Tactile Extinction

Tactile extinction is a neuropsychological phenomenon in which a person fails to perceive a touch stimulus on one side of the body when two touches are applied simultaneously—one to each side—even though they can detect each touch individually. It typically occurs after damage to the parietal lobes, most often from stroke, trauma, or neurodegenerative disease. In tactile extinction, the intact hemisphere “dominates” perception, and the contralesional stimulus (usually left side after right-hemisphere injury) is “extinguished” when competing bilateral inputs occur. Extinction reveals subtle sensory–attentional deficits that standard sensory testing might miss, making it crucial for comprehensive neurological assessment.

Tactile extinction is a curious sensory problem that appears after damage—usually a stroke or trauma—to one side of the brain’s parietal lobe. When someone with this condition closes their eyes and is touched on the right hand alone or the left hand alone, they notice the touch every time. But when both hands are touched at the same moment, the person reports feeling only the hand on the same side as their healthy brain hemisphere (the “ipsilesional” side). The touch delivered to the opposite (contralesional) hand is “extinguished.” It is not a skin or nerve fault—the issue lies in the brain’s attention network struggling to weight simultaneous sensory signals. Studies show that the presence and severity of tactile extinction can predict how well a survivor will function day-to-day after a stroke.pubmed.ncbi.nlm.nih.gov

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Types of Tactile Extinction

1. Simple Tactile Extinction
   The basic form involves simultaneous bilateral light touch. A patient may report feeling a single touch on one hand but fail to report the contralateral touch when both are delivered together.

2. Graded Tactile Extinction
   Severity ranges from mild (misses only very light touches) to severe (misses even firm touches), indicating the extent of attentional imbalance between hemispheres.

3. Crossmodal Extinction
   Here, a touch on one side is extinguished when a visual or auditory stimulus is presented simultaneously on the other side, demonstrating competition across sensory modalities.

4. Modality-Specific Extinction
   Extinction may occur only for tactile stimuli, or extend to extinction of thermal, pain, or vibration sensations, depending on lesion location and extent.

5. Spatially-Specific Extinction
   The deficit can be stronger in proximal (shoulder/upper arm) versus distal (hands/fingers) regions, reflecting topographical organization in somatosensory cortex.

6. Temporal Extinction
   When two touches are separated by a very brief interval (e.g., 50 ms), the second may be extinguished; this reveals temporal processing limits.

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Causes of Tactile Extinction

1. Ischemic Stroke in Right Parietal Lobe
   Loss of blood flow damages the region responsible for integrating bilateral touch.

2. Hemorrhagic Stroke
   Bleeding into parietal cortex disrupts neural circuits involved in spatial attention.

3. Traumatic Brain Injury
   Focal contusions or diffuse axonal injury tearing parietal networks.

4. Brain Tumors
   Lesions in superior parietal lobule can impinge on tactile integration areas.

5. Neurosurgical Resection
   Surgery for epilepsy or tumor removal may unintentionally damage somatosensory cortex.

6. Alzheimer’s Disease
   Early parietal atrophy can manifest extinction prior to overt dementia.

7. Lewy Body Dementia
   Parietal Lewy body deposition disrupts attentional networks.

8. Multiple Sclerosis
   Demyelinating plaques in parietal white matter interrupt tactile processing.

9. Parkinson’s Disease
   Posterior cortical involvement in advanced stages can yield extinction.

10. Traction Injuries
    Stretching of parietal lobe after skull fractures or rapid acceleration–deceleration.

11. Subdural Hematoma
    Mass effect compresses cortical tissue.

12. Hydrocephalus
    Increased intracranial pressure impairs parietal function.

13. Encephalitis
    Viral or autoimmune inflammation targets parietal regions.

14. Chronic Epilepsy
    Recurrent seizures produce gliosis in parietal cortex.

15. Cortical Dysplasia
    Developmental malformations impair tactile integration.

16. Stroke in Posterior Cerebral Artery
    Extends into parietal territory when posterior watershed zones are affected.

17. Arteriovenous Malformation
    Vascular steal phenomenon in parietal tissue.

18. Neurosyphilis
    Tabes dorsalis may involve dorsal columns but also cortical assimilation.

19. Posterior Reversible Encephalopathy Syndrome
    Reversible parietal dysfunction under hypertensive episodes.

20. Radiation Necrosis
    Post-radiotherapy injury to parietal cortex in cancer patients.

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Symptoms Associated with Tactile Extinction

