Lumbar Disc Migrated Sequestration

A migrated sequestered lumbar disc is the most advanced stage of disc herniation: a piece of nucleus pulposus has pushed through a torn annulus fibrosus, lost all continuity with its parent disc, and then travelled (migrated) some distance up, down, or sideways inside—or occasionally outside—the spinal canal. Because the fragment is free-floating, it can compress nerve roots at a level different from the original disc space and may trigger an inflammatory cascade that amplifies pain beyond simple mechanical pressure. In modern nomenclature it is classed as an “extruded → sequestered” herniation and further described by migration zone (far-up, near-up, near-down, far-down) or by grade 1-6 on high-resolution MRI, where grades 4-6 represent low-, high-, and very-high-grade inferior migration respectively.RadiopaediaPubMed Central

Epidemiologically the lesion peaks in people aged 30-50 who perform repetitive flexion-loading work, but it is also seen in elite athletes and in older adults with cumulative disc degeneration. The annual incidence of symptomatic lumbar disc herniation across all types is estimated at ≈0.5 %; migrated sequestration accounts for roughly 10-15 % of those cases, with L4–L5 and L5–S1 levels predominating.Verywell Health

Pathophysiologically three processes matter:

  1. Mechanical displacement of neural tissue by the fragment.

  2. Chemical irritation: the exposed nucleus pulposus is rich in cytokines and phospholipase A2, provoking radicular pain even when compression is modest.

  3. Auto-immune-like reaction: once the disc material is outside the annulus it is “foreign” to the immune system, inciting macrophage infiltration and neovascularisation, phenomena visible as rim enhancement on contrast MRI.


Anatomy Relevant to Migration

 Structure & Location of the Lumbar Intervertebral Disc

A lumbar disc is a fibrocartilaginous cushion situated between the vertebral bodies from L1/L2 to L5/S1. It has three gross zones:

  • Nucleus pulposus – a gelatinous, proteoglycan-rich core that holds water and transmits hydrostatic pressure.

  • Annulus fibrosus – concentric lamellae of type I collagen angled ≈30 ° alternately, resisting torsion and shear.

  • Cartilaginous end-plates – thin hyaline layers anchoring the disc to vertebral bodies and serving as a semi-permeable membrane for nutrient diffusion.Radiology Assistant

With age, the nucleus dehydrates, and radial fissures may appear in the annulus; a fissure that reaches the posterior longitudinal ligament (PLL) provides the exit path for sequestration.

Muscular Origin, Attachments & Synergy

Although discs are not muscles, understanding the deep lumbar muscles is crucial because their tension patterns influence disc stresses and influence postoperative rehabilitation.

  1. Multifidus – Arises from mammillary processes of each lumbar vertebra, sacrum, and iliac crest; inserts onto spinous processes 2–4 levels above, filling the laminar gutter.PubMed CentralRadiopaedia | Acts as segmental stabiliser; atrophy correlates with recurrent sequestration. |
  2. Erector spinae (iliocostalis, longissimus, spinalis) – Broad origin from thoracolumbar fascia and iliac crest; fibres ascend to ribs and transverse processes.Radiopaedia | Provides gross extension torque; overload drives posterior shear on discs.
  3. Quadratus lumborum – Iliac crest and iliolumbar ligament → transverse processes L1–L4 and 12th rib.NCBI | Frontal-plane stabiliser—unbalanced contraction can provoke asymmetric migration. |
  4. Psoas major –  Transverse processes and vertebral bodies T12–L5 → lesser trochanter of femur; crosses disc surfaces anteriorly. | Hip flexion synergy; spasm raises intradiscal pressure. |
  5. Intertransversarii & rotatores – Short fibres bridging adjacent transverse and laminar elements; richly proprioceptive.Radiopaedia | Fine-tunes vertebral motion; dysfunction impairs protective reflexes.|
  6. Multifidus in sentence form: The multifidus originates as short tendinous slips from each lumbar mammillary process, sacrum and iliac crest, then ascends two to four segments to insert on the spinous process above, filling the space between laminae. This stacked arrangement gives it enormous leverage over segmental motion; when the muscle atrophies—something MRI often reveals after acute radiculopathy—the disc loses a stabilising corset and is more prone to further migration.PubMed Central

Blood Supply

Each lumbar disc is avascular in its centre and receives nutrition by diffusion through cartilage end-plates. The surrounding structures share a robust arterial network:

  • Lumbar segmental arteries (branches of the abdominal aorta) give off periosteal and equatorial branches to the vertebral bodies, then dorsal branches to posterior muscles, and radicular/medullary branches to the dura and nerve roots.NCBIKenhub

  • The artery of Adamkiewicz (usually arising at L1 or L2) reinforces the anterior spinal artery, explaining why extreme caudal migration can threaten vascular supply as well as mechanical integrity.

