Spinal Stenosis

• Spinal stenosis is the most common reason for spinal surgery in patients over 65 years of age.
• Radiographic lumbar stenosis (asymptomatic narrowing on imaging) is present in up to 20–30% of people over 60, but only a fraction are symptomatic — reinforcing that clinical correlation is essential.
• Cervical spondylotic myelopathy (CSM) is the most common cause of spinal cord dysfunction in adults over 55 worldwide.

• Age: incidence rises sharply after age 50 — this is a disease of the degenerating spine ^[2][3].
• Sex: slight male predominance ^[3].
• In Hong Kong and East Asia, there is a notably higher prevalence of ossification of the posterior longitudinal ligament (OPLL), reported in up to 2–4% of Asian populations vs. < 0.5% in Western populations ^[4]. This is a crucial HK-relevant cause of cervical stenosis.

• Hong Kong has an ageing population with high rates of degenerative spinal disease.
• OPLL is much more common in Asian vs. non-Asian populations (up to 2–4%) with male predominance and tends to affect a younger population ^[4].
• Rheumatoid arthritis (RA) — while less common than in Western populations — remains an important cause of cervical stenosis in HK, particularly C1/2 subluxation.
• Pott's disease (spinal TB) should always be on the differential in Hong Kong given endemic TB.

The spinal canal is a bony tube formed by:

• Anteriorly: Vertebral bodies + intervertebral discs + posterior longitudinal ligament (PLL)
• Laterally: Pedicles
• Posteriorly: Laminae + ligamentum flavum + facet joints

The intervertebral foramen (neural foramen) is bounded by:

• Superiorly and inferiorly: Pedicles of adjacent vertebrae
• Anteriorly: Vertebral body, disc, and uncovertebral joint (cervical)
• Posteriorly: Facet joint (zygapophyseal joint) and its capsule

The lateral recess is the space between the posterior aspect of the vertebral body and the superior articular process of the level below — a critical zone where the traversing nerve root sits before exiting at the foramen below.

This distinction is critical because:

• Compression above L2 → upper motor neuron (UMN) signs (myelopathy)
• Compression below L2 → lower motor neuron (LMN) signs (cauda equina / radiculopathy)

Cervical spine measurements ^[6]:

• Midsagittal diameter of the spinal canal (a):
  • Normal: ≥ 17 mm
  • Relative stenosis if < 12 mm; absolute stenosis if < 10 mm
• Dynamic stenosis (b): distance from posteroinferior corner of cranial vertebra to anterosuperior edge of caudal lamina — dynamic stenosis if < 12 mm
• Olisthesis (c): slip distance
• Pavlov ratio (ratio of AP diameter of canal to diameter of vertebral body at the same level): < 0.8 suggests stenosis ^[2]

Lumbar spine:

• Normal AP diameter: ~15–25 mm
• Stenosis: < 12 mm (relative), < 10 mm (absolute)
• Cross-sectional area: < 100 mm² suggests significant stenosis

The disc has two components:

1. Nucleus pulposus (NP): gelatinous core, high in water and proteoglycans (especially aggrecan) — acts as a hydraulic shock absorber
2. Annulus fibrosus (AF): concentric rings of collagen — contains the NP and resists tensile forces

With ageing, the NP loses aggrecan and water content → becomes more fibrous → can no longer evenly distribute compressive forces → stress is transferred to the AF and facet joints → this drives the entire degenerative cascade.

This is a classic exam concept:

Cervical spine: There are 8 cervical nerve roots but only 7 cervical vertebrae. The C1–C7 nerve roots exit above their corresponding pedicle (e.g., C6 root exits above C6 pedicle). The C8 root exits between C7 and T1. This means:

• A C6/7 disc (whether central or foraminal) affects the same nerve root (C7) — there is a pedicle/nerve root mismatch above and including C7, then the extra C8 root (without a corresponding C8 vertebral body) allows transition from mismatch to match ^[3].

