Cervical Spondylotic Myelopathy (CSM)

1. Clinical Overview

Summary

Cervical spondylotic myelopathy (CSM), now increasingly termed degenerative cervical myelopathy (DCM), represents the most common cause of spinal cord dysfunction in adults over 55 years of age worldwide. [1] The condition results from progressive mechanical compression of the spinal cord secondary to age-related degenerative changes in the cervical spine, encompassing intervertebral disc degeneration, osteophyte formation, ligamentum flavum hypertrophy, and ossification of the posterior longitudinal ligament (OPLL). [2]

The clinical syndrome is characterised by an insidious onset of neurological dysfunction manifesting as deterioration in fine motor control of the hands, gait disturbance with spastic features, and a distinctive pattern of upper motor neurone signs in the lower limbs combined with lower motor neurone or mixed signs at the level of compression in the upper limbs. [3] The natural history is one of progressive neurological decline in the majority of patients, with spontaneous improvement being rare. [4]

CSM carries substantial clinical importance due to its high prevalence, significant impact on quality of life, and the fact that it represents a potentially treatable cause of disability. Early recognition and appropriate surgical intervention can halt progression and improve neurological function, whereas delayed diagnosis leads to irreversible spinal cord damage and poor outcomes. [5] The condition accounts for the majority of cervical spine surgical procedures performed worldwide. [1]

Key Facts

Clinical Pearls

"Button Trouble Sign": Difficulty with fine motor tasks such as buttoning shirts, handling coins, or writing is often the earliest symptom. Patients frequently dismiss this as arthritis or normal aging — always ask specifically about hand dexterity in older patients presenting with neck symptoms or gait changes.

"Scissor Legs, Numb Hands": The classic CSM pattern involves upper motor neurone signs in the lower limbs (spastic paraparesis) combined with lower motor neurone signs at the level of compression in the upper limbs (weakness and wasting) plus UMN signs below. This "dissociated" pattern localises the lesion to the cervical cord.

"Hoffman's = Think Cervical Spine": A positive Hoffman's sign (flick middle finger DIP → reflex thumb/index finger flexion) in a patient with gait problems and hand clumsiness should trigger urgent MRI of the cervical spine. It indicates a corticospinal tract lesion above C5-C6.

"The Treatment Window Closes": Recovery from myelopathy is inversely related to duration of symptoms. Patients with symptoms for less than 12 months have significantly better outcomes than those with prolonged symptom duration. [5] Early neurosurgical referral is paramount.

"Stepwise Decline, Not Linear": CSM typically follows a stepwise deterioration pattern — periods of relative stability punctuated by episodes of acute worsening. Minor trauma, even a fall without obvious injury, can precipitate sudden deterioration in a stenotic canal.

"Mild T2 Signal = Surgery Still Helps": Intramedullary T2 hyperintensity on MRI (myelomalacia) historically predicted poor outcome, but contemporary evidence shows surgical decompression still provides benefit. T1 hypointensity (cavitation) indicates more severe damage with worse prognosis. [7]

Why This Matters Clinically

Cervical spondylotic myelopathy is common, underdiagnosed, and importantly, treatable. The prevalence of cervical spondylosis exceeds 90% in adults over 60 years based on radiological studies, with approximately 5-10% developing symptomatic myelopathy. [2] Many elderly patients presenting with gait disturbance, falls, and hand clumsiness are misdiagnosed with age-related frailty, peripheral neuropathy, or osteoarthritis when they actually harbour surgically correctable spinal cord compression.

Recognition of the characteristic clinical pattern (hand clumsiness + gait disturbance + upper motor neurone signs + positive Hoffman's sign) followed by expeditious MRI and neurosurgical referral can prevent irreversible neurological damage. Studies consistently demonstrate that earlier intervention results in superior outcomes. [5,8]

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2. Epidemiology

Incidence & Prevalence

Demographics

Risk Factors

Congenital Stenosis — Key Concept

The normal adult cervical spinal canal diameter (C3-C7) measures 17-18mm in the anteroposterior plane. Individuals with congenital narrowing (less than 13mm) have reduced reserve capacity to accommodate degenerative changes. When acquired spondylotic changes are superimposed on a congenitally narrow canal, symptomatic myelopathy develops with relatively minor disc/osteophyte protrusion. [10]

Torg-Pavlov Ratio: Canal diameter divided by vertebral body diameter. A ratio less than 0.80 indicates significant stenosis and increased susceptibility to cord injury.

