Spinal Stenosis

1. Clinical Overview

Summary

Lumbar Spinal Stenosis (LSS) is a degenerative narrowing of the spinal canal, lateral recess, or neural foramina, leading to compression of the neural elements. It is the leading cause of spinal surgery in patients > 65 years and represents one of the most common indications for elective spinal procedures in the elderly population. [1,2] The classic symptom is Neurogenic Claudication: leg pain, numbness, or heaviness precipitated by walking and standing, and characteristically relieved by flexion (sitting, squatting, or leaning forward). This distinguishes it from Vascular Claudication, which is relieved simply by standing still. [3,4]

The pathoanatomy involves a classic triad of degenerative changes:

1. Disc Bulge/Herniation (Anterior compression)
2. Facet Joint Hypertrophy (Posterolateral compression)
3. Ligamentum Flavum Buckling/Hypertrophy (Posterior compression)

These combined degenerative processes transform the normally oval spinal canal into a characteristic "Trefoil" (cloverleaf) shape on axial MRI imaging. [5,6] Management ranges from conservative strategies (physiotherapy, epidural steroid injections, analgesics) to surgical intervention via Decompression (Laminectomy), with or without fusion depending on the presence of instability. [7,8]

Key Facts

The "Shopping Trolley Sign": Approximately 85-90% of patients with LSS report symptomatic relief by leaning forward on a shopping trolley or walking aid. This occurs because spinal flexion increases the canal diameter by 12-15% through stretching and thinning of the Ligamentum Flavum, reducing compression of neural elements. [9] Conversely, extension (such as walking downhill or standing erect) causes the ligamentum to buckle anteriorly into the canal, exacerbating symptoms.

The "Simian Stance": Patients characteristically adopt a stooped, forward-flexed posture during ambulation (hips and knees flexed, lumbar kyphosis) to maintain maximal canal capacity and minimize neural compression. This compensatory gait pattern is pathognomonic for neurogenic claudication.

Neurogenic vs Vascular Claudication Differentiation:

• Vascular: "I have to stop and stand still" (Pulses absent/diminished, ankle-brachial index less than 0.9)
• Neurogenic: "I have to sit down or bend over" (Pulses present, normal vascular examination)

The Bicycle Test: A pathognomonic clinical sign where a patient who cannot walk 100 yards on flat ground can cycle 3-5 miles without symptoms. Cycling maintains spinal flexion (keeping the canal open), whereas walking involves extension. Vascular claudication patients cannot cycle due to metabolic ischemia regardless of posture. [10]

Clinical Pearls

"Degenerative Spondylolisthesis Association": Lumbar spinal stenosis frequently coexists with degenerative spondylolisthesis (most commonly L4 on L5 slip). The pathophysiology is interconnected: facet joint degeneration causes both canal narrowing AND loss of the mechanical restraint preventing anteroposterior translation. These patients often require instrumented fusion in addition to decompression to prevent progressive slip and post-operative instability. [11,12]

"It's Arthritis of the Spine": When counseling elderly patients, framing stenosis as "internal arthritis of the spine pressing on nerves" is less anxiety-provoking than terms like "spinal compression" or "nerve damage," improving patient understanding and compliance.

"The Two-Level Rule": Symptomatic stenosis is most commonly multilevel (L3-L4 and L4-L5). Single-level stenosis should prompt careful evaluation for alternative diagnoses or contributory pathology such as synovial cysts or conjoined nerve roots.

---

2. Epidemiology

Demographics

Age Distribution: Lumbar spinal stenosis is predominantly a disease of the elderly, with peak incidence between 60-75 years. Onset before age 50 should raise suspicion of congenital short pedicles, achondroplasia, or early-onset degenerative changes. [13]

Prevalence:

• Radiological stenosis is detected in 20-30% of asymptomatic individuals over 60 on MRI imaging
• Symptomatic stenosis requiring intervention occurs in approximately 8-11% of the general population over 50
• The key principle: "Treat the patient, not the MRI" - imaging findings must correlate with clinical presentation [14,15]

Gender: Slight male predominance for central stenosis (M:F ratio 1.2:1), but degenerative spondylolisthesis with stenosis shows strong female predominance (F:M ratio 4:1) due to hormonally-influenced ligamentous laxity. [16]

Risk Factors

Congenital/Developmental:

• Congenitally short pedicles (trefoil canal from birth) - presents with symptoms 15-20 years earlier (age 40-45)
• Achondroplasia - severe congenital narrowing
• Developmental spinal canal stenosis - interpedicular distance less than 16mm on AP radiograph

Acquired/Degenerative:

• Advanced age (strongest predictor)
• Occupation: Heavy manual labor, repetitive flexion-extension loading
• Obesity (BMI > 30) - increases mechanical loading and accelerates facet degeneration
• Previous lumbar spine surgery - altered biomechanics
• Genetic predisposition - familial clustering observed [17]

Rare Causes:

• Acromegaly - soft tissue and bony hypertrophy
• Paget's Disease - bony expansion
• Fluorosis - ligamentous ossification
• Diffuse Idiopathic Skeletal Hyperostosis (DISH) - ligamentous calcification

---

3. Pathophysiology

Anatomical Changes

The pathogenesis of lumbar spinal stenosis is a progressive, multifactorial degenerative cascade:

Stage 1: Disc Degeneration (Age 30-50)

• Loss of proteoglycan content and hydration
• Disc height loss and bulging
• Transfer of axial load to posterior elements (facet joints)

Stage 2: Facet Joint Arthropathy (Age 40-60)

• Increased facet joint loading → synovitis and cartilage degeneration
• Osteophyte formation and capsular hypertrophy
• Facet joint effusions and synovial cysts
• Lateral recess and foraminal narrowing

Stage 3: Ligamentous Changes (Age 50-70)

• Ligamentum Flavum hypertrophy (most significant dynamic factor)
• Mechanical buckling during extension
• Microscopic: elastin fiber degeneration, collagen deposition, fibrosis
• Thickness increases from normal 3-5mm to 6-8mm in severe stenosis [18,19]

Stage 4: Canal Remodeling (Age 60+)

• Combination of anterior (disc), lateral (facets), and posterior (ligamentum flavum) encroachment
• Transformation from oval to "Trefoil" (three-lobed cloverleaf) canal morphology
• Critical stenosis threshold: less than 100mm² cross-sectional area (normal 150-300mm²)

The "Trefoil" Canal Morphology

The normal lumbar spinal canal is oval or circular. In stenosis, encroachment from three directions creates the pathognomonic trefoil appearance on axial T2 MRI:

1. Anterior: Disc bulge, posterior osteophytes, endplate spurring
2. Posterior: Ligamentum Flavum hypertrophy and buckling (thickness > 5mm abnormal)
3. Posterolateral (Bilateral): Superior articular facet hypertrophy, facet joint effusion, synovial cysts

This three-dimensional narrowing creates a "triple crush" phenomenon on the cauda equina and nerve roots. [20]

Vascular Hypothesis ("Neurogenic Claudication")

The symptoms of neurogenic claudication are not purely mechanical compression but involve ischemic injury to neural elements:

Cauda Equina Blood Flow:

• Extension reduces epidural venous drainage and causes venous congestion
• Arterial supply to nerve roots becomes compromised below critical perfusion pressure
• Metabolic demand during walking exceeds ischemic supply → claudication symptoms
• Flexion restores venous drainage and arterial flow → symptom relief [21,22]

This explains why:

• Symptoms worsen with activity (increased metabolic demand)
• Relief requires sitting (not just stopping walking) to restore flow
• Epidural steroid injections provide temporary benefit by reducing venous congestion

