Spinning migraine causes are often misunderstood, leading to ineffective treatments.TL;DR: Vestibular migraine is a spinning form of migraine where vertigo and imbalance are often more disabling than the headache, and standard pain drugs like triptans frequently fail to control the dizziness. Effective treatment usually needs a 4‑pillar plan: strict trigger and diet control, daily preventive migraine medicines (including newer CGRP therapies when needed), customized vestibular rehabilitation, and psychological support such as CBT to retrain the brain’s balance and pain networks. For patients in Hardoi, working with a vertigo‑focused migraine specialist allows this full protocol to be tailored to your specific triggers, comorbid anxiety, and lifestyle so that attacks become shorter, less intense, and less frightening over time

External Resources & References

For further reading on vestibular migraine and related conditions, please refer to these authoritative medical resources:

These resources provide evidence-based information on vestibular migraine pathophysiology, diagnosis, and treatment options recommended by leading international organizations.

ENGLISH VERSION

The Migraine That Spins: Why Headache Medications Fail (And What Actually Works)

Understanding Vestibular Migraine: A Hidden Epidemic

Dizziness and balance disorders are among the most common reasons patients seek medical advice, yet they remain some of the most misunderstood conditions in modern medicine. For millions of people worldwide, a migraine is not just a severe headache; it is a violent, spinning experience known as vestibular migraine (VM).

This condition is now recognized as the second most common cause of recurrent vertigo, affecting approximately 1% of the general population (though some estimates suggest higher prevalence in patients who visit balance clinics). Despite its prevalence, patients often find that standard headache treatments—triptans, NSAIDs, even opioids—do little to stop the world from spinning. This creates a frustrating cycle: the patient endures days of disability while conventional medications fail, leaving them confused about why treatments that work for regular migraines are ineffective for their dizziness.

This article explores the unique nature of the “spinning migraine,” why traditional approaches fail, and the multidisciplinary strategies that actually provide relief.

What is Vestibular Migraine?

Diagnostic Criteria: Moving Beyond the Headache-Centric Definition

Vestibular migraine is a specialized form of migraine where the primary symptoms are balance-related rather than pain-centered. This is the critical distinction that most physicians and patients miss.

The Bárány Society and the International Headache Society have established strict diagnostic criteria to help clinicians identify this elusive disorder. To be diagnosed with definite vestibular migraine, a patient must meet the following criteria:

At least five episodes of vestibular symptoms of moderate or severe intensity
Duration: Symptoms lasting between 5 minutes and 72 hours
Migraine history: Current or past history of migraine with or without aura
Migrainous features: At least one migrainous feature during at least 50% of the vertigo episodes

Migrainous features include:

Photophobia (sensitivity to light)
Phonophobia (sensitivity to sound)
Visual aura (flashing lights, zigzag patterns)
Headache (though notably absent in up to 30% of VM attacks)
Nausea or vomiting

The Diversity of Vestibular Migraine Presentations

Remarkably, vestibular migraine presents in four distinct clinical subtypes, and many patients cycle through multiple types throughout their lives:

Type 1: Spontaneous Vertigo

Patient feels they are spinning while sitting perfectly still
Often the most distressing form because there is no obvious environmental trigger
Can last from 5 minutes to days
May be accompanied by nausea so severe the patient cannot stand

Type 2: Positional Vertigo

Triggered by specific head movements (rolling in bed, tilting head back)
Can mimic BPPV (Benign Paroxysmal Positional Vertigo), leading to misdiagnosis
Unlike BPPV, the vertigo in VM is often longer-lasting (minutes to hours, not seconds)
May occur in clusters (repeated episodes over hours or days)

Type 3: Head-Motion Dizziness

A distorted sensation of spatial orientation during self-motion
Patient feels “off-balance” or as if the floor is tilting while walking or moving the head
Particularly disabling because it prevents normal daily activities like walking, driving, or exercise

Type 4: Visual Vertigo (Visual Dependence)

Symptoms triggered by complex or moving visual environments
Classic triggers: busy supermarket aisles, escalators, striped patterns, moving cars
Watching action movies or scrolling through social media can provoke attacks
Often overlooked because patients don’t link environmental visuals to their dizziness

The Science of the Spin: Why Vestibular Migraine Feels Different

The Neurobiological Basis: Beyond Simple Pain

The reason vestibular migraine is so disorienting—and why it responds differently to medications—lies in how it affects the brain’s processing centers.

Standard Migraines primarily involve:

The trigeminovascular system (trigeminal nerve + blood vessel interactions)
Release of CGRP (calcitonin gene-related peptide) and other inflammatory mediators
Activation of pain pathways in the thalamus and cortex
Result: severe headache, photophobia, nausea

Vestibular Migraines involve a broader activation:

The vestibular nuclei in the brainstem (balance processing centers)
The cerebellum (coordination and fine-tuning of balance)
The vestibular cortex in the temporal lobe (perception of motion and spatial orientation)
The visual-vestibular integration pathways (how the brain combines eye and balance signals)
Result: vertigo, imbalance, visual disturbances, and sometimes headache

Three Leading Theories of Vestibular Migraine Pathophysiology

Theory 1: Cortical Spreading Depression

The most accepted theory suggests that vestibular migraine involves a “spreading depression” of neuronal activity that cascades across the brain.

In regular migraines, spreading depression occurs in the cortex, causing the aura (visual symptoms) and triggering trigeminal activation
In VM, this wave of reduced neuronal activity spreads to include the vestibular cortex and cerebellar regions
As neural activity “quiets down,” the brain loses its ability to integrate balance signals properly, leading to vertigo
This explains why VM attacks can last hours to days—the spreading depression is slower to resolve than in typical migraines

Theory 2: Vasospasm of the Internal Auditory Artery

An alternative theory proposes that the internal auditory artery (IAA), which supplies blood to the inner ear and portions of the brainstem, may undergo vasospasm (temporary narrowing).

This leads to transient dysfunction of the vestibular sensors and balance processing centers
The attack resolves as blood flow is restored
This theory would explain why some VM patients experience sudden hearing loss during an attack—a symptom that overlaps with another condition, sudden sensorineural hearing loss (SSNHL)
However, this theory is less widely accepted because most VM patients do not have confirmed vasospasm on imaging

Theory 3: Channelopathy (Ion Channel Dysfunction)

Emerging evidence suggests that some patients with VM may have a genetic defect in ion channels—the cellular “gates” that regulate how nerves fire.

Mutations in potassium or calcium channels can make neurons hyperexcitable
This “hyperexcitability” lowers the threshold for migraine activation
In these patients, vestibular neurons are particularly sensitive to triggering stimuli
This explains why some families have multiple members with VM (genetic predisposition)
It also explains why some VM patients respond to anticonvulsants (which stabilize ion channels) when other medications fail

The Signal-to-Noise Problem

Imagine a radio receiver in a noisy room. When the radio works properly, it filters out background noise and focuses on the signal. In vestibular migraine, the brain’s ability to filter out irrelevant balance information becomes impaired. The signal-to-noise ratio becomes permanently altered, making the brain hypersensitive to:

Normal head movements
Visual motion
Changes in body position
Even subtle shifts in air pressure or temperature

This is why VM patients often report that triggers become more sensitive over time and why environmental modifications (staying in quiet, dimly lit spaces) provide temporary relief.

Why Standard Headache Medications Often Fail in Vestibular Migraine

Understanding the failures of conventional migraine treatments is crucial to appreciating why a different approach is needed.

Reason 1: The Timing Mismatch

Traditional migraine auras (visual symptoms, tingling) typically last between 5 and 60 minutes. Vestibular symptoms in VM can persist for days or even weeks.

Triptans and other abortive medications are designed for short bursts of pain (3-24 hours)
When taken during a VM attack, they may abort the headache component (if present) but leave the vertigo untouched
The patient experiences “partial relief”—the head pain resolves, but the world continues spinning
By the time the patient realizes the triptan didn’t work on the dizziness, the medication has already been absorbed and metabolized

Clinical Example: A patient takes sumatriptan at the onset of a migraine. The headache resolves within 30 minutes. However, the vertigo that began simultaneously persists for 3 more days. The patient attributes this to “incomplete response” when, in fact, they needed a different medication strategy.

Reason 2: Lack of Specific Vestibular Evidence in Clinical Trials

Most major clinical trials for migraine medications—including trials for triptans, beta-blockers, and anticonvulsants—focused on headache reduction as the primary outcome measure.

Researchers measured pain scores, photophobia, nausea
Few trials specifically measured vertigo severity or balance function
While triptans are excellent at constricting blood vessels and stopping head pain, their effect on the complex neuronal “overdrive” in the vestibular system remains unclear and often inconclusive
This creates a treatment gap: medications are approved for migraine but never tested for vestibular symptoms specifically

Reason 3: The Absorption Problem

VM attacks are frequently accompanied by severe nausea and vomiting, which disrupts normal stomach function.

Gastric motility (the stomach’s ability to move food and medication forward) decreases dramatically during a vestibular migraine attack
A patient swallows a pill during an attack hoping for relief, but the medication sits in the stomach and never gets absorbed
By the time nausea subsides (hours or days later), the acute attack has already passed
The patient concludes the medication “didn’t work” when, in fact, it was never absorbed

This is why rescue medications for VM are increasingly prescribed as:

Suppositories (absorbed through rectal tissue, bypassing the stomach)
Nasal sprays (absorbed through nasal mucosa, rapid onset)
Subcutaneous injections (injected directly under the skin for immediate delivery)

Reason 4: Misdiagnosis Leading to Wrong Treatment

Because vestibular migraine can mimic other conditions, patients often receive the wrong diagnosis and therefore the wrong treatment.

Example 1: BPPV Misdiagnosis

Patient presents with positional vertigo lasting hours
Doctor performs the Dix-Hallpike test (positive result)
BPPV is assumed, Epley maneuver is performed
The Epley maneuver may provide temporary relief (due to placebo effect or concurrent resolution of the migraine) but doesn’t address the underlying migraine
Attack recurs days later; patient is told to repeat the Epley maneuver
Correct treatment (preventative migraine medication) is never started

Example 2: Menière’s Disease Misdiagnosis

Patient experiences attacks of vertigo + hearing loss + tinnitus
Doctor assumes Menière’s disease and recommends salt restriction
Patient follows a strict low-sodium diet but attacks continue
The underlying migraine (which can cause temporary hearing loss) is never treated

Reason 5: Over-Reliance on Vestibular Suppressants

Many patients—and unfortunately, some well-intentioned physicians—reach for vestibular suppressants like meclizine (Dramamine), dimenhydrinate, or even diazepam.

Why this is problematic:

While these medications can quiet symptoms during a violent 24-hour attack, they work by suppressing the balance system’s activity
The brain’s natural ability to “re-calibrate” and compensate for balance deficits requires intact vestibular signaling
Long-term use of suppressants prevents this compensation process from occurring
The patient becomes dependent on the medication, and when they stop taking it, symptoms return—sometimes worse than before
This creates a vicious cycle: more dizziness → more suppressants → less compensation → persistent dizziness

The paradox: The medication that provides short-term relief may actually delay long-term recovery.

The 4-Step Approach That Actually Works

Success in managing vestibular migraine requires a paradigm shift from “stopping the spin” once it starts to “preventing the spin” from occurring in the first place.

Step 1: The Foundation—Lifestyle Modification and Trigger Management

The most effective long-term strategy for VM is establishing a “migraine lifestyle.” The brain of a VM patient is hyperexcitable and thrives on regularity and consistency.

