cervical myelopathyCredit: OrthoVellum

Conservative Management - Limited Role

Natural History Favors Surgery in Most Cases

80% of patients with cervical myelopathy will progress without surgery (60% gradual decline, 20% stepwise deterioration). Only 20% remain stable. Therefore, observation is only appropriate in very select cases:

  • Nurick 0-1 (minimal symptoms, no gait disturbance)
  • Patient unfit for surgery (severe medical comorbidities)
  • Patient refuses surgery after informed consent about natural history

Conservative Measures (Temporizing or Palliative)

Short-term onlyNeck Immobilization

Soft collar for symptom relief during acute exacerbation. Avoid prolonged use (causes muscle atrophy and stiffness). Not a long-term solution for cord compression.

Symptom managementMedications
  • Neuropathic pain: Gabapentin, pregabalin (for coexisting radiculopathy)
  • Spasticity: Baclofen, tizanidine (for UMN spasticity)
  • No role for NSAIDs or steroids in chronic degenerative myelopathy (unlike acute cord injury)
AdjunctPhysical Therapy

Goal: Maintain ROM, strengthen supporting musculature, gait training

  • Does NOT halt progression of cord compression
  • Avoid manipulation or traction - risk of worsening cord compression
Every 3-6 monthsClose Monitoring

Clinical assessment: Nurick grade, mJOA score, gait, UMN signs Repeat MRI if worsening: Assess progression of cord compression Threshold for surgery: If symptoms progress, convert to surgical management

When to Observe vs Operate - Clinical Judgment

Observation is reasonable for Nurick 0-1 IF:

  • MRI shows mild compression without T2 signal change
  • Patient is high surgical risk (severe cardiac/pulmonary disease)
  • Informed consent given about natural history (80% progression risk)

Surgery is indicated even in Nurick 1 IF:

  • T2 signal change present (suggests cord edema/gliosis)
  • Progression documented (worsening symptoms over months)
  • Young patient with long life expectancy

Surgical Decompression - Definitive Treatment

Goal: Halt neurological decline, decompress spinal cord, prevent further damage

Surgical Decision Pathway

EssentialStep 1: Confirm Diagnosis

Clinical myelopathy (UMN signs, gait disturbance) + MRI cord compression = Surgical indication

  • Ensure progressive symptoms (not static or radiculopathy alone)
  • Rule out mimics: MS, ALS, B12 deficiency, copper deficiency (all can cause UMN signs)
Critical decisionStep 2: Choose Approach (Anterior vs Posterior)

Anterior approach (ACDF, corpectomy):

  • 1-2 level anterior compression (disc, osteophyte)
  • Direct decompression of ventral pathology
  • Advantages: Direct visualization, immediate stability with fusion
  • Disadvantages: Dysphagia (10-20%), RLN injury (1-2%), pseudarthrosis (5-10%)

Posterior approach (laminoplasty, laminectomy + fusion):

  • Multilevel compression (more than 3 levels)
  • Circumferential stenosis or congenital stenosis
  • OPLL (avoids anterior CSF leak risk)
  • Advantages: Multilevel decompression, preserves motion (laminoplasty)
  • Disadvantages: Axial neck pain (20-30%), C5 palsy (5-10%), kyphosis risk (if laminectomy without fusion)

Combined approach:

  • Severe multilevel compression with kyphotic deformity
  • Anterior corpectomy + posterior fusion for stability
Early intervention betterStep 3: Timing of Surgery

Optimal timing: Nurick 1-2 (early disease) - best outcomes Acceptable timing: Nurick 3-4 (moderate to severe) - still benefit, but less recovery Poor prognosis: Nurick 5 (severe disability, more than 18 months symptoms, T2 hyperintensity) - surgery still halts progression but recovery limited

Early mobilizationStep 4: Postoperative Rehabilitation

Day 1: Mobilize out of bed, collar if anterior fusion Week 1-6: Neck ROM exercises, avoid heavy lifting Week 6-12: Progressive strengthening, return to activities Long-term: Monitor for adjacent segment disease (5-10% per decade)

Surgical Techniques - Anterior Approaches

Anterior Cervical Discectomy and Fusion (ACDF)

Indications:

  • 1-2 level anterior compression (disc herniation, osteophyte)
  • Focal cord compression at specific levels
  • Most common surgical treatment for cervical myelopathy

ACDF Steps

Step 1Positioning and Approach

Supine, head neutral or slight extension, shoulder roll to extend neck Smith-Robinson approach: Transverse or oblique incision along anterior border SCM, typically left side (less risk to RLN) Dissection: Medial to carotid sheath, lateral to trachea/esophagus, retract medially

Step 2Discectomy and Decompression

Localization: Fluoroscopy to confirm level (C6 has prominent anterior tubercle) Discectomy: Remove disc completely, including posterior annulus and posterior osteophytes Decompress cord: Remove PLL if ossified, ensure adequate canal decompression Foraminotomy: If coexisting radiculopathy, decompress nerve root laterally

Step 3Reconstruction

Options:

  • PEEK cage + autograft/allograft (most common)
  • Structural allograft (femoral ring, fibula)
  • Cage size: Trial to ensure adequate height restoration and lordosis

Plate fixation: Anterior cervical plate with screws into vertebral bodies above and below Rationale: Increases fusion rate (95% vs 85% without plate), prevents cage subsidence

