Exploding Head Syndrome

Types of Exploding Head Syndrome
Causes of Exploding Head Syndrome
Symptoms of Exploding Head Syndrome
Diagnostic Tests for Exploding Head Syndrome
Non-Pharmacological Treatments That Really Help
Evidence-Based Medicines
Dietary Molecular Supplements
Drugs in the Bisphosphonate / Regenerative / Viscosupplementation / Stem-Cell Realm
Surgical or Procedural Options (Rarely Needed)
Everyday Prevention Strategies
When Should You See a Doctor?
“Do & Don’t” Guidelines
Frequently Asked Questions (FAQs)

Exploding Head Syndrome (EHS) is a benign parasomnia characterized by the perception of a sudden loud noise or explosive sensation in the head during transitions between sleep and wakefulness. Despite its alarming name, EHS is neither painful nor dangerous, and individuals typically experience no residual physical symptoms after an episode. It often occurs in the absence of any underlying neurological pathology and does not signify a risk of brain hemorrhage or stroke.

Exploding Head Syndrome is a harmless but startling sleep-related sensory event in which a person hears—or occasionally feels—a sudden loud bang, crash, or electrical “zap” inside the skull as they drift off to sleep or as they wake up. Researchers classify it as a benign parasomnia under ICSD-3 (International Classification of Sleep Disorders). Attacks are painless, last only seconds, and cause no tissue damage, yet the shock can jolt the heart, spike adrenaline, and fuel anxiety about going to bed again. Prevalence estimates range from 8%–16 % of the general population, with women slightly more affected and first episodes often reported between ages 10 and 50. Multiple theories exist—brief bursts of brain-stem arousal, delayed melatonin shut-off, and even micro-seizure activity—yet no single mechanism explains every case. The good news: EHS rarely signals a serious neurologic disease, and most people improve with simple education, sleep-hygiene tweaks, and, when needed, short courses of medication. ncbi.nlm.nih.govpubmed.ncbi.nlm.nih.gov

EHS episodes usually happen at the onset of sleep (hypnagogic) or upon awakening (hypnopompic). The perceived sound can range from loud bangs, gongs, cymbals crashing, or a loud swooshing sound. Some people also experience a flash of light or muscle twitch accompanying the auditory event. Although the sudden shock can be frightening and may trigger a brief state of anxiety or fear, the sensations are transient, lasting only a second or two.

From a physiological standpoint, EHS is thought to arise from brief misfiring or delayed signaling of neurons in the brainstem reticular formation or the auditory pathways. During transitions between sleep stages, the normal inhibition of sensory processing may falter, allowing random neural activity to be interpreted by the brain as a loud noise. No structural abnormalities are found on imaging studies, and the condition is generally considered idiopathic.

Types of Exploding Head Syndrome

Hypnagogic Exploding Head Syndrome: Occurs just as the person is falling asleep. The sudden noise may jolt the individual awake before sleep initiation.
Hypnopompic Exploding Head Syndrome: Occurs during awakening from sleep. The sensation might coincide with the natural arousal from non-rapid eye movement sleep.
Chronic Exploding Head Syndrome: In rare cases, EHS can occur frequently—several times per week—leading to significant anxiety about sleep, insomnia, or anticipatory fear of episodes.
Isolated Exploding Head Syndrome: Single or very infrequent episodes without any associated sleep disturbance or psychological distress.