1. Missed Contralateral Touch
   Fails to report touch on affected side when both sides are stimulated.

2. Inattention to Affected Side
   Ignoring objects or sensations on the contralesional side.

3. Impaired Bimanual Coordination
   Difficulty coordinating both hands at once due to uneven sensory feedback.

4. Difficulty Dressing
   Struggles to sense garments on the affected side during dressing tasks.

5. Asymmetric Grip Force
   Applies less force with the hand on the side of extinction.

6. Clumsiness
   Increased dropping of objects in bilateral tasks.

7. Unawareness of Contralateral Limb
   Patient may not recognize their own limb when both are touched.

8. Bumping into Objects
   Colliding with items on the affected side when both sides receive input.

9. Reduced Sensory Thresholds
   Altered perception thresholds on the affected vs. intact side.

10. Neglect-Like Behaviors
    Overlap with hemispatial neglect, such as eating only from one side of the plate.

11. Difficulty in Braille Reading
    Fails to detect simultaneous raised dots when reading with both hands.

12. Pain Extinction
    May not report pain on one side when painful stimuli delivered bilaterally.

13. Thermal Extinction
    Misses temperature changes on the affected side under competition.

14. Vibration Extinction
    Fails to perceive tuning-fork vibration bilaterally.

15. Tactile Localization Errors
    Mislocalizes touches toward the intact side under dual stimulation.

16. Discomfort in Noisy Environments
    Crossmodal extinction worsens when noise or visual stimuli compete.

17. Headache or Discomfort
    Due to constant effort to attend bilaterally.

18. Anxiety or Frustration
    Emotional response to inability to perceive touches normally.

19. Delayed Reaction Times
    Slower responses to stimuli on the affected side.

20. Fatigue
    Increased cognitive load to compensate for sensory imbalance.

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Diagnostic Tests

A. Physical Exam

1. Light Touch Test
   Stroke a cotton wisp on each palm individually and then simultaneously; note extinction.

2. Pinprick Test
   Use a blunt pin for pressure sensation; test unilateral then bilateral.

3. Temperature Discrimination
   Alternate cold and warm stimuli on each forearm, then both together.

4. Vibration Sense
   Apply tuning fork to bony prominences; compare bilateral perception.

5. Proprioception Test
   Move fingers up/down; ask patient to report position when both hands moved.

6. Two-Point Discrimination
   Touch with two points at varying distances unilaterally then bilaterally.

7. Stereognosis
   Place a familiar object in each hand separately, then both; assess recognition.

8. Graphesthesia
   Trace letters on each palm individually and simultaneously; detect extinction.

B. Manual Tests

1. Simultaneous Bilateral Touch
   Examiner touches both hands at once; ask patient to point to each.

2. Cross-Body Stimulation
   Touch left hand and right leg simultaneously; assess cross-limb extinction.

3. Bilateral Shoulder Touch
   Apply touch to shoulders together; note if patient misses one.

4. Bilateral Trunk Touch
   Simultaneous tactile stimuli on both sides of torso; check reporting.

5. Dual-Finger Tapping
   Tap index fingers of both hands at same time; record which tapped.

6. Palm vs. Dorsal Surface
   Touch palm and back of hand simultaneously; see if back-of-hand touch is missed.

7. Finger Web Space Test
   Touch between fingers on each hand in unison; detect extinction.

8. Face vs. Hand Stimulation
   Simultaneous touch to cheek and hand; note competitive suppression.

C. Lab & Pathological Tests

1. Complete Blood Count
   Rule out infection or anemia affecting cognition.

2. Metabolic Panel
   Check electrolytes and glucose; metabolic derangements can mimic extinction.

3. Inflammatory Markers
   ESR and CRP for underlying inflammatory causes like vasculitis.

4. Autoimmune Panel
   Antiphospholipid, ANCA to detect autoimmune encephalitis.

5. CSF Analysis
   Lumbar puncture if encephalitis suspected; assess cells, proteins.

6. Toxin Screens
   Identify heavy metals or drugs affecting parietal function.

7. Genetic Testing
