1 Vertigo

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Balance the imbalance

DIAGNOSIS & MANAGEMENT OF VERTIGO - PRESENT SENARIO

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Dizziness 4 varients of dizziness -A definite rotational sensation or vertigo -A sensation of faintness or impending loss of

consiousness -Desequilibrium or sense of imbalance -An illdefined sense of dizziness or light headedness

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VERTIGO

-A subjective sensation of movement

-May feel either that him involving in space or that objects in the environment are moving around him.

-It also include feeling of swaying movement of body

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OTHER TYPE OF DIZZINESS Faintness- generally indicates hemodynamic factors

causing brain ischemia . Disequilibrium- refers to a sense of unsteadiness or

imbalance & occure during ambulation ,especially when stressed like rapid turning, in the dark & suggests cerebellar incordination, muscle weakness & peripheral sensory impairment .

Light headedness- is a frequently a neurologoic complaints & may have no stereotyped condition for its prepitation or aggravation other than emotional stress .

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ANATOMY AND PHYSIOLOGY*

*RELATED TO VERTIGO

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Utricularnerve

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ry

ve

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Central projection of peripheral vestibular system

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CAUSES OF VERTIGO

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What causes vertigo?

Contradictory information fromThe vestibular system (ears)2The visual system (eyes)The Proprioceptive system

(muscles, joints)

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Causes of Vertigo PERIPHERAL – Meniere’s disease Labyrinthitis Vestibular neuropathy BPPV Trauma CENTRAL- referred to mnemonic “ VERTIGO”

V – vascular causes like Stroke , Vertebrobasilar insufficiency , migraine , vasculitis & vascular elements like decreased cardiac output , orthostatic hypotension,anemia,hypoxia,hypoglycemia

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CAUSES OF CENTRAL VERTIGO E – Epilepsy(vertiginous)

R – Rx or drug related like ANTIBIOTICS- aminoglycosides, ANTIHYPERTENSIVES HYPNOTIC-SEDATIVE DRUGS- phenytoin, barbiturates, & alcohol. TRANQUILLIZERS –Phenothiazine,Benzodiazepines & Tricyclic antidepressants ASPIRIN QUININE

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CAUSES OF CENTRAL VERTIGO T – TUMOUR – Primary like Acoustic neuroma, Glioma, intraventricular tumours and secondary metastatic tumours of brain. - TRAUMA - THYROID- Hypothyroidism

I – INFECTIONS – viral, syphilis, vestibular neuronitis.

G – GLIAL DISEASE – Multiple sclerosis

O – OULAR PATHOLOGY- weakness of extra ocular muscles .

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Vertigo: Traditional Classification Peripheral

(arises in vestibule) Intermediate

(arises in vestibular nerve)

Central (arises in vestibular nuclei)

Non-vestibular (arises outside the vestibular system)

Vertigo

Vestibular

19Sites of Vertigo

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Physiology of Peripheral Vertigo Vestibular apparatus consist of – semicircular canal - utricle - sacculeAll these have sensory hair cells having stereocilia arranged in

ascending fashion. The longest steriocilia is k/a Kinocilia.Movement of steriocilia towards kinocilia- StimulationMovement of steriocilia opposite to kinocilia- Inhibition

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Conditions resulting in stimulation of only one labyrinth results in unequal impulses reaching to brain leading to state of dysequilibrium & manifest as vertigo or dizziness.

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Causes of Peripheral Vertigo

Benign Paroxysmal Positional Vertigo Meniere’s Disease Labyrinthitis Head Injuries & Surgical Trauma Pressure Vertigo

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Causes of Intermediate Vertigo

Vestibular neuronitis

Acoustic neuroma

Drugs –alcohal, aminoglycosides, anticonvulsants, antidepressanta, antihypertensive, barbiturates, cocaine .

