Lumbar Disc Trans-ligamentous Sequestration

Anatomy of the lumbar intervertebral disc
Types of transligamentous sequestration
Common causes and contributory factors
Symptoms
Diagnostic tests and investigations
Non-pharmacological treatments
Drugs (dosage – class – timing – key side-effects)
Drugs & biologics
Dietary molecular supplements
Common surgical options (when other care fails)
Prevention habits
When should you see a doctor fast?
Do’s and don’ts
FAQs

Lumbar disc trans-ligamentous sequestration happens when a soft inner fragment of a lumbar inter-vertebral disc squirts through the tough outer ring and then breaks right through the posterior longitudinal ligament (PLL). The loose bit migrates into the spinal canal, where it can press on nerves or even drift a little before your immune system slowly “eats” it away.
Research shows that the position and exposure of the fragment (through the torn PLL) matter more to natural shrinkage than its size. Patients whose fragment protrudes beyond the ligament are the most likely to improve without surgery. PubMedPubMed Central

A lumbar disc transligamentous sequestration happens when a piece of the jelly-like centre of an intervertebral disc (the nucleus pulposus) first bursts through the outer fibrous ring (annulus fibrosus), then ruptures the posterior longitudinal ligament (PLL) that lines the back of the vertebral bodies, and finally breaks completely free of the parent disc. The liberated fragment migrates into the spinal canal or epidural space, where it may compress nearby nerve roots or even the cauda equina. Radiologists also call it a “free fragment” or “sequestered extrusion.” RadiopaediaPubMed Central

Unlike a contained protrusion, the sequestered fragment no longer shares continuity with the disc, which explains why symptoms can wax and wane as the piece shifts position or undergoes spontaneous resorption by the immune system. Approximately 25-30 % of all lumbar disc herniations show some degree of sequestration, and fragments most often drift caudally and paracentrally because the PLL attachments funnel material in that direction. Journal of Korean Neurosurgical SocietyRadiopaedia

Anatomy of the lumbar intervertebral disc

Structure and location

Each lumbar disc sits between neighbouring vertebral bodies from L1/L2 down to L5/S1. It is a fibro-cartilaginous symphysis made of two main parts:

Annulus fibrosus – concentric collagen lamellae arranged in a criss-cross fashion that resist torsion and contain the nucleus.
Nucleus pulposus – a water-rich gel that behaves hydraulically to spread compressive forces.
The healthy adult lumbar disc is ~7–10 mm high anteriorly, tapering posteriorly to maintain the lumbar lordosis and to house the cauda equina safely. PhysiopediaWikipedia

Muscle origins that blend with the disc

Although a disc is not a muscle, some deep trunk flexors take partial origin from the anterior surfaces of the discs and adjoining bodies:

Psoas major – arises from the sides of T12–L4 vertebral bodies and the intervening discs as well as the transverse processes of L1–L5 before inserting on the lesser trochanter of the femur. This intimate contact explains why psoas spasm often accompanies acute disc injury. Kenhub

Related muscle attachments

Posteriorly, segmental stabilisers such as the multifidus and erector spinae attach to spinous and mammillary processes, anchoring to the same vertebrae that sandwich the disc. Contraction of these muscles modulates shear forces across the disc, protecting it during bending and lifting. NCBI

Blood supply

Mature discs are almost avascular. Capillaries terminate in the vertebral end plates and the outermost annulus; the inner two-thirds rely on diffusion of nutrients through tiny pores. This limited blood flow explains the disc’s poor healing capacity once torn. OrthobulletsDeuk Spine

Nerve supply

Only the outer annulus is innervated, chiefly by the sinuvertebral (recurrent meningeal) nerve, with sympathetic fibres entering via the grey rami communicantes. Irritation of these nociceptors produces the classic deep, aching discogenic pain. PubMed CentralNCBI

Key functions of the lumbar disc

Shock absorption – dissipates vertical loads during walking and jumping. ScienceDirect
Load distribution – converts a point load into uniform pressure on the vertebral endplates. JOSPT
Spacer for neural structures – maintains foraminal height to protect exiting nerve roots. Physiopedia
Facilitator of motion – allows controlled flexion, extension, lateral bending, and rotation between vertebrae. NCBI
Contribution to spinal curves – its wedge shape supports the lumbar lordosis required for upright posture. Center for Specialty Care
Hydraulic reservoir – the proteoglycan-rich nucleus draws in water overnight, restoring disc height and nutrition. StudySmarter UK

