Cavernous Sinus Syndrome (CSS) is a collection of signs and symptoms that appear when the structures running through, or lying next to, the cavernous sinus become damaged or compressed. The cavernous sinus is a hollow, blood‑filled channel tucked deep behind each eye, on either side of the pituitary gland. Inside this small space run the internal carotid artery, a venous plexus, and five critical nerves (cranial nerves III, IV, V division 1, V division 2, and VI). When disease, infection, bleeding, a tumor, or inflammation disturb this area, patients develop a predictable set of neurological and eye‑related problems. CSS is not itself a single disease; it is the shared end result of many possible disorders that injure the cavernous sinus or its contents.
The cavernous sinuses are two small, hollow veins that sit on either side of the pituitary gland, behind the eyes. They act like busy traffic hubs for blood and for five key cranial nerves (III, IV, V1, V2 and VI) plus part of the sympathetic nerve chain and the internal carotid artery. Cavernous Sinus Syndrome (CSS) is the name doctors give to the cluster of problems that appear when anything—blood clot, infection, tumour, trauma or inflammation—presses on, blocks or grows inside this space. Typical red‑flag signs are new double vision, bulging eye, droopy eyelid, eye pain, facial numbness or Horner‑type pupil changes. Rapid diagnosis matters because untreated causes such as septic cavernous sinus thrombosis can be life‑threatening. NCBI
Anatomy
Think of the cavernous sinus as an “under‑the‑bridge tunnel” for nerves and a major artery. The artery (the internal carotid) brings blood to the brain, while the cranial nerves act like high‑speed data cables controlling eye movement, eyelid elevation, pupil size, and facial sensation. If any disorder narrows the tunnel or fills it with clot, infection, tumor, or leaked blood, those cables and the artery are squeezed. Because the space is rigid, even a small swelling can quickly pinch the nerves, block venous outflow, and threaten blood supply to the brain and eye.
Most causes of CSS fall into four broad mechanisms:
Mass effect – something bulky (tumor, aneurysm, abscess) crowds the sinus.
Vascular event – a clot (thrombosis) or abnormal connection (fistula) alters pressure and flow.
Inflammation or infection – swelling from microbes or autoimmune attack thickens sinus walls and inflames nerves.
Trauma – fractures or surgical injury bruise or tear the contents.
Regardless of the trigger, the shared outcome is nerve dysfunction and venous congestion, which then create the clinical picture we call CSS.
Main Types of Cavernous Sinus Syndrome
Although clinicians may slice the pie differently, five broad “types” help organize thinking and guide treatment:
Infectious CSS – Driven by bacteria, fungi, or viruses that reach the sinus by bloodstream or from nearby facial or sinus infections.
Neoplastic CSS – Caused by benign or malignant tumors such as meningioma, pituitary adenoma, lymphoma, metastasis, or schwannoma.
Vascular CSS – Results from cavernous sinus thrombosis, carotid‑cavernous fistula, or internal carotid artery aneurysm pressing from within.
Inflammatory/Auto‑immune CSS – Includes Tolosa‑Hunt syndrome, granulomatosis with polyangiitis, sarcoidosis, IgG4‑related disease, and idiopathic orbital inflammatory disease.
Traumatic/Post‑surgical CSS – Occurs after skull base fractures, penetrating injury, or neurosurgical or ENT procedures in the region.
Each type follows the same anatomic rules but requires different tests and treatments.
Common Causes
Bacterial cavernous sinus thrombosis – A deep‑seated blood‑clot and infection often starting from boils or sinusitis spreads through facial veins, causing pus‑filled clot that blocks venous drainage.
Mucormycosis – A fast‑moving fungal infection, especially in diabetics, grows along blood vessels, invades the sinus walls, and can destroy tissue within days.
Pituitary macroadenoma – A benign but bulky tumor beneath the sinus bulges sideways and presses on the lateral walls, crushing cranial nerves.
Meningioma of the sphenoid wing – This slow‑growing lining tumor thickens the bone and directly invades the cavernous sinus, leading to gradual nerve failure.
Carotid‑cavernous fistula (CCF) – A tear between artery and venous sinus shoots high‑pressure arterial blood into the low‑pressure sinus, causing pulsating congestion and eye redness.
