Lumbar disc circumferential herniation—often referred to as a circumferential annular tear or global disc bulge—is a form of intervertebral disc injury in which the disc material (nucleus pulposus and inner annulus fibrosus) extends uniformly around more than 25% of the circumference of the disc, without focal rupture of the outer annular fibers. In contrast to focal protrusions, which involve limited portions of the annulus fibrosus, a circumferential herniation reflects degeneration or tearing of the disc ring in a 360° pattern, leading to a more diffuse bulging that may impinge on adjacent neural structures at multiple points. This pathology is commonly seen in advanced degenerative disc disease, where cumulative microtrauma and biochemical alterations weaken the annulus, allowing the nucleus to press against it circumferentially. Patients with circumferential herniation may present with a broader distribution of symptoms compared to focal herniations, and imaging often reveals a uniform “bulge” of the disc margin on MRI or CT myelography.
Anatomy of the Lumbar Intervertebral Disc
Understanding circumferential herniation begins with a thorough grasp of normal disc anatomy. Below are the key anatomical features, each detailed in its own section.
Structure
The intervertebral disc is a fibrocartilaginous joint composed of two major components: the central, gelatinous nucleus pulposus and the surrounding lamellar annulus fibrosus. The nucleus pulposus contains a high concentration of proteoglycans and water (up to 80% in youth), granting it hydrostatic properties to absorb compressive loads. The annulus fibrosus consists of 15–25 concentric rings of collagen fibers arranged obliquely, providing tensile strength and containing the nucleus. Together, these structures allow the disc to function as both a mechanical cushion and a flexible pivot between vertebral bodies.
Location
Lumbar intervertebral discs are situated between the vertebral bodies of L1–L2 through L5–S1. They occupy the space from the anterior margin of each vertebral body to the posterior annulus adjacent to the spinal canal. This positioning places them directly anterior to the spinal canal and nerve roots, making herniations clinically significant when disc material impinges on neural elements.
Attachment (Origin & Insertion)
Unlike muscles, discs do not “originate” and “insert” but rather are anchored superiorly and inferiorly to the vertebral endplates via Sharpey’s fibers—perforating collagen fibers that extend from the outer annulus into the subchondral bone. These attachments ensure that compressive forces are transmitted evenly across the endplate and into the vertebral bodies, and also guide nutrient diffusion into the largely avascular disc.
Blood Supply
Intervertebral discs are essentially avascular structures. Nutrient and gas exchange occur by diffusion from the capillaries in the vertebral endplates and the outer third of the annulus. As people age, endplate calcification and decreased capillary density further impair diffusion, accelerating disc degeneration.
Nerve Supply
Sensory innervation of the disc is provided primarily by the sinuvertebral (recurrent meningeal) nerves, which penetrate the outer one-third of the annulus fibrosus. Additional innervation arises from the ventral rami of spinal nerves and the gray rami communicantes. When annular tears extend into the innervated outer fibers, they may generate pain signals that are perceived as deep, axial back pain.
Functions
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Shock Absorption: The high water content of the nucleus allows the disc to compress under load, distributing forces evenly across the vertebral bodies and protecting the spine from impact.
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Load Distribution: Hydrostatic pressure within the nucleus transmits axial forces radially to the annulus, which bears tensile stress, balancing spinal loads during upright posture.
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Spinal Flexibility: The disc permits controlled movements of flexion, extension, lateral bending, and rotation between adjacent vertebrae.
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Spacing & Foramina Patency: By maintaining intervertebral height, the discs preserve space for nerve roots to exit through the intervertebral foramina.
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Preventing Bone-on-Bone Contact: Discs cushion the vertebral bodies, preventing osteoarthritic changes by reducing direct bony friction.
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Contribution to Spinal Stability: Through interaction with ligaments and facet joints, the disc helps stabilize the motion segment, preventing excessive movement.
Classification (Types) of Lumbar Disc Herniation
Lumbar disc herniations are categorized by shape, extent, and location of the displaced material.
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Bulging Disc: A generalised extension of disc material beyond the vertebral margins affecting >25% of the circumference; often symmetrical.
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Focal Protrusion: Localized annular bulge involving <25% of the disc circumference, with the base of the herniation broader than its depth.
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Extrusion: Focal herniation where the depth (distance the displaced material extends) exceeds the base width; annular fibers are disrupted.