  • Venous drainage flows into the internal vertebral venous plexus—valveless and therefore sensitive to intra-abdominal pressure.

Nerve Supply

The sinuvertebral (recurrent meningeal) nerve, a mixed somatic-sympathetic branch of the ventral ramus, innervates the outer annulus, PLL and dura. Signal molecules from a sequestered fragment irritate this nerve, producing deep axial pain that radiates poorly and persists even in the absence of frank compression.PubMed Central

Key Functions of a Healthy Lumbar Disc Unit

  1. Shock absorption—the hydrostatic nucleus distributes compressive loads.

  2. Weight bearing—transfers 80-90 % of axial load in neutral posture.

  3. Facilitation of motion—allows flexion, extension, lateral bending and rotation while constraining extremes.

  4. Maintenance of foraminal height—preserves the window through which spinal nerves exit.

  5. Load sharing with facet joints—in flexion the disc bears more load; in extension facets bear more, reducing disc stress.

  6. Protection of neural tissues—working in concert with ligaments and muscles to shield the cauda equina from sudden forces.

When the annulus tears and the nucleus migrates, every one of these six functions is partially lost, which is why migrated sequestration produces such dramatic symptoms.


Types of Migrated Sequestration

Radiologists describe four direction-distance zones (far-up, near-up, near-down, far-down) and, more recently, six migration grades (0 = intradiscal, 1-3 = extruded but not far-migrated; 4 = low-grade inferior; 5 = high-grade inferior; 6 = very-high-grade inferior) measured against pedicle height on sagittal T2 MRI.PubMedPubMed Central

Less commonly, fragments can migrate posteriorly behind the dural sac—a surgical emergency because the PLL no longer restricts the mass—intra-dural migration, or extraforaminal migration where the fragment sits in the lateral recess or even anterior to the psoas.PubMed CentralPubMed Central


Causes

  1. Age-related degeneration – proteoglycan loss dries out the nucleus, promoting fissures that let fragments escape.

  2. Repetitive heavy lifting and twisting in occupations such as warehousing rapidly cycles intradiscal pressure and shearing.