   In suspected degenerative disorders with parietal atrophy.

8. Thyroid Function Tests
   Hypothyroidism can impair cognitive and sensory integration.

D. Electrodiagnostic Tests

1. Somatosensory Evoked Potentials (SSEPs)
   Record cortical response to peripheral nerve stimulation bilaterally.

2. Electroencephalography (EEG)
   Evaluate for focal slowing or epileptiform discharges in parietal region.

3. Nerve Conduction Studies
   Rule out peripheral neuropathy contributing to sensory deficits.

4. Event-Related Potentials
   Assess cognitive–sensory integration when bilateral stimuli delivered.

5. Magnetoencephalography (MEG)
   Map tactile processing areas and interhemispheric timing differences.

6. Transcranial Magnetic Stimulation (TMS)
   Probe cortical excitability in somatosensory cortex.

7. Cortical Evoked Potential Mapping
   Pinpoint exact lesion location within parietal cortex.

8. Electrocorticography (ECoG)
   In surgical candidates, direct cortical recording of evoked responses.

E. Imaging Tests

1. Magnetic Resonance Imaging (MRI)
   High-resolution view of parietal lesions causing extinction.

2. Diffusion-Weighted MRI
   Detect acute ischemic changes in parietal lobe within minutes.

3. Computed Tomography (CT) Scan
   Rapid identification of hemorrhage or mass effect.

4. CT Angiography
   Visualize vascular occlusions in parietal branches.

5. Positron Emission Tomography (PET)
   Measure regional brain metabolism; hypometabolic parietal areas.

6. Single-Photon Emission CT (SPECT)
   Assess cerebral blood flow to parietal cortex.

7. Functional MRI (fMRI)
   Observe real-time activation patterns during bilateral touch tasks.

8. Diffusion Tensor Imaging (DTI)
   Evaluate white-matter tract integrity connecting parietal regions.

Non-Pharmacological Treatments

Below are evidence-based options divided into four friendly groups. For each, you’ll see: What it is, Why it’s done, How it is thought to work.

A. Physiotherapy & Electro-therapy

1. Sensory Re-education (Texture hunts, temperature games)
   Description: Therapist guides the patient through graded touch tasks—silk vs. sandpaper, warm-cool blocks.
   Purpose: Re-map tactile discrimination and sharpen attention.
   Mechanism: Repeated, salient stimulation drives Hebbian plasticity in perilesional parietal cortex.lifeweavers.org

2. Mirror Therapy
   Watching the healthy hand in a mirror positioned to appear as the affected hand tricks the brain into “seeing” symmetrical touch and movement. Visual feedback recruits bilateral parietal activation, helping normalise sensory weighting.

3. Constraint-Induced Sensory Therapy (CIST)
   The stronger hand is gently restrained, forcing the weak side to explore objects; repeated use lowers extinction rates by boosting cortical representation.

4. Prism Adaptation Therapy (PAT)
   Wearing right-shifting goggles while pointing realigns visuomotor maps; extinction drops because spatial attention recalibrates leftward. Benefits can last weeks with 10-minute daily sessions.pubmed.ncbi.nlm.nih.govneurology.orgfrontiersin.org

5. Repetitive Peripheral Magnetic Stimulation (RPMS)
   A handheld coil delivers painless pulses over skin and muscles of the affected limb, making the area “stand out” in the somatosensory cortex. Randomised trials show reduced extinction and better grasp strength.pubmed.ncbi.nlm.nih.gov

6. Repetitive Transcranial Magnetic Stimulation (rTMS)
   Low-frequency (1 Hz) pulses to the intact parietal lobe or high-frequency pulses to the damaged side rebalance inter-hemispheric inhibition, letting contralesional touch win fairer battles.pubmed.ncbi.nlm.nih.govacademic.oup.com

7. Transcranial Direct-Current Stimulation (tDCS)
   20 minutes of 2 mA anodal tDCS over the injured parietal cortex during training raises cortical excitability and short-term gains; multi-session courses may lock in improvement.mdpi.compmc.ncbi.nlm.nih.gov

8. Thermal Stimulation Cycling (alternating warm/cold packs) intensifies sensory salience and may prime neuroplasticity.

9. Transcutaneous Electrical Nerve Stimulation (TENS) delivers gentle pulses through skin pads to reactivate A-beta fibres, promoting cortical re-mapping.