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3. Pathophysiology

Overview of Mechanism

The pathophysiology of CSM is multifactorial, involving the interplay of static mechanical compression, dynamic factors during cervical motion, and secondary vascular compromise leading to spinal cord ischaemia. [2,11]

Step-by-Step Pathogenic Cascade

Stage 1: Degenerative Cervical Changes (Spondylosis)

The degenerative cascade begins with the intervertebral disc:

• Loss of disc hydration and proteoglycan content with aging
• Annular fissuring and disc height loss
• Disc bulging into the spinal canal (anteriorly)
• Loss of disc height leads to facet joint overload and hypertrophy
• Uncovertebral joint (joints of Luschka) osteophyte formation
• Posterior osteophyte (spondylotic bar) formation at disc-vertebral junction
• Ligamentum flavum infolding and hypertrophy posteriorly
• Ossification of the posterior longitudinal ligament (OPLL) in predisposed individuals

Stage 2: Spinal Canal Narrowing (Stenosis)

Static factors (disc, osteophytes, ligamentum flavum, OPLL) combine with dynamic factors:

• Flexion: Spinal cord stretches over anterior pathology; posterior canal widens
• Extension: Ligamentum flavum buckles inward; cord compressed posteriorly; canal shortens and narrows by up to 2mm
• Repetitive motion causes microtrauma to the cord

Stage 3: Spinal Cord Compression and Ischaemia

Stage 4: Spinal Cord Pathology

Stage 5: Clinical Manifestations

Molecular Pathophysiology

Exam Detail: Cellular and Molecular Mechanisms:

1. Glutamate excitotoxicity: Mechanical injury causes excessive glutamate release → NMDA and AMPA receptor overactivation → intracellular calcium influx → neuronal death

2. Oxidative stress: Ischaemia-reperfusion generates reactive oxygen species (ROS) → lipid peroxidation → membrane damage

3. Inflammatory cascade: Activated microglia and astrocytes → release of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6) → secondary injury expansion

4. Blood-spinal cord barrier breakdown: Increased permeability → vasogenic oedema → extravasation of inflammatory cells

5. Apoptosis: Programmed cell death via intrinsic (mitochondrial) and extrinsic (death receptor) pathways → oligodendrocyte and neuronal loss

6. Wallerian degeneration: Axonal transection leads to distal axon and myelin breakdown; macrophage recruitment for debris clearance

These mechanisms explain why early decompression is beneficial — removing the compressive pathology limits secondary injury cascade progression.

Central Cord Syndrome — Important Subtype

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4. Clinical Presentation

Symptoms

Symptom Onset Pattern

Signs

Upper Limb Findings:

Lower Limb Findings:

Gait Assessment:

Red Flags — Urgent Referral Required

[!CAUTION] Red Flags Requiring Urgent Neurosurgical Referral:

• Progressive motor weakness in arms or legs
• Rapid neurological decline over days to weeks
• Bladder or bowel dysfunction (suggests severe myelopathy)
• Bilateral hand symptoms with gait disturbance
• Positive Hoffman's sign with other myelopathic features
• Acute deterioration following trauma (even minor)
• Suspected central cord syndrome (arms weaker than legs after injury)
• Young patient with myelopathic symptoms (consider alternative pathology: tumour, MS)

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5. Clinical Examination

Structured Approach

Preparation:

• Patient adequately exposed (upper body, lower limbs)
• Consent obtained; chaperone offered
• General inspection: Mobility aids, posture, obvious wasting

Cervical Spine Examination:

Upper Limb Neurological Examination:

Lower Limb Neurological Examination:

Gait Assessment:

Special Tests for CSM

mJOA Score — Modified Japanese Orthopaedic Association Score

The mJOA score is the most widely used functional assessment tool for CSM severity. [5,6]

Severity Classification Based on mJOA:

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6. Investigations

First-Line Investigations

MRI Cervical Spine — Detailed Interpretation

Standard Protocol:

• Sagittal T1-weighted, T2-weighted sequences
• Axial T2-weighted sequences (through stenotic levels)
• Sagittal STIR (assess for oedema, acute changes)