Sleep Hygiene

Target: 7–9 hours of consistent sleep per night, same bedtime and wake time daily
Mechanism: Sleep deprivation lowers the migraine threshold; irregular sleep triggers cascades of dysregulation
Practical: No sleeping in on weekends; maintain consistency even during vacation

Stress Management

Target: Identify personal stress triggers and develop coping mechanisms
Mechanism: Stress hormones (cortisol, adrenaline) activate the fight-or-flight response, priming the nervous system for migraine
Practical methods: Meditation, yoga, progressive muscle relaxation, cognitive behavioral therapy, exercise

Hormonal Triggers in Menstruating Individuals

Pattern: Many women report migraines clustered around menstruation (menstrual migraine)
Timing: Attacks often occur 2 days before to 3 days after the start of menstruation
Mechanism: Fluctuating estrogen levels destabilize the neurochemical balance
Management options:
Timed preventative medication starting 2 days before expected menstruation
Continuous hormonal contraception (to avoid hormonal fluctuations)
Consultation with gynecologist to optimize hormone timing

Migraine Trigger Foods (See Downloadable Table Below)

Certain foods and beverages contain chemical compounds that trigger migraines in susceptible individuals:

High-Tyramine Foods:

Aged cheeses (cheddar, blue cheese, feta)
Fermented foods (sauerkraut, kimchi, miso)
Cured meats (salami, pepperoni, bacon)
Alcohol (red wine, beer, aged spirits)

High-Nitrite Foods:

Processed meats (hot dogs, deli meats, sausages)
Smoked foods (smoked salmon, bacon)

MSG and Food Additives:

Monosodium glutamate (MSG)—common in Asian cuisine, processed foods
Aspartame (artificial sweetener)
Tartrazine (yellow food coloring)

Caffeine Paradox:

Acute use: Caffeine can abort a developing migraine by constricting blood vessels
Chronic use: Regular caffeine consumption raises the baseline migraine frequency; withdrawal causes rebound headaches
Recommendation for VM: Limit to ≤100mg per day (roughly one cup of weak tea or half a cup of coffee) and maintain consistent daily intake

Hydration and Meals

Dehydration: Even 2–3% dehydration can trigger a migraine in susceptible individuals
Hypoglycemia: Skipping meals causes blood sugar drops, destabilizing the nervous system
Practical: Eat small, regular meals (every 3–4 hours) and drink 2–3 liters of water daily

Environmental Triggers

Visual: Flickering lights (some people are sensitive to 60Hz fluorescent lights), high-contrast patterns, busy visual scenes
Auditory: Loud or sudden noises, particular frequencies
Olfactory: Strong perfumes, chemical smells
Weather: Barometric pressure changes, extreme heat or cold

Step 2: Prophylactic (Preventative) Medications

When attacks are frequent (more than two per month) or severely disabling, preventative medication becomes necessary. These medications are taken every day to raise the “seizure-like” threshold of the brain, making it less reactive to triggers.

Key principle: Preventative medications take 4–12 weeks to show benefit; they are not meant to abort individual attacks.

First-Line: Beta-Blockers

Mechanism: Reduce heart rate, blood pressure, and nervous system hyperreactivity

Most Common Agents:

Drug	Starting Dose	Typical Maintenance	Advantages	Side Effects	Dr Prateek Porwal
Propranolol	40 mg daily	120–240 mg/day (divided)	Long track record, also effective for hypertension	Fatigue, depression, sexual dysfunction, bradycardia	Often first choice; non-selective beta-blocker
Metoprolol	25 mg daily	100–200 mg/day	Selective for heart (β1), fewer lung side effects	Similar to propranolol but slightly less CNS side effects	Good for patients with asthma/COPD
Timolol	5 mg daily	20–30 mg/day	Short half-life, easy to adjust	Fatigue, dizziness (ironic for VM patients), bradycardia	Use cautiously in VM; dizziness can worsen symptoms

Success Rate: 40–60% reduction in migraine frequency
Timeline to Benefit: 4–8 weeks
Contraindications: Asthma, COPD, uncontrolled diabetes, bradycardia, decompensated heart failure

Second-Line: Tricyclic Antidepressants

Mechanism: Block reuptake of serotonin and norepinephrine; modulate pain pathways; have anticholinergic effects

Most Common Agents:

Drug	Starting Dose	Typical Maintenance	Advantages	Side Effects	Dr Prateek Porwal
Amitriptyline	10–25 mg at bedtime	50–150 mg/day (usually single dose at night)	Dual benefit: prevents migraine AND improves insomnia/anxiety	Drowsiness (often desired for sleep), dry mouth, weight gain, urinary retention, anticholinergic effects	Excellent choice if patient also has insomnia; helps with anxiety-related dizziness
Nortriptyline	10–25 mg at bedtime	50–100 mg/day	Similar to amitriptyline but slightly less sedating, fewer anticholinergic effects	Dry mouth, drowsiness, weight gain	Alternative if amitriptyline causes excessive sedation

Success Rate: 40–60% reduction in migraine frequency
Timeline to Benefit: 6–12 weeks (slower than beta-blockers but equally effective)
Special Consideration: Particularly useful in VM patients with comorbid Persistent Postural-Perceptual Dizziness (PPPD) due to anxiety/catastrophizing component

Third-Line: Anticonvulsants

Mechanism: Stabilize neuronal electrical activity; block ion channels; reduce excitatory neurotransmission

Most Common Agents:

Drug	Starting Dose	Typical Maintenance	Advantages	Side Effects	Dr Prateek Porwal
Topiramate	25 mg daily (increase slowly)	75–200 mg/day (divided)	Cognitive benefits (weight loss, possible mood improvement); particularly effective for VM; once-daily dosing available	Cognitive dulling (“topiramate fog”—slowed thinking, word-finding difficulties), numbness/tingling, kidney stone risk, narrow-angle glaucoma risk	EXCELLENT for VM; start slowly to minimize cognitive effects; monitor hydration to prevent stones
Valproate (Depakote)	250 mg daily	500–1500 mg/day (divided)	Highly effective for migraines; FDA-approved for migraine prevention	Tremor, hair loss, weight gain, liver toxicity (monitor LFTs), teratogenicity in pregnancy, blood dyscrasias	High efficacy but more side effects; requires regular lab monitoring
Levetiracetam	250 mg daily	500–1500 mg/day (divided)	Fewer drug interactions; no liver metabolism	Behavioral changes, irritability, dizziness (can paradoxically worsen VM), somnolence	Use cautiously in VM; monitor for mood changes

Success Rate: 40–70% reduction in migraine frequency
Timeline to Benefit: 4–12 weeks
Special Consideration for Topiramate in VM: Multiple mechanisms benefit balance—stabilizes ion channels, reduces neuronal hyperexcitability, and may improve cerebellar function

Fourth-Line: Calcium Channel Blockers

Mechanism: Block calcium entry into cells; reduce vascular reactivity; modulate neurotransmitter release

Most Common Agents:

Drug	Starting Dose	Typical Maintenance	Advantages	Side Effects	Dr Prateek Porwal
Verapamil	120 mg daily (sustained-release)	240–480 mg/day	FDA-approved for migraine; excellent for migraine with aura; also effective for hypertension	Constipation (can be severe), bradycardia, hypotension, ankle edema, drug interactions	PARTICULARLY EFFECTIVE for VM; less side-effect burden than other prophylactics in some patients
Flunarizine	5 mg at bedtime	5–10 mg/day	Highly effective for migraine and VM; unique mechanism; once-daily dosing	Drowsiness, weight gain, depression, tardive dyskinesia risk (with long-term use), slower onset	NOT FDA-approved in USA but widely used internationally; excellent efficacy in VM

Success Rate: 40–60% reduction in migraine frequency
Timeline to Benefit: 4–8 weeks for verapamil; 2–4 weeks for flunarizine
Special Note: Verapamil may be underutilized in VM despite strong evidence of efficacy

Step 3: Vestibular Rehabilitation Therapy (VRT) and Visual Desensitization

VRT is an exercise-based program that retrains the brain to ignore the incorrect signals it receives during a migraine. It is NOT a cure, but it significantly accelerates compensation and recovery.

The Mechanism: Habituation

The brain’s balance system relies on three inputs:

Vestibular system (inner ear)
Visual system (eyes)
Proprioceptive system (body position sensors)

In VM, the vestibular system sends corrupted signals. Through repeated, controlled exposure to the stimuli that cause dizziness, the brain learns to:

Downweight the corrupted vestibular input
Rely more heavily on vision and proprioception
Eventually stop producing the vertigo response altogether

This process is called habituation, and it requires consistent, graduated exposure to the dizziness-inducing stimulus.

Visual Desensitization Exercises

For patients whose VM is triggered by complex visual environments:

Week 1–2: Look at simple moving patterns (e.g., scrolling vertical lines on a screen) for 1–2 minutes, multiple times daily
Week 3–4: Progress to more complex moving patterns (checkerboards, horizontal motion)
Week 5–6: Introduce real-world visual stimuli (watching busy crowds via video, moving vehicles)
Week 7+: Gradual exposure to actual triggering environments (supermarkets, traffic, crowded spaces)

Key principle: Exercises should produce mild dizziness (3–4/10 intensity), not severe vertigo. The brain needs to habituate, not be overwhelmed.

Gaze Stabilization Exercises

Improves the vestibulo-ocular reflex (VOR), the reflex that keeps your eyes fixed on a target while your head moves.

Simple Exercise:

Fixate on a target (wall poster, mark on wall)
Move head side-to-side (or up-and-down) at increasing speeds while keeping eyes on target
5 minutes daily

Balance and Proprioceptive Training

Standing on progressively unstable surfaces (foam, balance ball)
Tandem stance (one foot in front of the other)
Single-leg stance
Walking heel-to-toe

Best Practice: VRT should be delivered by a physical therapist trained in vestibular disorders. PRIME ENT Center can provide referrals to certified vestibular rehabilitation specialists.

VRT + Medication Synergy

Patients who undergo VRT while on proper preventative medication often report significantly better outcomes (60–80% improvement) than those using medication alone (40–50% improvement). The medication stabilizes the nervous system while VRT retrains it.

Step 4: Addressing the Psychological Component

Persistent dizziness creates a “threat response” in the brain, leading to health anxiety, fear of falling, and avoidance behaviors.

Understanding PPPD (Persistent Postural-Perceptual Dizziness)

PPPD is a condition that develops in up to 25% of VM patients. Characterized by:

Constant unsteadiness between migraine attacks
“Phantom” dizziness (feeling dizzy without active migraine)
Catastrophizing: “Will this ever end?” “Am I having a stroke?” “I’ll never be normal again”
Avoidance: Stopping exercise, staying home, avoiding driving

The cycle:

VM attack occurs (legitimate neurological cause)
Patient experiences severe dizziness (real)
Fear and health anxiety develop (psychological amplification)
Patient avoids activities, becomes sedentary (deconditioning)
Deconditioning and muscle weakness worsen dizziness (vicious cycle)
Between attacks, patient feels “on edge,” anticipating the next one

Cognitive Behavioral Therapy (CBT) for VM and PPPD

CBT helps patients:

Recognize the thought-feeling-behavior loop: “I feel dizzy → I think I’m having a stroke → I avoid activity → I feel worse”
Challenge catastrophic thoughts: “What is the actual evidence that I’m having a stroke? The neurologist said my imaging is normal. My heart rate is fine. This is a migraine, not a stroke.”
Gradually re-engage in activities: Using “graded exposure” similar to VRT, but for psychological resilience
Develop acceptance: Understanding that some dizziness may persist, but it is not dangerous and can be managed

Outcome: Patients who combine VRT + preventative medication + CBT often report the best results. The medication stabilizes the nervous system, VRT retrains balance, and CBT removes the psychological amplification.