Internal carotid artery aneurysm – A balloon‑like bulge at the artery curve inside the sinus presses on adjacent nerves, often causing isolated eye muscle palsy.
Metastatic breast or lung cancer – Cancer cells traveling in blood settle in the sinus, forming infiltrative masses that mimic meningioma but progress faster.
Lymphoma – Malignant lymphocytes infiltrate the sinus walls, thickening them and reducing nerve function; steroids may shrink the mass temporarily.
Tolosa‑Hunt syndrome – A rare, idiopathic inflammation that causes painful eye movement and resolves with steroids but may recur.
Granulomatosis with polyangiitis – An autoimmune attack on small vessels deposits granulomas in the sinus region, leading to nerve ischemia and necrosis.
Sarcoidosis – Clumps of immune cells build up in the sinus walls or cranial nerves, causing chronic, painless ophthalmoplegia.
Tuberculous pachymeningitis – Tuberculosis infection thickens the dura lining; granulomatous tissue can extend into the cavernous sinus.
Traumatic skull base fracture – Bone shards or hematoma directly injure the venous channel and its nerves, producing acute CSS after head injury.
Iatrogenic injury after trans‑sphenoidal surgery – Navigating too laterally while removing pituitary tumors may nick the internal carotid or nerves, leading to immediate CSS.
Idiopathic orbital inflammatory disease – A non‑infectious swelling behind the eye can extend to the sinus, creating pressure and nerve inflammation without detectable systemic disease.
Symptoms
Double vision (diplopia) – Because eye muscles lose their nerve control, the two eyes no longer point together, so images split.
Drooping eyelid (ptosis) – Weakness of the oculomotor nerve leaves the upper lid without its lifting muscle, causing a partial or complete droop.
Eye movement paralysis (ophthalmoplegia) – Some or all directions of gaze become impossible, making the eye “frozen” or sluggish.
Protruding eye (proptosis) – Congestion and pressure push the eyeball forward, giving a bulged‑eye appearance.
Eye redness and swelling (chemosis) – Stagnant venous blood engorges conjunctival vessels, making the white of the eye red, swollen, and tender.
Facial pain or numbness – Injury to the first two branches of the trigeminal nerve (V1 and V2) causes sharp pain, tingling, or loss of touch in the forehead, nose, cheek, and upper teeth.
Pulsatile noise in ear (subjective bruit) – With a carotid‑cavernous fistula, patients hear a whooshing sound matching their heartbeat, created by turbulent blood flow.
Headache behind the eye – Venous congestion stretches pain‑sensitive coverings around the sinus and artery, producing deep, boring pain that worsens when bending forward.
Blurred or lost vision – Pressure on the optic nerve or reduced arterial flow can dim sight; delayed treatment may cause permanent blindness.
Systemic signs of infection (fever, chills) – When CSS is infectious, bacteria or fungi trigger high temperature, malaise, and elevated white‑cell count.
Diagnostic Tests
A. Physical‑Examination‑Based Tests
Cranial‑nerve eye‑movement assessment – The clinician asks the patient to follow a finger in six directions. Restricted motion or double vision pinpoints which cranial nerve (III, IV, VI) is weak.
Pupil light reaction – Shining a light in each eye shows if the oculomotor nerve is intact; a blown (dilated) or sluggish pupil suggests compressive lesion or aneurysm.
Corneal‑blink reflex – Touching the cornea with a sterile wisp should trigger a blink; loss points to trigeminal (V1) involvement.
Facial‑sensation mapping – Light touch or pin‑prick tests across forehead, cheeks, and upper gum reveal numb zones, guiding suspicion to V1 or V2 compression.
B. Manual or Bedside Tests
Hess chart plotting – A grid test where patients align dots records eye muscle strength; asymmetry maps nerve palsies quantitatively.
Fundoscopy for papilledema – Using an ophthalmoscope, the doctor looks for swollen optic discs, hinting at raised intracranial pressure linked to venous blockage.
Hand‑held Doppler auscultation – A pocket Doppler probe over the closed eyelid detects turbulent arterialized flow, supporting a fistula diagnosis.
C. Laboratory & Pathological Tests
Complete blood count (CBC) – High white cells flag bacterial infection, anemia may point to chronic disease or blood loss from trauma.