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Causes of Central Vertigo

VBI (Vertebrobasilar Insufficiency)

Arteriosclerosis

Cervical Spondylosis

Whiplash injuries of Neck

Brain Tumors

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Head injuries Epilepsy Multiple sclerosis Hypoglycemia Migraine

Non-Vestibular Causes of Vertigo

Ocular vertigo Anemia Cardiovascular

(orthostatic hypotension) Cerebrovascular disorders Psychogenic Brain tumors

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Another classification of vertigo

Paroxysmal Vertigo - sudden attack comes on quickly, lasts for a short time

The single attack - sudden intense attack fading away slowly

Chronic vertigo - not severe Positional vertigo - occurs following sudden

movements of head in certain positions Dizzy spells - lasting a few seconds occurring

irregularly

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DIAGNOSIS OF VERTIGO

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Medical History Description of symptoms by patient Classification of vertigo attacks (Which type, how debilitating, frequency, duration,

vegetative symptoms) Influencing circumstances (Injuries, drugs taken, stress, eating pattern, Illnesses) Secondary symptoms Tinnitus, Hearing loss, Headache, nausea/ vomiting

Biswas A., ‘Neurotological History Taking’ IN An Introduction to Neurotology, 1998, 8-11

31Adapted from Biswas A.,’Clinical tests in Neurotology’ IN An Introduction to Neurotology, 1998, 13-25

Vestibular Function Tests

Vestibulo spinal reflexRomberg testUnterberger testModified Sikatani testBabinski-weill testBarany Pointing test

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Vestibulo ocular reflex←Cold caloric test (Kobrak test)←Bithermal test ( Fitzgerald-Hallpike test)←Air caloric test←Dundas Grant air caloric test←Fistula test←ENG←Optokinetic test←Rotation test

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•Patient closes eyes and stretches arms out in front

•Walks on spot for a minute

•Patients with vertigo will start to turn his axis in particular direction

•The knees raised as high as possible

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•Deviation to one side in pointing occurs in patients with vertigo

BARANY’S

36Patient with vertigo starts to walk in a star shape

Babinsky- Weill TestPatient closes his eyes and takes 5 steps forward and 5 steps back for 30 seconds

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FITZGERALD- HALLPIKE / BITHERMAL CALORIC TEST

Patient in supine position with head flexed at 30⁰ with horizontal. Ear is irrigated with water at 44⁰ C & 30⁰ C separately for periode of

40 Sec each with the gap of 5 minute between both irrigations. Duration & character of nystagmus is observed .

Normal duration of nystagmus is 90-120 Sec with direction for cold water towards opposite ear & for warm water for same side. (mnemonic – COWS)

If time,duration & severity decreases on one side – CANAL PARESIS If no reaction is observed on one side – DEAD LABYRINTH

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OTHER CALORIC TESTS KOBRAK’S/ COLD CALORIC TEST- Position similar to

bithermal test with irrigation with 10-15cc of ice cold water.

AIR CALORIC TEST- Air at different temperature like 17.5 ⁰C,45.5⁰ C is passed into ear & nustafmus is noted.

DUNDAS GRANT AIR CALORIC TEST –Ethyle chloride is sprayed on a copper tube & then air from the tube is passed into the ear . Ntstagmus is noted .

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FISTULA TEST Pressure is increased in EAC with Siegle’s speculum or by

applying pressure over tragus & occurance of any nystagmus or vertigo is noted.

POSITIVE FISTULA TEST- indicates fistula in labyrinth especially in LSC .

NEGATIVE FISTULA TEST-Normal labyrinth or dead labyrinth .

FALSE POSITIVE TEST- Also K/a Hannebert’s Sign is seen in Meniere’s disease and Congenital syphilis.

FALSE NEGATIVE TEST- Seen in cases of dead labyrinth

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ELECTRONYSTAGMOGRAPHYENG measures the function of the vestibular system,

through the occulormotor pathways rather than the auditory pathways.

In ENG we compare slow; phase velocity and fast phase velocity of the nystagmus , of which slow phase velocity is more important .

Standerd Deviation (SD) between two ear should not be more than 30 % for a normal person .

Practically without ENG we use a costless procedure to count fast componant in 10 Sec. Of maximum nystagmus periode which is known as a cumulative velocity .

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ELECTRONYSTAGMOGRAPHY A battery of 6 tests are performed.

Saccade Test: Patient looks back and forth at a visual target on a screen.