Types of transligamentous sequestration

Clinicians describe sequestered fragments by direction of migration:

Cranial (upward)
Caudal (downward) — most common, often settling behind the adjacent vertebral body.
Paracentral — drifting slightly lateral to the midline, potentially trapping the L5 or S1 root.
Far-lateral / foraminal — escaping through the lateral recess or foramen, irritating the exiting nerve.
Posterior epidural (rare) — crosses the midline septum to lie behind the thecal sac, sometimes mimicking a tumour or abscess. RadiopaediaJKSR Online

Common causes and contributory factors

A lumbar disc never fails for one reason alone; rather, multiple stressors accumulate until the annulus and PLL rupture. Below are 20 well-documented contributors, each in plain language:

Age-related disc degeneration – dehydration and stiffening weaken the annulus. Spine-health
Occupational heavy lifting – repetitive forward bending with load spikes disc pressure. Spine-health
Sudden axial trauma – falls or road traffic collisions can burst an already fragile disc.
Poor sitting posture – sustained flexion raises nucleus pressure and strains posterior fibres. PubMed Central
Prolonged daily sitting > 6 h – decreases diffusion of nutrients and accelerates degeneration. PubMed Central
Obesity (BMI > 30) – extra body weight chronically compresses lumbar discs. drfanaee.comVerywell Health
Smoking – nicotine reduces disc blood supply, impairing repair. drfanaee.com
Genetic collagen IX and aggrecan polymorphisms – inherited weak structural proteins predispose to herniation. PubMede-Century Publishing Corporation
Male sex – men show roughly double the incidence, possibly due to occupational exposure. riverhillsneuro.com
Family history of herniation – first-degree relatives share both genes and lifestyle. riverhillsneuro.com
Sedentary lifestyle – de-conditioned core muscles offer less dynamic support to the disc. riverhillsneuro.com
Repetitive twisting sports such as golf or rowing – create annular micro-tears.
Vibration exposure – professional drivers experience higher disc degeneration.
Poor muscular endurance of the multifidus – leads to segmental instability.
Previous lumbar surgery – alters biomechanics and load distribution.
Congenital lumbarisation or sacralisation – abnormal segment counts shift stress to remaining discs.
Vitamin D deficiency – impairs collagen synthesis and bone-disc interface health.
Systemic inflammatory states – elevate cytokines that degrade disc matrix. BioMed Central
End-plate nutritional failure – sclerosis blocks diffusion, starving the nucleus.
Acute valsalva events (sneezing, heavy dead-lift) – transient pressure spike ruptures a thin annulus.

Symptoms

Sudden low-back “pop” followed by sharp pain after bending or lifting.
One-sided leg pain (sciatica) radiating below the knee in a dermatomal strip.
Tingling or “pins-and-needles” in the calf, foot, or toes.
Numb patch on the dorsum of the foot or lateral calf.
Electric-shock pain on coughing, sneezing, or straining (positive Valsalva).
Night or early-morning pain that eases when walking about.
Difficulty straightening up after sitting (“locked” posture).
Hamstring tightness that is really neural tension.
Weak foot dorsiflexion—tripping over the toes (L5 root).
Loss of ankle reflex (S1 root).
Calf muscle wasting over weeks if compression persists.
Saddle-area numbness in severe central fragments.
Urinary hesitancy or retention—a red flag for cauda equina syndrome.
Bowel incontinence in extreme compression.
Sexual dysfunction due to sacral root involvement.
Pain relief when lying supine with knees bent (opens foramina).
Increased pain when sitting—highest disc pressure position.
Stabbing pain on trunk rotation at the waist.
Spasm of deep paraspinal muscles palpable as knots beside the spinous processes.
Episodes of dramatic improvement followed by relapse as the free fragment migrates. Spine-health

Diagnostic tests and investigations

Physical-examination manoeuvres

Inspection & posture – list the patient watches for asymmetric waist folds and a trunk list to one side, often leaning away from the compressed nerve root.
Lumbar range of motion – flexion usually limited; extension may reproduce leg pain.
Gait analysis – antalgic limp or foot-drop noted.
Palpation for paraspinal spasm – guarding muscles flank the involved segment.
Dermatomal sensory test – light-touch pinwheel maps numb areas along L4, L5, S1.
Myotome strength test – heel walk (L5), toe walk (S1), squat-rise (L4).

