Cervical Myelopathy

• 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:

1. Anterior structures (front):

   • Vertebral bodies
   • Intervertebral discs
   • Posterior longitudinal ligament (PLL) — runs along the posterior aspect of the vertebral bodies inside the canal ^[1][2]
     • Ossification of PLL (OPLL) is very common in Japanese and Chinese — a common cause of cervical myelopathy ^[2]

2. Posterior structures (back):

   • Laminae
   • Ligamentum flavum (LF) — connects adjacent laminae ^[1][2]
     • Dynamic compression: osteophytes + buckled LF during extension — this is why extension worsens myelopathy ^[2]
     • Ossification of LF (OLF) can also contribute ^[2]
   • Spinous processes
   • Supraspinous and interspinous ligaments

3. Lateral structures:

   • Pedicles
   • Facet (apophyseal/zygapophyseal) joints
   • Neural foramina — where nerve roots exit

This is critical for understanding the clinical signs:

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.

• 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)

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.

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:

(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 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

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)

Radiculopathy level-by-level clinical features ^[1]:

Differential diagnosis of cervical radiculopathy includes: cervical myelopathy (symptoms may overlap and patients can have myeloradiculopathy), peripheral nerve compression, and shoulder pathology ^[1].

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).

• 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:

Central cord syndrome ^[1][4]:

• 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

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:
  • Myelopathy: hyperreflexia, myelopathic hand signs e.g. Hoffmann sign, finger escape sign ^[2]
  • Radiculopathy: hyporeflexia, dermatomal numbness, Spurling sign ^[2]
• Trunk: sensory level (T4: nipple; T10: umbilicus) ^[2]
• LL:
  • Clonus, hyperreflexia, upgoing plantar reflex ^[2]
  • Straight leg raise test ^[2]
  • Gait ^[2]

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]:

• 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.

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)

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

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]:

• Difficult to arrange ^[3]
• Shows soft-tissue lesion, cord oedema ^[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 Sequences and What They Show:

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:

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)

• 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

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.

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:

1. Decompress the spinal cord — remove the compressive pathology
2. Restoration of lordosis ^[2] — restore normal cervical alignment
3. Stabilise the spine — if instability is present or created by the decompression
4. 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]:

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:
  • 1–2 level cervical spondylotic myelopathy
  • Disc protrusions into the spinal cord ^[1]
  • Fixed kyphotic deformity ^[1] (can correct alignment)
  • Concurrent radiculopathy (anterior cervical discectomy and fusion ^[1])
• 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)

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).

• 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:

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:

Organ system complications following spinal cord injury ^[1]:

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.