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Summary Table

Category	Details
Risk Factors	Age 30 to 50 years, male sex, obesity, sedentary lifestyle, repetitive heavy lifting, prolonged sitting, smoking (impairs disc nutrition), occupational vibration exposure, tall stature
Etiology	Degenerative weakening of the annulus fibrosus leading to herniation of the nucleus pulposus, often precipitated by axial loading with flexion or rotation
Patient Presentation	Acute onset of radiating pain in a dermatomal distribution (sciatica for lumbar, brachialgia for cervical), worsened by Valsalva maneuvers (coughing, sneezing, straining), sitting, or forward flexion
Classic Physical Exam	Positive straight leg raise (SLR) test at 30 to 70 degrees (lumbar), crossed SLR (highly suggestive), Spurling test (cervical), dermatomal sensory loss, focal motor weakness, diminished deep tendon reflexes corresponding to the affected nerve root
Key Diagnostic Results	MRI of the spine showing disc material extending beyond the annulus with nerve root compression; EMG/nerve conduction studies (NCS) for chronic or equivocal cases
Management	Conservative therapy first (NSAIDs, activity modification, physical therapy) for 4 to 6 weeks; epidural corticosteroid injection for refractory pain; surgical microdiscectomy for progressive neurological deficit, failed conservative management beyond 6 weeks, or cauda equina syndrome
Keywords	"Shooting pain down the leg," "positive straight leg raise," "worse with coughing/sneezing," "foot drop," "saddle anesthesia," "urinary retention"

1. Pathophysiology

The intervertebral disc is composed of two structures: a tough outer ring called the annulus fibrosus and a gelatinous core called the nucleus pulposus. The nucleus pulposus functions as a hydraulic shock absorber, distributing compressive forces across the vertebral endplates. With aging and repetitive mechanical stress, the annulus fibrosus undergoes degenerative changes including desiccation, fissuring, and weakening of its concentric collagen layers. When the annulus is sufficiently compromised, the nucleus pulposus can herniate through the defect and protrude into the spinal canal or neural foramen.

The posterolateral direction is the most common site of herniation because the posterior longitudinal ligament is thinnest and narrowest at its lateral edges, offering the least structural resistance. This posterolateral herniation places the disc material directly adjacent to the traversing nerve root within the lateral recess.

A critical concept for exam purposes is the distinction between the traversing (descending) nerve root and the exiting nerve root. In a typical posterolateral lumbar herniation, the disc compresses the traversing nerve root, which is numbered one level below the disc. For example, an L4-L5 disc herniation compresses the L5 nerve root, and an L5-S1 herniation compresses the S1 nerve root. The exception is a far lateral (foraminal) herniation, which instead compresses the exiting nerve root at the same level (an L4-L5 far lateral herniation would compress the L4 root). This distinction is a frequent source of exam questions.

The compressed nerve root generates pain through two mechanisms: direct mechanical compression causing ischemia and demyelination, and a secondary chemical radiculitis mediated by inflammatory cytokines (TNF-alpha, IL-1, IL-6, phospholipase A2) released from the herniated nucleus pulposus material. This chemical irritation explains why some patients with small herniations on imaging can have severe radicular symptoms, while others with large herniations remain asymptomatic.

Cauda equina syndrome represents the most feared complication. A large central disc herniation (most commonly at L4-L5 or L5-S1) can compress multiple sacral nerve roots simultaneously, producing bilateral leg symptoms, saddle anesthesia (S2-S4 dermatomes), urinary retention with overflow incontinence, fecal incontinence, and decreased rectal tone. This is a surgical emergency requiring decompression within 24 to 48 hours to prevent permanent neurological damage.

2. Classification and Clinical Manifestation

Morphological Classification

Type	Description	Clinical Significance
Bulge	Diffuse, circumferential extension of the disc beyond the vertebral body margin (>50% of disc circumference)	Usually asymptomatic, often an incidental finding; does not typically compress nerve roots
Protrusion	Focal extension of disc material through a defect in the annulus; the base at the parent disc is wider than the herniated fragment	Symptomatic when it contacts a nerve root; annulus is partially intact
Extrusion	Disc material extends through the annulus; the neck of the herniation is narrower than the body of the fragment	More likely to cause severe radiculopathy; fragments may migrate superiorly or inferiorly
Sequestration	A free fragment of disc material separates completely from the parent disc and lies within the spinal canal	Often causes acute, severe symptoms; paradoxically, free fragments may resorb spontaneously over time