The New Frontier: CGRP Monoclonal Antibodies

What are CGRP Inhibitors?

CGRP (Calcitonin Gene-Related Peptide) is a neuropeptide released during migraine attacks. It causes:

Vasodilation (blood vessel widening)
Inflammation in the meninges (brain covering)
Sensitization of pain pathways

CGRP monoclonal antibodies are laboratory-engineered proteins that bind to CGRP (or its receptor) and block its activity. Four are currently FDA-approved for migraine prevention:

Drug	Target	Dosing	Mechanism
Erenumab (Aimovig)	CGRP Receptor	Monthly subcutaneous injection (70 or 140 mg)	Binds receptor, blocks CGRP signaling
Fremanezumab (Ajovy)	CGRP Peptide	Monthly or quarterly subcutaneous injection	Monoclonal antibody against CGRP
Galcanezumab (Emgality)	CGRP Peptide	Monthly subcutaneous injection	Humanized monoclonal antibody
Eptinezumab (Vyepti)	CGRP Peptide	Quarterly IV infusion	Humanized monoclonal antibody

Efficacy in Vestibular Migraine

Emerging research suggests CGRP inhibitors may be particularly effective for VM:

Study Findings:

VM patients treated with CGRP inhibitors show 50–70% reduction in vestibular symptoms
This exceeds the typical 40–50% reduction seen with traditional preventatives
Benefit emerges within 4 weeks (faster than most other medications)
Both headache AND vertigo improve simultaneously (unlike triptans)

Proposed Mechanism in VM:

CGRP is released not just in pain pathways but also in vestibular nuclei
Blocking CGRP may directly stabilize the neuronal hyperexcitability in balance centers
This explains superior efficacy compared to medications that primarily target pain or blood vessels

Practical Advantages

Once-monthly or quarterly dosing (excellent adherence)
Subcutaneous or IV administration (bypasses absorption issues)
Well-tolerated with few systemic side effects
No significant drug-drug interactions
No cognitive side effects (unlike topiramate or anticonvulsants)

Disadvantages and Limitations

Cost: Extremely expensive ($500–800 per month); often requires insurance approval
Delayed onset: Benefits typically emerge at 4 weeks; full effect by 12 weeks
Not a cure: Requires ongoing treatment; symptoms often recur if stopped
Limited long-term data: CGRP inhibitors have been available for only 5 years; long-term safety data still emerging
Injection/infusion burden: Monthly or quarterly clinic visits for some patients

CGRP Inhibitors at PRIME ENT Center Hardoi

If you are considering CGRP therapy for vestibular migraine:

Confirm the diagnosis with a vestibular specialist (HINTS exam, audiometry, MRI if indicated)
Discuss with your neurologist or headache specialist whether you qualify (typically reserved for patients with ≥4 migraine days per month despite prophylactic medication trials)
PRIME ENT Center can provide coordination with your neurologist to monitor vestibular outcomes during CGRP therapy

Abortive (Rescue) Strategies: What to Do During an Active Attack

While prevention is key, patients still need a plan for managing an acute vestibular migraine attack.

Anti-Nausea Medication

Critical principle: Because gastric motility is severely impaired during an attack, oral pills are often ineffective.

Preferred formulations:

Medication	Route	Advantages	Limitations
Ondansetron (Zofran)	IV, IM, or rectal suppository	Highly effective, no sedation, fast onset	Requires clinic/ER access for IV; constipation possible
Metoclopramide (Reglan)	IV, IM, or oral (dissolved under tongue)	Aids stomach emptying, allowing other meds to absorb; helps nausea	Dystonic reactions rare but scary; tardive dyskinesia with long-term use
Dimenhydrinate (Dramamine)	Suppository or IM injection	Antihistamine + anticholinergic; helps nausea and dizziness	Sedation (can be beneficial or unwanted); anticholinergic side effects

Vestibular Sedatives for Acute Attack

Use only for short term (≤3 days) during peak attack intensity.

Medication	Route	Dose	Use in VM
Dimenhydrinate	IM, IV, or rectal	50–100 mg every 4–6 hours	Short-term relief; anticholinergic effects help nausea
Meclizine	Oral (if tolerated)	25–50 mg every 4–6 hours	Better tolerated than dimenhydrinate but less effective
Diazepam	IV (ER only), oral, or rectal	2–5 mg every 6 hours	Muscle relaxant; GABA agonist; use only for severe, disabling attacks

Important caveat: These medications should NOT be used long-term because they prevent the brain’s natural compensation mechanisms.

Early Intervention: The “Prodrome Window”

Many VM patients experience a “prodrome” (warning period) before a full attack:

Ear fullness
Mild dizziness
Visual symptoms (flickering lights, shimmering)
Neck stiffness

If you take rescue medication during the prodrome (before vomiting starts), the attack may be aborted or significantly reduced.

Optimal rescue plan:

At first sign of prodrome, take metoclopramide (to enhance stomach emptying) + anti-nausea medication (suppository preferred)
Lie down in a dark, quiet room
Apply ice pack to back of neck
If attack escalates despite these measures, go to ER for IV anti-nausea and vestibular sedative

Conclusion: Reclaiming Your Balance and Your Life

Vestibular migraine is a complex, multisensory syndrome that requires a completely different approach than treating a typical headache. If you suffer from spinning sensations that do not respond to standard painkillers or if you experience dizziness that seems disconnected from any headache, it is time to reevaluate your diagnosis and treatment strategy.

The “Three-Legged Stool” of Effective VM Management consists of:

Lifestyle optimization (sleep, stress, diet, trigger avoidance)
Preventative medication (beta-blockers, tricyclics, anticonvulsants, or calcium channel blockers—ideally with CGRP inhibitors for severe cases)
Vestibular rehabilitation therapy (retraining the brain’s balance pathways)
Psychological support (CBT to address health anxiety and PPPD)

Expected outcomes: Most patients achieve a 50–70% reduction in symptom frequency and severity within 3–6 months of starting a comprehensive program. Some achieve complete remission, while others maintain low-frequency attacks that are manageable with lifestyle modification alone.

The key is early diagnosis, targeted treatment, and patience. There is no instant cure for a migraine that spins, but there is a pathway back to a steady, confident life. By understanding the mechanical, chemical, and neurological roots of the spin, you transform from a victim of the dizziness into an informed patient who can advocate for the right treatment and reclaim your balance.

vestibular migraine spinning treatment prevention

HINGLISH VERSION

The Migraine That Spins: Kyun Headache Medicines Fail Aur Kya Actually Kaam Karti Hai

Vestibular Migraine: Ek Hidden Problem

Lakhon logo ke liye, migraine sirf ek severe headache nahi hota. Yeh ek violent, spinning experience hota hai—vestibular migraine (VM).

Yeh second most common cause of recurrent vertigo hai aur lagbhag 1% of population ko affect karti hai. Dikkat yeh hai: standard headache medicines bilkul kaam nahi karti spinning ko rokne ke liye. Patient ko triptans dete ho, patient 3 days tak ghat spinning mein rehta hai. Frustration!

Yeh article samjhata hai: vestibular migraine kya hai, kyun normal migraine medicines fail karti hain, aur kya actually kaam karti hai.

Vestibular Migraine Kya Hota Hai?

Diagnostic Criteria: Pain Ke Baad Balance

Vestibular migraine = migraine jismein primary problem balance hai, pain nahi.

Strict criteria:

Minimum 5 episodes of vestibular symptoms (moderate-severe)
Duration: 5 minutes to 72 hours
Migraine history: Current or past migraine
Migrainous features: Light sensitivity, sound sensitivity, visual aura, headache (sometimes absent), nausea

Four Types of Vestibular Migraine

Type 1: Spontaneous Vertigo

Bilkul still baithe bhi spinning lag rahi hai
Most distressing kyunke no clear trigger

Type 2: Positional Vertigo

Bed se roll over, head tilt → spinning
BPPV mimic kar sakti hai (misdiagnosis risk)
Lekin BPPV se longer duration (minutes-hours, not seconds)

Type 3: Head-Motion Dizziness

Walking mein “off-balance” feel
Floor tilting jaise lag raha hai
Prevents normal activity

Type 4: Visual Vertigo

Busy supermarket aisle, moving cars, action movies → dizzy
Visual environment trigger karti hai

Science of the Spin: Kya Different Hota Hai

Why Vestibular Migraine Alag Hota Hai

Normal migraine:

Trigeminovascular system activate
CGRP release
Pain pathways trigger
Headache

Vestibular migraine:

Vestibular nuclei (balance centers) activate
Cerebellum (coordination) activate
Vestibular cortex (spatial orientation) activate
Visual-vestibular pathways affect
Result: spinning, imbalance, sometimes pain

Three Theories

Theory 1: Spreading Depression

Wave of reduced neuronal activity spreads to vestibular cortex
Brain loses balance signal integration
Days tak chalti hai attack

Theory 2: Vasospasm (Blood Vessel Narrowing)

Internal auditory artery (inner ear supply) narrows
Inner ear + brainstem dysfunction
Blood flow restore hote hi theek hota hai

Theory 3: Channelopathy (Ion Channel Defect)

Genetic mutation = neurons overexcitable
Family history possible
Anticonvulsants kaam karti hain

Kyun Standard Migraine Medicines Fail

Reason 1: Timing Mismatch

Aura = 5–60 minutes
VM = days-weeks
Triptans = short attacks ke liye designed
Long VM attacks mein headache go karti hai, spinning rehti hai

Reason 2: Trials Mein Headache Hi Measure Karte Hain

Vertigo ko specifically test nahi karte
Medicines “work” head pain ke liye lekin vertigo pe proven nahi

Reason 3: Nausea = No Absorption

Severe nausea mein stomach work nahi karti
Pill swallow → stomach mein sit karti hai → absorb nahi hoti
By time nausea theek, attack over

Solution: Suppositories, nasal sprays, injections use karte hain

Reason 4: Misdiagnosis

BPPV assume: Epley maneuver do (helps temporarily, doesn’t address migraine)
Menière’s assume: Salt restrict kro (kaam nahi karti, real problem = migraine)

Reason 5: Over-Suppressant Use

Meclizine, diazepam = short-term help
Lekin long-term use = brain compensation slow
Patient dependent ban jaata hai medications pe
Stop karti ho toh symptoms worse

4-Step Approach That Works

Step 1: Lifestyle—The Foundation

Sleep

7–9 hours, same time daily
Irregular sleep = migraine trigger

Stress

Meditation, yoga, exercise
Stress hormones = migraine priming

Hormonal (Women)

Menstruation = migraine cluster
Solution: Timed meds or continuous contraception

Migraine Trigger Foods (See Table Below)

Aged cheese, cured meats, MSG
Alcohol (red wine, beer)
Caffeine = paradox (short-term help, long-term worse)

Hydration + Meals

2–3 liters water daily
Eat every 3–4 hours (blood sugar drops trigger migraine)

Environment

Flickering lights, busy visuals, loud noise
Barometric pressure, extreme heat/cold

Step 2: Preventative Medications

Take every day to raise migraine threshold. Benefits in 4–12 weeks.