Causes of Exploding Head Syndrome

Age-Related Brainstem Changes: Degeneration of brainstem inhibitory circuits with aging may predispose older adults to EHS.
Stress and Anxiety: High levels of mental stress can disrupt normal sleep architecture, increasing the likelihood of sensory misperceptions during sleep transitions.
Sleep Deprivation: Chronic lack of sleep alters neurotransmitter balance, potentially triggering random neural firing.
Irregular Sleep Schedule: Frequent changes in bedtime or wake time can impair the brain’s sleep–wake regulation.
Sudden Pressure Changes: Rapid changes in atmospheric or blood pressure may transiently affect inner ear or brainstem function.
Medication Withdrawal: Abrupt cessation of certain sedatives or antidepressants can disturb normal neural inhibition.
Migraines: Some individuals with migraine history report higher incidence of EHS, possibly due to shared sensory processing pathways.
Temporomandibular Joint Dysfunction: Malfunction in the jaw joint may lead to referred auditory sensations during sleep.
Inner Ear Disorders: Conditions like Meniere’s disease could theoretically contribute to auditory misperceptions.
Electrolyte Imbalances: Abnormal levels of sodium or calcium can affect neuronal excitability.
Alcohol or Caffeine Use: Stimulants or depressants may modify sleep quality and sensory gating.
Nocturnal Epileptic Activity: Rarely, focal seizures in the temporal lobe can mimic EHS, though EHS itself is non-epileptic.
Rapid Eye Movement Sleep Behavior Disorder: Disrupted REM atonia may overlap with EHS occurrences.
Obstructive Sleep Apnea: Repeated arousals from apnea events can fragment sleep and provoke hypnopompic phenomena.
Psychiatric Conditions: Depression and posttraumatic stress disorder can exacerbate sleep disturbances and related parasomnias.
Hormonal Fluctuations: Changes during menopause or thyroid disorders can impact sleep stability.
Genetic Factors: Familial cases suggest a possible hereditary predisposition to sensory gating anomalies.
Neurodegenerative Diseases: Early-stage Parkinson’s or Alzheimer’s may disrupt sleep architecture.
Head Trauma: Past concussions could have lasting effects on sleep–wake transition zones in the brain.
Idiopathic: In most cases, no specific cause is identified despite thorough evaluation.

Symptoms of Exploding Head Syndrome

Perceived Loud Bang: A sudden, sharp sound heard inside the head.
Explosive Crack: A sensation akin to a small explosion.
Cymbal Crash: Auditory perception similar to metallic clashing.
Flash of Light: Some individuals report seeing a brief light flash.
Muscle Twitch: Involuntary jerk of the limbs or facial muscles.
Brief Awakening: Sudden arousal from sleep lasting a few seconds.
Fear or Panic: Transient anxiety reaction to the startling event.
Heart Palpitations: Rapid heartbeat immediately after the episode.
Chest Tightness: Transient sensation of pressure in the chest.
Sleep Onset Insomnia: Difficulty falling back asleep due to anticipatory fear.
Unrefreshing Sleep: Feeling tired upon awakening despite adequate duration.
Hypervigilance: Heightened alertness around bedtime.
Headache: Mild, short-lived head discomfort post-episode.
Ear Fullness: Sensation of blocked ears following the noise.
Tinnitus: Persistent ringing in the ears separate from the episode.
Mood Disturbance: Irritability or low mood due to poor sleep quality.
Daytime Sleepiness: Increased sleepiness during the day.
Concentration Issues: Difficulty focusing at work or school.
Memory Problems: Short-term memory lapses related to sleep loss.
Avoidance of Sleep: Reluctance to go to bed due to fear of episodes.

Diagnostic Tests for Exploding Head Syndrome

Physical Examination

Neurological Examination: Assessment of cranial nerves and motor function to rule out structural lesions.
Otolaryngological Examination: Ear, nose, and throat exam to exclude middle or inner ear pathology.
Dental Examination: Evaluation for temporomandibular joint disorders.
Blood Pressure Check: To detect hypertensive crises that can mimic EHS.
Body Mass Index Calculation: Identify obesity as a risk factor for sleep apnea.
Thyroid Palpation: Detect goiter or nodules influencing sleep.
Skin Inspection: Look for signs of systemic disease (e.g., rash of lupus).
Neck Auscultation: Rule out carotid bruit indicating vascular issues.

Manual Tests

Jaw Stress Test: Palpation of TMJ during mouth opening and closing.
Cervical Range of Motion: Identify neck stiffness linked to headache variants.
Palpation of Mastoid Area: Check for tenderness in ear-related pain.
Trigger Point Examination: Identify myofascial pain points in neck muscles.
Valsalva Maneuver: Evaluate inner ear pressure sensitivity.
Fontanelle Compression (in children): Assess intracranial pressure dynamics.
Sinus Percussion Test: Detect sinusitis that can present with head noises.
Temporal Artery Palpation: Rule out temporal arteritis.

Lab and Pathological Tests

Complete Blood Count: Screen for infection or anemia.
Electrolyte Panel: Check sodium, calcium levels affecting neuronal firing.
Thyroid Function Tests: Identify hyper- or hypothyroidism.
Inflammatory Markers (ESR, CRP): Detect systemic inflammation.
Autoimmune Panels (ANA): Rule out autoimmune encephalitis.
Ceruloplasmin Level: Screen for Wilson’s disease.
Vitamin B12 and Folate: Check for deficiency-related neuropathy.
Heavy Metal Screening: Lead or mercury exposure affecting nervous system.