Manual nerve-tension tests

Straight-Leg-Raise (SLR) test – supine hip flexion reproducing radicular pain at 30–70°. Sensitivity ~80 %. NCBIFamily Practice Notebook
Crossed SLR – raising the contralateral leg provokes pain on the affected side; highly specific (90–98 %). Family Practice Notebook
Slump test – seated slouch, neck flexion, knee extension; more sensitive (0.84) than SLR for sequestration. PubMed
Femoral nerve stretch test – prone hip extension with knee flexion reproduces anterior-thigh pain in upper-lumbar disc lesions (L2–L4). Orthobullets
Bragard’s sign – dorsiflex the ankle at the pain limit of SLR; increase confirms neural tension. Orthobullets
Valsalva manoeuvre – patient bears down; increased intrathecal pressure shoots pain down the leg, supporting discogenic compression.

Laboratory & pathology markers

High-sensitivity C-reactive protein (hs-CRP) – mild elevation reflects inflammatory cytokines around the fragment. PubMed Central
Erythrocyte sedimentation rate (ESR) – usually normal but rises if sequestration triggers epidural phlegmon or discitis; helps rule out infection. PubMed CentralPatient
White blood cell count – normal in simple herniation, elevated if abscess masks as a fragment. Consultant360
Serum phospholipase A2 – experimental biomarker of disc inflammation. PubMed Central
Pro-inflammatory cytokine panels (IL-6, TNF-α) – research tests predicting pain severity. BioMed Central
Vitamin D levels – low levels correlate with disc degeneration and poor healing.

Electrodiagnostic studies

Needle electromyography (EMG) – looks for spontaneous fibrillations in paraspinal and limb muscles, confirming root axon loss; sensitivity 49–86 %. NCBIPM&R KnowledgeNow
Nerve-conduction studies (NCS) – measure electrical speed along the sciatic branches; slowed signals imply demyelination from compression. Wiley Online Library
H-reflex latency – prolonged in S1 root compression, useful when EMG is borderline.
F-wave persistence – assesses proximal conduction along motor axons; asymmetry hints at radiculopathy.
Quantitative EMG (motor-unit number estimation) – counts surviving axons to grade severity. JCN
Sympathetic skin response – evaluates small-fibre involvement; abnormal in chronic root injury. JCN

Imaging techniques

MRI (T1/T2 sequences) – gold standard; shows the free fragment’s size, location, and degree of nerve impingement. Radiopaedia
Contrast-enhanced MRI – helps differentiate a fragment (non-enhancing rim) from epidural abscess or tumour. JKSR Online
Diffusion-weighted imaging (DWI/ADC) – high signal predicts spontaneous shrinkage potential. PubMed Central
CT myelography – indicated when MRI is contraindicated; contrast outlines dural sac indentation by the fragment. PubMedRadiopaedia
Plain CT – useful to detect calcified fragments or bony sequestra.
Dynamic flexion–extension X-rays – rule out gross segmental instability that may need fusion during surgery. PubMed

Non-pharmacological treatments

Below, every item is a mini-paragraph so Google can index each keyword.

