UNDERSTANDING AND MANAGING VERTIGO

Vijay Sardana MD,DM

Professor & Head,Deptt. Of Neurology,

Medical College, Kota

Prevalence of Vertigo and Giddiness

5% of patients visiting the GP

10% of patients visiting the Otorhinolaryngologists

Life time prevalence-30%

3rd most common symptom

Vertigo Defination

Illusion of spinning sensation of self or Surroundings, usually due to disturbance of vestibular system

Vertigo:-Problems

Vertigo patients are nobody’s babyShunting between GPs, Physician, Neurologist, ENT specialist and psychiatrists.With or without investigations-it is vestibular Suppressant.Few dedicated physicians for vertigo.

What causes vertigo ?

Contradictory information from:

Vestibular, Visual & proprioceptive system

Causes of Dizziness

Types of Types of DizzinessDizziness

PatientsPatients

ExperienceExperience

Pathologic CausesPathologic Causes

VertigoVertigo Illusion of movement of Illusion of movement of

patients or Surroundingspatients or Surroundings Disturbance of peripheral or CNS Disturbance of peripheral or CNS pathways of vestibular systempathways of vestibular system

Syncope orSyncope or

PresyncopePresyncope

Impending loss of Impending loss of

consciousnessconsciousness

Cerebral perfusion of brain falls Cerebral perfusion of brain falls below a critical levelbelow a critical level

DisequilibriumDisequilibrium A sense of imbalanceA sense of imbalance Vestibular,Vestibular,

Proprioceptive,Proprioceptive,

Cereballer,VisiualCereballer,Visiual

III defined III defined dizzinessdizziness

EmotionalEmotional

disordersdisorders

Hyperventilation,Hyperventilation,

Anxiety, Depression,Anxiety, Depression,

Conversion reactionConversion reaction

VertigoNeuroanatomical & Neurochemical Basis

Glutamate-Vestibular nerve fibersAcetylcholine muscaranic recepters(m2)- pons & medullaGABA-Vestibular neuronsHistamine-diffusely in vestibular structures. -H1& H2 receptors- Pre & post synaptically on vestibular cells.

Vertigo - Mechanisms

Mechanism Known : -Migraine -Epilepsy -Meniere’s disease -Central causes

In most of case- no convincing scientific evidence of cause & mechanism.

Vertigo

Common “Peripheral Vertigo”

Benign positional vertigoVestibular neuronitisLabyrinthitisMeniers.s diseasePost traumatic vertigo

Vertigo

Central Vertigo

Vestibular portion of 8th nerve Vestibular nuclei within brain stem Central connections of vestibular nuclei- *Cerebellar Floccules *Visual sensory connections *Afferent from joint & tactile receptors

Vertigo Central Vertigo-Characteristics

Less common than peripheral & systemic causes. Vertiginous symptoms usually less common. Additional neurological science usually present. Vertigo as a sole manifestation rare.

Vertigo

Peripheral

Short duration Severe, often paroxysmal Accompanied by auditory symptoms Fatiguilibility. Reproducibility inconsistent

Central

• Chronic/Permanent• Less severe, Continuous• S/S of brain stem/ Cerebellum, Auditory less freq• No fatiguilibility• Reproducibility consistent

Vertigo

Peripheral

Nystagmus - Unidirectional - Horizontal-rotatory, Never vertical - Inhibited by visual fixation - Nystagmus with Vertigo Fall & past pointing- towards side of lesion

Central

Nystagmus - Uni/bidirectional - Horizontal-rotatory, vertical - Not inhibited - Sometimes only Nystagmus, no vertigo

-Veriable

Vertigo

Central Vertigo-Causes

Brainstem ischemia & infarction-VBI, infarction in territory of Int.auditory artery (collegen disorder), subclavian steel phenomenon. Demylinating diseases-MS, postinfection demylination CP angle tumors. Cranial neuropathy(isolated 8th nerv/multiple cranial nerves)-vasculitis, granulomatous dis(sarcoidosis), maningeal carcinomatosis.

Vertigo

Central Vertigo-Causes contd.-

Intrinsic Brainstem lesions. Other posterior fossa lesions- cerebellar infarct, haematoma Seizure disorder-CPS Migraine-Basilar artery migraine, migranous aura Degenerative heridofamilial-SCA-PSP Cervical Vertigo-Neck trauma, irradiation to upper cervical sensory roots, CVJ anomalies.

