33.biological basic of equilibrium

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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 .

http://patients.uptodate.com/author.asp?ID=848394

http://patients.uptodate.com/author.asp?ID=848394



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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



OTOLOGICAL CAUSES OF IMBALANCE (DHILLON, 1999)

Middle ear disease

trauma

BPPV (Benign paroxysmal positionalvertigo)

Meniere’s didease

labyrinthitis ototoxic drugs

otosclerosis



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



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



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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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




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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33.biological basic of equilibrium

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