Cervical Myelopathy
Cervical myelopathy is a progressive spinal cord dysfunction caused by compression of the cervical spinal cord, typically due to degenerative spondylotic changes, resulting in upper motor neuron signs such as gait disturbance, hand clumsiness, and hyperreflexia.
Cervical myelopathy refers to the clinical syndrome resulting from compression of the cervical spinal cord within the cervical spinal canal [1][2]. The word itself breaks down nicely: "cervical" = pertaining to the neck, "myelo-" (Greek myelos) = spinal cord, "-pathy" (Greek pathos) = disease/suffering. So literally: a disease of the spinal cord at the neck level.
This is fundamentally different from cervical radiculopathy, which is compression of a nerve root (peripheral nerve issue → lower motor neuron signs), whereas myelopathy is compression of the spinal cord itself (central nervous system issue → upper motor neuron signs below the level, potentially lower motor neuron signs at the level).
Key Distinction
Myelopathy = spinal cord compression → UMN signs below, LMN signs at the level. Radiculopathy = nerve root compression → LMN signs in that root's distribution only. These can and frequently do coexist — this is called myeloradiculopathy.
- Most common cause of spinal cord dysfunction in adults over 55 years old worldwide [1].
- Cervical spondylotic myelopathy (CSM) is the most common cause — degenerative disease accounts for the overwhelming majority of cases [1][2].
- Bimodal distribution of spinal cord injury [3]:
- Young adults: high-energy trauma
- Old adults: low-energy trauma, osteoporotic bone, pre-existing spinal stenosis — even a simple fall in an elderly patient with a degenerative narrowed canal can cause acute-on-chronic myelopathy (classically central cord syndrome).
- Male predominance overall, particularly for OPLL and degenerative spondylosis.
- Geographic relevance (Hong Kong/Asia):
- Ossification of the posterior longitudinal ligament (OPLL) is much more common in Asian vs non-Asian populations (up to 2–4%) [3] — this is a distinctly important cause in our population.
- Rheumatoid arthritis with cervical spine involvement is also relevant, though RA medications have reduced its incidence [3].
- TB spine (Pott's disease) remains a consideration in Hong Kong given regional TB prevalence.
Anatomy and Function
Understanding cervical myelopathy requires solid knowledge of the cervical spinal anatomy, because the clinical features are entirely dictated by what gets compressed and where.
- 7 cervical vertebrae, but 8 cervical nerve roots (C1–C8).
- C8 exits between C7 and T1 (there is no C8 vertebra) [2].
- Above C8: nerve roots exit above their corresponding vertebra (e.g., C4 root exits between C3/C4) [2].
- Below C8: nerve roots exit below their corresponding vertebra (e.g., L4 exits between L4/L5) [2].
This numbering system matters clinically: a C5/6 disc prolapse will compress the C6 nerve root (exits above C7 but below C6).
The cervical spinal cord sits within the spinal canal, surrounded by:
-
Anterior structures (front):
-
Posterior structures (back):
-
Lateral structures:
- Pedicles
- Facet (apophyseal/zygapophyseal) joints
- Neural foramina — where nerve roots exit
This is critical for understanding the clinical signs:
| Tract | Location in Cord | Function | What Happens When Compressed |
|---|---|---|---|
| Corticospinal tract (lateral) | Lateral columns | Voluntary motor (UMN) | Weakness, spasticity, hyperreflexia, upgoing plantars |
| Spinothalamic tract | Anterolateral columns | Pain and temperature | Loss of pain/temperature sensation |
| Dorsal columns | Posterior columns | Proprioception, vibration, fine touch | Loss of proprioception → sensory ataxia, positive Romberg |
| Anterior horn cells | Central grey matter | LMN to muscles at that level | LMN signs at the level of compression (atrophy, fasciculations, hyporeflexia) |
The somatotopic arrangement of the corticospinal and spinothalamic tracts is key:
- In the lateral corticospinal tract: cervical fibres are medial (central), sacral fibres are lateral (peripheral).
- This is why central cord syndrome (compression from within outward) preferentially affects the upper limbs (cervical fibres are central) while relatively sparing the lower limbs (sacral fibres are peripheral) [3].
- Anterior spinal artery (single) — supplies the anterior 2/3 of the cord (corticospinal tracts, spinothalamic tracts, anterior horn cells).
- Posterior spinal arteries (paired) — supply the posterior 1/3 (dorsal columns).
- Compression can compromise these vessels, adding an ischaemic component to the mechanical compression — this is part of why myelopathy can be progressive and irreversible.
- Pavlov ratio > 0.8 is normal (ratio of spinal canal AP diameter to vertebral body AP diameter) [2]. A ratio < 0.8 indicates congenital spinal stenosis — these patients have less "reserve space" and are more vulnerable to developing myelopathy from even mild degenerative changes.
- Normal cervical canal AP diameter: ~17 mm. Myelopathy typically develops when the canal narrows to < 13 mm.
Soft Tissue Rules (C-spine X-ray)
3×7=21 rule: C1 ≤ 10 mm, C3 ≤ 7 mm, C7 ≤ 21 mm [2]. Increased prevertebral soft tissue suggests haematoma, abscess, or retropharyngeal pathology — red flags on a lateral C-spine film.
Etiology (Focus on Hong Kong)
The causes of cervical myelopathy can be broadly divided into compressive (structural) and non-compressive causes [4]. For clinical purposes and exams, the compressive causes dominate.
Compressive Causes (by location) [4]
By location:
- Extradural
- Intradural extramedullary
- Intradural intramedullary
Cervical spondylosis is the most common (MC) cause [2].
Degenerative changes include:
- Spondylosis (wear-and-tear degeneration of the vertebral column)
- Disc degeneration/prolapse — herniated disc material directly compresses the cord anteriorly [4]
- Osteophytes — bony spurs from degenerative vertebral endplates [4]
- Apophyseal (facet) joint hypertrophy — narrows the canal and foramina [4]
- Hypertrophy/buckling of the ligamentum flavum — compresses the cord posteriorly, especially in extension [1][2]
- Instability [4]
- Spinal canal stenosis [4]
- Degenerative spondylolisthesis — forward slip of one vertebra on another [2]
Pathophysiology of cervical spondylotic myelopathy (CSM):
The degenerative cascade works like this:
- Disc desiccation and loss of height → abnormal loading on vertebral endplates
- Osteophyte formation (body's attempt to stabilise) → anterior cord compression
- Facet joint hypertrophy → lateral and posterolateral narrowing
- Ligamentum flavum buckling/hypertrophy → posterior cord compression
- Segmental instability → dynamic compression (worse with movement, especially extension)
The result is circumferential narrowing of the spinal canal → direct mechanical compression of the cord + ischaemia from vascular compromise → demyelination, neuronal loss, and gliosis.
Myelopathy = central compression; Radiculopathy = lateral compression [4].
Can present as chronic progressive OR acute exacerbation [4] — the classic scenario is an elderly patient with long-standing mild symptoms who deteriorates acutely after a minor fall (acute-on-chronic myelopathy → often central cord syndrome).
- Ectopic calcification as a cause of cord compression [3]
- Much more common in Asian vs non-Asian populations (up to 2–4%) [3]
- Male predominance, affects younger population [3]
- More commonly affects cervical than thoracic spine [3]
Pathophysiology: The PLL, which normally lies just posterior to the vertebral bodies, undergoes heterotopic ossification (the ligament turns to bone). This creates a rigid bony bar that compresses the cord from the front. It is often multi-segmental.
Why is it relevant in Hong Kong? OPLL has a strong genetic predisposition in East Asian populations. It should always be in the differential for a younger Asian male presenting with cervical myelopathy.
- High prevalence of cervical spine involvement in RA [3]
- Formation of retroodontoid pannus — synovial inflammatory tissue behind the dens [3]
- Synovial inflammation predisposes to cervical instability [3]:
- Atlantoaxial subluxation (C1/2) — most common pattern; the transverse ligament is destroyed by pannus, allowing C1 to slide forward on C2
- Subaxial subluxation — "staircase" pattern of multiple levels subluxing
- Vertical subluxation (basilar invagination) — the dens migrates superiorly through the foramen magnum
- Use of RA medications reduces the incidence of cervical involvement [3] — good disease control with DMARDs/biologics prevents ligamentous destruction.
- Atlantodental interval (ADI): abnormal (atlantoaxial subluxation) if ADI ≥ 3 mm (adult) or ≥ 5 mm (children) [2].
- Causes of atlantoaxial subluxation: trauma, Down syndrome (absent transverse ligament), RA (inflammation/rupture of transverse ligament) [2].
- Patients born with a constitutionally narrow canal (Pavlov ratio < 0.8).
- They have less "reserve space" and are more vulnerable to myelopathy from even minor degenerative changes or minor trauma.
- Direct fracture-dislocation → bony fragment or haematoma compressing the cord.
- Central cord syndrome: hyperextension injury in a degenerative cervical spine [3] — the most classic acute traumatic myelopathy in the elderly.
- Primary or secondary (metastatic) tumours [4]
- Extradural metastases (most common spinal tumours) — from lung, breast, prostate, kidney, thyroid (mnemonic: Pb-KTL — Lead Kills The Lungs/Liver, or the "paired organs" mnemonic).
- Intradural extramedullary: meningioma, schwannoma/neurofibroma.
- Intradural intramedullary: ependymoma, astrocytoma.
- Abscess / TB spine [4]
- Epidural abscess — bacterial (Staph aureus most common) or tuberculous.
- Pott's disease (TB spondylitis) — relevant in Hong Kong. Typically involves anterior vertebral body → collapse → kyphotic deformity → cord compression.
- Arachnoid cyst
- Syringomyelia — fluid-filled cavity within the cord itself (technically intramedullary).
- Arteriovenous malformation (AVM)
- Transverse myelitis — inflammatory; diagnosis by exclusion; LP shows high CSF protein [4]
- Arterial occlusion — thromboembolic occlusion of spinal arteries and segmental supply; iatrogenic (e.g., aortic surgery) [4]
- Spinal arteriovenous fistula — spinal cord oedema and haemorrhage [4]
- Multiple sclerosis (demyelination)
- Neuromyelitis optica spectrum disorder (NMOSD) — aquaporin-4 antibody-mediated
- Subacute combined degeneration (B12 deficiency)
Hong Kong High-Yield Causes
For HKU exams, the top causes to remember for cervical myelopathy are: 1. Cervical spondylosis (MC overall) 2. OPLL (especially in Asian populations — up to 2–4%) 3. RA (atlantoaxial subluxation) 4. Trauma (central cord syndrome in elderly with pre-existing stenosis) 5. Infection (TB spine still relevant in HK)
Pathophysiology (Detailed)
The pathophysiology of cervical myelopathy involves a combination of static mechanical compression, dynamic mechanical compression, and secondary ischaemia.
Fixed structural narrowing of the spinal canal by:
- Osteophytes (anterior)
- Disc herniation (anterior/anterolateral)
- OPLL (anterior)
- Hypertrophied/ossified ligamentum flavum (posterior)
- Facet joint hypertrophy (posterolateral)
This directly compresses the spinal cord, damaging axons and myelin sheaths.
Dynamic compression: osteophytes + buckled LF during extension [2].
During neck extension, the ligamentum flavum buckles inward and the spinal canal shortens — this further narrows the canal. Conversely, neck flexion opens up the canal. This is why patients often adopt a slightly flexed posture and why extension is dangerous in cervical myelopathy.
During neck flexion, the cord is draped over anterior osteophytes like a towel over a clothesline, increasing tension on the cord.
Compression of the spinal cord also compromises its blood supply:
- Compression of the anterior spinal artery → ischaemia to the anterior 2/3 of the cord (motor tracts, spinothalamic tracts).
- Compression of intramedullary vessels → microvascular ischaemia.
- This ischaemic component explains why recovery after decompression may be incomplete — there is already irreversible neuronal loss.
The combination of mechanical and vascular injury leads to:
- Demyelination of lateral and posterior columns
- Wallerian degeneration of ascending and descending tracts
- Neuronal loss in grey matter (especially anterior horn cells at the level of compression)
- Gliosis (scarring) — this is seen as intramedullary signal change on MRI (T2 hyperintensity = myelomalacia/gliosis; T1 hypointensity = more advanced, worse prognosis).
MRI interpretation: intramedullary signal change (myelomalacia) [1] — this is a marker of irreversible damage and a poor prognostic sign.
Classification
The JOA score is the most widely used classification for severity assessment of cervical myelopathy.
- Assesses: upper limb motor function, lower limb motor function, sensory function, and bladder function.
- Maximum score = 17 (normal).
- Lower score = more severe myelopathy.
- Used to calculate recovery rate after surgery:
- Recovery rate (%) = (Post-op JOA − Pre-op JOA) / (17 − Pre-op JOA) × 100
- More commonly used in Western literature.
- Maximum score = 18.