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Sequestration: Free fragment of nucleus that has separated completely from the parent disc and may migrate within the spinal canal.
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Circumferential Annular Tear (Global Circumferential Herniation): A full 360° radial tear of the annulus allowing uniform bulge of the nucleus; may involve high-grade annular fissuring.
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Focal vs. Broad-Based: Herniations affecting <25% (focal) versus 25–50% (broad-based) of the circumference; influences surgical approach.
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Central (Medial): Located in the midline directly posterior; can compress the cauda equina in severe cases.
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Paracentral (Paramedian): Just off midline; most common—compresses exiting nerve roots.
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Foraminal (Lateral Recess): Within the intervertebral foramen; affects the exiting nerve root at that level.
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Extraforaminal (Far Lateral): Beyond the foramen; compresses the nerve root at the level above.
Causes of Lumbar Disc Circumferential Herniation
Below are twenty contributing factors, each shown in a separate paragraph:
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Age-Related Degeneration: Progressive loss of proteoglycans in the nucleus reduces water binding, leading to decreased disc height and annular fissuring.
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Repetitive Mechanical Stress: Chronic overloading through occupation (e.g., heavy lifting) induces microtrauma and annular fiber fatigue.
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Acute Trauma: A sudden axial load or flexion injury (e.g., fall or motor vehicle accident) can create radial tensile stress exceeding annular strength.
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Genetic Predisposition: Polymorphisms in genes for collagen types I and IX correlate with early disc degeneration and predisposition to circumferential tears.
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Smoking: Nicotine induces vasoconstriction in vertebral endplates, impairing nutrient diffusion and accelerating disc degeneration.
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Obesity: Excess body weight increases axial compressive forces on the lumbar discs, hastening structural breakdown.
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Poor Posture: Sustained flexion or lateral bending (e.g., slouched sitting) shifts load to the anterior annulus, promoting fissure formation.
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Sedentary Lifestyle: Weak paraspinal musculature fails to offload discs effectively, increasing intradiscal pressures during daily activities.
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Vibration Exposure: Whole-body vibration (e.g., heavy machinery) repeatedly strains spinal discs, contributing to annular damage.
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Core Muscle Weakness: Inadequate support from the transverse abdominis and multifidus raises disc load during movement.
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Metabolic Disorders: Diabetes mellitus alters disc matrix turnover and increases glycation, weakening annular fibers.
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Inflammatory Cytokines: Elevated interleukin-1β and tumor necrosis factor-α in degenerated discs promote matrix metalloproteinase activity, breaking down collagen.
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Endplate Calcification: Bony sclerosis of vertebral endplates impedes nutrient flow, triggering nucleus dehydration and annular fissures.
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Disc Desiccation: Water loss lowers disc turgor, reducing load-bearing capacity and fostering circumferential annular cracks.
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Autoimmune Reactions: Exposed nucleus pulposus antigens may elicit autoimmune inflammation, weakening annular integrity.
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Occupational Bending/Twisting: Jobs requiring frequent torso rotation place shear forces on the annulus, predisposing to global tears.
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Previous Spinal Surgery: Altered biomechanics after laminectomy or fusion can overload adjacent levels, accelerating degeneration.
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Hormonal Factors: Post-menopausal estrogen deficiency is linked to reduced proteoglycan synthesis in discs.
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Nutritional Deficiencies: Low intake of vitamin D and calcium may impair endplate microcirculation and disc health.
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Genetic Connective Tissue Disorders: Conditions like Ehlers-Danlos syndrome yield inherently weak collagen, facilitating annular rupture.
Symptoms of Lumbar Disc Circumferential Herniation
Each clinical feature is elaborated below:
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Chronic Axial Low Back Pain: Deep, aching discomfort localized to the lumbar region; often worse with prolonged standing or bending.
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Mechanical Stiffness: Morning rigidity or transient loss of lumbar flexion, reflecting decreased disc height and facet joint stress.
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Radicular Leg Pain (Sciatica): Sharp, shooting pain radiating from the buttock to the posterior thigh or calf, corresponding to nerve root irritation.
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Numbness & Paresthesia: “Pins and needles” or loss of sensation in a dermatomal distribution, indicative of sensory fiber compromise.
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Muscle Weakness: Reduced strength in myotomal muscles (e.g., dorsiflexors in L4–L5 lesions), reflecting motor root involvement.