Gaze Test: Patient gazes right, left, up, down and center. Tracking Test: Patient follows a visual target on an horizontal plane. Optokinetic Test: Patient follows a series of moving lights on a

horizontal plane. Position Test: Patient moves in various position focusing on one target. Caloric Test: Patient’s ears are stimulated 2x each with warm and cool

air or water

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ROTATION TEST There are two kinds of computerized rotation tests: auto head

rotation and rotary chair. In auto head rotation tests, the person being tested is asked to

look at a fixed target and move his/her head back and forth or up and down for short periods of time.

During rotary-chair tests, the computerized chair moves for the person being tested.

Less usfull than caloric test because it stimulates both the ear simultaneously.

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OPTOKINETIC TEST The person sits in front of a rotating drum with

alternate white and black vertical strips .

Nowdays a computerised horizontal bar with traking light has replaced a rotatory drum stimulation optokinetic test .

The nystagmus induced is recorded

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INVESTIGATIONSHEMATOLOGIC INVESTIGATIONS - CBC - CHEMICAL SCREENING LIKE BUN,ALBUMIN & GLOBULIN - T3 & TSH - FTA – ABSURINE ANALYSISRADIOLOGICAL STUDIES - MASTOID & INTERNAL ACOUSTIC CANAL VIEWS - CT SCAN - SKULL & CERVICAL SPINE RADIOLOGY

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INVESTIGATIONSOPTIONAL TESTS- -five hour glucose tolerance test - polycyclic tomograms of the petrous bone - ECG - EEG - Psychometric testing

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Nystagmus

Spontaneous Induced

When When When When When When WhenLooking focusing looking following head changing turningstraight on fixed sideways moving is in position the headahead spot object particular of head

position

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Induced nystagmus

Positional nystagmus Any nystagmus that occurs when the head is in position other than normal upright

Positioning nystagmusoccurs when change of head position and used to diagnose BPPV

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Differentiation of Peripheral and Central Vertigo Sign / Symptoms Pheripheral Central

Latency 2- 10 second none

Duration Stopes in 30 Sec or less Continuous for more than 1 minute

Fatiguability present absent

Adaptation disappears in 50 Sec Persist

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Differentiation of Peripheral and Central VertigoSign / Symptom Peripheral (Labyrinth) Central (Brainstem or

Cerebellum)

Vertigo Always present, Severe May be mild or Absent

Direction of spin Toward fast phase VariedDirection of fall Toward slow phase VariableDuration of Finite (minutes, days, May be chronicsymptoms weeks) but recurrentTinnitus and /or Often present Usually absentdeafnessAssociated central None Extremely commonabnormalitiesCommon causes Infection (labyrinthitis), Vascular, demyelinating,

Meniere's, neuronitis, neoplasmischemia, trauma, toxinDaroff R. B., ‘Faintness Syncope, Dizziness and vertigo IN Harrisons Principles of Internal Medicine, 14th Edition, 105

(Contd.)

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MANEGMENT OF

PERIPHERAL VERTIGO

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If Ménière is due to a secondary cause (ie, Ménière syndrome), primary first-line management is the diagnosis and treatment of the primary disease (eg, thyroid disease).

MEDICAL MANEGMENT- Vestibulosuppressants (eg, meclizine) Diuretics or diuretic-like medications (eg,

hydrochlorothiazide). Steroids

MANEGMENT OF MENIRE’S DISEASE

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MANEGMENT OF MENIRE’S DISEASE In an acutely vertiginous patient, management

is directed toward vertigo control.

Intravenous (IV) or intramuscular (IM) diazepam provides excellent vestibular suppression and antinausea effects.

Steroids can be given for anti-inflammatory effects in the inner ear.

IV fluid support can help prevent dehydration and replaces electrolytes.

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MANEGMENT OF MENIRE’S DISEASE

SURGICAL MANEGMENT-CONSERVATIVE SURGERY- If serviceable hearing

present.I. ENDOLYMPHATIC SAC DECOPMRESSIONII. SHUNT PROCEDURE – Between sac & mastoid cavity or

subarachnoid space.

DESTRUCTIVE SURGERY-If hearing is not serviceable.I. LABYRINTHECTOMYII. VESTIBULAR NEURECTOMY

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The Dix-Hallpike test, along with the patient's history, aids in the diagnosis of BPV.

