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Vertigo

The document discusses various types of dizziness and vertigo including their causes, anatomy, physiology, diagnosis, and investigations. It covers peripheral, central, and non-vestibular causes of vertigo and describes tests used in diagnosis like caloric, rotation, and optokinetic tests. The document provides detailed information on evaluating and classifying different types of vertigo.

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0% found this document useful (0 votes)
194 views111 pages

Vertigo

The document discusses various types of dizziness and vertigo including their causes, anatomy, physiology, diagnosis, and investigations. It covers peripheral, central, and non-vestibular causes of vertigo and describes tests used in diagnosis like caloric, rotation, and optokinetic tests. The document provides detailed information on evaluating and classifying different types of vertigo.

Uploaded by

jetone472
Copyright
© Attribution Non-Commercial (BY-NC)
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF, TXT or read online on Scribd

Balance the imbalance DIAGNOSIS & MANAGEMENT OF VERTIGO - PRESENT SENARIO

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

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

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 .

ANATOMY AND PHYSIOLOGY*

*RELATED TO VERTIGO
5

Utricular nerve e

ry

ve
10

Central projection of peripheral vestibular system

11

12

CAUSES OF VERTIGO

13

What causes vertigo?


Contradictory
The

information from

vestibular system (ears) visual system (eyes)

2The The

Proprioceptive system (muscles, joints)

14

Causes of Vertigo
PERIPHERAL Menieres disease Labyrinthitis Vestibular neuropathy BPPV Trauma CENTRAL- referred to mnemonic VERTIGO

15

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

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
16

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

17

O OULAR PATHOLOGY- weakness of extra ocular muscles .

Vertigo: Traditional Classification


Peripheral (arises Vestibular

in vestibule)

Intermediate
(arises

in vestibular nerve)
Central in vestibular nuclei)

Vertigo (arises

Non-vestibular
(arises
18

outside the vestibular system)

19

Sites of Vertigo

Physiology of Peripheral Vertigo


apparatus consist of semicircular canal - utricle - saccule All these have sensory hair cells having stereocilia arranged in ascending fashion. The longest steriocilia is k/a Kinocilia. Movement of steriocilia towards kinocilia- Stimulation Movement of steriocilia opposite to kinocilia- Inhibition
Vestibular

20

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.
21

Causes of Peripheral Vertigo


Benign

Paroxysmal Positional Vertigo

Menieres

Disease

Labyrinthitis

Head

Injuries & Surgical Trauma


Vertigo

Pressure

22

Causes of Intermediate Vertigo


Vestibular Acoustic Drugs

neuronitis

neuroma

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

23

Causes of Central Vertigo


VBI

(Vertebrobasilar Insufficiency)

Arteriosclerosis Cervical

Spondylosis injuries of Neck

Whiplash Brain
24

Tumors

Non-Vestibular Causes of Vertigo


Ocular

vertigo

Head injuries Epilepsy

Anemia Cardiovascular

Multiple sclerosis
Hypoglycemia Migraine

(orthostatic hypotension)
Cerebrovascular

disorders
Psychogenic Brain
25

tumors

Another classification of vertigo


Paroxysmal

Vertigo - sudden attack comes on quickly, lasts for a short time single attack - sudden intense attack fading away slowly vertigo - not severe

The

Chronic

Positional

vertigo - occurs following sudden movements of head in certain positions


spells - lasting a few seconds occurring irregularly

Dizzy
26

27

DIAGNOSIS OF VERTIGO

28

29

Medical History
Description

of symptoms by patient of vertigo attacks

Classification

(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


30

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

Vestibular Function Tests


Vestibulo

spinal reflex
test test test Sikatani test

Romberg

Unterberger Modified

Babinski-weill Barany

Pointing test

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

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

32

33

Patient closes eyes and stretches arms out in front

Walks on spot for a minute


The knees raised as high as possible Patients with vertigo will start to turn his axis in particular direction
34

BARANYS

Deviation to one side in pointing occurs in patients with vertigo

35

Babinsky- Weill Test


Patient closes his eyes and takes 5 steps forward and 5 steps back for 30 seconds

36

Patient with vertigo starts to walk in a star shape

FITZGERALD- HALLPIKE / BITHERMAL CALORIC TEST


Patient in supine position with head flexed at 30 with horizontal. Ear is irrigated with water at 44 C & 30 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

37

OTHER CALORIC TESTS


KOBRAKS/

COLD CALORIC TEST- Position similar to bithermal test with irrigation with 10-15cc of ice cold water. CALORIC TEST- Air at different temperature like 17.5 C,45.5 C is passed into ear & nustafmus is noted. 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 .

