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BIOLOGICAL BASIC OF EQUILIBRIUM DISEASE
BAMBANG UDJI DJOKO RIANTO
EAR, NOSE & THROAT DEPARTMENT
DR. SARDJITO GENERAL HOSPITAL/FACULTY OF MEDICINE GADJAH MADA UNIVERSITY
YOGYAKARTA2007
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REFFERENCES
1. Simpson, J.F.,Robin, I.G., 1993. Ballantyne,J.C. & Grove, J. A synopsis of
otolaryngology.
2. Boies,L.R., Hilger,J.A. and Priest,R.E., 2000. Fundamentals of otolaryngology. A
textbook of ear, nose and throat disease.
3. Bailey, BJ., Calhoun, KH., Healy, GB., Pillsbury, HC., Johnson, JT., et al. 2001,
2006. Head & neck surgery otolaryngology 3rd (eds).4. Becker W., Naumann H.H., Pfaltz C.R. 1993. Ear, Nose, and Throat Disease.
5. Katz. 2001. Hand book of clinical audiology.
6. van der Velde G.1999.M. Benign paroxysmal positional vertigo: Background and
clinical presentation. J Can Chiropr Assoc ; 43(1)
7. Neuhauser & Hannelore.2007.Epidemiology of vertigo. Neuro-ophthalmology and
neuro-otology. Current Opinion in Neurology. 20(1):40-46
8. Furman, JM . 2007. Pathophysiology, etiology, and differential diagnosis of vertigo.
The literature review .
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PHYSIOLOGY OF EQUILIBRIUM
Equilibrium is maintained primarily by thevestibular part of the labyrinth
It is aided by eyes and propioceptivesenses distributed all over the body
Final controlling of equilibrium is done by
the cerebellum and cerebrum which areconnected with each other and all the end-organs mentioned above.
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INTERACTING COMPONENTS OF THE VESTIBULAR
SYSTEM (GRAY, 1992)
.
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TERMINOLOGY IMBALANCES
(DHILLON, 1999)
Vertigo :an illusion of rotarymovement,worse in the dark.Causes byperipheral vest,disease, rarely central
vest. Lightheadedness : a feeling of fainting.
Causes by CV,ototoxic drugs,psychiatriccondition)
Unsteadiness; difficulty with gait, atendency to fallor veer to one side(ageingprocess)
Loss of conciousness: usually clear out
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OTOLOGICAL CAUSES OF IMBALANCE (DHILLON, 1999)
Middle ear disease
trauma
BPPV (Benign paroxysmal positionalvertigo)
Meniere’s didease
labyrinthitis ototoxic drugs
otosclerosis
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CAUSES OF PERIPHERAL VERTIGO
1. Benign positional vertigo 2. Vestibular neuronitis
3. Labyrinthitis 4. Meniere's disease 5. Ramsay-Hunt syndrome 6. Ototoxic drugs e.g., Aminoglycosides 7. Air travel 8. Trauma 9. Motion sickness
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CRITERION VERTIGO VESTIBULER & BPPVDIAGNOSIS
Vestibuler vertigo:
1. Spontaneous positional vertigo2. Positional vertigo
3. Recurrent dizziness + nausea & either oscillopsia/imbalance
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BPPV:
20-30% cause vestibular vertigoepidemiology in population not certainly known
(Brevern et al ., 2007)
incidence: 10-100/ 100.000/ yearincidence increase with age
- range: 11-84 yo
- uncommon in children- majority: no antecedent history
(Cohrane review, 2004)
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n Total % (95% CI) % women % men
Lifetime prevalence
BPPV
Severe BPPV
80
69
2.4 (1.9-3.0)
2.1 (1.6-2.6)
3.2
2.9
1.6
1.3
1 y prevalence BPPV
13-39 y
40-59 y
≥ 60 y
53
7
21
25
1.6 (1.3-2.1)
0.5 (0.2-1.0)
1.7 (1.1-2.6)
3.4 (2.5-5.0)
2.3
0.7
2.5
4.2
0.9
0.3
0.7
3.4
4 weeks prevalence BPPV 23 0.7 (0.5-1.1) 1.0 0.4
Population incidence (1 y) BPPV 20 0.6 (0.4-0.9) 0.8 0.4
Table 1. Population prevalence & incidence of BPPV
Severe BPPV: leading to medical consultation, interruption of daily activities or
sick leave
(Brevern et al ., 2007) 12
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Table 2. Duration episodes in 80 samples
Duration of episode %
< 1 week 45.0
1-2 weeks 11.2
2-4 weeks 12.5
4-12 weeks 18.8
> 12 weeks 12.5
Duration of the last episode of BPPV
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(Brevern et al ., 2007)
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Table 3. Clinical characteristics in 80 sample of BPPV
Characteristics of BPPV %
Rotational vertigo 86
Oscilopsia 31
Nausea 33
Vomiting 14
Imbalance 49
Awakening due to BPPV 49Fear of falling 36
Fall due to BPPV 1
Precipitating head movement
Turning over in bed 85
Lying down 74
Rising up from supine position 58
Bending forward 55
Reclining the head 4114
(Brevern et al ., 2007)
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BPPV Control group OR (95% CI) multivariate
Women 74 51 2.4 (1.3-4.5) 1.8 (0.9-3.4)
Age (y)
18-39
40-59
60+
12
40
48
43
38
19
Secondary school ed.