MANEGMENT OF BPPV

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MANEGMENT OF BPPV TREATMENT- Medications-Antiemetic - Antihistaminic -Anticholinergic

The Canalith Repositioning Procedure (CRP)

Surgery

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Canalith Repositioning Procedure ( CRP ) The treatment of choice for BPPV. Also known as the Epley maneuver. The patient is positioned in a series of steps so as to slowly move the

otoconia particles from the posterior semicircular canal back into the utricle.

Takes approximately 5 minutes. The patient is instructed to wear a neck brace for 24 hours and to not

bend down or lay flat for 24 hours after the procedure. One week after the CRP, the Dix-Hallpike test is repeated.

If the patient does experience vertigo and nystagmus, then the CRP is repeated with a vibrator placed on the skull in order to better dislodge the otoconia.

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Canalith Repositioning Procedure ( CRP )

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THE T/T OF BPPV IS CRP MANEUVERS AS DESCRIBED BY SEMONT AND EPILEY FOR POSTERIOR CANAL AND HAMID AND LEMPERT FOR HORIZONTAL CANAL . SEMONT MANEUVER IS EFFECTIVE IN TREATING PC CUPOLITHIASIS, EPILEY FOR PC CANALITHIASIS, LEMPERT FOR HC CANALITHIASIS & HAMID FOR HC CUPULOLITHIASIS. LEMPERT AND HAMID MANEUVERS IN SOME CENTRE KNOWN AS BARBIQUE PROCEDURES

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SYNDROME CHARACTERIZED BY SOUND OR PRESSURE INDUCED VERTIGO

DEFINITIVE TREATMENT ISRESURFACING OR PLUGGING THE BONY DEFECT VIA MIDDLE FOSSA OR TRANSMASTOID APPROACH

PRESSURE EQUALIZING (PE) TUBE ,DIAMOX AND TOPAMAX TO CONTROL SYMPTOMS

DEHISCENCE OF SUPERIOR SEMICIRCULAR CANAL SYNDROME

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LARGE VESTIBULAR AQUEDUCT SYNDROME

DEVELOPMENTAL ANOMALY OF INNER EAR PRESENT WITH SUDDEN SENORINEURAL OR FLUCTUATING HEARING LOSS IN CHILDHOOD

DEFINITIVE T/T IS COCHLEAR IMPLANTS SYMPTOMS STABILZED WITH LOW SALT

DIET, HYDROCHLOROTHIAZIDE AND VESTIBULAR SUPPRESSANTS

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LARGE COCHLEAR AQUEDUCT SYNDROMES

CLINICAL,AUDIOLOGIC AND VESTIBULAR FINDING IN PATIENTS CONSISTENT WITH “HYDROPS”, ON THE SIDE IDENTIFIED BY CT

RESPOND TO T/T WITH DIAMOX AND/OR TOPAMAX

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Brandt-Daroff Exercises method of treating BPPV, usually used when the

office treatment fails. These exercises should be performed

for two weeks, three times per day for three weeks, twice per day.

In each time, one performs the maneuver as shown five times.

1 repetition = maneuver done to each side in turn (takes 2 minutes)

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Brandt-Daroff Exercises

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SURGICAL MANEGMENT OF BPPV

Singular neurectomy

Vestibular Neurectomy

Posterior Canal Plugging Procedure

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Posterior Canal Plugging ProcedureRecently developed procedure Replaced the singular neurectomy. A mastoidectomy is performed through an incision made

behind the ear. The balance center is then uncovered . The posterior semicircular canal is opened, exposing the

delicate membranous channel in which the crystalline debris is floating.

The canal is then gently, but firmly packed off with tissue so the debris can no longer move within the canal and strike against the nerve endings.

The canal is then sealed and the incision closed.

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MANEGMENT OF LABYRINTHITIS Bed rest & maintanance of hydration Antiemetic & antivertigo. Benzodiazepenes in case of sever vomiting & vertigo. Steroids Antibiotics in case of bacterial labyrinthitis Antiviral drugs- role is not well documented. Surgical- if it is secondary to middle ear disease requiring

surgical treatment. Antioxidents Vestibular rehabilitation exercises.