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Reflex Changes: Hyporeflexia or areflexia (e.g., diminished Achilles reflex in S1 compression), observed on neurological exam.
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Neurogenic Claudication: Leg pain and fatigue during walking or standing that is relieved by sitting or flexion, common with central canal compromise.
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Gait Disturbance: Antalgic or waddling gait to minimize painful lumbar motion or nerve stretch.
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Postural Changes: Antalgic lean away from the side of pain, spinal list, or flattened lumbar lordosis to reduce nerve tension.
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Positive Straight Leg Raise (SLR): Reproduction of leg pain between 30°–70° of hip flexion, signifying nerve root stretch.
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Crossed SLR: Contralateral leg rise eliciting ipsilateral pain—a highly specific sign of large disc herniation.
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Pain Worsened by Valsalva Maneuver: Increased intrathecal pressure exacerbates nerve root compression, intensifying symptoms.
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Pain with Cough/Sneeze: Transmitted pressure spikes provoke radicular pain when dural sac is compressed.
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Limited Flexion/Extension: Guarding and muscle spasm restrict lumbar motion in any plane.
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Sleep Disturbance: Nocturnal pain awakens patients, reflecting persistent nerve irritation.
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Bowel or Bladder Dysfunction: New-onset incontinence signals cauda equina syndrome and requires emergency evaluation.
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Sexual Dysfunction: Neuropathic disruption of pelvic plexus fibers may impair sexual function.
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Lower Extremity Edema or Venous Stasis: Secondary to neurogenic vascular dysregulation in severe cases.
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Hyperalgesia or Allodynia: Painful response to normally non-painful stimuli, due to central sensitization from chronic root irritation.
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Constitutional Symptoms (rare): Low-grade fever or weight loss may occur if inflammatory mediators are prominent.
Diagnostic Tests for Lumbar Disc Circumferential Herniation
Below is an exhaustive list, grouped by category, each with an expanded description.
A. Physical Examination
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Inspection: Observe spinal alignment, muscle bulk, and presence of scoliosis or lateral shift; global bulges often alter normal lumbar curvature.
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Palpation: Gentle pressure along the spinous processes and paraspinal muscles reveals trigger points, spasm, or tenderness over the disc level.
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Range of Motion (ROM): Active and passive flexion, extension, lateral bending, and rotation assess pain-limited motion arcs.
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Gait Analysis: Watch for antalgic gait (shortened stance phase on the painful side), Trendelenburg sign if hip abductor weakness coexists.
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Adam’s Forward Bend Test: Assesses spinal alignment and reveals compensatory curves when patient bends forward.
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Leg Length Measurement: Disparities may mimic or exacerbate symptoms, so true versus apparent leg length is compared.
B. Manual Provocative Tests
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Straight Leg Raise (Lasegue’s Test): Passive hip flexion with knee extended stretches the sciatic nerve; pain between 30°–70° suggests nerve root tension.
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Crossed Straight Leg Raise: Raising the asymptomatic leg reproduces pain on the symptomatic side—high specificity for large herniations.
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Slump Test: Patient seated with neck and thoracic flexion plus knee extension creates neural tension; symptom reproduction supports nerve root involvement.
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Femoral Nerve Stretch Test: Prone knee flexion stretches the femoral nerve; anterior thigh pain indicates upper lumbar root irritation (L2–L4).
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Kemp’s Test: With patient standing, examiner applies extension and rotation; ipsilateral pain suggests facet or foraminal pathology.
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Bowstring Test: During SLR, knee flexion to relieve pain then pressure on the popliteal fossa re-elicits it—confirms sciatic nerve tension.
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Valsalva Maneuver: Asking the patient to bear down increases intrathecal pressure; worsened radicular pain implies intraspinal lesion.
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Bragard’s Sign: Following a positive SLR, the examiner lowers the leg until pain subsides, then dorsiflexes the foot; return of pain further implicates nerve root.
C. Laboratory & Pathological Tests
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Complete Blood Count (CBC): Screens for infection; elevated white blood cells suggest discitis rather than simple tear.
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Erythrocyte Sedimentation Rate (ESR): Elevated in inflammatory or infectious processes of the spine.
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C-Reactive Protein (CRP): More sensitive marker for acute inflammation; helps differentiate aseptic annular tear from septic discitis.
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HLA-B27 Testing: Assesses for ankylosing spondylitis or spondyloarthropathy that may mimic discogenic pain.