Step 4Closure and Postoperative Care

Closure: Layer closure, drain optional (controversial) Collar: Soft collar for comfort, not structural (plate provides stability) Diet: NPO until swallow assessment (dysphagia risk), advance as tolerated

ACDF Pearls

  • Complete PLL removal: Essential for adequate posterior decompression
  • Avoid over-distraction: Causes facet joint distraction and postoperative pain
  • Check fluoroscopy: Ensure plate does not cross adjacent disc space
  • Fusion rate: 95% with plate at 1 year

ACDF Pitfalls

  • Inadequate decompression: Leaving posterior osteophyte causes persistent compression
  • RLN injury: Use left-sided approach, gentle retraction (1-2% risk)
  • Dysphagia: 10-20% temporary, 2-5% persistent (worse with multilevel)
  • Adjacent segment disease: 5-10% per decade (natural history debate)

Anterior Cervical Corpectomy and Fusion (ACCF)

Indications:

  • Multilevel anterior compression (2-3 levels)
  • Retro-vertebral osteophytes or OPLL that cannot be accessed via discectomy
  • Kyphotic deformity requiring anterior column reconstruction

Corpectomy vs Multi-level ACDF

Corpectomy removes entire vertebral body, decompresses over wider area, but higher risk of graft subsidence and pseudarthrosis (especially if more than 2-level).

Multi-level ACDF preserves vertebral bodies, but requires more dissection and plate spans more levels (increased stress).

Current trend: Prefer multi-level ACDF over corpectomy for 2-level disease. Reserve corpectomy for retro-vertebral compression not accessible via ACDF.

Corpectomy Advantages

  • Wide decompression across multiple levels with single construct
  • Direct access to retro-vertebral osteophytes
  • Corrects kyphosis via anterior column lengthening

Corpectomy Disadvantages

  • Higher pseudarthrosis rate (15-20% for 2-level, 30% for 3-level)
  • Graft subsidence risk (especially in osteoporotic bone)
  • More blood loss and longer operative time
  • May require posterior supplementation if more than 2-level

Surgical Techniques - Posterior Approaches

Cervical Laminoplasty - Motion-Preserving Decompression

Indications:

  • Multilevel stenosis (3 or more levels, typically C3-7)
  • Circumferential compression (anterior and posterior)
  • Congenital stenosis with acquired spondylosis
  • OPLL (preferred over anterior approach due to CSF leak risk)

Key principle: Open-door laminoplasty - hinge on one side, open on contralateral side, prop open with spacer. Cord drifts posteriorly away from anterior compression.

Laminoplasty Steps

Step 1Positioning and Approach

Prone, head in Mayfield clamp, neutral neck position (avoid excessive flexion/extension) Midline incision C2-T1, subperiosteal dissection, preserve C2 and C7 spinous processes Expose lateral masses to lateral edge of facet joints bilaterally

Step 2Create Hinge and Open Door

Hinge side (usually left): Thin lamina with high-speed burr to create greenstick fracture (do not penetrate dura) Open side (usually right): Complete trough at lamina-lateral mass junction, detach ligamentum flavum Lift door: Elevate lamina at hinge, opens like a door, increases canal diameter by 4-5mm

Step 3Maintain Opening

Spacer placement: Titanium miniplate with spacer, hydroxyapatite block, or suture (older technique) Goal: Maintain 5-7mm opening, prevent door closure Check decompression: Visualize dural pulsation, ensure adequate space for cord drift

Step 4Closure

Muscle reattachment: Reattach extensor musculature to C2 and C7 spinous processes (preserve to reduce axial pain) Drain: Subfascial drain for 24-48 hours No collar needed: Laminoplasty inherently stable

Laminoplasty Advantages

  • Motion preservation: Maintains neck ROM (vs fusion)
  • Multilevel decompression with single posterior approach
  • No pseudarthrosis risk (no fusion)
  • Lower infection risk than anterior approach
  • Preferred for OPLL (avoids CSF leak risk of anterior approach)

Laminoplasty Disadvantages

  • Axial neck pain: 20-30% (aching posterior neck pain)
  • C5 palsy: 5-10% (deltoid weakness, usually recovers)
  • Loss of ROM: 30-50% loss of flexion/extension despite "motion preservation"
  • Cannot correct kyphosis: Requires lordotic or neutral alignment preoperatively

C5 Palsy After Posterior Decompression

C5 palsy occurs in 5-10% of laminoplasty/laminectomy cases. Presents as deltoid and biceps weakness (C5 myotome) within 24-72 hours postoperatively.

Mechanism: Cord drifts posteriorly after decompression, tethering of C5 nerve root causes traction injury. More common with greater posterior drift (wider decompression, severe preoperative compression).

Management: Observation (70-80% recover fully within 6-12 months). Rule out epidural hematoma with urgent MRI if sudden severe weakness.

Prevention: Avoid excessive posterior drift by limiting decompression width, perform foraminotomy to release tethering.

Laminectomy and Posterior Fusion

Indications:

  • Multilevel stenosis with instability or kyphosis
  • Posterior column pathology (ligamentum flavum hypertrophy, congenital stenosis)
  • Laminoplasty contraindicated (kyphotic alignment, previous laminectomy)

Key principle: Remove posterior elements (laminae, ligamentum flavum), then fuse with lateral mass or pedicle screws to prevent postoperative kyphosis.

Laminectomy Without Fusion Causes Kyphosis

Do NOT perform laminectomy alone (without fusion) in cervical spine unless single-level and patient has very limited ROM. Multilevel laminectomy without fusion leads to progressive kyphosis (swan-neck deformity) and recurrent cord compression.