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MANEGMENT OF VESTIBULAR NEUROPATHY

Symptomatic

Steroids

Antibiotics in case of active middle ear disease.

Vestibular rehabilitation exercises

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EXERCISES IN VESTIBULAR

HABITUATION THERAPY

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EXERCISES IN BED : EYE MOVEMENTS

Looking up and then down

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Looking alternately left and right

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Convergence exercise

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EXERCISES IN BED : HEAD MOVEMENTS

Bending alternately forward and backward

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EXERCISES IN BED : HEAD MOVEMENTS

Turning alternatively to the left and then right

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EXERCISES IN SITTING POSITION

Shrugging and rotating shoulders

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Bending forward and picking up objects from the floor

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Turning head and trunk alternately to the left and the right

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EXERCISES IN STANDING POSITION

Changing from sitting to standing, initially with eyes open and then with the eyes closed

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Throwing a small (ping pong) ball in, an arc from hand to hand and following it with the eyes

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Throwing a small ball from hand to hand under the knee

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EXERCISES WHILE WALKING

Throwing and catching the ball while walking

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Walking around in the room with eyes open and closed

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Walking up and down a flight of stairs

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Playing any game involving bending, stretching and aiming with the ball

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Pharmacotherapy(Antivertigo drugs)

Vasodilators

Antiemetics

Labyrinthine sedatives

Anxiolytics

Diuretics

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Anti- emetics

Antihistamines Anti Phenothiazines MiscellaneousCholinergics

Large overlap between the effects produced by antihistamines, anticholinergics and phenothiazines.

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Phenothiazines(Prochlorperazine, Thiethylperazine)

Prochlorperazine is less sedating than some other phenothiazines but drowsiness still occurs

Also causes hypotension, Parkinsonian side effects--Betts T et al, Brit. J. Clin. Pharmac, 1991, 32, 455-8,

--Curley JWA, E N T Journal, 1984, 65, 555-560

“The drug which most commonly causes parkinsonism in general practice is Prochlorperazine”

--Chaplin S, Geriatric Medicine, 1989, Feb, 13-14

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Anxiolytics (Tranquilizers)(Benzodiazepines such as diazepam, Lorazepam)

No effect on the underlying vertigo

Helps patient endure the symptoms by allaying anxiety

Many side effects drowsiness and sedation, dependence and addiction abuse potential, psychomotor impairment, memory loss, interactions with alcohol

Harris T, Ear Nose Throat J, 1984, 65, 551-5

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Diuretics(e.g. Furosemide, Hydrochlorthiazide)

Used in vertigo and meniere’s disease

Reduce the volume of endolymph by promoting urine flow and reducing fluid retention.

Use mainly associated with electrolyte imbalance

Ludman H, Brit. Med. J., 1981, 282, 454-457, Harris T, Ear Nose Throat J, 1984, 65, 551-5

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Cinnarizine, Collin Dollery Therapeutic Drugs, C240-3, Godfraind T et al, Drugs of Today, 1982, XVIII(1), 27-42, Venkataraman S, Neurosciences Today, 1997, Vol. I, 3&4, 205-6, Norre M E, Crit Rev. Phy. Rehab. Med., 1990, 2,2,101-20

Labyrinthine Sedative With Antihistaminic action

Cinnarizine, Flunarizine, Cyclizine Drowsiness and blurred vision (Difficult for patients who

drive or operate machinery) Delay normal vestibular compensation process Cinnarizine and Flunarizine act via calcium antagonism,

unspecific action may cause side effects Weight gain & depression (serotonergic effects) Extrapyramidal symptoms (dopaminergic effects) G.I. upset

95Data on file

Betahistine

Trusted therapy for more than

41 million

Vertigo patients worldwide

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Betahistine - Chemistry

Histamine Betahistine

N

N

H

CH2CH2NH2

NCH2CH2NHCH3

Histamine analogue, can be given orally with no histamine like side effects

Van Cauwenberge P B, et al, Acta Otolaryngol, 1997, suppl. 526, 43-6, Venkataraman S, Neurosciences Today, 1998, II, 1 & 2, 56-8

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Betahistine : Pharmacokinetics