Beta-Blockers (First-Line)

Drug	Dose Range	Good For	Bad Effect
Propranolol	120–240 mg/day	High BP + migraine	Fatigue, depression
Metoprolol	100–200 mg/day	Asthma patients	Similar to propranolol
Timolol	20–30 mg/day	Quick adjustment	Can worsen VM dizziness

Efficacy: 40–60% reduction, 4–8 weeks

Tricyclic Antidepressants (Second-Line)

Drug	Dose	Good For	Bad Effect
Amitriptyline	50–150 mg bedtime	Insomnia + migraine	Drowsy, dry mouth, weight gain
Nortriptyline	50–100 mg bedtime	Less sedating option	Dry mouth, weight gain

Efficacy: 40–60% reduction, 6–12 weeks
Special: Great if anxiety + PPPD (fear-based dizziness)

Anticonvulsants (Third-Line)

Drug	Dose	Good For	Bad Effect
Topiramate	75–200 mg/day	Weight loss + VM	“Topiramate fog” (slow thinking), numbness, kidney stones
Valproate	500–1500 mg/day	High efficacy	Hair loss, tremor, liver monitoring needed
Levetiracetam	500–1500 mg/day	Fewer interactions	Dizziness, mood changes

Efficacy: 40–70% reduction, 4–12 weeks
VM-Specific: Topiramate = EXCELLENT; stabilizes ion channels + improves cerebellar function

Calcium Channel Blockers (Fourth-Line)

Drug	Dose	Good For	Bad Effect
Verapamil	240–480 mg/day	VM + high BP	Constipation, bradycardia
Flunarizine	5–10 mg/day	Highly effective VM	Drowsy, weight gain, depression

Efficacy: 40–60% reduction, 4–8 weeks
VM-Specific: Verapamil PARTICULARLY effective for VM

Step 3: Vestibular Rehabilitation Therapy (VRT)

VRT = exercise program jo brain ko dizziness signals ko ignore karna sikhati hai.

Visual Desensitization

Week 1–2: Simple moving patterns (scrolling lines)
Week 3–4: Complex patterns (checkerboards)
Week 5–6: Real-world visuals (busy crowds video)
Week 7+: Actual environments (supermarket)

Key: Mild dizziness (3–4/10), not severe. Brain habituation needed.

Gaze Stabilization

Target fix karo, head move karo side-to-side
5 min daily

Balance Training

Unstable surfaces, tandem stance, single-leg
Best with certified vestibular therapist

VRT + Medication = BEST

60–80% improvement (vs. 40–50% with meds alone)

Step 4: Psychology—CBT for Health Anxiety

Problem: Persistent dizziness = health anxiety, fear of falling, avoidance
Result: PPPD (constant dizziness between attacks)

PPPD Cycle

VM attack (real)
Fear (real)
Avoidance (behavior)
Deconditioning (worse dizziness)
Constant anticipation (anxiety)

CBT Solution

Recognize loop: Dizzy → Stroke? → Avoid activity → Worse
Challenge thoughts: “MRI normal. Doctor says migraine. Heart rate fine. Not stroke.”
Gradual re-engagement: Slow exposure to activities
Acceptance: Dizziness possible lekin manageable, not dangerous

Best outcome: VRT + meds + CBT = 70–80% improvement

CGRP Monoclonal Antibodies: New Frontier

What Are They?

CGRP = neuropeptide released in migraine. Causes vasodilation, inflammation, pain sensitization.

CGRP inhibitors = antibodies jo CGRP ko block karti hain.

FDA-Approved Drugs

Drug	Target	How	Dosing
Erenumab (Aimovig)	CGRP Receptor	Blocks receptor	Monthly injection
Fremanezumab (Ajovy)	CGRP Peptide	Monoclonal antibody	Monthly or quarterly
Galcanezumab (Emgality)	CGRP Peptide	Humanized antibody	Monthly
Eptinezumab (Vyepti)	CGRP Peptide	Humanized antibody	Quarterly IV

Efficacy in Vestibular Migraine

50–70% reduction in vestibular symptoms (better than traditional meds!)
Benefits within 4 weeks (faster)
Both headache AND spinning improve

Why It Works in VM

CGRP released in pain pathways AND vestibular nuclei
Blocking CGRP stabilizes neuronal hyperexcitability in balance centers
Direct effect on vestibular system (not just pain)

Advantages

Monthly/quarterly dosing (adherence good)
Injection/IV (bypasses stomach issues)
Well-tolerated, no cognitive side effects
No drug interactions

Disadvantages

Cost: $500–800/month (insurance approval needed)
Delayed onset: 4 weeks to benefit; 12 weeks for full effect
Not permanent: Symptoms return if stopped
Limited long-term data: Only 5 years available

Abortive (Rescue) Strategies: Active Attack

Anti-Nausea Medication

Principle: Pills fail (stomach motility down). Use suppositories/injections!

Med	Route	Why
Ondansetron (Zofran)	IV/IM/suppository	Highly effective, no sedation
Metoclopramide (Reglan)	IV/IM/sublingual	Aids stomach, helps nausea
Dimenhydrinate (Dramamine)	Suppository/IM	Antihistamine + anticholinergic

Vestibular Sedatives (Short-Term Only)

Med	Dose	Use
Dimenhydrinate	50–100 mg every 4–6 hrs	IM/IV/rectal, short-term
Meclizine	25–50 mg every 4–6 hrs	Oral if tolerated
Diazepam	2–5 mg every 6 hrs	ER only, severe attacks

Important: Don’t use long-term! Prevents brain compensation.

Early Intervention: Prodrome Window

Prodrome (warning):

Ear fullness
Mild spinning
Visual flashing
Neck stiffness

If meds taken during prodrome, attack may be aborted or reduced!

Optimal plan:

Prodrome sign → Take metoclopramide + anti-nausea (suppository)
Dark, quiet room + ice pack
If worse → ER for IV meds

Conclusion: Apna Balance Wapas Paao

Vestibular migraine = complex, multisensory syndrome. Different approach needed.

“Three-Legged Stool” of Management:

Lifestyle (sleep, stress, diet, trigger avoidance)
Preventative meds (beta-blockers, tricyclics, anticonvulsants, CCB, CGRP inhibitors)
VRT (brain retraining)
CBT (psychology support)

Expected outcome: 50–70% improvement in 3–6 months. Some get complete remission; others manage with lifestyle alone.

Key: Early diagnosis + targeted treatment + patience = back to steady, confident life!

HINDI VERSION

जो माइग्रेन घूमता है: क्यों सिरदर्द की दवाएं विफल होती हैं (और क्या वास्तव में काम करता है)

Vestibular Migraine: एक छिपी समस्या

लाखों लोगों के लिए, माइग्रेन सिर्फ एक गंभीर सिरदर्द नहीं है। यह एक हिंसक, घूमने वाला अनुभव है—vestibular migraine (VM)।

यह दूसरा सबसे आम कारण है आवर्ती vertigo का और लगभग 1% जनसंख्या को प्रभावित करता है। समस्या: मानक सिरदर्द की दवाएं घूमने को रोकने में बिल्कुल काम नहीं करती। डॉक्टर triptans देते हैं, रोगी 3 दिन तक घूमने में रहता है। निराशा!

यह लेख समझाता है: vestibular migraine क्या है, क्यों सामान्य माइग्रेन दवाएं विफल होती हैं, और क्या वास्तव में काम करता है।

Vestibular Migraine क्या होता है?

निदान मानदंड: दर्द के बाद संतुलन

Vestibular migraine = माइग्रेन जिसमें प्राथमिक समस्या संतुलन है, दर्द नहीं।

कठोर मानदंड:

कम से कम 5 एपिसोड vestibular लक्षणों का (मध्यम-गंभीर)
अवधि: 5 मिनट से 72 घंटे
माइग्रेन इतिहास: वर्तमान या पिछला माइग्रेन
माइग्रेन विशेषताएं: प्रकाश संवेदनशीलता, ध्वनि संवेदनशीलता, दृश्य aura, सिरदर्द (कभी-कभी अनुपस्थित), मतली

चार प्रकार का Vestibular Migraine

Type 1: Spontaneous Vertigo

बिल्कुल स्थिर बैठे भी घूमना महसूस हो रहा है
सबसे परेशान करने वाला क्योंकि कोई स्पष्ट ट्रिगर नहीं

Type 2: Positional Vertigo

बिस्तर से पलट जाना, सिर झुकाना → घूमना
BPPV का नकल कर सकता है (गलत निदान का जोखिम)
लेकिन BPPV से लंबी अवधि (मिनट-घंटे, सेकंड नहीं)

Type 3: Head-Motion Dizziness

चलने में “असंतुलित” महसूस
फर्श झुकता जैसा लगता है
सामान्य गतिविधि को रोकता है

Type 4: Visual Vertigo

व्यस्त सुपरमार्केट aisle, चलती कारें, action movies → चक्कर
दृश्य environment ट्रिगर करता है

घूमने का विज्ञान: क्या अलग होता है

Vestibular Migraine अलग क्यों होता है

सामान्य माइग्रेन:

Trigeminovascular system सक्रिय
CGRP release
दर्द पथ ट्रिगर
सिरदर्द

Vestibular माइग्रेन:

Vestibular nuclei (संतुलन केंद्र) सक्रिय
Cerebellum (समन्वय) सक्रिय
Vestibular cortex (स्थानिक अभिविन्यास) सक्रिय
दृश्य-vestibular पथ प्रभावित
Result: घूमना, असंतुलन, कभी-कभी दर्द

तीन सिद्धांत

सिद्धांत 1: Spreading Depression

न्यूरॉनल गतिविधि में कमी की wave vestibular cortex तक फैलती है
दिमाग संतुलन संकेत integration खो देता है
दिनों तक attack चलती है

सिद्धांत 2: Vasospasm (Blood Vessel Narrowing)

Internal auditory artery (आंतरिक कान supply) संकीर्ण हो जाती है
आंतरिक कान + ब्रेनस्टेम dysfunction
Blood flow restore हो जाता है तो ठीक हो जाता है

सिद्धांत 3: Channelopathy (Ion Channel Defect)

आनुवंशिक उत्परिवर्तन = neurons overexcitable
Family history संभव
Anticonvulsants काम करती हैं

क्यों सामान्य माइग्रेन दवाएं विफल होती हैं

कारण 1: समय Mismatch

Aura = 5–60 मिनट
VM = दिन-हफ्ते
Triptans = छोटे attacks के लिए डिज़ाइन किए गए
Long VM attacks में headache चली जाती है, spinning रहती है

कारण 2: Trials में Headache ही Measure करते हैं

Vertigo को विशेष रूप से परीक्षण नहीं करते
दवाएं “काम” head pain के लिए लेकिन vertigo पर proven नहीं

कारण 3: Nausea = No Absorption

गंभीर मतली में stomach काम नहीं करता
Pill निगल → stomach में बैठ जाता है → absorb नहीं होता
By time नausea ठीक, attack खत्म

समाधान: Suppositories, nasal sprays, injections use करते हैं

कारण 4: Misdiagnosis

BPPV assume: Epley maneuver दो (अस्थायी मदद, migraine address नहीं)
Menière’s assume: नमक restrict करो (काम नहीं करता, असली समस्या = माइग्रेन)