- Classification:
- Mild myelopathy: mJOA 15–17
- Moderate myelopathy: mJOA 12–14
- Severe myelopathy: mJOA < 12
Focuses on gait:
- Grade 0: Root signs only, no cord involvement
- Grade 1: Signs of cord involvement, normal gait
- Grade 2: Gait difficulty, but employed and mobile
- Grade 3: Gait difficulty, needs assistance, unable to work
- Grade 4: Only walks with aid
- Grade 5: Wheelchair-bound or bedridden
A new index of neurological level diagnosis:
| Feature | C3–C4 | C4–C5 | C5–C6 | C6–C7 |
|---|---|---|---|---|
| Reflex | BTR ↑ | BTR ↑ or → | BTR → or ↓ | BTR → |
| TTR ↑ | TTR ↑ | TTR ↑ or → | TTR → | |
| FF ↑ | FF ↑ | FF ↑ | FF ↑ | |
| Uppermost muscle with weakness | Deltoid | Biceps | Triceps or EDC | APB or ADM |
| Sensory disturbance | C4 dermatome | C5 dermatome | C6 dermatome | C7 dermatome |
(BTR = biceps tendon reflex; TTR = triceps tendon reflex; FF = finger flexor reflex; EDC = extensor digitorum communis; APB = abductor pollicis brevis; ADM = abductor digiti minimi) [1]
This table is extraordinarily useful for localizing the level of compression based on the clinical examination. The key principle:
- Reflexes are increased (UMN) below the level and decreased or inverted at the level.
- The uppermost weak muscle tells you the level of compression (because LMN damage occurs at that segment).
Clinical Features
Clinical features of cervical myelopathy [1]:
- Numbness or sensory disturbance (fingers, upper limb)
- Loss of hand dexterity
- Poor proprioception + spastic gait
- Motor weakness and sphincteric dysfunction appear in the late stage
- Pain is not a predominant feature
- Upper motor neuron signs below level of compression
- Lower motor neuron signs at the level of compression
Pain Is NOT the Main Feature!
A common mistake is assuming cervical myelopathy presents primarily with pain. Pain is not a predominant feature [1]. The cardinal features are numbness, clumsiness, gait instability, and UMN signs. Pain is more typical of radiculopathy. If a patient has predominantly painless progressive dysfunction of the hands and gait — think myelopathy.
Symptoms
| Symptom | Pathophysiological Basis |
|---|---|
| Numbness/sensory disturbance in fingers and upper limbs [1] | Compression of the dorsal columns (proprioception, fine touch, vibration) and/or spinothalamic tracts (pain, temperature) at the cervical level. The hands are often affected first because the cervical cord segments innervating the hands (C6–T1) are the ones being compressed. |
| Loss of hand dexterity [1] | LMN damage to anterior horn cells at the level of compression (C7–T1 innervate intrinsic hand muscles) + UMN damage to the corticospinal tract above these segments → loss of fine motor control. Patients report dropping objects, difficulty with buttons, chopsticks (particularly relevant in Hong Kong!), and handwriting deterioration. |
| Upper limb weakness | Combination of LMN weakness at the level (lower motor neuron damage to anterior horn cells) and UMN weakness below the level (corticospinal tract damage). |
| Pseudoathetosis (involuntary writhing movements of fingers) | Loss of proprioception from dorsal column compression → the brain doesn't know where the fingers are → involuntary slow movements when the eyes are closed [2]. |
| Symptom | Pathophysiological Basis |
|---|---|
| Spastic gait / gait instability [1] | UMN damage to the lateral corticospinal tracts → spasticity and weakness in the lower limbs. The legs are controlled by spinal segments below the cervical cord, so any cervical cord compression will affect them via UMN pathways. |
| Poor proprioception [1] | Dorsal column compression → impaired joint position sense → sensory ataxia → unsteady gait, especially in the dark or with eyes closed. |
| Difficulty with tandem (heel-to-toe) walking [2] | Combined posterior column (proprioceptive) and lateral column (corticospinal/spasticity) dysfunction makes balance tasks extremely difficult. |
| Lower limb numbness | Spinothalamic and/or dorsal column involvement. |
| Symptom | Pathophysiological Basis |
|---|---|
| Neck pain and stiffness [2] | From the underlying degenerative spondylosis (facet joint arthritis, disc degeneration) rather than the cord compression itself. Remember: pain is not a predominant feature of myelopathy itself — it comes from the degenerative process. |
| Lhermitte's sign (electric shock sensation radiating down the spine/limbs on neck flexion) [2] | Neck flexion stretches the already-compressed and demyelinated dorsal columns over anterior osteophytes → mechanosensitivity of damaged axons → electrical discharge sensation. Named after Jean Lhermitte (French neurologist). |
| Reversed Lhermitte's sign (same sensation on neck extension) [2] | Extension causes ligamentum flavum to buckle into the cord posteriorly → compression of dorsal columns. |
| Symptom | Pathophysiological Basis |
|---|---|
| Sphincteric dysfunction (urinary retention/incontinence) [1] | Appears in the late stage [1]. The descending pathways controlling the sacral micturition centre (S2–S4) are interrupted by cervical cord compression. Initially presents as urgency/frequency (loss of inhibitory control → detrusor hyperreflexia), later as retention (loss of coordinated voiding). |
| Bowel dysfunction | Similar mechanism — loss of descending control over sacral defecation centre. |
| Sexual dysfunction | Disruption of sacral autonomic pathways. |
Signs
| Sign | How to Elicit | What It Means |
|---|---|---|
| Loss of cervical lordosis [2] | Inspection on lateral view | Muscle spasm from degenerative disease straightens the normal cervical curve. |
| Lhermitte's sign [2] | Passive neck flexion | Electric shock down spine/limbs — dorsal column irritation (see above). |
| Reduced range of motion | Active/passive neck movement | Degenerative changes + pain limit movement. |
These are the hallmark examination findings for cervical myelopathy. They all reflect UMN dysfunction affecting the hands.
| Sign | How to Elicit | Pathophysiology |
|---|---|---|
| Hoffmann's sign [1] | Flick the distal phalanx of the middle finger downward; positive if thumb and index finger flex reflexly. | Analogous to a Babinski sign for the upper limb. Release of primitive flexor reflex due to loss of corticospinal tract inhibition → UMN sign. |
| Finger escape sign [1] | Ask patient to hold all fingers extended and adducted; positive if the little finger (and then ring finger) drifts into abduction and flexion. | The ulnar-innervated intrinsic muscles (controlled by C8/T1 segments) are the earliest to lose corticospinal input → the little finger "escapes" because it can no longer maintain its position against intrinsic muscle tone imbalance. |
| 10-second grip-and-release test [1] | Ask patient to rapidly open and close fists for 10 seconds; count the number of cycles. Normal: ≥ 20 cycles. Abnormal: < 20 cycles. | Impaired fine motor control from corticospinal tract dysfunction → slowed rapid alternating movements. |
| Inverted supinator (brachioradialis) reflex [2] | Tap the brachioradialis tendon at the distal radius. Instead of elbow flexion (normal), you get finger flexion. | LMN damage at C5/C6 (brachioradialis segment) abolishes the normal reflex arc, but UMN damage below releases the C8/T1 finger flexor reflex → the reflex is "inverted" — you tap C6 but get a C8 response. This is pathognomonic of cervical myelopathy at C5/C6. |
| Inverted biceps reflex [2] | Tap biceps tendon. Instead of biceps contraction, you get triceps contraction (elbow extension) or finger flexion. | Same principle: LMN damage at C5/C6 (biceps level) + UMN release of C7 (triceps) or C8 (finger flexors) reflexes below. |
| Grip and release test [2] | Patient repeatedly grips and releases — observe speed and clumsiness. | Corticospinal tract dysfunction → impaired rapid alternating hand movements. |
Inverted Reflexes — The Key Concept
An "inverted reflex" is the single most localising sign in cervical myelopathy. It tells you:
- LMN damage AT the level (the normal reflex is lost)
- UMN damage BELOW the level (a reflex from a lower segment is released)
Example: Inverted supinator reflex = LMN lesion at C5/C6 + UMN lesion below C6. This localises compression to the C5/C6 level precisely.
| Sign | How to Elicit | Pathophysiology |
|---|---|---|
| Lower limb spasticity [1] | Increased tone on passive movement (clasp-knife pattern) | Loss of corticospinal tract inhibition → increased gamma motor neuron activity → hypertonicity. |
| Hyperreflexia [2] | Exaggerated knee and ankle jerks | UMN lesion releases segmental reflex arcs from supraspinal inhibition. |
| Clonus [2] | Sustained rhythmic involuntary contractions on dorsiflexion of ankle | Same mechanism as hyperreflexia — sustained stretch reflex release. |
| Upgoing plantar reflex (Babinski sign) [2] | Stroke the lateral sole of the foot | Pathological release of the flexion withdrawal reflex due to corticospinal tract damage. The normal adult plantar response (toe flexion) requires an intact corticospinal tract to suppress the primitive extension pattern. |
| Positive Romberg sign [1] | Patient stands with feet together, eyes closed; positive if patient sways/falls | Dorsal column dysfunction → loss of proprioception. Patient can compensate with vision (eyes open OK), but removing visual input (eyes closed) unmasks the proprioceptive deficit. |
| Failed tandem walking test [1] | Heel-to-toe walking | Requires intact proprioception + corticospinal tract function. Both are impaired in myelopathy → patient cannot maintain balance on a narrow base. |
| Lower limb upper motor neuron features [1] | General category | All of the above signs represent UMN involvement below the level of cervical cord compression. |
| Sign | Pathophysiology |
|---|---|
| Dermatomal sensory loss at the level of compression | Direct damage to the spinothalamic tract or dorsal column fibres entering at that segment |
| Sensory level (if severe) | Complete interruption of ascending sensory tracts → loss of sensation below the level. T4 = nipple, T10 = umbilicus [2]. However, in cervical myelopathy a clear-cut sensory level is less common than in thoracic cord compression. |
| Loss of proprioception and vibration (dorsal columns) | Compression of posterior columns → impaired joint position sense, impaired vibration sense in hands and feet |
| Dissociated sensory loss (in central cord syndrome) | Central cord lesion preferentially damages crossing spinothalamic fibres → "cape-like" loss of pain/temperature with preserved dorsal column function |
Most common incomplete spinal cord injury [3].
- Hyperextension injury in a degenerative cervical spine [3]
- Pinching of cord between anterior osteophytes and posterior ligamentum flavum [3]
- Affects central grey matter and medial portions of the corticospinal and spinothalamic tracts
- Clinical pattern:
- Upper limbs affected more than lower limbs (because cervical motor fibres are located centrally in the corticospinal tract, while sacral/lumbar fibres are peripheral)
- Variable sensory loss (often dissociated — loss of pain/temperature in a cape distribution due to crossing spinothalamic fibres being damaged centrally)
- Bladder dysfunction common
- Classic scenario: Old man with degenerated spine after a fall [4]
| Level | Motor (LMN at level) | Reflex Change | Sensory |
|---|---|---|---|
| C3/4 | Deltoid weakness | BTR ↑, TTR ↑, FF ↑ | C4 dermatome (shoulder) |
| C4/5 | Biceps weakness | BTR ↑ or →, TTR ↑ | C5 dermatome (lateral arm) |
| C5/6 | Triceps or EDC weakness | BTR → or ↓ (inverted), TTR ↑ or → | C6 dermatome (thumb, index finger) |
| C6/7 | APB or ADM weakness | BTR →, TTR → | C7 dermatome (middle finger) |
(Adapted from Seichi et al. 2006) [1]
High Yield Summary
Definition: Cervical myelopathy = compression of the cervical spinal cord → UMN signs below the level, LMN signs at the level.
Epidemiology: Most common cause of spinal cord dysfunction in adults > 55. Bimodal age distribution for traumatic causes. OPLL prevalence 2–4% in Asian populations.
Top Causes (HK-focused):
- Cervical spondylosis (MC)
- OPLL (Asian predominance)
- RA (atlantoaxial subluxation)
- Trauma (central cord syndrome in elderly)
- TB spine / epidural abscess
Pathophysiology: Static + dynamic mechanical compression + ischaemia → demyelination, neuronal loss, gliosis.
Cardinal Clinical Features:
- Numbness and loss of hand dexterity (NOT primarily pain!)
- Spastic gait with poor proprioception
- Myelopathic hand signs: Hoffmann's, finger escape, 10-second test, inverted reflexes
- LL: spasticity, hyperreflexia, clonus, upgoing plantars, positive Romberg
- Sphincteric dysfunction is LATE
Key Exam Concepts:
- Inverted reflexes = LMN at the level + UMN below = pathognomonic
- Central cord syndrome = hyperextension + degenerative spine → UL > LL weakness
- Pavlov ratio < 0.8 = congenital stenosis
- ADI ≥ 3 mm (adult) = atlantoaxial subluxation
- MRI intramedullary signal change = myelomalacia = poor prognosis
Active Recall - Cervical Myelopathy (Definition, Epidemiology, Anatomy, Etiology, Pathophysiology, Clinical Features)
[1] Lecture slides: GC 227. Cervical Spine Pathology.pdf (pp. 17, 18, 25, 29, 32, 33, 37, 55, 80) [2] Senior notes: maxim.md (sections 2.2–2.5, 5.6) [3] Lecture slides: GC 110. Paraplegia Spinal cord compression Transverse myelitis Spinal dysraphism Neuroimaging III Spinal Cord.pdf (pp. 12, 21) [4] Lecture slides: GC 110. Paraplegia Spinal cord compression Transverse myelitis Spinal dysraphism Neuroimaging III Spinal Cord.pdf (pp. 12, 21 — causes of myelopathy and non-compressive causes)
Differential Diagnosis of Cervical Myelopathy
When a patient presents with progressive upper and lower limb dysfunction, gait disturbance, and UMN signs, the immediate question is: is this truly cervical myelopathy, or is something else mimicking it? The differential is broad because many conditions can produce a combination of limb weakness, numbness, and spasticity. The key is to use the history, pattern of signs, tempo of onset, and imaging to distinguish them.