C‑reactive protein & erythrocyte sedimentation rate (ESR) – These inflammation markers climb in infection, vasculitis, or Tolosa‑Hunt syndrome.
Blood cultures – Growing bacteria from blood confirms septic cavernous sinus thrombosis and guides antibiotic choice.
Auto‑antibody panel (ANCA, ACE, IgG4) – Positive tests help diagnose granulomatosis with polyangiitis, sarcoidosis, or IgG4‑related inflammatory CSS.
Pituitary hormone profile – If a pituitary tumor is suspected, measuring prolactin, growth hormone, ACTH, and thyroid hormones clarifies functional status and guides surgery.
D. Electrodiagnostic Tests
Visual evoked potentials (VEP) – Electrodes record brain responses to flashing lights; slowed signals imply optic pathway compromise from cavernous lesions.
Electromyography (EMG) of extra‑ocular muscles – Fine‑needle recordings detect denervation patterns, distinguishing neuropathic from myopathic eye movement failure.
E. Imaging Tests
Magnetic resonance imaging (MRI) with contrast – The gold standard: high‑resolution pictures show soft‑tissue masses, inflammatory thickening, venous clot, and arterial flow voids inside the sinus.
MR venography (MRV) – Special MRI sequence visualizes venous channels; absence of flow or filling defects confirms thrombosis.
MR angiography (MRA) – Highlights arteries, revealing aneurysms or fistulas feeding the cavernous sinus.
Computed‑tomography (CT) scan of head and orbit – Faster than MRI, CT detects bone fractures, acute hemorrhage, and calcified meningiomas.
Digital subtraction angiography (DSA) – An invasive catheter study injects dye into vessels; it remains the most precise way to map fistulas and plan endovascular repair.
Positron‑emission tomography‑CT (PET‑CT) – Combines metabolic and anatomic imaging, helpful when searching for lymphoma or distant metastases that seed the cavernous sinus.
Non‑Pharmacological Treatments
Below are scientifically informed approaches grouped into exercise therapies, mind‑body methods, and educational/self‑management tools. Each paragraph states what it is, why it is used and how it works.
Oculomotor gaze‑stability training – Guided eye‑movement drills (pursuits, saccades, convergence) strengthen weakened extra‑ocular muscles, reduce diplopia and help the brain remap gaze control. Studies show measurable gains in eye‑alignment and symptom relief within 6–8 weeks. Mechanism: repetitive activation promotes neuromuscular plasticity of cranial nerves III, IV and VI. PubMed Central
Facial‑muscle neuromotor retraining – Gentle resistance exercises for frontalis, orbicularis oculi and masseter muscles improve symmetry and chewing comfort when trigeminal branches are affected. Purpose: regain strength, prevent synkinesis. Mechanism: proprioceptive feedback boosts motor‑unit recruitment in CN V and VII circuits.
Vestibulo‑ocular reflex (VOR) drills – Head‑turn‑with‑target tasks recalibrate balance between inner‑ear, eye and cerebellar inputs, easing oscillopsia and dizziness often triggered by rapid eye movements.
Prism adaptation sessions – Temporary Fresnel prisms rearrange incoming light, letting the visual cortex suppress diplopic images. Over weeks, neural adaptation can partially maintain single vision even after the prism is removed.
Postural core‑stability training – Pilates‑style core work and proprioceptive balance board routines support cervical alignment, reducing referred neck strain that may worsen headache in CSS.
Graduated aerobic conditioning – Cycling or brisk walking (≥150 min/week) improves cerebral blood flow and reduces systemic risk factors (e.g., hypercoagulability) linked to venous thrombosis.
Mindfulness‑Based Stress Reduction (MBSR) – An 8‑week course combining breath‑awareness meditation and gentle yoga dampens limbic pain processing and lowers anxiety that magnifies visual symptoms. Neuro‑imaging shows activation of anterior cingulate and orbitofrontal cortices, areas that gate pain signals. PubMed Central
Guided imagery for neuropathic pain – Visualising warm, soothing light across the face and eyes can down‑regulate sympathetic outflow, decreasing burning or stabbing sensations in V1/V2 dermatomes.