  3. Single high-energy trauma – a fall from height can rupture annulus and PLL in one event.

  4. Sedentary posture (prolonged sitting) weakens the posterior annulus through static flexion creep.

  5. Poor core muscular endurance (multifidus and transverse abdominis atrophy) removes dynamic stability.

  6. Smoking – nicotine‐induced micro-ischemia impairs disc nutrition.

  7. Obesity increases compressive load day-in, day-out.

  8. Genetic collagen variants (e.g., COL9A2 polymorphisms) weaken annulus tensile strength.

  9. Occupational whole-body vibration (truck driving, heavy machinery) accelerates disc delamination.

  10. Previous lumbar surgery can leave stress risers in the annulus.

  11. Systemic corticosteroid use delays collagen repair.

  12. Vitamin D deficiency alters bone–disc end-plate interface, encouraging Schmorl’s nodes and annular tears.

  13. Pregnancy-related ligamentous laxity combined with weight gain stresses the lower lumbar discs.

  14. Repetitive hyperflexion sports (rowing, gymnastics) place cyclical stress on the posterior annulus.

  15. Hyperparathyroidism drives calcium resorption in vertebral bodies, altering load distribution.

  16. Connective-tissue disorders such as Marfan syndrome produce weaker annular fibres.

  17. Chronic cough or valsalva (e.g., COPD) spikes venous and intradiscal pressures.

  18. Diabetes mellitus induces glycation of annular collagen, making it brittle.

  19. Thoracolumbar scoliosis shifts load vectors to one side of the annulus.

  20. Sedative or muscle-relaxant overuse reduces protective muscular reflexes during sudden loads.


Cardinal Symptoms

  1. Sharp unilateral low-back pain that started suddenly during a bend or lift suggests fragment extrusion.

  2. Radiating leg pain (sciatica) follows a dermatomal path, worst with sitting because the fragment moves posteriorly.

  3. Paresthesia—tingling or “pins and needles” down the leg—reflects partial sensory root compression.

  4. Numbness in foot or toes indicates more severe afferent blockade.

  5. Weakness in ankle dorsiflexion (foot drop) when the L4/L5 fragment impinges L5 root.

  6. Loss of plantar-flexion power if S1 root is compressed.

  7. Reflex changes—diminished patellar or Achilles reflex on the affected side.

  8. Positional pain relief in extension because extension reduces posterior fragment pressure.

  9. Pain provoked by coughing or sneezing (Valsalva) due to transient CSF pressure rise driving root contact.

  10. Antalgic lean—patient leans away from the compressed root to enlarge foraminal volume.

  11. Night pain when lying in fetal position that partly eases when standing.

  12. Difficulty straightening after sitting (disc hydration rebounds overnight, causing morning stiffness).

  13. Positive straight-leg raise at ≤45 ° indicating root tension.

  14. Crossed straight-leg sign—raising the healthy leg exacerbates pain in the symptomatic limb.

  15. Saddle dysesthesia if central migration encroaches on S2–S4 fibres.

  16. Urinary hesitancy or retention—a red-flag symptom for cauda-equina involvement.

  17. Sexual dysfunction (erectile or orgasmic difficulty) from autonomic fibre irritation.

  18. Rapid-onset lumbar muscle spasm acting as a protective splint.

  19. Perceived limb “giving way” caused by root motor compromise.

  20. Psychological distress—fear-avoidance behaviour amplifies chronicity.


Diagnostic Tests with Long Descriptions

 Physical Examination Tests

  1. Observation & posture analysis – note scoliosis, flat-back, pelvic tilt; migration often forces a list called “sciatic scoliosis.”

  2. Lumbar palpation – tenderness over paraspinals; paradoxically the original disc level may be non-tender if fragment has moved.

  3. Active range-of-motion (ROM) testing – flexion ↑ pain; extension ↓ pain.

  4. Straight-Leg Raise (SLR) – passive hip flexion stretches the sciatic nerve; pain at < 45 ° suggests root irritation.

  5. Crossed SLR – pain reproduces on affected side when contralateral leg is lifted; highly specific for sequestration.

  6. Slump Test – seated neural tension test; adds cervical flexion and ankle dorsiflexion to sensitize.

  7. Prone Knee Bend – detects high lumbar (L2–L3) migrated fragments by stressing femoral nerve.

  8. Gait analysis – foot drop or antalgic pattern correlates with EMG findings.

  9. Neurological screen – myotomes, dermatomes, deep-tendon reflexes.

  10. Peripheral pulse palpation – to exclude vascular claudication masquerading as radicular pain.

Manual / Orthopaedic Tests

  1. Prone Instability Test – patient lifts legs while examiner presses on spinous processes; pain decrease suggests ancillary instability.

  2. Segmental Spring Test – gentle PA pressure over vertebrae detects hypo- or hyper-mobility at the injured level.

  3. Kemp’s Test – combined extension-rotation narrows foramen; pain indicates extraforaminal fragment.

  4. Femoral Nerve Stretch – side-lying hip extension stresses upper-lumbar roots.

  5. Heel-Toe Walk – functional test revealing dorsiflexor / plantar-flexor weakness.

Laboratory & Pathological Tests

  1. Complete blood count (CBC) – baseline prior to surgery; elevated WBC suggests infection, not sequestration.

  2. Erythrocyte sedimentation rate (ESR) & C-reactive protein (CRP) – normal in mechanical lesions; high levels hint at discitis or epidural abscess.

  3. HLA-B27 assay – screens for spondyloarthropathy in differential diagnosis.

  4. Serum calcium, PTH, vitamin D – detect metabolic bone disease influencing recurrent migration.

  5. Histopathology of removed fragment – collagenous annulus with central myxoid degeneration confirms disc origin.

Electrodiagnostic Tests

  1. Needle Electromyography (EMG) – fibrillation potentials in myotomes corresponding to compressed root within 3 weeks of onset.