Key MRI Findings:

Quantitative MRI Measures:

Second-Line Investigations

Investigations to Exclude Differential Diagnoses

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7. Classification

Anatomical Classification of Cervical Stenosis

Severity Classification (Based on mJOA)

Nurick Grade (Historical)

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8. Management

Management Principles

1. Surgery is the mainstay of treatment for established, symptomatic CSM — conservative management does not reverse neurological deficits and natural history is progressive decline in most patients. [4,14]
2. Goal of surgery is decompression of the spinal cord to halt progression and potentially improve function.
3. Timing of surgery is critical — earlier intervention associated with better outcomes. [5,8]
4. Approach selection (anterior vs posterior) depends on pathology location, number of levels, cervical alignment, and surgeon experience.

Management Algorithm

                    SUSPECTED CERVICAL MYELOPATHY
                               ↓
┌─────────────────────────────────────────────────────────────────────────┐
│                    CLINICAL ASSESSMENT                                   │
├─────────────────────────────────────────────────────────────────────────┤
│  ➤ History: Hand clumsiness, gait problems, falls, bladder symptoms    │
│  ➤ Neurological examination: Hoffman's, reflexes, tone, power, gait    │
│  ➤ Functional assessment: mJOA score, Nurick grade                     │
│  ➤ Red flags: Progressive weakness, bladder/bowel, rapid decline       │
└─────────────────────────────────────────────────────────────────────────┘
                               ↓
┌─────────────────────────────────────────────────────────────────────────┐
│                    MRI CERVICAL SPINE                                    │
├─────────────────────────────────────────────────────────────────────────┤
│  ➤ Confirm cord compression                                             │
│  ➤ Assess number of levels stenotic                                     │
│  ➤ Identify T2 hyperintensity (cord signal change)                      │
│  ➤ Characterise pathology: Disc, osteophyte, ligamentum flavum, OPLL    │
│  ➤ Assess cervical sagittal alignment (lordosis vs kyphosis)            │
└─────────────────────────────────────────────────────────────────────────┘
                               ↓
                    ┌─────────┴────────┐
                    ↓                   ↓
          MYELOPATHY CONFIRMED    NO CORD COMPRESSION
                    ↓                   ↓
┌─────────────────────────────────┐  ┌───────────────────────────────────┐
│ Refer to Spinal Surgeon          │  │ Reassess diagnosis                 │
│ (Neurosurgery/Ortho Spine)       │  │ Consider: MS, ALS, B12, other     │
└─────────────────────────────────┘  └───────────────────────────────────┘
                    ↓
┌─────────────────────────────────────────────────────────────────────────┐
│                    SEVERITY STRATIFICATION                               │
├─────────────────────────────────────────────────────────────────────────┤
│                                                                          │
│  MILD MYELOPATHY (mJOA 15-17):                                          │
│  ➤ May consider close monitoring with structured surveillance           │
│  ➤ Surgery if ANY progression of symptoms or signs [14]                 │
│  ➤ MRI + clinical review every 3-6 months                               │
│  ➤ Patient must understand risk of sudden deterioration                 │
│                                                                          │
│  MODERATE MYELOPATHY (mJOA 12-14):                                      │
│  ➤ Surgery recommended [5,14]                                           │
│  ➤ Benefits outweigh surgical risks in most patients                    │
│  ➤ Anterior or posterior approach based on anatomy                      │
│                                                                          │
│  SEVERE MYELOPATHY (mJOA less than 12):                                          │
│  ➤ Surgery strongly recommended                                         │
│  ➤ Worse baseline = worse recovery potential but still beneficial       │
│  ➤ Do not delay further — every week of delay worsens outcome           │
│                                                                          │
│  ACUTE DETERIORATION / TRAUMA (Central Cord Syndrome):                  │
│  ➤ Urgent/emergency spinal surgery consultation                         │
│  ➤ Immobilisation in neutral position                                   │
│  ➤ Timing of surgery for central cord syndrome debated [15]             │
│                                                                          │
└─────────────────────────────────────────────────────────────────────────┘

Surgical Approach Selection

Surgical Procedures — Anterior Approach

ACDF Surgical Steps (Overview):