कारण 5: Over-Suppressant Use

Meclizine, diazepam = short-term मदद
लेकिन long-term use = brain compensation धीमा
रोगी medications पर निर्भर बन जाता है
बंद करने से लक्षण बदतर

4-Step Approach जो काम करती है

Step 1: Lifestyle—आधार

नींद

7–9 घंटे, same time daily
अनियमित नींद = माइग्रेन ट्रिगर

तनाव

Meditation, yoga, exercise
Stress hormones = माइग्रेन priming

हार्मोनल (महिलाएं)

Menstruation = माइग्रेन cluster
समाधान: Timed meds या continuous contraception

Migraine Trigger Foods (नीचे तालिका देखें)

Aged cheese, cured meats, MSG
Alcohol (red wine, beer)
Caffeine = विरोधाभास (short-term मदद, long-term बदतर)

Hydration + Meals

2–3 लीटर पानी daily
हर 3–4 घंटे खाएं (blood sugar drops माइग्रेन trigger करते हैं)

Environment

Flickering lights, busy visuals, loud noise
Barometric pressure, extreme heat/cold

Step 2: Preventative दवाएं

हर दिन लें migraine threshold बढ़ाने के लिए। 4–12 weeks में लाभ।

Beta-Blockers (First-Line)

Drug	Dose Range	अच्छा है	बुरा असर
Propranolol	120–240 mg/day	High BP + माइग्रेन	Fatigue, depression
Metoprolol	100–200 mg/day	Asthma रोगी	Propranolol जैसा
Timolol	20–30 mg/day	जल्दी adjustment	VM को बदतर कर सकता है

Efficacy: 40–60% reduction, 4–8 weeks

Tricyclic Antidepressants (Second-Line)

Drug	Dose	अच्छा है	बुरा असर
Amitriptyline	50–150 mg bedtime	Insomnia + माइग्रेन	Drowsy, dry mouth, weight gain
Nortriptyline	50–100 mg bedtime	कम sedating विकल्प	Dry mouth, weight gain

Efficacy: 40–60% reduction, 6–12 weeks
विशेष: Anxiety + PPPD (fear-based dizziness) के लिए बेहतरीन

Anticonvulsants (Third-Line)

Drug	Dose	अच्छा है	बुरा असर
Topiramate	75–200 mg/day	Weight loss + VM	“Topiramate fog” (slow thinking), numbness, kidney stones
Valproate	500–1500 mg/day	High efficacy	Hair loss, tremor, liver monitoring
Levetiracetam	500–1500 mg/day	कम interactions	Dizziness, mood changes

Efficacy: 40–70% reduction, 4–12 weeks
VM-विशिष्ट: Topiramate = EXCELLENT; ion channels को stabilize करता है + cerebellar function improve करता है

Calcium Channel Blockers (Fourth-Line)

Drug	Dose	अच्छा है	बुरा असर
Verapamil	240–480 mg/day	VM + high BP	Constipation, bradycardia
Flunarizine	5–10 mg/day	Highly effective VM	Drowsy, weight gain, depression

Efficacy: 40–60% reduction, 4–8 weeks
VM-विशिष्ट: Verapamil PARTICULARLY VM के लिए प्रभावी

Step 3: Vestibular Rehabilitation Therapy (VRT)

VRT = व्यायाम कार्यक्रम जो दिमाग को dizziness signals को ignore करना सिखाता है।

Visual Desensitization

Week 1–2: सरल moving patterns (scrolling lines)
Week 3–4: Complex patterns (checkerboards)
Week 5–6: Real-world visuals (busy crowds video)
Week 7+: वास्तविक environments (supermarket)

Key: हल्का dizziness (3–4/10), गंभीर vertigo नहीं। Brain habituation चाहिए।

Gaze Stabilization

Target fix करो, head move करो side-to-side
5 min daily

Balance Training

Unstable surfaces, tandem stance, single-leg
certified vestibular therapist के साथ सर्वश्रेष्ठ

VRT + Medication = BEST

60–80% improvement (vs. 40–50% with meds alone)

Step 4: Psychology—CBT for Health Anxiety

समस्या: Persistent dizziness = health anxiety, falling का डर, avoidance
Result: PPPD (attacks के बीच constant dizziness)

PPPD Cycle

VM attack (वास्तविक)
डर (वास्तविक)
Avoidance (व्यवहार)
Deconditioning (बदतर dizziness)
Constant anticipation (चिंता)

CBT समाधान

Loop recognize करो: Dizzy → Stroke? → Activity avoid → बदतर
Thoughts challenge करो: “MRI सामान्य है। डॉक्टर कहते हैं माइग्रेन। Heart rate ठीक है। Stroke नहीं है।”
Gradual re-engagement: Activities के लिए slow exposure
Acceptance: Dizziness संभव लेकिन manageable, dangerous नहीं

सर्वश्रेष्ठ परिणाम: VRT + meds + CBT = 70–80% improvement

vestibular migraine spinning treatment prevention

CGRP Monoclonal Antibodies: नया Frontier

वे क्या हैं?

CGRP = neuropeptide माइग्रेन में release होता है। Vasodilation, inflammation, दर्द sensitization करता है।

CGRP inhibitors = antibodies जो CGRP को block करते हैं।

FDA-Approved ड्रग्स

Drug	Target	कैसे	Dosing
Erenumab (Aimovig)	CGRP Receptor	Receptor को block	Monthly injection
Fremanezumab (Ajovy)	CGRP Peptide	Monoclonal antibody	Monthly या quarterly
Galcanezumab (Emgality)	CGRP Peptide	Humanized antibody	Monthly
Eptinezumab (Vyepti)	CGRP Peptide	Humanized antibody	Quarterly IV

Vestibular Migraine में Efficacy

50–70% reduction vestibular लक्षणों में (traditional meds से बेहतर!)
4 weeks में लाभ (faster)
Both headache AND spinning improve

VM में कैसे काम करता है

CGRP release होता है pain pathways में AND vestibular nuclei में
CGRP को block करना stabilize करता है neuronal hyperexcitability को balance centers में
Vestibular system पर direct असर (केवल pain नहीं)

फायदे

Monthly/quarterly dosing (अच्छी adherence)
Injection/IV (stomach issues bypass)
Well-tolerated, कोई cognitive side effects नहीं
कोई drug interactions नहीं

नुकसान

Cost: $500–800/month (insurance approval चाहिए)
Delayed onset: 4 weeks लाभ; 12 weeks full effect
Permanent नहीं: बंद करने से लक्षण return
Limited long-term data: केवल 5 साल

Abortive (Rescue) रणनीतियां: सक्रिय Attack

Anti-Nausea दवा

सिद्धांत: Pills fail (stomach motility down)। Suppositories/injections use करो!

Med	Route	क्यों
Ondansetron (Zofran)	IV/IM/suppository	Highly effective, कोई sedation नहीं
Metoclopramide (Reglan)	IV/IM/sublingual	Stomach मदद, nausea में मदद
Dimenhydrinate (Dramamine)	Suppository/IM	Antihistamine + anticholinergic

Vestibular Sedatives (केवल Short-Term)

Med	Dose	Use
Dimenhydrinate	50–100 mg हर 4–6 hr	IM/IV/rectal, short-term
Meclizine	25–50 mg हर 4–6 hr	Oral if tolerated
Diazepam	2–5 mg हर 6 hr	ER only, गंभीर attacks

महत्वपूर्ण: Long-term न करो! Brain compensation को रोकता है।

Early Intervention: Prodrome Window

Prodrome (चेतावनी):

Ear fullness
Mild spinning
दृश्य flashing
Neck stiffness

Prodrome के दौरान meds लिए गए तो attack abort या कम हो सकता है!

Optimal plan:

Prodrome sign → Metoclopramide + anti-nausea लो (suppository)
Dark, quiet room + ice pack
Worse होने पर → ER for IV meds

निष्कर्ष: Apna Balance Wapas Paao

Vestibular migraine = complex, multisensory syndrome। अलग approach चाहिए।

“Three-Legged Stool” of Management:

Lifestyle (नींद, तनाव, आहार, trigger avoidance)
Preventative meds (beta-blockers, tricyclics, anticonvulsants, CCB, CGRP inhibitors)
VRT (brain retraining)
CBT (psychology support)

अपेक्षित परिणाम: 3–6 महीनों में 50–70% सुधार। कुछ को complete remission; अन्य lifestyle से ही manage करते हैं।

कुंजी: शीघ्र निदान + targeted treatment + धैर्य = steady, confident life वापसी!

MIGRAINE TRIGGER FOODS REFERENCE

(Downloadable Table)

🚫 Foods to Avoid or Limit for Vestibular Migraine Prevention

Category	High-Risk Foods	Chemical	Avoid/Limit	Safer Alternatives
CHEESES	Aged/Hard Cheeses	Tyramine	Cheddar, Blue, Feta, Swiss, Parmesan, Aged Mozzarella	Fresh mozzarella, Cream cheese, Ricotta, Cottage cheese
CURED MEATS	Processed Meats	Nitrites/Nitrates	Salami, Pepperoni, Bacon, Ham, Hot dogs, Deli meats, Sausages, Prosciutto	Fresh chicken breast, Turkey, Lean beef, Fish
FERMENTED FOODS	Pickled/Fermented	Tyramine	Sauerkraut, Kimchi, Miso, Tempeh, Soy sauce, Tamari, Marmite	Fresh vegetables, Homemade salads
ALCOHOL	Alcoholic Beverages	Tyramine/Histamine	Red wine, Beer, Aged spirits, Sherry, Vermouth	White wine (occasional), Vodka (occasional, use cautiously)
CHOCOLATE	Dark Chocolate, Cocoa	Phenylethylamine, Caffeine	Dark chocolate (>70%), Cocoa powder, Hot chocolate	Milk chocolate (occasional), Carob
CAFFEINE	Coffee, Tea, Energy Drinks	Caffeine	High-caffeine coffee (>100mg/serving), Energy drinks, Strong tea	Decaf coffee (<25mg), Herbal tea, Water
ARTIFICIAL SWEETENERS	Artificial Additives	Aspartame, Saccharine	Diet sodas, Sugar-free desserts with aspartame	Stevia, Honey, Sugar (in moderation)
FOOD ADDITIVES	MSG, Dyes	Monosodium Glutamate, Tartrazine, Food colorings	Asian restaurant food (high MSG), Processed foods, Yellow/Red #5/#40 dyed foods	Home-cooked meals, Natural foods, Organic products
CITRUS	Acidic Fruits	Citric acid (in some individuals)	Excess orange juice, Lemon, Lime	Apples, Pears, Berries, Bananas, Grapes
CURED/SMOKED FISH	Smoked Salmon, Sardines	Histamine, Tyramine	Smoked salmon, Anchovies, Sardines, Herring	Fresh salmon, White fish, Tuna (fresh, not canned)
SOY PRODUCTS	Fermented Soy	Tyramine	Soy sauce, Miso, Tempeh	Fresh tofu (occasional), Edamame (fresh)
NUTS	Certain Nuts	Tyramine, Phenylethylamine	Peanuts, Peanut butter, Almonds (large quantities)	Sunflower seeds, Macadamia nuts (small amounts)
YEAST	Yeast-Containing Foods	Tyramine	Bread, Donuts, Yeast extracts, Nutritional yeast	Fresh bread, Yeast-free alternatives
DAIRY	Full-Fat Dairy (in some)	Fat, Tyramine	Full-fat milk, Whole milk yogurt	Low-fat or non-fat versions, Plant-based milk alternatives