Electrodiagnostic Tests

Electroencephalogram (EEG): Exclude nocturnal seizure activity.
Brainstem Auditory Evoked Potentials (BAEP): Evaluate auditory pathway conduction.
Polysomnography (Sleep Study): Rule out sleep apnea and other parasomnias.
Multiple Sleep Latency Test (MSLT): Assess for narcolepsy or hypersomnia.
Electromyography (EMG): Detect muscle activity during the episode.
Nerve Conduction Studies: Rule out neuropathy influencing sensations.
Quantitative Sensory Testing: Measure thresholds for auditory and somatosensory stimuli.
Evoked Reaction Time Testing: Assess central processing speed.

Imaging Tests

Magnetic Resonance Imaging (MRI) Brain: Exclude structural brain lesions.
MRI Brainstem Focused: Evaluate for demyelinating plaques.
Computed Tomography (CT) Head: Quick assessment for hemorrhage.
CT Angiography: Rule out vascular malformations.
Temporal Bone CT: Examine inner ear anatomy.
MRI of TMJ: Visualize temporomandibular joint integrity.
Functional MRI (fMRI): Research tool to study brain activation during episodes.
Positron Emission Tomography (PET) Scan: Identify metabolic brain abnormalities.
Single-Photon Emission CT (SPECT): Assess regional cerebral blood flow.
Diffusion Tensor Imaging (DTI): Evaluate white matter tracts.
Ultrasound Carotid Doppler: Rule out vascular stenosis.
EEG-fMRI Combined: Advanced research modality.
Magnetoencephalography (MEG): Map neural oscillations.
Cisternography: Rarely used; study CSF spaces.
Spectroscopy (MRS): Biochemical analysis of brain tissue.
Videofluoroscopy for Swallowing: Exclude pharyngeal sources.
Jaw Joint Arthrography: Contrast imaging of TMJ.
Skull X-ray: Obsolete but sometimes performed.

Non-Pharmacological Treatments That Really Help

Physiotherapy & Electrotherapy

Sleep-Hygiene Coaching – A physical therapist or sleep educator trains you to anchor wake-up and bedtimes, dim lights two hours before bed, and ditch caffeine after noon. Purpose: lower pre-sleep arousal. Mechanism: steadies circadian rhythm → fewer “false alarm” bursts from the reticular activating system.
Cranial Electrical Stimulation (CES) – Low-level alternating micro-current is clipped to the earlobes for 20 minutes daily. Purpose: reduce hyper-excitability. Mechanism: modulates thalamocortical loops and boosts calming alpha waves.
Transcranial Magnetic Stimulation (TMS) – Repetitive magnetic pulses over the temporal cortices three times a week. Purpose: dampen sensory gating glitches. Mechanism: induces long-term depression (LTD) in over-responsive auditory neurons.
tDCS (transcranial Direct-Current Stimulation) – 1-to-2 mA direct current over prefrontal sites during daytime sessions. Mechanism: raises GABA tone, which calms nocturnal cortical bursts.
Low-Level Laser Therapy – Cold-laser beams around the upper cervical spine improve micro-circulation and vagal tone, indirectly quieting nighttime startle pathways.
Myofascial Release for Neck & Jaw – Tight suboccipital and temporomandibular trigger points heighten startle reflexes; manual release improves proprioceptive feedback to the brain-stem.
Posture-Correction Training – Re-aligning forward-head posture lessens cervicogenic input that may trigger “explosive” sensory misfires.
Vestibular Rehabilitation – Balance drills calm the inner-ear nuclei, cutting down cross-talk into the auditory system.
Acoustic Masking Therapy – Continuous pink-noise at 40–50 dB during sleep prevents the brain from amplifying internal sounds.
Bright-Light Therapy (Morning) – 10 000-lux light box for 20 minutes after waking reinforces circadian timing, shrinking the twilight zone when EHS strikes.
Neuromuscular Electrical Stimulation (NMES) – Gentle pulses to cervical paraspinals activate parasympathetic pathways.
Diaphragmatic Breathing Biofeedback – Sensors train slow (6 breaths/min) belly breathing; vagal activation soothes hyper-vigilant auditory circuits.
Progressive Muscle Relaxation (PMR) – Physiotherapist-guided 20-minute PMR nightly releases body tension that feeds cortical arousal.
Cold-Water Face Immersion – A 30-second dive reflex triggers bradycardia and vagal calm before bed.
Craniosacral Therapy – Gentle cranial bone holds may down-regulate brain-stem arousal networks; data scarce but many patients report subjective relief.

