Apraxia of Eyelid Opening (ALO)

Apraxia of Eyelid Opening (ALO) is a non-paralytic motor disorder in which a person cannot initiate the voluntary act of lifting the upper eyelid after it has been closed, despite normal eyelid function at other times. Unlike true ptosis—where the eyelid itself is weak—or blepharospasm—where there is involuntary squeezing of the eyelids—ALO stems from a breakdown in the neural commands that coordinate the muscles responsible for opening the eye. Patients typically have no structural eyelid abnormality and can maintain their eyelids open once lifted manually Wikipedia.

Apraxia of eyelid opening (AEO) is a non-paralytic motor disorder in which a person has difficulty initiating the upward movement of the eyelids despite intact muscle strength and no structural abnormality of the lids or extraocular muscles MedscapeEyeWiki. Patients often report that after a blink or forced closure, their eyelids “stick” shut for several seconds, even though they are trying to open them. Unlike true apraxia—where the brain’s intention to move is lost—AEO arises from abnormal inhibition of the levator palpebrae superioris muscle and/or prolonged contraction of the orbicularis oculi muscle, leading to failed eyelid elevation under voluntary command EyeWiki.

Clinically, AEO commonly occurs in association with blepharospasm (involuntary lid‐closure spasms) or other extrapyramidal syndromes such as progressive supranuclear palsy and dystonic parkinsonism EyeWikiE-ARM. However, isolated cases have been reported after focal brain injuries, frontal lobe hypometabolism, and even certain medications (e.g., lithium, sulpiride) E-ARMEyeWiki. Patients characteristically use a “forehead push” or finger to lift the lids, or sustain frontalis muscle contraction, in an effort to overcome the apraxia and reopen their eyes.

At its core, eyelid opening requires two simultaneous actions: activation of the levator palpebrae superioris muscle to lift the eyelid and inhibition of the orbicularis oculi muscle to prevent closure. In ALO, there is either involuntary inhibition of the levator, prolonged contraction of the orbicularis, or both, leading to an inability to “kick-start” the opening process EyeWiki.

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Types

While ALO is a single clinical phenomenon, it can be categorized by its underlying association:

1. Primary (Idiopathic) ALO
   Occurs in isolation without any identifiable neurological disease or external trigger. Patients have normal imaging and laboratory studies.

2. Dystonic ALO
   Seen in conjunction with focal dystonias, especially blepharospasm. Here, abnormal muscle contractions of the orbicularis oculi play a central role.

3. Parkinsonian ALO
   Develops in patients with Parkinson’s disease, sometimes fluctuating with “on” and “off” medication states.

4. Progressive Supranuclear Palsy (PSP)-Associated ALO
   ALO is an early and characteristic sign in PSP, reflecting midbrain and basal ganglia pathology.

5. Multiple System Atrophy (Shy-Drager) ALO
   Occurs as part of widespread autonomic and extrapyramidal degeneration.

6. Multiple Sclerosis-Related ALO
   Results from demyelinating lesions affecting supranuclear pathways essential for eyelid control.

7. Post-Surgical ALO
   Follows interventions such as stereotactic surgery or deep brain stimulation that may disrupt neural circuits.

8. Medication-Induced ALO
   Triggered by dopamine-blocking agents (e.g., antipsychotics such as sulpiride) or other drugs that alter basal ganglia function.

9. Structural Lesion ALO
   Caused by tumors, strokes, or hemorrhages in frontal lobes, basal ganglia, or brainstem areas controlling eyelid movement.