✅ SAFE, MIGRAINE-FRIENDLY FOODS

Proteins:

Chicken breast (fresh)
Turkey (fresh)
Fish (fresh: salmon, white fish, tuna—fresh, not canned/smoked)
Eggs (preparation methods vary; some tolerate better than others)
Lean beef (fresh)
Plant-based: Lentils, chickpeas, fresh tofu

Grains:

White rice, Brown rice
Oats
Whole wheat bread (fresh, yeast-free versions if sensitive)
Pasta

Fruits:

Apples, Pears
Berries (fresh)
Bananas
Grapes, Watermelon
Peaches, Plums

Vegetables:

Leafy greens (spinach, lettuce)
Broccoli, Cauliflower
Carrots, Bell peppers
Zucchini, Green beans
Potatoes

Dairy (if tolerated):

Low-fat or non-fat milk
Low-fat yogurt (plain, no additives)
Fresh mozzarella, Ricotta, Cottage cheese

Fats/Oils:

Olive oil
Coconut oil
Avocado (moderate)

Beverages:

Water (primary)
Herbal tea (chamomile, peppermint—caffeine-free)
Decaffeinated coffee (limit)
Coconut water

📋 CAFFEINE CONTENT GUIDE (Keep ≤100mg/day for VM)

Beverage	Serving	Caffeine Content
Coffee (brewed, regular)	8 oz	80–100 mg
Coffee (brewed, strong)	8 oz	120–180 mg
Espresso	1 shot (1 oz)	63–75 mg
Tea (black, brewed)	8 oz	25–50 mg
Tea (green, brewed)	8 oz	25–35 mg
Tea (herbal, caffeine-free)	8 oz	0 mg ✅
Chocolate (dark, 70%+)	1 oz	12–26 mg
Soft drink (cola)	12 oz	30–40 mg
Energy drink	8–12 oz	80–300 mg
Coffee (decaffeinated)	8 oz	2–5 mg ✅

🎯 PRACTICAL TIPS FOR TRIGGER MANAGEMENT

Keep a Food Diary for 2–4 weeks:

Note foods eaten each day
Record migraine attacks (date, time, severity)
Identify patterns

Elimination Phase (4 weeks):

Avoid all high-risk foods simultaneously
Track if migraine frequency decreases

Reintroduction Phase:

Reintroduce one food every 3–5 days
Observe if attack occurs
Identify personal triggers (not everyone reacts the same way)

Create a Personal Trigger List:

Document which foods trigger your attacks
Share with family and healthcare providers

Read Labels Carefully:

Look for MSG, artificial sweeteners, food dyes
Check for hidden tyramine sources in processed foods

Restaurant Navigation:

Ask about preparation methods
Request no MSG, no added salt
Specify fresh (not aged) cheese

MIGRAINE TRIGGERS PERSONAL CHECKLIST

(Personal Tracking Tool)

📊 MIGRAINE TRIGGER IDENTIFICATION & TRACKING

Use this checklist to identify YOUR personal triggers over 4 weeks. Not all triggers affect all people—this helps you find YOUR specific pattern.

WEEK: | TRACKING PERIOD: to __

DAILY TRACKING SHEET

Day/Date: ____

☑️ Sleep & Circadian Rhythm

☐ Slept < 6 hours last night
☐ Slept > 10 hours last night
☐ Woke at different time than usual
☐ Took nap today (unusual)
☐ Jet lag or shift work today
Notes: _____________________

☑️ Food & Drink

☐ Aged cheese consumed
☐ Cured/processed meat consumed
☐ Alcohol consumed (type: ) (amount: drinks)
☐ High-caffeine beverage (coffee, strong tea, energy drink)
☐ MSG-containing food (Asian food, processed food, restaurant meal)
☐ Artificial sweetener consumed (aspartame, saccharine)
☐ Skipped meals or ate late
☐ Dehydrated (< 2 liters water consumed)
Notes: _____________________

☑️ Stress & Emotions

☐ High stress day (work, family, finances)
☐ Major life event (positive or negative)
☐ Anxiety/panic symptoms present
☐ Depression/low mood present
☐ Arguments or conflicts
☐ Public speaking or performance
Stress level (1–10): _
Notes: _____________________

☑️ Hormonal (Women/Menstruating Individuals)

☐ Menstruation started today (day _ of cycle)
☐ Period expected within 3 days
☐ Premenstrual symptoms (bloating, mood change)
☐ Hormonal contraceptive taken today
☐ Missed contraceptive dose
Notes: _____________________

☑️ Environmental Factors

☐ Fluorescent lights present (office, store)
☐ Flickering lights
☐ High-contrast or striped patterns viewed
☐ Busy/crowded environment
☐ Loud sounds or noise exposure
☐ Strong perfumes or chemical smells
☐ Weather change (temperature, humidity, barometric pressure shift)
☐ Screen time > 3 hours
Notes: _____________________

☑️ Physical Activity & Exercise

☐ Intense exercise performed
☐ No exercise (sedentary day)
☐ Unusual physical exertion
☐ Neck/shoulder tension present
Type of activity: _____________
Duration: ____
Notes: _____________________

☑️ Medications & Supplements

☐ New medication started
☐ Medication dose changed
☐ Skipped usual medication
☐ Supplement taken (which: ______)
Notes: _____________________

☑️ Illness & Health

☐ Cold or flu symptoms
☐ Fever
☐ Allergies present (nasal congestion, itching)
☐ Sinus issues (congestion, pressure)
Notes: _____________________

☑️ MIGRAINE OUTCOME TODAY

☐ No migraine ✅
☐ Mild dizziness (1–3/10 intensity) – no vertigo
☐ Moderate dizziness (4–6/10) – some vertigo
☐ Severe migraine (7–10/10) – disabling vertigo
☐ Attack characteristics:
Duration: __ hours
Type: ☐ Spontaneous spinning ☐ Positional ☐ Head-motion dizziness ☐ Visual vertigo
Associated headache: ☐ Yes ☐ No
Nausea/vomiting: ☐ Yes ☐ No
Hearing loss: ☐ Yes ☐ No
Visual symptoms (flashing, aura): ☐ Yes ☐ No
Time of onset: __
Time of resolution: __
Medications taken: __________________
What helped: __________________
What made it worse: __________________

WEEKLY SUMMARY (End of Each Week)

Week #: _

Trigger Category	Days Present (0–7)	Confidence Level (Low/Medium/High)	Personal Notes
Sleep issues	_ days	☐ Low ☐ Med ☐ High	*____*
Food triggers	_ days	☐ Low ☐ Med ☐ High	*____*
Stress	_ days	☐ Low ☐ Med ☐ High	*____*
Hormonal	_ days	☐ Low ☐ Med ☐ High	*____*
Environmental	_ days	☐ Low ☐ Med ☐ High	*____*
Exercise	_ days	☐ Low ☐ Med ☐ High	*____*
Medications	_ days	☐ Low ☐ Med ☐ High	*____*
Illness/Allergies	_ days	☐ Low ☐ Med ☐ High	*____*

Migraine frequency this week: _ attacks
Average severity: _ /10
Total hours disabled: __

4-WEEK PATTERN ANALYSIS

After 4 weeks of tracking, review your data:

Most Common Triggers (Rank by Frequency)

____ (appeared _ times in 4 weeks)
____ (appeared _ times in 4 weeks)
____ (appeared _ times in 4 weeks)

Strongest Correlations

(Which triggers ALWAYS preceded attacks?)

____
____

Safe Days (No Migraine)

What did you do differently on days with NO migraine?

____
____
____

Personal Trigger Severity Ranking

(Rate your top 3 triggers from WORST to LEAST WORST)

____ – AVOID COMPLETELY
____ – LIMIT/REDUCE
____ – MONITOR

ACTION PLAN (Based on Your Tracking)

Primary Triggers to Eliminate:

__________________
__________________
__________________

Secondary Triggers to Limit:

__________________
__________________

Lifestyle Changes to Implement:

☐ Sleep schedule: bedtime _ wake time _
☐ Stress management: _ minutes daily (activity: ______)
☐ Hydration goal: __ liters per day
☐ Caffeine limit: ≤ 100 mg/day (__ servings max)
☐ Exercise routine: _ minutes, _ days/week
☐ Other: __________________

SUBMIT TO PRIME ENT CENTER HARDOI

Print or photograph this completed 4-week tracking sheet and bring it to your appointment. Dr. Prateek Porwal and Dr. Harshita Singh will review your personal trigger patterns to create a targeted prevention plan.

This takes your treatment from “generic migraine management” to “YOUR migraine management.”

FAQs

ENGLISH FAQs (20 Questions)

1. What is the main difference between regular migraine and vestibular migraine?

Answer: Regular migraine is pain-centered; the primary symptom is headache. Vestibular migraine is balance-centered; the primary symptom is vertigo or dizziness. Notably, up to 30% of vestibular migraine patients have NO headache at all—only spinning. This distinction is crucial because treatments differ: pain medications are ineffective for balance-centered attacks, requiring instead preventative medications and vestibular rehabilitation.

2. Why don’t triptans work for vestibular migraine?

Answer: Triptans are designed to abort short-duration attacks (pain resolves within 2–4 hours). Vestibular migraine symptoms last hours to days. While a triptan may reduce headache, the vertigo persists because: (1) the medication may not absorb properly due to nausea, (2) the vestibular nucleus requires different neurochemical intervention than pain pathways, and (3) triptans haven’t been tested specifically for vertigo outcomes in clinical trials.

3. What is CGRP and how do CGRP inhibitors help vestibular migraine?

Answer: CGRP (Calcitonin Gene-Related Peptide) is a neuropeptide released during migraine attacks. It causes blood vessel dilation, inflammation, and sensitization of pain pathways—but also affects vestibular nuclei in the brainstem. CGRP inhibitors (monoclonal antibodies) block this peptide, reducing both headache AND vestibular dysfunction. Studies show 50–70% symptom reduction in vestibular migraine patients, superior to traditional prophylactic medications.

4. How long does it take for preventative medications to work in vestibular migraine?

Answer: Most preventative medications take 4–12 weeks to show benefit. Beta-blockers and calcium channel blockers typically show benefit within 4–8 weeks. Tricyclic antidepressants and anticonvulsants may take 6–12 weeks. CGRP inhibitors show benefit within 4 weeks. Importantly, these medications do not work by aborting individual attacks; they raise the overall “seizure threshold” of the brain, making it less reactive to triggers.

5. Is topiramate (Topamax) specifically beneficial for vestibular migraine?

Answer: Yes. Topiramate is particularly effective for vestibular migraine because it: (1) stabilizes ion channels (beneficial for the “channelopathy” theory), (2) reduces neuronal hyperexcitability specifically in vestibular nuclei, (3) may improve cerebellar function, and (4) can cause weight loss (beneficial if weight is a contributing factor). Typical dose range is 75–200 mg/day. The main drawback is cognitive side effects (“topiramate fog”), which improve if the dose is increased slowly.

6. What is the role of vestibular rehabilitation therapy (VRT) in vestibular migraine?

Answer: VRT retrains the brain to ignore or “habituate” to the incorrect balance signals it receives during a migraine. Through graduated exposure to dizziness-inducing stimuli (starting mild and progressing), the brain learns to downweight corrupted vestibular input and rely more on vision and proprioception. Patients on VRT combined with preventative medication show 60–80% improvement vs. 40–50% with medication alone. VRT should be delivered by a certified vestibular rehabilitation specialist.