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Discography (Provocative Discography): Injection of contrast into the nucleus under pressure reproduces concordant pain and visualizes annular tears on fluoroscopy or CT.
D. Electrodiagnostic Studies
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Electromyography (EMG): Detects denervation potentials in paraspinal or limb muscles, indicating chronic nerve root compression.
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Nerve Conduction Studies (NCS): Measures electrical conduction velocity; slowed signals in sensory or motor nerves confirm peripheral involvement.
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F-Wave Latency: Prolonged F-wave responses suggest proximal nerve root compromise.
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H-Reflex Testing: Analogous to Achilles reflex; extended latency supports S1 root entrapment.
E. Imaging Studies
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Plain Radiography (X-ray): Lateral and anteroposterior views assess disc space narrowing, endplate sclerosis, and osteophytes as indirect signs of degeneration.
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Magnetic Resonance Imaging (MRI): Gold standard for soft-tissue visualization; T2-weighted images reveal annular tears, disc bulges, and nerve root compression.
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Computed Tomography (CT): Superior for bony detail; with CT myelography, contrast outlines the thecal sac and root sleeves to show impingement.
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CT Discography: Combines provocative discography with CT imaging to pinpoint symptomatic disc and visualize internal fissures.
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Ultrasound (Limited): High-resolution probes can image paraspinal muscles and superficial soft tissues but have limited disc penetration.
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Bone Scan (Technetium-99m): Detects increased osteoblastic activity in endplates (“Modic changes”) adjacent to degenerated discs.
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Diffusion Tensor Imaging (DTI): Advanced MRI technique mapping nerve fiber integrity; reduced fractional anisotropy indicates root compromise.
Non-Pharmacological Treatments
Evidence-based clinical guidelines recommend beginning management of lumbar disc herniation with conservative therapies before considering medications or surgery .
A. Physiotherapy & Electrotherapy
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Heat Therapy (Moist Hot Packs)
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Description: Application of moist heat to the lumbar region.
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Purpose: Relieves muscle spasm and pain.
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Mechanism: Increases local blood flow, promotes tissue extensibility, and reduces muscle tension .
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Cryotherapy (Ice Packs)
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Description: Local cold application to inflamed areas.
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Purpose: Reduces acute inflammation and pain.
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Mechanism: Vasoconstriction decreases edema and nerve conduction velocity .
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Transcutaneous Electrical Nerve Stimulation (TENS)
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Description: Low-voltage electrical currents via skin electrodes.
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Purpose: Modulates pain perception.
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Mechanism: Activates the gate-control mechanism and stimulates endorphin release .
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Ultrasound Therapy
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Description: High-frequency sound waves delivered via a transducer.
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Purpose: Promotes tissue healing and pain relief.
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Mechanism: Mechanical vibrations enhance cellular metabolism and blood flow .
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Shortwave Diathermy
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Description: Deep heating using electromagnetic waves.
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Purpose: Reduces deep muscular pain and stiffness.
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Mechanism: Increases tissue temperature, enhancing circulation and collagen extensibility .
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Interferential Current Therapy
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Description: Medium-frequency currents that intersect in tissues.
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Purpose: Alleviates deep-seated pain.
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Mechanism: Stimulates nerve fibers to inhibit pain signals .
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Low-Level Laser Therapy
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Description: Application of low-intensity laser beams.
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Purpose: Reduces pain and inflammation.
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Mechanism: Photobiomodulation enhances mitochondrial function and modulates cytokine release .
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Spinal Traction Therapy
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Description: Mechanical or manual stretching of the spine.
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Purpose: Decompresses nerve roots and reduces disc pressure.
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Mechanism: Increases intervertebral space, decreases intradiscal pressure .
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Massage Therapy (Deep Tissue)
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Description: Manual kneading of paraspinal muscles.
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Purpose: Relieves muscle tension and improves flexibility.
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Mechanism: Enhances circulation, breaks adhesions, and stimulates mechanoreceptors .
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Manual Therapy (Spinal Mobilization)
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Description: Therapist-applied passive movements of spinal joints.
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Purpose: Improves joint mobility and reduces pain.
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Mechanism: Modulates mechanoreceptor input and reduces nociceptive signaling .
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Spinal Manipulation (Chiropractic)
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Description: High-velocity, low-amplitude thrusts.
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Purpose: Restores joint function and alleviates radicular pain.
