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 nobodys baby

Shunting between GPs, Physician, Neurologis
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 Patients Pathologic Causes

Dizziness Experience
Vertigo Illusion of movement of Disturbance of peripheral or CNS
pathways of vestibular system
patients or Surroundings

Syncope or Impending loss of

consciousness
Cerebral perfusion of brain falls
below a critical level
Presyncope
Disequilibrium A sense of imbalance Vestibular,
Proprioceptive,
Cereballer,Visiual

III defined Emotional

disorders
Hyperventilation,
Anxiety, Depression,
dizziness Conversion reaction
 Vertigo
Neuroanatomical & Neurochemical Basis

Glutamate-Vestibular nerve fibers

Acetylcholine muscaranic recepters(m2)-
pons & medulla
GABA-Vestibular neurons
Histamine-diffusely in vestibular structures.
-H1& H2 receptors- Pre &
post synaptically on vestibular cells.
 Vertigo - Mechanisms

Mechanism Known :
-Migraine
-Epilepsy
-Menieres disease
-Central causes

In most of case- no convincing scientific

evidence of cause & mechanism.
 Vertigo

Common Peripheral Vertigo

Benign positional vertigo

Vestibular neuronitis
Labyrinthitis
Meniers.s disease
Post 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 Central

Short duration Chronic/Permanent

Severe, often Less severe,
paroxysmal Continuous
Accompanied by S/S of brain stem/
auditory Cerebellum,
symptoms Auditory less freq
Fatiguilibility. No fatiguilibility
Reproducibility Reproducibility
inconsistent consistent
 Vertigo
Peripheral Central

Nystagmus Nystagmus
- Unidirectional - Uni/bidirectional
- Horizontal-rotatory, - Horizontal-rotatory,
Never vertical vertical
- Inhibited by visual - Not inhibited
fixation - Sometimes only
- Nystagmus with Nystagmus, no verti
Vertigo
Fall & past pointing- -Veriable
towards side of lesion
 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 evaluation

Good history

To diagnose 90%
-
- 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 menieres 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 vertigo
Vestibular 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 Rehabilitation
Adaptation
a phenomenon which helps a patient with
persisting peripheral dysfunctional state to regain
normal balance.
Habituation
repeated exposure of the body to mismatched
sensory input.
Compensation
a goal directed process induced by some
recognized errors, 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.
Vestibular compensation
Right labyrinth damaged Left Labyrinth normal
Less electrical discharge Normal electrical discharge
Imbalance between two sides- Vertigo
Sensation of unequal inputs from two sides by CNS

Habituation and adaptation to the error

possible ways

increasing elect. discharge fromDecreasing electrical discharge

from
damaged labyrinth normal labyrinth

Not possible Cerebellar Clamp or Vestibular shutdown

Acute compensation by cerebellar clamp
or vestibular shutdown
Cerebellum through connections with Vestibular
nuclei induces reduction in resting electrical
discharge- cerebellum induced vestibular shutdown
Reduces inequality between electrical discharge
between the two sides by lowering electrical
discharge of normal vestibular labyrinth

Advantages Disadvantage
symptomatic relief of reduced vestibular
vertigo in acute case sensitivity
Inhibited vestibular system
At rest, no vertigo
fails to react normally to
vestibular assault
Sudden head movement
Chronic
Mechanism
leads
compensation
chronic
to vertigo
is essential .
compensation is needed
 Chronic compensation for vertigo
Normal situation
Right vestibule equal Left vestibule

Right vestibular nuclei Left vestibular

nuclei

Vertigo
Right vestibule damaged Left vestibule
normal
Less electrical normal electrical.
Discharge discharge

Right vestibular nuclei left vestibular nuclei

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

Chronic Compensation

Chronic compensation

Right vestibule damaged Left vestibul

normal
normal
electrical discharge
Right vestibular
equal nuclei
synapse Left vestibular
equal
nuclei

brain
Chronic compensation
Inhibitory effect of cerebellum on vestibular nuclei is
gradually removed and requisite anatomical
restructuring of central vestibular pathways takes
place
Cerebellum monitors afferent ( sensory) and efferent
(motor) inputs form the two sides
Vestibular nuclei on damaged vestibular side gets
connected anatomically and functionally to vestibular
nuclei on normal vestibular side.
Capacity of cerebellum to adapt to the affected or
changed vestibular scenario is called plasticity of CNS.
Chronic compensation

Whole compensatory mechanism controlled by CNS ,

mediated by cerebellum. Compensatory mechanism
ineffective if cerebellum malfunctioning, (Cerebellar
degeneration)
If after the above compensatory mechanisms, still
errors in vestibular functioning, corrected by other
afferent such as propioceptive and visual system.
Central compensation initiated and enhanced by head
movements- adaptation exercises and vestibular
habituation therapy

.
 Vastibular Rehabilitation
General Principles

Decrease centrally sedating or vestibular

suppressant drugs
Exercise must provoke vertigo
Initiate as early as possible
Exercise should simulate real life situations
Maintenance 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 Effects Neurological Effect
(in inner ear & brain) (in brain)
 Betahistine-Vascular Effects
H3 autoreceptor H1 Agonist
Antagonist

Inhibits autoregulation
of histamine release

Improve cochlear micro circulation

Improve cerebral/vertibrobasilar blood flow
Betahistine-Neurological Effects

Blocks H3 Receptors

Regulates firing activity of

Vestibular Nuclei
 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)

Flunarizine(1985)
Mechanism

? Vestibular hair cells

-H1 antihistamnic
endowed with ca
properties
channels
-Sedative
-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
avoided
Vestibular 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