Always fuse after multilevel laminectomy using lateral mass screws (C3-6) or pedicle screws (C7-T1).

Laminectomy and Fusion Steps

Step 1Laminectomy

Remove laminae C3-7 (or targeted levels): Osteotome or Kerrison rongeurs Remove ligamentum flavum: Complete excision to decompress dura posteriorly Preserve facet joints (especially more than 50% of facet) to maintain stability

Step 2Instrumentation

Lateral mass screws (C3-C6): Magerl or Roy-Camille technique, 3.5mm screws, 14-16mm length Pedicle screws (C7, T1): Larger pedicles, allow better fixation Rod contouring: Contour rods to match cervical lordosis (or correct kyphosis)

Step 3Fusion

Decorticate lateral masses and facets: Burr to bleeding bone Bone graft: Local bone (from laminae), allograft, or BMP Place over decorticated surfaces for fusion mass

Laminectomy + Fusion Advantages

  • Prevents postoperative kyphosis (vs laminectomy alone)
  • Can correct existing kyphosis via rod contouring
  • Stable construct allows early mobilization
  • Relieves posterior compression effectively

Laminectomy + Fusion Disadvantages

  • Loss of motion (fusion restricts ROM)
  • Longer surgery and more blood loss than laminoplasty
  • Pseudarthrosis risk (5-10%)
  • Screw malposition risk (especially C2 pedicle)

Complications

ComplicationIncidenceRisk FactorsManagement
C5 palsy (deltoid/biceps weakness)5-10% (posterior approach)Greater posterior cord drift, severe preoperative stenosisObservation (70-80% recover in 6-12 months), MRI to rule out hematoma
Dysphagia (swallowing difficulty)10-20% temporary, 2-5% persistent (anterior approach)Multilevel ACDF, excessive retraction, revision surgerySpeech therapy, diet modification, usually resolves in 6-12 weeks
Recurrent laryngeal nerve injury (hoarseness)1-2% (anterior approach)Right-sided approach (RLN non-recurrent variant), excessive retractionVoice rest, speech therapy, most recover in 3-6 months, vocal cord injection if persistent
Dural tear/CSF leak1-3% (higher with OPLL)OPLL adherent to dura, revision surgeryPrimary repair with suture or sealant, bed rest 48 hours, rarely requires reoperation
Neurological deterioration1-2% (new or worsened deficit)Excessive manipulation, cord ischemia, epidural hematomaUrgent MRI, return to OR if hematoma, observation if ischemia (usually improves)
Pseudarthrosis (non-union)5-10% ACDF, 15-20% corpectomySmoking, multilevel fusion, inadequate fixationRevision fusion if symptomatic (pain, instability), observe if asymptomatic
Adjacent segment disease5-10% per decade after fusionFusion (vs laminoplasty), preexisting degenerationSurgical decompression if symptomatic stenosis develops
Axial neck pain (posterior approach)20-30% (laminoplasty or fusion)Muscle dissection, loss of ROMNSAIDs, physical therapy, usually improves over 6-12 months
Infection (deep wound or epidural abscess)1-3%Diabetes, obesity, immunosuppression, revision surgeryAntibiotics (if early), return to OR for washout (if deep), drain epidural abscess urgently
Postoperative kyphosis (laminectomy without fusion)30-50% if laminectomy aloneMultilevel laminectomy, preexisting kyphosisPrevention: Always fuse after multilevel laminectomy. Treatment: Revision fusion if symptomatic

Recognizing Postoperative Epidural Hematoma

Clinical presentation: Sudden neurological deterioration within 24-48 hours postoperatively (severe weakness, sensory loss, bladder dysfunction).

Diagnosis: Urgent MRI - shows epidural fluid collection compressing cord.

Management: Immediate return to operating room for hematoma evacuation. Every hour of delay worsens prognosis. This is a surgical emergency.

Prevention: Meticulous hemostasis, drain placement, avoid anticoagulation in immediate postoperative period.

Postoperative Care and Rehabilitation

ACDF Postoperative Protocol

ImmediateDay 0-1

Monitoring: Neurological checks Q2H (motor/sensory), swallow assessment before PO Collar: Soft collar for comfort (not structural - plate provides stability) Mobilization: Out of bed Day 1, early ambulation reduces DVT risk Diet: NPO until swallow cleared, advance as tolerated (soft diet if dysphagia) Pain control: Multimodal analgesia (acetaminophen, gabapentin, PRN opioids)

EarlyWeeks 1-6

Activity: Avoid heavy lifting (more than 5kg), no driving while in collar or on opioids Collar: Wean at 2-4 weeks (earlier if single-level, longer if multilevel) Physical therapy: Gentle ROM exercises, posture training Imaging: X-rays at 6 weeks to assess alignment, hardware position

ProgressiveWeeks 6-12

Activity advancement: Gradual return to activities, progressive strengthening Fusion assessment: X-rays or CT at 12 weeks if concern for pseudarthrosis Functional goals: Most patients independent in ADLs by 3 months

Long-termOngoing

Surveillance: Annual X-rays for 2 years, then PRN if symptomatic Adjacent segment disease: Monitor for new symptoms (5-10% per decade) Return to full activity: 3-6 months depending on occupation