Classification Systems

Schizas MRI Grading (Based on T2 Axial - Rootlet Morphology)

• Grade A: CSF clearly visible anterior and posterior to cauda equina - Mild stenosis
• Grade B: Rootlets occupy entire dural sac but remain distinguishable - Moderate stenosis
• Grade C: No CSF visible, rootlets not individually distinguishable - Severe stenosis
• Grade D: Extreme compression, "bone on bone" appearance - Extreme stenosis [23]

Anatomical Classification

• Central canal stenosis - sagittal diameter less than 10mm, area less than 100mm²
• Lateral recess stenosis - depth less than 3mm (normal 5mm), nerve root compression
• Foraminal stenosis - narrowing of intervertebral foramen, exiting root compression

Etiological Classification

• Congenital/Developmental - idiopathic, achondroplasia
• Acquired/Degenerative - most common (> 95% of cases)
• Combined - congenital narrowing + superimposed degeneration
• Iatrogenic - post-laminectomy, post-fusion adjacent segment disease

---

4. Clinical Presentation

Cardinal Symptom: Neurogenic Claudication

Definition: Position-dependent leg pain, numbness, heaviness, or weakness precipitated by lumbar extension (walking, standing) and relieved by lumbar flexion (sitting, squatting, leaning forward). [24]

Classic Description: "Walking through treacle" or "legs turning to concrete." Patients describe a progressive heaviness and fatigue in the legs during ambulation, often bilateral but may be asymmetric.

Key Distinguishing Features:

Associated Symptoms

Lower Limb Symptoms:

• Pain: Typically bilateral, buttock/thigh/calf distribution, non-dermatomal
• Paresthesias: "Pins and needles," electric shocks (more common than in vascular disease)
• Weakness: Insidious, worse with walking, improves with rest
• Leg "giving way": Functional weakness from pain/ischemia

Lumbar Spine Symptoms:

• Axial low back pain: Present in 70-80%, often long-standing mechanical pain
• Morning stiffness: Common (coexistent degenerative changes)
• Reduced spinal mobility: Loss of lumbar lordosis, fixed flexed posture

Positional Characteristics:

• Aggravating: Walking, standing erect, lumbar extension, walking downhill, lying prone
• Relieving: Sitting, squatting, leaning forward (shopping trolley), walking uphill, lying supine with hips flexed

Radiculopathy vs Claudication

Radiculopathy (lateral recess/foraminal stenosis affecting specific root):

• Dermatomal pain distribution (e.g., L5 → dorsum of foot, L4 → anterior thigh)
• Myotomal weakness (e.g., L5 → foot drop, L4 → quadriceps weakness)
• Reflex changes (L4 → knee jerk, S1 → ankle jerk)
• Often unilateral

Claudication (central canal stenosis):

• Non-dermatomal, bilateral leg heaviness
• Activity-related onset
• Position-dependent

Many patients have mixed presentations with central stenosis causing claudication and lateral recess stenosis superimposing radiculopathy.

Physical Examination

At Rest (Supine/Sitting):

• Examination is characteristically NORMAL in most cases
• Peripheral pulses: Palpable (differentiates from PVD)
• Straight leg raise: Usually negative (unlike acute disc herniation)
• Motor/sensory examination: Often normal or subtle deficits
• Reflexes: May be preserved or symmetrically diminished (age-related)

Provocative Tests:

Extension Test:

1. Ask patient to stand and extend lumbar spine (lean backwards)
2. Hold position for 30-60 seconds
3. Positive test: Reproduces leg symptoms (pain, numbness, weakness)
4. Sensitivity ~60%, Specificity ~70% [25]

Walking Test:

1. Ask patient to walk normally in corridor until symptoms develop
2. Measure distance to onset of claudication
3. Ask patient to sit/flex spine → symptoms should resolve within 2-5 minutes
4. High clinical utility for confirming neurogenic claudication

The "Stoop Test":

1. Patient walks until symptoms develop
2. Patient stoops forward (flexes spine) while standing
3. Symptom relief without sitting confirms neurogenic etiology

Specific Neurological Findings (if severe/chronic):

• L4 root: Quadriceps weakness (difficulty rising from chair), diminished knee jerk
• L5 root: Foot drop (weakness of ankle/toe dorsiflexion), numbness first web space
• S1 root: Plantarflexion weakness (cannot tiptoe walk), absent ankle jerk, numbness lateral foot

Red Flag Symptoms (Require Urgent Assessment)

1. Cauda Equina Syndrome:

   • Urinary retention or incontinence
   • Fecal incontinence or severe constipation
   • Saddle anaesthesia (perineal numbness)
   • Progressive bilateral leg weakness
   • Action: MRI within 24 hours, urgent neurosurgical/spinal referral

2. Rapidly Progressive Motor Deficit:

   • Acute foot drop or quadriceps weakness over days
   • Suggests acute-on-chronic compression or vascular event
   • Action: Urgent MRI, consider surgical decompression

3. Cervical Stenosis/Myelopathy (if neck involvement):

   • Upper limb symptoms, hand clumsiness
   • Gait ataxia (wide-based, unsteady)
   • Hyperreflexia, Babinski sign, clonus
   • Action: Cervical spine MRI, risk of spinal cord injury with minor trauma

---

5. Investigations

Imaging

MRI Lumbar Spine (Gold Standard) [26]

Sequences:

• T2 Sagittal: Overall canal assessment, disc hydration, spinal alignment
• T2 Axial: Cross-sectional area measurement, trefoil morphology, Schizas grading
• T1 Sagittal: Bony anatomy, facet joints, foraminal stenosis assessment

Quantitative Assessment:

• Normal canal area: 150-300 mm²
• Stenosis: less than 100 mm²
• Severe stenosis: less than 75 mm²
• Critical stenosis: less than 50 mm²

Qualitative MRI Signs:

"Sedimentation Sign" (High Specificity for Severe Stenosis):

• Normally, nerve rootlets float posteriorly (dorsally) in CSF in supine position due to gravity
• In severe stenosis, rootlets remain clumped centrally or anteriorly (no CSF space to "sediment")
• Positive sign = Severe stenosis (Schizas C/D) [27]

Other MRI Findings:

• Ligamentum flavum thickness: Normal 3-5mm; stenosis > 5mm; severe > 7mm
• Facet joint effusion/hypertrophy: "Facet arthropathy"
• Disc bulging/herniation: Anterior compression component
• Lateral recess depth: Normal 5mm; stenosis less than 3mm
• Foraminal stenosis: Grading 0 (normal) to III (severe root compression)

T2 Signal Changes (Poor Prognostic Signs):

• Cauda equina high T2 signal: Chronic compression/ischemia
• Ligamentum flavum signal change: Calcification/ossification

Standing AP/Lateral Lumbar Radiographs

Purpose: Assess for spondylolisthesis and overall spinal alignment

Key Measurements:

• Meyerding Grading of spondylolisthesis: Grade I (0-25% slip), II (25-50%), III (50-75%), IV (> 75%)
• Interpedicular distance (AP view): less than 16mm suggests congenital stenosis
• Disc height loss: Indirect marker of degeneration
• Facet joint arthropathy: Sclerosis, osteophytes

Flexion-Extension Lateral Radiographs:

• Purpose: Detect dynamic instability
• Measurement: Anterior-posterior translation between flexion and extension
• Instability definition: > 3-4mm translation or > 10° angular change
• Clinical significance: Instability mandates fusion in addition to decompression [28]

CT Lumbar Spine

Indications:

• MRI contraindicated (pacemaker, claustrophobia)
• Superior bony detail (facet anatomy, calcification, ossification)
• Pre-operative planning for complex deformity