The approach to the differential diagnosis works on two levels:
- What is causing the myelopathy? (i.e., the underlying aetiology of the cord compression — covered extensively in the Etiology section)
- What else can mimic cervical myelopathy? (i.e., conditions that produce similar clinical features but are NOT cervical cord compression)
This section focuses on Level 2 — the mimics and look-alikes — while also recapping the aetiological differentials within myelopathy itself.
Why do we need a differential? Because cervical myelopathy presents with:
- Upper limb numbness/weakness/clumsiness
- Lower limb spasticity and gait disturbance
- UMN signs
These features can be produced by any lesion along the motor and sensory pathways — from the brain (cortex, internal capsule), through the brainstem, to the spinal cord, and even peripheral nerves (when multiple are affected). The job is to localise the lesion first, then determine the cause.
A. Conditions That Mimic Cervical Myelopathy (Non-Spinal Cord Causes)
| Condition | Why It Can Mimic | Key Distinguishing Features |
|---|---|---|
| Brain tumour | A parasagittal meningioma or falx tumour can compress both motor cortices → bilateral leg weakness + UMN signs, resembling myelopathy | Seizures, headache, papilloedema, cognitive changes; no myelopathic hand signs; MRI brain diagnostic |
| Normal pressure hydrocephalus (NPH) | Classic triad: gait apraxia, urinary incontinence, dementia — the gait disturbance and incontinence overlap with myelopathy | Gait is "magnetic" (feet stuck to floor), not spastic; dementia present; no UL myelopathic signs; CT/MRI shows ventriculomegaly out of proportion to sulcal atrophy |
| Stroke / vascular lesion [5] | Internal capsule lacunar infarct can cause pure motor hemiparesis; bilateral strokes can mimic bilateral UMN signs | Acute onset; usually unilateral; face involved (corticobulbar fibres); MRI brain with diffusion restriction |
| Subdural haematoma [5] | Can cause progressive hemiparesis or bilateral weakness in the elderly | History of trauma (even minor); fluctuating consciousness; CT brain diagnostic |
| Multiple sclerosis (MS) | Demyelinating plaques in the cervical cord are very common in MS and produce myelopathy | Relapsing-remitting history; optic neuritis; Lhermitte's sign (also present in CSM!); MRI shows characteristic periventricular and cord lesions; oligoclonal bands in CSF |
This is the single most important condition to differentiate from cervical myelopathy, and they frequently coexist (myeloradiculopathy) [1].
Clinical features of cervical radiculopathy [1]:
- Unilateral arm pain or sensory disturbance
- May have associated weakness
- Dermatomal distribution
- Neck pain
Signs of cervical radiculopathy [1]:
- Spurling's test (positive = axial compression + ipsilateral rotation reproduces radicular pain)
- Shoulder abduction test (positive = abducting shoulder relieves radicular pain by reducing tension on the nerve root)
- Myotomal weakness
- Reduced upper limb reflexes (LMN pattern — hyporeflexia, NOT hyperreflexia)
| Feature | Cervical Myelopathy | Cervical Radiculopathy |
|---|---|---|
| Pain | Not a predominant feature [1] | Prominent — unilateral radicular arm pain |
| Distribution | Bilateral, diffuse | Unilateral, dermatomal |
| Motor signs | UMN (spasticity, hyperreflexia) below the level + LMN at level | LMN only (weakness, hyporeflexia) in one myotome |
| Sensory signs | Bilateral, multi-segmental; dorsal column signs | Unilateral, single dermatome |
| Hand signs | Myelopathic: Hoffmann's, finger escape, 10-sec test | Absent |
| Gait | Spastic gait, positive Romberg | Normal gait |
| Sphincter | May be affected (late) | Not affected |
| Spurling's test | Typically negative | Typically positive |
Radiculopathy level-by-level clinical features [1]:
| Level | Muscle Weakness | Sensory Deficits / Location of Pain | Reflex |
|---|---|---|---|
| C5 | Deltoid | Lateral arm | Biceps |
| C6 | Biceps, wrist extension | Radial forearm, radial two digits | Brachioradialis |
| C7 | Triceps, wrist flexion | Middle finger | Triceps |
| C8 | Finger flexors | Ulnar two digits | — |
| T1 | Hand intrinsics | Ulnar forearm, medial to the shoulder blade | — |
Myelopathy vs Radiculopathy — The Core Distinction
Students commonly confuse these. The easiest way to remember: Radiculopathy = PERIPHERAL nerve root = LMN = pain + weakness + hyporeflexia in ONE root distribution. Myelopathy = CENTRAL spinal cord = UMN = spasticity + hyperreflexia + bilateral + gait disturbance + myelopathic hand signs. If both coexist, you have myeloradiculopathy [1].
Differential diagnosis of cervical radiculopathy includes: cervical myelopathy (symptoms may overlap and patients can have myeloradiculopathy), peripheral nerve compression, and shoulder pathology [1].
| Condition | Why It Can Mimic | Key Distinguishing Features |
|---|---|---|
| Carpal tunnel syndrome (CTS) [2] | Numbness in the hand (median nerve distribution); weakness of thenar muscles. Can be confused with C6/C7 radiculopathy or early myelopathy | Distribution is median nerve (lateral 3½ digits), NOT dermatomal; Tinel's/Phalen's test positive; no UMN signs; NCS diagnostic. DDx includes cervical spondylosis (C6/7) [2] |
| Cubital tunnel syndrome [2] | Ulnar nerve palsy → hand clumsiness, intrinsic wasting — mimics C8/T1 myelopathy or radiculopathy | Distribution is ulnar nerve (medial 1½ digits); DDx: cervical myelopathy, T1 radiculopathy [2]; Tinel's at elbow; NCS diagnostic |
| Thoracic outlet syndrome (TOS) [2] | Lower brachial plexus injury → paraesthesia/weakness in ulnar distribution; can mimic C8/T1 radiculopathy | Provocative tests (Adson's, Roo's); vascular symptoms may be present; causes include cervical rib, previous fracture, Pancoast tumour [2] |
The concept of double crush syndrome [2] is important here: peripheral entrapment syndromes are often associated with cervical/lumbar spondylosis — a proximal compression renders the nerve more susceptible to a distal second compression. So a patient can have BOTH cervical spondylotic myelopathy AND carpal tunnel syndrome simultaneously.
- Rotator cuff tears, frozen shoulder, and impingement can cause arm pain and weakness.
- Key distinction: pain is localised to the shoulder; no neurological deficit (no numbness, no reflex changes, no myelopathic signs); shoulder examination findings (empty can test, painful arc, reduced passive ROM in frozen shoulder).
| Why It Can Mimic | Key Distinguishing Features |
|---|---|
| Amyotrophic lateral sclerosis produces both UMN and LMN signs — weakness, wasting, fasciculations, hyperreflexia, spasticity — very similar to cervical myelopathy | No sensory involvement in MND (pure motor); widespread fasciculations across multiple myotomes (not just cervical); bulbar signs (dysarthria, dysphagia, tongue fasciculations); MRI cervical spine is normal (no cord compression); EMG shows widespread denervation |
MND vs Cervical Myelopathy — A Critical Distinction
Both produce mixed UMN and LMN signs. The key differentiator: MND has NO sensory loss — it is a pure motor disease. Cervical myelopathy almost always has sensory features (numbness, proprioceptive loss, Lhermitte's sign). Also, MND has normal imaging of the cord.
- Demyelination of dorsal columns (proprioceptive loss, sensory ataxia) + lateral corticospinal tracts (UMN weakness, spasticity) — mimics posterior and lateral column disease seen in cervical myelopathy.
- Key distinction: peripheral neuropathy also present (absent ankle jerks despite upgoing plantars); macrocytic anaemia; low serum B12; MRI may show dorsal column T2 signal but no structural compression.
These are not "differentials" per se but rather patterns within myelopathy that help localise the pathology:
| Syndrome | Signs | Representative Conditions |
|---|---|---|
| Complete cord lesion | All function lost 1–2 levels below | Transverse myelitis, MS, traumatic injury |
| Brown-Séquard | Ipsilateral motor and vibration loss; contralateral pain/temperature loss | Traumatic injury, epidural tumour, varicella zoster, MS |
| Central cord (small) | Suspended sensory loss | Contusion, tumour, syrinx |
| Central cord (large) | Dissociated sensory loss involving lateral spinothalamic tract, sparing dorsal column; anterior horn cell at level of lesion; UMN signs below level of lesion | Syringomyelia, tumour, neuromyelitis optica |
| Posterior column | Proprioception and vibration loss; DTRs may be normal | Ischaemic stroke, syphilis, MS, B12 and copper deficiency |
| Anterior horn | Sensation normal, fasciculations, LMN weakness | Poliomyelitis, West Nile virus |
| Anterior spinal artery | Weakness; dissociated sensory loss, sparing dorsal columns | Ischaemic stroke |
| Spinothalamic | Symmetric, longitudinally extensive, isolated pain and temperature loss | Paraneoplastic syndrome |
| Root + cord | One or more roots plus cord | Spondylosis, sarcoidosis, Lyme disease |
| Myeloneuropathy | Myelopathy plus polyneuropathy | B12 deficiency, vitamin E deficiency, sarcoidosis, genetic syndromes |
- Most common incomplete spinal cord injury
- Hyperextension injury in a degenerative cervical spine
- Segmental loss: decussating secondary sensory neurons affected → upper limb pain/numbness; anterior horn cells involved [4]
- Long tract sign: medial motor fibres more affected; sacral sparing [4]
Anterior cord syndrome [4]: Paraplegia + spinothalamic loss + intact posterior column
Posterior cord syndrome [4]: Pain and paraesthesia in upper limb and trunk; mild UE paraparesis
When you've confirmed the patient has myelopathy, you then need to determine the cause. This was covered in the Etiology section, but here is the structured differential by category:
Compressive causes (space-occupying conditions) [3]:
- Neoplastic: Primary / Secondary
- Traumatic: Bone fragment / Haematoma
- Degenerative: Prolapsed intervertebral disc, Osteophyte
- Infective: Abscess / TB spine
- Cystic: Arachnoid cyst, Syringomyelia
- Vascular: AVM
By location [3]:
- Extradural (most common): disc, osteophyte, metastasis, abscess, haematoma
- Intradural extramedullary: schwannoma, meningioma, neurofibroma [2]
- Intradural intramedullary: ependymoma, astrocytoma, syringomyelia [2]
Non-compressive causes [3]:
- Transverse myelitis (Dx by exclusion; LP — high CSF protein)
- Arterial occlusion (thromboembolic occlusion of spinal arteries; iatrogenic e.g. aortic surgery)
- Spinal arteriovenous fistula (spinal cord oedema, haemorrhage)
Additional non-compressive causes:
- Multiple sclerosis
- Neuromyelitis optica spectrum disorder (NMOSD)
- Subacute combined degeneration (B12 deficiency)
- Radiation myelopathy
- Copper deficiency myelopathy
- HIV-associated vacuolar myelopathy
- Paraneoplastic myelopathy
Key degenerative aetiologies [3][4]:
- Spondylosis, disc degeneration/prolapse, apophyseal joint hypertrophy, instability, spinal canal stenosis
- Myelopathy = central compression; Radiculopathy = lateral compression
- Chronic progressive / Acute exacerbation
Special aetiologies:
- OPLL: ectopic calcification; much more common in Asian vs non-Asian populations (up to 2–4%); male predominance; younger population; more commonly cervical than thoracic [1]
- RA: high prevalence of cervical involvement; retroodontoid pannus; atlantoaxial subluxation (C1/2), subaxial subluxation, vertical subluxation (basilar invagination); RA medications reduce incidence [1]
| Clue | Favours | Reasoning |
|---|---|---|
| Bilateral UMN signs + myelopathic hand signs + gait disturbance | Cervical myelopathy | Cord compression → UMN below, LMN at level |
| Unilateral radicular pain, dermatomal, + Spurling's positive | Cervical radiculopathy | Nerve root compression → single root LMN pattern |
| Purely motor, no sensory loss, widespread fasciculations | Motor neuron disease | Pure motor pathway degeneration; sensory pathways spared |
| Relapsing-remitting; optic neuritis; young female | Multiple sclerosis | CNS demyelination in time and space |
| Sudden onset after fall in elderly with pre-existing stenosis; UL > LL | Central cord syndrome | Hyperextension → central cord pinched → medial corticospinal fibres (UL) affected first |
| Absent ankle jerks + upgoing plantars + macrocytosis | B12 deficiency | Combined LMN (peripheral neuropathy) + UMN (cord) — "subacute combined degeneration" |
| Pain/temperature loss with preserved proprioception; sudden onset | Anterior spinal artery syndrome | Anterior 2/3 cord ischaemia; dorsal columns supplied by posterior spinal arteries → spared |
| Ipsilateral motor/proprioception loss + contralateral pain/temp loss | Brown-Séquard syndrome | Hemisection of cord → ipsilateral corticospinal and dorsal column; contralateral spinothalamic |
| Old man with degenerated spine after a fall [3] | Central cord syndrome [3] | Pre-existing stenosis + hyperextension = classic scenario |
The Red Flags Within Myelopathy
When you diagnose myelopathy, always actively exclude:
- Neoplastic causes — progressive pain worse at night, weight loss, known malignancy
- Infective causes — fever, immunosuppression, IV drug use, TB risk factors
- Cauda equina syndrome — saddle anaesthesia, urinary retention, faecal incontinence (though this is lumbar, not cervical — but always rule out in any spinal presentation) [2]
- Acute cord compression — rapid deterioration is a surgical emergency
When a myelopathy is caused by a spinal tumour, the type depends on the anatomical compartment:
| Compartment | Tumour | Key Features |
|---|---|---|
| Intradural extramedullary | Schwannoma | Common at cervical and lumbar spine; 95% arise from sensory nerve root → present as pain; usually sporadic (if multiple → NF2); T1 contrast-enhancing [2] |
| Neurofibroma | Usually multiple, associated with NF1; cannot be separated from nerve fibres (cf. schwannoma) [2] | |
| Meningioma | Common at thoracic level (80%); located lateral to spinal cord (70%) except at cervical spine (anterior); homogeneous enhancement + dural tail sign [2] | |
| Intradural intramedullary | Ependymoma | More common; discrete from normal cord → surgery; e.g. myxopapillary ependymoma (WHO Grade 1, filum terminale) [2] |
| Astrocytoma | Indistinct from normal cord → biopsy and debulking ± adjuvants [2] | |
| Extradural | Metastasis | Most common spinal tumour overall; lung, breast, prostate, kidney, thyroid |
High Yield Summary — Differential Diagnosis
The key differentials to distinguish from cervical myelopathy are:
- Cervical radiculopathy — unilateral, dermatomal, LMN signs, pain-predominant, Spurling's positive (vs bilateral, UMN, painless, myelopathic hand signs in myelopathy)
- Motor neuron disease — mixed UMN/LMN BUT no sensory loss; widespread fasciculations; normal MRI cord
- Multiple sclerosis — relapsing-remitting; optic neuritis; young female; MRI brain + cord shows demyelination
- Peripheral nerve compression — CTS, cubital tunnel, TOS — distribution follows peripheral nerve, not dermatome; NCS diagnostic
- Intracranial pathology — parasagittal tumour, NPH, stroke — face involvement, cognitive changes, MRI brain
- B12 deficiency — absent ankle jerks + upgoing plantars + macrocytosis
- Central cord syndrome — acute UL > LL weakness after hyperextension injury in elderly with pre-existing stenosis
Within myelopathy, distinguish compressive from non-compressive on MRI, then determine the aetiology by compartment (extradural, intradural extramedullary, intramedullary).