10. Genetic-Mutation ALO
    Linked to POLG1 gene mutations, often with mitochondrial dysfunction.

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Causes

1. Idiopathic Dysfunction
   No identifiable cause on imaging or labs; likely subtle neurotransmitter imbalance.

2. Blepharospasm
   Persistent orbicularis overactivity inhibits levator activation.

3. Parkinson’s Disease
   Dopaminergic neuron loss disrupts supranuclear eyelid pathways.

4. Progressive Supranuclear Palsy
   Midbrain degeneration impairs lid opening circuitry.

5. Multiple System Atrophy
   Combined autonomic and extrapyramidal damage includes eyelid control centers.

6. Multiple Sclerosis
   Demyelination in frontal or brainstem regions interrupts signals.

7. Hydrocephalus
   Raised intracranial pressure and ventricular dilation damage periventricular fibers.

8. Motor Neuron Disease
   Rare involvement of supranuclear tracts controlling eyelids.

9. Stroke
   Infarcts in frontal cortex or basal ganglia can produce ALO.

10. Brain Tumors
    Space-occupying lesions in midbrain or frontal lobes.

11. Deep Brain Stimulation or Lesioning
    Surgical targeting of basal ganglia disrupts eyelid–opening circuits.

12. Antipsychotic Medication
    Dopamine receptor blockade (e.g., sulpiride) may precipitate ALO.

13. Valproate Toxicity
    Rare reports link high–dose valproic acid to ALO.

14. Mitochondrial POLG1 Mutations
    Genetic syndromes presenting with isolated ALO.

15. Inflammatory Encephalitis
    Autoimmune or infectious inflammation affecting eyelid control regions.

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Symptoms

1. Failure to Open Eyelids at Will
   Patients report being “locked” in eye closure after blinking or deliberate closure.

2. Manual Lifting Required
   Many use their fingers to physically raise the lid before vision is restored.

3. Backward Head Thrust
   To engage frontalis muscle more effectively, patients tilt their head back.

4. Forehead Muscle Contraction
   Visible wrinkling as the frontalis tries to compensate and lift the lids.

5. Normal Blinking Reflex
   Blinks occur spontaneously; only voluntary opening is impaired.

6. Intermittent Vision Obstruction
   Transient “blackouts” as the eyelids fail to open.

7. Eye Strain and Fatigue
   Increased effort to open the lids leads to fatigue around the forehead.

8. Reading and Driving Difficulty
   Tasks requiring sustained visual attention become challenging.

9. Social Anxiety
   Embarrassment or frustration in social or workplace settings.

10. Associated Blepharospasm
    In some, concurrent eyelid squeezing episodes exacerbate the opening delay.

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Diagnostic Tests

Physical Examination

1. Cranial Nerve Assessment
   Rules out CN III palsy (ptosis) and confirms intact motor pathways.

2. Eyelid Behavior Observation
   Watch spontaneous vs. voluntary opening after prolonged closure.

3. Frontalis Activation Test
   Ask patient to lift eyebrows; observe if this aids eyelid opening.

4. Orbicularis Oculi Palpation
   Feel for persistent contraction around the eye.

5. Ptosis Differentiation
   Determine whether eyelid droop is due to muscle weakness or apraxia.

6. General Neurological Exam
   Check tone, reflexes, and signs of extrapyramidal involvement.

Manual Tests

1. Manual Lid Elevation
   Gently lifting the eyelid by hand; if vision restores and lid stays open, supports ALO.

2. Closure-Reopening Challenge
   Have patient close eyes for 10 seconds then open; inability to initiate opening indicates ALO.