7. What is PPPD and how does it relate to vestibular migraine?

Answer: PPPD (Persistent Postural-Perceptual Dizziness) is a condition where patients feel constantly unsteady or dizzy between migraine attacks due to health anxiety and catastrophizing. It develops when the original vestibular migraine (legitimate neurological cause) triggers psychological fear (“Will I ever recover?” “Am I having a stroke?”), leading to avoidance and deconditioning, which perpetuates dizziness. Cognitive Behavioral Therapy (CBT) combined with VRT is essential for breaking this cycle.

8. Can vestibular migraine be cured?

Answer: There is no permanent cure, but most patients achieve 50–70% reduction in symptom frequency and severity with comprehensive management (lifestyle optimization + preventative medication + VRT + psychological support). Some achieve complete remission and require no medication. Others maintain low-frequency attacks that are manageable with lifestyle modification alone. The goal is functional improvement, not complete elimination.

9. Are there specific foods that trigger vestibular migraine?

Answer: Yes. Common triggers include aged cheeses (tyramine), cured meats (nitrites), MSG, artificial sweeteners, alcohol (especially red wine and beer), and chocolate. However, triggers are highly individual—not all people with VM are sensitive to the same foods. Keeping a 4-week food and migraine diary (see Downloadable Migraine Triggers Checklist) helps identify YOUR personal triggers, which is more valuable than following generic “migraine diet” rules.

10. How does stress trigger vestibular migraine and what can be done about it?

Answer: Stress activates the sympathetic nervous system, releasing cortisol and adrenaline. These hormones prime the nervous system for migraine by destabilizing neurotransmitter balance. Stress reduction techniques (meditation, yoga, regular exercise, cognitive behavioral therapy) lower baseline nervous system hyperexcitability. Even 10–15 minutes of daily stress management can significantly reduce attack frequency. The key is consistency; irregular stress management is less effective than daily practice.

11. Why do some vestibular migraine patients have hearing loss during attacks?

Answer: The internal auditory artery (IAA) supplies both the inner ear (cochlea) and portions of the brainstem involved in balance. During a migraine, vasospasm of this artery can cause temporary sensorineural hearing loss alongside vertigo. This is particularly relevant because sudden hearing loss + vertigo may suggest AICA (Anterior Inferior Cerebellar Artery) stroke, requiring urgent differentiation from vestibular migraine through medical evaluation and possible imaging.

12. What is the difference between abortive and preventative treatment in vestibular migraine?

Answer: Abortive medication is taken during an active attack to stop or reduce symptoms. Preventative medication is taken daily, regardless of whether an attack is occurring, to reduce overall attack frequency and severity. In vestibular migraine, prevention is more effective than abortion because: (1) absorption issues due to nausea make abortive pills unreliable, (2) vestibular symptoms are harder to abort than headache, and (3) preventative medications directly stabilize the hyperexcitable nervous system.

13. Can caffeine be beneficial for vestibular migraine?

Answer: Caffeine has a paradoxical effect in VM. Acute caffeine use (1 cup of coffee) at the start of an attack may temporarily reduce headache through vasoconstriction. However, chronic daily caffeine use actually increases baseline migraine frequency because it chronically overstimulates the nervous system. For VM patients, the recommendation is to limit caffeine to ≤100 mg/day (roughly one cup of weak tea) and maintain consistent daily intake to avoid withdrawal-induced rebound migraines.

14. How do hormonal fluctuations trigger vestibular migraine in women?

Answer: Estrogen fluctuations during the menstrual cycle destabilize serotonin and other neurotransmitter systems. Many women with VM report attack clusters 2 days before to 3 days after menstruation begins. Management strategies include: (1) timed preventative medication starting 2 days before expected menstruation, (2) continuous hormonal contraception (to avoid monthly fluctuations), or (3) consultation with a gynecologist to optimize hormone timing. Some women benefit from steady-dose hormone replacement rather than fluctuating cycles.

15. What should patients with vestibular migraine do if they cannot tolerate preventative medications?

Answer: If medication side effects are intolerable, the first step is dose optimization—starting with lower doses and increasing gradually often improves tolerability. If medication truly cannot be tolerated, alternative approaches include: (1) intensive lifestyle modification (strict sleep, stress management, trigger diet), (2) aggressive vestibular rehabilitation therapy, (3) cognitive behavioral therapy for anxiety/PPPD, and (4) discussion with your neurologist about trialing a different medication class. CGRP inhibitors, while expensive, have fewer side effects than many traditional preventatives.

16. Is there a connection between migraine with aura and vestibular migraine?

Answer: Yes. Migraine with aura and vestibular migraine likely share the same underlying mechanism: “spreading depression” of neuronal activity. In migraine with aura, spreading depression occurs in the visual cortex (causing visual symptoms). In VM, it occurs in the vestibular cortex (causing balance symptoms). Some patients experience both aura and vestibular symptoms in the same attack. Migraine with aura is a risk factor for stroke, which is why careful neuroimaging is sometimes warranted in VM patients.

17. Can vestibular migraine be diagnosed with imaging (MRI or CT)?

Answer: Imaging is typically normal in vestibular migraine. However, MRI may be warranted to rule out other causes of vertigo (stroke, tumors, multiple sclerosis) if the clinical presentation is atypical or if red flag symptoms are present. Diagnosis of VM is primarily clinical, based on strict diagnostic criteria (5+ attacks, 5 minutes to 72 hours duration, migraine history, and migrainous features). Imaging serves to rule out alternatives, not to confirm VM.

18. How should a vestibular migraine attack be managed if the patient is vomiting and cannot take oral medication?

Answer: Severe nausea and vomiting impair stomach function, making oral medication ineffective. Alternatives include: (1) anti-nausea suppositories (ondansetron, dimenhydrinate), (2) nasal sprays (some formulations of triptans, anti-nausea medications), (3) IV or IM medications (administered in an emergency department), or (4) subcutaneous injections (some triptans, other rescue medications). Many patients benefit from taking metoclopramide (which improves stomach emptying) with anti-nausea medication at the first sign of prodromal symptoms, before severe vomiting develops.

19. What is the “prodrome” in vestibular migraine and why is early intervention important?

Answer: The prodrome is a warning period before a full migraine attack, lasting minutes to hours. Symptoms include ear fullness, mild dizziness, visual flickering, or neck stiffness. Early intervention during the prodrome (before severe symptoms or vomiting develops) can significantly reduce attack severity or abort it entirely. This is why maintaining a “rescue medication kit” and recognizing your personal prodromal symptoms is valuable.

20. How can patients differentiate between vestibular migraine and other causes of recurrent vertigo (BPPV, Menière’s disease)?

Answer: Key differentiators include: (1) Duration—BPPV: seconds to minutes; VM: minutes to days; Menière’s: minutes to hours; (2) Triggers—BPPV: position-dependent; VM: spontaneous or migraine triggers; Menière’s: unpredictable; (3) Hearing loss—BPPV: no; VM: sometimes; Menière’s: yes, often progressive; (4) Migraine history—VM: always present (current or past); (5) Response to treatments—BPPV: Epley maneuver curative; VM: needs preventative medication; Menière’s: salt restriction, diuretics. A vestibular specialist (ENT or neurologist) can differentiate these conditions through clinical examination and diagnostic testing.

HINGLISH FAQs (20 Questions)

1. Regular migraine aur vestibular migraine mein main difference?

Answer: Regular = pain-centered (headache). Vestibular = balance-centered (vertigo/dizziness). Up to 30% VM patients ko headache hi nahi hota—sirf spinning. Different treatment: pain meds fail, preventative + VRT chahiye.

2. Triptans vestibular migraine ke liye kyun fail karti hain?

Answer: (1) Short duration ke liye design (2–4 hrs pain). VM = hours-days. (2) Nausea se absorption fail. (3) Headache to theek karti hain lekin vertigo nahi. (4) Triptans haven’t been tested for vertigo specifically.

3. CGRP kya hai aur CGRP inhibitors vestibular migraine mein kaise help karti hain?

Answer: CGRP = neuropeptide migraine mein release hota hai. Blood vessels dilate, inflammation, pain sensitization—lekin vestibular nuclei bhi affected. Inhibitors = antibodies jo CGRP block karti hain. 50–70% reduction in VM symptoms.

4. Preventative medications kitne time mein work karti hain?

Answer: 4–12 weeks. Beta-blockers/CCB = 4–8 weeks. Tricyclics/anticonvulsants = 6–12 weeks. CGRP inhibitors = 4 weeks. Daily lena padta hai; individual attacks ko nahi roktein, overall threshold badh jaati hai.

5. Topiramate (Topamax) vestibular migraine ke liye particularly beneficial?

Answer: Haan. Ion channels stabilize, neuronal hyperexcitability reduce, cerebellar function improve, weight loss possible. 75–200 mg/day. Downside: cognitive fog (improves slow-dose increase mein).

6. VRT vestibular migraine mein kya role?

Answer: Brain ko train karti hai dizziness signals ko ignore karne. Graduated exposure se habituation. Medication + VRT = 60–80% improvement (vs. 40–50% meds alone). Certified therapist chahiye.

7. PPPD kya hai aur vestibular migraine se relation?

Answer: Persistent PosturalPerceptual Dizziness = constant dizziness between attacks due to health anxiety. Original migraine → fear → avoidance → deconditioning → perpetuated dizziness. Solution: VRT + CBT.

8. Vestibular migraine cure ho sakta hai?

Answer: Cure nahi, lekin 50–70% improvement 3–6 months mein. Some complete remission; others low-frequency + manageable. Goal = functional improvement.

9. Specific foods vestibular migraine trigger karti hain?

Answer: Aged cheese (tyramine), cured meats (nitrites), MSG, artificial sweeteners, alcohol, chocolate. Lekin individual—not everyone reacts same. 4-week food diary = YOUR triggers find karti hai.

10. Stress vestibular migraine ko trigger kaise karti hai?

Answer: Sympathetic nervous system activate → cortisol, adrenaline → neurotransmitter imbalance. Meditation, yoga, exercise 10–15 min daily = stress hormones reduce. Consistent practice key.

11. VM mein hearing loss attacks ke time kyun?

Answer: Internal auditory artery (inner ear + brainstem supply) vasospasm hote hi temporary hearing loss + vertigo. Important: sudden hearing loss + vertigo = possible stroke, urgent evaluation chahiye.

12. Abortive aur preventative treatment difference?

Answer: Abortive = during attack (relieves active symptoms). Preventative = daily (reduces frequency/severity). VM mein prevention better kyunke absorption issues + vestibular symptoms harder to abort.

13. Caffeine vestibular migraine ke liye beneficial hai?

Answer: Paradox. Acute = short-term headache relief possible. Chronic = increases migraine frequency. Recommendation: ≤100 mg/day, consistent intake (avoid withdrawal).

14. Women mein hormonal fluctuations vestibular migraine trigger kaise karti hain?

Answer: Menstrual cycle mein estrogen changes → serotonin instability → attacks cluster menstruation around. Solutions: timed meds, continuous contraception, gynecologist consultation.

15. Agar preventative meds tolerate nahi kar sakte?

Answer: (1) Slow dose increase try karo. (2) Different medication class try. (3) Lifestyle + VRT + CBT aggressive. (4) CGRP inhibitors (fewer side effects, expensive).