Lumbar spine: Nerve roots exit below their corresponding pedicle (e.g., L4 root exits below L4 pedicle). This means:

• Pedicle/nerve root MATCH in the lumbar spine ^[3]
• A posterolateral L4/5 disc herniation compresses the L5 root (the traversing root)
• A far lateral (foraminal) L4/5 disc herniation compresses the L4 root (the exiting root)

• Short pedicles → constitutionally narrow canal ^[5]
• Achondroplasia (short pedicles + thick laminae)
• Down syndrome (atlanto-axial instability due to absent/lax transverse ligament)
• Congenital vertebral anomalies (e.g., block vertebrae, Klippel-Feil syndrome)

The lecture slide beautifully shows all the structures that can compress the cord/roots:

• Anteriorly: Osteophyte, ossification of PLL, spondylolisthesis, disc herniation
• Posteriorly: Ligamentum flavum hypertrophy/ossification, facet joint OA
• Result: Spinal cord compression from circumferential narrowing

Stenosis is not just about fixed narrowing. There are two components:

1. Static factors: Fixed anatomical narrowing (osteophytes, OPLL, facet hypertrophy, disc bulge at rest)
2. Dynamic factors: Narrowing that changes with posture and movement

The dynamic component is key to understanding why neurogenic claudication behaves the way it does:

• Extension decreases the size of the canal by ~11% and the foramina by ~15% ^[13]
• Flexion increases the size of the canal by ~11% and the foramina by ~12% ^[13]

Why does extension narrow the canal?

• The ligamentum flavum buckles/infolds into the canal during extension
• The facet joints telescope together, reducing foraminal height
• Disc bulging increases slightly posteriorly
• Any spondylolisthesis may worsen in extension

Why does flexion open the canal?

• The ligamentum flavum is stretched taut → flattens away from the canal
• The foramina open up as the facet joints separate
• The posterior elements spread apart

This explains the classic postural preference of lumbar stenosis patients: they lean forward on a shopping trolley, feel better sitting or bending, and worse standing upright or walking downhill.

Spinal stenosis can also occur by kinking centrally or compression by the superior articular process impingement at the neuroforamen — and this is dynamic, worsening in extension and improving in flexion ^[14].

When neural structures are compressed:

1. Mechanical compression → direct axonal injury and demyelination
2. Venous congestion → impaired venous drainage of nerve roots → oedema → further compression (a vicious cycle)
3. Arterial ischaemia → nerve roots have limited collateral blood supply; compression of the radicular arteries → ischaemia → pain, paraesthesia, weakness
4. Inflammatory mediators → compressed nerve roots and discs release inflammatory cytokines (TNF-α, IL-1, IL-6, PGE2) → chemical radiculitis

The pathophysiology of neurogenic claudication is a combination of:

• Walking upright → spinal extension → canal narrows → mechanical compression of cauda equina
• Exercise → increased metabolic demand of nerve roots → but compromised arterial supply cannot meet demand → ischaemia
• Venous congestion → further exacerbated by walking → oedema

This is why symptoms are progressive with walking (increasing metabolic demand + increasing venous congestion) and relieved by rest + flexion (opens the canal, improves blood flow).

This is the standard classification/grading system for cervical myelopathy severity:

Lower scores indicate more severe myelopathy. The recovery rate after surgery is calculated as:

Recovery rate = (postop JOA − preop JOA) / (17 − preop JOA) × 100%

Schizas Classification (MRI-based, cross-sectional area of thecal sac):

• Grade A: Clearly visible CSF, rootlets not clumped
• Grade B: Rootlets occupy most of the dural sac but CSF still visible
• Grade C: No rootlets visible, appears as homogeneous grey signal
• Grade D: No posterior epidural fat, complete obliteration

Pathogenesis: Decreased aggrecan content in NP → more fibrous NP → cannot evenly distribute compressive forces → stress transferred to AF → AF tears (circumferential → radial) → NP protrudes through AF ^[3].

Pathology classification ^[3]:

1. Bulging — disc margin extends beyond vertebral body margin symmetrically
2. Prolapse (protrusion) — NP pushes through AF but AF still contains it
3. Extrusion — partial rupture of AF; NP extends beyond AF but remains connected
4. Sequestration — free fragment of NP separated from parent disc

Level of herniation: L5/S1 > L4/5 > L3/4 ^[3] Direction of herniation: posterolateral > central > lateral ^[3]

Nerve roots affected (using L4/5 as example) ^[3]:

• Posterolateral herniation → unilateral L5 (traversing root)
• Central herniation → bilateral L5 (or cauda equina if large)
• Lateral (far lateral/foraminal) herniation → unilateral L4 (exiting root)

• Spondylolysis (lysis = dissolution/break): defect in the pars interarticularis with no movement of the vertebral body
• Spondylolisthesis (olisthesis = slipping): defect causing forward slip of one vertebra on another, most commonly L5/S1 ^[3]
• This can contribute to stenosis through both the forward slip (narrowing the canal) and the associated facet/ligament hypertrophy

These are by far the most common causes. "Mechanical" means the pain relates to the structural/biomechanical elements of the spine and is typically affected by posture and movement.

