# Lumbar Disc Herniation and Spinal Stenosis

## Introduction

Lumbar disc herniation and lumbar spinal stenosis are the two most common degenerative conditions causing low back and leg pain. Together, they account for the majority of lumbar spine surgeries performed annually. Understanding the pathoanatomy, natural history, and evidence-based management is fundamental for every orthopedic resident.

## Lumbar Disc Herniation

### Anatomy and Pathophysiology

The intervertebral disc consists of the nucleus pulposus (a gelatinous core) and the annulus fibrosus (concentric collagen lamellae). Disc herniation results from annular disruption with extrusion of nucleus pulposus material. The most common levels are L4-L5 and L5-S1, which together account for over 95% of lumbar herniations. Herniation is classified as protrusion (broad-based bulging with the base wider than the dome), extrusion (dome wider than base, extending beyond the annulus but still connected to the disc space), or sequestration (free fragment separated from the parent disc that may migrate cranially or caudally). Posterolateral herniation, the most common type, compresses the traversing nerve root (for example, an L4-L5 disc compresses the L5 root). Far lateral (foraminal) herniation compresses the exiting nerve root (for example, an L4-L5 disc compresses the L4 root).

### Clinical Presentation

Sciatica presents as radicular leg pain that is worse than back pain, following a dermatomal distribution. Pain is exacerbated by sitting, bending, and the Valsalva maneuver. Numbness, paresthesias, and weakness occur in the affected nerve root distribution. Cauda equina syndrome is a surgical emergency presenting with bilateral leg pain and weakness, saddle anesthesia, bowel and bladder dysfunction, and decreased rectal tone.

### Physical Examination

The straight leg raise (SLR) is positive if radicular pain is reproduced at 30 to 70 degrees of hip flexion, with a sensitivity of 91%. The crossed SLR is positive when contralateral leg raise reproduces ipsilateral symptoms, with high specificity of 88%. The femoral stretch test, performed with hip extension and knee flexion in the prone position, detects upper lumbar herniations (L2 to L4). | Root | Motor | Sensory | Reflex | Common Disc Level |
| --- | --- | --- | --- | --- | --- |
| L4 | Tibialis anterior (ankle dorsiflexion) | Medial leg/ankle | Patellar | L3-L4 |  |
| L5 | EHL, hip abductors (great toe dorsiflexion) | Lateral leg, dorsum of foot | None reliable | L4-L5 |  |
| S1 | Gastrocnemius, peroneus longus (plantarflexion) | Lateral foot, sole | Achilles | L5-S1 |  |

Motor testing evaluates L4 (tibialis anterior), L5 (EHL, hip abductors), and S1 (gastrocnemius, peroneus longus). Reflex testing evaluates L4 (patellar) and S1 (Achilles).

### Imaging

MRI is the gold standard, assessing disc morphology, nerve root compression, canal stenosis, and cord or cauda equina compression. Radiographs assess alignment, disc space height, and instability on flexion-extension views. CT myelography is used when MRI is contraindicated and provides excellent visualization of neural compression. Incidental disc herniations on MRI in asymptomatic individuals are common, exceeding 50% at age 40.

### Management

Nonoperative management is first-line, as the natural history is favorable with 85 to 90% of patients improving within 6 to 12 weeks. Treatment includes NSAIDs, short courses of oral steroids, neuropathic agents (gabapentin), physical therapy (McKenzie exercises, core stabilization, nerve gliding techniques), and epidural steroid injections (transforaminal preferred for short-term relief and diagnostic value). Prolonged bed rest should be avoided.

Operative management is indicated for cauda equina syndrome (emergency), progressive motor deficit, or failure of 6 to 12 weeks of conservative care with persistent disabling symptoms. Microdiscectomy is the gold standard, with removal of the herniated disc fragment under magnification achieving greater than 85% success and a recurrence rate of 5 to 15%. Endoscopic discectomy is a minimally invasive alternative with equivalent outcomes for appropriate candidates. The SPORT trial demonstrated faster improvement with surgery but similar long-term outcomes at 4 to 8 years.

