Peripheral vestibular disorders

1. PERIPHERAL VESTIBULAR
DISORDERS
PRESENTOR : KANICK COSTANTINE
29/07/2019

2. OUTLINE
Introduction.
Vestibular anatomy and function.
Epidemiology.
Clinical classification of PVDs
Etiology
Pathogenesis.
Diagnosis and management of PVDs
Examples Peripheral Vestibular Disorders
Diagnostic workout
Treatment

3. INTRODUCTION
• Peripheral vestibular disorders (PVD) include pathology of inner ear
vestibular structures as well as vestibular portion of the eighth cranial
nerve.
• Such pathology diminishes available sensory information regarding head
position and movement.
• Central vestibular disorders(CVD) involve the vestibular nucleus complex
and its second order neural pathways ,cerebellum and the vestibular cortex
• Pathology of the central vestibular structures affects integration and
processing of sensory input from the vestibular, visual and somatosensory
systems.

4. PERIPHERAL VESTIBULAR
SYSTEM
• Includes the vestibular sensory end-organs of the three semi-
circular canals (SCCs) , the otolithic organs (utricle and
saccule) and the vestibular nerve.
• It is housed within the right and left inner ears.
• The bony labyrinth is filled with a fluid called perilymph (high
concentration of sodium ions).
• The membranous labyrinth, found suspended inside the bony
labyrinth, contains a fluid called endolymph (high concentration
of potassium ions).

6. • Cristae is a group of hair cells located in the ampullated ends of
the three semicircular canals, it detects angular acceleration of
the head
• Maculae is a group of hair cells located in utricle and saccule, it
detects linear acceleration of the head
• The nerve impulses generated by hair cells in the maculae and
cristae are picked by vestibular nerve
The peripheral vestibular system ct

8. How ssc sense rotation
•When the head is
turned, the
membranous
labyrinth moves
with it, but the
endolymph fluid in the
semicircular canal
has an inertia mass
that tends to oppose
the turning motion.

9. • This causes pressure
build up across the
cupula, in turn deflects
the hair cells that are
attached to the base of
the cupula, generating
an impulse that is sent
along the nerve
pathways to the brain
about direction and
speed of head
movement.

10. •As the cupula is
deflected, the
stereocilia bend either
toward the kinocilium
causing an increase in
firing rate of the
vestibular nerve, or
they move away from
kinocilium, decreasing
the firing.

11. How otolith organs sense linear motion
•When we bend down or move forward, the
statoconia embedded on the otolithic membrane
will causes a relative drag or resistance to
motion due to inertia.
•This action in turn deflects the hair cells that
are attached to the base of the otolithic
membrane, causing them to send impulses
along the nerve pathways to the brain about
linear (vertical or horizontal) or gravitational
(tilt or lean) changes.

13. •Nerve fibers from the crista and the
maculae send movement-related
information to brain via the superior and
inferior vestibular nerves.
•The superior vestibular nerve sends
information from the lateral and superior
semi-circular canals, and the utricle.
•The inferior vestibular nerve sends
information from the posterior semi-circular
canal and saccule.

14. Central pathways
• Electrical activity generated within the inner
ear travels along the vestibular nerve to the
central vestibular nuclei of the brainstem,
forming second-order neuronal pathways that
become:
-the vestibulo-ocular reflex (VOR),
-the vestibulospinal tracts,
-the vestibulocerebellar tracts

15. Epidemiology
The incidence of peripheral vestibular disorders is not well
known.
One large epidemiological study estimates that as many as
35% of adults aged 40 years or older in the United
States have experienced some form of vestibular
dysfunction).
( Agrawal Y etal in 2009)
In patients aged <50yrs peripheral vestibular disorders are
more likely to be responsible for the dizziness whereas in
older patients central disturbances are more common
.

16. Clinical classification
• Sudden onset unilateral disorders
• Sudden onset bilateral disorders
• Gradual onset unilateral disorders
• Gradual onset bilateral disorders
• Unilateral fluctuating disorders

17. AETIOLOGY PVDs
•Sudden onset unilateral disorders
Vestibular neuronitis
Trauma both iatrogenic & accidents
Unilateral ototoxicity
Vascular lesion
Cholesteatoma

18. Aetiology ct
• Sudden onset bilateral disorders
Ototoxicity
Labyrinthitis from meningitis
Bilateral trauma.

19. Gradual onset unilateral disorders
Eighth nerve neoplasm

20. Gradual onset bilateral disorders
•Aging
•Ototoxicity
•Autoimmune disease
•Syphilis
•Degenerative disorders [vestibular neuronitis].

21. Unilateral fluctuating disorders
 Benign paroxysmal positional vertigo
Meniere’s disease

22. Unilateral Disorders of Sudden Onset
pathopysiology
A lesion involving one labyrinth reduces the action
potential going to the CNS from the affected
labyrinth.
This results in a reduction of activity in the ipsilateral
vestibular nucleus and a reduction in the tonic
activity of oculomotor nerves that produce contra
lateral eye movements.