Progressive muscle relaxation (PMR) – Systematic tensing and releasing of muscle groups lowers blood pressure and reduces sympathetic surges that may aggravate arterial aneurysm leaks into the sinus.
Biofeedback‑assisted blink training – Electromyographic sensors teach patients to normalise blink rate, cutting exposure keratopathy when eyelid closure is incomplete.
Cognitive‑behavioural therapy (CBT) for health anxiety – CBT sessions reframe catastrophic thoughts (“I’m going blind”) and improve adherence to treatment regimens.
Patient‑directed diary tracking – Logging daily diplopia severity, headache scores and medication times helps clinicians fine‑tune therapy and catches early relapse.
Peer‑support groups (online or local) – Sharing experiences reduces isolation, provides coping tips, and reinforces healthy habits such as eye‑shield use during sleep.
Ergonomic workstation adjustment – Elevating monitors, adding anti‑glare filters and scheduling 20‑20‑20 vision breaks minimise eye‑strain.
Protective eye‑patch scheduling – Short, alternating monocular occlusion prevents suppression amblyopia while giving temporary relief from double vision.
Moist‑heat facial packs – Warm compresses loosen tight orbicularis and temporalis muscles, easing pain while improving sinus drainage.
Manual lymph‑drainage massage – Light strokes toward pre‑auricular nodes lower periorbital edema that can worsen proptosis.
Transcutaneous electrical nerve stimulation (TENS) – Low‑frequency pulses over trigeminal trigger zones modulate spinal trigeminal nucleus activity, dulling neuropathic pain.
Mindful breathing ‘box’ technique – 4‑4‑4‑4 breathing balances autonomic tone, lessening stress‑induced blood‑pressure spikes that might enlarge carotid aneurysms.
Educational workshops on early‑infection care – Teaching prompt treatment of sinusitis, facial boils and dental abscesses directly reduces the incidence of septic cavernous sinus thrombosis.
Evidence‑Based Drugs
Safety note: Dosages are adult averages; always individualise and monitor renal/hepatic function.
Vancomycin – Glycopeptide antibiotic; 15 mg/kg IV every 12 h for presumed MRSA in septic cavernous sinus thrombosis. Side effects: nephro‑ and ototoxicity, “red‑man” flushing. Medscape
Ceftriaxone – Third‑generation cephalosporin; 2 g IV every 12 h, broad Gram‑negative and streptococcal coverage. Beware biliary sludging.
Metronidazole – Nitroimidazole; 500 mg IV every 8 h adds anaerobic coverage for sinus pathogens. Metallic taste, peripheral neuropathy with >4 wk use.
Low‑Molecular‑Weight Heparin (Enoxaparin) – Anticoagulant; 1 mg/kg SC every 12 h for 5–10 days, then bridge to oral agent. Monitors factor Xa in renal impairment; watch for heparin‑induced thrombocytopenia. AHA Journals
Warfarin – Vitamin‑K antagonist; initial 5 mg PO daily, titrate to INR 2‑3 for 3–6 months. Interacts with many foods/drugs; risk of bleeding.
Dexamethasone – Corticosteroid; 4 mg IV every 6 h for acute edema from tumour or inflammatory pseudotumor. Taper over 1–2 weeks to avoid adrenal crisis.
Aspirin – Antiplatelet; 81–325 mg PO daily for long‑term secondary prevention after thrombosis resolves. GI irritation, bleeding hazard.
Clopidogrel – P2Y 12 inhibitor; 75 mg PO daily when aspirin alone insufficient or contraindicated. Check CYP2C19 metabolism.
Carbamazepine – Sodium‑channel blocker; start 100 mg PO twice daily, titrate to 400–800 mg/day for trigeminal neuralgia pain. Monitor liver enzymes, watch for hyponatremia.
Gabapentin – Calcium‑channel modulator; 300 mg PO night‑time, uptitrate to 900–2400 mg/day for neuropathic facial pain. Drowsiness and weight gain are common.
Dietary Molecular Supplements
Omega‑3 Fish‑oil (EPA + DHA) – 1000 mg twice daily. Function: anti‑thrombotic, reduces vascular inflammation; mechanism: competitive COX‑2 inhibition and pro‑resolving mediator production.
