MIGRAINOUS VERTIGOMIGRAINOUS VERTIGOAN UNDERDIAGNOSED ENTITYAN UNDERDIAGNOSED ENTITY

DR.ANITA BHANDARIDR.ANITA BHANDARICONSULTANT NEUROTOLOGIST CONSULTANT NEUROTOLOGIST VERTIGO AND EAR CLINICVERTIGO AND EAR CLINICJAIPURJAIPUR

Vertigo, imbalance, dizziness, Vertigo, imbalance, dizziness, disequilibrium – these are all terms used disequilibrium – these are all terms used by the pt. to describe a sensation of by the pt. to describe a sensation of altered orientation to the environment.altered orientation to the environment.

They are all symptoms , not diagnoses.They are all symptoms , not diagnoses.

A careful history ,physical examination & A careful history ,physical examination & investigations can help in establishing the investigations can help in establishing the cause in most pts.cause in most pts.

The vestibular system operates The vestibular system operates below the level of consciousness. below the level of consciousness. Only when it is abnormal does the pt. Only when it is abnormal does the pt. recognize that something is wrong. recognize that something is wrong. Because a person is so rarely Because a person is so rarely conscious of his own vestibular conscious of his own vestibular system, he has a great deal of system, he has a great deal of trouble describing his symptoms.trouble describing his symptoms.

CLASSIFICATION OF VERTIGOCLASSIFICATION OF VERTIGO

OTOLOGICALOTOLOGICAL CENTRALCENTRAL MEDICAL / SYSTEMICMEDICAL / SYSTEMIC UNLOCALIZEDUNLOCALIZED

CENTRALCENTRAL

DYSFUNCTION OF CENTRAL DYSFUNCTION OF CENTRAL STR.THAT PROCESS SENSORY INPUT STR.THAT PROCESS SENSORY INPUT FROM THE INNER EARFROM THE INNER EAR

2 to 23% OF VERTIGO DIAGNOSES 2 to 23% OF VERTIGO DIAGNOSES DEPENDING ON THE SPECIALITY DEPENDING ON THE SPECIALITY SETTINGSETTING

MIGRAINE RELATED VERTIGO / MIGRAINE RELATED VERTIGO / VERTIGINOUS MIGRAINEVERTIGINOUS MIGRAINE

MYTH OR REALITY ?MYTH OR REALITY ? ADAM & VICTORADAM & VICTOR’’S PRINCIPLES OF S PRINCIPLES OF

NEUROLOGY [ 2005] – The putative NEUROLOGY [ 2005] – The putative relationship of migraine & vertigo was relationship of migraine & vertigo was mentioned earlier. This refers to otherwise mentioned earlier. This refers to otherwise mundane migraine in which vertigo is mundane migraine in which vertigo is perhaps an aura.perhaps an aura.

However literature supported by several However literature supported by several standard neurotological textbooks & standard neurotological textbooks & publications fully recognize MRV as a distinct publications fully recognize MRV as a distinct entity.entity.

DIAGNOSTIC CRITERIADIAGNOSTIC CRITERIA

Vertigo is not included in the IHS Vertigo is not included in the IHS Classification as a migrainous Classification as a migrainous symptom except in basilar migrainesymptom except in basilar migraine

Hence most pts. who have MV Hence most pts. who have MV cannot be classified with the current cannot be classified with the current IHS criteriaIHS criteria

PROPOSED DIAGNOSTIC PROPOSED DIAGNOSTIC CRITERIACRITERIA

DEFINITE MIGRAINOUS VERTIGODEFINITE MIGRAINOUS VERTIGO• Episodic vestibular symptoms of at Episodic vestibular symptoms of at

least mod. Severityleast mod. Severity• H/O migraine acc. to IHS criteriaH/O migraine acc. to IHS criteria• One of the following migrainous One of the following migrainous

symptoms during 2 or more vertigo symptoms during 2 or more vertigo attacks: migrainous headache , attacks: migrainous headache , photophobia , phonophobia, visual or photophobia , phonophobia, visual or other aurasother auras

• Other causes ruled outOther causes ruled out

PROBABLE MIGRAINOUS PROBABLE MIGRAINOUS VERTIGOVERTIGO

Episodic vestibular symptoms of at least Episodic vestibular symptoms of at least moderate severity moderate severity

One of the followingOne of the following• Current or previous H/o migraineCurrent or previous H/o migraine• Migrainous symptoms during vestibular Migrainous symptoms during vestibular

symptomssymptoms• Migraine precipitants of vertigo in more than Migraine precipitants of vertigo in more than

50% of attacks : food triggers , sleep 50% of attacks : food triggers , sleep irregularities, hormonal changeirregularities, hormonal change

• Response to migraine T/t in >50% of attacksResponse to migraine T/t in >50% of attacks Other causes ruled outOther causes ruled out

CLASSIFICATION OF MIGRAINECLASSIFICATION OF MIGRAINE

COMMONCOMMON CLASSICALCLASSICALWITHOUT AURAWITHOUT AURA WITH AURAWITH AURA

90%90% 10%10%

HEADACHE – 4-72 HRSHEADACHE – 4-72 HRS PRECEDED BY REVERSIBLE CNS PRECEDED BY REVERSIBLE CNS DYSFUNCTION < 60 MIN.DYSFUNCTION < 60 MIN.