Manual lumbar mobilisation – A physiotherapist gently glides one vertebra on another. Purpose: unstick facet joints and improve fluid exchange. Mechanism: stretches joint capsules and down-regulates pain signals via mechanoreceptors.
Spinal manipulation (high-velocity thrust) – A quick, controlled “crack.” Works by reflex-relaxing tight muscles and giving a small disc vacuum that can ease nerve root pressure.
McKenzie extension protocol – Repeated press-ups train the disc fragment to migrate forward, away from the nerve. Evidence shows centralisation of pain improves outcomes. Spine-health
Mulligan SNAGs – Sustained Natural Apophyseal Glides add active motion while the therapist glides the facet. Good for people who fear movement.
Nerve-root mobilisation (“flossing”) – Gentle sliding of the sciatic nerve reduces adhesions.
Mechanical traction / non-surgical decompression – A table gently pulls the spine, lowering intradiscal pressure and allowing bulged material to retract. Protocols of 20-30 sessions showed disc-size reduction on MRI. Journal of Contemporary Chiropractic
TENS – Portable pads send painless electric pulses that scramble pain messages before they reach the brain.
Interferential current – Two medium-frequency currents cross to bathe deep tissues, boosting blood flow and endorphin release.
Therapeutic ultrasound – Sound waves warm deep tissues, speeding nutrient diffusion into the disc rim.
Low-level laser – Photons trigger mitochondrial repair in the nerve root.
Pulsed electromagnetic field therapy – Low-energy fields promote anti-inflammatory cytokines (IL-10).
Dry needling – A thin needle de-activates painful trigger points in the paraspinals, reducing protective spasm.
Cryotherapy (cold packs) – Fifteen-minute ice sessions blunt local nerve conduction and cut swelling.
Moist heat packs – Warmth relaxes muscles and increases collagen stretchability before exercise.
Instrument-assisted soft-tissue mobilisation (IASTM) – Metal tools break cross-link adhesions in fascia.

Exercise therapies

Core-stabilisation training (Pilates-inspired) – Teaches the deep transverse abdominis and multifidus to fire first, relieving disc load.
Dynamic lumbar stabilisation – Adds resistance bands so stabilisers work through range, not just static holds.
Aquatic therapy – Water cuts body-weight by up to 80 %, letting you move without jarring the disc.
Graded walking program – Builds aerobic endurance and pumps nutrition into the disc through cyclic loading.
Stationary cycling – Keeps the spine in slight flexion, reducing nerve tension while raising heart-rate.
Flexion-distraction exercises – Gentle flexion on a special table opens the posterior disc space.
Yoga (e.g., cat-camel, sphinx pose) – Combines mobility, breathing, and awareness; RCTs show pain and disability drops >30 %.
Tai Chi – Slow, weight-shifting moves improve proprioception and reduce fear of movement.
Resistance training with neutral spine – Strong glutes and lats off-load the lumbar segment.
Motor-control retraining – Real-time ultrasound or EMG teaches correct muscle timing.

Mind-Body & Educational self-management

Mindfulness-Based Stress Reduction (MBSR) – Eight-week program lowers pain catastrophising and cortisol.
Cognitive-Behavioural Therapy (CBT) – Reframes “hurt equals harm,” cutting disability scores.
Guided imagery & progressive relaxation – Ten-minute audio scripts calm the sympathetic nervous system.
Biofeedback – Surface EMG lets patients see and then down-train muscle tension.
Pain neuroscience education – Plain-language sessions explain how nerves sensitise, empowering safe activity. Guidelines highlight education as core to every care plan. PubMed CentralPubMed Central

Drugs (dosage – class – timing – key side-effects)

Paracetamol 500–1 000 mg every 6 h (Analgesic) – Liver strain if >4 g/day.
Ibuprofen 400 mg 3× / day (NSAID) – Stomach upset, raise BP.
Naproxen 250–500 mg twice daily (NSAID) – Heartburn, fluid retention.
Diclofenac SR 75 mg twice daily (NSAID) – Higher CV risk long term.
Etoricoxib 60–90 mg once daily (COX-2 inhibitor) – Safer on gut, watch BP.
Celecoxib 200 mg once daily (COX-2) – Same as above.
Ketorolac 10 mg 4× / day ≤5 days (Potent NSAID) – Renal strain, GI bleed risk.
Methylprednisolone dose-pack (Oral corticosteroid taper over 6 days) – Insomnia, mood swing.
Prednisone 40 mg daily for 5 days then taper (Corticosteroid) – Same plus blood-sugar spike.
Gabapentin 300 mg night-time ↑ to 900 mg TID (Anti-neuropathic) – Drowsiness, dizziness.
Pregabalin 75 mg twice daily ↑ to 150 mg (Neuropathic) – Weight gain, oedema.
Duloxetine 30 mg daily ↑ to 60 mg (SNRI) – Nausea, dry mouth.
Amitriptyline 10 mg night ↑ to 25 mg (TCA) – Dry mouth, next-day grogginess.
Cyclobenzaprine 5 mg 3× / day (Muscle relaxant) – Drowsy, anticholinergic.
Tizanidine 2 mg 3× / day (Muscle relaxant) – Hypotension, dry mouth.
Baclofen 5 mg 3× / day (GABA-B agonist) – Weakness, sedation.
Tramadol 50 mg every 6 h PRN (Weak opioid) – Nausea, dependency.
Tapentadol 50–100 mg 12-hourly (Dual opioid/NE re-uptake) – Same, less itch.
Topical diclofenac gel 1 % 4× daily on sore segment – Minimal systemic effects.
Lidocaine 5 % patch 12 h on / 12 h off – Local numbness only.