Laboratory and Pathological Tests

1. Acetylcholine Receptor Antibodies
   Exclude myasthenia gravis.

2. Anti-MuSK Antibody
   Further refine myasthenia evaluation.

3. ANA and Inflammatory Markers (ESR/CRP)
   Screen for autoimmune or inflammatory encephalitis.

4. CSF Analysis
   Look for oligoclonal bands suggestive of multiple sclerosis.

5. Genetic Testing (POLG1)
   In familial or early-onset cases to identify mitochondrial mutations.

Electrodiagnostic Tests

1. Electromyography (EMG) of Orbicularis Oculi
   Detects sustained involuntary contractions.

2. EMG of Levator Palpebrae Superioris
   Assesses failure of muscle activation during attempted opening.

3. Blink Reflex EMG
   Evaluates neural circuitry integrity between trigeminal and facial nerves.

4. Facial Nerve Conduction Study
   Rules out peripheral neuropathy affecting orbicularis function.

Imaging Tests

1. Magnetic Resonance Imaging (MRI) of Brain
   Identifies strokes, tumors, demyelination, or neurodegenerative changes.

2. Computed Tomography (CT) Scan
   Rapid screening for hemorrhage or mass lesions.

3. Positron Emission Tomography (PET)
   Shows basal ganglia or cortical hypometabolism in conditions like PSP.

Non-Pharmacological Treatments

Effective management of AEO often starts with non-drug approaches that aim to retrain eyelid control, reduce muscle overactivity, and empower patients to self-manage symptoms. Below are 20 evidence-based interventions, grouped into Exercise Therapies, Mind-Body Techniques, and Educational Self-Management.

Exercise Therapies

1. Blinking Retraining
   Description: Guided practice of slow, deliberate blinks.
   Purpose: Improve timing and coordination between orbicularis and levator muscles.
   Mechanism: Repetitive, slow eyelid closure and slow opening reinforces proper neural circuits governing eyelid movements.

2. Mirror-Assisted Feedback
   Description: Performing lid-opening exercises in front of a mirror.
   Purpose: Increase visual awareness of eyelid position and movement.
   Mechanism: Visual feedback engages sensorimotor cortex, strengthening levator activation pathways.

3. Frontalis Activation Drills
   Description: Repeatedly contracting the forehead muscles to assist eye opening.
   Purpose: Harness frontalis-levator synergy to overcome orbicularis inhibition.
   Mechanism: Co-activation reinforces alternative neural routes for lid elevation.

4. Orbicularis Stretching
   Description: Gentle manual stretching of the muscle around the eye.
   Purpose: Reduce hypertonicity of orbicularis oculi.
   Mechanism: Muscle stretching increases length-tension capacity and lowers involuntary contraction.

5. Neuromuscular Re-education
   Description: Biofeedback-guided eyelid coordination training.
   Purpose: Restore normal muscle recruitment patterns.
   Mechanism: Electromyographic feedback helps patients learn to inhibit orbicularis while activating levator.

6. Eye-Movement Coupling Exercises
   Description: Coordinating eyelid opening with saccadic eye movements.
   Purpose: Facilitate natural synchronous movement of eyes and lids.
   Mechanism: Linking eye movement commands with eyelid circuits enhances central motor planning.

7. Proprioceptive Tapping
   Description: Light tap on the upper eyelid during attempted opening.
   Purpose: Provide sensory cue to trigger levator contraction.
   Mechanism: Cutaneous stimulation can unmask latent levator activation in dystonic conditions.

Mind-Body Techniques

8. Progressive Muscle Relaxation
   Description: Systematic tensing and relaxing of facial and neck muscles.
   Purpose: Lower overall muscle tone and reduce dystonic overactivity.
   Mechanism: Activates parasympathetic system, decreasing involuntary orbicularis firing.

9. Guided Imagery
   Description: Visualization of smooth eyelid opening.
   Purpose: Prime motor cortex for proper movement sequences.
   Mechanism: Mental rehearsal strengthens synaptic connections without physical strain.

10. Mindfulness Meditation
    Description: Focused breathing and awareness of eyelid sensations.
    Purpose: Reduce anxiety and breaking the cycle of dystonic reflexes.
    Mechanism: Lowers stress-related neurotransmitters that can exacerbate muscle spasms.

11. Biofeedback Therapy
    Description: Real-time feedback on muscle activity via sensors.
    Purpose: Teach voluntary control over orbicularis inhibition.
    Mechanism: Enhanced interoceptive awareness allows patients to consciously suppress unwanted contractions.

12. Hypnotherapy
    Description: Guided trance to reprogram involuntary lid closure.
    Purpose: Access subconscious motor patterns for correction.
    Mechanism: Alters cortical excitability thresholds, easing motor initiation.

13. Cognitive Behavioral Therapy (CBT)
    Description: Identifying and reframing thoughts that worsen symptoms.
    Purpose: Decrease anxiety-driven dystonic responses.
    Mechanism: Reduces maladaptive neural loops between emotion centers and motor cortex.