PHOTOPHOBIAPHOTOPHOBIA

PHONOPHOBIAPHONOPHOBIA

ABSENTABSENT

N/VN/V ABSENTABSENT

BASILAR MIGRAINEBASILAR MIGRAINE

VARIANT OF CLASSICAL MIGRAINEVARIANT OF CLASSICAL MIGRAINE FEATURES OF BASILAR ART. INV. FEATURES OF BASILAR ART. INV.

• VERTIGO VERTIGO • TINNITUS TINNITUS • DYSARTHRIA DYSARTHRIA • ATAXIA ATAXIA • VISUAL SYMPTOMS VISUAL SYMPTOMS • TINGLING , NUMBNESS, WEAKNESS OF TINGLING , NUMBNESS, WEAKNESS OF

LIMBSLIMBS

GENESIS OF THE MIGRAINE GENESIS OF THE MIGRAINE SYNDROMESYNDROME

OLDER HYPOTHESIS : VASCULAR REACTIVITYOLDER HYPOTHESIS : VASCULAR REACTIVITY

Reduced regional blood flow through cortexReduced regional blood flow through cortex

AURAAURA

Dilatation of scalp arteriesDilatation of scalp arteries

HEADACHEHEADACHE

NEURONAL THEORY NEURONAL THEORY

Welch & Ramadan , 1995Welch & Ramadan , 1995

Systemic and brain Magnesium Systemic and brain Magnesium deficiencydeficiency

MAGNESIUM DEFICIENCYMAGNESIUM DEFICIENCY

Abnormal mitochondrial oxidative Abnormal mitochondrial oxidative phosphorylationphosphorylation

Gain in NMDA receptor functionGain in NMDA receptor function

• Instability of neuronal polarizationInstability of neuronal polarization

• Neuronal hyperexcitabilityNeuronal hyperexcitability• Lower threshold for spontaneous Lower threshold for spontaneous

depolarizationdepolarization

MAGNESIUM DEFICIENCYMAGNESIUM DEFICIENCY

Mitochondrial dysfunctionMitochondrial dysfunction Impairment of energy metabolismImpairment of energy metabolism Prolonged hypometabolismProlonged hypometabolism Enhanced neuronal excitabilityEnhanced neuronal excitability Susceptability to spontaneous Susceptability to spontaneous

depolarizationdepolarization Changes in blood vessel caliberChanges in blood vessel caliber

MIGRAINE CASCADEMIGRAINE CASCADECHANGE IN NEURAL ACTIVITY OF BRAIN IN AREAS WHICH CONTROL CHANGE IN NEURAL ACTIVITY OF BRAIN IN AREAS WHICH CONTROL

CEREBRAL & EXTRA CRANIAL ART. BL. FLOWCEREBRAL & EXTRA CRANIAL ART. BL. FLOW

EFFERENT NEURONS OF V N. STIMULATEDEFFERENT NEURONS OF V N. STIMULATED VASODIL OF DURAL ART.VASODIL OF DURAL ART.

EXTRA VASATION OF PLASMAEXTRA VASATION OF PLASMA

RELEASE OF SEROTONIN, SUB.P, NEUROPEPTIDESRELEASE OF SEROTONIN, SUB.P, NEUROPEPTIDES

RELEASE & ACTIVATION OF PROSTOGLANDINSRELEASE & ACTIVATION OF PROSTOGLANDINS INFL. OF ART .IN DURA WHICH ARE INFL. OF ART .IN DURA WHICH ARE

CONNECTED BY AFFERENT FIBRES TO V NCONNECTED BY AFFERENT FIBRES TO V N

HEADACHE MEDIATED BY V NUCLEUSHEADACHE MEDIATED BY V NUCLEUS

NEUROGENIC INFLAMMATIONNEUROGENIC INFLAMMATION

Supported by the fact that Supported by the fact that medications that block neurogenic medications that block neurogenic inflammation & mediate inflammation & mediate vasoconstriction are successfully vasoconstriction are successfully used to abort attackused to abort attack

MRV 42

INCIDENCEINCIDENCE

Total 256

CLINICAL PRESENTATIONCLINICAL PRESENTATION AGEAGE

• ANY AGE ANY AGE • OFTEN STARTS EARLY IN LIFEOFTEN STARTS EARLY IN LIFE• BENIGN PAROXYSMAL VERTIGO OF BENIGN PAROXYSMAL VERTIGO OF

CHILDHOOD IS AN EARLY MANIFESTATION OF CHILDHOOD IS AN EARLY MANIFESTATION OF MVMV

0

2

4

6

8

10

12

14

16

0-10 11-20 20-30 31-40 41-50 51-60 > 61

MALE : FEMALE MALE : FEMALE

FEMALE PREPONDERANCEFEMALE PREPONDERANCE

FEMALE

MALE

CLINICAL PRESENTATIONCLINICAL PRESENTATION

Headache – only 50% pts. presented Headache – only 50% pts. presented with H/o headache along with or with H/o headache along with or after vertigo .Several patients had after vertigo .Several patients had headaches earlier in life but now headaches earlier in life but now vertigo was the predominant vertigo was the predominant symptomsymptom

Duration – usually few hrs.Duration – usually few hrs.