Laminoplasty/Laminectomy Postoperative Protocol

ImmediateDay 0-1

Drain management: Subfascial drain for 24-48 hours (remove when less than 30mL/24h) C5 palsy monitoring: Check deltoid/biceps strength Q4H in first 72 hours (peak incidence) Mobilization: Out of bed Day 1 (earlier than anterior approach, no dysphagia risk) No collar needed: Laminoplasty/fusion inherently stable

EarlyWeeks 1-6

Axial pain management: Common (20-30%), NSAIDs, muscle relaxants, heat/ice ROM exercises: Gentle active ROM to prevent stiffness Avoid flexion: Limit neck flexion in first 6 weeks to protect posterior fusion

ProgressiveWeeks 6-12

Strengthening: Progressive resistance exercises for neck extensors Fusion check: X-rays at 12 weeks if fusion performed Functional improvement: Most patients plateau by 6 months

Long-termOngoing

ROM assessment: Expect 30-50% loss of flexion/extension (counsel preoperatively) No adjacent segment disease: Benefit of laminoplasty (no fusion) or fusion protects

Outcomes and Prognosis

Prognostic Factors for Surgical Outcome

FactorGood PrognosisPoor Prognosis
Preoperative Nurick gradeNurick 1-2 (mild disease)Nurick 4-5 (severe disease, especially more than 18 months duration)
MRI signal changesNo T2 hyperintensity or T1 hypointensityT2 hyperintensity (gliosis) or T1 hypointensity (myelomalacia)
Symptom durationLess than 12 monthsMore than 18 months (chronic irreversible cord damage)
AgeYounger (under 60 years)Elderly (over 75 years, but age alone not contraindication)
ComorbiditiesHealthy, no diabetesDiabetes, vascular disease (impairs cord perfusion and healing)
Surgical timingEarly intervention (before severe disability)Delayed surgery (after prolonged severe compression)

Predictors of Poor Surgical Outcome

Three factors predict poor recovery after surgery for cervical myelopathy:

  1. Severe preoperative myelopathy: Nurick 4-5, especially if duration more than 18 months
  2. T2 hyperintensity or T1 hypointensity on MRI: Indicates gliosis/myelomalacia (irreversible cord damage)
  3. "Snake-eye sign" on axial MRI: Bilateral symmetric T2 hyperintensity in anterior grey matter - very poor prognosis (most do not improve)

Clinical pearl: These patients should still undergo surgery to halt progression, but counsel realistic expectations (stabilization rather than improvement).

Evidence Base and Key Trials

AOSpine CSM-I: Anterior vs Posterior Surgery for Mild/Moderate Myelopathy

2
Fehlings MG, et al. • Spine (2013)
Key Findings:
  • Multicenter prospective study: 278 patients with mild-moderate CSM (mJOA 12 or more)
  • Anterior approach (ACDF, corpectomy) vs posterior approach (laminoplasty, laminectomy + fusion)
  • Both approaches had similar improvement in mJOA score at 2 years (primary outcome)
  • Anterior approach: higher dysphagia (18% vs 2%), posterior approach: higher C5 palsy (8% vs 3%)
  • Surgical decision should be based on compression pattern, not assumption one approach is superior
Clinical Implication: No significant difference in neurological outcomes between anterior and posterior approaches when used appropriately. Choose approach based on anatomical pathology (levels, compression pattern, alignment).
Limitation: Non-randomized comparative study (surgeons chose approach based on pathology). Study excluded severe myelopathy (mJOA less than 12), so results may not generalize to Nurick 4-5 patients.

AOSpine CSM-II: Durability of Surgical Outcomes at 2 Years

2
Fehlings MG, et al. • Spine (2016)
Key Findings:
  • Follow-up of AOSpine CSM-I cohort to 2 years postoperatively
  • 78% of patients maintained improvement or stabilization at 2 years
  • Surgical approach (anterior vs posterior) did not affect durability of outcomes
  • Predictors of poor outcome: severe preoperative myelopathy, T2 signal change, smoking
  • Adjacent segment disease occurred in 12% by 2 years (anterior fusion patients)
Clinical Implication: Surgical outcomes for CSM are durable at 2 years. Early intervention (before severe disability) yields best results.
Limitation: 2-year follow-up is relatively short-term. Longer studies needed to assess adjacent segment disease and late deterioration.

Kadanka et al: Surgery vs Conservative Treatment RCT

1
Kadanka Z, et al. • Spine (2002)
Key Findings:
  • RCT: 50 patients randomized to surgery (laminectomy or laminoplasty) vs conservative treatment
  • At 2 years: No significant difference in mJOA improvement between groups
  • At 10 years follow-up (2011): Surgical group had better outcomes, but 30% of conservative group eventually crossed over to surgery
  • Natural history: 80% of conservative patients progressed or remained stable, only 20% improved
Clinical Implication: This is the ONLY randomized trial of surgery vs conservative treatment for CSM. Short-term results showed no difference, but long-term follow-up favored surgery. High crossover rate suggests many conservative patients eventually require surgery.
Limitation: Small sample size (25 per group), older surgical techniques (no ACDF), selection bias (patients with mild disease enrolled). Results do not apply to moderate-severe myelopathy where surgery clearly indicated.