16. Migraine with aura aur vestibular migraine connection?

Answer: Same mechanism—spreading depression. Aura = visual cortex. VM = vestibular cortex. Some patients dono mein experience both. Aura = stroke risk, so imaging sometimes warranted.

17. Imaging (MRI/CT) se vestibular migraine diagnose ho sakta hai?

Answer: Normal imaging usually. Lekin MRI stroke, tumors, MS rule out karne ke liye use hoti hai (red flags mein). Diagnosis = clinical, based on strict criteria.

18. Agar vomiting aa raha hai aur oral medication nahi le sakte?

Answer: Suppositories, nasal sprays, IV/IM medications, subcutaneous injections use karte hain. Metoclopramide + anti-nausea at prodrome start (before severe vomiting).

19. “Prodrome” kya hai aur early intervention important kyun?

Answer: Warning period minutes-hours pehle = ear fullness, mild dizziness, visual flickering. Early meds = attack abort or reduce possible. Prodromal symptoms recognize karti ho toh rescue kit ready rakhो.

20. BPPV, Menière’s, Vestibular Migraine mein difference?

Answer: Duration: BPPV = seconds-minutes, VM = minutes-days, Menière’s = minutes-hours. Triggers: BPPV = position, VM = migraine triggers, Menière’s = unpredictable. Hearing: BPPV = no, VM = sometimes, Menière’s = yes. Migraine history: VM = always. Treatment: BPPV = Epley, VM = preventative meds, Menière’s = salt restriction.

HINDI FAQs (20 Questions)

1. Regular migraine और vestibular migraine में मुख्य अंतर?

Answer: Regular = pain-centered (सिरदर्द)। Vestibular = balance-centered (vertigo/चक्कर)। 30% VM रोगियों को सिरदर्द ही नहीं—सिर्फ घूमना। अलग उपचार: pain meds fail, preventative + VRT चाहिए।

2. Triptans vestibular migraine के लिए क्यों विफल होती हैं?

Answer: (1) Short duration के लिए design (2–4 hrs)। VM = दिन-हफ्ते। (2) Nausea से absorption fail। (3) Headache ठीक करती हैं लेकिन vertigo नहीं। (4) Vertigo के लिए specifically परीक्षण नहीं।

3. CGRP क्या है और CGRP inhibitors vestibular migraine में कैसे मदद करती हैं?

Answer: CGRP = neuropeptide माइग्रेन में release होता है। Blood vessels dilate, inflammation, दर्द sensitization—लेकिन vestibular nuclei भी affected। Inhibitors = antibodies जो CGRP को block करती हैं। VM लक्षणों में 50–70% कमी।

4. Preventative medications कितने समय में काम करती हैं?

Answer: 4–12 सप्ताह। Beta-blockers/CCB = 4–8 सप्ताह। Tricyclics/anticonvulsants = 6–12 सप्ताह। CGRP inhibitors = 4 सप्ताह। Daily लेना पड़ता है; individual attacks को नहीं रोकती, overall threshold बढ़ जाती है।

5. Topiramate (Topamax) vestibular migraine के लिए विशेष रूप से लाभकारी?

Answer: हाँ। Ion channels को stabilize करता है, neuronal hyperexcitability कम करता है, cerebellar function improve करता है, weight loss संभव है। 75–200 mg/day। कमी: cognitive fog (धीरे-धीरे dose बढ़ाने से improves)।

6. VRT vestibular migraine में क्या भूमिका है?

Answer: दिमाग को dizziness signals को ignore करना सिखाता है। Graduated exposure से habituation। Medication + VRT = 60–80% improvement (vs. 40–50% meds alone)। Certified therapist चाहिए।

7. PPPD क्या है और vestibular migraine से संबंध?

Answer: Persistent PosturalPerceptual Dizziness = attacks के बीच constant dizziness health anxiety के कारण। Original migraine → डर → avoidance → deconditioning → perpetuated dizziness। समाधान: VRT + CBT।

8. Vestibular migraine ठीक हो सकता है?

Answer: ठीक नहीं, लेकिन 50–70% सुधार 3–6 महीनों में। कुछ को complete remission; अन्य low-frequency + manageable। लक्ष्य = functional improvement।

9. विशिष्ट खाद्य पदार्थ vestibular migraine को ट्रिगर करते हैं?

Answer: Aged cheese (tyramine), cured meats (nitrites), MSG, artificial sweeteners, alcohol, chocolate। लेकिन individual—हर किसी को same react नहीं करते। 4-week food diary = YOUR triggers पता चलते हैं।

10. Stress vestibular migraine को कैसे ट्रिगर करता है?

Answer: Sympathetic nervous system activate → cortisol, adrenaline → neurotransmitter imbalance। Meditation, yoga, exercise 10–15 min daily = stress hormones कम। Consistent practice key।

11. VM में hearing loss attacks के समय क्यों?

Answer: Internal auditory artery (inner ear + brainstem supply) vasospasm हो तो temporary hearing loss + vertigo। महत्वपूर्ण: sudden hearing loss + vertigo = संभावित stroke, urgent evaluation चाहिए।

12. Abortive और preventative treatment में अंतर?

Answer: Abortive = during attack (active symptoms राहत)। Preventative = daily (frequency/severity कम)। VM में prevention बेहतर है क्योंकि absorption issues + vestibular symptoms abort करना कठिन।

13. Caffeine vestibular migraine के लिए लाभकारी है?

Answer: विरोधाभास। Acute = short-term headache relief संभव। Chronic = migraine frequency बढ़ता है। सिफारिश: ≤100 mg/day, consistent intake (withdrawal से बचें)।

14. महिलाओं में हार्मोनल fluctuations vestibular migraine को कैसे ट्रिगर करते हैं?

Answer: Menstrual cycle में estrogen changes → serotonin instability → attacks menstruation के आसपास cluster। समाधान: timed meds, continuous contraception, gynecologist consultation।

15. अगर preventative meds tolerate नहीं कर सकते?

Answer: (1) Slow dose increase try करो। (2) Different medication class try करो। (3) Lifestyle + VRT + CBT aggressive। (4) CGRP inhibitors (कम side effects, expensive)।

16. Migraine with aura और vestibular migraine का संबंध?

Answer: Same mechanism—spreading depression। Aura = visual cortex। VM = vestibular cortex। कुछ रोगियों को दोनों एक ही attack में। Aura = stroke risk, तो कभी-कभी imaging warranted।

17. Imaging (MRI/CT) से vestibular migraine diagnose हो सकता है?

Answer: Normal imaging usually। लेकिन MRI stroke, tumors, MS rule out करने के लिए use होती है (red flags में)। Diagnosis = clinical, strict criteria पर based।

18. अगर vomiting आ रही है और oral medication नहीं ले सकते?

Answer: Suppositories, nasal sprays, IV/IM medications, subcutaneous injections use करते हैं। Metoclopramide + anti-nausea prodrome शुरुआत में (severe vomiting से पहले)।

19. “Prodrome” क्या है और early intervention महत्वपूर्ण क्यों?

Answer: Warning period minutes-hours पहले = ear fullness, mild dizziness, visual flickering। Early meds = attack abort या reduce संभव। Prodromal symptoms पहचानो तो rescue kit ready रखो।

20. BPPV, Menière’s, Vestibular Migraine में अंतर?

Answer: Duration: BPPV = सेकंड-मिनट, VM = मिनट-दिन, Menière’s = मिनट-घंटे। Triggers: BPPV = position, VM = migraine triggers, Menière’s = unpredictable। Hearing: BPPV = नहीं, VM = कभी-कभी, Menière’s = हाँ। Migraine history: VM = always। Treatment: BPPV = Epley, VM = preventative meds, Menière’s = salt restriction।

The Migraine That Spins: Why Headache Medications Fail (And What Actually Works) | Dr Prateek Porwal

ENGLISH VERSION

The Migraine That Spins: Why Headache Medications Fail (And What Actually Works)

Understanding Vestibular Migraine: A Hidden Epidemic

What is Vestibular Migraine?

Diagnostic Criteria: Moving Beyond the Headache-Centric Definition

The Diversity of Vestibular Migraine Presentations

The Science of the Spin: Why Vestibular Migraine Feels Different

The Neurobiological Basis: Beyond Simple Pain

Three Leading Theories of Vestibular Migraine Pathophysiology

Theory 1: Cortical Spreading Depression

Theory 2: Vasospasm of the Internal Auditory Artery

Theory 3: Channelopathy (Ion Channel Dysfunction)

The Signal-to-Noise Problem

Why Standard Headache Medications Often Fail in Vestibular Migraine

Reason 1: The Timing Mismatch

Reason 2: Lack of Specific Vestibular Evidence in Clinical Trials

Reason 3: The Absorption Problem

Reason 4: Misdiagnosis Leading to Wrong Treatment

Reason 5: Over-Reliance on Vestibular Suppressants

The 4-Step Approach That Actually Works

Step 1: The Foundation—Lifestyle Modification and Trigger Management

Sleep Hygiene

Stress Management

Hormonal Triggers in Menstruating Individuals

Migraine Trigger Foods (See Downloadable Table Below)

Hydration and Meals

Environmental Triggers

Step 2: Prophylactic (Preventative) Medications

First-Line: Beta-Blockers

Second-Line: Tricyclic Antidepressants

Third-Line: Anticonvulsants

Fourth-Line: Calcium Channel Blockers

Step 3: Vestibular Rehabilitation Therapy (VRT) and Visual Desensitization

The Mechanism: Habituation

Visual Desensitization Exercises

Gaze Stabilization Exercises

Balance and Proprioceptive Training

VRT + Medication Synergy

Step 4: Addressing the Psychological Component

Understanding PPPD (Persistent Postural-Perceptual Dizziness)

Cognitive Behavioral Therapy (CBT) for VM and PPPD

The New Frontier: CGRP Monoclonal Antibodies

What are CGRP Inhibitors?

Efficacy in Vestibular Migraine

Practical Advantages

Disadvantages and Limitations

CGRP Inhibitors at PRIME ENT Center Hardoi

Abortive (Rescue) Strategies: What to Do During an Active Attack

Anti-Nausea Medication

Vestibular Sedatives for Acute Attack

Early Intervention: The “Prodrome Window”

Conclusion: Reclaiming Your Balance and Your Life

HINGLISH VERSION

The Migraine That Spins: Kyun Headache Medicines Fail Aur Kya Actually Kaam Karti Hai

Vestibular Migraine: Ek Hidden Problem

Vestibular Migraine Kya Hota Hai?

Diagnostic Criteria: Pain Ke Baad Balance

Four Types of Vestibular Migraine

Science of the Spin: Kya Different Hota Hai

Why Vestibular Migraine Alag Hota Hai

Three Theories

Kyun Standard Migraine Medicines Fail

Reason 1: Timing Mismatch

Reason 2: Trials Mein Headache Hi Measure Karte Hain

Reason 3: Nausea = No Absorption

Reason 4: Misdiagnosis

Reason 5: Over-Suppressant Use

4-Step Approach That Works

Step 1: Lifestyle—The Foundation

Sleep

Stress

Hormonal (Women)

Migraine Trigger Foods (See Table Below)

Hydration + Meals

Environment

Step 2: Preventative Medications

Beta-Blockers (First-Line)

Tricyclic Antidepressants (Second-Line)

Anticonvulsants (Third-Line)