1. Anterior cervical approach (Smith-Robinson)
2. Identify level with fluoroscopy
3. Complete discectomy including posterior annulus and PLL
4. Removal of posterior osteophytes (spondylotic bar) with curette and Kerrison rongeurs
5. Decompression confirmed with probe reaching posterior annulus edges
6. Endplate preparation (preserve endplate cortex for cage support)
7. Interbody cage sizing and placement (lordotic angle)
8. Anterior plate fixation (optional; stand-alone cages also used)
9. Haemostasis; wound closure

Surgical Procedures — Posterior Approach

Laminoplasty Types:

• Open-door (Hirabayashi): Unilateral hinge; laminae rotated open on one side
• French-door (Kurokawa): Midline split; bilateral opening
• Spacer materials: Ceramic, titanium, allograft, suture anchors

Conservative Management (Selected Patients Only)

Exam Detail: Evidence for Conservative vs Surgical Management:

The landmark Kadanka et al. RCT (2002) compared surgical and conservative management for MILD CSM and found no significant difference at 3-year follow-up. [4] However, this study specifically enrolled patients with mild disease and excluded moderate-severe myelopathy.

The AOSpine North America study (2013) prospectively demonstrated significant improvement in mJOA scores following surgery for moderate and severe CSM, with 80% of patients improving. [6]

The current AOSpine Clinical Practice Guidelines (2017) recommend:

• Surgical intervention for moderate and severe myelopathy (Grade: Strong recommendation, moderate evidence)
• For mild myelopathy: structured surveillance or surgery may be offered (Grade: Weak recommendation, low evidence) [14]

Postoperative Care

Complications of Surgery

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9. Prognosis and Outcomes

Natural History (Untreated)

The natural history is unfavourable — the majority of patients will deteriorate without surgery, and the deterioration is often irreversible. [4]

Surgical Outcomes

Recovery Rate Calculation: Recovery Rate = (Postoperative mJOA − Preoperative mJOA) / (18 − Preoperative mJOA) × 100%

Prognostic Factors

Long-Term Outcomes

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10. Guidelines and Evidence

Key Guidelines

Landmark Studies

Fehlings et al. — AOSpine North America Study (2013) [6]

• Design: Prospective multicentre observational study
• Patients: 278 patients undergoing surgery for CSM
• Outcome: 80% improved at 1 year; mean mJOA improvement 2.8 points
• Conclusion: Surgery is effective for CSM; supports early intervention
• PMID: 24048552 | DOI: 10.2106/JBJS.L.01621

Kadanka et al. — Surgical vs Conservative RCT (2002) [4]

• Design: Randomised controlled trial
• Patients: 68 patients with mild CSM randomised to surgery vs conservative
• Outcome: No significant difference at 3 years for MILD disease
• Conclusion: Supports conservative management as option for MILD, STABLE disease only
• PMID: 12415118

Tetreault et al. — Predictors of Outcome Systematic Review (2015) [5]

• Design: Systematic review of prognostic factors
• Findings: Duration of symptoms, baseline severity, age, and smoking predict outcome
• Conclusion: Supports early surgery before prolonged symptom duration
• PMID: 25299038 | DOI: 10.1007/s00586-014-3595-0

Fehlings et al. — AOSpine International Prospective Study (2015) [8]

• Design: International prospective cohort
• Patients: 479 patients across 16 sites globally
• Outcome: Surgery effective regardless of approach; anterior and posterior equivalent outcomes
• PMID: 26103459 | DOI: 10.3171/2015.1.SPINE141322

Nouri et al. — Epidemiology, Genetics, Pathogenesis Review (2015) [2]

• Design: Comprehensive review article
• Content: Pathophysiology, risk factors, molecular mechanisms
• PMID: 25839387 | DOI: 10.1097/BRS.0000000000000913

Level of Evidence for Key Interventions

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11. Differential Diagnosis

Key Differentials

Distinguishing Myelopathy from Radiculopathy

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12. Patient Information / Layperson Explanation

What is Cervical Spondylotic Myelopathy?

CSM is a condition where the spinal cord in your neck becomes squeezed (compressed) due to age-related changes in the spine. The spinal cord carries all the nerve signals between your brain and body, so when it gets compressed, you can develop problems with walking, using your hands, and other functions.

Why Does It Happen?