Limitations:

• Inferior soft tissue contrast (neural elements, ligamentum flavum)
• Radiation exposure
• Does not visualize dynamic (positional) changes

CT Myelography

Indications:

• Cannot tolerate MRI
• Discordant MRI and clinical findings
• Post-operative assessment (artifact from metalwork)

Technique:

• Intrathecal contrast injection
• CT imaging with contrast in thecal sac outlining nerve roots
• Can perform in extension to assess dynamic stenosis

Electrodiagnostic Studies

Nerve Conduction Studies (NCS) / Electromyography (EMG):

Indications:

• Differentiate stenosis from peripheral neuropathy (e.g., diabetic neuropathy)
• Distinguish stenosis from motor neuron disease
• Identify specific root level involvement if imaging equivocal

Findings in LSS:

• Chronic radiculopathy: Denervation (fibrillations, positive sharp waves), reduced recruitment
• Multi-level involvement: Multiple lumbosacral root abnormalities
• NCS: Typically normal (pure axonal nerve root lesion proximal to DRG)

Limitations:

• Normal EMG does not exclude stenosis (many patients have normal studies)
• Cannot differentiate stenosis from other causes of radiculopathy

Vascular Studies (To Exclude PVD)

Ankle-Brachial Index (ABI):

• Normal: 0.9-1.3
• PVD: less than 0.9
• Critical ischemia: less than 0.5
• Utility: First-line test to exclude vascular claudication in patients with atypical features

Duplex Ultrasound / CT Angiography:

• If ABI abnormal or high clinical suspicion of concurrent PVD
• 10-15% of elderly patients have concurrent stenosis AND PVD ("tandem pathology")

Laboratory Tests

Not routinely indicated, but consider:

• Inflammatory markers (ESR, CRP): If suspected infection, malignancy, inflammatory arthropathy
• Calcium/PTH/Vitamin D: If osteoporosis concern (pre-operative fusion planning)
• PSA (men > 50): Screen for prostate cancer (can metastasize to spine)

---

6. Differential Diagnosis

Vascular Claudication (PAD)

Lumbar Disc Herniation

• Acute onset (stenosis is insidious)
• Positive SLR (stenosis usually negative)
• Single dermatomal radiculopathy (stenosis often bilateral/multi-level)
• Younger age (30-50 vs 60+ for stenosis)

Degenerative Spondylolisthesis

• Often coexists with stenosis
• Axial low back pain more prominent
• Radiographs demonstrate slip
• May require fusion

Trochanteric Bursitis / Hip Arthritis

• Lateral hip pain radiating to lateral thigh
• Worse with hip abduction, lying on affected side
• Tenderness over greater trochanter
• Hip examination/radiographs diagnostic

Diabetic/Peripheral Neuropathy

• Symmetrical distal stocking-glove distribution
• Constant symptoms (not position-dependent)
• Absent ankle reflexes bilaterally
• EMG/NCS: diffuse sensorimotor polyneuropathy

Spinal Tumor/Infection

• Progressive constant pain, worse at night
• Systemic features (fever, weight loss)
• Elevated inflammatory markers
• MRI: focal lesion, marrow signal change, epidural collection

---

7. Management Algorithm

                 LEG PAIN / CLAUDICATION SYMPTOMS
                              ↓
                   CLINICAL ASSESSMENT
            (History, Examination, Pulses, ABI)
                              ↓
                 NEUROGENIC OR VASCULAR?
             (Bicycle Test / Stoop Test / Flexion Relief)
            ┌─────────────────┴─────────────────┐
        VASCULAR                           NEUROGENIC
      (Refer Vascular)                          ↓
                                    SYMPTOMS LIMIT QoL?
                                    (Walking distance less than 200m)
                                    ┌──────────┴──────────┐
                                   NO                    YES
                                    ↓                     ↓
                              REASSURE              MRI LUMBAR SPINE
                              MONITOR                     ↓
                           (Annual review)      STENOSIS CONFIRMED?
                                                ┌────────┴────────┐
                                               NO                YES
                                                ↓                 ↓
                                         (Alternative Dx)   CONSERVATIVE TRIAL
                                                          (Physio + Analgesia)
                                                                  ↓
                                                           3-6 MONTHS
                                                                  ↓
                                                      ADEQUATE SYMPTOM CONTROL?
                                                      ┌──────────┴──────────┐
                                                     YES                   NO
                                                      ↓                     ↓
                                               CONTINUE              EPIDURAL INJECTION
                                                                    (If severe, short-term)
                                                                            ↓
                                                                    SURGICAL ASSESSMENT
                                                                            ↓
                                                                 FIT FOR SURGERY?
                                                                 IMAGING-CLINICAL MATCH?
                                                                 ┌──────────┴──────────┐
                                                                NO                    YES
                                                                 ↓                     ↓
                                                          OPTIMIZE MEDICAL    ASSESS FOR INSTABILITY
                                                                              (Flexion-Extension XR)
                                                                              ┌──────────┴──────────┐
                                                                     STABLE                   UNSTABLE
                                                                              ↓                     ↓
                                                                       DECOMPRESSION       DECOMPRESSION
                                                                         ALONE                + FUSION
                                                                      (Laminectomy)        (TLIF/PLIF)

---

8. Management Protocols

Conservative Management

Indication: First-line for all patients without red flags, duration 3-6 months minimum trial [29]

1. Physiotherapy

Flexion-Based Exercise Program:

• Core stability training: Transversus abdominis, multifidus strengthening
• Flexion exercises: Posterior pelvic tilt, pelvic tilts, knee-to-chest stretches
• Avoid extension: McKenzie extension exercises (used for disc herniation) worsen stenosis
• Aerobic conditioning: Stationary cycling, swimming (maintains flexed spine)
• Postural education: Avoid prolonged standing, use of walking aids with handles to maintain flexion

Efficacy: 30-40% symptom improvement in appropriately selected patients, primarily in mild-moderate stenosis

2. Pharmacological Management

Analgesics:

• Paracetamol: 1g QDS (first-line, limited efficacy for neuropathic pain)
• NSAIDs: Ibuprofen 400mg TDS, Naproxen 500mg BD (caution in elderly: GI, renal, CVS risk)
• Weak opioids: Codeine, Tramadol (short-term only, addiction risk, limited evidence)

Neuropathic Pain Agents:

• Gabapentin: Start 300mg OD, titrate to 300-600mg TDS (sedation, dizziness common)
• Pregabalin: Start 75mg BD, titrate to 150-300mg BD (fewer drug interactions than gabapentin)
• Duloxetine: 60mg OD (SNRI, also treats coexistent depression)
• Amitriptyline: 10-25mg nocte (sedating, anticholinergic side effects in elderly)

Limited Evidence:

• Calcitonin: Previously used, no longer recommended (no proven benefit) [30]
• Methylcobalamin (Vitamin B12): Popular in Asia, weak evidence

3. Epidural Steroid Injections

Technique:

• Interlaminar approach: Midline entry between laminae, contrast confirms epidural spread
• Transforaminal approach: Targets specific nerve root, higher risk but more targeted delivery
• Caudal approach: Via sacral hiatus, less precise but safest

Medication: Triamcinolone 80mg or Methylprednisolone 80mg + Local anesthetic (Bupivacaine 0.25%)

Mechanism:

• Reduces venous congestion and neural edema
• Anti-inflammatory effect on inflamed nerve roots
• Does NOT reverse structural stenosis

Efficacy:

• Short-term benefit (3-6 months) in 50-60% of patients
• No long-term alteration of disease progression
• May serve as "diagnostic block" to confirm pain generator
• Can delay surgery or provide temporary relief for non-operative candidates [31]