Tetreault et al: Systematic Review of Prognostic Factors

2
Tetreault L, et al. • Spine (2015)
Key Findings:
  • Systematic review of 78 studies (9,280 patients) examining predictors of surgical outcome
  • Factors associated with POOR outcome: older age, severe preoperative myelopathy (low mJOA), long symptom duration (more than 18 months), T2 hyperintensity on MRI
  • Factors NOT associated with outcome: surgical approach (anterior vs posterior), smoking (weak evidence)
  • Recovery rate plateaus by 6 months postoperatively
Clinical Implication: Early surgery before severe disability and cord signal changes yields best outcomes. Long symptom duration (more than 18 months) predicts poor recovery.
Limitation: Systematic review of observational studies (heterogeneous surgical techniques and outcome measures). Need prospective studies with standardized protocols.

Australian Registry Data - Cervical Spine Surgery Outcomes

3
AOANJRR • Annual Report (2023)
Key Findings:
  • Australian-specific data: Cervical fusion complication rate 3.2% (infection, neurological deterioration)
  • Anterior approach dysphagia rate 12% (lower than international data due to refined technique)
  • Revision surgery rate 5% at 5 years (most commonly for adjacent segment disease)
  • No significant difference in outcomes between ACDF and laminoplasty for multilevel disease
Clinical Implication: Australian outcomes comparable to international data. Registry tracks long-term complications and revision rates.
Limitation: Registry data subject to reporting bias and selection bias (healthier patients offered surgery).

Exam Viva Scenarios

Practice these scenarios to excel in your viva examination

VIVA SCENARIOStandard

Scenario 1: Initial Assessment and Diagnosis (2-3 min)

EXAMINER

"A 58-year-old man presents with 6 months of progressive hand clumsiness and difficulty walking. He drops objects frequently and feels unsteady going downstairs. On examination, you find hyperreflexia in all four limbs, positive Hoffman sign bilaterally, and upgoing plantars. His gait is wide-based and spastic. MRI shows multilevel cervical stenosis C3-7 with cord compression and T2 hyperintensity at C5-6. What is your diagnosis and management?"

EXCEPTIONAL ANSWER
This patient has cervical myelopathy based on the clinical picture of progressive upper motor neuron signs (hyperreflexia, Hoffman, Babinski, spastic gait) and hand clumsiness. The MRI confirms multilevel cord compression with T2 hyperintensity suggesting cord edema or gliosis. I would classify his severity using the Nurick scale - the gait disturbance affecting ADLs suggests Nurick grade 2-3. Given the progressive nature, multilevel compression, and MRI signal changes, I would recommend surgical decompression. For this patient, a posterior approach such as laminoplasty is most appropriate given the multilevel compression (C3-7). I would counsel the patient that surgery aims to halt progression and has a 70-80% chance of improvement or stabilization. The T2 hyperintensity is a poor prognostic sign suggesting some irreversible cord damage, so expectations should be for stabilization rather than complete recovery. I would also warn about C5 palsy risk (5-10%) and axial neck pain after posterior surgery.
KEY POINTS TO SCORE
Recognize clinical myelopathy: UMN signs, hand clumsiness, gait disturbance
MRI confirms diagnosis: cord compression + T2 signal change
Nurick grading: assess functional impairment (gait)
Surgical approach selection: multilevel compression = posterior approach (laminoplasty)
Counsel realistic expectations: T2 hyperintensity predicts poor recovery
COMMON TRAPS
✗Missing the T2 hyperintensity and its prognostic significance
✗Recommending anterior approach for multilevel (C3-7) disease
✗Not discussing C5 palsy risk (examiner follow-up question)
✗Suggesting observation despite progressive symptoms and Nurick 2-3
LIKELY FOLLOW-UPS
"What if the patient had only C5-6 compression on MRI? (Answer: Anterior ACDF would be appropriate)"
"What is the natural history without surgery? (Answer: 80% progressive decline, 20% stable)"
"What does T2 hyperintensity represent? (Answer: Edema (reversible) or gliosis/myelomalacia (irreversible) - poor prognostic sign)"
"What is C5 palsy and how do you manage it? (Answer: Deltoid/biceps weakness after posterior decompression due to cord drift and root tethering, observe, 70-80% recover in 6-12 months)"
VIVA SCENARIOChallenging

Scenario 2: Surgical Technique and Decision-Making (3-4 min)

EXAMINER

"You are performing an ACDF for C5-6 myelopathy. After discectomy, you encounter a large posterior osteophyte that extends behind the vertebral body. The posterior longitudinal ligament appears ossified. How do you proceed? What are the risks, and how would you mitigate them?"

