Lumbar Disc Herniation and Radiculopathy
Contents (8)
Herniation of the nucleus pulposus through a weakened annulus compresses or inflames a nerve root, producing radicular leg pain that dominates over back pain. Most resolve without surgery; the exam focus is root localisation and red flags.
- Anatomy of compression: herniations are usually posterolateral, because the posterior longitudinal ligament reinforces the midline. In the lumbar spine, a posterolateral herniation typically compresses the traversing root — the one numbered below the disc, so an L4–L5 disc affects L5, and L5–S1 affects S1.
- Root patterns:
- L4 — anterior thigh and medial shin, weak knee extension, reduced patellar reflex.
- L5 — lateral leg and dorsum of foot, weak great toe and ankle dorsiflexion (foot drop), reflexes preserved.
- S1 — posterior leg and lateral foot, weak plantarflexion, reduced Achilles reflex.
- Examination: straight leg raise is sensitive; the crossed straight leg raise is more specific.
- Red flags demanding urgent imaging: cauda equina syndrome (saddle anaesthesia, urinary retention then overflow incontinence, bilateral leg symptoms — a surgical emergency), progressive or severe motor deficit, fever with back pain, history of malignancy, and unexplained weight loss.
- Imaging is not indicated in the first six weeks without red flags — MRI findings are common in asymptomatic people and drive unnecessary intervention.
- Management: most improve within 6–12 weeks with continued activity, analgesia and physiotherapy. Surgery is for cauda equina, progressive deficit, or persistent disabling radiculopathy after conservative care.
(Seed article — remaining sections to be written and reviewed.)
Mechanism of the herniation itself
- Age-related disc degeneration: the dominant cause. Loss of proteoglycan and water from the nucleus pulposus shifts axial load onto the annulus fibrosus, which develops radial fissures through which nuclear material extrudes.
- Acute mechanical overload: flexion combined with axial compression and rotation (lifting a heavy object with a rounded back) generates the peak posterior annular stress; a discrete lifting event is the classic stem trigger but is superimposed on pre-existing degeneration.
- Repetitive microtrauma: occupational bending, twisting, and whole-body vibration (long-haul drivers, heavy machinery operators).
- Rare structural causes: trauma with endplate fracture, and heritable collagen disorders producing a structurally weak annulus.
Non-modifiable risk factors
- Age 30–50: peak incidence. The nucleus still has enough turgor to extrude; in the elderly the desiccated disc more often produces spinal stenosis and neurogenic claudication instead.
- Male sex and tall stature.
- Genetics: polymorphisms in genes encoding collagen IX, aggrecan, and matrix metalloproteinases; a strong family history of early disc disease is a recognised risk marker.
- Prior herniation or prior discectomy: the annular defect persists and predisposes to recurrence at the same level.
Modifiable risk factors
- Smoking: nicotine-induced vasoconstriction impairs diffusion of nutrients across the avascular endplate, accelerating disc desiccation; it also predicts worse post-operative outcomes.
- Obesity and truncal deconditioning: increased compressive load with poor paraspinal and abdominal support.
- Occupational lifting and prolonged sitting/driving.
- Sedentary behaviour and poor lifting mechanics.
Anatomic predilection: over 90% of herniations occur at L4–L5 and L5–S1, where segmental motion, lordotic angulation, and lever-arm forces are greatest, and where the posterior longitudinal ligament is narrowest — reinforcing the posterolateral pattern described above. Pregnancy is often planted in the stem as a contributor through weight gain, lordosis, and relaxin-mediated ligamentous laxity.
From disc to root
- Normal disc architecture: an outer annulus fibrosus of concentric type I collagen lamellae contains a hydrated, proteoglycan-rich nucleus pulposus (type II collagen, notochordal origin) that behaves as an incompressible fluid, distributing load evenly across the endplates.
- Degeneration: proteoglycan loss lowers the imbibition pressure, the nucleus dehydrates, disc height falls, and load is transferred eccentrically to the annulus. Repetitive shear opens radial fissures, most often posterolaterally where the posterior longitudinal ligament gives no reinforcement.
- Herniation grades: bulge → protrusion (base wider than dome) → extrusion (dome wider than base) → sequestration (free fragment). Extruded and sequestered fragments are the most symptomatic but paradoxically the most likely to resorb, because exposed nuclear material is phagocytosed by macrophages and neovascularised.
Why the leg hurts more than the back
- Mechanical compression deforms the root and, more importantly, obstructs its intraneural microcirculation, producing venous congestion, endoneurial oedema, and ischaemia. Large-diameter myelinated fibres are most vulnerable, so paraesthesia, weakness, and hyporeflexia appear out of proportion to pinprick loss.