10. Functional Electrical Stimulation (FES) contracts hand muscles in sync with detected touch, creating strong sensorimotor pairing.

11. Vibration Therapy (e.g., 80 Hz palm plates) excites Pacinian corpuscles and drives sensory cortex engagement.

12. Low-Level Laser Therapy increases local blood flow, indirectly supporting nerve recovery.

13. Interactive Metronome Training synchronises bilateral tapping to metronome beats, enhancing timing maps across hemispheres.

14. Virtual Reality Sensory Rooms immerse patients in 360° multi-sensory challenges demanding detection on both sides.

15. Task-Oriented Bilateral Training (folding towels, kneading dough) offers real-life, symmetrical tasks that continuously expose both hands to touch.

B. Exercise-Based Approaches

16. Graded Hand-Arm Bimanual Exercises—using therapy balls, resistive putty, or dumbbells—force equal tactile attention.

17. Fine Motor Workshops (piano-style finger tapping, bead threading) heighten fingertip acuity and boost representation density.

18. Locomotor Sensory Feedback—walking while tapping both thighs with soft sticks—trains leg sensory extinction (often an overlooked variant).

19. Cross-Education Drills—rapid, complex patterns with the healthy hand can “spill over” activation to the injured hemisphere.

20. Aerobic Cardio (30 min brisk cycling)—increases brain-derived neurotrophic factor (BDNF), fertilising neural plasticity for any concurrent tactile training.

C. Mind-Body Techniques

21. Mindfulness-Based Sensory Attention—guided meditation directs gentle focus sequentially to each limb, priming awareness.

22. Motor Imagery of Bilateral Touch—patients visualise both hands being brushed; fMRI shows parietal activation even without physical contact.

23. Clinical Hypnosis for Neglect—short scripts suggest vivid, balanced body awareness.

24. Biofeedback of Galvanic Skin Response—seeing skin-conductance spikes reinforces detection success.

25. Yoga with Eyes Closed—slow symmetrical poses expose the neglected side to weight-bearing touch in a calming, plasticity-friendly environment.

D. Educational Self-Management Tools

26. Home Sensory Diaries track daily touch wins and misses, building metacognition.

27. Mobile Apps with Haptic Alerts deliver random buzzes to each hand, encouraging real-time testing.

28. Caregiver Skill Training—family learn how to cue simultaneous bilateral touches during grooming and mealtimes.

29. Safety Education—practical steps (e.g., hold mug in detected hand, place hot items centrally) reduce injury risk.

30. Goal-Setting & Motivational Interviewing—evidence shows that clear, personally meaningful goals improve adherence and neuro-rehab outcomes.

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Key Drugs

Important: No medicine is currently licensed specifically for tactile extinction. The following drugs are used off-label to enhance stroke recovery, attention, or cortical plasticity. Always discuss risks and benefits with a licensed physician.

1. Citicoline (CDP-choline) – Neuroprotective nutrient/drug. 500–2,000 mg oral daily, split doses. May boost phospholipid repair and dopamine release. Mild insomnia, GI upset.

2. Piracetam – Nootropic (GABA analogue). 2.4–4.8 g oral in 2–3 doses. Improves membrane fluidity and microcirculation. Side-effects: nervousness, weight gain.

3. Levodopa + Carbidopa – Dopamine precursor. 100/25 mg bid for six weeks in some stroke trials. Dopaminergic drive enhances learning. Nausea, dyskinesia.