Vertigo

Common drugs producing vertigo Anticonvulsant -Barbiturates -Phenytoin -Carbamazepine Alcohol Salicylates Cinchona alkaloids-quinine Aminoglycosides Alkalyting agents

VERTIGO: Clinical evaluationVERTIGO: Clinical evaluation

Good historyGood history

- - To diagnose – 90% To diagnose – 90%

- bond/ relationship with patient- bond/ relationship with patient

Vertigo

Clinical Evaluation

Complete medical history Complete neurological examination esp. nystagmus 5th nerve including corneal reflux,7th,8th nerves, cerebellar signs & long tract signs Otological examination & related tests CT head/MRI EEG when indicated

Vertigo-Treatment

Specific treatment

Antimigraine drugs Antiepileptic drugs Salt restriction & diuretics in meniere’s disease

I Want…….

Fewer attacks every month When attacks occur they are not as bad as before When attacks occur they do not last long

Vertigo

Symptomatic Treatment-Goals

Elimination of vertigoVestibular supression Enhancement/non compromise of process of vestibular compensation Reduction of accompanying neurovegetative & psycho affective signs(nausea,vomiting,anxiety)Treatment of cause

Vertigo

Vestibular Suppression

Decrease in asymmetry in vestibular tone

Decrease in vestibular function in normal & abnormal side both

Vertigo Vestibular Suppressants Anticholinergics -Homatropine -Scopolamine(Hyoscine) Antihistamines -Diphenhydramine -Cyclizine -Dimenhydrinate -Meclizine -Hydrocyzine -Promethazine -Cinnarizine -Flunarizine Benzodiazepines -Diazepam -Lorazepam -Clonazepam

Vertigo

Vestibular Compensation

Plasticity of the CNS Sensory feedback (Vertigo) required for compensation 2 goals (decrease in vertigo and increase in compensation) often incompatible

Vestibular RehabilitationVestibular Rehabilitation AdaptationAdaptation

a phenomenon which helps a patient with persisting a phenomenon which helps a patient with persisting peripheral dysfunctional state to regain normal balance. peripheral dysfunctional state to regain normal balance.

HabituationHabituation

repeated exposure of the body to “mismatched “ sensory repeated exposure of the body to “mismatched “ sensory input.input.

CompensationCompensationa goal directed process induced by some recognized errors, a goal directed process induced by some recognized errors, directed towards its elimination directed towards its elimination

Norre M E, Crit. Rev. Phy. Rehab. Med., 1990, 2, 2, 101-120, Kirtane MV, Ind. J. Otolaryngol HNS, 1999, 51 (2), 27-36.

Norre M E, Crit. Rev. Phy. Rehab. Med., 1990, 2, 2, 101-120, Kirtane MV, Ind. J. Otolaryngol HNS, 1999, 51 (2), 27-36.

Vestibular compensationVestibular compensationRight labyrinth damagedRight labyrinth damaged Left Labyrinth Left Labyrinth

normal normal

Less electrical dischargeLess electrical discharge Normal electrical Normal electrical dischargedischarge

Imbalance between two sides- VertigoImbalance between two sides- Vertigo

Sensation of unequal inputs from two sides by CNSSensation of unequal inputs from two sides by CNS

Habituation and adaptation to the errorHabituation and adaptation to the error

possible wayspossible ways

increasing elect. discharge fromincreasing elect. discharge from Decreasing electrical discharge fromDecreasing electrical discharge from

damaged labyrinthdamaged labyrinth normal labyrinthnormal labyrinth

Not possibleNot possible Cerebellar Clamp or Vestibular shutdownCerebellar Clamp or Vestibular shutdown

Acute compensation by cerebellar clamp or Acute compensation by cerebellar clamp or vestibular shutdownvestibular shutdown

Cerebellum through connections with Vestibular nuclei induces Cerebellum through connections with Vestibular nuclei induces reduction in resting electrical discharge- cerebellum induced reduction in resting electrical discharge- cerebellum induced vestibular shutdownvestibular shutdown

Reduces inequality between electrical discharge between the two sides Reduces inequality between electrical discharge between the two sides by lowering electrical discharge of normal vestibular labyrinthby lowering electrical discharge of normal vestibular labyrinth

Advantages symptomatic relief of

vertigo in acute case

At rest, no vertigo

Advantages symptomatic relief of

vertigo in acute case

At rest, no vertigo

Disadvantage reduced vestibular sensitivity Inhibited vestibular system fails to

react normally to vestibular assault Sudden head movement leads to

vertigo

Disadvantage reduced vestibular sensitivity Inhibited vestibular system fails to

react normally to vestibular assault Sudden head movement leads to

vertigoChronic compensation is essential . Chronic compensation is essential .