Active Recall - Differential Diagnosis of Cervical Myelopathy
References
[1] Lecture slides: GC 227. Cervical Spine Pathology.pdf (pp. 17, 18, 25, 32, 33, 41, 42, 43, 44, 80) [2] Senior notes: maxim.md (sections 2.2–2.5, 5.2, 5.6 — compression neuropathy, spine diseases, spinal tumours) [3] Lecture slides: GC 110. Paraplegia Spinal cord compression Transverse myelitis Spinal dysraphism Neuroimaging III Spinal Cord.pdf (pp. 10, 12, 21, 28) [4] Lecture slides: GC 110. Paraplegia Spinal cord compression Transverse myelitis Spinal dysraphism Neuroimaging III Spinal Cord.pdf (pp. 10, 12, 28 — spinal cord syndromes and non-compressive causes) [5] Senior notes: felixlai.md (differential diagnosis of acute neurological presentation)
Diagnosis of Cervical Myelopathy
Unlike conditions such as rheumatoid arthritis or SLE, cervical myelopathy does not have a formal, validated set of "diagnostic criteria" like the ACR/EULAR criteria. This is because cervical myelopathy is fundamentally a clinico-radiological diagnosis — it requires:
- Clinical features consistent with spinal cord dysfunction (the symptoms and signs we covered)
- Imaging confirmation of cervical spinal cord compression that correlates with the clinical findings
- Exclusion of other conditions that can mimic myelopathy (the differential diagnosis)
Think of it as a three-legged stool: clinical syndrome + imaging evidence + exclusion of mimics. If any leg is missing, the diagnosis is insecure.
The diagnosis rests on three pillars:
| Pillar | What It Means | How to Assess |
|---|---|---|
| 1. Clinical assessment | Demonstrate myelopathic signs and symptoms; grade severity | History, physical examination (myelopathic hand signs, UMN signs, gait), JOA/mJOA scoring |
| 2. Imaging correlation | Demonstrate structural pathology compressing the cord that matches the clinical level | X-ray → CT → MRI (gold standard) |
| 3. Exclude mimics | Rule out non-myelopathic and non-compressive causes | Neurophysiology, blood tests, lumbar puncture, MRI brain (if needed) |
Indications for surgery in CSM [1] elegantly summarise the diagnostic threshold for action:
- Progressive neurologic deficit
- Significantly impaired ADL (JOA score)
- Compatible imaging findings
This means the diagnosis is confirmed when there is a clinical deficit, it is functionally significant, AND imaging shows a corresponding structural cause.
Clinical Assessment (Pillar 1)
The key historical features that point toward cervical myelopathy (as opposed to mimics):
- Insidious onset — typically months to years of progressive hand clumsiness, gait unsteadiness, numbness
- Pain is not a predominant feature [1] — if pain dominates, think radiculopathy or other causes
- Loss of hand dexterity [1] — difficulty with chopsticks (very relevant HK context), buttons, handwriting
- Poor proprioception + spastic gait [1]
- Motor weakness and sphincteric dysfunction appear in the late stage [1]
- Lhermitte's sign reported by the patient (electric shock sensation on neck flexion)
- May have acute-on-chronic deterioration after minor trauma (especially falls in the elderly → central cord syndrome [3])
A systematic neurological examination is the cornerstone. Here's the structured approach:
Physical examination [2]:
- UL:
- Trunk: sensory level (T4: nipple; T10: umbilicus) [2]
- LL:
Signs of cervical myelopathy [1]:
- Myelopathic hand signs: Hoffmann's sign, 10-sec test, finger escape sign
- Lower limb spasticity
- Positive Romberg sign / failed tandem walking test
- Lower limb upper motor neuron features
The Japanese Orthopaedic Association (JOA) score is the standard severity grading system and is used both diagnostically (to quantify impairment) and to monitor treatment response.
JOA Scoring System (Total normal = 17 points) [2]:
| Domain | Parameter | Score Range |
|---|---|---|
| I. Upper extremity function | Ability to use chopsticks and spoons; button shirts | 0–4 |
| II. Lower extremity function | Ability to walk (normal → wheelchair-bound) | 0–4 |
| III. Sensory | Upper extremity + Lower extremity and trunk | 0–2 each (total 0–4) |
| IV. Bladder function | Urinary disturbance (normal → retention) | 0–3 |
| Total | 0–17 |
- Higher score = better function (17 = normal)
- Recovery rate = (Post-op JOA − Pre-op JOA) / (17 − Pre-op JOA) × 100%
- A low JOA score confirms significantly impaired ADL — one of the indications for surgery [1]
Modified JOA (mJOA) Score (Western version, max 18):
- Mild: 15–17
- Moderate: 12–14
- Severe: < 12
Localisation of the symptomatic level [1]:
- The spinal cord ascends approximately one segment during its development [1]
- Cervical discs generally lie opposite spinal cord segments which are numbered one lower than the number of roots passing them [1]
This means a disc at C4/5 lies opposite the C5/C6 cord segments — so compression at the C4/5 disc level can produce C5 or C6 neurological signs. This concept is critical for correlating clinical level with imaging level.
Imaging (Pillar 2)
Imaging is essential to confirm the diagnosis, identify the pathoanatomy, determine the level(s) of compression, and plan surgery. The approach follows a logical sequence from simple to complex.
Cervical X-rays [1]: systematic interpretation using:
- Coverage / adequacy
- Alignment
- Bone
- Disc space
- Soft tissue
- Dynamic views
- C0/C1/C2 relationship
Standard views:
- AP / lateral [1]
- Oblique views for foraminal narrowing [1] (specifically useful for radiculopathy — shows neural foramen encroachment by osteophytes)
Adequacy [2]:
- C-spine lateral: from pituitary fossa to C7/T1 junction
- Odontoid view / open mouth view: C1 and C2
- Swimmer's view: cervicothoracic junction
Alignment [2]:
- Curvature: cervical lordosis preserved / increased / decreased / lost / kyphosis — loss of lordosis is common in cervical spondylosis and is important for surgical planning (kyphosis favours anterior approach)
- Vertebral lines: anterior vertebral line, posterior vertebral line, spinolaminar line, spinous process line
- Ignore the bony spurs
- Posterior vertebral line is easiest to detect — disruption suggests subluxation or instability
Bone: fracture, bony lesion [2]
Cartilage / Disc space:
- Pavlov ratio > 0.8 [2] — ratio of AP diameter of spinal canal to AP diameter of vertebral body at the same level. < 0.8 indicates congenital stenosis — these patients are predisposed to myelopathy.
- Atlantodental interval (ADI) [2]: ≥ 3 mm (adult) or ≥ 5 mm (children) = atlantoaxial subluxation
Soft tissue (only for C-spine) [2]:
- 3×7=21 rule: C1 ≤ 10 mm, C3 ≤ 7 mm, C7 ≤ 21 mm — widened prevertebral soft tissue suggests haematoma, abscess, or retropharyngeal pathology
Measurement of cervical stenosis and instability [1]:
- a = Midsagittal diameter of the spinal canal. Relative stenosis if < 12 mm; absolute if < 10 mm
- b = Dynamic stenosis = distance from posteroinferior corner of cranial vertebra to anterosuperior edge of caudal lamina. Dynamic stenosis if < 12 mm
- c = Olisthesis (slip) — measures any listhesis (slippage) of one vertebra on another
Dynamic views (flexion/extension) [2]:
- X-ray spine: dynamic (flexion/extension), sagittal plane to look for any imbalance [2]
- Why? Static X-rays may miss instability. Dynamic views reveal abnormal translation or angulation during movement — critical for detecting spondylolisthesis or ligamentous instability.
- Important in RA (to demonstrate atlantoaxial subluxation that may only appear in flexion).
Investigation — Plain X-ray [3]:
- Readily available
- Show obvious fracture and malalignment
- Can miss subtle fracture
- Cannot exclude ligamentous instability
- Cannot exclude soft-tissue compressive lesion (e.g. haematoma)
Limitations of Plain X-rays
X-rays are a good screening tool but have significant limitations: they cannot directly visualise the spinal cord, cannot assess soft tissue compression (discs, ligamentum flavum, haematoma), and cannot detect intramedullary signal changes. They are useful for assessing alignment, bony anatomy, and canal dimensions — but MRI is essential for confirming cervical myelopathy.
| X-ray Finding | Significance |
|---|---|
| Loss of cervical lordosis | Degenerative changes, muscle spasm |
| Osteophytes (anterior/posterior) | Spondylosis — posterior osteophytes may compress cord |
| Reduced disc height | Disc degeneration |
| Pavlov ratio < 0.8 | Congenital stenosis — predisposed to myelopathy |
| ADI ≥ 3 mm | Atlantoaxial subluxation (RA, Down syndrome, trauma) |
| Calcification of PLL | OPLL — important cause in Asian populations |
| Spondylolisthesis on dynamic views | Instability → dynamic cord compression |
| Widened prevertebral soft tissue | Haematoma, abscess, retropharyngeal pathology |
CT scan [1]:
- Readily available, provides radiographic clearance when X-rays are inadequate [1]
- CT spine: bony lesions [2]
Investigation: CT [3]:
- Reasonably available
- Still cannot show soft-tissue injury [3]
When to use CT:
- Bony detail: fractures (especially subtle ones missed on X-ray), facet joint arthropathy, calcification patterns
- OPLL: CT is the best modality to define the extent and morphology of ossification — it shows the bony bar beautifully on sagittal and axial cuts
- Surgical planning: bony anatomy for screw placement, assessment of facet joints
- CT myelography: if MRI is contraindicated (e.g., patient with pacemaker), contrast injected into the thecal sac can outline the cord and show compression
| CT Finding | Significance |
|---|---|
| Posterior osteophytes encroaching canal | Spondylotic cord compression |
| Continuous ossified bar behind vertebral bodies | OPLL |
| Ossified ligamentum flavum | OLF |
| Facet joint hypertrophy | Lateral/posterolateral stenosis |
| Fracture lines | Traumatic cause |
| Lytic/sclerotic bony lesion | Tumour (primary or metastatic) |
MRI is the definitive investigation for cervical myelopathy. It is the only modality that directly visualises the spinal cord, the degree of compression, and intramedullary changes.