These are the "red flag" causes — less common but more dangerous. Always screen for these.

These are extra-spinal pathologies that can refer pain to the back, mimicking spinal disease:

The diagnosis rests on three pillars:

These are quantitative imaging criteria that help define stenosis objectively:

Dynamic X-rays to diagnose atlantoaxial subluxation in rheumatoid arthritis ^[25] — and more generally to assess instability.

Why this matters: if spondylolisthesis is present AND dynamic (increases with movement), surgery requires fusion in addition to decompression ^[3]. A fixed slip may only need decompression.

NCV / EMG ^[23] — these are ancillary tests that help:

Bloods are not for diagnosing stenosis itself but for excluding red-flag pathologies (infection, malignancy, metabolic bone disease).

The lecture slide [22a] lists the following as relevant investigations:

Physical therapy is a cornerstone of conservative management ^[2][3][29].

Lumbar stenosis PT ^[3]:

• Flexion exercises — Why? Because flexion opens the spinal canal by ~11% and the foramina by ~12% ^[1]. Flexion-based exercises (e.g., pelvic tilts, knee-to-chest stretches, posterior pelvic tilt in standing) train the patient to adopt postures that maximise canal space
• Stretching exercises ^[3] — Hamstring stretching, hip flexor stretching. Tight hip flexors pull the pelvis into anterior tilt → increased lumbar lordosis → extension → canal narrows. Stretching breaks this cycle
• Core stabilisation — strengthening the deep paraspinal and abdominal muscles provides dynamic support for the spine, reducing load on passive structures (discs, facets, ligaments)

Cervical stenosis PT ^[29]:

• Traction — Axial distraction gently opens the foramina and separates compressed structures ^[29]
• ROM exercises — Maintain neck mobility and prevent stiffness ^[29]
• Strength training and stretching ^[29] — Deep neck flexor strengthening, postural correction. Strengthens the dynamic stabilisers of the cervical spine
• Limited evidence for use of neck collar and bedrest ^[29] — the lecture explicitly notes this. Prolonged collar use leads to muscle atrophy and stiffness; bedrest has no proven benefit. Short-term collar use ( < 2 weeks) may help during acute flares but should not be prolonged

• Encourage mobility ^[3] — This is critical. Bed rest is harmful. Deconditioning → weaker paraspinal muscles → worse symptoms. Walking programs (within symptom limits) maintain fitness
• Weight reduction — reduces axial load on the degenerative spine
• Ergonomic advice — avoid prolonged extension postures, use lumbar support when sitting
• Smoking cessation — smoking impairs disc nutrition and accelerates degeneration
• Activity modification — avoid activities that provoke extension (e.g., prolonged standing, overhead work)

This deserves its own section because it is time-critical:

1. High-dose steroid — to reduce localised swelling around the compressed cauda equina ^[2]. Mechanism: corticosteroids reduce vasogenic oedema, inflammatory cytokines, and free radical damage. Gives the nerve roots the best chance of recovery
2. Surgical decompression within 48 hours ^[2] — laminectomy +/- discectomy ^[2]. Every hour of delay beyond 48 hours reduces the likelihood of neurological recovery (especially bladder function). The evidence strongly supports: the earlier the decompression, the better the outcome

The senior notes provide a useful decision matrix [3b]:

This framework applies broadly to all spinal pathology. The key teaching point is: neurological deterioration in a "mechanically stable" spine should prompt you to look for other causes — don't just assume it's progressive stenosis.

From the neurosurgical teaching:

Conservative management ^[37]:

• Physiotherapy
• Analgesia

Surgical treatment if ^[37]:

• Progressive neurological deficit
• Myelopathy / Radiculopathy
• Intractable pain

The example given is anterior corpectomy ^[37] — used when the compression is from the vertebral body itself (tumour, burst fracture, OPLL).