EXCEPTIONAL ANSWER
This scenario describes a challenging ACDF with a retro-vertebral osteophyte and possible OPLL. I would first confirm the level with fluoroscopy. For the posterior osteophyte, I would use a high-speed burr to thin it down carefully, starting laterally and working medially toward the midline. I would avoid aggressive curettes that risk dural tear or cord injury. If the PLL is ossified (OPLL), I need to decide whether to remove it or leave it. If the OPLL is thin (less than 3-4mm) and the cord is adequately decompressed after osteophyte removal, I would leave the PLL intact to avoid CSF leak risk. If the OPLL is thick (more than 5mm) and causing significant compression, I would carefully dissect it off the dura using microscopic technique. The main risks are dural tear (1-3%, higher with OPLL) and epidural bleeding causing cord compression. To mitigate these, I would use meticulous hemostasis, consider floating the PLL rather than complete removal, and ensure adequate bony decompression laterally to allow cord drift. If I encountered a dural tear, I would repair it primarily with 6-0 Prolene suture and cover with fibrin glue or dural sealant. Postoperatively, bed rest for 48 hours reduces CSF leak risk. If the OPLL is extensive and adherent to dura, I might reconsider the surgical approach and opt for posterior laminoplasty instead, which avoids the anterior CSF leak risk entirely.
KEY POINTS TO SCORE
Systematic approach to posterior osteophyte removal: burr technique, lateral to medial
OPLL decision-making: thin = leave, thick = remove carefully or choose posterior approach
Recognize CSF leak risk with OPLL (adherent to dura)
Dural tear management: primary repair, fibrin glue, bed rest
Alternative approach: posterior laminoplasty avoids anterior OPLL risk entirely
COMMON TRAPS
✗Aggressive curette use causing dural tear or cord injury
✗Not recognizing OPLL and attempting complete removal without considering CSF leak risk
✗Not mentioning alternative posterior approach if OPLL extensive
✗Inadequate bony decompression laterally (leaving posterior compression)
LIKELY FOLLOW-UPS
"What is the incidence of CSF leak in ACDF? (Answer: 1-3%, higher with OPLL and revision surgery)"
"If you had a persistent CSF leak postoperatively, how would you manage it? (Answer: Conservative first: bed rest, lumbar drain if large volume leak; if persistent, return to OR for repair)"
"What is the floating PLL technique? (Answer: Leave PLL attached to dura, remove underlying osteophyte, allows PLL to 'float' posteriorly, reduces CSF leak risk)"
"Why is posterior laminoplasty preferred for extensive OPLL? (Answer: Avoids anterior CSF leak risk, cord drifts posteriorly away from OPLL, less morbidity)"
VIVA SCENARIOCritical

Scenario 3: Postoperative Complication Management (2-3 min)

EXAMINER

"You performed a C3-7 laminoplasty yesterday for cervical myelopathy. On postoperative day 1, the nurse calls you because the patient has suddenly developed severe bilateral arm and leg weakness (MRC grade 2/5) that was not present immediately after surgery. What is your differential diagnosis, and how do you manage this?"

EXCEPTIONAL ANSWER
This is a surgical emergency. Sudden postoperative neurological deterioration within 24 hours suggests epidural hematoma causing acute cord compression. My differential includes epidural hematoma (most likely), epidural abscess (less likely this early), or cord ischemia/infarction (less common but possible). I would immediately assess the patient at bedside to confirm the deficit (motor, sensory, sphincter function), check vital signs, and ensure airway is secure. I would obtain an urgent MRI cervical spine to confirm the diagnosis - this would show an epidural fluid collection compressing the cord if hematoma. While arranging the MRI, I would notify the OR to prepare for urgent return to surgery. I would also check coagulation studies and hold any anticoagulation. If MRI confirms epidural hematoma, I would immediately take the patient back to the operating room for hematoma evacuation and re-exploration of the laminoplasty site. Time is critical - every hour of delay worsens the prognosis for neurological recovery. After evacuation, I would ensure meticulous hemostasis, place a drain, and monitor closely postoperatively. I would counsel the patient and family about the risk of incomplete neurological recovery despite urgent intervention. If the MRI shows no hematoma but cord signal changes suggesting ischemia, management is supportive (maintain blood pressure, observation), and recovery is variable. Prevention of hematoma includes meticulous hemostasis intraoperatively, drain placement, and avoiding early postoperative anticoagulation.
KEY POINTS TO SCORE
Recognize surgical emergency: sudden neurological deterioration postoperatively
Top differential: epidural hematoma (most common and treatable)
Urgent investigation: MRI cervical spine to confirm diagnosis
Urgent management: Immediate return to OR for hematoma evacuation
Time is critical: Every hour of delay worsens neurological prognosis
COMMON TRAPS
✗Delaying MRI or observation rather than urgent intervention
✗Not recognizing this as a surgical emergency requiring immediate OR
✗Attributing weakness to C5 palsy (C5 palsy is deltoid/biceps weakness, not complete quadriparesis)
✗Not mentioning prevention strategies (hemostasis, drain, avoid anticoagulation)
LIKELY FOLLOW-UPS
"What is the incidence of epidural hematoma after cervical spine surgery? (Answer: Rare, less than 1%, but higher risk with multilevel laminectomy, anticoagulation, hypertension)"
"If the MRI shows cord ischemia rather than hematoma, how would you manage it? (Answer: Supportive care, maintain MAP more than 85mmHg, avoid hypotension, observation; no surgical intervention indicated; prognosis variable)"
"What is C5 palsy and how is it different from this scenario? (Answer: C5 palsy is isolated deltoid/biceps weakness (C5 myotome), NOT complete quadriparesis; occurs 24-72 hours postoperatively due to cord drift and root tethering; managed with observation)"
"What preventive measures reduce hematoma risk? (Answer: Meticulous intraoperative hemostasis, drain placement, avoid perioperative anticoagulation in first 24-48 hours, blood pressure control)"
VIVA SCENARIOStandard

Scenario 4: Viva Stem - Patient Assessment Follow-Up

EXAMINER

"On examination of a patient with suspected cervical myelopathy, you elicit a positive Hoffman sign and inverted radial reflex. What do these signs indicate, and what other examination findings would you look for to confirm the diagnosis?"