- Chemical radiculitis: nucleus pulposus is immune-privileged; when exposed it triggers TNF-α, IL-6, and phospholipase A2 release. These sensitise the dorsal root ganglion and can generate florid radicular pain with minimal compression — this explains why symptom severity correlates poorly with the size of the herniation on MRI, and why many patients improve as inflammation subsides without any change in disc morphology.
- Ectopic discharge from the sensitised DRG produces spontaneous shooting pain, and mechanical tethering explains why manoeuvres that stretch the root (straight leg raise) or raise intrathecal pressure (Valsalva, coughing, sneezing, sitting) reproduce it.
Localisation logic: the traversing root is compressed by the usual posterolateral herniation, while an uncommon far-lateral (foraminal) herniation compresses the exiting root — so an L4–L5 far-lateral disc gives an L4 rather than L5 syndrome. Below the conus (~L1–L2), herniations compress the cauda equina rather than the cord, giving flaccid, areflexic, lower-motor-neuron deficits.
The classic stem: a working-age adult (30–50), often a smoker or someone with an occupational lifting history, who develops sudden lancinating leg pain after bending or lifting.
Symptoms
- Sciatica: sharp, electric, burning pain radiating from buttock down the posterior or lateral leg below the knee, following a dermatome. Pain below the knee is the discriminating feature — pain confined to the buttock and thigh is more often referred somatic pain from facet or muscle.
- Leg pain > back pain: the hallmark distinguishing radiculopathy from mechanical low back pain.
- Aggravation with Valsalva, coughing, sneezing, and sitting (sitting raises intradiscal pressure); relief with lying supine with hips and knees flexed.
- Paraesthesia and numbness in the dermatome; weakness in the myotome, reported functionally as tripping (foot drop, L5) or difficulty pushing off/climbing stairs (S1).
Signs
- Positive straight leg raise: radicular pain reproduced below the knee between roughly 30° and 70° of passive hip flexion with the knee extended — tension on the L5/S1 roots. Sensitive, not specific.
- Crossed straight leg raise: raising the asymptomatic leg reproduces pain in the affected leg; highly specific for a large, usually central-to-posterolateral herniation.
- Femoral stretch (reverse SLR): prone knee flexion/hip extension reproduces anterior thigh pain — upper lumbar roots (L2–L4).
- Focal LMN findings: dermatomal sensory loss, myotomal weakness, and depressed reflex per the root patterns already outlined. Reflexes are preserved in L5 lesions, a favourite discriminator.
- Antalgic gait, list away from the side of pain, paraspinal spasm.
Red-flag presentation: bilateral radicular symptoms, saddle anaesthesia, urinary retention with overflow incontinence, faecal incontinence or loss of rectal tone signal cauda equina syndrome. Fever, night pain, unexplained weight loss, immunosuppression, IV drug use, or a malignancy history point instead to infection or tumour and mandate immediate evaluation.
Step 1 — clinical diagnosis, no imaging: in a patient with dermatomal radicular pain and no red flags, the diagnosis is clinical. The ACP and ACR Appropriateness Criteria both advise against imaging in the first six weeks, because degenerative disc findings and asymptomatic herniations are extremely common on MRI in pain-free adults and drive unnecessary procedures. Document a focused neurological exam (root-specific strength, sensation, reflexes) and straight leg raise as the baseline against which progression is judged.
Step 2 — when to image urgently: suspected cauda equina syndrome, progressive or severe motor deficit, or suspicion of infection or malignancy. Obtain an emergent MRI lumbar spine without contrast; add contrast if infection, tumour, or prior lumbar surgery (to distinguish recurrent disc from post-operative scar, which enhances). Check a post-void residual — a markedly elevated residual volume is the most useful bedside screen for cauda equina and a normal residual makes it unlikely.
Step 3 — confirmatory imaging
- MRI is the gold standard: shows the herniated fragment, its position (central, posterolateral/subarticular, foraminal, far-lateral), the compressed root, and the degree of thecal sac effacement.
- CT myelography: the alternative when MRI is contraindicated (pacemaker, retained hardware, severe claustrophobia).
- Plain radiographs: no role in diagnosing herniation; useful only for suspected fracture, spondylolisthesis, or instability.
Step 4 — adjuncts when the picture is atypical
- EMG/nerve conduction studies: reserve for distinguishing radiculopathy from peripheral mononeuropathy (e.g. common peroneal palsy at the fibular head mimicking L5, but sparing hip abduction and inversion) or polyneuropathy; denervation changes take weeks to appear.
- ESR, CRP, CBC if infection or malignancy is suspected; ESR/CRP are the entry point for vertebral osteomyelitis or epidural abscess.
The rule examiners test: imaging findings must correlate anatomically with the clinical root level. An MRI abnormality that does not match the exam does not explain the symptoms.
Immediate triage: identify cauda equina syndrome or a progressive/severe motor deficit first. Cauda equina is a surgical emergency — emergent MRI and urgent surgical decompression; delay correlates with permanent bladder, bowel, and sexual dysfunction. Everything below applies only after red flags are excluded.