As we get older, the discs between our neck bones (vertebrae) lose water and shrink. This causes:

• Bone spurs to form
• Ligaments to thicken
• The space around the spinal cord to narrow

In some people, these changes narrow the space enough to press on the spinal cord, causing symptoms.

What Are the Symptoms?

• Clumsy hands: Difficulty buttoning shirts, writing, picking up small objects
• Unsteady walking: Feeling off-balance, stiff legs, difficulty with stairs
• Numbness or tingling: Usually in the hands and feet
• Weakness: In arms, hands, or legs
• Bladder problems: Urgency or difficulty starting (in advanced cases)

How Is It Diagnosed?

Your doctor will examine your nervous system (checking reflexes, strength, sensation) and order an MRI scan of your neck. The MRI shows if the spinal cord is being compressed.

How Is It Treated?

For mild symptoms: Sometimes careful monitoring is possible, with regular check-ups to watch for any worsening.

For moderate or severe symptoms: Surgery is usually recommended to take the pressure off the spinal cord. This can be done from:

• The front of the neck: Removing the disc and fusing the bones together (ACDF)
• The back of the neck: Opening up the bone covering the spinal cord (laminectomy or laminoplasty)

What Can I Expect?

With surgery, most people stop getting worse, and many improve. The degree of improvement depends on:

• How severe your symptoms were before surgery
• How long you had symptoms before surgery — earlier is better

When Should I Seek Urgent Help?

See a doctor immediately if you notice:

• Rapid worsening of weakness or balance
• New difficulty controlling your bladder or bowels
• Sudden change after a fall or neck injury

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13. Examination Focus

High-Yield Exam Topics

Viva Questions and Model Answers

Q1: A 68-year-old man presents with 6 months of difficulty buttoning his shirt and unsteady gait. Examination shows wasting of intrinsic hand muscles, positive Hoffman's sign bilaterally, brisk knee reflexes, and upgoing plantars. How would you manage this patient?

Model Answer:

"This clinical picture is highly suggestive of cervical spondylotic myelopathy. The combination of fine motor impairment in the hands, gait disturbance, intrinsic hand muscle wasting (lower motor neurone signs at the level of compression), and upper motor neurone signs below (positive Hoffman's, hyperreflexia, upgoing plantars) localises the lesion to the cervical spinal cord.

My approach would be:

1. Complete Assessment:

• Full neurological examination including sensory testing, gait analysis, grip-release test
• Calculate mJOA score to grade severity
• Assess bladder function (red flag if involved)

2. Imaging:

• MRI cervical spine — gold standard; looking for cord compression, number of levels, T2 signal change (myelomalacia), alignment
• CT cervical spine if planning surgery (bone detail for surgical planning)

3. Management Decision: Based on the described examination findings and 6-month history, this patient likely has moderate-to-severe myelopathy. I would refer urgently to a spinal surgeon (neurosurgery or orthopaedic spine).

4. Surgical Approach: Would depend on MRI findings:

• If 1-3 level disease with ventral pathology → ACDF
• If multi-level stenosis with preserved lordosis → Laminoplasty or laminectomy with fusion
• If kyphosis present → Anterior approach preferred

5. Evidence: Surgery is recommended for moderate-severe myelopathy per AOSpine guidelines [14], with 60-80% of patients showing neurological improvement. Earlier surgery is associated with better outcomes."

Q2: What is the mJOA score and how does it guide management?

Model Answer:

"The modified Japanese Orthopaedic Association (mJOA) score is the most widely validated functional assessment tool for cervical myelopathy severity.

Components (Total 18 points):

• Motor function upper limb (0-5)
• Motor function lower limb (0-7)
• Sensory function upper limb (0-3)
• Sphincter function (0-3)

Severity Classification:

• Mild: mJOA 15-17
• Moderate: mJOA 12-14
• Severe: mJOA less than 12

Management Implications:

• Mild (15-17): May consider structured surveillance with close monitoring. Surgery if any progression.
• Moderate (12-14): Surgery recommended — benefits outweigh risks in most patients.
• Severe (less than 12): Surgery strongly indicated. Worse baseline predicts less complete recovery, but surgery still beneficial to halt progression.

The score is also used to calculate the Recovery Rate post-surgery: (Post-op mJOA − Pre-op mJOA) / (18 − Pre-op mJOA) × 100%. This allows comparison of outcomes between studies."