Lumbar Root Level

Root	Disc Level	Motor Deficit	Sensory Loss	Reflex Change	Distinguishing Feature
L3	L2-L3	Hip flexion, knee extension (quadriceps)	Anterior thigh	Diminished patellar reflex	Anterior thigh pain, difficulty climbing stairs
L4	L3-L4	Knee extension (quadriceps), tibialis anterior	Medial leg, medial malleolus	Diminished patellar reflex	Pain radiating to medial leg below the knee
L5	L4-L5	Great toe dorsiflexion (EHL), ankle dorsiflexion (tibialis anterior), hip abduction	Lateral leg, dorsum of foot, first web space	None reliably tested (tibialis posterior reflex inconsistent)	Foot drop is the hallmark; pain radiating to dorsum of foot
S1	L5-S1	Ankle plantarflexion (gastrocnemius/soleus), hip extension	Lateral foot, posterior calf, sole	Diminished Achilles reflex	Difficulty with toe walking; pain radiating to lateral foot and sole

Cervical Root Level

Root	Disc Level	Motor Deficit	Sensory Loss	Reflex Change
C5	C4-C5	Deltoid weakness (shoulder abduction), biceps	Lateral arm (deltoid region)	Diminished biceps reflex
C6	C5-C6	Wrist extension (extensor carpi radialis), biceps	Lateral forearm, thumb, index finger	Diminished brachioradialis reflex
C7	C6-C7	Wrist flexion, elbow extension (triceps), finger extension	Middle finger	Diminished triceps reflex
C8	C7-T1	Finger flexion, grip strength, intrinsic hand muscles	Medial forearm, ring and little finger	None reliably tested

Cauda Equina Syndrome

Feature	Description
Saddle anesthesia	Numbness in the perineal region (S2-S4 distribution)
Urinary retention	Inability to void with overflow incontinence (most consistent early finding)
Fecal incontinence	Loss of anal sphincter tone
Bilateral lower extremity weakness	Often asymmetric but involves both legs
Progressive neurological deficit	Rapid worsening of motor function

3. Diagnostic Workup

Test	Role	Key Findings
Clinical examination (SLR, neurological exam)	Best initial assessment	Positive SLR at 30 to 70 degrees reproduces radicular pain; crossed SLR is less sensitive but more suggestive of true herniation
MRI of the spine (without contrast)	Gold standard imaging	Demonstrates disc herniation, nerve root compression, and excludes alternative pathology (tumor, infection, fracture)
CT myelography	Alternative when MRI is contraindicated	Shows filling defects in the thecal sac indicating disc compression
Plain radiographs (X-ray)	Limited role	Cannot visualize soft tissue; useful only to rule out fractures, spondylolisthesis, or bony lesions
EMG / Nerve conduction studies	Adjunctive for chronic or equivocal cases	Confirms radiculopathy, localizes affected nerve root, distinguishes from peripheral neuropathy; abnormalities appear 2 to 3 weeks after onset
Post-void residual (PVR) ultrasound	When cauda equina syndrome is suspected	Elevated PVR (>100 to 200 mL) supports the diagnosis of neurogenic bladder

The diagnosis of HNP is fundamentally clinical. In a patient presenting with acute radicular pain in a dermatomal pattern, the best initial step is a thorough history and neurological examination. The straight leg raise (SLR) test is performed with the patient supine; passive elevation of the extended leg that reproduces radiating pain below the knee between 30 and 70 degrees of hip flexion is considered positive. The crossed SLR (raising the unaffected leg reproduces symptoms in the affected leg) has lower sensitivity (~25%) but higher clinical value because it is rarely positive in non-discogenic conditions.

Imaging is not indicated in the first 4 to 6 weeks for patients with uncomplicated radiculopathy who respond to conservative management and have no red flags. This is a high-yield testing point: ordering an MRI on day one for a young patient with sciatica and no neurological deficits is the wrong answer on an exam.

MRI without contrast is the imaging study of choice and should be ordered when any of the following are present: symptoms persisting beyond 4 to 6 weeks of conservative therapy, progressive motor weakness, clinical suspicion for cauda equina syndrome, or red flags suggesting malignancy or infection (unexplained weight loss, fever, history of cancer, IV drug use, immunosuppression). MRI provides excellent visualization of soft tissue structures including the disc, nerve roots, and spinal cord.