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Mechanism: Releases entrapped synovial folds and activates descending inhibitory pathways .
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Kinesio Taping
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Description: Elastic therapeutic tape applied along paraspinal muscles.
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Purpose: Supports muscles and reduces pain.
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Mechanism: Improves lymphatic drainage and proprioceptive feedback.
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Neuromuscular Electrical Stimulation (NMES)
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Description: Electrical currents to evoke muscle contraction.
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Purpose: Strengthens core musculature.
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Mechanism: Enhances muscle recruitment and prevents atrophy .
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Aquatic Therapy
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Description: Exercises performed in water.
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Purpose: Minimizes gravitational load and facilitates movement.
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Mechanism: Buoyancy reduces joint stress; hydrostatic pressure improves proprioception .
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Extracorporeal Shockwave Therapy (ESWT)
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Description: High-energy acoustic pulses delivered to tissues.
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Purpose: Promotes tissue repair and reduces chronic pain.
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Mechanism: Induces microtrauma, stimulating neovascularization and growth factor release.
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B. Exercise Therapies
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McKenzie Extension Exercises – Centralize pain by teaching end-range lumbar extension movements. Mechanism: Mobilizes nucleus pulposus away from nerve roots.
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Core Stabilization – Isometric activation of transversus abdominis and multifidus. Mechanism: Enhances spinal support and load distribution.
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Lumbar Flexion Exercises – Double knee-to-chest stretches to reduce posterior disc pressure.
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Swiss Ball Stabilization – Dynamic core strengthening on an unstable surface.
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Pilates-Based Training – Focuses on controlled, precise movements to improve posture and flexibility.
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Yoga Postures (e.g., Cobra Pose) – Enhances spinal extension and stretches paraspinal muscles.
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Low-Impact Aerobics (Walking, Cycling) – Promotes circulation and overall conditioning.
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Hamstring & Hip Flexor Stretching – Reduces posterior chain tightness contributing to lumbar load .
C. Mind-Body Therapies
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Yoga Therapy – Integrates postures, breathwork, and meditation for holistic pain management.
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Tai Chi – Gentle, flowing movements improve balance and reduce stress.
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Mindfulness Meditation – Teaches nonjudgmental awareness of pain, reducing its perceived intensity.
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Biofeedback – Uses real-time EMG feedback to teach muscle relaxation techniques.
D. Educational & Self-Management
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Back School (Posture Education) – Teaches proper body mechanics for daily activities.
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Self-Pacing & Activity Modification – Guides gradual activity increases to prevent flare-ups.
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Ergonomic & Workplace Instruction – Optimizes seating, lifting, and workstation setup to minimize lumbar strain.
Pharmacological Treatments
Drug | Class | Dosage & Timing | Major Side Effects |
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Ibuprofen | NSAID (non-selective COX-1/2 inhibitor) | 200–800 mg orally every 4–6 h as needed (max 3,200 mg/day) Verywell Health | GI upset, ulceration, renal impairment |
Naproxen | NSAID (non-selective) | 220–500 mg orally every 8–12 h (max 1,500 mg/day) Verywell Health | GI bleeding, edema, cardiovascular risk |