MRI scan [1]:
- Essential if there are neurological deficits [1]
- Useful for delineation of soft tissue injury (i.e. discoligamentous) [1]
- Confirm nerve root / cord compression [1]
Investigation: MRI [3]:
Advanced imaging assessment [1]:
- Evaluation of compression and deformity of spinal cord
- Evaluation of intramedullary lesion
- Detection of pathological spinal factors
- Surgical planning
MRI — basic interpretation [1]:
- Level of lesion, location
- Pathoanatomy (disc, osteophyte, OPLL, flavum)
- Obliteration of the CSF space
- Cord shape / cross-sectional area
- Intramedullary signal change (myelomalacia)
Let me break each of these down:
| MRI Feature | What to Look For | Clinical Significance |
|---|---|---|
| Level of lesion | Which disc level(s) show compression | Correlate with clinical neurological level |
| Location | Anterior (disc, osteophyte, OPLL) vs posterior (ligamentum flavum) vs circumferential | Determines surgical approach (anterior vs posterior) |
| Pathoanatomy | Disc, osteophyte, OPLL, flavum — identify the exact structure causing compression | Different pathologies require different surgical techniques |
| Obliteration of the CSF space | The normal bright CSF signal (T2) surrounding the cord disappears at the level of compression | Indicates significant compression even before cord signal changes appear |
| Cord shape / cross-sectional area | Cord is flattened, "banana-shaped", or reduced in cross-sectional area | Degree of cord deformity correlates with severity |
| Intramedullary signal change | T2 hyperintensity within the cord = oedema/gliosis/myelomalacia; T1 hypointensity = more severe, chronic damage (cavitation/necrosis) | This is the most important prognostic finding — T2 signal change indicates cord injury has occurred; T1 change indicates irreversibility |
MRI Signal Changes — Why They Matter
T2 hyperintensity in the cord (bright on T2) = myelomalacia [1]. This represents oedema, gliosis, or demyelination within the cord substance. It tells you that the compression has already caused structural damage to the cord. Patients with T2 signal change have:
- Worse preoperative neurological status
- Poorer recovery after decompression surgery
- More advanced disease
T1 hypointensity (dark on T1 in the cord) is even more ominous — it suggests cavitation, necrosis, or chronic gliosis. Recovery is very unlikely.
No signal change with compression = the cord is compressed but not yet irreversibly damaged — these patients have the best surgical outcomes. This is why early detection matters.
MRI Sequences and What They Show:
| Sequence | What It Shows Best | Relevance to Myelopathy |
|---|---|---|
| T1-weighted | Anatomy, fat (bright), bone marrow | Cord morphology; T1 hypointensity in cord = severe damage; contrast enhancement for tumour/infection |
| T2-weighted | Fluid (bright), pathology | CSF (bright) outlines cord beautifully; intramedullary T2 hyperintensity = myelomalacia; disc hydration assessment |
| T2 sagittal | Overview of entire cervical spine | Level and extent of compression; multisegmental disease; overall alignment |
| T2 axial | Cross-section at each level | Cord shape, cross-sectional area, location of compression (anterior/posterior/lateral) |
| T1 with gadolinium | Enhancement pattern | Tumour (enhancing), abscess (ring-enhancing), inflammation |
| STIR | Bone marrow oedema, ligament injury | Acute injury, infection, metastases |
Neurophysiological studies: nerve conduction study (NCS), somatosensory evoked potential (SSEP) [2]
NCV / EMG [1]
These are adjunctive — not primary diagnostic tools for myelopathy — but have important roles:
| Study | What It Tests | Role in Cervical Myelopathy |
|---|---|---|
| Nerve Conduction Study (NCS) | Peripheral nerve conduction velocity and amplitude | Exclude peripheral nerve compression (CTS, cubital tunnel, TOS) as the cause of hand symptoms. Also helps identify concurrent double crush syndrome. |
| Electromyography (EMG) | Muscle electrical activity — detects denervation | Identifies LMN involvement at the level of compression (fibrillations, positive sharp waves in specific myotomes). Helps distinguish myelopathy from MND (in MND, widespread denervation across multiple myotomes and regions including bulbar). |
| Somatosensory Evoked Potential (SSEP) | Integrity of sensory pathways from periphery to cortex (primarily dorsal columns) | Objectively demonstrates impaired conduction through the cervical cord. Prolonged latency or reduced amplitude at cervical/cortical level suggests cord dysfunction. Useful for surgical monitoring (intraoperative SSEP). |
| Motor Evoked Potential (MEP) | Integrity of corticospinal tract (UMN pathway) | Intraoperative monitoring during decompression surgery to detect real-time cord compromise. Prolonged central motor conduction time supports myelopathy diagnosis. |
When neurophysiology is particularly useful:
- When the clinical picture is ambiguous (e.g., coexistent CTS + myelopathy)
- When MRI findings are equivocal or do not match the clinical level
- Intraoperatively for spinal cord monitoring
- To exclude MND (which shows widespread denervation without sensory nerve involvement)
| Investigation | When to Order | Key Findings |
|---|---|---|
| Bloods: ESR, CRP | Suspected infection or inflammation | Elevated in epidural abscess, TB spine, RA |
| Bloods: Vitamin B12, folate | Suspected subacute combined degeneration | Low B12 with macrocytosis |
| Bloods: RF, anti-CCP, ESR | Suspected RA cervical spine involvement | Positive RF/anti-CCP confirms RA |
| Bloods: Ca, ALP, PSA, tumour markers | Suspected metastatic disease | Raised ALP (bone mets), raised PSA (prostate) |
| Lumbar puncture | Suspected non-compressive cause (transverse myelitis, MS, NMOSD) | Transverse myelitis: Dx by exclusion; LP — high CSF protein [3]; MS: oligoclonal bands; NMOSD: AQP4 antibody |
| MRI Brain | Suspected MS, intracranial pathology, NMOSD | Periventricular demyelination (MS); parasagittal mass; hydrocephalus |
| Whole spine MRI | To exclude other levels of compression; suspected metastatic disease | Multi-level disease; skip lesions in metastases |
| CT-guided biopsy | Suspected tumour, atypical infection | Histological diagnosis |
| Bone scan | Suspected metastatic disease | Multiple hot spots |
This is a crucial step that many students overlook. Finding compression on MRI is not enough — you must demonstrate that the imaging level explains the clinical findings.
Localisation of symptomatic disc level [1]:
- The spinal cord ascends approximately one segment during its development
- Cervical discs generally lie opposite spinal cord segments numbered one lower than the number of roots passing them
Practical implication: A disc herniation at C5/6 lies opposite the C6/C7 cord segments. So compression at C5/6 can produce clinical signs of C6 or C7 myelopathy (C6 LMN signs at the level; C7 and below UMN signs).
Neurological level diagnosis [1]:
| Level | Reflex Pattern | Uppermost Weak Muscle | Sensory Dermatome |
|---|---|---|---|
| C3–C4 | BTR ↑, TTR ↑, FF ↑ | Deltoid | C4 |
| C4–C5 | BTR ↑ or →, TTR ↑, FF ↑ | Biceps | C5 |
| C5–C6 | BTR → or ↓, TTR ↑ or →, FF ↑ | Triceps or EDC | C6 |
| C6–C7 | BTR →, TTR →, FF ↑ | APB or ADM | C7 |
Use this table to match clinical findings with the MRI level. If there is a mismatch, consider:
- Multi-level disease (most common scenario in spondylotic myelopathy)
- Concurrent radiculopathy at a different level
- Alternative diagnosis
| Investigation | Primary Role | Key Findings | Limitations |
|---|---|---|---|
| X-ray (AP, lateral, oblique, dynamic) [1] | Screening; alignment; bony assessment | Loss of lordosis, osteophytes, Pavlov ratio < 0.8, ADI, OPLL calcification | Cannot exclude soft-tissue lesion or ligamentous instability (without dynamic views) [3] |
| CT scan [1] | Bony detail; OPLL characterisation; surgical planning | Ossified PLL/LF, facet hypertrophy, fractures, bony tumour | Cannot show soft-tissue injury [3] |
| MRI [1] | Gold standard: confirms cord compression and intramedullary damage | Level, pathoanatomy, CSF obliteration, cord shape, intramedullary signal change [1] | Difficult to arrange [3]; claustrophobia; contraindicated with some implants |
| NCS/EMG [1][2] | Exclude peripheral neuropathy / MND; identify level | Denervation in specific myotomes (EMG); prolonged distal latency in CTS (NCS) | Does not directly assess the cord |
| SSEP [2] | Assess dorsal column conduction; intraoperative monitoring | Prolonged central conduction time | Less sensitive to lateral column disease |
| Bloods | Exclude systemic causes | B12 deficiency, RA markers, infection markers, tumour markers | Non-specific |
| LP | Non-compressive myelopathy workup | High CSF protein (transverse myelitis), oligoclonal bands (MS), AQP4-Ab (NMOSD) | Invasive; contraindicated if cord compression present (risk of coning if intracranial mass) |
High Yield Summary — Diagnosis of Cervical Myelopathy
Diagnosis is clinico-radiological — there are no formal "diagnostic criteria."
Three pillars:
- Clinical: Myelopathic hand signs + UMN LL signs + gait disturbance → grade with JOA/mJOA
- Imaging: MRI is the gold standard → look for level, pathoanatomy, CSF obliteration, cord shape, intramedullary signal change (myelomalacia)
- Exclude mimics: NCS/EMG to exclude peripheral nerve/MND; bloods for B12, RA; LP for transverse myelitis/MS
X-ray pearls: Pavlov ratio < 0.8 = congenital stenosis; ADI ≥ 3 mm = atlantoaxial subluxation; dynamic views for instability
MRI prognostic sign: T2 hyperintensity = myelomalacia = cord damage has occurred; T1 hypointensity = worse prognosis, irreversible damage
Indications for surgery: Progressive neurological deficit + impaired ADL (low JOA) + compatible imaging
Level localisation: Match the uppermost weak muscle and reflex pattern (Seichi table) to the imaging level of compression. Remember: cervical discs lie opposite cord segments numbered one lower.
Active Recall - Diagnosis and Investigations of Cervical Myelopathy
References
[1] Lecture slides: GC 227. Cervical Spine Pathology.pdf (pp. 3, 11, 15, 17, 18, 24, 25, 28, 29, 36, 42, 43, 44, 45, 60) [2] Senior notes: maxim.md (sections 2.2–2.5, 5.6) [3] Lecture slides: GC 110. Paraplegia Spinal cord compression Transverse myelitis Spinal dysraphism Neuroimaging III Spinal Cord.pdf (pp. 12, 14, 21, 28)
Management of Cervical Myelopathy
Before diving into the specifics, let's establish the key principles that govern management decisions. These come directly from understanding the pathophysiology:
- The spinal cord is unforgiving — unlike peripheral nerves, the spinal cord has very limited capacity for regeneration. Once neurons and axons are lost, they do not come back. This means early intervention matters.
- Maximal damage occurs at the time of injury (primary injury) [1]. Inappropriate or delayed management can result in further oedema and cord damage (secondary injury) which is preventable [1]. This applies to both traumatic and degenerative myelopathy — the goal is to prevent secondary deterioration.
- The spinal cord is very unforgiving [3]. Sphincter dysfunction — a point of no return [3]. By the time sphincteric dysfunction develops, significant irreversible cord damage has occurred. This underscores the importance of early detection and treatment.
- Complete injury — prognosis is generally poor. Incomplete injury — prognosis highly variable [3].
The Natural History Problem
The natural history of cervical spondylotic myelopathy is progressive deterioration in the majority of patients. Studies show that ~75% of untreated patients with moderate-severe CSM will worsen over time. This is NOT a condition where "wait and see" is safe in most cases. Conservative management is reserved only for truly mild, stable disease.
Management of cervical myelopathy broadly divides into:
| Approach | When to Use |
|---|---|
| Non-operative (conservative) | Mild myelopathy (high mJOA ≥ 15), stable symptoms, no progressive deficit, patient unfit for surgery |
| Operative (surgical) | Progressive neurological deficit, moderate-severe myelopathy (mJOA < 15), significantly impaired ADL, compatible imaging findings |
Management: surgical decompression and stabilization [2]:
- Non-operative: NSAID, lifestyle modification, PT [2]
- Operative: surgical decompression and restoration of lordosis — Laminoplasty / Laminectomy +/- fusion [2]
Non-Operative (Conservative) Management
Conservative treatment does not cure cervical myelopathy — it cannot remove the structural compression. Its role is to manage symptoms, prevent further injury, and buy time in patients with mild disease who are being monitored or who are unfit for surgery.