First-line (the vast majority): the ACP 2017 guideline recommends starting with non-pharmacologic care — remain active, avoid bed rest beyond a day or two (immobility worsens deconditioning and outcomes), superficial heat, and structured physical therapy. Reassure the patient that most radiculopathy improves substantially within 6–12 weeks.
- NSAIDs (e.g. naproxen) are the first-line pharmacologic option; use the lowest effective dose for the shortest period.
- Skeletal muscle relaxants (e.g. cyclobenzaprine) may be added short-term for spasm, with counselling about sedation.
Escalation / second-line
- Duloxetine or, selectively, tramadol are ACP second-line options for persistent pain.
- Epidural glucocorticoid injection (transforaminal or interlaminar): NASS supports it for short-term relief of radicular pain; it does not alter the natural history or reduce the eventual need for surgery.
- Systemic glucocorticoids are not recommended — trials show no meaningful benefit for pain in acute low back pain and, at best, marginal functional benefit in sciatica.
- Gabapentinoids have weak and largely negative evidence for sciatica; not routinely recommended.
- Opioids are a last resort given limited efficacy and addiction risk, in line with the CDC opioid prescribing guideline.
Definitive/surgical: microdiscectomy (or open discectomy) for cauda equina, progressive or profound motor deficit, or radiculopathy that remains disabling after roughly six weeks of appropriate conservative care with concordant MRI findings. The SPORT trial showed surgery gives faster relief of leg pain and functional recovery, while long-term outcomes converge with non-operative care — so surgery is an accelerator, not a requirement.
Contraindicated/avoid: prolonged bed rest, traction, routine early imaging, and fusion for uncomplicated single-level herniation without instability.
Emergencies
- Cauda equina syndrome: a large central herniation compresses multiple lumbosacral roots. Signalled by saddle anaesthesia, urinary retention with overflow incontinence, bilateral leg pain/weakness, and loss of anal sphincter tone. Retention is the most sensitive early feature; once established, incontinence often means the deficit is permanent. Emergent MRI and decompression.
- Conus medullaris syndrome: an upper lumbar (L1–L2) lesion producing early, symmetric bladder/bowel dysfunction with mixed upper and lower motor neuron signs — distinguished from cauda equina, which is purely LMN, asymmetric, and pain-predominant.
- Spinal epidural abscess or haematoma: post-procedural (injection or surgery), presenting with severe back pain, fever (abscess) and rapidly progressive deficit; emergent MRI and decompression.
Disease-related
- Persistent foot drop from prolonged L5 compression — axonal loss means recovery may be incomplete even after decompression; the sign is weak great-toe and ankle dorsiflexion with a steppage gait.
- Chronic neuropathic pain and central sensitisation from sustained DRG irritation.
- Disuse atrophy and deconditioning from inappropriate bed rest.
Treatment-related
- NSAIDs: GI ulceration/bleeding, acute kidney injury (prostaglandin-dependent afferent arteriolar dilation lost), hypertension, fluid retention.
- Opioids: sedation, constipation, tolerance, dependence.
- Epidural steroid injection: dural puncture with post-dural-puncture headache, transient hyperglycaemia and HPA suppression, infection; rarely, vascular injury with cord ischaemia.
- Discectomy: recurrent herniation at the same level (most common late complication, heralded by recurrence of the original radicular pain after a pain-free interval), incidental durotomy with CSF leak, nerve root injury, discitis, and arachnoiditis. Persistent pain despite technically successful surgery is termed failed back surgery syndrome.
- Fusion, when performed, adds adjacent segment degeneration from transferred biomechanical load.
- Leg pain > back pain, radiating below the knee, worse with sitting, coughing, and Valsalva is the signature of radiculopathy. Pain that stops at the buttock or thigh is usually referred somatic pain, not root compression.
- Reflex is the fastest localiser: depressed patellar = L4, depressed Achilles = S1, normal reflexes with foot drop = L5. L5 has no routinely tested deep tendon reflex — the commonest distractor is expecting a diminished reflex in an L5 lesion.
- Posterolateral herniation hits the traversing root (number below the disc): L4–L5 → L5; L5–S1 → S1. A far-lateral/foraminal herniation hits the exiting root (L4–L5 → L4) — this is the exception examiners hide in the stem.
- Straight leg raise is sensitive; crossed straight leg raise is specific. If asked which finding best confirms a clinically significant herniation, choose the crossed SLR.
- Single best next step with no red flags = conservative management, not MRI. Imaging in the first six weeks is a wrong answer per the ACP and ACR Appropriateness Criteria, because asymptomatic disc findings are ubiquitous.
- Single best next step with saddle anaesthesia, urinary retention, or bilateral leg symptoms = emergent MRI followed by surgical decompression. Check a post-void residual at the bedside while arranging imaging. Do not