Higher level
Middle level
Lower level
28
29
43
39
35
26
1
1.0 (0.5-2.1)
1.3 (0.7-2.7)
Co-morbidity
depression
hypertension
high blood lipid
diabetes
coronary HD
stroke
14
52
55
14
18
10
9
22
24
5
5
1
1.4 (0.6-3.2)
2.2 (1.2-4.0)
2.5 (1.4-4.4)
1.6 (0.7-3.8)
2.1 (0.9-4.6)
6.9 (1.8-19.2)
1.9 (1.0-3.6)
2.0 (1.1-3.7)
4.7 (2.5-13.8)
Body mass index
(kg/m2)
< 25
25- < 30 (overweight)
30+ (obese)
32
52
16
58
33
9
1
2.4 (1.3-4.6)
2.2 (0.9-5.1)
Smoking (current daily) 10 27 0.5 (0.2-1.1)
Migraine 34 10 7.5 (3.9-14.2) 8.6 (4.3-17.3)
Table 4. Co-morbidity & socioepidemographic factors associated with prevalence
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AETIOLOGY BPPV
Still under debate
Labyrinthine trauma
Stapes surgeryViral neurolabyrinthitis
Chronic supurative otitis mediaMastoiditis
Vestibular neuronitis
(Velde, 1999)
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Tabel 5. Comparison of two pathophysiological theories for BPPV
Theory Cupulolithiasis Canalithiasis
Originator Schuknecht, 1969 Hall,et al.,1979
Location of lesion Posterior semicircular canal
(PSC)
PSC
Proposed
pathophysiology
Cupulolithiasis (basophilic
densities adhered to the PSC
cupula) alter the specific
gravity of the cupula making
it sensitive to gravitational
changes
Canalith (free-floating psc
endolympathic densities)
create a hydrodynamic drag
which displaces & stimulates
the cupula
Supportive evidence 1. Histological observation of
cupular basophilic
densities2. Reports of positive
responses to physical
treatment inspired by this
pathophysical theory
1. Operative observation of
free-floating
endolymphatic densities2. Reports of positive
responses to physical
treatment inspired by this
pathophysical theory
(Velde, 1999)
E
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KRITERIA DIAGNOSIS BPPV:
a. Recurrent vestibuler vertigo
b. Duration of attack always < 1 minute
c. Symptoms invariably provoked by the followingchanges of head position:
- lying down, or- turning over in the supine position- or at least 2 of the following manouvres:
- reclining the head- rising up from supine position- bending forward
d. Not attributable to another disorder(Brevern et al ., 2007)
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Duration of symptom in relation to aetiology(Dhillon, 1999)
Second
Minutes tohours
Hours to days
BPPV
Cervical spondilosys
Postural hypotension
Meniere’s disease
Labyrinthitis
Labyrinthine failure
Ototoxicity
Central vestibular disease
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DIX-HALLPIKE MANEUVER
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TREATMENT BPPV
Non surgicalSpontaneous resolution within several monthsVestibular habituation position of maximal stimulationwith the affected ear in the dependent positionLiberatory maneuvers displace the heavy debris on the
cupula away from the ampula of PCS(Young & Quin, 1994)
Expectant observation self limiting natural history of
BPPVMedicationPhysical treatment inspired by canalithiasis theoryOperative procedures for intractable case
(Velde, 1999)
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Hain, 2007:
No active tretment (wait & see)- modification daily activities- use 2 pillows at night- avoid sleeping on the bedside- get up slowly & sit on the edge of the bed for a minute- avoid bending down to pick up things, extending
the head, such as to get something out of a cabinet
Motion sickness medications for nausea associated with
BPPV
Office treatment of BPPV:- The Epley and Semont maneuvers
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EPLEY
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Reclined head hanging 45 degree turn
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Rotate 45 degrees contralateral
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Head and body rotated to 135 degrees from
supine
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Keep head turn and to sitting
Turn forward chin down 20 degrees
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SEMONT
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BRANDT & DAROFF EXCERCISES
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RESULTS
EPLEY
100% with multiple maneuvers,
Herdmann: 90%
SEMONT 84% after one tx, 93% after two tx
BRANDT & DAROFF 98% after 3-14 days of tx
(Herdmanet al
., 1993)
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Thank you
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Epley CPR procedure
Canaliths theory
Head maneuvers and vibration move particles Target canal determined
Sum of latency and duration
Estimate of 90 degree time Premedicated
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