4. Modafinil – Wakefulness promoter. 100–200 mg AM. Heightens noradrenergic-dopaminergic focus. Headache, anxiety.

5. Methylphenidate – Stimulant. 5–10 mg bid. Increases attention and reward-based learning. Appetite loss, tachycardia.

6. Donepezil – Acetylcholinesterase inhibitor. 5–10 mg nightly. Acetylcholine sharpens sensory gating. Night-time cramps, vivid dreams.

7. Galantamine – Similar cholinergic drug; 8–24 mg/day. Adds nicotinic modulation.

8. Memantine – NMDA modulator. 10 mg bid. Lowers excitotoxicity while permitting plasticity. Dizziness, constipation.

9. Sertraline – SSRI. 50 mg/day may indirectly aid neurogenesis and mood. Sexual dysfunction, nausea.

10. Bupropion – NDRI antidepressant. 150 mg AM; boosts dopamine, helping attention. Dry mouth, insomnia.

11. Amphetamine (d-AMP) – 5 mg AM under close supervision; has shown transient neglect improvement in trials. BP elevation, addiction risk.

12. Atomoxetine – Selective norepinephrine reuptake inhibitor. 40 mg AM. Improves vigilance. Possible palpitations.

13. Bromocriptine – Dopamine agonist. 1.25 mg titrated; used in post-stroke apathy studies. Nausea, orthostatic hypotension.

14. Selegiline (MAO-B inhibitor) – 5 mg AM; raises dopamine without tyramine risk at low dose. Insomnia.

15. Nimodipine – Calcium-channel blocker. 60 mg q4h × 3 weeks post-SAH; improves cortical perfusion; limited evidence for extinction.

16. Ampakine CX-717 (research) – 500 mg used in trial settings; enhances AMPA-receptor signalling. Yet to be approved; headache.

17. Dexamphetamine/Levoamphetamine mix – 2.5–5 mg; stronger than d-AMP alone, but higher CV risk.

18. Nicotine (transdermal patch 7 mg) – Short-term cholinergic up-tuning; watch dependence.

19. Rotigotine (transdermal) – 2 mg/24 h; steady dopamine agonism; skin rash.

20. Caffeine (200 mg) – Everyday adenosine antagonist; moderate doses right before therapy can heighten alertness without major risk.

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Dietary Molecular Supplements

(Supplements do not replace balanced diet or medications; check pharmacist for interactions.)

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Additional Drug-Level Interventions

(Bisphosphonates etc. are not core tactile-extinction drugs but may be part of holistic survivor care.)

1. Alendronate (Bisphosphonate) – 70 mg once weekly keeps bones strong in hemiparetic patients prone to falls. Limits osteoclast activity.

2. Zoledronic Acid IV – Annual infusion for severe osteoporosis; same mechanism.

3. Hyaluronic Acid Viscosupplement (intra-articular knee) – Reduces joint pain so bilateral stance exercises are possible; improves compliance with rehab.

4. Platelet-Rich Plasma (PRP) Injections – Under study for peripheral nerve recovery; growth factors may accelerate sensory remapping.

5. Recombinant Human Nerve Growth Factor (rh-NGF) – Experimental subcutaneous delivery; fosters axonal sprouting.

6. Cerebrolysin – Porcine brain-derived peptide mix; 10 mL IV daily × 10 days shown to improve neglect scores in small trials.

7. Stem-Cell-Derived Exosomes – Research intravenous therapy delivering micro-RNA cargo to enhance neuroplasticity.

8. Autologous Bone-Marrow–Derived Stem Cell Infusion – Exploratory; aims to replace lost neurons and release trophic factors.

9. Erythropoietin (high-dose neuro-EPO) – 30,000 IU IV in acute stroke trials; anti-apoptotic, pro-angiogenic.

10. Fesoterodine (M3 antagonist) – Treats post-stroke bladder urgency, improving comfort during long therapy sessions.

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Surgical or Procedural Options

1. Decompressive Craniectomy – Lifesaving in malignant MCA infarct; preventing herniation preserves parietal tissue that could still relearn touch.