## Lumbar Spinal Stenosis

### Pathophysiology

Central stenosis involves narrowing of the central canal caused by disc bulging, facet and ligamentum flavum hypertrophy, and spondylolisthesis. Lateral recess stenosis narrows the lateral recess, compressing the traversing nerve root. Foraminal stenosis narrows the neural foramen, compressing the exiting nerve root. Stenosis typically affects patients over 50 years through a degenerative process. Neurogenic claudication results from venous congestion and nerve root ischemia within the stenotic canal.

### Clinical Presentation

Neurogenic claudication produces bilateral leg pain, heaviness, weakness, and numbness with standing and walking, relieved by sitting or forward flexion (the "shopping cart sign"). It must be distinguished from vascular claudication, which improves with standing still, while neurogenic claudication requires a positional change. Back pain may or may not be present, and patients adopt a forward-flexed posture that increases canal diameter.

### Physical Examination

The examination is often remarkably normal at rest. Neurological deficits may only appear after provocative walking. Peripheral pulses are assessed to rule out vascular claudication. Gait is wide-based with difficulty in tandem walking. Spondylolisthesis may be detected by a palpable step-off.

### Imaging

MRI is the gold standard, assessing central canal area, lateral recess dimensions, foraminal stenosis, and disc pathology. CT myelography is an alternative for patients who cannot undergo MRI and provides dynamic assessment. Standing radiographs with flexion-extension views evaluate for dynamic instability or spondylolisthesis. A cross-sectional area below 100 mm squared indicates relative stenosis, and below 75 mm squared indicates absolute stenosis.

### Management

Nonoperative management includes physical therapy (flexion-based exercises, core strengthening, aerobic conditioning), epidural steroid injections (modest short-term benefit with limited evidence for long-term efficacy), NSAIDs, gabapentin for neuropathic symptoms, and activity modification for mild symptoms.

Operative management is indicated for failure of conservative management over 3 to 6 months, progressive neurological deficit, or significantly impaired quality of life and walking capacity. Decompressive laminectomy is the standard procedure, involving removal of the lamina, ligamentum flavum, and medial facetectomy to decompress neural elements. Laminectomy with fusion is added when concomitant instability or spondylolisthesis is present, using pedicle screw instrumentation with interbody fusion (PLIF or TLIF). Minimally invasive decompression with bilateral decompression via a unilateral approach preserves midline structures, with growing evidence supporting this technique. The SPORT trial demonstrated greater improvement with surgery than conservative care at 4 years for lumbar stenosis with or without spondylolisthesis.

## Cauda Equina Syndrome

Cauda equina syndrome is a surgical emergency requiring decompression ideally within 48 hours of symptom onset, with the best outcomes achieved within 24 hours. It presents with bilateral radiculopathy, saddle anesthesia, urinary retention or incontinence, bowel dysfunction, and decreased rectal tone. It is most commonly caused by a large central disc herniation but may also result from tumor, epidural abscess, or hematoma. Emergent MRI and surgical decompression are required.

## Clinical Pearls

Cauda equina syndrome is a surgical emergency requiring decompression within 24 to 48 hours. Most lumbar disc herniations resolve with nonoperative management; surgery provides faster relief but similar long-term outcomes. Neurogenic claudication (stenosis) is distinguished from vascular claudication by relief with flexion and sitting, not just standing still. Far lateral disc herniations compress the exiting nerve root, one level higher than expected. Correlation between imaging findings and clinical symptoms is essential, as asymptomatic MRI abnormalities are extremely common.

## References
1. Weinstein JN, Tosteson TD, Lurie JD, et al. "Surgical vs Nonoperative Treatment for Lumbar Disk Herniation: The Spine Patient Outcomes Research Trial (SPORT)." *JAMA*. 2006;296(20):2441-2450.
2. Weinstein JN, Tosteson TD, Lurie JD, et al. "Surgical Versus Nonsurgical Therapy for Lumbar Spinal Stenosis." *New England Journal of Medicine*. 2008;358(8):794-810.
3. Kreiner DS, Shaffer WO, Baisden JL, et al. "An Evidence-Based Clinical Guideline for the Diagnosis and Treatment of Degenerative Lumbar Spinal Stenosis." *Spine Journal*. 2013;13(7):734-743.
4. Ahn UM, Ahn NU, Buchowski JM, et al. "Cauda Equina Syndrome Secondary to Lumbar Disc Herniation: A Meta-Analysis of Surgical Outcomes." *Spine*. 2000;25(12):1515-1522.