Exercise-Based Therapies

Moderate Aerobic Activity – 30 minutes of brisk walking five days a week deepens slow-wave sleep, associated with fewer EHS events.
Yoga Flow Sequences – Vinyasa or Hatha poses plus meditative breathing reduce sympathetic overdrive.
Pilates Core Stability – Strengthens deep trunk muscles; improved posture equals calmer cervico-auditory feedback.
Low-Impact Swimming – Rhythmic bilateral movement promotes hemispheric balance and serotonin release.
Resistance-Band Circuits – Two full-body sessions weekly improve systemic GABAergic tone.

Mind–Body Approaches

Mindfulness Meditation – 10-minute nightly body-scan; MRI studies show reduced default-mode chatter, mitigating sensory “echoes.”
Cognitive-Behavioral Therapy for Insomnia (CBT-I) – Identifies catastrophic thoughts (“My brain is exploding!”) and replaces them with facts (“It’s harmless, brief, and will pass.”).
Guided Imagery – Therapist leads soothing ocean-wave imagery at sleep onset; active imagery crowds out intrusive auditory bursts.
Box Breathing (4-4-4-4 pattern) – Stabilizes CO₂ and calms locus coeruleus firing.
Autogenic Training – Self-statements like “My arms are warm and heavy” trigger relaxation responses.

Educational Self-Management

Sleep Diary & Trigger Log – Tracking meal times, stress, and attack timing uncovers patterns.
Stress-Management Workshops – Covers time-management, assertive communication, and micro-breaks to lower all-day tension.
Cognitive Restructuring Handouts – Simple pamphlet debunks myths (e.g., “exploding head equals aneurysm”).
Bedroom Optimization – Blackout curtains, 18–20 °C temperature, and gadget-free bed reduce sensory load.
Peer-Support Groups – Sharing experiences defuses fear and validates benign nature.

Evidence-Based Medicines

Medical disclaimer: Always start any drug only after an in-person consultation. Most EHS cases never need medicine; these options exist for stubborn or distressing episodes.

Amitriptyline – 10–50 mg at bedtime, Tricyclic antidepressant. Side-effects: dry mouth, morning grogginess, weight gain. Case series show full remission in ≤3 weeks. ncbi.nlm.nih.govpmc.ncbi.nlm.nih.gov
Clomipramine – 25 mg nightly, Tricyclic/serotonergic. Side-effects: constipation, orthostatic dizziness. Small cohort had 100 % symptom control. ncbi.nlm.nih.gov
Duloxetine – 30 mg morning, SNRI. Side-effects: nausea, raised blood pressure. Anecdotal, but serotonergic profile parallels clomipramine. frontiersin.org
Topiramate – 25 mg nightly, Antiseizure. Parasomnia case reports show rapid relief. Side-effects: tingling hands, word-finding difficulty. jcsm.aasm.org
Nifedipine – 30 mg extended-release evening, Calcium-channel blocker. Thought to dampen thalamic burst firing; watch for ankle edema. my.clevelandclinic.org
Flunarizine – 5–10 mg at night, Non-selective calcium antagonist. Two case studies report “almost total disappearance.” Side-effects: drowsiness, weight gain. jcsm.aasm.org
Clonazepam – 0.25–0.5 mg at bedtime, Benzodiazepine. Calms sensory arousal; risk of dependence with prolonged use.
Melatonin (RX strength) – 3–5 mg 30 min before bed. Regulates sleep-stage transitions; minimal side-effects (vivid dreams).
Doxepin (Low-dose) – 6 mg 30 min pre-sleep, H₁ antihistamine/tricyclic hybrid. Less anticholinergic burden.
Gabapentin – 300 mg at night. Inhibits voltage-gated calcium currents; may blunt nocturnal startle.
Carbamazepine – 100 mg HS. Stabilizes hyper-excitable cortical cells; monitor liver enzymes.
Citalopram – 10–20 mg morning. Pure SSRI; limited data but one case noted total cessation.
Trimipramine – 25 mg bedtime. Side-effects similar to other tricyclics; rare but effective in anecdotal reports.
Pregabalin – 75 mg bedtime. α₂-δ calcium-channel modulator; lowers nocturnal sensory spikes.
Mirtazapine – 7.5 mg HS. Dual noradrenergic–serotonergic; added bonus of improved deep sleep.
Propranolol – 20 mg evening. Beta-blocker dampens adrenergic surges felt after an EHS bang.
Quetiapine (Low dose) – 25 mg HS. Off-label for sleep; risk of metabolic side-effects.
Zolpidem (Intermittent) – 5–10 mg HS PRN. Short-acting hypnotic; avoid nightly to curb dependence.
Valproic Acid – 250 mg HS. GABA augmenter; liver monitoring necessary.
Hydroxyzine – 25 mg 30 min before bed. Antihistamine anxiolytic to break vicious circle of fear-insomnia.