Complications (Rare less than 1%):

• Dural puncture headache
• Infection (epidural abscess)
• Bleeding (epidural hematoma)
• Transient neurological deficit

Contraindications:

• Active infection
• Coagulopathy/anticoagulation
• Severe spinal deformity (technical difficulty)

4. Walking Aids / Assistive Devices

• Rolling walker with handles: Maintains flexion, reduces symptoms, improves walking distance
• Lumbosacral corset: Limited evidence, may provide proprioceptive feedback
• Cane/Crutches: Less effective (do not maintain flexion)

Surgical Management

General Indications: [32,33]

1. Failure of conservative management (3-6 month trial)
2. Significant functional impairment (walking distance less than 200m, severe QoL impact)
3. Progressive neurological deficit
4. Cauda equina syndrome (absolute emergency indication)

Contraindications to Surgery:

• Severe medical comorbidity (ASA IV-V)
• Active infection
• Severe osteoporosis (relative - requires careful surgical planning)
• Lack of imaging-clinical correlation (symptoms do not match MRI level)

---

Surgical Options

1. Decompression Alone (No Fusion)

Indications:

• Central canal or lateral recess stenosis
• No instability (stable spondylolisthesis Grade I or less, less than 3mm translation on dynamic XR)
• Minimal facet joint resection required (less than 50% bilateral)

Procedures:

Laminectomy (Open Decompression):

• Technique: Remove spinous process + lamina + ligamentum flavum + medial facets
• Extent: Typically 1-2 levels (L3-L4, L4-L5 most common)
• Goal: Adequate decompression of neural elements, preserve facet joint integrity
• Success rate: 70-80% good/excellent outcomes for leg pain at 2-4 years [34]

Laminotomy / Fenestration (Minimally Invasive):

• Technique: Undercutting laminotomy, preserve midline structures
• Benefits: Less tissue disruption, faster recovery, less postoperative instability
• Limitations: Limited visualization, technically demanding, not suitable for severe/multilevel stenosis

Bilateral Decompression via Unilateral Approach:

• Technique: Ipsilateral decompression, then undercut to contralateral side
• Benefits: Preserve interspinous ligaments, reduce instability risk
• Requires: Experienced surgeon, appropriate instrumentation

Outcomes (Weinstein SPORT Trial - 2008): [35]

• Surgery group showed significantly greater improvement in pain and function vs non-operative at 2 and 4 years
• Effect size moderate to large (SF-36 bodily pain: 22-point difference favoring surgery)
• Unlike disc herniation (which often improves spontaneously), stenosis is structural and mechanical - rarely improves without surgery
• Crossover common: 40% of non-op patients eventually had surgery

Predictors of Success:

• ✅ Severe stenosis on imaging (Schizas C/D)
• ✅ Classic neurogenic claudication
• ✅ Absence of significant back pain (leg pain primary complaint)
• ✅ Younger age (less than 75)
• ✅ Absence of significant medical comorbidity
• ❌ Predominantly axial back pain (poor surgical outcome)
• ❌ Mild stenosis (imaging-clinical mismatch)
• ❌ Depression, chronic pain syndrome, litigation

2. Decompression + Fusion

Indications: [36]

1. Degenerative spondylolisthesis with stenosis (especially Grade II or greater)
2. Dynamic instability: > 3-4mm translation on flexion-extension radiographs
3. Iatrogenic instability risk: > 50% bilateral facet resection required for adequate decompression
4. Degenerative scoliosis: > 10° Cobb angle with rotational component
5. Recurrent stenosis: Previous decompression with instability

Fusion Techniques:

Posterolateral Fusion (PLF):

• Bone graft in lateral gutters
• With instrumentation (pedicle screws + rods) - modern standard
• Without instrumentation - rarely performed (high pseudarthrosis rate)

Posterior Lumbar Interbody Fusion (PLIF):

• Cage placement in disc space from posterior approach
• Better sagittal alignment restoration
• Indirect foraminal decompression
• Risk of nerve root traction injury

Transforaminal Lumbar Interbody Fusion (TLIF):

• Unilateral approach to disc space
• Less nerve retraction than PLIF
• Cage + posterolateral fusion
• Most common technique for single-level stenosis with spondylolisthesis

Lateral Lumbar Interbody Fusion (LLIF/XLIF):

• Retroperitoneal transpsoas approach
• Large cage footprint (excellent subsidence resistance)
• Indirect decompression via disc height restoration
• Risk of psoas/lumbar plexus injury

Fusion Outcomes:

• Arthrodesis rate: 85-95% with instrumented fusion
• Clinical success: 70-85% good/excellent outcomes
• Complication rate: Higher than decompression alone (10-20% vs 5-10%)

Controversy: Fusion vs Decompression Alone in Degenerative Spondylolisthesis:

• SLIP Trial (Sweden, 2017): No difference in patient-reported outcomes between fusion + decompression vs decompression alone at 2 years for low-grade spondylolisthesis [37]
• Usual practice: Most surgeons fuse Grade II slips, debate continues for Grade I

---

9. Complications

Intra-operative Complications

Dural Tear (Durotomy)

Incidence: 5-15% (higher in revision surgery, severe stenosis, ossified ligamentum flavum) [38]

Causes:

• Adherent dura to hypertrophied/ossified ligamentum flavum
• Thin, friable dura in elderly
• Excessive traction on nerve roots
• Unrecognized lateral recess extension

Recognition:

• CSF leak visualization
• "Wet field" that doesn't clear with irrigation/suction
• Nerve root herniation through defect

Management:

• Primary repair: 5-0/6-0 suture, watertight closure
• Patch: If large defect, use dural substitute/autograft (fat, muscle)
• Fibrin glue: Adjunct sealant
• Post-op: Flat bed rest 24-48 hours (controversial - some advocate early mobilization)

Complications of Unrecognized Durotomy:

• Pseudomeningocele (CSF collection)
• CSF fistula (persistent leak)
• Meningitis (rare)
• Nerve root entrapment in pseudomeningocele

Nerve Root Injury

Incidence: 1-3%

Mechanisms:

• Direct trauma (sharp dissection, pedicle screw malposition)
• Traction injury (excessive retraction)
• Thermal injury (cautery, burr heat)
• Ischemia (excessive dissection of root vasculature)

Presentation: Immediate post-operative dermatomal sensory/motor deficit

Management: Observation (most are neurapraxia and recover), re-exploration if complete deficit

Vascular Injury

Rare (less than 1%): Great vessels anterior to spine (aorta, IVC, iliac vessels)

Mechanism: Anterior perforation during disc space preparation (PLIF/TLIF) or pedicle screw placement

Presentation: Hemodynamic instability, expanding retroperitoneal hematoma

Management: Immediate vascular surgery consultation, anterior approach for repair, resuscitation

Post-operative Complications

Surgical Site Infection (SSI)

Incidence:

• Decompression alone: 1-3%
• Instrumented fusion: 3-8% [39]

Risk Factors: Diabetes, obesity (BMI > 35), prolonged operative time, revision surgery, immunosuppression

Classification:

• Superficial: Skin/subcutaneous tissue within 30 days
• Deep: Muscle/fascia within 30-90 days
• Hardware infection: May present late (months to years)

Organisms: Staphylococcus aureus (50%), S. epidermidis (30%), Propionibacterium acnes (late infections)

Management:

• Superficial: Antibiotics ± wound care
• Deep: Surgical debridement + 6 weeks IV antibiotics (retain hardware if possible)
• Hardware infection: Debridement, consider hardware retention vs removal (depends on fusion status)

Adjacent Segment Disease (ASD)