Drugs & biologics

Agent (category)	Typical dose / route	Main function	How it works
Alendronate (bisphosphonate)	70 mg orally once weekly	Strengthens vertebrae, may damp disc-derived bone pain	Inhibits osteoclasts, lowering inflammatory cytokines.
Ibandronate	150 mg monthly tablet	Same plus fracture prevention in osteoporotic backs	Longer half-life in bone resorption pits.
Minodronate	50 mg once monthly	RCTs show less low-back pain in post-menopausal women. PubMed	Potent nitrogen-containing bisphosphonate, reduces acidic osteoclast secretion.
Zoledronic acid	5 mg IV once yearly	Helpful when oral drugs fail or intolerance exists	Single infusion suppresses resorption for 12 months.
Platelet-Rich Plasma (PRP) (regenerative)	2–3 mL intradiscal	Growth factors spark cell repair	α-granules release PDGF, TGF-β, VEGF.
Hydrogel-based nucleus pulposus augment	1 mL via 18-gauge needle	Re-hydrates disc, restores height	Attracts water, shares load.
Hyaluronic acid (viscosupplement)	1–2 mL intradiscal every 6 months	Lubricates, buffers nerve irritation	Visco-elastic matrix traps inflammatory mediators.
DiscGenics IDCT (allogeneic progenitor cells)	Single 1 mL injection	Phase-I/II data show pain ↓ and disability ↓. PR Newswire	Cells secrete anti-inflammatory and matrix-building proteins.
BRTX-100 (autologous stem cell product)	40 million BMC cells / disc	FDA-cleared phase-2 trial underway. WSJ	Mesenchymal cells modulate immune response and rebuild disc matrix.
Bone-marrow-derived MSC concentrate	2 mL aspirate under fluoro-guidance	Case-series show pain and ODI improvement. PubMed Central	MSCs differentiate into nucleus-like cells, secrete proteoglycans.

Dietary molecular supplements

Omega-3 fish oil 1 000 mg EPA + DHA daily – Lowers prostaglandin E2, easing nerve root inflammation.
Curcumin 500 mg twice daily with black pepper – Blocks NF-κB signalling, an inflammatory master switch.
Boswellia serrata extract 150 mg thrice daily – Reduces 5-LOX mediated leukotrienes linked to disc pain.
Glucosamine sulfate 1 500 mg daily – Supplies building blocks for proteoglycans inside the disc.
Chondroitin sulfate 1 200 mg daily – Synergises with glucosamine to hold water in the nucleus.
Collagen peptides 10 g daily powder – Provides amino acids for annulus repair.
Methyl-sulfonyl-methane (MSM) 2 g daily – Anti-oxidant sulfur donor for connective-tissue enzymes.
Resveratrol 250 mg daily – Activates SIRT1, protecting disc cells from apoptosis.
Vitamin D3 2 000 IU daily – Modulates immune cells; deficiency predicts worse back-pain scores.
Magnesium glycinate 300 mg nightly – Relaxes paraspinal muscle cramps and regulates nerve firing.

Common surgical options (when other care fails)

Micro-discectomy – Small key-hole removes only the sequestered fragment. Benefits: fastest pain relief, keeps most disc tissue intact.
Endoscopic transforaminal discectomy – 7-mm skin incision, local anaesthesia; less muscle damage, day-case.
Sequestrectomy – Surgeons extract only loose free fragment, preserving annulus – lower re-herniation risk in selected cases.
Laminotomy – Tiny bone window to reach the fragment when it has migrated upward or downward.
Laminectomy – Removes the lamina to decompress wide-level stenosis plus the sequestration.
Facet-sparing micro-tubular discectomy – Uses 18-mm tube; keeps facet joint for spine stability.
Percutaneous nucleoplasty (coblation) – Radio-frequency ablates small nucleus channels, reducing pressure.
Artificial disc replacement – For young patients with disc collapse; keeps motion, avoids fusion.
Instrumented posterolateral fusion – Screws and rods stop painful motion when instability co-exists.
Annular repair device (Barricaid) – Plugs large annular defect after fragment removal, cutting re-herniation risk.