AIR

DUNDAS

38

39

FISTULA TEST
Pressure

is increased in EAC with Siegles 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 Hanneberts Sign is seen in Menieres disease and Congenital syphilis. FALSE NEGATIVE TEST- Seen in cases of dead labyrinth
40

ELECTRONYSTAGMOGRAPHY
ENG

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 .

41

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: Patients ears are stimulated 2x each with warm and cool air or water

42

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.

43

OPTOKINETIC TEST
The

person sits in front of a rotating drum with alternate white and black vertical strips . a computerised horizontal bar with traking light has replaced a rotatory drum stimulation optokinetic test . nystagmus induced is recorded

Nowdays

The

44

INVESTIGATIONS
HEMATOLOGIC INVESTIGATIONS - CBC - CHEMICAL SCREENING LIKE BUN,ALBUMIN & GLOBULIN - T3 & TSH - FTA ABS URINE ANALYSIS RADIOLOGICAL STUDIES - MASTOID & INTERNAL ACOUSTIC CANAL VIEWS - CT SCAN - SKULL & CERVICAL SPINE RADIOLOGY
45

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

46

Nystagmus
Spontaneous
When Looking straight ahead When When focusing looking on fixed sideways spot When following moving object When head is in particular position

Induced
When When changing turning position the head of head

47

Induced nystagmus
Positional

nystagmus Any nystagmus that occurs when the head is in position other than normal upright
nystagmus occurs when change of head position and used to diagnose BPPV

Positioning

48

Differentiation of Peripheral and Central Vertigo


Sign / Symptoms
Latency Duration

Pheripheral
2- 10 second Stopes in 30 Sec or less

Central
none Continuous for more than 1 minute absent Persist

Fatiguability Adaptation

present disappears in 50 Sec

49

(Contd.)

Differentiation of Peripheral and Central Vertigo


Sign / Symptom Vertigo Direction of spin Direction of fall Duration of symptoms Tinnitus and /or deafness Associated central abnormalities Common causes Peripheral (Labyrinth) Central (Brainstem or Cerebellum)

Always present, Severe May be mild or Absent Toward fast phase Varied Toward slow phase Variable Finite (minutes, days, May be chronic weeks) but recurrent Often present Usually absent None Infection (labyrinthitis), Meniere's, neuronitis, ischemia, trauma, toxin Extremely common Vascular, demyelinating, neoplasm

50

Daroff R. B., Faintness Syncope, Dizziness and vertigo IN Harrisons Principles of Internal Medicine, 14th Edition, 105

MANEGMENT OF
PERIPHERAL VERTIGO
51

MANEGMENT OF MENIRES DISEASE


If Mnire is due to a secondary cause (ie, Mnire 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
52

MANEGMENT OF MENIRES 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.

53

MANEGMENT OF MENIRES DISEASE


SURGICAL MANEGMENTCONSERVATIVE SURGERY- If serviceable hearing
I. II.

present. ENDOLYMPHATIC SAC DECOPMRESSION SHUNT PROCEDURE Between sac & mastoid cavity or subarachnoid space.

DESTRUCTIVE SURGERY-If hearing is not serviceable.


I. II.
54

LABYRINTHECTOMY VESTIBULAR NEURECTOMY

MANEGMENT OF BPPV

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

55

MANEGMENT OF BPPV
TREATMENT

Medications-Antiemetic - Antihistaminic -Anticholinergic The Canalith Repositioning Procedure (CRP) Surgery


56

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.

57

Canalith Repositioning Procedure

( CRP )

58

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 59

60

61

62

DEHISCENCE OF SUPERIOR SEMICIRCULAR CANAL SYNDROME


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
63

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
64

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

65

66

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)
67

Brandt-Daroff Exercises

68

SURGICAL MANEGMENT OF BPPV


Singular

neurectomy
Neurectomy

Vestibular Posterior

Canal Plugging Procedure

69

Posterior Canal Plugging Procedure


Recently 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.
70

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.
71

MANEGMENT OF VESTIBULAR NEUROPATHY


Symptomatic
Steroids Antibiotics Vestibular
72

in case of active middle ear disease. rehabilitation exercises

EXERCISES IN
VESTIBULAR HABITUATION THERAPY

73

EXERCISES IN BED : EYE MOVEMENTS

Looking up and then down


74

Looking alternately left and right

75

Convergence exercise
76

EXERCISES IN BED : HEAD MOVEMENTS

Bending alternately forward and backward


77

EXERCISES IN BED : HEAD MOVEMENTS

Turning alternatively to the left and then right

78

EXERCISES IN SITTING POSITION

Shrugging and rotating shoulders


79

EXERCISES IN SITTING POSITION

Bending forward and picking up objects from the floor


80

EXERCISES IN SITTING POSITION

Turning head and trunk alternately to the left and the right
81

EXERCISES IN STANDING POSITION

Changing from sitting to standing, initially with eyes open and then with the eyes closed
82

