PERIFERAL VERTIGO

BAMBANG UDJI DJOKO RIANTO

EAR, NOSE & THROAT DEPARTMENT

DR. SARDJITO GENERAL HOSPITAL/
FACULTY OF MEDICINE GADJAH MADA UNIVERSITY
YOGYAKARTA
2013

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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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 Equilibrium is maintained primarily by the
vestibular part of the labyrinth
 It is aided by eyes and propioceptive senses
distributed all over the body
 Final controlling of equilibrium is done by the
cerebellum and cerebrum which are connected
with each other and all the end-organs
mentioned above.

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 .

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 Vertigo: an illusion of rotary movement, worse in
the dark, caused by peripheral vest,disease, rarely
central vest.
 Lightheadedness : a feeling of fainting. Caused by
CV disturbance, ototoxic drugs, psychiatric
condition)
 Unsteadiness; difficulty with gait, a tendency to
fallor veer to one side(ageing process)
 Loss of conciousness: usually clear out history
(neurological, cardiac arythmia)

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 Middle ear disease
 trauma
 BPPV
 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 VESTIBULAR & BPPV DIAGNOSIS

vestibular vertigo:

1. Spontaneous positional vertigo

2. Positional vertigo
3. Recurrent dizziness + nausea & either oscillopsia/
imbalance

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 BPPV:

20-30% causes vestibular vertigo

epidemiology in population not certainly known

(Brevern et al., 2007)

incidence: 10-100/ 100.000/ year

incidence increase with age
- range: 11-84 yo
- uncommon in children
- majority: no antecedent history
(Cohrane review, 2004)

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 Table 1. Population prevalence & incidence of BPPV

n Total % (95% CI) % women % men

Lifetime prevalence
BPPV 80 2.4 (1.9-3.0) 3.2 1.6
Severe BPPV 69 2.1 (1.6-2.6) 2.9 1.3

1 y prevalence BPPV 53 1.6 (1.3-2.1) 2.3 0.9

13-39 y 7 0.5 (0.2-1.0) 0.7 0.3
40-59 y 21 1.7 (1.1-2.6) 2.5 0.7
≥ 60 y 25 3.4 (2.5-5.0) 4.2 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

Severe BPPV: leading to medical consultation, interruption of daily activities or

sick leave
(Brevern et al., 2007)
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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

(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 49
Fear 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 41
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(Brevern et al., 2007)
Table 4. Co-morbidity & socioepidemographic factors associated with prevalence BPPV
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 12 43
40-59 40 38
60+ 48 19
Secondary school ed.
Higher level 28 39 1
Middle level 29 35 1.0 (0.5-2.1)
Lower level 43 26 1.3 (0.7-2.7)

Co-morbidity
depression 14 9 1.4 (0.6-3.2)
hypertension 52 22 2.2 (1.2-4.0) 1.9 (1.0-3.6)
high blood lipid 55 24 2.5 (1.4-4.4) 2.0 (1.1-3.7)
diabetes 14 5 1.6 (0.7-3.8)
coronary HD 18 5 2.1 (0.9-4.6)
stroke 10 1 6.9 (1.8-19.2) 4.7 (2.5-13.8)
Body mass index (kg/m2)
< 25 32 58 1
25- < 30 (overweight) 52 33 2.4 (1.3-4.6)
>30 (obese) 16 9 2.2 (0.9-5.1)

Smoking (current daily) 10 27 0.5 (0.2-1.1)

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Migraine 34 10 7.5 (3.9-14.2) 8.6 (4.3-17.3)
 AETIOLOGY BPPV

Still under debate

Labyrinthine trauma
Stapes surgery
Viral neurolabyrinthitis
Chronic supurative otitis media
Mastoiditis
Vestibular neuronitis

(Velde, 1999)
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Tabel 5. Comparison of two pathophysiological theories for BPPV
Theory Cupulolithiasis
Originator Schuknecht, 1969
Location of lesion Posterior semicircular canal
(PSC)
Proposed Cupulolithiasis (basophilic
pathophysiology densities adhered to the PSC
cupula) alter the specific gravity
of the cupula making it sensitive
to gravitational changes
Supportive evidence 1. Histological observation of
cupular basophilic densities
2. Reports of positive
responses to physical
treatment inspired by this
pathophysical theory
Canalithiasis
Hall,et al.,1979
PSC
Canalith (free-floating psc
endolympathic densities) create
a hydrodynamic drag which
displaces & stimulates the
cupula
1. Operative observation of
free-floating endolymphatic
densities
2. Reports of positive
responses to physical
treatment inspired by this
pathophysical theory
(Velde, 1999)
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KRITERIA DIAGNOSIS BPPV:

a.Recurrent vestibular vertigo

b.Duration of attack always < 1 minute

c. Symptoms invariably provoked by the following

changes 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) 18
 Duration of symptom in relation to aetiology
(Dhillon, 1999)

 Second  BPPV
 Cervical spondilosys
 Postural hypotension

 Meniere’s disease
 Minutes to
hours
 Labyrinthitis

 Labyrinthine failure
 Hours to days  Ototoxicity
 Central vestibular disease

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DIX-HALLPIKE MANEUVER

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 TREATMENT BPPV

Non surgical
Spontaneous resolution within several months
Vestibular habituation  position of maximal stimulation
with the affected ear in the dependent position
Liberatory maneuvers  displace the heavy debris on the
cupula away from the ampula of PCS
(Young & Quin, 1994)

Expectant observation  self limiting natural history of

BPPV
Medication
Physical treatment inspired by canalithiasis theory
Operative 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

(Herdman et 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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