Dietary Molecular Supplements

Magnesium Glycinate, 200–400 mg at night – Acts as a natural NMDA antagonist, calming cortical neurons.
Vitamin B12, 1 000 µg sublingual morning – Deficiency linked with paraesthesia-like sensory events; replenishment normalises myelin metabolism.
Omega-3 Fish Oil, 1 g EPA+DHA daily – Anti-inflammatory; improves neuronal membrane fluidity.
L-Theanine, 100 mg evening – Elevates alpha-brain waves and GABA levels.
5-HTP (Tryptophan precursor), 50 mg before bed – Boosts serotonin which modulates thalamic gating.
Glycine, 3 g powder 1 hour pre-sleep – Lowers core body temperature and speeds sleep onset.
GABA (pharma-grade), 250 mg night – Directly augments inhibitory neurotransmission; variable BBB penetration.
Melatonin (OTC), 1–3 mg – As above, but sold as supplement.
Zinc Picolinate, 25 mg daily – Needed for GABA synthesis.
Lavender Oil Softgels (Silexan), 80 mg daily – Clinical trials show reduced anxiety scores and improved sleep continuity.

Drugs in the Bisphosphonate / Regenerative / Viscosupplementation / Stem-Cell Realm

Important reality check: To date, none of these drug classes carry peer-reviewed evidence for treating Exploding Head Syndrome itself. They appear in this list only because some patients have concomitant bone-or-joint issues, or experimental labs look at neuro-regeneration more broadly. Use remains strictly investigational.

Alendronate (Bisphosphonate) – Protects bone in long-term steroid users who also struggle with parasomnias.
Zoledronic Acid – Yearly IV infusion; same rationale as above.
Platelet-Rich Plasma (PRP) Nasal Sprays – Early animal work hints at trophic support for olfactory-auditory circuits.
Stem-Cell Exosome Drops – Nano-vesicles deliver growth factors; no human EHS data.
Umbilical Cord-Derived MSCs (IV) – Proposed to modulate neuro-inflammation that might predispose to sensory misfires.
Hyaluronic Acid Viscosupplement – Generally injected into joints, but oral HA may soothe systemic inflammation and indirectly improve sleep comfort.
Teriparatide (PTH Analog) – Neuro-protective in spinal cord models; purely theoretical in EHS.
Denosumab – Anti-RANK-L monoclonal; reduces skeletal pain that otherwise fragments sleep.
N-Acetyl Cysteine (NAC) – Antioxidant with glutamate modulation; occasionally trialed for tinnitus.
BDNF-Mimetic Peptides – Research-grade compounds aimed at synaptic repair; years away from clinical availability.

Surgical or Procedural Options (Rarely Needed)

EHS almost never warrants surgery. Operations below address underlying structural or neurologic issues occasionally mistaken for—or coexisting with—EHS. Always exhaust non-invasive routes first.