23. Unilateral Disorders of Sudden Onset…
If the right labyrinth is affected, this results in
fast phase nystagmus towards the left and a
sensation of clockwise rotation and falling to the
right.
The severity of symptoms depends on how much
labyrinthine function is lost and how much central
compensation has taken place since the lesion.

24. Unilateral Disorders of Sudden Onset…
In severe losses of function, changes in
vestibular nucleus activity spill over to other brain
stem nucleus and nausea, vomiting, sweating,
and bradycardia also occur.
Initially nystagmus is present in all positions of
gaze.
• It is always suppressed by fixation.
• Is fastest when looking away from the lesion.
• Least when looking towards the lesion.

25. Unilateral Disorders of Sudden Onset…
With time, the vegetative symptoms of vertigo
and nausea diminish, and nystagmus first
disappears in gaze toward the lesion,
later in central gaze, and finally also in gaze
away from the lesion.
Nystagmus may still be present in the dark or
with closed eyes for a longer period of time.

26. BILATERAL VESTIBULAR LESIONS {Sudden Onset }
• In bilateral vestibular lesions, there is symmetrical
reduction of vestibular sensory inputs to the brain
stem.
• Patients commonly complain of visual disturbances
instead of vertigo.

27.  Symptoms after a partial bilateral loss usually
disappear in a few days due cerebellar adjustment
mechanisms.
With severe loss of bilateral vestibular function, the
vestibuloocular reflexes stops working and patients
experience severe visual disturbances with head
movements.
This condition, called oscillopsia, refers to an
oscillating environment during head movements.

28. Unilateral disorders of gradual
onset
Lesions of gradual onset may not produce
severe symptoms because the
vestibulooculomotor reflex is continuously
monitored and adjusted to perform its task of
compensatory eye movements for head
movements.
Gain is adjusted by the lateral cerebellum
(nodulus and flocculus).
If the progression of the lesion is slow enough,
vestibular symptoms may be so mild

29. Bilateral disorders of gradual onset
Gradual onset bilateral lesions cause very few
symptoms because of cerebellar compensatory
mechanisms (nodulus and flocculus).
Until most of the sensation is lost, the oscillopsia
symptoms occur.

30. Unilateral fluctuating disorders
When the sensitivity of the vestibular system
changes episodically, as in Meniere's disease and
BPPV, the CNS does not have time to
compensate.

31. DIAGNOSIS
The management of peripheral vestibular disorders
depends on an accurate diagnosis.
The evaluation that will establish the diagnosis will
determine the location, severity, duration, and
etiology of the disorder.
Evaluation of other sensory systems, the CNS
integrity, and the integrity of compensatory
mechanisms is important.
The history and Physical examination are the most
important evaluation methods.

32. Diagnosis ctd.
The examination includes a complete head and
neck examination, cranial nerve examination ,eye
movement examination, and of gait and posture.
A complete otologic examination, including
pneumatic otoscopy and hearing tests should be
done
Evaluation of eye movements using Frenzel glasses
should be performed at the office evaluation.

33. Positional nystagmus and pneumatic otoscopy
with positive and negative pressure and frenzel
glasses should be used to assess Hennebert’s
symptom and sign.
• Vertigo and abnormal eye movements
with positive or negative pressure in the
ear canal
In patients with a history of visual impairment, the
eyes vision, and visual fields should be evaluated.

34. Diagnosis ctd
• Tests of vestibular function should assess the
labyrinth as well as eye movement control
systems, posture and postural control.
• Studies of vestibular function include evaluation
of spontaneous and gaze nystagmus with and
without fixation.

35. Dx and Investigation
Electronystagmography
CT or MRI can aid in telling the location of the
lesion in selected cases or rule out other CNS
disorders
The final Dx should include etiologic Dx and
provide information about site of lesion and
integrity of CNS

37. Treatment
Is aimed at decreasing symptoms and restoring
function.
Treatment consist of
• Vestibulosuppresant medication,
• Ablative
• Vestibular rehabilitation.
In some disorders treatment is aimed at the
disease process itself.
Operative and antibiotic therapy should be
considered in emergency basis.

38. Rx CTD
I/v PHENOTHIAZINE can stop the severe
vertigo, nausea and vomiting caused by severe
unilateral loss of vestibular function.eg IV
Promethazine 25mg 4-6hrly, IV Prochlorperazine
10mg 8hrly
Once the symptoms are over, movements
exercises must be started to rehabilitate the
remaining functions.
Rehabilitation requires active head movements
with visual function.

39. Ablation
Ablation of labyrinthine function has high rate of
success in relieving symptoms of episodic
vertigo.
It is done by systemic use of ototoxic drugs or
labyrinthectomy, or vestibular nerve section.
Both methods put at risk the remaining auditory
function.

40. Surgery
Indicated in incapacitating episodic vertigo with
no useful hearing in the affected ear.
Labyrinthectomy can be performed via the ear
canal or posterior tympanomeatal flap.
Transmastoid approach can be done in more
extensive removal of vestibular labyrinth and in
vestibular neurectomy.