  2. Nerve conduction studies (NCS) – evaluate sensory latency in sural or peroneal nerves; helps grade severity.

  3. H-reflex testing – prolonged latency in S1 radiculopathy.

  4. F-wave persistence – reduced in chronic L5 compression.

  5. Somatosensory evoked potentials (SSEP) – delayed peaks when central canal compromise co-exists.

Imaging Tests

  1. Lumbar MRI (gold standard) – T2 hyperintense fragment separate from disc, sometimes with rim enhancement; explains “far-migrated” level.PubMed CentralUConn Health

  2. Gadolinium-enhanced MRI – differentiates sequestered disc (peripheral enhancement) from abscess (central).

  3. CT myelography – useful when MRI contraindicated; shows filling defect opposite the exiting nerve root.

  4. Lumbar CT without contrast – excellent for calcified fragments; aids surgical planning for anterior migrations.

  5. Plain radiographs – limited in soft tissue detail but reveal alignment, spondylolisthesis, or vacuum phenomenon.

Non-pharmacological treatments

Physiotherapy and Electrotherapy / Exercise therapies

  1. McKenzie Directional Exercises – repeated extension drives nucleus anterior; centralises pain.

  2. Core-stabilisation training – transversus abdominis activation lowers intradiscal pressure.

  3. Lumbar traction (mechanical or manual) – creates negative pressure, may retract fragment.

  4. Therapeutic ultrasound – micro-massage increases nutrient diffusion.

  5. Interferential current (IFC) – medium-frequency currents gate pain transmission.

  6. Transcutaneous Electrical Nerve Stimulation (TENS) – activates A-beta fibres to damp pain.

  7. High-intensity laser therapy – photobiomodulation modulates inflammatory cytokines.

  8. Pulsed-electromagnetic field therapy – alters ion binding, easing oedema.

  9. Aquatic therapy – buoyancy unloads spine while permitting range-of-motion gains.

  10. Suspension training (TRX-type) – closed-chain exercises build core endurance; recent RCT shows VAS drop of 2 points at 8 weeks Frontiers.

  11. Swiss-ball lumbar mobility drills – improves proprioception.

  12. Neuromuscular re-education via biofeedback – normalises firing patterns.

  13. Soft-tissue manual therapy – reduces paraspinal tone guarding.

  14. Thermotherapy (moist heat packs) – vasodilates and relaxes muscle spasm.

  15. Graduated walking program – maintains disc nutrition through cyclic loading.

Mind-body & Educational Self-Management

  • Cognitive-behavioural therapy (CBT) – reframes pain catastrophising.

  • Mindfulness meditation – down-regulates limbic pain circuits.

  • Progressive muscle relaxation – breaks sympathetic loop.

  • Iyengar-based restorative yoga – gentle traction combined with breath.

  • Tai-Chi or Qigong – slow weight-shift improves spinal proprioception.

  • Acceptance & Commitment Therapy – fosters values-driven activity despite pain.

  • Pain neuroscience education – explains central sensitisation, reducing fear.

  • Ergonomic workplace training – chairs at 90 °, monitor at eye level.

  • Back-school classes – teaches hip hinge, log-roll, safe lifting.

  • Self-monitoring apps – daily posture reminders.

  • Goal-setting coaching – SMART activity targets.

  • Peer-support groups – social modelling of recovery.

  • Smoking-cessation counselling – nicotine vasoconstriction reversal.

  • Sleep-hygiene modules – pain and mood improvement.

  • Weight-management dietician sessions – every 5 kg lost reduces disc load by ~20 kg during bend.

A 2023 umbrella review concluded that multimodal physiotherapy plus education provides the largest effect size for pain and disability in lumbar disc herniation (standardised mean difference −0.77, 95 % CI −1.32 to −0.22). PubMed CentralPubMed


Common drugs

(Always follow your prescriber’s advice; doses below are adult averages.)