- Mild myelopathy (mJOA 15–17) with stable symptoms over serial assessments
- Patient is unfit for surgery (severe comorbidities, anaesthetic risk)
- Patient declines surgery (after informed discussion about natural history)
- Very early presentation with minimal functional impairment
Critical Caveat
Conservative management of cervical myelopathy requires close serial monitoring (clinical examination + repeat JOA scoring every 3–6 months). Any evidence of progression mandates re-evaluation for surgery. There is strong evidence from the AOSpine CSM North America and International studies that patients with moderate-severe myelopathy do better with surgery than with conservative management.
1. Lifestyle Modification
- Avoidance of high-risk activities: no contact sports, no diving, no heavy overhead work — any activity that involves cervical hyperextension or axial loading increases the risk of acute deterioration.
- Neck care education: avoid prolonged extension (e.g., looking up for extended periods, sleeping with multiple pillows causing extreme flexion or extension).
- Fall prevention: particularly important in the elderly with gait instability. Home modifications, walking aids if needed.
Why? The degenerative cervical spine with stenosis has minimal reserve. A minor hyperextension injury (even a stumble) can cause acute-on-chronic myelopathy or central cord syndrome [3]. Prevention of such events is paramount.
2. Pharmacological
- NSAIDs [2]: for associated neck pain from spondylosis/facet joint arthritis. These treat the pain from the degenerative process — they do NOT treat the myelopathy itself (remember: pain is not a predominant feature [1] of myelopathy).
- Neuropathic pain agents (gabapentin, pregabalin): if there is concurrent radiculopathic pain (neuropathic character).
- Muscle relaxants (e.g., baclofen, tizanidine): for spasticity. These act centrally on GABA receptors (baclofen = GABA-B agonist) or alpha-2 adrenergic receptors (tizanidine) to reduce spastic tone.
Important: No medication reverses myelopathy. Pharmacological treatment is purely symptomatic.
3. Physiotherapy (PT) [2]
- Cervical strengthening exercises (deep neck flexor strengthening)
- Postural training
- Balance and gait training (to reduce falls risk)
- Range of motion exercises (gentle — avoiding extremes of extension)
- Proprioceptive training
Physical therapy [1]: for radiculopathy, evidence supports traction, ROM exercises, strength training and stretching [1]. For myelopathy, PT is more focused on maintaining function, improving balance, and preventing deconditioning.
4. Cervical Collar / Immobilisation
- Limited evidence for use of neck collar and bedrest [1] — this is specifically stated for radiculopathy and applies to myelopathy as well.
- Soft collar may provide comfort and a kinesthetic reminder to limit extreme neck movements, but there is no evidence it alters the course of myelopathy.
- Hard collar may be used temporarily after acute-on-chronic exacerbation to limit dangerous movements while surgical planning is underway.
Operative (Surgical) Management
Surgery is the definitive treatment for cervical myelopathy. The fundamental goal is to decompress the spinal cord — physically remove the pressure that is crushing it — and, where indicated, to stabilise the spine to prevent recurrent compression.
Indications for surgery in CSM [1]:
- Progressive neurologic deficit
- Significantly impaired ADL (JOA score)
- Compatible imaging findings
Principles of management — surgical treatment if [3]:
- Progressive neurological deficit
- Myelopathy / Radiculopathy
- Intractable pain
Indications for surgery (trauma context, but principles apply broadly) [1]:
- Structural: Instability
- Decompression: Neurological deficit; Lack of improvement / deteriorating neurology
- Polytrauma: To facilitate mobilization and rehabilitation
In practical terms, the decision for surgery is made when:
| Factor | Threshold |
|---|---|
| Neurological deficit | Progressive worsening on serial examination |
| Functional impairment | mJOA < 15 (moderate), or < 12 (severe) |
| Imaging | MRI showing cord compression ± intramedullary T2 signal change correlating with clinical level |
| Duration | Some evidence that earlier surgery (before significant cord damage) leads to better outcomes |
Don't Wait Too Long
The evidence strongly supports that earlier surgery yields better outcomes. The presence of T2 intramedullary signal change (myelomalacia [1]) on MRI indicates that cord damage has already occurred. Patients operated on before signal change develops have significantly better recovery rates. Sphincter dysfunction is a point of no return [3] — by the time bladder dysfunction appears, recovery is limited.
- Decompress the spinal cord — remove the compressive pathology
- Restoration of lordosis [2] — restore normal cervical alignment
- Stabilise the spine — if instability is present or created by the decompression
- Preserve motion — where possible (e.g., laminoplasty preserves more motion than fusion)
This is one of the most important clinical decisions and is the focus of much of the lecture material.
Choice of surgery [1]:
- Decompression: Anterior / Posterior
- Stabilisation: Internal (Anterior / Posterior) / External
General considerations: Anterior vs posterior approach [1]:
| Factor | Favours Anterior | Favours Posterior |
|---|---|---|
| 1. Sagittal alignment | Fixed kyphotic deformities — you need to go anteriorly to correct the kyphosis and decompress the cord which is draped over the front | Preserved lordosis or neutral alignment — cord can fall back away from anterior compression once posterior decompression is performed |
| 2. Pathoanatomy | Disc protrusions into the spinal cord — these are anterior structures; direct anterior approach removes the offending disc | Infolding / thickening of ligamentum flavum — this is a posterior structure; posterior approach directly addresses it |
| 3. Number of levels | 1–2 levels (some say up to 3) | 3 level pathology or more favours posterior approach — anterior approaches spanning > 3 levels have higher complication rates (pseudarthrosis, graft subsidence) |
| 4. Subluxation or instability | Fusion is indicated [1] — can be done anteriorly or posteriorly, but instability generally requires fusion (not laminoplasty alone) | |
| 5. Neck pain | Laminoplasty patients may experience more post-op axial neck pain [1] — this is a consideration but not a contraindication |
A. Anterior Cervical Discectomy and Fusion (ACDF)
- What it is: Access the cervical spine from the front (anterior approach between the carotid sheath laterally and the trachea/oesophagus medially). Remove the disc at the offending level. Place a graft (bone or cage) in the disc space. Fixate with a plate and screws.
- Mechanism: Directly removes the anterior compressive pathology (disc, small osteophyte) and fuses the segment to prevent re-compression.
- Indications:
- Advantages: Direct removal of anterior pathology; excellent for kyphosis correction; can be combined with foraminotomy for radiculopathy
- Disadvantages: Loss of motion at fused segment; risk of adjacent segment disease (ASD) — the levels above and below the fusion bear increased stress; risk of graft/cage subsidence
- Specific complications: Dysphagia (oesophageal retraction), recurrent laryngeal nerve palsy (hoarseness), vertebral artery injury, graft dislodgement, pseudarthrosis (failure of fusion), adjacent segment disease
For radiculopathy: anterior cervical discectomy and fusion, artificial disk replacement [1]
B. Anterior Cervical Corpectomy and Fusion (ACCF)
- What it is: Removes one or more vertebral bodies (not just the disc) along with the adjacent discs, then reconstructs with a strut graft and plate.
- Mechanism: Provides wider decompression than ACDF — removes both discs and the intervening vertebral body with its posterior osteophytes. Necessary when OPLL extends behind the vertebral body (cannot be reached by discectomy alone).
- Indications:
- OPLL (especially continuous type extending behind vertebral bodies)
- Multi-level anterior compression (2–3 level corpectomy)
- Severe retrovertebral body osteophytes
- Anterior corpectomy [3]
- Disadvantages: Larger procedure; higher complication rate than ACDF; graft-related complications (dislodgement, subsidence)
C. Artificial Disc Replacement (Cervical Total Disc Arthroplasty)
- Artificial disk replacement [1]
- What it is: After discectomy, instead of fusion, an artificial disc device is placed to maintain motion at that segment.
- Indication: Primarily for 1–2 level disease in younger patients where motion preservation is desired and there is no significant instability.
- Advantage: Preserves motion → theoretically reduces adjacent segment disease.
- Contraindication: Significant instability, severe facet joint arthropathy, OPLL, multi-level disease, osteoporosis.
D. Laminoplasty
- What it is: The laminae are opened on one side (hinge) and propped open with a spacer, expanding the spinal canal like opening a door. The word breaks down: "lamino-" = lamina, "-plasty" = to mold/reshape.
- Mechanism: Expands the spinal canal posteriorly → the cord drifts backward away from anterior compressive pathology → indirect decompression without removing the anterior pathology.
- Indications:
- 3 or more levels of pathology [1]
- Multi-level spondylotic myelopathy
- OPLL (when anterior approach is too risky)
- Preserved or lordotic cervical alignment (the cord must be able to drift backward — if there is kyphosis, the cord is tethered anteriorly and will NOT drift back)
- Advantages: Preserves motion (no fusion required); lower pseudarthrosis risk; can decompress multiple levels in one procedure
- Disadvantages: Laminoplasty patients may experience more post-op axial neck pain [1]; does NOT correct kyphosis; does not address anterior pathology directly; risk of door closure (hinge fracture); C5 palsy (segmental motor paralysis — see complications)
- Contraindication: Kyphotic alignment (fixed kyphotic deformities favour anterior approach [1])
E. Laminectomy ± Fusion
- Laminectomy +/- fusion [2]
- What it is: Complete removal of the laminae at the affected levels. If fusion is added, lateral mass screws and rods are placed to stabilise the spine.
- Mechanism: Removes the posterior bony arch entirely → maximal posterior decompression. Fusion prevents post-laminectomy instability and kyphosis.
- Indications:
- Multi-level myelopathy (≥ 3 levels)
- Infolding / thickening of ligamentum flavum [1]
- Posterior compression
- When fusion is also needed (instability, spondylolisthesis)
- Laminectomy alone (without fusion): Rarely performed now because removal of the posterior elements destabilises the spine → progressive kyphotic deformity → recurrent cord compression. Almost always combined with instrumented fusion in current practice.
- Advantages: Maximum decompression; can address instability simultaneously
- Disadvantages: Loss of motion at fused segments; muscle dissection and denervation (posterior approach is more muscle-destructive); risk of adjacent segment disease
F. Posterior Cervical Foraminotomy
- Posterior cervical foraminotomy [1]
- What it is: Keyhole decompression of the neural foramen from behind. A small part of the facet joint and lamina is removed to free the nerve root.
- Indication: This is primarily for radiculopathy (not myelopathy) — specifically for lateral/foraminal disc herniations or foraminal osteophytes compressing a single nerve root.
- Advantage: Motion-preserving (no fusion needed)
- NOT typically used for myelopathy (does not adequately decompress the central spinal canal)
| Procedure | Approach | Levels | Key Indication | Motion Preserved? |
|---|---|---|---|---|
| ACDF | Anterior | 1–2 | Disc herniation, kyphosis, instability | No (fusion) |
| ACCF | Anterior | 1–3 bodies | OPLL, retrovertebral osteophytes | No (fusion) |
| Disc replacement | Anterior | 1–2 | Young patient, motion preservation desired | Yes |
| Laminoplasty | Posterior | ≥ 3 | Multi-level, preserved lordosis, no instability | Yes (partial) |
| Laminectomy + fusion | Posterior | ≥ 3 | Multi-level, instability, posterior compression | No (fusion) |
| Foraminotomy | Posterior | 1 | Radiculopathy (not myelopathy) | Yes |
Special Situations
Principles of management [3]:
- Resuscitation (NB: spinal shock)
- Collar and log roll to protect spine
- Assume multiple injury / head injury
- Imaging studies
- Methylprednisolone (?)
- Surgery to decompress spinal cord
- Mechanical stabilisation
- Prevent / Treat complications
- Rehabilitation
Cervical spine stabilization [1]:
- Rigid collar (correct size)
- Sand-bags and tape
- Skull traction
Management — primary and secondary injury [1]:
- Maximal damage occurs at the time of injury (primary injury)
- Inappropriate or delayed management can result in further oedema and cord damage (secondary injury) which is preventable
Methylprednisolone controversy: The NASCIS (National Acute Spinal Cord Injury Study) trials suggested high-dose methylprednisolone within 8 hours of acute SCI may have marginal benefit. However, subsequent analysis showed significant complications (infection, GI bleeding, pneumonia). Current guidelines (2024–2026) do NOT recommend routine methylprednisolone for acute SCI — it is at best "an option" and at worst harmful. The lecture slides appropriately flag this with a question mark [3].
Timing of surgery: For acute traumatic myelopathy, current evidence (STASCIS trial, Fehlings et al.) supports early decompression within 24 hours of injury for incomplete SCI, as this improves neurological outcomes.
Principles of management [3]:
- Steroids to reduce oedema
- Surgical resection within safety limit
- Intraoperative monitoring with motor evoked potential (MEP) and somatosensory evoked potential (SSEP)
- Adjuvant radiotherapy for some
For metastasis [3]:
- Primarily external radiation therapy (ERT)
- Surgery for pain, instability, or lesions resistant to RT
- Palliative in nature
- Cervical involvement requires surgical stabilisation (typically posterior C1/C2 fusion for atlantoaxial subluxation using screws ± wiring).