Alpha‑Lipoic Acid (ALA) – 600 mg once daily. Function: antioxidant; shown in meta‑analysis to improve neuropathic pain scores. Mechanism: scavenges free radicals, restores mitochondrial glutathione. PubMed
Curcumin (bio‑enhanced) – 500 mg three times daily with black‑pepper extract. Function: neuro‑protective; mechanism: inhibits NF‑κB and activates Nrf2, reducing neuro‑inflammation. PubMed Central
Vitamin B12 (Methylcobalamin) – 1000 µg sublingual daily or 1 mg IM weekly. Supports myelin repair and nerve conduction.
Acetyl‑L‑Carnitine – 500 mg twice daily; improves mitochondrial energy in damaged nerves.
Coenzyme Q10 (Ubiquinone) – 100 mg twice daily; enhances oxidative phosphorylation, may improve fatigue.
Magnesium Glycinate – 200 mg nightly; calms neuronal hyper‑excitability, helps headache prevention.
N‑Acetyl Cysteine (NAC) – 600 mg twice daily; boosts glutathione, mitigates oxidative stress secondary to infection‑related cytokine surge.
Resveratrol – 150 mg daily; activates SIRT1, modulates endothelial nitric‑oxide synthase, supporting vascular health.
Ginkgo biloba extract (EGb 761) – 120 mg daily; improves micro‑circulation, may aid residual visual‑field perfusion.
Regenerative / Stem‑Cell‑Based Therapies
Autologous Mesenchymal Stem‑Cell (MSC) Intrathecal Infusion – Typical protocol: 1–2 × 10⁶ cells/kg delivered via lumbar puncture every 3 months. Purpose: secrete neurotrophic factors and modulate inflammation to encourage cranial‑nerve regeneration. Early phase‑I trials in peripheral nerve injury report safety and modest functional gains. PubMed Central
MSC‑Derived Exosome IV Infusion – 100 µg exosomal protein weekly for 4 weeks. Nano‑vesicles carry micro‑RNAs that stimulate Schwann‑cell remyelination. Dove Medical Press
Adipose‑Derived Stem‑Cell Injection Around Cavernous Sinus – 5 × 10⁶ cells, image‑guided via trans‑foraminal approach; investigated for repairing stretch‑injured cranial nerves. ClinicalTrials.gov
Schwann‑Cell Graft with Fibrin Scaffold – One‑time surgical placement of autologous Schwann cells seeded on fibrin matrix along damaged nerve segment; promotes axonal guidance. PubMed Central
Intranasal Neural Progenitor ‘Nerve Bridge’ Implant – Harvested olfactory mucosal cells cultured into 3‑D bridge and implanted to span cranial‑nerve gap; dosage: ~2 cm matrix length carrying 1 × 10⁷ cells. Early human trial announced 2024. The Australian
AAV‑BDNF Gene‑Therapy Micro‑Injection – Delivers brain‑derived neurotrophic factor gene to cavernous sinus region (single 10¹¹ vg dose). Aim: long‑term trophic support; pre‑clinical only.
All regenerative options remain investigational; access limited to accredited trials with rigorous consent.
Surgical / Interventional Procedures
Endovascular Balloon or Coil Embolization for Carotid‑Cavernous Fistula (CCF) – A micro‑catheter fed through the femoral artery places detachable balloons or coils to seal the arterial leak. Success ≥80 % with rapid relief of eye congestion; benefits: minimally invasive, short stay. PubMed
Decompressive Resection of Cavernous Sinus Meningioma – Neurosurgeon removes tumour piecemeal through lateral skull‑base window, sparing critical nerves while reducing mass effect. Benefit: preserves vision and extra‑ocular movement; possible cranial‑nerve improvement >70 %. PubMed
Stereotactic Radiosurgery (Gamma Knife®) – Focused cobalt‑60 beams (12–14 Gy) shrink residual or inoperable lesions over 6–12 months with ≤5 % cranial‑nerve toxicity. ScienceDirect
Endoscopic Endonasal Trans‑Sphenoidal Removal of Pituitary Adenoma – Through nasal corridors, surgeons debulk adenomas invading the cavernous sinus; advantages: no brain retraction, faster recovery. EyeWiki
Catheter‑Directed Thrombolysis / Mechanical Thrombectomy – For extensive septic thrombosis not responding to heparin: interventional radiologist aspirates clot or infuses urokinase directly into the sinus. Used selectively due to hemorrhage risk. Medscape
Ways to Prevent Cavernous Sinus Problems
Treat facial and sinus infections promptly with proper antibiotics.