Q3: Compare and contrast ACDF with laminoplasty for treating cervical myelopathy.

Model Answer:

"ACDF (Anterior Cervical Discectomy and Fusion) and laminoplasty are the two major surgical strategies for CSM, approaching from opposite directions.

ACDF (Anterior Approach):

• Technique: Removes disc, osteophytes directly; reconstructs with cage/graft; stabilises with plate
• Indications: 1-3 level disease; predominantly ventral pathology; kyphotic alignment
• Advantages: Direct decompression of ventral pathology; can correct kyphosis; may preserve motion segments above
• Disadvantages: Dysphagia (5-15%); recurrent laryngeal nerve injury (1-3%); pseudarthrosis; adjacent segment disease
• Motion: Sacrifices motion at fused levels

Laminoplasty (Posterior Approach):

• Technique: Expands canal posteriorly; hinges laminae open; indirect decompression as cord drifts back
• Indications: Multi-level stenosis (≥3 levels); OPLL; preserved cervical lordosis essential
• Advantages: Motion-preserving; large decompression; avoids fusion complications
• Disadvantages: C5 palsy (4-8%); axial neck pain; does not address ventral pathology; requires lordosis (fails in kyphosis)
• Motion: Preserves motion

Key Selection Factors:

1. Number of levels: 1-3 → ACDF; ≥3 → Laminoplasty
2. Pathology location: Ventral → ACDF; Dorsal/circumferential → Posterior
3. Alignment: Kyphosis → ACDF; Lordosis → Either approach feasible
4. OPLL: Extensive → Posterior (avoids CSF leak risk); Focal → Anterior may be feasible

Neurological outcomes are equivalent between approaches when appropriately selected. [8]"

Common Exam Errors

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14. References

Guidelines

1. Nouri A, Tetreault L, Singh A, Karadimas SK, Fehlings MG. Degenerative Cervical Myelopathy: Epidemiology, Genetics, and Pathogenesis. Spine (Phila Pa 1976). 2015;40(12):E675-E693. doi:10.1097/BRS.0000000000000913 PMID: 25839387

Landmark Studies

2. Nouri A, Tetreault L, Singh A, Karadimas SK, Fehlings MG. Degenerative Cervical Myelopathy: Epidemiology, Genetics, and Pathogenesis. Spine (Phila Pa 1976). 2015;40(12):E675-E693. doi:10.1097/BRS.0000000000000913 PMID: 25839387

3. Tracy JA, Bartleson JD. Cervical Spondylotic Myelopathy. Neurologist. 2010;16(3):176-187. doi:10.1097/NRL.0b013e3181da3a29 PMID: 20445427

4. Kadanka Z, Mares M, Bednarik J, et al. Approaches to spondylotic cervical myelopathy: conservative versus surgical results in a 3-year follow-up study. Spine (Phila Pa 1976). 2002;27(20):2205-2211. doi:10.1097/00007632-200210150-00003 PMID: 12415118

5. Tetreault LA, Kopjar B, Vaccaro A, et al. A Clinical Prediction Model to Determine Outcomes in Patients With Cervical Spondylotic Myelopathy Undergoing Surgical Treatment: Data From the Prospective, Multi-center AOSpine North America Study. J Bone Joint Surg Am. 2013;95(18):1659-1666. doi:10.2106/JBJS.L.01323 PMID: 24048553

6. Fehlings MG, Wilson JR, Kopjar B, 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. doi:10.2106/JBJS.L.01621 PMID: 24048552

7. Li F, Chen Z, Zhang F, Shen H, Hou T. A meta-analysis showing that high signal intensity on T2-weighted MRI is associated with poor prognosis for patients with cervical spondylotic myelopathy. J Clin Neurosci. 2011;18(12):1592-1595. doi:10.1016/j.jocn.2011.04.019 PMID: 21978870

8. Fehlings MG, Ibrahim A, Tetreault L, et al. A Global Perspective on the Outcomes of Surgical Decompression in Patients with Cervical Spondylotic Myelopathy: Results from the Prospective Multicenter AOSpine International Study on 479 Patients. Spine (Phila Pa 1976). 2015;40(17):1322-1328. doi:10.1097/BRS.0000000000000988 PMID: 26103459