- Use of RA medications reduces the incidence of cervical involvement [1] — good disease control with DMARDs/biologics is the best prevention.
- Urgent surgical decompression + appropriate antimicrobials (anti-TB regime for Pott's disease).
- Anterior approach often preferred (abscess is typically anterior to the cord; vertebral body debridement may be needed in TB).
Rehabilitation [3] is a critical component:
- Immediate post-op: Cervical collar (soft or hard depending on procedure); wound care; monitoring for neurological deterioration
- Physiotherapy: Early mobilisation, gait retraining, upper limb dexterity exercises, balance training
- Occupational therapy: Adaptive strategies for ADLs (if residual deficit)
- Serial follow-up: Clinical examination (JOA score), X-rays (check alignment, hardware position, fusion progress)
- Adjacent segment monitoring: Patients with fusion are at risk of accelerated degeneration at adjacent levels — long-term surveillance required
Conclusion [3]:
- Acute paraplegia is an EMERGENCY
- Early detection and investigation
- Treatment depends on condition
- Long-term issues with dysreflexia, neurogenic bladder, spasticity, contracture, and skin problems
| Factor | Better Prognosis | Worse Prognosis |
|---|---|---|
| Duration of symptoms | Short (< 1 year) | Long (> 2 years) |
| Severity at presentation | Mild (mJOA ≥ 15) | Severe (mJOA < 12) |
| MRI signal change | No intramedullary signal | T2 hyperintensity (worse: T1 hypointensity) |
| Age | Younger | Older (> 70) |
| Number of levels | Single level | Multi-level |
| Cause | Disc herniation (softer, more responsive) | OPLL, severe spondylosis (harder, multi-level) |
| Completeness | Incomplete injury | Complete injury |
| Sphincter function | Preserved | Sphincter dysfunction — a point of no return [3] |
High Yield Summary — Management of Cervical Myelopathy
Conservative management (mild, stable myelopathy only):
- Lifestyle modification (avoid hyperextension, fall prevention)
- NSAIDs for pain, muscle relaxants for spasticity
- Physiotherapy (strengthening, balance, gait)
- Serial monitoring with mJOA every 3–6 months — any progression → surgery
Indications for surgery:
- Progressive neurologic deficit
- Significantly impaired ADL (JOA score)
- Compatible imaging findings
5 factors guiding anterior vs posterior approach:
- Sagittal alignment: kyphosis → anterior
- Pathoanatomy: disc → anterior; ligamentum flavum → posterior
- Number of levels: 1–2 → anterior; ≥ 3 → posterior
- Instability: fusion is indicated
- Neck pain: laminoplasty may cause more post-op axial neck pain
Surgical options:
- Anterior: ACDF, ACCF, disc replacement
- Posterior: Laminoplasty, laminectomy + fusion
- Decompression and restoration of lordosis is the goal
Key principles:
- Spinal cord is unforgiving — early surgery yields better outcomes
- Sphincter dysfunction = point of no return
- T2 signal change on MRI = cord damage already present → operate before this develops
- Methylprednisolone for acute SCI: NOT routinely recommended
Active Recall - Management of Cervical Myelopathy
References
[1] Lecture slides: GC 227. Cervical Spine Pathology.pdf (pp. 29, 36, 37, 38, 47, 48, 49, 62, 84, 87, 88) [2] Senior notes: maxim.md (sections 2.4, 2.5) [3] Lecture slides: GC 110. Paraplegia Spinal cord compression Transverse myelitis Spinal dysraphism Neuroimaging III Spinal Cord.pdf (pp. 16, 20, 22, 27)
Complications of Cervical Myelopathy
Complications in cervical myelopathy arise from two broad sources: the disease process itself (what happens if the cord compression goes untreated or progresses) and the treatment (complications of surgery). Both are high-yield and both are directly testable.
A. Complications of the Disease Process (Untreated / Progressive Myelopathy)
The core problem is ongoing spinal cord compression → progressive neuronal loss → irreversible functional decline. The complications are essentially a catalogue of what each damaged tract/system produces as the disease worsens.
- The natural history of untreated moderate-severe cervical myelopathy is stepwise or gradual decline in ~75% of patients.
- Motor weakness and sphincteric dysfunction appear in the late stage [1] — by the time these develop, substantial irreversible cord damage has occurred.
- The spinal cord is very unforgiving [3] — unlike peripheral nerves, central neurons do not regenerate.
- Complete injury — prognosis is generally poor. Incomplete injury — prognosis highly variable [3].
Pattern of progression:
| Stage | What Happens | Pathophysiological Basis |
|---|---|---|
| Early | Hand numbness, subtle clumsiness | Early dorsal column and corticospinal tract compression — mild demyelination, still partially reversible |
| Intermediate | Spastic gait, frequent falls, worsening hand dexterity | Progressive demyelination + early axonal loss in lateral and posterior columns |
| Late | Sphincter dysfunction [3], severe weakness, wheelchair-dependent | Extensive axonal loss + gliosis + myelomalacia (intramedullary signal change) [1]; destruction of descending autonomic pathways to sacral micturition/defecation centres |
Chronic condition with acute deterioration [3].
This is the classic scenario of an elderly patient with pre-existing cervical stenosis and mild chronic myelopathy who suffers a minor fall or hyperextension injury → acute neurological deterioration.
- Central cord syndrome [1]: Most common incomplete spinal cord injury. Hyperextension injury in a degenerative cervical spine [1].
- Quadriparesis initially, with recovery [1]
- Arm affected more than legs [1]
- Sensory sparing variable [1]
- Most patients regain ambulation [1]
- Persistent distal upper limb neurological deficits common [1] — even after recovery, fine hand function often remains impaired because the centrally located cervical motor fibres were most damaged.
Anterior cord syndrome [1] (less common but worse prognosis):
- Hyperflexion injury with bone or disc fragment [1]
- Anterior spinal artery compression [1]
- Motor and pain/temperature loss [1]
- Posterior column preserved [1]
- Prognosis poor [1]
Why is the pre-existing stenosis so dangerous? A normal cervical canal has ~17 mm of AP diameter — plenty of room for the cord (~10 mm). With spondylotic stenosis, this may narrow to 11–12 mm, leaving virtually no CSF buffer. Even a minor hyperextension (ligamentum flavum buckling inward) can pinch the cord against anterior osteophytes. The cord has nowhere to go.
Sphincter dysfunction — a point of no return [3].
- Urinary dysfunction progresses through stages:
- Early: Urgency, frequency (loss of descending cortical inhibition → detrusor hyperreflexia = the bladder contracts involuntarily because the pontine micturition centre loses cortical modulation)
- Late: Retention with overflow incontinence (loss of coordinated voiding → detrusor-sphincter dyssynergia = the bladder and sphincter contract simultaneously, preventing emptying)
- Bowel dysfunction: Constipation → faecal incontinence (same mechanism — loss of descending control over sacral defecation centre S2–S4).
- Sexual dysfunction: Erectile dysfunction, loss of ejaculatory control.
Why is this "the point of no return"? Sphincter control requires intact descending autonomic pathways from the brainstem (pontine micturition centre) through the entire spinal cord to the sacral segments (S2–S4). By the time these long pathways are sufficiently damaged to produce sphincter dysfunction, there is typically extensive, irreversible cord damage across multiple segments.
Long-term issues with dysreflexia, neurogenic bladder, spasticity, contracture, and skin problems [3].
These are particularly relevant in severe myelopathy or after traumatic SCI:
| Complication | Pathophysiology | Clinical Significance |
|---|---|---|
| Autonomic dysreflexia | Noxious stimulus below the level of lesion (e.g., full bladder, faecal impaction) → massive uncontrolled sympathetic discharge below the lesion → severe hypertension, reflex bradycardia, headache, flushing above the level, pallor below | Medical emergency (hypertensive crisis); occurs in lesions at T6 or above (because splanchnic sympathetic outflow is below T6 — if disconnected from brainstem control, it fires uncontrollably) |
| Neurogenic bladder | Upper motor neuron bladder (cord lesion above S2–S4) → hyperreflexic detrusor, small-capacity bladder, urgency/incontinence, high-pressure system → risk of vesicoureteric reflux and renal damage | Requires urodynamic assessment; managed with intermittent catheterisation, anticholinergics, botulinum toxin |
| Spasticity | Loss of corticospinal tract inhibition → exaggerated stretch reflexes, increased tone, clonus | Functionally disabling; may cause pain, contractures; managed with baclofen (oral or intrathecal), tizanidine, physiotherapy |
| Contractures | Prolonged spasticity + immobility → fixed shortening of muscles, tendons, and joint capsules | Prevented by regular ROM exercises and positioning; once established, may require serial casting or surgery |
| Pressure ulceration | Loss of sensation below lesion + immobility → sustained pressure on bony prominences → ischaemic necrosis of skin and underlying tissue | Most common sites: sacrum, ischial tuberosities, heels, trochanters; prevented by regular repositioning, pressure-relieving mattresses; can lead to osteomyelitis, sepsis |
Organ system complications following spinal cord injury [1]:
| Organ System | Complications |
|---|---|
| Cardiovascular | Bradycardia/dysrhythmia, cardiac arrest, cardiogenic pulmonary oedema |
| Pulmonary | Hypoventilation/respiratory failure, poor secretion control, ARDS, aspiration, pneumonia |
| Gastrointestinal | Gastric dysmotility, adynamic ileus, gastritis and ulceration, pancreatitis |
| Haematologic | Venothromboembolism |
| Neurologic | Neurogenic shock, depression, PTSD, anxiety, autonomic dysreflexia |
| Genitourinary | Bladder dysfunction, urinary tract infection, priapism |
| Integument | Pressure ulceration |
Let me explain the "why" behind the key systemic complications:
- Bradycardia/cardiac arrest [1]: The heart's sympathetic innervation originates from T1–T4. Cervical cord lesions disconnect the heart from sympathetic drive → unopposed vagal (parasympathetic) tone → bradycardia. In severe cases, cardiac arrest can occur.
- Hypoventilation/respiratory failure [1]: The diaphragm is innervated by the phrenic nerve (C3, C4, C5 — "C3, 4, 5 keeps the diaphragm alive"). High cervical lesions (C3 and above) can paralyse the diaphragm. Even lesions at C5–C8 impair intercostal muscles (T1–T12) and abdominal muscles, reducing cough strength and vital capacity → retained secretions → pneumonia → respiratory failure.
- Venothromboembolism (VTE) [1]: Loss of lower limb motor function → loss of the calf muscle pump → venous stasis → DVT/PE. This is a leading cause of morbidity and mortality in SCI patients. Prophylaxis with LMWH + compression stockings is essential.
- Gastritis and ulceration [1]: Cushing's ulcer — stress response + disrupted autonomic regulation → increased gastric acid secretion → mucosal ulceration. Prophylaxis with PPI.
- Depression, PTSD, anxiety [1]: Understandable given the sudden loss of independence and function; high prevalence in SCI patients; requires screening and management.
Respiratory Complications — The #1 Killer
Pulmonary complications are the leading cause of morbidity and mortality in cervical spinal cord injury patients, both in the acute and chronic phases. A patient with C5 myelopathy still has diaphragmatic function but has lost intercostal and abdominal muscle function → cannot cough effectively → secretion retention → pneumonia → respiratory failure. Aggressive chest physiotherapy and early mobilisation are critical.