Definition: Symptomatic degeneration at level above or below fusion

Incidence: 10-20% over 10 years post-fusion [40]

Pathophysiology:

• Increased biomechanical stress at adjacent mobile segment
• Accelerated facet degeneration and disc degeneration
• Debate: true iatrogenic vs natural history of degenerative process

Presentation: Recurrent stenosis symptoms 5-10 years post-fusion

Management: Revision surgery (extend fusion) if conservative measures fail

Prevention: Minimize fusion levels, preserve facet joints, maintain sagittal alignment

Epidural Hematoma

Incidence: 1-2%

Risk Factors: Inadequate hemostasis, anticoagulation, hypertension, large dead space

Presentation: Acute neurological deterioration within 24-48 hours post-op (leg weakness, cauda equina symptoms)

Diagnosis: Urgent MRI

Management: Emergent re-exploration and evacuation if symptomatic

Pseudarthrosis (Non-union)

Definition: Failure of fusion mass to consolidate (> 12 months)

Incidence:

• Instrumented PLF: 5-10%
• Non-instrumented fusion: 30-40%

Risk Factors: Smoking, diabetes, obesity, NSAIDs, multilevel fusion, revision surgery

Presentation: Persistent mechanical back pain, hardware failure (screw breakage)

Diagnosis: CT scan (bridging bone assessment), dynamic radiographs (motion > 3mm)

Management: Revision fusion if symptomatic

Hardware Complications

Pedicle Screw Malposition: 5-10%

• Medial breach: Risk nerve root injury (usually recognized intra-op)
• Lateral breach: Usually clinically silent
• Anterior breach: Risk vascular injury

Screw Loosening/Breakage: Suggests pseudarthrosis or inadequate fixation

Proximal Junctional Kyphosis: Fracture or collapse at upper instrumented vertebra (long fusions)

Medical Complications

Cardiovascular: MI, DVT/PE (elderly population, prolonged surgery, immobility)

Pulmonary: Pneumonia, atelectasis (general anesthesia, pain limiting deep breathing)

Urinary: Retention (common in elderly, instrumentation), UTI

Delirium: 10-20% in elderly post-operatively (multifactorial: anesthesia, opioids, unfamiliar environment)

---

10. Prognosis

Natural History (Untreated)

Lumbar spinal stenosis is a chronic progressive condition:

• Stable symptoms: 30-40% (do not worsen significantly over years)
• Gradual deterioration: 50-60% (slow progression, increasing disability)
• Spontaneous improvement: 10-15% (rare, usually related to activity modification) [41]

Progression to Cauda Equina: Rare (less than 1%), but risk increases with severe stenosis

Walking Distance: Median decline ~30m per year in symptomatic untreated patients

Surgical Outcomes

Short-term (1-2 years):

• Pain improvement: 70-85% significant reduction in leg pain
• Walking distance: Median improvement 200-400m
• Quality of life: Significant improvement in SF-36 physical function, bodily pain domains
• Return to activities: 60-70% return to desired activity level

Long-term (5-10 years): [42]

• Sustained benefit: 60-70% maintain good outcomes
• Deterioration: 20-30% experience gradual symptom recurrence (adjacent segment disease, re-stenosis, general degeneration)
• Re-operation rate: 10-20% over 10 years

Comparative Studies: Surgical outcomes superior to conservative management in appropriately selected patients with severe symptomatic stenosis and imaging correlation

Predictors of Poor Outcome

Patient Factors:

• Age > 80 years (increased comorbidity, frailty)
• BMI > 35 (higher complication rate)
• Smoking (impaired fusion, wound healing)
• Diabetes (infection risk, neuropathy confounds symptoms)
• Depression, chronic pain syndrome (central sensitization)
• Workers' compensation/litigation

Disease Factors:

• Predominantly axial back pain (vs leg pain) - strongest negative predictor
• Mild stenosis (imaging-clinical mismatch)
• Multilevel stenosis (> 3 levels)
• Significant spinal deformity (scoliosis > 30°)

Surgical Factors:

• Inadequate decompression (residual stenosis)
• Iatrogenic instability (excessive facet resection without fusion)
• Complications (infection, durotomy, nerve injury)

---

11. Patient Counseling

What is Spinal Stenosis?

"Spinal stenosis is a narrowing of the spinal canal - the tunnel in your backbone that carries nerves to your legs. It's caused by 'wear and tear' arthritis, similar to arthritis in a knee or hip, but it affects the inside of the spine. Over many years, bone spurs, thickened ligaments, and bulging discs gradually narrow this tunnel and squeeze the nerves."

Why Do My Legs Hurt When I Walk?

"The nerves in your spine need blood flow to work properly. When you stand up and walk, your back naturally arches slightly, which further narrows the already tight tunnel and reduces blood flow to the nerves. This causes your legs to feel heavy, numb, or painful - similar to how your heart muscle hurts if it doesn't get enough blood (angina)."

Why Does Bending Forward Help?

"Bending forward, sitting, or leaning on a shopping trolley opens up the spinal tunnel by 10-15%. This is like un-kinking a garden hose - it allows better blood flow to reach the nerves again. That's why you can lean on a shopping trolley for an hour but can't stand upright for 5 minutes."

Will It Get Worse?

"Spinal stenosis is usually a slowly progressive condition. Most people stay stable or gradually worsen over years. Sudden worsening is uncommon. We can manage symptoms with physiotherapy, pain medications, and sometimes injections. Surgery is reserved for people whose quality of life is significantly affected despite conservative treatment."

What Does Surgery Involve?

"The operation is called 'decompression.' We remove some of the thickened bone and ligament from the back of the spine to create more room for the nerves - like widening a tunnel. Most patients notice improvement in leg pain and walking distance. However, it does not cure arthritis in your back, so some back pain may persist."

Will I Need Fusion?

"Most patients need only decompression. However, if your spine is unstable (one bone slipping on another), we may need to 'fuse' the bones together with screws and rods to prevent the bones shifting after surgery. This is a bigger operation with a longer recovery, but it prevents the spine collapsing after decompression."

Recovery Timeline

• Hospital stay: 1-3 days (decompression alone), 3-7 days (fusion)
• Walking: Encourage walking day 1 post-op, gradually increase distance
• Return to sedentary work: 4-6 weeks (decompression), 8-12 weeks (fusion)
• Return to heavy manual work: 3-6 months
• Driving: 2-4 weeks (when comfortable with emergency stop)
• Maximum improvement: 6-12 months

Risks of Surgery

"All surgery carries risks. For spinal decompression, the main risks are:

• Infection (2-3%): May require antibiotics or further surgery
• Nerve damage (1-2%): Rarely, a nerve root may be injured, causing weakness or numbness
• CSF leak (5-10%): Tear in the nerve covering, usually repaired during surgery, may require extra bed rest
• Blood clot (1-2%): DVT or pulmonary embolism, prevented with blood thinners and early mobilization
• No improvement (15-20%): Some patients do not benefit from surgery

For fusion, risks are higher due to more extensive surgery, longer operative time, and implant-related complications."