Diclofenac | NSAID (non-selective) | 50 mg orally 2–3 times/day (max 150 mg/day) Drugs.com | GI bleeding, hypertension, hepatic dysfunction |
Ketorolac | NSAID (non-selective) | 10–20 mg IV/IM initial, then 10 mg every 4–6 h (max 40 mg/day) MedicineNet | Renal toxicity, GI bleeding |
Celecoxib | NSAID (COX-2 selective) | 200 mg once daily or 100–200 mg BID (max 200 mg/day) WikEM | Cardiovascular risk, GI ulceration |
Acetaminophen | Analgesic (non-opioid) | 325–500 mg every 4–6 h (max 3,250 mg/day) Verywell Health | Hepatotoxicity (overdose) |
Tramadol | Opioid-analgesic & SNRI | 50–100 mg orally every 4–6 h PRN (max 400 mg/day) Drugs.com | Nausea, dizziness, seizures, dependence |
Morphine | Opioid-analgesic | 15–30 mg orally every 4 h PRN (opioid-naïve) NCBI | Respiratory depression, constipation |
Gabapentin | Anticonvulsant (gabapentinoid) | 300 mg orally TID (may titrate up to 1,200 mg/day) WikEM | Drowsiness, dizziness, edema |
Pregabalin | Anticonvulsant (gabapentinoid) | 75 mg orally BID (may increase to 300 mg/day) Mayo Clinic | Dizziness, weight gain, somnolence |
Duloxetine | SNRI (serotonin-norepinephrine RI) | 60 mg once daily (initial and maintenance; max 120 mg/day) Drugs.com | Nausea, insomnia, dry mouth |
Amitriptyline | TCA (tricyclic antidepressant) | 10–25 mg once daily at bedtime (neuropathic pain) | Sedation, anticholinergic effects |
Cyclobenzaprine | Muscle relaxant | 5–10 mg TID (short-term) | Sedation, dry mouth |
Baclofen | Muscle relaxant (GABA_B agonist) | 5 mg TID (increase to 20–80 mg/day) | Drowsiness, weakness |
Prednisone | Corticosteroid | 5–60 mg once daily (taper per protocol) | Weight gain, hyperglycemia |
Methylprednisone | Corticosteroid | 16–48 mg once daily (short-course taper) | Immunosuppression, osteoporosis |
Diazepam | Benzodiazepine | 2–10 mg TID (short-term) | Sedation, dependence |
Codeine | Opioid | 15–60 mg every 4–6 h PRN (max 360 mg/day) | Constipation, drowsiness |
Oxycodone | Opioid | 5–10 mg every 4 h PRN (max 60 mg/day) | Nausea, respiratory depression |
Meloxicam | NSAID (preferential COX-2) | 7.5 mg once daily (may increase to 15 mg) | GI upset, edema |
Hydrocodone | Opioid | 5–10 mg every 4–6 h PRN (max 60 mg/day) | Nausea, sedation |
Dietary & Molecular Supplements
Supplement | Dosage | Function | Mechanism |
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Glucosamine | 1,500 mg/day | Joint support | Stimulates proteoglycan synthesis |
Chondroitin | 1,200 mg/day | Cartilage health | Inhibits degradative enzymes |
MSM (Methylsulfonylmethane) | 2,000 mg/day | Anti-inflammatory | Donates sulfur for connective tissue repair |
Collagen (Type II) | 10 g/day | Disc matrix support | Provides amino acids for ECM synthesis |
Omega-3 Fatty Acids | 1,000 mg/day | Anti-inflammatory | Inhibits NF-κB and cytokine production |
Vitamin D | 1,000–2,000 IU/day | Bone health | Regulates calcium homeostasis |
Magnesium | 300 mg/day | Muscle relaxation | Modulates NMDA receptor and Ca²⁺ channels |
Curcumin | 500 mg BID | Anti-inflammatory | Inhibits COX-2 and cytokines |
Resveratrol | 200 mg/day | Antioxidant | Activates SIRT1, reduces oxidative stress |
Collagen Peptides | 10 g/day | Connective tissue support | Stimulates fibroblast proliferation |
Advanced & Regenerative Drugs
Drug Class | Drug & Dosage | Function | Mechanism |
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Bisphosphonates | Alendronate 70 mg weekly | Bone density maintenance | Inhibits osteoclasts |
Regenerative Peptides | BPC-157 200 µg daily (off-label) | Tissue repair | Promotes angiogenesis and fibroblast growth |
Viscosupplementation | Hyaluronic acid injection (2 mL) | Joint lubrication | Restores synovial fluid viscosity |
Platelet-Rich Plasma | 3 mL epidural injection | Regenerative therapy | Releases growth factors |
Stem Cell Therapeutics | MSC injection (off-label protocols) | Disc regeneration | Differentiation into nucleus pulposus cells |
Growth Factors | rhBMP-2 (off-label) | Bone fusion | Stimulates osteogenesis |
Autologous Chondrocytes | 1 × 10⁶ cells injection | Cartilage repair | Cartilage matrix synthesis |
Nucleoplasty | Plasma disc decompression (single session) | Minimally invasive decompression | Uses coblation to remove disc material |
Extracellular Vesicles | EV-rich injectate (protocol dependent) | Regenerative signaling | Delivers microRNAs and proteins |
Collagen Scaffold | Disc scaffold implantation (surgical) | Structural support | Provides ECM framework for regeneration |
Surgical Options
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Microdiscectomy
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Procedure: Removal of herniated disc fragment via a small incision and microscope.
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Benefits: Rapid pain relief, short hospital stay.