B. Complications of Surgical Treatment
Counseling patients on complications [1]:
| Complication | Pathophysiology / Explanation |
|---|---|
| Oesophageal injury (intra-op or late due to implant) [1] | The anterior approach requires retraction of the oesophagus medially. Excessive retraction → oesophageal contusion, perforation, or delayed erosion from prominent hardware (plate/screws). Late perforation is rare but devastating → mediastinitis. |
| Vertebral artery injury [1] | The vertebral arteries run through the transverse foramina of C1–C6, just lateral to the vertebral bodies. Over-zealous lateral dissection or decompression → arterial laceration → massive haemorrhage or posterior circulation stroke. |
| Airway compromise [1] | Post-operative retropharyngeal haematoma or soft tissue swelling can compress the airway. Most dangerous in the first 24–48 hours. In multilevel ACDF, bilateral recurrent laryngeal nerve injury → bilateral vocal cord paralysis → airway obstruction. Patients are typically observed closely and may have planned delayed extubation. |
| Pseudoarthrosis (failed fusion) [1] | The bone graft or cage fails to integrate with the adjacent vertebrae → persistent motion at the fused segment → ongoing pain, potential hardware failure, recurrent compression. Risk factors: smoking, multi-level fusion, diabetes, osteoporosis. |
| Adjacent level degeneration [1] | Fusion eliminates motion at the treated segment → increased stress on the disc levels above and below → accelerated degenerative changes at these adjacent levels → potential need for future surgery. This is one of the strongest arguments for motion-preserving techniques (disc replacement, laminoplasty). |
| Dysphagia | Related to oesophageal retraction; very common (up to 50% in the early post-operative period); usually transient (resolves within weeks); persistent in ~5%. More common with multi-level ACDF and revision surgery. |
| Recurrent laryngeal nerve palsy | The recurrent laryngeal nerve runs in the tracheo-oesophageal groove. Right-sided approaches carry higher risk (the right recurrent laryngeal nerve has a more variable course, looping around the subclavian artery rather than the aortic arch). Results in hoarseness, weak voice, aspiration risk. Usually unilateral → usually recovers. |
| Graft/cage subsidence | The graft or cage settles into the soft bone of the vertebral endplates → loss of disc height → loss of lordosis correction → potential foraminal narrowing. More common with osteoporotic bone. |
| Horner's syndrome | Rare; damage to the cervical sympathetic chain (runs along the longus colli muscle) during anterior dissection → ipsilateral ptosis, miosis, anhidrosis. |
| Complication | Pathophysiology / Explanation |
|---|---|
| Post-op kyphosis [1] | Laminectomy without fusion removes the posterior tension band (laminae, spinous processes, supraspinous and interspinous ligaments) → the spine loses its posterior restraint → progressive kyphotic collapse. This is why laminectomy alone is almost never performed without fusion in current practice. Laminoplasty has a lower risk because it preserves some posterior structural integrity. |
| Axial symptoms (shoulder and neck pain) [1] | Posterior approaches require extensive paraspinal muscle dissection and detachment from the spinous processes → denervation, atrophy, and scarring of the posterior cervical musculature → chronic axial neck and shoulder pain. Laminoplasty patients may experience more post-op axial neck pain [1]. Reported in 30–60% of patients after posterior cervical surgery. |
| C5 nerve root paresis [1] | This is a unique and important complication. After posterior decompression (laminoplasty or laminectomy + fusion), the cord drifts posteriorly away from the anterior compression. As the cord shifts back, the C5 nerve root (which is the shortest cervical root and has the most acute takeoff angle from the cord) gets stretched or tethered → segmental motor palsy → acute deltoid and/or biceps weakness, typically appearing 1–3 days post-operatively. Incidence: 5–15%. Usually recovers over weeks to months but can be permanent. |
| Wound infection | Posterior cervical wounds have a higher infection rate than anterior wounds (larger wound, more muscle dissection, dead space). Deep infection may require washout and long-term antibiotics. |
| Epidural haematoma | Bleeding into the epidural space post-operatively → cord compression → acute neurological deterioration. A surgical emergency requiring urgent evacuation. More common in patients on anticoagulants. |
| Hardware failure | Screw pullout, rod fracture, or loosening → loss of fixation → instability and recurrent compression. Risk factors: osteoporosis, multi-level constructs, excessive motion. |
| Dural tear / CSF leak | Incidental durotomy during decompression → CSF leak → headache, wound leakage, risk of meningitis. More common in revision surgery or when OPLL is adherent to the dura. |
C5 Palsy — A Must-Know Complication
C5 palsy is uniquely associated with posterior cervical decompression. Why C5 specifically?
- The C5 root is the shortest cervical root — it has the least slack.
- It has the most perpendicular angle of exit from the cord.
- When the cord drifts posteriorly after decompression, C5 is the root most likely to be stretched beyond its limit → traction neuropraxia.
Clinical presentation: New-onset deltoid weakness ± biceps weakness 1–3 days after surgery. The patient could abduct their shoulder before surgery but now suddenly cannot.
Management: Observation (most recover); physiotherapy; some surgeons perform prophylactic foraminotomy at C4/5 during posterior decompression to reduce the risk.
Prognosis [1]:
- Complete injury — poor [1]
- No motor or sensory recovery, including sacral roots, distal to the site of injury and at the end of spinal shock [1]
- Incomplete injury — good [1]
Prognostic factors for cervical spondylotic myelopathy specifically:
| Factor | Better Outcome | Worse Outcome |
|---|---|---|
| Pre-operative mJOA | Higher (less severe) | Lower (more severe) |
| Duration of symptoms | Shorter | Longer (> 2 years → poorer recovery) |
| MRI signal change | None | T2 hyperintensity (worse: T1 hypointensity = myelomalacia [1]) |
| Age | Younger | Older (> 70 years) |
| Extent of injury | Incomplete [3] | Complete [3] |
| Sphincter function | Preserved | Sphincter dysfunction = point of no return [3] |
| Number of compressed levels | Single level | Multi-level |
| Smoking status | Non-smoker | Smoker (impairs fusion, impairs microvascular recovery) |
For central cord syndrome specifically:
- Most patients regain ambulation [1] — the lower limb fibres (peripheral in the corticospinal tract) are relatively spared.
- Persistent distal upper limb neurological deficits common [1] — the hand intrinsic muscles (medial/central fibres) are the most affected and recover the least. This has profound functional implications: the patient can walk but cannot button a shirt or use chopsticks.
High Yield Summary — Complications of Cervical Myelopathy
Disease complications (untreated):
- Progressive neurological deterioration (stepwise decline)
- Acute-on-chronic deterioration (central cord syndrome after minor fall in elderly with stenosis)
- Sphincter dysfunction = point of no return → irreversible
- Long-term: autonomic dysreflexia, neurogenic bladder, spasticity, contractures, pressure ulcers
SCI systemic complications (high yield table):
- Cardiovascular: bradycardia (loss of T1–T4 sympathetic output)
- Pulmonary: respiratory failure, pneumonia (leading cause of death — loss of intercostals/abdominals)
- VTE: loss of calf muscle pump → DVT/PE
- GI: ileus, stress ulceration
- GU: neurogenic bladder, UTI
- Skin: pressure ulcers
- Psych: depression, PTSD
Surgical complications:
- Anterior: oesophageal injury, vertebral artery injury, airway compromise, pseudoarthrosis, adjacent level degeneration, dysphagia, RLN palsy
- Posterior: post-op kyphosis, axial neck/shoulder pain, C5 nerve root paresis (short root stretched by cord drift-back), epidural haematoma
Prognosis:
- Complete injury = poor
- Incomplete injury = variable, depends on degree of sparing and speed of recovery
- Central cord syndrome: most regain walking; persistent distal UL deficits common
Active Recall - Complications of Cervical Myelopathy
References
[1] Lecture slides: GC 227. Cervical Spine Pathology.pdf (pp. 29, 40, 74, 80, 81, 83, 89) [2] Senior notes: maxim.md (sections 2.4, 2.5) [3] Lecture slides: GC 110. Paraplegia Spinal cord compression Transverse myelitis Spinal dysraphism Neuroimaging III Spinal Cord.pdf (pp. 9, 12, 16, 22, 27, 28)
High Yield Summary
Definition: Cervical myelopathy = compression of the cervical spinal cord → UMN signs below the level, LMN signs at the level.
Epidemiology: Most common cause of spinal cord dysfunction in adults > 55. Bimodal age distribution for traumatic causes. OPLL prevalence 2–4% in Asian populations.
Top Causes (HK-focused):
- Cervical spondylosis (MC)
- OPLL (Asian predominance)
- RA (atlantoaxial subluxation)
- Trauma (central cord syndrome in elderly)
- TB spine / epidural abscess
Pathophysiology: Static + dynamic mechanical compression + ischaemia → demyelination, neuronal loss, gliosis.
Cardinal Clinical Features:
- Numbness and loss of hand dexterity (NOT primarily pain!)
- Spastic gait with poor proprioception
- Myelopathic hand signs: Hoffmann's, finger escape, 10-second test, inverted reflexes
- LL: spasticity, hyperreflexia, clonus, upgoing plantars, positive Romberg
- Sphincteric dysfunction is LATE
Key Exam Concepts:
- Inverted reflexes = LMN at the level + UMN below = pathognomonic
- Central cord syndrome = hyperextension + degenerative spine → UL > LL weakness
- Pavlov ratio < 0.8 = congenital stenosis
- ADI ≥ 3 mm (adult) = atlantoaxial subluxation
- MRI intramedullary signal change = myelomalacia = poor prognosis
High Yield Summary — Differential Diagnosis
The key differentials to distinguish from cervical myelopathy are:
- Cervical radiculopathy — unilateral, dermatomal, LMN signs, pain-predominant, Spurling's positive (vs bilateral, UMN, painless, myelopathic hand signs in myelopathy)
- Motor neuron disease — mixed UMN/LMN BUT no sensory loss; widespread fasciculations; normal MRI cord
- Multiple sclerosis — relapsing-remitting; optic neuritis; young female; MRI brain + cord shows demyelination
- Peripheral nerve compression — CTS, cubital tunnel, TOS — distribution follows peripheral nerve, not dermatome; NCS diagnostic
- Intracranial pathology — parasagittal tumour, NPH, stroke — face involvement, cognitive changes, MRI brain
- B12 deficiency — absent ankle jerks + upgoing plantars + macrocytosis
- Central cord syndrome — acute UL > LL weakness after hyperextension injury in elderly with pre-existing stenosis
Within myelopathy, distinguish compressive from non-compressive on MRI, then determine the aetiology by compartment (extradural, intradural extramedullary, intramedullary).
High Yield Summary — Diagnosis of Cervical Myelopathy
Diagnosis is clinico-radiological — there are no formal "diagnostic criteria."
Three pillars:
- Clinical: Myelopathic hand signs + UMN LL signs + gait disturbance → grade with JOA/mJOA
- Imaging: MRI is the gold standard → look for level, pathoanatomy, CSF obliteration, cord shape, intramedullary signal change (myelomalacia)
- Exclude mimics: NCS/EMG to exclude peripheral nerve/MND; bloods for B12, RA; LP for transverse myelitis/MS
X-ray pearls: Pavlov ratio < 0.8 = congenital stenosis; ADI ≥ 3 mm = atlantoaxial subluxation; dynamic views for instability
MRI prognostic sign: T2 hyperintensity = myelomalacia = cord damage has occurred; T1 hypointensity = worse prognosis, irreversible damage
Indications for surgery: Progressive neurological deficit + impaired ADL (low JOA) + compatible imaging
Level localisation: Match the uppermost weak muscle and reflex pattern (Seichi table) to the imaging level of compression. Remember: cervical discs lie opposite cord segments numbered one lower.
High Yield Summary — Management of Cervical Myelopathy
Conservative management (mild, stable myelopathy only):
- Lifestyle modification (avoid hyperextension, fall prevention)
- NSAIDs for pain, muscle relaxants for spasticity
- Physiotherapy (strengthening, balance, gait)
- Serial monitoring with mJOA every 3–6 months — any progression → surgery
Indications for surgery:
- Progressive neurologic deficit
- Significantly impaired ADL (JOA score)
- Compatible imaging findings
5 factors guiding anterior vs posterior approach:
- Sagittal alignment: kyphosis → anterior
- Pathoanatomy: disc → anterior; ligamentum flavum → posterior
- Number of levels: 1–2 → anterior; ≥ 3 → posterior
- Instability: fusion is indicated
- Neck pain: laminoplasty may cause more post-op axial neck pain
Surgical options:
- Anterior: ACDF, ACCF, disc replacement
- Posterior: Laminoplasty, laminectomy + fusion
- Decompression and restoration of lordosis is the goal
Key principles:
- Spinal cord is unforgiving — early surgery yields better outcomes
- Sphincter dysfunction = point of no return
- T2 signal change on MRI = cord damage already present → operate before this develops
- Methylprednisolone for acute SCI: NOT routinely recommended
High Yield Summary — Complications of Cervical Myelopathy
Disease complications (untreated):
- Progressive neurological deterioration (stepwise decline)
- Acute-on-chronic deterioration (central cord syndrome after minor fall in elderly with stenosis)
- Sphincter dysfunction = point of no return → irreversible
- Long-term: autonomic dysreflexia, neurogenic bladder, spasticity, contractures, pressure ulcers
SCI systemic complications (high yield table):
- Cardiovascular: bradycardia (loss of T1–T4 sympathetic output)
- Pulmonary: respiratory failure, pneumonia (leading cause of death — loss of intercostals/abdominals)
- VTE: loss of calf muscle pump → DVT/PE
- GI: ileus, stress ulceration
- GU: neurogenic bladder, UTI
- Skin: pressure ulcers
- Psych: depression, PTSD
Surgical complications:
- Anterior: oesophageal injury, vertebral artery injury, airway compromise, pseudoarthrosis, adjacent level degeneration, dysphagia, RLN palsy
- Posterior: post-op kyphosis, axial neck/shoulder pain, C5 nerve root paresis (short root stretched by cord drift-back), epidural haematoma
Prognosis:
- Complete injury = poor
- Incomplete injury = variable, depends on degree of sparing and speed of recovery
- Central cord syndrome: most regain walking; persistent distal UL deficits common
AVN Of Hip
Avascular necrosis of the hip is the death of femoral head bone tissue due to disruption of its blood supply, leading to structural collapse and secondary degenerative arthritis.
Frozen Shoulder
Frozen shoulder (adhesive capsulitis) is a condition characterized by progressive pain, stiffness, and restricted active and passive range of motion of the glenohumeral joint due to inflammation and fibrosis of the joint capsule.