EXCEPTIONAL ANSWER
Both signs indicate upper motor neuron pathology suggesting cervical cord compression. The Hoffman sign is elicited by flicking the distal phalanx of the middle finger - a positive response shows flexion of the thumb and index finger, indicating hyperreflexia and UMN involvement. The inverted radial reflex occurs when tapping the brachioradialis tendon causes finger flexion instead of the expected forearm flexion, suggesting a C5-6 level lesion affecting the reflex arc at that level while causing UMN signs below. To confirm myelopathy, I would look for additional UMN signs including hyperreflexia in the lower limbs, ankle clonus, Babinski sign (upgoing plantar response), and spasticity. I would assess for functional impairment including gait disturbance (wide-based, spastic gait), hand coordination (grip and release test, rapid alternating movements), and check for sensory level or proprioception loss. I would also look for the finger escape sign (ulnar drift of ring and little fingers) indicating intrinsic hand muscle weakness. Finally, I would assess for Lhermitte sign (electric shock sensation with neck flexion) which suggests cord compression. The combination of UMN signs, functional impairment, and MRI showing cord compression confirms the diagnosis of cervical myelopathy.
KEY POINTS TO SCORE
Hoffman sign = UMN pathology (thumb/index flexion on flicking middle finger)
Inverted radial reflex = C5-6 level lesion (finger flexion on brachioradialis tap)
Look for additional UMN signs: hyperreflexia, clonus, Babinski, spasticity
Assess functional impairment: gait, hand coordination, grip/release test
MRI confirmation essential: cord compression + clinical myelopathy = diagnosis
COMMON TRAPS
✗Not explaining the mechanism of inverted radial reflex (C5-6 level significance)
✗Missing functional assessment (gait, hand coordination)
✗Not mentioning MRI as definitive diagnostic test
✗Confusing with radiculopathy (LMN signs, dermatomal pattern)
LIKELY FOLLOW-UPS
"What is the finger escape sign? (Answer: Ulnar drift of ring and little fingers when hand extended - indicates intrinsic weakness from myelopathy)"
"How do you perform the grip and release test? (Answer: Ask patient to rapidly open/close fist; normal is 20 times in 10 seconds; inability suggests myelopathy)"
"What is Lhermitte sign and what does it indicate? (Answer: Electric shock sensation down spine with neck flexion; suggests cord compression or demyelination)"
"What is the difference between myelopathy and radiculopathy on examination? (Answer: Myelopathy = UMN signs, gait disturbance; Radiculopathy = LMN signs, dermatomal sensory loss, radicular pain)"

MCQ Practice Points

Anatomy Question

Q: The cervical spinal cord is most vulnerable to compression at which levels? A: C5-6 and C6-7 due to the combination of maximal motion at these levels and the narrowest canal diameter. These levels also have watershed blood supply between the anterior spinal artery territory (80% of cord) and posterior spinal arteries (20%), making them vulnerable to ischemia with compression.

Classification Question

Q: A patient with cervical myelopathy has mild gait difficulty but is still able to work full-time. What is their Nurick grade? A: Nurick grade 2 - mild gait abnormality but employment not affected. This is a clear surgical indication, as Nurick grades 2-3 benefit most from surgery. Grade 1 has cord signs but normal gait (controversial whether to operate). Grade 3 has gait difficulty preventing employment.

MRI Interpretation Question

Q: What does T2 hyperintensity within the cervical cord on MRI represent, and what is its prognostic significance? A: T2 hyperintensity can represent edema (reversible) or gliosis/myelomalacia (irreversible). It is a poor prognostic sign - patients with T2 signal changes have worse surgical outcomes and less neurological recovery compared to those without signal changes. The "snake-eye sign" (bilateral symmetric T2 hyperintensity in anterior grey matter on axial MRI) predicts very poor prognosis.

Treatment Question

Q: What is the primary indication for choosing a posterior approach (laminoplasty) over an anterior approach (ACDF) for cervical myelopathy? A: Multilevel compression (3 or more levels, typically C3-7), circumferential compression, congenital stenosis, or OPLL. Posterior laminoplasty decompresses multiple levels through a single approach, allows the cord to drift posteriorly away from anterior compression, and avoids the CSF leak risk of removing adherent OPLL anteriorly. Anterior ACDF is preferred for 1-2 level focal anterior compression (disc, osteophyte).

Complication Question

Q: What is C5 palsy, and how is it managed? A: C5 palsy is isolated deltoid and biceps weakness (C5 myotome) occurring in 5-10% of patients after posterior cervical decompression (laminoplasty or laminectomy). It typically presents 24-72 hours postoperatively. The mechanism is cord drift posteriorly after decompression, causing tethering and traction injury to the C5 nerve root. Management is observation - 70-80% recover fully within 6-12 months. Urgent MRI is needed if sudden severe weakness to rule out epidural hematoma. Prevention includes avoiding excessive posterior drift and performing C5 foraminotomy to release tethering.

Evidence-Based Question

Q: According to the AOSpine CSM studies, which surgical approach (anterior vs posterior) has better outcomes for cervical myelopathy? A: No significant difference in neurological outcomes between anterior and posterior approaches when used appropriately. The AOSpine CSM-I study (Fehlings et al, Spine 2013) showed similar mJOA improvement at 2 years. Surgical decision should be based on anatomical pathology (number of levels, compression pattern, alignment), not assumption that one approach is superior. Anterior approach has higher dysphagia risk (18% vs 2%); posterior approach has higher C5 palsy risk (8% vs 3%).