41. Rx ctd
Psychological counseling is the part of management of these
patients.
Since psychogenic disorders frequently accompany vertigo disorders.

42. BPPV - Benign Paroxysmal Positional Vertigo.
This is the most common Peripheral vestibular
disorder.
It is characterized by sudden onset of brief
spells of often severe vertigo that are
experienced only with specific head
movements/position.

43. Epidemiology
It represents 20-40% of patients with PVD.
The incidence ranges from 10-100 per 100000
persons per year
Has a peak incidence in 5th decade
Has no gender bias

44. Pathogenesis
Canalolithiasis-free floating (debris) otoconia from utricle float
in the semicircular canals perilymph
Cupulolithiosis- occurs when otoconia dislodge from the
utricle and stuck on the cupula of SCC
The posterior canal is most commonly affected, although
involvement of other canals can occur

45. Essentials of Diagnosis
Sudden vertigo lasting seconds with certain head positions.
No associated hearing loss.
Characteristic nystagmus (latent, geotropic, fatigable) with Dix-
Hallpike test.

46. Dx
Depends on Hx and PE.
The Dix-Hallpike maneuver is the standard clinical test for
BPPV.
The finding of classic rotatory nystagmus with latency and
limited duration is considered pathognomonic.

47. Dix-Hallpike Maneuver
Used to provoke nystagmus and
vertigo commonly associated with
BPPV
Head turned 45 degrees to
maximally stimulate posterior
semicircular canal

48. Head supported and rapidly placed into head
hanging position
Frenzel glasses eliminate visual fixation
suppression of response

50. Dix Hallpike test

51. Dix-Hallpike Maneuver ctd
Positive test
•rotatory nystagmus
•Nystagmus to the stimulated side
•Rotatory component to the affected ear
•Lasts 15-45 seconds
•Latency of 2-15 seconds
•Fatigues easily

52. Rx
Treatment options include;
• Watchful waiting
• Vestibulosuppressant medication
• Canalithis repositioning (Epley maneuver)
• Surgery -the primary surgical option is
posterior semicircular canal occlusion,
using fascia, muscle or laser collapsing.

53. EPLEY MANEURVER

55. Prognosis
• The natural history of BPPV includes an
acute onset and remission over a few
months.
• However, up to 30% of patients may have
symptoms for longer than one year.
• Patients may have unpredictable
recurrences and remissions, and the rate of
recurrence may be 10–15% per year.

56. Prognosis
These patients may be retreated with a repositioning
maneuver.
A subset of patients who have adapted by not using
certain positions in order to avoid the vertigo or who
have other balance disorders can benefit from balance
rehabilitation therapy

57. VESTIBULAR NEURONITIS
Is described as acute, sustained
dysfunction of the peripheral vestibular
system with secondary nausea, vomiting,
and vertigo.
Essentials of Diagnosis
Vertigo lasting days after an upper
respiratory infection.
No hearing loss.
No other neurologic signs or symptoms

58. • As this condition is not clearly inflammatory in
nature, neurologists often refer to it as vestibular
neuropathy
• Is the third most common cause of PVD after
BPPV and Meniere's d’se.
• Typically present with dramatic, sudden onset of
vertigo, nausea and vomiting.

59. • The dizziness lasts days with gradual, definite
improvement throughout the course
• This syndrome occurs most commonly in middle-
aged adults; mean age of onset is 41 years .

60. Pathophysiology
The proposed etiologies for vestibular neuronitis
include
• Viral infection of vestibular nerve/labrinthyne
• Vascular occlusion
• Immunologic mechanisms
Vestibular neuronitis appears to be a sudden
disruption of afferent neuronal input from 1 of the 2
vestibular apparatuses.

61. Rx
• The primary management includes
 symptomatic and supportive care (acute phase).
 vestibular suppressants and antiemetic (control
vestibular sx)
• Tapering /withdraw medication (central vestibular
compensation).
• Recent data suggest a 3-week course of
methylprednisolone tapered from 100 mg down to 10
mg daily may reduce long-term loss of vestibular
function. ( Ator GA etal. Vertigo—Evaluation and
Treatment in the Elderly)

62. •Despite the evidence of viral infection
valacyclovir was found not to be
helpful alone or in combination with
methylprednisolone in the study.

63. Prognosis
The natural history of vestibular neuronitis
includes an acute attack of vertigo that lasts a
few days with complete or at least partial
recovery within a few weeks to months.
 Some patients (15% in one study) may have
significant vestibular symptoms even after 1 year.
Recurrent attacks in the same or contralateral
ear have been reported but are unusual.
Some patients may later develop BPPV.
Vestibular rehabilitation is of benefit in patients
with residual symptoms.

64. References
• Head and neck surgery-Otorhinolaryngology 4th ed.by B.J.Bailey.
• Ballenger’s Otorhinolaryngology Head and neck surgery 16th ed.by
James .B.Snow.
• Current Diagnosis&Treatment Otorhinolaryngology 2nd ed. By Anil
k.Lalwani
• http://www.unboundmedicine.com/medline
• www.Medscape.com
• www.utube.com