Oral administration Rapid and complete absorption Mean plasma half life :- 3-4 Hrs. Complete excretion via urine in 24 hours Very low plasma protein binding One metabolite (2-aminoethyl pyridine) is found

to be active

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Betahistine : Mode of Action

Vascular Effects Neurological Effects(in inner ear & brain) (in brain)

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H3-AUTORECEPTORS … CONTROLLING THE RELEASE OF HISTAMINE

Adapted Van Cauweneberge PB, Acta Otolaryngol, 1997, suppl. 526, 43-6, Venkataraman S, Neurosciences Today, 1998, II, 1 & 2, 56-8

H1 H2

H3 autoreceptor

Histaminergic Neuron

100 Venkataraman S, Neurosciences Today, 1998, II (1 & 2), 56-8

EFFECTS OF BETAHISTINE

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Betahistine - Vascular Effects

H3 autoreceptors antagonist H1 agonist

Inhibits autoregulation of histamine release

Venkataraman S, Neurosciences Today, 1998, II (1 & 2), 56-8

Improves cochlear microcirculation Improves cerebral / vertebrobasilar blood flow

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Blocks H3 heteroreceptors

Increases release of other neurotransmitters e.g. serotonin

Regulates firing activity of vestibular nuclei

Venkataraman S, Neurosciences Today, 1998, II (1 & 2), 56-8, Biswas A, Ind. J. Otolaryngol H N S, 1997, 49(2), 179-81

Betahistine - Neurological Effects

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Betahistine : Mode of actionBlocks

H3 heteroreceptors H3 autoreceptors

stimulates release of other neurotransmitter e.g.

serotonin

Stimulates release of histamine

Regulatory effect on vestibular nuclei

H1 receptor

Symptomatic relief of vertigo

Prophylactic effect of vertigo

improvement of cochlear & cerebral blood flow

direct stimulatory effect

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BETAHISTINE

Therapeutic Indications Vertigo Meniere’s Syndrome

Dosage Recommendations 24-48 mg /day

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Betahistine -Tolerance

No sedation

No gastric side effects

No anticholinergic effects

No extrapyramidal side effects

Bradoo RA et al, Ind. J. Otolaryngol HNS, 2000, 52(2), 151-8,Biswas A, Ind. J. Otolaryngol H N S, 1997, 49(2), 179-81

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Betahistine: No affinity for H2 receptors

H2 receptors predominate in stomach and control gastric secretion

Betahistine has no effect on H2 receptors.

Betahistine is generally free of gastric side effects

Betahistine, Collin Dollery Therapeutic Drugs, B 62-5Van Cauwenberge PB, Acta Otolaryngol, 1997, Suppl. 526, 43-6

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Betahistine

Contraindications - Not known

Precaution / Caution for useBetahistine, being a histamine analogue, should be used with caution in patients with pheochromocytoma, peptic ulcer, bronchial asthma, concurrent use of antihistamines

Bradoo RA et al, Ind. J. Otolaryngol HNS, 2000, 52(2), 151-8

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Betahistine

Contraindications - Not known

Precaution / Caution for useBetahistine, being a histamine analogue, should be used with caution in patients with pheochromocytoma, peptic ulcer, bronchial asthma, concurrent use of antihistamines

Bradoo RA et al, Ind. J. Otolaryngol HNS, 2000, 52(2), 151-8

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Betahistine No antagonistic effect on H1 receptors

Antihistamines block H1 receptors in brain, causing sedation or drowsiness

Betahistine, stimulates H1 receptors

Betahistine, does not slow down vestibular compensation, unlike antihistamines. Hence is suitable for use with vestibular habituation therapy.

Kirtane MV, Ind. J. Otolaryngol HNS, 1999, 51(2),27-36

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Betahistine - Summary Pharmacokinetics: Rapid and complete absorption after

oral route Pharmacology: It is a H1 agonist and H3 receptor

antagonist. It increases cochlear and cerebral blood flow and regulates firing activity of vestibular nuclei.

Dose: 24-48 mg /day Indication: vertigo, meniere’s syndrome Contraindications: not known Precaution for use: pheochromocytoma, peptic ulcer,

bronchial asthma

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1 Vertigo