Prevention habits

Lift with hips, not the back.
Maintain a healthy body-weight to cut disc compression.
Strength-train the core twice weekly.
Quit smoking – nicotine starves disc cells of oxygen.
Break up long sitting every 30 min.
Use ergonomic chairs and lumbar rolls.
Stay hydrated – discs are 80 % water.
Sleep on a medium-firm mattress.
Treat coughing or sneezing fits quickly – repeated spikes stress the disc.
Schedule annual movement-screen check-ups with a physiotherapist.

When should you see a doctor fast?

• Numbness around the groin or bladder trouble (possible cauda equina).
• Leg weakness that worsens day by day.
• Fever, chills, or recent cancer plus new back pain.
• Severe night pain or weight loss.
• Pain not settling after 6–8 weeks of good conservative care.*

Do’s and don’ts

Do keep walking short distances; Don’t stay in bed for days.
Do practise controlled belly-breathing; Don’t hold your breath while lifting.
Do use a lumbar roll when driving; Don’t slump in the seat.
Do warm-up with gentle cat-camel; Don’t bounce into deep toe-touch stretches cold.
Do log your pain triggers; Don’t push through sharp leg pain.
Do follow your exercise plan even on low-pain days; Don’t over-do weekend DIY projects.
Do keep a healthy calcium & vitamin-D intake; Don’t rely on fizzy sodas (they leach calcium).
Do ask about early MRI only if red flags; Don’t insist on imaging for every ache.
Do practise mindful posture checks; Don’t stare at a laptop on the sofa for hours.
Do celebrate small gains; Don’t catastrophise flare-ups—they are normal.

FAQs

Can an LTS fragment disappear on its own? Yes—because it lies outside the PLL, immune cells can reach and dissolve it; MRI studies show up to 60 % shrinkage within 6 months. PubMed Central
Is bed rest best? No. Short (<48 h) rest may calm spasms, but longer rest weakens muscles.
Will exercise push the fragment further out? Properly guided movements actually coax it away from the nerve.
Do I need an MRI immediately? Imaging is reserved for red-flag signs or if you’re not better after 6 weeks.
Are steroid shots mandatory? Not always; they help rapid pain control but don’t fix the disc.
Can I drive? Yes, if you can brake safely; use a cushion to support the curve.
Is surgery the only cure? No—most people improve with non-surgical care first.
How long before I’m back at work? Light office work often 2-4 weeks; heavy manual 6 – 12 weeks, depending on progress.
Does cracking my back cause LTS? Routine self-cracking is unlikely to tear the PLL but poor lifting technique does.
Are stem-cell injections approved? They’re still in clinical trials; early data look promising but not yet mainstream. PR Newswire
Why does coughing hurt my leg? Each cough spikes disc pressure, momentarily boosting nerve pinch.
Do bisphosphonates heal the disc? They mainly strengthen bone but may also cool disc-related inflammatory pain.
Which mattress is best? Medium-firm foam or hybrid springs that keep your spine neutral.
Is it safe to lift weights again? Yes—once pain is controlled and technique is re-trained under supervision.
Can diet really help? Anti-inflammatory foods and supplements trim chemical irritants that keep nerves hypersensitive.

Disclaimer: Each person’s journey is unique, treatment plan, life style, food habit, hormonal condition, immune system, chronic disease condition, geological location, weather and previous medical history is also unique. So always seek the best advice from a qualified medical professional or health care provider before trying any treatments to ensure to find out the best plan for you. This guide is for general information and educational purposes only. Regular check-ups and awareness can help to manage and prevent complications associated with these diseases conditions. If you or someone are suffering from this disease condition bookmark this website or share with someone who might find it useful! Boost your knowledge and stay ahead in your health journey. We always try to ensure that the content is regularly updated to reflect the latest medical research and treatment options. Thank you for giving your valuable time to read the article.

The article is written by Team Rxharun and reviewed by the Rx Editorial Board Members

Last Updated: May 19, 2025.

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