14. Yoga and Deep Breathing
    Description: Slow stretching and diaphragmatic breathing exercises.
    Purpose: Overall stress reduction to diminish dystonic exacerbations.
    Mechanism: Shifts autonomic balance away from muscle-tightening sympathetic activity.

Educational Self-Management

15. Symptom Diaries
    Description: Daily logging of symptom severity, triggers, and relief measures.
    Purpose: Identify patterns and effective self-care strategies.
    Mechanism: Empowers patients through data-driven adjustments of daily routines.

16. Action Planning
    Description: Predefined steps to take at each symptom onset.
    Purpose: Improve response speed and reduce panic.
    Mechanism: Creates automatic routines that bypass stress-induced hesitation.

17. Goal Setting
    Description: Specific, measurable objectives (e.g., reduce delay in lid opening by 50%).
    Purpose: Maintain motivation and track progress.
    Mechanism: Reinforces reward circuits when goals are met, boosting adherence.

18. Educational Workshops
    Description: Group classes on AEO physiology and management.
    Purpose: Increase health literacy and coping skills.
    Mechanism: Knowledge reduces uncertainty-driven stress amplifying dystonia.

19. Peer Support Groups
    Description: Regular meetings with other AEO patients.
    Purpose: Share tips, emotional support, and normalize experiences.
    Mechanism: Social reinforcement strengthens commitment to therapy.

20. Digital Self-Management Apps
    Description: Mobile tools for reminders, diaries, and exercise guides.
    Purpose: Foster consistency and easy access to resources.
    Mechanism: Push notifications automate adherence, reducing cognitive load.

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Key Pharmacological Treatments

While non-drug approaches are foundational, several medications can reduce orbicularis overactivity or facilitate levator function. Below are ten evidence-based drugs, with typical dosage, class, timing, and side effects.

1. Botulinum Toxin Type A

   • Class: Neuromuscular blocker

   • Dosage: 2.5–5 U per injection site, typically 3–5 sites per eye every 12 weeks

   • Timing: Inject every 3 months as needed

   • Side Effects: Ptosis, dry eye, double vision EyeWiki.

2. Clonazepam

   • Class: Benzodiazepine

   • Dosage: 0.25–1 mg orally at bedtime

   • Timing: 1–2 times daily

   • Side Effects: Drowsiness, dizziness, dependency.

3. Baclofen

   • Class: GABA_B agonist

   • Dosage: 5–10 mg orally 3 times daily

   • Timing: With meals

   • Side Effects: Weakness, sedation, fatigue.

4. Tetrabenazine

   • Class: Dopamine depleter

   • Dosage: Start 12.5 mg once daily, titrate up to 50 mg day

   • Timing: Divided doses

   • Side Effects: Depression, parkinsonism, insomnia.

5. Trihexyphenidyl

   • Class: Anticholinergic

   • Dosage: 1–2 mg orally 2–3 times daily

   • Timing: With meals

   • Side Effects: Dry mouth, blurred vision, urinary retention.

6. Diazepam

   • Class: Benzodiazepine

   • Dosage: 2–5 mg orally at bedtime

   • Timing: Once daily

   • Side Effects: Sedation, ataxia, dependence.

7. Zolpidem

   • Class: Non-benzodiazepine hypnotic

   • Dosage: 5–10 mg at bedtime

   • Timing: Once nightly

   • Side Effects: Dizziness, headache, sleepwalking.

8. Levodopa/Carbidopa

   • Class: Dopaminergic agent

   • Dosage: 100/25 mg orally 3 times daily

   • Timing: With meals

   • Side Effects: Nausea, orthostatic hypotension, dyskinesia.

9. Tizanidine

   • Class: α₂-adrenergic agonist

   • Dosage: 2–4 mg orally every 6–8 h

   • Timing: Up to 3 doses daily

   • Side Effects: Dry mouth, hypotension, sedation.

