Post on 29-Aug-2014
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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
e
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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
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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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EXERCISES IN SITTING POSITION
Bending forward and picking up objects from the floor
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EXERCISES IN SITTING POSITION
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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EXERCISES IN STANDING POSITION
Throwing a small (ping pong) ball in, an arc from hand to hand and following it with the eyes
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EXERCISES IN STANDING POSITION
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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EXERCISES WHILE WALKING
Walking around in the room with eyes open and closed
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EXERCISES WHILE WALKING
Walking up and down a flight of stairs
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EXERCISES WHILE WALKING
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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