EXERCISES IN STANDING POSITION

Throwing a small (ping pong) ball in, an arc from hand to hand and following it with the eyes
83

EXERCISES IN STANDING POSITION

Throwing a small ball from hand to hand under the knee

84

EXERCISES WHILE WALKING

Throwing and catching the ball while walking


85

EXERCISES WHILE WALKING

Walking around in the room with eyes open and closed


86

EXERCISES WHILE WALKING

Walking up and down a flight of stairs


87

EXERCISES WHILE WALKING

Playing any game involving bending, stretching and aiming with the ball
88

Pharmacotherapy (Antivertigo drugs)


Vasodilators
Antiemetics Labyrinthine Anxiolytics Diuretics

sedatives

89

Anti- emetics
Antihistamines Anti Phenothiazines Miscellaneous Cholinergics

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

90

Phenothiazines (Prochlorperazine, Thiethylperazine)


Prochlorperazine

is less sedating than some other phenothiazines but drowsiness still occurs
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

Also

The

drug which most commonly causes parkinsonism in general practice is Prochlorperazine


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

91

Anxiolytics (Tranquilizers)
(Benzodiazepines such as diazepam, Lorazepam)
No

effect on the underlying vertigo patient endure the symptoms by allaying anxiety

Helps Many

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

92

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

Diuretics
(e.g. Furosemide, Hydrochlorthiazide)
Used

in vertigo and menieres disease

Reduce

the volume of endolymph by promoting urine flow and reducing fluid retention. mainly associated with electrolyte imbalance

Use

Ludman H, Brit. Med. J., 1981, 282, 454-457, Harris T, Ear Nose Throat J, 1984, 65, 551-5
93

Cinnarizine, Flunarizine, Cyclizine

Labyrinthine Sedative With Antihistaminic action

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
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

94

Betahistine
Trusted therapy for more than

41 million
Vertigo patients worldwide

95

Data on file

Betahistine - Chemistry
Histamine
N

Betahistine
CH2CH2NH2 CH2CH2NHCH3

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

96

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


metabolite (2-aminoethyl pyridine) is found to be active

One

97

Betahistine : Mode of Action


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

98

H3-AUTORECEPTORS CONTROLLING THE RELEASE OF HISTAMINE


Histaminergic Neuron

H3 autoreceptor

H1
99

H2

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

EFFECTS OF BETAHISTINE

100

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

Betahistine - Vascular Effects


H3 autoreceptors antagonist Inhibits autoregulation of histamine release H1 agonist

Improves cochlear microcirculation Improves cerebral / vertebrobasilar blood flow


101

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

Betahistine - Neurological Effects


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

102

Betahistine : Mode of action


Blocks H3 heteroreceptors stimulates release of other neurotransmitter e.g. serotonin H3 autoreceptors Stimulates release of histamine direct stimulatory effect Regulatory effect on vestibular nuclei H1 receptor improvement of cochlear & cerebral blood flow Symptomatic relief of vertigo Prophylactic effect of vertigo

103

BETAHISTINE
Therapeutic Indications
Vertigo Menieres

Syndrome

Dosage Recommendations
24-48

mg /day

104

Betahistine -Tolerance
No
No

sedation
gastric side effects

No
No

anticholinergic effects
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
105

Betahistine: No affinity for H2 receptors


H2

receptors predominate in stomach and control gastric secretion


has no effect on H2 receptors. is generally free of gastric side

Betahistine Betahistine

effects

Betahistine, Collin Dollery Therapeutic Drugs, B 62-5 Van Cauwenberge PB, Acta Otolaryngol, 1997, Suppl. 526, 43-6
106

Betahistine
Contraindications - Not known

Precaution /

Caution for use

Betahistine, 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

107

Betahistine
Contraindications - Not known

Precaution /

Caution for use

Betahistine, 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

108

Betahistine No antagonistic effect on H1 receptors


Antihistamines

block H1 receptors in brain, causing sedation or drowsiness


stimulates H1 receptors

Betahistine, Betahistine,

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

109

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

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. 24-48 mg /day vertigo, menieres syndrome

Dose:

Indication:

Contraindications:
Precaution

not known

for use: pheochromocytoma, peptic ulcer, bronchial asthma

110

111

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