Practise meticulous dental hygiene; dental abscesses can seed the sinus.
Wear protective headgear during contact sports to avoid skull‑base fractures.
Keep blood‑sugar and blood‑pressure in target range to shrink aneurysm risk.
Stop smoking—nicotine damages vessel walls and thickens blood.
Stay hydrated; sluggish blood flow promotes clotting.
Move every hour on long flights or car trips to reduce venous stasis.
Manage hormonal states (e.g., contraceptive pills) wisely; discuss thrombosis risk with your doctor.
Vaccinate against sinus‑loving pathogens (e.g., pneumococcus, influenza).
Attend routine eye exams; subtle nerve palsies caught early lead to quicker work‑ups.
When to See a Doctor Urgently
Call or visit an emergency department the same day if you notice any of these sudden changes:
new double vision or eye that cannot move in all directions
rapidly bulging, red, painful eye
severe, one‑sided headache around the eye or temple
numbness or tingling in the forehead or cheek
eyelid droop with unequal pupils
fever or facial infection followed by worsening eye pain
Early treatment prevents permanent vision loss, stroke or even death in septic cases. NCBI
Practical Do’s and Don’ts
Do
Keep your head slightly elevated when sleeping to ease venous drainage.
Apply sterile warm compresses to promote sinus clearing if infection ruled out.
Wear UV‑blocking sunglasses outdoors to reduce photophobia.
Follow all antibiotic and anticoagulant doses exactly—missing doses endangers recovery.
Log symptoms daily to spot patterns and share with your clinician.
Don’t
6. Don’t pick or squeeze facial pimples in the “danger triangle” (nose to mouth corners).
7. Don’t drive until your ophthalmologist confirms safe binocular vision.
8. Avoid contact sports until vascular lesions are fully treated.
9. Skip follow‑up scans; some aneurysms re‑expand silently.
10. Never stop steroids suddenly; tapering prevents adrenal crisis.
Frequently Asked Questions (FAQs)
Is cavernous sinus syndrome the same as cavernous sinus thrombosis?
No. CSS is the umbrella term for any problem in the cavernous sinus; thrombosis is just one cause.Can CSS heal on its own?
Some mild traumatic cases improve spontaneously, but most underlying causes need active therapy to protect vision and life.How long will double vision last?
If the nerve compression is relieved quickly, diplopia can fade within weeks; long‑standing damage may take months of rehabilitation.Are antibiotics always required?
Only when infection or thrombosis from infection is suspected—your doctor decides after imaging and blood work.Is anticoagulation dangerous for brain bleeds?
Heparin is safe for venous sinus clots in experienced hands; bleeding risk is monitored with scans and lab tests.Can I fly after treatment?
Most people can fly when stable; wait at least two weeks after endovascular procedures and confirm with your specialist.Do blue‑light‑filter glasses help?
They reduce eye‑strain but do not treat the underlying nerve issue; combine with prescribed therapy.Can diet alone cure CSS?
No, but anti‑inflammatory nutrients support healing alongside medical care.What are the long‑term complications?
Persistent cranial‑nerve palsy, chronic headache, partial vision loss or relapse of the original lesion.Is stem‑cell therapy available now?
Only through regulated clinical trials; commercial “stem‑cell clinics” are unproven and risky.How often will I need MRI scans?
Typically at diagnosis, 3 months, 1 year and then yearly if residual lesion remains.Will my insurance cover Gamma Knife surgery?
Many plans do when conventional surgery is unsuitable—pre‑authorisation is essential.Can children develop CSS?
Yes, usually from infection or congenital tumours; they need prompt paediatric neuro‑ophthalmology referral.What if I’m pregnant?
Treatment choices balance maternal eye‑brain health and fetal safety; MRI without contrast is usually safe; some antibiotics and anticoagulants are preferred.Where can I find support?
Neuro‑ophthalmology patient groups, the Cavernous Angioma Community and rare disease networks offer peer help and resources.
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: July 15, 2025.