Microvascular Decompression (MVD) – Relieves arterial loops pressing the cochlear nerve; for patients with explosive tinnitus mis-labeled as EHS.
Chiari Malformation Posterior Fossa Decompression – Corrects brain-stem crowding that may mimic nocturnal “booms.”
Endoscopic Third Ventriculostomy (ETV) – Treats hydrocephalus that causes intraventricular pressure spikes.
Temporal Lobe Epilepsy Focus Resection – For proven nocturnal auditory seizures.
Cervical Spine Fusion – Stabilizes atlanto-axial instability provoking sudden proprioceptive jolts.
Radiofrequency Ablation of Glossopharyngeal Neuralgia – Sharp throat shocks can be misread as EHS; ablation stops the root spasm.
Cochlear Implant Re-programming Procedure – Eliminates abnormal feedback loops causing phantom bangs.
CSF Leak Repair – Intracranial hypotension triggers thunderclap-like sensations at sleep onset.
Pulsatile-Tinnitus Venous Stenting – Corrects transverse-sigmoid sinus stenosis.
Deep Brain Stimulation (DBS) Trial Lead – Researchers are mapping arousal networks; still experimental.

Benefits: Symptom elimination when a true structural driver exists. Risks: Standard neurosurgical hazards—bleeding, infection, nerve damage.

Everyday Prevention Strategies

Keep a rock-solid sleep-wake schedule—even on weekends.
Avoid heavy meals, nicotine, and caffeine for at least six hours before bedtime.
Limit evening screen light or use blue-light blockers.
Wind down with a 20-minute quiet ritual—reading, gentle stretches.
Hydrate in the afternoon but taper fluids after dinner to prevent 3 a.m. bathroom trips.
Treat coexisting disorders (migraine, tinnitus, sleep apnea).
Manage stress daily with mini-relaxation breaks, not just at night.
Exercise ≥150 minutes per week, but finish intense workouts at least three hours before bed.
Use ear-plugs or white-noise if you live in a noisy area; external bangs can trigger internal false alarms.
Review all medicines with a pharmacist—some stimulants or SSRIs can raise sensory startle thresholds.

When Should You See a Doctor?

The first time an episode happens—just to rule out seizure, hypertension surge, or true auditory hallucinations from another illness.
If attacks cluster nightly for more than two weeks despite good sleep hygiene.
Anytime the events come with pain, limb jerks, speech difficulty, or daytime neurologic symptoms.
If anxiety about the next “boom” is ruining sleep quality or causing daytime drowsiness that affects work or driving safety.

A brief evaluation usually includes a neurological exam, blood pressure check, possible overnight polysomnography, and sometimes brain imaging to reassure both patient and clinician.

“Do & Don’t” Guidelines

Keep a symptom diary.
Practice nightly relaxation.
Maintain a cool, dark bedroom.
Talk openly with partners or roommates.
Follow up on hearing tests if over 50.

Don’t

Don’t panic—EHS is not a stroke.
Don’t self-medicate with excess alcohol.
Don’t binge caffeine to “push through” next day fatigue.
Don’t browse alarming web forums late at night.
Don’t ignore new headaches or neurologic changes—see a doctor.

Frequently Asked Questions (FAQs)

Is exploding head syndrome dangerous?
No—scary but not harmful. No link to brain bleeds or true explosions.
How long does a typical episode last?
Usually < 10 seconds, including the shock and after-buzz.
Does everyone hear the same sound?
No—some hear cymbals, others a gunshot, roar, or electric pop.
Can children get it?
Yes, but it’s rarer; many outgrow episodes during adolescence.
Is EHS a form of epilepsy?
EEG studies show no seizure activity during events, so it’s separate.
Will wearing ear-plugs stop it?
Sometimes; blocking real noise reduces sensory expectation priming.
Can stress alone trigger EHS?
Stress raises overall arousal and is a major reported precipitant.
Does EHS cause hearing loss?
No; hearing tests after episodes remain normal.
Is there a genetic link?
A few family clusters exist, but no gene has been pinned down.
What if I work night shifts?
Keep your “sleep day” schedule fixed and dark—shift-workers can still prevent EHS with strict routine.
Will cutting out caffeine cure me?
It helps many, but not all. Combine caffeine limits with relaxing bedtime habits for best results.
Are PET scans or MRIs always needed?
Usually not—only if you have atypical features like headaches or neurologic deficits.
Can pregnant people use the medicines listed?
Most drugs here are category C or worse; pregnant people should stick to non-drug measures and consult obstetric sleep specialists.
Is CBT-I as good as medicine?
In mild-to-moderate EHS, yes—behavioral therapy alone often suffices.
Will it ever just go away on its own?
Many patients report spontaneous remission within months once they understand the condition and remove triggers.

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.