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Laminectomy
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Procedure: Removal of the lamina to decompress the spinal canal.
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Benefits: Relieves central canal stenosis.
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Foraminotomy
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Procedure: Widening of the neural foramen.
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Benefits: Reduces nerve root compression.
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Spinal Fusion
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Procedure: Permanent joining of two vertebrae using bone grafts and instrumentation.
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Benefits: Stabilizes unstable segments.
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Disc Replacement
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Procedure: Implantation of an artificial disc.
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Benefits: Preserves motion at the disc level.
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Endoscopic Discectomy
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Procedure: Minimally invasive removal via endoscope.
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Benefits: Less tissue trauma, faster recovery.
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Percutaneous Nucleoplasty
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Procedure: Radiofrequency removal of nucleus pulposus.
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Benefits: Minimally invasive, quick recovery.
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Facet Joint Fusion (RF Ablation)
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Procedure: Radiofrequency ablation of facet joints.
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Benefits: Reduces facet-mediated pain.
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Minimally Invasive Transforaminal Lumbar Interbody Fusion (MIS-TLIF)
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Procedure: Fusion via small tubular retractors.
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Benefits: Less muscle damage, quicker rehab.
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Anterior Lumbar Interbody Fusion (ALIF)
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Procedure: Fusion through an anterior abdominal approach.
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Benefits: Restores disc height, indirect decompression.
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Preventive Measures
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Regular Core Strengthening – Maintains spinal support.
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Ergonomic Workstations – Reduces repetitive lumbar stress.
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Proper Lifting Techniques – Bend knees, keep spine neutral.
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Weight Management – Minimizes axial load.
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Smoking Cessation – Improves disc nutrition.
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Postural Awareness – Prevents abnormal spinal loading.
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Regular Low-Impact Exercise – Promotes circulation and disc health.
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Adequate Hydration – Maintains disc turgor.
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Stretching Routines – Reduces muscular tension.
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Use of Supportive Footwear – Improves overall posture.
When to See a Doctor
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Severe or Progressive Neurological Deficits: Such as muscle weakness or loss of sensation.
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Cauda Equina Signs: Bowel/bladder dysfunction, saddle anesthesia.
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Intractable Pain: Unresponsive to 6–12 weeks of conservative therapy.
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Systemic Symptoms: Fever, weight loss, or night sweats suggesting infection or malignancy.
Frequently Asked Questions
1. What causes circumferential herniation?
A combination of age-related degeneration, elevated intradiscal pressure, and annular fiber tears leads to diffuse bulging of the disc around its circumference.
2. How is it diagnosed?
MRI is the gold standard, demonstrating disc bulge >180° and assessing nerve root impingement.
3. Can conservative treatment reverse it?
While the bulge itself may not fully regress, most patients experience significant symptom relief with conservative care.
4. What is the role of spinal traction?
Traction temporarily increases intervertebral space and can alleviate nerve root compression.
5. When is surgery indicated?
Surgery is considered for progressive neurological deficits, cauda equina syndrome, or pain refractory to 6–12 weeks of conservative management.
6. Are steroids useful?
Short-course oral steroids may reduce inflammation, but they’re not a long-term solution.
7. How effective is epidural steroid injection?
It can provide short-term pain relief but may not alter long-term outcomes.
8. What lifestyle changes help prevention?
Regular exercise, weight control, ergonomic adjustments, and smoking cessation are key.
9. Is weightlifting contraindicated?
Heavy lifting can exacerbate symptoms; proper technique and progressive loading are crucial.
10. Can yoga worsen the condition?
When guided by a trained instructor, yoga can be beneficial; uncontrolled deep flexion or twisting may aggravate symptoms.
11. How long does recovery take after microdiscectomy?
Most patients return to light activities within 4–6 weeks, with full recovery by 3 months.
12. Are regenerative therapies proven?
Most are experimental; platelet-rich plasma and stem cell injections show promise but lack large-scale evidence.
13. What supplements support disc health?
Glucosamine, chondroitin, omega-3, and collagen peptides may help, though evidence varies.
14. Can mind-body therapies reduce pain?
Yes—meditation, Tai Chi, and biofeedback help modulate pain perception and cope with chronic pain.
15. When should I suspect cauda equina syndrome?
Loss of bowel/bladder control, saddle anesthesia, or significant lower limb weakness require immediate assessment.
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 16, 2025.