  1. Ibuprofen 400 mg orally 8-hourly (NSAID) – gastritis, renal strain.

  2. Naproxen 500 mg 12-hourly (NSAID) – photosensitivity, fluid retention.

  3. Diclofenac 50 mg 8-hourly (NSAID) – hepatotoxicity risk.

  4. Ketorolac 10 mg 6-hourly (NSAID) – limit to 5 days, GI bleeding.

  5. Celecoxib 200 mg daily (COX-2 selective) – less GI, but CV caution.

  6. Paracetamol 1 g 6-hourly (analgesic) – safe if <4 g/day; liver risk in overdose.

  7. Tramadol 50–100 mg 6-hourly (weak opioid) – nausea, dependence.

  8. Oxycodone 5–10 mg 6-hourly (opioid) – constipation, respiratory depression.

  9. Gabapentin 300–900 mg nightly (antineuropathic) – dizziness, weight gain.

  10. Pregabalin 75 mg 12-hourly – peripheral oedema.

  11. Amitriptyline 10–25 mg at night (TCA) – dry mouth, QT prolongation.

  12. Duloxetine 30 mg daily (SNRI) – sweating, nausea.

  13. Diazepam 5 mg night (muscle-relaxant) – sedation.

  14. Cyclobenzaprine 10 mg night – anticholinergic effects.

  15. Methylprednisolone 125 mg IV one-off (epidural or systemic steroid) – mood changes, glucose rise.

  16. Dexamethasone taper 6 mg → 0 mg over 7 days – adrenal suppression.

  17. Topical diclofenac gel 2 % q.i.d. – local rash.

  18. Lidocaine 5 % patch 12 h on / 12 h off – skin irritation.

  19. Etanercept 25 mg subcut weekly (off-label anti-TNF) – infection risk.

  20. Calcitonin 200 IU intranasal daily – flushing, rhinitis.


Dietary molecular supplements

  1. Omega-3 fish oil 2 g/day – anti-inflammatory eicosanoid shift.

  2. Curcumin (turmeric extract) 1 g/day with pepperine – NF-κB inhibition.

  3. Vitamin D3 2,000 IU/day – modulates bone mineral, down-regulates IL-6.

  4. Magnesium citrate 250 mg/day – muscle relaxation, NMDA antagonism.

  5. Collagen peptides 10 g/day – provides glycine & proline for matrix repair.

  6. Glucosamine sulphate 1,500 mg/day – substrate for proteoglycan synthesis.

  7. Chondroitin sulphate 800 mg/day – augments aggrecan water-holding.

  8. Boswellia serrata resin 300 mg 8-hourly – 5-LOX blockade, less leukotriene.

  9. Methylsulfonylmethane (MSM) 1 g twice daily – antioxidant sulfur donor.

  10. Resveratrol 250 mg/day – SIRT-1 activation, anti-oxidative.


Advanced or “disease-modifying” injectables / biologics

  • Bisphosphonates

    • Alendronate 70 mg once weekly – slows end-plate micro-erosion; may reduce Modic-related pain.

    • Zoledronic acid 5 mg IV yearly – stronger but flu-like post-dose.

  • Regenerative agents

    • Platelet-rich plasma (PRP) 2–4 ml intradiscal – growth factors spark matrix repair.

    • UPAL hydrogel (clinical trial) – biomaterial scaffold recruits native NP progenitors jmaj.jp.

    • Gene-edited NP cell therapy (pre-clinical) – drives aggrecan expression.

  • Viscosupplementations

    • Hyaluronic acid 2 ml facet-joint injection – mixed evidence in lumbar spine PubMed.

    • Cross-linked HA + PRP hybrid – experimental synergy.

  • Stem-cell products

    • Autologous bone-marrow MSCs 1 × 10^7 cells intradiscal – early trials show VAS −4 at 1 yr PubMed Central.

    • Hypoxic cultured MSC “BRTX-100” – fast-tracked phase 2 study for chronic disc disease CGTlive™.

    • Allogeneic umbilical cord MSCs – off-the-shelf, immuno-modulatory.

Mechanistically these biologics aim to restore disc hydration and tamp down catabolic cytokines (IL-1β, TNF-α), potentially reversing the cascade toward degeneration.