---

12. Special Populations

Stenosis in Younger Patients (less than 50 years)

Causes:

• Congenital short pedicles (developmental stenosis)
• Achondroplasia (severe congenital stenosis)
• Early degenerative changes (heavy labor, genetic predisposition)
• Post-traumatic (fracture malunion)

Management: Similar principles, but higher threshold for surgery (longer life expectancy, cumulative surgical burden)

Stenosis in the Very Elderly (> 80 years)

Considerations:

• Higher perioperative risk (ASA III-IV)
• Medical comorbidities (cardiac, respiratory, renal)
• Polypharmacy, anticoagulation
• Frailty, cognitive impairment, limited mobility goals

Approach:

• Rigorous patient selection
• Optimize medical comorbidities pre-operatively
• Anesthetic assessment (consider regional vs general)
• Shorter procedures (limit fusion to 1-2 levels)
• Enhanced recovery protocols
• Multidisciplinary care (geriatrician, physiotherapist)

Outcomes: Age alone is not a contraindication - appropriately selected fit elderly patients benefit from surgery

Cervical Stenosis (Cervical Spondylotic Myelopathy)

Key Differences:

• Spinal cord compression (not cauda equina) → myelopathy (not claudication)
• Upper limb symptoms: Hand clumsiness, fine motor impairment
• Gait disturbance: Ataxic, wide-based (vs claudication in LSS)
• Upper motor neuron signs: Hyperreflexia, Babinski, clonus
• Lhermitte's sign: Electric shocks down spine with neck flexion

Management: Surgical decompression (anterior discectomy + fusion or posterior laminoplasty) recommended for moderate-severe myelopathy (progressive condition, does not improve spontaneously)

Tandem Stenosis (Cervical + Lumbar)

Incidence: 5-10% of LSS patients have coexistent cervical stenosis

Clinical Challenge: Differentiating symptoms (upper limb = cervical, lower limb = lumbar, but gait can be affected by both)

Management: Treat symptomatic/severe level first, staged procedures if both symptomatic

---

13. Evidence & Guidelines

Landmark Trials

SPORT Trial (Spine Patient Outcomes Research Trial) - 2008 [35]

Design: Multicenter RCT + observational cohort, 289 patients with LSS, surgery vs non-operative treatment

Findings:

• Primary outcome (SF-36 bodily pain, physical function): Significant improvement favoring surgery at 2 and 4 years
• Effect size: Moderate to large (bodily pain improvement: 22 points greater in surgical group)
• Crossover: High rate (30-40% non-op → surgery), suggesting conservative failure common
• Conclusion: Surgery provides greater benefit than conservative care for symptomatic severe LSS

Limitations: High crossover rate limits pure RCT interpretation (as-treated analysis showed stronger surgical benefit)

Maine Lumbar Spine Study - 2000 [43]

Design: Prospective cohort, 148 patients, surgical vs non-operative, 8-10 year follow-up

Findings:

• Surgical group superior outcomes at 1, 4, and 8-10 years
• Gap narrows over time (re-stenosis, adjacent segment disease, aging)
• Conclusion: Long-term benefit of surgery sustained but diminishes over time

Swedish Spinal Stenosis Study - 2013

Design: RCT, 94 patients, decompression vs decompression + fusion for degenerative spondylolisthesis

Findings:

• No difference in patient-reported outcomes (ODI, back/leg pain) at 2 years
• Higher complication rate in fusion group
• Conclusion: Routine fusion not superior to decompression alone for stable low-grade spondylolisthesis

SLIP Trial - 2017 [37]

Design: RCT, 247 patients, Sweden, decompression vs decompression + fusion for degenerative spondylolisthesis

Findings:

• No difference in primary outcome (Oswestry Disability Index) at 2 and 5 years
• Fusion group: longer operative time, more blood loss
• Conclusion: Challenges routine use of fusion for all spondylolisthesis cases

Clinical Guidelines

North American Spine Society (NASS) - 2011 [44]

Recommendations:

• Imaging: MRI is diagnostic gold standard (Grade A recommendation)
• Conservative management: Initial 3-6 month trial for most patients (Grade B)
• Epidural steroid injections: May provide short-term relief, no long-term benefit (Grade B)
• Surgery: Recommended for patients with persistent symptoms despite conservative care (Grade A)
• Fusion: Add fusion if instability present (Grade B)

National Institute for Health and Care Excellence (NICE) - UK

Recommendations:

• Consider surgery if conservative management fails and quality of life significantly impaired
• Shared decision-making regarding surgical risks/benefits
• Routine fusion not recommended for all cases

---

14. Examination Focus (FRCS/FRACS Viva)

Core Knowledge

Q1: Describe the pathoanatomy of lumbar spinal stenosis.

Model Answer: "Lumbar spinal stenosis is a degenerative condition causing narrowing of the spinal canal, lateral recess, or neural foramina. The pathoanatomy involves a triad of degenerative changes:

1. Disc degeneration: Loss of disc height and bulging encroaches anteriorly
2. Facet joint hypertrophy: Increased loading causes facet arthropathy with osteophytes and synovial hypertrophy, narrowing the lateral recess
3. Ligamentum flavum hypertrophy and buckling: The posterior ligament thickens (> 5mm) and buckles into the canal during extension

This creates the characteristic 'trefoil' canal morphology on axial MRI. The critical stenosis threshold is less than 100mm² cross-sectional area, compared to normal 150-300mm²."

Q2: What is the "Sedimentation Sign" on MRI and what does it indicate?

Model Answer: "The sedimentation sign is a qualitative MRI finding indicating severe stenosis. Normally, on supine T2 axial imaging, the cauda equina nerve rootlets float dorsally (posteriorly) in CSF due to gravity, creating a visible CSF space anteriorly. In severe stenosis, there is insufficient CSF space, so the rootlets remain clumped centrally or cannot sediment posteriorly. A positive sedimentation sign correlates with Schizas Grade C/D stenosis and indicates severe canal compromise. It has high specificity for clinically significant stenosis."

Q3: How do you differentiate neurogenic from vascular claudication clinically?

Model Answer: "There are several key differentiating features:

The bicycle test is pathognomonic: neurogenic patients can cycle (maintains flexion) but cannot walk, whereas vascular patients cannot perform either activity due to metabolic ischemia."

Q4: What are the indications for adding fusion to decompression in lumbar spinal stenosis?

Model Answer: "Fusion is indicated when there is instability or high risk of post-operative instability:

1. Pre-existing instability: Degenerative spondylolisthesis Grade II or greater, or dynamic instability (> 3-4mm translation on flexion-extension radiographs)
2. Iatrogenic instability risk: Decompression requiring > 50% bilateral facet resection
3. Degenerative scoliosis: Significant coronal deformity (> 10-15° Cobb angle) with rotational component
4. Recurrent stenosis: Previous decompression with post-operative instability

The rationale is that removing posterior stabilizing structures (lamina, facets) in an already unstable or at-risk spine will lead to progressive slip and mechanical back pain. However, recent trials (SLIP Trial 2017) suggest that routine fusion for all low-grade spondylolisthesis may not be necessary - careful patient selection is required."

Q5: Why do we avoid extension exercises in spinal stenosis physiotherapy?

Model Answer: "Extension exercises worsen stenosis symptoms through a mechanical mechanism. The hypertrophied and thickened ligamentum flavum (6-8mm in stenosis vs 3-5mm normal) buckles anteriorly into the spinal canal during extension, further reducing the already compromised canal diameter. This exacerbates neural compression and vascular compromise.

In contrast, flexion exercises are prescribed because flexion stretches and thins the ligamentum flavum, increasing canal diameter by 12-15% and reducing compression. This is the opposite of disc herniation management, where McKenzie extension exercises push the disc anteriorly away from the nerve root. Confusing these two conditions can lead to inappropriate physiotherapy and worsening symptoms."

Q6: Describe the Weinstein SPORT trial and its significance.

Model Answer: "The Spine Patient Outcomes Research Trial (SPORT), published in 2008 in the New England Journal of Medicine, was a landmark multicenter study comparing surgical decompression versus non-operative management for lumbar spinal stenosis. It included 289 patients followed for 2-4 years.