Photophobia & phonophobia were Photophobia & phonophobia were common symptoms.common symptoms.

AUDIOLOGICAL PRESENTATIONAUDIOLOGICAL PRESENTATION

Most had normal hearingMost had normal hearing

Any SNHL was not related to MVAny SNHL was not related to MV

MOTION SICKNESSMOTION SICKNESS

Has been reported to occur Has been reported to occur commonly in MV due to a optokinetic commonly in MV due to a optokinetic stimulation.stimulation.

5 in our series5 in our series

BPPV AND MVBPPV AND MV

5 cases had BPPV5 cases had BPPV BPPV is a well documented sequelae BPPV is a well documented sequelae

to ischemic damage of the inner ear to ischemic damage of the inner ear presumably d/t release of otoconia presumably d/t release of otoconia from the macular membrane.from the macular membrane.

The vasospasm associated with The vasospasm associated with classical visual aura is secondary to a classical visual aura is secondary to a primary neuronal metabolic defectprimary neuronal metabolic defect

MANAGEMENTMANAGEMENT

Lifestyle changesLifestyle changes• Explaining to the pt. what is going onExplaining to the pt. what is going on• Avoidance of irregular lifestyle and Avoidance of irregular lifestyle and

stress. Migrainous and nonmigrainous stress. Migrainous and nonmigrainous brains are wired differently. Migraine brains are wired differently. Migraine pts. are more susceptable to the effects pts. are more susceptable to the effects of overexertion – mental & physical , of overexertion – mental & physical , irregular eating and sleeping habits.irregular eating and sleeping habits.

AVOIDANCE OF TRIGGER AVOIDANCE OF TRIGGER FACTORSFACTORS

A personal vertigo and diet diaryA personal vertigo and diet diary Common triggers Common triggers

• bright and blinking lights bright and blinking lights • monosodium glutamate monosodium glutamate • caffeine caffeine • cheese cheese • chocolates chocolates • alcohol alcohol • pills pills • strong smells strong smells

TREATMENT OF ACUTE MVTREATMENT OF ACUTE MV TriptansTriptans – Sumatriptan – Sumatriptan Vestibular suppressantsVestibular suppressants

• promethazine promethazine • dimenhydrinate dimenhydrinate • meclizinemeclizine

PROPHYLACTIC TREATMENTPROPHYLACTIC TREATMENT

INDICATIONSINDICATIONS• 3 or more attacks per month3 or more attacks per month• Attacks which are incapacitating & Attacks which are incapacitating &

impair normal activities impair normal activities • Cannot tolerate or are not helped by Cannot tolerate or are not helped by

abortive therapyabortive therapy• Cannot psychologically cope with Cannot psychologically cope with

attacksattacks

PROPHYLACTIC TREATMENTPROPHYLACTIC TREATMENT Beta blockers Beta blockers

• Propanolol – 40 -240 mg / dayPropanolol – 40 -240 mg / day• Metoprolol – 50 -120 mg / dayMetoprolol – 50 -120 mg / day

Side effects –fatigue , hypotension , impotence , Side effects –fatigue , hypotension , impotence , depression , nightmares , bronchial constrictiondepression , nightmares , bronchial constriction

Calcium channel blockersCalcium channel blockers• Flunerizine – 5-10 mg / dayFlunerizine – 5-10 mg / day• Verapamil -120 -240 mg / dayVerapamil -120 -240 mg / day

Tricyclic antidepressantsTricyclic antidepressants• Nortryptiline – 10 mg initially , upto 25 mg / day Nortryptiline – 10 mg initially , upto 25 mg / day

Second line of drugs include Valproic acid and Second line of drugs include Valproic acid and methysergide.methysergide.

PROPHYLAXIS TREATMENTPROPHYLAXIS TREATMENT

Acetazolamide Acetazolamide • Beneficial effect results from its altering Beneficial effect results from its altering

the pH within the cerebellum thus the pH within the cerebellum thus stabilizing the mutated calcium channel stabilizing the mutated calcium channel [Baloh][Baloh]

• Dose -250 mg BDDose -250 mg BD• Side effects – paraesthesias ,inability to Side effects – paraesthesias ,inability to

drink carbonated drinks , long term risk drink carbonated drinks , long term risk of renal stonesof renal stones

PROPHYLAXIS TREATMENTPROPHYLAXIS TREATMENT

Botulinum toxoid [Botox] injections Botulinum toxoid [Botox] injections into the scalp or neckinto the scalp or neck• Mechanism – inhibition of acetylcholine Mechanism – inhibition of acetylcholine

in brainin brain• Efficacy after pericranial injection can Efficacy after pericranial injection can

last for 3 or more monthslast for 3 or more months• Used in case studies and trials , not yet Used in case studies and trials , not yet

approvedapproved