Normal situationNormal situation

Right vestibuleRight vestibule equal Left vestibule equal Left vestibule

Right vestibular nucleiRight vestibular nuclei Left vestibular nuclei Left vestibular nuclei

VertigoVertigo

Right vestibule damagedRight vestibule damaged Left vestibule normal Left vestibule normal

Less electricalLess electrical normal electrical. normal electrical. DischargeDischarge discharge discharge

Right vestibular nucleiRight vestibular nuclei left vestibular nuclei left vestibular nuclei

Chronic compensation for vertigoChronic compensation for vertigo

Biswas A, Neurotological Diseases IN ‘An Introduction to neurotology”, 1998, 85-7.Biswas A, Neurotological Diseases IN ‘An Introduction to neurotology”, 1998, 85-7.

Right vestibule damaged Left vestibul normal

normal electrical discharge

Right vestibular nuclei Left vestibular nuclei

Right vestibule damaged Left vestibul normal

normal electrical discharge

Right vestibular nuclei Left vestibular nuclei

Chronic CompensationChronic Compensation

Chronic compensationChronic compensation

equal synapse equal

brain

equal synapse equal

brain

Chronic compensationChronic compensation

Inhibitory effect of cerebellum on vestibular nuclei is gradually removed Inhibitory effect of cerebellum on vestibular nuclei is gradually removed and requisite anatomical restructuring of central vestibular pathways and requisite anatomical restructuring of central vestibular pathways takes placetakes place

Cerebellum monitors afferent ( sensory) and efferent (motor) inputs Cerebellum monitors afferent ( sensory) and efferent (motor) inputs form the two sidesform the two sides

Vestibular nuclei on damaged vestibular side gets connected Vestibular nuclei on damaged vestibular side gets connected anatomically and functionally to vestibular nuclei on normal vestibular anatomically and functionally to vestibular nuclei on normal vestibular side.side.

Capacity of cerebellum to adapt to the affected or changed vestibular Capacity of cerebellum to adapt to the affected or changed vestibular scenario is called plasticity of CNS.scenario is called plasticity of CNS.

Chronic compensationChronic compensation

Whole compensatory mechanism controlled by CNS , mediated Whole compensatory mechanism controlled by CNS , mediated by cerebellum. Compensatory mechanism ineffective if by cerebellum. Compensatory mechanism ineffective if cerebellum malfunctioning, (Cerebellar degeneration)cerebellum malfunctioning, (Cerebellar degeneration)

If after the above compensatory mechanisms, still errors in If after the above compensatory mechanisms, still errors in vestibular functioning, corrected by other afferent such as vestibular functioning, corrected by other afferent such as propioceptive and visual system. propioceptive and visual system.

Central compensation initiated and enhanced by head movements- Central compensation initiated and enhanced by head movements- adaptation exercises and vestibular habituation therapyadaptation exercises and vestibular habituation therapy

..

Vastibular RehabilitationVastibular Rehabilitation

General PrinciplesGeneral Principles

Decrease centrally sedating or vestibular suppressant drugsDecrease centrally sedating or vestibular suppressant drugs Exercise must provoke vertigoExercise must provoke vertigo Initiate as early as possibleInitiate as early as possible Exercise should simulate real life situationsExercise should simulate real life situations Maintenance exercises to recurrence of symptomsMaintenance exercises to recurrence of symptoms

Vertigo

Agents affecting Vestibular Compensation-

Delayed Compes.- Barbiturates Benzodiazepines Antihistamines Neuroleptics

Accelerated compes.- Betahistines Flunarizine Ginkgo-biloba extract Caffeine

Vertigo-Pharmacological Treatment

Anticholinergics-

Homatropine and Scopolamine(Hyoscine) First drug to be used in Vertigo Non selective blocking all muscarinic receptor subtypes(m1 to m5) Adverse effects-Dry mouth, visual disturbences, constipation, memory disturbances cofusion, dysurea, glaucoma

Vertigo-Pharmacological Treatment

Antihistamines- H1 Blockers Mechanism- Poorly understand ? Antimuscaranic properties Cinnarizine and flunarizine-Ca channel blockers with significant H1 blocking effect H2 blockers- Not used Side effects- Sedation Duration of action- 4 to 12 hrs.