2. Hematoma Evacuation – Early removal of intracerebral bleed lessens cortical damage.

3. Revascularisation (CEA or Stenting) – Restores blood flow where carotid stenosis threatens further parietal ischemia.

4. Cortical Reorganisation Surgery (research) – Electrocorticography-guided resection of inhibitory scar, rare.

5. Deep Brain Stimulation (DBS) of Thalamus – Experimental for sensory network modulation.

6. Epidural Cortical Stimulation – Implanted electrodes over injured parietal cortex deliver patterned pulses syncing with tactile rehab.

7. Peripheral Nerve Transfer – In brachial plexus injuries causing extinction-like deficits, rerouting donor nerves restores bilateral sensation.

8. Vagus-Nerve Stimulation Paired with Rehab – FDA-cleared for stroke arm weakness; may spill over to tactile networks.

9. Selective Dorsal Rhizotomy – For severe spasticity hindering sensory training; reduces overactive afferent barrage.

10. Robotic-Assisted Micro-Neurolysis – Removes fibrotic cuffs around cutaneous nerves to improve peripheral input quality.

Each procedure carries its own risks; only a neurosurgeon or interventionalist can advise suitability.

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Prevention Strategies

1. Control Blood Pressure (<130/80 mm Hg)

2. Manage Atrial Fibrillation (anticoagulation)

3. Treat Diabetes (HbA1c < 7%)

4. Lower LDL (<70 mg/dL)

5. Quit Smoking

6. Exercise 150 min/week

7. Mediterranean-Style Diet

8. Limit Alcohol (≤2 units/day)

9. Regular Carotid & Cardiac Check-ups

10. Immediate ER visit for FAST symptoms (Face droop, Arm weakness, Speech slur, Time to call).

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When to See a Doctor

• Immediately if new numbness, weakness, speech change, confusion, or vision loss appears—could signal a fresh stroke.

• Within 24 hours if existing extinction suddenly worsens, you feel new headaches, or cannot perform daily tasks safely.

• Every 3–6 months for routine neuro-rehab reviews, medication checks, bone health, mood screening, and driver-safety assessments.

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Key “Do’s and Don’ts”

Do

1. Practise daily bilateral touch drills.

2. Keep a sensory progress journal.

3. Use contrasting textures (rough towel vs. smooth mug) during tasks.

4. Wear a smartwatch on the affected wrist for haptic cues.

5. Involve family in simultaneous touch games.

Don’t

1. Ignore unexplained burns or cuts on the numb hand.

2. Place hot drinks on the neglected side.

3. Perform kitchen knife work without adaptive devices.

4. Skip antihypertensives—stroke risk piles up.

5. Feel discouraged—plasticity can last years.

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Frequently Asked Questions (FAQs)

1. Is tactile extinction the same as numbness?
   No. Skin nerves work, but the brain’s attention filter discards one of two simultaneous inputs.

2. Will it go away on its own?
   Many people improve within months, especially with targeted therapy; some need longer.

3. What tests confirm it?
   Simple bedside “double simultaneous stimulation” plus MRI of the parietal lobe.

4. Does the problem affect vision too?
   It can co-exist with visual extinction—missing one of two brief flashes.

5. Can children get it?
   Rarely, usually after traumatic brain injury.

6. Is there a cure?
   No single cure, but combined neuro-rehabilitation and brain-stimulation pack strong evidence.

7. Are drugs compulsory?
   Not always; many gains come from physiotherapy alone.

8. Can I drive?
   Only after formal occupational therapy assessment of attention and sensory integration.

9. Does coffee help?
   Moderate caffeine before therapy may boost focus, but avoid excess jitters.

10. Are wearable tech gloves worth it?
    Early trials show vibrotactile gloves can cue the neglected hand; ask your therapist.

11. Could virtual reality worsen dizziness?
    Some do experience cyber-sickness; sessions should be brief and progressive.

12. Do supplements replace medication?
    No—think of them as nutritional support that may enhance brain repair.

13. Is surgery a last resort?
    Yes; most surgeries aim at the stroke cause not extinction itself.

14. What about CBD oil?
    Evidence is scant; discuss legality and interactions first.

15. How do I explain this to friends?
    “My brain is still rewiring. If you touch both my hands at once, the left one sometimes goes unnoticed.”

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: June 24, 2025.