CT myelography serves as the alternative when MRI is contraindicated (pacemakers, certain metallic implants, severe claustrophobia). It provides good bony detail and can demonstrate nerve root compression through contrast column filling defects.

EMG and nerve conduction studies are reserved for cases where the clinical picture is equivocal, when imaging findings do not correlate with symptoms, or when peripheral neuropathy must be excluded. Results are most reliable when performed at least 3 weeks after symptom onset, as Wallerian degeneration takes time to produce detectable electrophysiological changes.

When cauda equina syndrome is suspected, the workup shifts to an emergency MRI without delay. A post-void residual bladder scan should be obtained concurrently. This is a time-critical diagnosis where delayed imaging is a management error.

4. Management and Treatment

Phase	Intervention	Details
Acute conservative (0 to 6 weeks)	NSAIDs	Ibuprofen 400 to 800 mg every 6 to 8 hours, or naproxen 250 to 500 mg twice daily; first-line pharmacotherapy
	Activity modification	Avoid prolonged bed rest (bed rest beyond 2 days worsens outcomes); encourage gentle activity as tolerated
	Short-course oral corticosteroids	Prednisone taper (e.g., 60 mg/day for 5 days then taper) for severe acute radiculopathy; limited evidence but commonly used
	Muscle relaxants	Cyclobenzaprine 5 to 10 mg at bedtime for paravertebral spasm; short-term adjunct only
Subacute (4 to 6 weeks)	Physical therapy	Core stabilization, McKenzie exercises (extension-based), nerve gliding exercises; cornerstone of non-surgical management
Subacute (4 to 6 weeks)	Epidural corticosteroid injection	Fluoroscopy-guided transforaminal or interlaminar injection; provides temporary pain relief (weeks to months); allows participation in physical therapy
Surgical	Microdiscectomy / discectomy	Standard surgical approach for failed conservative therapy (>6 weeks), progressive motor deficit, or cauda equina syndrome
Emergency	Surgical decompression	Cauda equina syndrome requires decompression within 24 to 48 hours

First-line conservative management is appropriate for the vast majority of patients because approximately 85 to 90% of lumbar disc herniations resolve spontaneously within 6 to 12 weeks through natural resorption of the herniated fragment. NSAIDs are the preferred analgesic class. Acetaminophen alone has not shown consistent benefit for radicular pain and is no longer recommended as monotherapy for this condition. Opioids should be avoided or used only as a very short course (less than 3 days) for severe, debilitating pain that prevents any mobility.

A commonly tested point is that prolonged bed rest is harmful. Patients should be advised to remain as active as tolerated. Strict bed rest beyond 1 to 2 days leads to deconditioning, muscle atrophy, and delayed recovery.

Gabapentin or pregabalin may be added for neuropathic pain (burning, tingling components) if NSAIDs alone are insufficient. Gabapentin is typically started at 300 mg at bedtime and titrated to 300 mg three times daily or higher as tolerated. However, recent evidence questions the efficacy of gabapentinoids for acute sciatica, so this is more commonly tested as an option for chronic radicular pain.

Physical therapy is the next step when initial pharmacotherapy provides partial relief. A structured program emphasizing core strengthening, lumbar stabilization, and extension-based exercises (McKenzie method) has demonstrated benefit. Physical therapy should begin once the acute pain is sufficiently controlled to allow participation, typically at 2 to 4 weeks.

Epidural corticosteroid injections are considered when 4 to 6 weeks of conservative therapy fails to provide adequate relief. The transforaminal approach is preferred for radicular symptoms as it delivers medication closest to the affected nerve root. These injections do not alter the natural history of the disease (they do not shrink the disc) but provide a window of pain relief that facilitates rehabilitation.

Surgical intervention with microdiscectomy is indicated in three situations: (1) failure of adequate conservative therapy beyond 6 to 8 weeks, (2) progressive neurological deficit (worsening foot drop, for instance), and (3) cauda equina syndrome, which is an absolute surgical emergency. Microdiscectomy provides faster pain relief compared to continued conservative care, though long-term outcomes at 1 to 2 years tend to equalize between surgical and non-surgical groups. This nuance is frequently tested.

For cauda equina syndrome, emergent surgical decompression within 24 to 48 hours is the standard of care. Delays beyond this window are associated with permanent bladder dysfunction, sexual dysfunction, and lower extremity weakness. The next best step when cauda equina syndrome is suspected is an emergency MRI, followed immediately by surgical consultation. Do not waste time with conservative measures.