Key Findings:

• Surgical group showed significantly greater improvement in SF-36 bodily pain and physical function scores (effect size: 22 points favoring surgery)
• High crossover rate (30-40% non-operative patients eventually underwent surgery)
• As-treated analysis showed stronger surgical benefit

Significance: The trial demonstrated that unlike disc herniation (which often improves spontaneously), spinal stenosis is a structural mechanical problem that rarely resolves without surgery. It provided Level I evidence supporting surgery for appropriately selected patients with symptomatic severe stenosis failing conservative management. This trial fundamentally shaped modern surgical indications for LSS."

Q7: What is adjacent segment disease and how do you minimize this risk?

Model Answer: "Adjacent segment disease (ASD) is symptomatic degeneration at the level above or below a spinal fusion, occurring in 10-20% of patients over 10 years. The pathophysiology involves increased biomechanical stress at the adjacent mobile segment, accelerating facet and disc degeneration. There is debate whether this is true iatrogenic disease or simply the natural history of degenerative spinal disease.

Risk Minimization Strategies:

1. Minimize fusion levels: Decompress only symptomatic levels, avoid prophylactic fusion of asymptomatic adjacent levels
2. Preserve facet joints: Limit facet resection to less than 50% to maintain segmental stability
3. Restore sagittal alignment: Maintain or restore lumbar lordosis (reduces compensatory hypermobility at adjacent segments)
4. Appropriate patient selection: Avoid fusion in patients with only mild instability

If ASD develops, treatment is initially conservative, but 50% eventually require revision surgery to extend the fusion."

---

15. Clinical Cases

Case 1: Classic Neurogenic Claudication

Presentation: 68-year-old male, retired postman, presents with 18-month history of bilateral leg heaviness and pain when walking. He can walk only 150 yards before having to sit down. He notices he can lean on a shopping trolley and walk around a supermarket for an hour without difficulty. Symptoms are worse walking downhill. Past medical history: hypertension, type 2 diabetes. No back pain.

Examination: BMI 31, all peripheral pulses palpable, no varicose veins, normal neurological examination at rest. Extension test reproduces bilateral calf pain after 45 seconds.

Investigations: MRI lumbar spine shows severe central canal stenosis L3-L4 and L4-L5 (Schizas Grade C), ligamentum flavum hypertrophy, no spondylolisthesis. Standing radiographs show degenerative changes, no instability on flexion-extension views.

Management:

1. Initial 3-month trial of physiotherapy (flexion exercises, core stability) + Pregabalin 150mg BD
2. Minimal improvement, walking distance unchanged
3. Epidural steroid injection → 6 weeks relief, then symptom recurrence
4. Surgical option discussed: L3-L4, L4-L5 decompression (bilateral laminectomy)
5. Patient opts for surgery, undergoes uneventful bilateral laminectomy
6. 6-month post-op: Walking distance > 1 mile, satisfied with outcome, ODI improved from 58 to 22

Teaching Points: Classic presentation, appropriate conservative trial, clear surgical indication (severe stenosis, functional impairment, imaging-clinical correlation), decompression alone appropriate (no instability).

Case 2: Stenosis with Degenerative Spondylolisthesis

Presentation: 72-year-old female, 2-year history of bilateral leg pain and back pain. Walking distance 100 yards. Difficulty standing to cook meals. She has tried physiotherapy and multiple medications with minimal benefit.

Examination: Stooped posture, reduced lumbar lordosis, tenderness L4-L5. Neurological examination normal. Pulses present.

Investigations: MRI shows severe L4-L5 central stenosis with Grade I degenerative spondylolisthesis (L4 on L5). Flexion-extension radiographs show 2mm translation (stable slip).

Management: Dilemma: Decompression alone vs decompression + fusion?

• Arguments for fusion: Spondylolisthesis present, back pain prominent
• Arguments against: Stable slip (less than 3mm), Grade I only, SLIP trial showed no benefit

Decision: After MDT discussion and shared decision-making with patient:

• Proceed with L4-L5 decompression + TLIF fusion (given patient's prominent back pain and preference for comprehensive treatment)

Outcome: 12-month post-op, solid fusion, ODI 18, back and leg pain significantly improved, walking unlimited.

Teaching Points: Fusion vs no fusion debate for low-grade spondylolisthesis remains controversial. Patient factors (back pain severity, expectations) and surgeon experience influence decision-making. SLIP trial suggests decompression alone may suffice in many cases, but fusion still appropriate in selected patients.

---

16. Key References

1. Katz JN, Harris MB. Lumbar spinal stenosis. N Engl J Med. 2008;358(8):818-825. doi:10.1056/NEJMcp0708097

2. Lurie J, Tomkins-Lane C. Management of lumbar spinal stenosis. BMJ. 2016;352:h6234. doi:10.1136/bmj.h6234

3. Genevay S, Atlas SJ. Lumbar spinal stenosis. Best Pract Res Clin Rheumatol. 2010;24(2):253-265. doi:10.1016/j.berh.2009.11.001

4. Benoist M. Natural history of the aging spine. Eur Spine J. 2003;12 Suppl 2:S86-89. doi:10.1007/s00586-003-0593-0

5. Steurer J, Roner S, Gnannt R, Hodler J. Quantitative radiologic criteria for the diagnosis of lumbar spinal stenosis: a systematic literature review. BMC Musculoskelet Disord. 2011;12:175. doi:10.1186/1471-2474-12-175

6. Abbas J, Hamoud K, May H, et al. Degenerative lumbar spinal stenosis and lumbar spine configuration. Eur Spine J. 2010;19(11):1865-1873. doi:10.1007/s00586-010-1516-5

7. Chou R, Loeser JD, Owens DK, et al. Interventional therapies, surgery, and interdisciplinary rehabilitation for low back pain: an evidence-based clinical practice guideline from the American Pain Society. Spine. 2009;34(10):1066-1077. doi:10.1097/BRS.0b013e3181a1390d

8. Ammendolia C, Stuber KJ, Rok E, et al. Nonoperative treatment for lumbar spinal stenosis with neurogenic claudication. Cochrane Database Syst Rev. 2013;(8):CD010712. doi:10.1002/14651858.CD010712

9. Takahashi K, Miyazaki T, Takino T, Matsui T, Tomita K. Epidural pressure measurements. Relationship between epidural pressure and posture in patients with lumbar spinal stenosis. Spine. 1995;20(6):650-653. doi:10.1097/00007632-199503150-00003

10. Fritz JM, Erhard RE, Vignovic M. A nonsurgical treatment approach for patients with lumbar spinal stenosis. Phys Ther. 1997;77(9):962-973. doi:10.1093/ptj/77.9.962

11. Sengupta DK, Herkowitz HN. Degenerative spondylolisthesis: review of current trends and controversies. Spine. 2005;30(6 Suppl):S71-81. doi:10.1097/01.brs.0000155579.88537.8e

12. Kalichman L, Hunter DJ. Diagnosis and conservative management of degenerative lumbar spondylolisthesis. Eur Spine J. 2008;17(3):327-335. doi:10.1007/s00586-007-0543-3

13. Ishimoto Y, Yoshimura N, Muraki S, et al. Prevalence of symptomatic lumbar spinal stenosis and its association with physical performance in a population-based cohort in Japan: the Wakayama Spine Study. Osteoarthritis Cartilage. 2012;20(10):1103-1108. doi:10.1016/j.joca.2012.06.018

14. Boden SD, Davis DO, Dina TS, Patronas NJ, Wiesel SW. Abnormal magnetic-resonance scans of the lumbar spine in asymptomatic subjects. J Bone Joint Surg Am. 1990;72(3):403-408.