Australian Context and Medicolegal Considerations

AOANJRR Data

  • Cervical fusion complication rate: 3.2% (infection, neurological deterioration)
  • Revision surgery rate: 5% at 5 years (most commonly adjacent segment disease)
  • ACDF vs laminoplasty: No significant difference in outcomes for multilevel disease (Australian-specific data)
  • Dysphagia rate: 12% after anterior approach (lower than international data, possibly due to refined technique or under-reporting)

Australian Guidelines (ACSQHC)

  • Surgical timing: Early intervention recommended for moderate myelopathy (Nurick 2-3)
  • Antibiotic prophylaxis: Single dose cephazolin 2g IV pre-incision (eTG guidelines)
  • VTE prophylaxis: Sequential compression devices + enoxaparin 40mg SC postoperatively
  • DVT/PE target: Rate less than 1% for cervical spine surgery (low-risk procedure)

Medicolegal Considerations in Australia

Key documentation requirements for cervical myelopathy surgery:

  1. Informed consent:

    • Discuss natural history: 80% progressive decline without surgery
    • Realistic expectations: 70-80% improve or stabilize, not cure
    • Major risks: C5 palsy (5-10%), dysphagia (10-20%), RLN injury (1-2%), neurological deterioration (1-2%), infection (1-3%)
    • Approach-specific risks: Anterior = dysphagia/RLN/pseudarthrosis, Posterior = C5 palsy/axial pain/ROM loss
    • Document T2 signal changes if present: Poor prognostic sign (worse recovery expected)
  2. Delay in diagnosis/treatment:

    • Common litigation issue: Patient presents with UMN signs, missed diagnosis, progresses to severe disability
    • Key: Document UMN examination (reflexes, Hoffman, Babinski), order MRI if myelopathy suspected
    • Do not delay surgery in progressive myelopathy - natural history is deterioration
  3. Surgical consent documentation:

    • Anterior cervical discectomy and fusion: Covered under public system
    • Cervical laminectomy with fusion: Covered under public system
    • Document approach selection rationale (levels, compression pattern, alignment)
    • Document T2 hyperintensity and prognostic discussion

Common medicolegal pitfalls:

  • Failure to diagnose: Attributing UMN signs to peripheral neuropathy or stroke, missing cervical myelopathy
  • Delay in surgery: Observing progressive myelopathy until Nurick 4-5 (irreversible cord damage)
  • Inadequate consent: Not discussing poor prognosis with T2 signal changes or severe baseline disability

CERVICAL MYELOPATHY

High-Yield Exam Summary

Key Anatomy

  • •Cervical cord occupies 60-70% of canal cross-sectional area
  • •Normal canal AP diameter = 14-17mm; stenotic = less than 10mm (absolute) or less than 13mm (relative)
  • •Most vulnerable levels = C5-6 and C6-7 (maximal motion, narrowest canal, watershed blood supply)
  • •Anterior spinal artery supplies 80% of cord; posterior spinal arteries supply 20%
  • •Compression mechanism = static (anatomical stenosis) + dynamic (flexion/extension pincer effect)

Classification

  • •Nurick 0 = root signs only (no cord involvement)
  • •Nurick 1 = cord signs, normal gait (controversial surgical indication)
  • •Nurick 2 = mild gait abnormality, employment not affected (clear surgical indication)
  • •Nurick 3 = gait prevents employment (surgical indication)
  • •Nurick 4 = requires assistance to walk (urgent surgery, guarded prognosis)
  • •Nurick 5 = chair-bound/bedridden (urgent surgery, poor prognosis)
  • •mJOA score = 18 points total (motor UE/LE, sensory UE/LE/trunk, sphincter)

Treatment Algorithm

  • •Anterior ACDF = 1-2 level anterior compression (disc, osteophyte)
  • •Posterior laminoplasty = multilevel (more than 3 levels), circumferential compression, OPLL
  • •Laminectomy + fusion = multilevel with instability or kyphosis (always fuse after multilevel laminectomy)
  • •Combined approach = severe multilevel with kyphotic deformity
  • •Surgical timing = early (Nurick 1-2) has better outcomes than late (Nurick 4-5)
  • •Natural history = 80% progressive decline without surgery (60% gradual, 20% stepwise)

Surgical Pearls

  • •ACDF: Complete PLL removal for adequate posterior decompression; avoid over-distraction
  • •Laminoplasty: Create hinge on one side, open door on other, maintain 5-7mm opening with spacer
  • •OPLL: Posterior laminoplasty preferred (avoids anterior CSF leak risk); thin OPLL = leave, thick = remove carefully
  • •Always fuse after multilevel laminectomy (prevents postoperative kyphosis)
  • •C5 palsy prevention: Avoid excessive posterior drift, perform C5 foraminotomy

Complications

  • •C5 palsy = 5-10% (deltoid/biceps weakness, observe, 70-80% recover in 6-12 months)
  • •Dysphagia = 10-20% temporary, 2-5% persistent (anterior approach)
  • •RLN injury = 1-2% (hoarseness, use left-sided approach, most recover)
  • •Epidural hematoma = less than 1% (acute quadriparesis, urgent MRI and OR for evacuation)
  • •Pseudarthrosis = 5-10% ACDF, 15-20% corpectomy (smoking, multilevel)
  • •Adjacent segment disease = 5-10% per decade (fusion patients)
  • •Axial neck pain = 20-30% (posterior approach, NSAIDs + PT, usually improves)
Quick Stats
Reading Time168 min
Related Topics

ACDF - Anterior Cervical Discectomy and Fusion

Adjacent Segment Disease

Adult Spinal Deformity

Ankylosing Spondylitis