10. Amantadine

    • Class: NMDA antagonist, antiviral

    • Dosage: 100 mg orally twice daily

    • Timing: Morning and noon

    • Side Effects: Livedo reticularis, peripheral edema, hallucinations.

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Dietary Molecular Supplements

Adjunctive nutritional support may modulate neural excitability and support muscle function. Typical dosages and proposed mechanisms include:

1. Magnesium Citrate (200–400 mg/day)

   • Function: Muscle relaxant

   • Mechanism: Inhibits NMDA receptors, reducing excitatory neurotransmission.

2. Vitamin D₃ (1,000–2,000 IU/day)

   • Function: Neuroprotective

   • Mechanism: Regulates calcium channels and neuronal growth.

3. Vitamin B₁₂ (500 µg/day)

   • Function: Nerve repair

   • Mechanism: Methylation cycles supporting myelin integrity.

4. Omega-3 Fatty Acids (1–2 g EPA/DHA daily)

   • Function: Anti-inflammatory

   • Mechanism: Modulates cytokines and neurotransmitter release.

5. Coenzyme Q₁₀ (100–200 mg/day)

   • Function: Mitochondrial support

   • Mechanism: Enhances ATP production in neurons.

6. Curcumin (500 mg twice daily)

   • Function: Antioxidant

   • Mechanism: Inhibits NF-κB, reducing oxidative stress.

7. Resveratrol (100 mg/day)

   • Function: Neuroprotective

   • Mechanism: Activates SIRT1, promoting neuronal resilience.

8. Acetyl-L-Carnitine (500 mg twice daily)

   • Function: Energy substrate

   • Mechanism: Transports fatty acids into mitochondria.

9. N-Acetylcysteine (600 mg twice daily)

   • Function: Glutathione precursor

   • Mechanism: Replenishes antioxidant defenses.

10. Vitamin B₆ (50 mg/day)

    • Function: Neurotransmitter synthesis

    • Mechanism: Cofactor for GABA and serotonin production.

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Advanced Therapeutic Agents

Though off-label and experimental in AEO, the following agents have been explored for their regenerative or structural effects:

1. Alendronate (70 mg once weekly)

   • Type: Bisphosphonate

   • Function: Reduces bone-mediated compression in orbital floor anomalies

   • Mechanism: Inhibits osteoclasts, preventing bone overgrowth.

2. Zoledronic Acid (5 mg IV once yearly)

   • Type: Bisphosphonate

   • Function: Similar to alendronate.

   • Mechanism: Potent osteoclast inhibition.

3. Hyaluronic Acid Injection (1 mL per lid, monthly)

   • Type: Viscosupplementation

   • Function: Lubricates tarsal-conjunctival interface.

   • Mechanism: Restores viscoelastic properties, easing mechanical lid opening.

4. Platelet-Rich Plasma (1–2 mL per eyelid, quarterly)

   • Type: Regenerative

   • Function: Promotes tissue healing.

   • Mechanism: Delivers growth factors to eyelid muscles and nerves.

5. Autologous Mesenchymal Stem Cells (1×10⁶ cells IV infusion monthly)

   • Type: Stem cell therapy

   • Function: Neurorestorative potential.

   • Mechanism: Paracrine release of neurotrophic factors.

6. Cerebrolysin (10 mL IV daily for 10 days)

   • Type: Neuroregenerative peptide mixture

   • Function: Supports neuronal repair.

   • Mechanism: Provides endogenous peptides that mimic nerve growth factor.

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Surgical Procedures

When conservative measures fail, surgery can provide lasting relief:

1. Pretarsal Orbicularis Myectomy

   • Procedure: Resection of pretarsal orbicularis oculi fibers.

   • Benefits: Reduces involuntary closure and apraxia episodes.

2. Selective Peripheral Denervation

   • Procedure: Isolates and cuts orbicularis motor branches.

   • Benefits: Precise reduction of dystonic overactivity with minimal tissue removal.

3. Frontalis Sling Suspension

   • Procedure: Connects forehead muscle to upper lid via autologous fascia lata or synthetic sling.

   • Benefits: Bypasses dysfunctional levator pathway, providing mechanical lift.