15. de Schepper EI, Overdevest GM, Suri P, et al. Diagnosis of lumbar spinal stenosis: an updated systematic review of the accuracy of diagnostic tests. Spine. 2013;38(8):E469-481. doi:10.1097/BRS.0b013e31828935ac

16. Kalichman L, Cole R, Kim DH, et al. Spinal stenosis prevalence and association with symptoms: the Framingham Study. Spine J. 2009;9(7):545-550. doi:10.1016/j.spinee.2009.03.005

17. Battié MC, Videman T, Levälahti E, Gill K, Kaprio J. Genetic and environmental effects on disc degeneration by phenotype and spinal level: a multivariate twin study. Spine. 2008;33(25):2801-2808. doi:10.1097/BRS.0b013e31818043b7

18. Sairyo K, Biyani A, Goel V, et al. Pathomechanism of ligamentum flavum hypertrophy: a multidisciplinary investigation based on clinical, biomechanical, histologic, and biologic assessments. Spine. 2005;30(23):2649-2656. doi:10.1097/01.brs.0000188203.87146.60

19. Kosaka H, Sairyo K, Biyani A, et al. Pathomechanism of loss of elasticity and hypertrophy of lumbar ligamentum flavum in elderly patients with lumbar spinal canal stenosis. Spine. 2007;32(25):2805-2811. doi:10.1097/BRS.0b013e31815b650f

20. Jenis LG, An HS. Spine update. Lumbar foraminal stenosis. Spine. 2000;25(3):389-394. doi:10.1097/00007632-200002010-00022

21. Porter RW. Spinal stenosis and neurogenic claudication. Spine. 1996;21(17):2046-2052. doi:10.1097/00007632-199609010-00024

22. Olmarker K, Rydevik B, Holm S. Edema formation in spinal nerve roots induced by experimental, graded compression. An experimental study on the pig cauda equina with special reference to differences in effects between rapid and slow onset of compression. Spine. 1989;14(6):569-573. doi:10.1097/00007632-198906000-00002

23. Schizas C, Theumann N, Burn A, et al. Qualitative grading of severity of lumbar spinal stenosis based on the morphology of the dural sac on magnetic resonance images. Spine. 2010;35(21):1919-1924. doi:10.1097/BRS.0b013e3181d359bd

24. Sirvanci M, Bhatia M, Ganiyusufoglu KA, et al. Degenerative lumbar spinal stenosis: correlation with Oswestry Disability Index and MR imaging. Eur Spine J. 2008;17(5):679-685. doi:10.1007/s00586-008-0646-5

25. Cook C, Brown C, Isaacs R, Roman M, Davis S, Richardson W. Clustered clinical findings for diagnosis of lumbar spinal stenosis. J Man Manip Ther. 2010;18(4):248-254. doi:10.1179/106698110X12804993426848

26. Jarvik JG, Deyo RA. Diagnostic evaluation of low back pain with emphasis on imaging. Ann Intern Med. 2002;137(7):586-597. doi:10.7326/0003-4819-137-7-200210010-00010

27. Barz T, Melloh M, Staub LP, et al. Nerve root sedimentation sign: evaluation of a new radiological sign in lumbar spinal stenosis. Spine. 2010;35(8):892-897. doi:10.1097/BRS.0b013e3181c7cf4b

28. Leone A, Guglielmi G, Cassar-Pullicino VN, Bonomo L. Lumbar intervertebral instability: a review. Radiology. 2007;245(1):62-77. doi:10.1148/radiol.2451051359

29. Atlas SJ, Keller RB, Wu YA, Deyo RA, Singer DE. Long-term outcomes of surgical and nonsurgical management of lumbar spinal stenosis: 8 to 10 year results from the Maine Lumbar Spine Study. Spine. 2005;30(8):936-943. doi:10.1097/01.brs.0000158953.77141.83

30. Podichetty VK, Segal AM, Lieber M, Mazanec DJ. Effectiveness of salmon calcitonin nasal spray in the treatment of lumbar canal stenosis: a double-blind, randomized, placebo-controlled, parallel group trial. Spine. 2004;29(21):2343-2349. doi:10.1097/01.brs.0000143807.78082.7e

31. Friedly JL, Comstock BA, Turner JA, et al. A randomized trial of epidural glucocorticoid injections for spinal stenosis. N Engl J Med. 2014;371(1):11-21. doi:10.1056/NEJMoa1313265

32. Kreiner DS, Shaffer WO, Baisden JL, et al. An evidence-based clinical guideline for the diagnosis and treatment of degenerative lumbar spinal stenosis (update). Spine J. 2013;13(7):734-743. doi:10.1016/j.spinee.2012.11.059

33. Watters WC 3rd, Baisden J, Gilbert TJ, et al. Degenerative lumbar spinal stenosis: an evidence-based clinical guideline for the diagnosis and treatment of degenerative lumbar spinal stenosis. Spine J. 2008;8(2):305-310. doi:10.1016/j.spinee.2007.10.033

34. Weinstein JN, Tosteson TD, Lurie JD, et al. Surgical versus nonoperative treatment for lumbar spinal stenosis four-year results of the Spine Patient Outcomes Research Trial. Spine. 2010;35(14):1329-1338. doi:10.1097/BRS.0b013e3181e0f04d

35. Weinstein JN, Tosteson TD, Lurie JD, et al. Surgical versus nonsurgical therapy for lumbar spinal stenosis. N Engl J Med. 2008;358(8):794-810. doi:10.1056/NEJMoa0707136

36. Matz PG, Meagher RJ, Lamer T, et al. Guideline summary review: an evidence-based clinical guideline for the diagnosis and treatment of degenerative lumbar spondylolisthesis. Spine J. 2016;16(3):439-448. doi:10.1016/j.spinee.2015.11.055

37. Försth P, Ólafsson G, Carlsson T, et al. A Randomized, Controlled Trial of Fusion Surgery for Lumbar Spinal Stenosis. N Engl J Med. 2016;374(15):1413-1423. doi:10.1056/NEJMoa1513721

38. Dafford EE, Anderson PA. Comparison of dural repair techniques. Spine J. 2015;15(5):1099-1114. doi:10.1016/j.spinee.2013.06.044

39. Pull ter Gunne AF, Cohen DB. Incidence, prevalence, and analysis of risk factors for surgical site infection following adult spinal surgery. Spine. 2009;34(13):1422-1428. doi:10.1097/BRS.0b013e3181a03013

40. Park P, Garton HJ, Gala VC, Hoff JT, McGillicuddy JE. Adjacent segment disease after lumbar or lumbosacral fusion: review of the literature. Spine. 2004;29(17):1938-1944. doi:10.1097/01.brs.0000137069.88904.03

41. Johnsson KE, Rosén I, Udén A. The natural course of lumbar spinal stenosis. Clin Orthop Relat Res. 1992;(279):82-86.

42. Atlas SJ, Deyo RA, Keller RB, et al. The Maine Lumbar Spine Study, Part III. 1-year outcomes of surgical and nonsurgical management of lumbar spinal stenosis. Spine. 1996;21(15):1787-1794. doi:10.1097/00007632-199608010-00012

43. Atlas SJ, Keller RB, Robson D, Deyo RA, Singer DE. Surgical and nonsurgical management of lumbar spinal stenosis: four-year outcomes from the Maine Lumbar Spine Study. Spine. 2000;25(5):556-562. doi:10.1097/00007632-200003010-00005

44. North American Spine Society. Evidence-Based Clinical Guidelines for Multidisciplinary Spine Care: Diagnosis and Treatment of Degenerative Lumbar Spinal Stenosis. 2011. https://www.spine.org/Documents/ResearchClinicalCare/Guidelines/LumbarStenosis.pdf

---