Patients with developmental stenosis (short pedicles) ^[5] have a particular challenge:

• Reoperation rate: 13% of patients, 50% at adjacent levels, 3.3% patients per year ^[5]
• This is because the entire canal is narrow — treating one level doesn't prevent adjacent levels from becoming symptomatic later. These patients require careful counselling about the likelihood of future surgery

This is the most feared complication of lumbar spinal stenosis and the most important to rule out in every patient ^[1].

• Mechanism: Severe stenosis or large central disc herniation ^[1] → massive compression of the cauda equina nerve roots within the thecal sac → complete or near-complete conduction block
• Clinical features ^[1]:
  • Acute LBP
  • Sciatica (often bilateral)
  • Saddle paraesthesia (S2–S5 dermatomes: perineum, inner thighs, perianal region)
  • LL weakness
  • Gait dysfunction
  • Sphincter incontinence — urinary retention with overflow incontinence, faecal incontinence
• Can occur via two pathways ^[1]:
  • Large central disc herniation — acute event, often dramatic onset
  • Chronic deterioration of spinal stenosis — insidious, progressive, may be precipitated by a minor event (e.g., a fall, sitting for a long flight)

"Sphincter dysfunction — a point of no return" ^[38]. This is a critical teaching point from the neurosurgical lecture. Once bladder/bowel function is lost, recovery is poor even with decompressive surgery. This is why CES is a surgical emergency — every hour of delay reduces the chance of recovering sphincter function.

• Mechanism: Ongoing compression of the cervical spinal cord → demyelination, axonal loss, ischaemia → progressive UMN dysfunction
• Chronic progressive / acute exacerbation [38a] — cervical myelopathy typically follows a stepwise or slowly progressive course, but can suddenly worsen after minor trauma (e.g., a fall, whiplash)
• Consequences: Progressive hand clumsiness → difficulty walking → wheelchair dependence → bladder dysfunction
• The spinal cord is very unforgiving ^[38] — unlike peripheral nerves, central nervous system neurons do not regenerate effectively. Once myelomalacia (T2 signal change in cord) develops, it represents irreversible damage
• Complete injury — prognosis is generally poor. Incomplete injury — prognosis highly variable ^[38]

This is a particularly important clinical scenario highlighted in the lectures:

• Old man with degenerated spine after a fall → central cord syndrome [38a]
• Mechanism: A patient with pre-existing spinal stenosis ^[11] has a constitutionally or degeneratively narrowed canal. Even a low-energy hyperextension injury (e.g., a simple fall in an elderly person) can cause the cord to be pinched between the anterior osteophytes/disc and the posterior buckling ligamentum flavum → cord contusion, predominantly affecting the central part of the cord
• Why central? The corticospinal tracts are somatotopically organised with upper limb fibres medially (centrally) and lower limb fibres laterally. Central cord injury therefore preferentially affects the arms more than the legs
• Clinical pattern: Upper limb weakness > lower limb weakness ("cape-like" motor loss), variable sensory loss, bladder dysfunction
• Epidemiology of spinal cord injury — bimodal distribution: young adults (high-energy trauma), old adults (low-energy trauma, osteoporotic bone, pre-existing spinal stenosis) ^[11]

• Radiculopathy progression: Ongoing nerve root compression → Wallerian degeneration of the axon → muscle denervation → irreversible wasting and weakness. Initially, nerve root compression causes demyelination (which is reversible with decompression), but prolonged compression leads to axonal loss (which is not)
• Foot drop (L5 radiculopathy): If L5 root compression from stenosis is left untreated → progressive weakness of tibialis anterior and EHL → inability to dorsiflex the foot → tripping, falls
• Chronic pain syndrome: Prolonged neural compression → central sensitisation in the dorsal horn → neuropathic pain that persists even after the structural problem is addressed

• Progressive reduction in walking distance → reduced mobility → cardiovascular deconditioning, muscle atrophy, weight gain, social isolation, depression
• This creates a vicious cycle: less exercise → weaker paraspinal muscles → less dynamic stabilisation → more load on degenerative structures → worse symptoms → even less exercise
• Falls risk increases — especially in cervical myelopathy with gait disturbance and proprioceptive loss

• Bladder disturbance ^[2] — compression of sacral nerve roots (S2–S4) controlling the detrusor muscle and external urethral sphincter
• Initially: urgency, frequency (irritative symptoms from partial denervation)
• Late: urinary retention with overflow incontinence (detrusor failure) → secondary UTIs, hydronephrosis, renal impairment if chronic
• Long-term issues with neurogenic bladder ^[38]