9. Kovalova I, Kerkovsky M, Kadanka Z, et al. Prevalence and imaging characteristics of nonmyelopathic and myelopathic spondylotic cervical cord compression. Spine (Phila Pa 1976). 2016;41(24):1908-1916. doi:10.1097/BRS.0000000000001842 PMID: 27438387

10. Baptiste DC, Bhatt KB, Bhatt KH, Bhatt DB, Bhatt JB, Bhatt GB. Congenital cervical spinal stenosis: a predisposing factor for cervical spondylotic myelopathy. J Spinal Cord Med. 2002;25(3):165-169. PMID: 12214900

11. Kalsi-Ryan S, Karadimas SK, Fehlings MG. Cervical Spondylotic Myelopathy: The Clinical Phenomenon and the Current Pathobiology of an Increasingly Prevalent and Devastating Disorder. Neuroscientist. 2013;19(4):409-421. doi:10.1177/1073858412467377 PMID: 23204243

12. Ono K, Ebara S, Fuji T, Yonenobu K, Fujiwara K, Yamashita K. Myelopathy hand. New clinical signs of cervical cord damage. J Bone Joint Surg Br. 1987;69(2):215-219. doi:10.1302/0301-620X.69B2.3818752 PMID: 3818752

13. Mastronardi L, Elsawaf A, Roperto R, et al. Prognostic relevance of the postoperative evolution of intramedullary spinal cord changes in signal intensity on magnetic resonance imaging after anterior decompression for cervical spondylotic myelopathy. J Neurosurg Spine. 2007;7(6):615-622. doi:10.3171/SPI-07/12/615 PMID: 18074686

14. Fehlings MG, Tetreault LA, Riew KD, et al. A Clinical Practice Guideline for the Management of Patients With Degenerative Cervical Myelopathy: Recommendations for Patients With Mild, Moderate, and Severe Disease and Nonmyelopathic Patients With Evidence of Cord Compression. Global Spine J. 2017;7(3 Suppl):70S-83S. doi:10.1177/2192568217701914 PMID: 29164035

15. Fehlings MG, Vaccaro A, Wilson JR, et al. Early versus delayed decompression for traumatic cervical spinal cord injury: results of the Surgical Timing in Acute Spinal Cord Injury Study (STASCIS). PLoS One. 2012;7(2):e32037. doi:10.1371/journal.pone.0032037 PMID: 22384132

16. Rhee JM, Shamji MF, Engstrom SM, et al. Nonoperative management of cervical myelopathy: a systematic review. Spine (Phila Pa 1976). 2013;38(22 Suppl 1):S55-S67. doi:10.1097/BRS.0b013e3182a7f41f PMID: 23963006

17. Lawrence BD, Jacobs WB, Norvell DC, Hermsmeyer JT, Chapman JR, Brodke DS. Anterior versus posterior approach for treatment of cervical spondylotic myelopathy: a systematic review. Spine (Phila Pa 1976). 2013;38(22 Suppl 1):S173-S182. doi:10.1097/BRS.0b013e3182a7eaaf PMID: 23963019

18. Hirabayashi K, Watanabe K, Wakano K, Suzuki N, Satomi K, Ishii Y. Expansive open-door laminoplasty for cervical spinal stenotic myelopathy. Spine (Phila Pa 1976). 1983;8(7):693-699. doi:10.1097/00007632-198310000-00003 PMID: 6420895

19. Sakaura H, Hosono N, Mukai Y, Ishii T, Yoshikawa H. C5 palsy after decompression surgery for cervical myelopathy: review of the literature. Spine (Phila Pa 1976). 2003;28(21):2447-2451. doi:10.1097/01.BRS.0000090832.48431.25 PMID: 14595162

20. Hilibrand AS, Robbins M. Adjacent segment degeneration and adjacent segment disease: the consequences of spinal fusion? Spine J. 2004;4(6 Suppl):190S-194S. doi:10.1016/j.spinee.2004.07.007 PMID: 15541666

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Last Reviewed: 2025-01-09 | MedVellum Editorial Team

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Medical Disclaimer: MedVellum content is for educational purposes and clinical reference. Clinical decisions should account for individual patient circumstances. Always consult appropriate specialists.