4. Levator Aponeurosis Advancement

   • Procedure: Reinforces levator tendon insertion on tarsus.

   • Benefits: Strengthens primary elevator to counteract inhibition.

5. Peripheral Orbicularis Oculi Myomectomy

   • Procedure: Extensive removal of overactive orbicularis muscle segments.

   • Benefits: Long-term reduction of lid-closure forces.

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Prevention Strategies

1. Wear UV-blocking sunglasses in bright light.

2. Take frequent “blink breaks” during screen use.

3. Practice daily eyelid stretching exercises.

4. Maintain regular sleep patterns.

5. Manage stress with yoga or meditation.

6. Limit caffeine and alcohol intake.

7. Ensure proper workstation ergonomics.

8. Stay hydrated.

9. Avoid neurotoxic medications when possible.

10. Attend regular follow-ups with a neurologist or ophthalmologist.

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When to See a Doctor

Seek medical attention if you experience any of the following:

• Persistent inability to open your eyes for more than a few seconds

• New or worsening vision impairment

• Significant interference with daily activities (e.g., reading, driving)

• Sudden onset of symptoms after head injury

• Associated facial spasms or pain

• No improvement with self-care measures

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What to Do—and What to Avoid

What to Do:

1. Apply warm compresses before exercises.

2. Use mirror feedback during lid-opening drills.

3. Keep a symptom diary.

4. Practice relaxation techniques daily.

5. Stay consistent with prescribed medications.

6. Use ergonomic lighting.

7. Blink deliberately every minute.

8. Stay hydrated.

9. Wear sunglasses outdoors.

10. Join a support group.

What to Avoid:

1. Prolonged screen scrolling without breaks.

2. Bright, flickering lights.

3. Excessive caffeine or alcohol.

4. Poor sleep habits.

5. High-stress situations without coping strategies.

6. Abrupt medication changes.

7. Rubbing eyes vigorously.

8. Driving at night without corrective lenses.

9. Ignoring early symptoms.

10. Using unprescribed topical eye drops.

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Frequently Asked Questions

1. What causes apraxia of eyelid opening?
   It arises from abnormal brain-to-muscle signaling that fails to inhibit orbicularis oculi or activate the levator palpebrae superioris.

2. How is AEO different from blepharospasm?
   Blepharospasm involves active, involuntary lid closure spasms; AEO is an inability to initiate lid opening despite intact muscles.

3. Who is at risk?
   Patients with dystonic neurological conditions, frontal lobe lesions, or on certain psychiatric medications.

4. How is it diagnosed?
   Clinical observation of delayed lid opening, electromyography to confirm orbicularis persistence, and exclusion of true paralysis.

5. Is AEO curable?
   There’s no definitive cure, but many patients achieve significant relief with botulinum toxin, therapy, or surgery.

6. Can exercises really help?
   Yes—rehabilitative exercises retrain neural circuits, improving lid elevation over weeks to months.

7. Are medications necessary?
   Medications like botulinum toxin or muscle relaxants often provide faster symptom control, especially when combined with exercises.

8. Do dietary supplements work?
   Supplements such as magnesium and omega-3 may support neural health but are best used alongside other treatments.

9. When should surgery be considered?
   If symptoms remain severe despite optimized non-surgical and pharmacological therapies for at least 6–12 months.

10. What are surgery risks?
    Possible over-correction leading to lagophthalmos (incomplete eye closure), infection, or scarring.

11. Will AEO come back after treatment?
    Some residual or recurrent symptoms are common; maintenance injections or follow-up exercises may be needed.

12. How can I prevent worsening?
    Avoid known triggers like bright lights, stress, and poor sleep, and maintain regular follow-up.

13. Is AEO painful?
    Usually it is not painful, though secondary eye strain or headache can occur.

14. Can children have AEO?
    It is rare in children; when present, it often follows brain injury or metabolic disorders.

15. Does stress make AEO worse?
    Yes—stress can amplify dystonic muscle activity, increasing apraxia episodes.

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 13, 2025.