Contraindications and Considerations

Situation	Modification
Renal insufficiency	Avoid NSAIDs; use acetaminophen with adjunctive gabapentin
Active peptic ulcer disease	Avoid NSAIDs; consider COX-2 inhibitors with gastroprotection or alternative analgesics
Pregnancy	Avoid NSAIDs in the third trimester (risk of premature ductus arteriosus closure); acetaminophen is the safest analgesic; MRI without gadolinium is safe for imaging
Anticoagulation therapy	Epidural injections carry elevated bleeding risk; coordinate with the prescribing physician regarding temporary cessation

5. Differential Diagnosis and Distractors

Differential	Why It Is Similar	Key Discriminator
Lumbar spinal stenosis	Also causes leg pain and neurological symptoms in older adults	Pain is caused by neurogenic claudication (bilateral, worse with walking and standing, relieved by sitting or leaning forward); SLR is typically negative; symptoms are positional, not dermatomal
Piriformis syndrome	Causes buttock pain radiating down the posterior leg resembling S1 radiculopathy	Pain worsened by hip internal rotation or prolonged sitting on hard surfaces; SLR is negative; MRI of the spine is normal; tenderness is deep in the buttock over the piriformis
Sacroiliac joint dysfunction	Produces low back and buttock pain that may radiate to the posterior thigh	Pain does not extend below the knee; FABER (Patrick) test is positive; no dermatomal neurological deficits; pain is reproduced by sacroiliac provocation maneuvers
Peripheral neuropathy (diabetic)	Causes leg pain, numbness, and weakness	Distribution is symmetric, distal ("stocking-glove"), and bilateral; not dermatomal; associated with diabetes, alcohol use; NCS shows diffuse polyneuropathy rather than single-root involvement
Vertebral compression fracture	Causes acute back pain, may have radicular component from fragment retropulsion	History of osteoporosis or trauma; pain is midline and focal over the spinous process; point tenderness on percussion; imaging shows vertebral body height loss
Spinal epidural abscess	Back pain with possible radiculopathy and neurological deficits	Fever, elevated ESR/CRP, leukocytosis; history of recent bacteremia, IV drug use, or spinal procedure; MRI shows enhancing epidural collection; progresses through stages from back pain to weakness to paralysis
Cauda equina syndrome (from tumor)	Saddle anesthesia, urinary retention, bilateral symptoms	Insidious onset (weeks to months rather than acute); constitutional symptoms (weight loss, night pain, fatigue); MRI shows intradural or extradural mass rather than disc herniation

6. Traps and High-Yield Pearls

The single most common way students answer HNP questions incorrectly is by misidentifying the compressed nerve root. The reflex to match the disc level to the same-numbered nerve root leads to consistent errors. Remember: a posterolateral L4-L5 herniation compresses the L5 nerve root (the traversing root), not the L4 root. The only exception is the far lateral herniation, which compresses the exiting root at the same level. Vignettes may test this by describing motor and sensory findings and asking you to identify the affected level.

The second major trap involves premature imaging. A question presenting a 35-year-old with 2 weeks of sciatica, a positive SLR, and no red flags will tempt you to choose MRI. The correct answer is to continue conservative management and reassess. MRI is not indicated until 4 to 6 weeks have passed or red flags appear. The exception is any presentation suggestive of cauda equina syndrome, where the correct answer is always emergency MRI followed by urgent surgical referral.

A third frequently tested concept is the distinction between lumbar spinal stenosis and HNP. Both cause leg pain, but the mechanism and clinical pattern differ. Stenosis presents with neurogenic claudication (bilateral, provoked by walking or standing, relieved by flexion or sitting). HNP presents with radiculopathy (unilateral, dermatomal, worsened by Valsalva, positive SLR). The classic distractor places an elderly patient with bilateral leg pain that improves when leaning on a shopping cart, and the wrong answer is disc herniation.

Finally, never forget cauda equina syndrome as a surgical emergency. Any vignette that includes urinary retention, saddle anesthesia, or bilateral progressive weakness in the setting of back pain demands immediate action. Choosing "conservative management" or "outpatient MRI in 2 weeks" in this scenario is always the wrong answer. The core competency being tested across HNP questions is the ability to localize a neurological deficit by nerve root level, to apply evidence-based timing for imaging, and to recognize the red flags that convert a conservative management plan into an emergency.

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