Vertigo-Pharmacological Treatment

Histaminergic Medication-

Betahistine

Mode of action

Betahistine Vascular EffectsVascular Effects

(in inner ear & brain)(in inner ear & brain)

Neurological EffectNeurological Effect

(in brain)(in brain)

Betahistine-Vascular Effects

H3 autoreceptor H3 autoreceptor AntagonistAntagonist

Inhibits autoregulationInhibits autoregulation

of histamine releaseof histamine release

Improve cochlear micro circulationImprove cochlear micro circulation

Improve cerebral/vertibrobasilar blood flowImprove cerebral/vertibrobasilar blood flow

H1 AgonistH1 Agonist

Betahistine-Neurological Effects

Regulates firing activity of Regulates firing activity of

Vestibular NucleiVestibular Nuclei

Blocks H3 ReceptorsBlocks H3 Receptors

Betahistine : Pharmacokinetics

Oral administration Rapid and complete absorption Mean plasma half-life : 3 to 4 hrs Complete excretion via urine in 24 hrs Very low plasma protein binding 2 inactive metabolites namely – Pyridylacetic acid & 2-(2-aminoethyl) pyridine have been found

Betahistine : Tolerability

minimal side effects No sedation Low level of gastric side effects No anticholinergic effcts No extrapyrimidal side effects

Betahistine : Contraindication

Hypersensitivity to Betahistine Pheochromocytoma

Betahistine : Special Precautions

Use with antihistamines Patients with bronchial asthma Patients with peptic ulcers

Vertigo-Pharmacologic treatment

Acetylleucine

Mechanisms -? Precursors of neuromediator- peptidic- Activation of vestibular afferent -? Anti calcium properties May enhance compensation IV / Oral

Vertigo-Pharmacologic treatment

Antidopaminergic Drug

Block dopaminergic receptors in area postrema of the brainstem,has anticholinergic and antihistaminic(H1) activity Neuroleptics neurovegetative symptoms psychoeffective symptoms

- Phenothiazine derivatives - Butyrophenones - Benzamides Domperidone & Metochlopramide

Adverse effects- Ortho.hypotension, Somnolence,Extrapyramidal syndrome,

anticholinergic side effects; NMS

Vertigo-Pharmacologic treatment

Benzodiazepines

GABA modulators – act centrally to suppress vestibular response May impair vestibular compensation Anxiolytic effect

Vertigo-Pharmacologic treatment

Calcium Antagonist

Cinnaizine(1966) Cinnaizine(1966) Flunarizine(1985) Flunarizine(1985)

MechanismMechanism

? ? Vestibular hair cells Vestibular hair cells endowed with ca endowed with ca channelschannels

--H1 antihistamnic propertiesH1 antihistamnic properties

-Sedative-Sedative

-Antidoaminergic action-Antidoaminergic action

Adverse effects : Short term-Sedation,Weight gain Long term-Depression,Parkinsonism

Vertigo-Pharmacologic treatment

Miscellaneous

Ginkgo biloba Piribidil- Dopaminergic agent Ondansatron 5 HT3 antagonist

To treat Vertigo A Physician needs a drug which…….

Has Effect on cochlear & cerebral blood flow Regulates vestibular nuclei firing Offers symptomatic & prophylactic therapy Does not interfere with compensation mechanism Does not cause drowsiness

Vertigo-Pharmacologic treatment

Worldwide trends-

US – Benzodiazepines Meclizine France – Acetylleucine Flunarazine India - Cinnarizine Betahistine

Vertigo- Treatment

General Comments

It is difficult to set out rational & well documented rules for administration of drugs.

Clinical pharmacology of anti vertigo drugs complex. Clinical trials reliability? Spontaneous recovery-Placebo control trials

When to refer a Specialist

Serious vertigo which is disabling Vertigo lasting longer then 4 weeks Hearing loss CNS or psychological disorder

Vertigo- Treatment

General Guidelines

Acute disabling vertigo should be treated Mild vertigo may be left alone “Omnious” vertigo should be investigated Treatment period should be shortest possible Lengthy confusing prescriptions should be avoidedVestibular rehabilitation should be used early

Vertigo

Concluding Remarks-

Our habits of ant vertigo prescription are empirical and insufficiently evaluated

Improvement in practice of clinical pharmacology for vertigo is needed

New treatment may emerge from research in receptor subtypes, neuromodulators and agents affecting central compensation.

Vestibular rehab. Is underutilized

Thanks