Surgical options

  1. Percutaneous endoscopic lumbar discectomy (PELD) – keyhole, removes fragment with 8 mm cannula; fast recovery.

  2. Microdiscectomy – gold standard open microscope-assisted; >90 % leg-pain relief at 1 year.

  3. Tubular retractors discectomy – muscle-splitting to spare multifidus.

  4. Minimally invasive transforaminal endoscopic discectomy – avoids dura retraction.

  5. Hemilaminectomy + fragmentectomy – for medial migrations.

  6. Laminectomy with flavectomy – decompresses multi-level stenosis plus disc.

  7. Posterior lumbar interbody fusion (PLIF) – adds stability in recurrent disc + spondylolisthesis.

  8. Total disc replacement – preserves motion; niche for young active.

  9. Annular repair device (“Barricaid”) – reduces re-herniation risk.

  10. Emergent decompression for cauda equina syndrome – restores bladder function if <48 h AANS.


Prevention habits

  1. Keep a neutral spine when lifting – bend the hips, not the back.

  2. Strengthen core three sessions weekly.

  3. Sit-stand work pattern every 30 minutes.

  4. Ergonomic mattress – medium-firm.

  5. Maintain healthy BMI < 25.

  6. Quit smoking – improves disc nutrition.

  7. Stay hydrated – discs lose water with dehydration.

  8. Use proper footwear with cushioning.

  9. Warm-up before sport; cool-down stretches.

  10. Treat minor back aches early – prevents compensatory overload.


When to see a doctor immediately

  • New loss of bladder or bowel control.

  • Numbness in the saddle area.

  • Progressive leg weakness, foot-drop.

  • Fever, chills, or weight loss with back pain.

  • Pain after severe trauma (fall, crash).

These may herald cauda equina syndrome, spinal infection, or fracture. Time to surgery can decide long-term nerve outcome. Cleveland Clinic


“Do’s” and “Avoids”

Helpful to do Important to avoid
Short, regular walks Long static sitting
Core-stability exercises Lifting & twisting together
Good lumbar support while driving Smoking
Heat packs for spasm Going totally bed-bound
Anti-inflammatory diet Rapid weight gain
Mindfulness or CBT Catastrophising pain
Ergonomic workspace Slouching on couch
Scheduled stretching breaks Heavy high-impact sport early
Sleep 7–8 h/night Skipping prescribed meds
Follow-up MRI if red flags Self-injecting “miracle” shots

Frequently Asked Questions

  1. Will my migrated sequestrated disc re-absorb on its own?
    Yes. Several MRI series show spontaneous shrinkage in 60 – 80 % within 12 months as the body’s macrophages digest the fragment.

  2. How long before I can return to work?
    Light desk duties: 2 – 4 weeks with graded sitting. Heavy manual: after physiotherapist and surgeon clear functional lifts, usually 6 – 12 weeks.

  3. Is it dangerous to exercise while I still have pain?
    Not if pain is kept below 4/10 and movements are guided; controlled exercise prevents de-conditioning.

  4. Do I need a corset brace?
    Short-term (≤2 weeks) bracing may ease acute pain but prolonged use weakens core muscles.

  5. Which sleeping position is best?
    Side-lying with a pillow between knees keeps lumbar spine neutral; or supine with small pillow under knees.

  6. Can a disc fragment “paralyse” me?
    Complete leg paralysis is very rare; the bigger fear is bladder/bowel nerve compression (cauda equina) which is still uncommon.

  7. Will chiropractic manipulation push the fragment back?
    High-velocity thrusts are controversial. Gentle mobilisations may relieve joint stiffness, but evidence for fragment reduction is limited.

  8. Are steroid epidurals safe?
    Most people tolerate them well; temporary sugar rise or insomnia are common. Spinal infection or dural puncture are rare (<1 : 10,000).

  9. Do stem-cell injections rebuild my disc?
    Early studies are promising for pain relief and hydration but long-term structural restoration is still being studied.

  10. What happens if I ignore the pain?
    Some discs settle, but constant nerve compression can cause chronic numbness or weakness.

  11. Is surgery a “quick fix”?
    Leg pain relief is usually quick, but rehab is still needed to restore muscle control and prevent recurrence.

  12. Can I travel by air?
    Yes, but stand and stretch every hour, and use a lumbar roll.

  13. Are inversion tables effective?
    They may provide short-term traction, yet evidence for lasting benefit is modest and caution is urged in glaucoma or hypertension.

  14. What diet helps disc healing?
    Protein for collagen, Omega-3 for inflammation, colourful produce for antioxidants.

  15. Could my child inherit my disc problem?
    Genetics play a role but lifestyle factors (fitness, weight, posture) modulate actual risk.

 

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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