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Vestibular Function and
Anatomy
Prof. Hamad Al-Muhaimeed
Professor/Consultant
Department of Otorhinolaryngology
King Abdulaziz University Hospital

System of balance
 Membranous and bony labyrinth embedded in
petrous bone
 5 distinct end organs
– 3 semicircular canals: superior, lateral,
posterior
– 2 otolith organs: utricle and saccule

Semicircular canals sense angular acceleration
 Otolithic organs (utricle and saccule) sense
linear acceleration
Embryology



3rd week of
embryonic
development
Otic placode formed
from neuroectoderm
and ectoderm
Otocyst or otic vesicle
4th week



Semicircular canals
are orthogonal to each
other
Lateral canal inclined
to 30 degrees
Superior/postereor
canals 45 degrees off
of sagittal plane


Utricle is in horizontal
plane
Saccule is in vertical
plane
Anatomy



There are five
openings into area of
utricle
Saccule in spherical
recess
Utricle in elliptical
recess

45% from AICA
 24% superior
cerebellar artery
 16% basilar
 Two divisions:
anterior vestibular and
common cochlear
artery


Superior vestibular
nerve: superior canal,
lateral canal, utricle
Inferior vestibular
nerve: posterior canal
and saccule


Membranous labyrinth is surrounded by
perilymph
Endolymph fills the vestibular end organs along
with the cochlea

Perilymph
– Similar to extracellular fluid
– K+=10mEQ, Na+=140mEq/L
– Unclear whether this is ultrafiltrate of CSF or
blood
– Drains via venules and middle ear mucosa

Endolymph
– Similar to intracellular fluid
– K+=144mEq/L, Na+=5mEq/L
– Produced by marginal cells in stria vascularis
from perilymph at the cochlea and from dark
cells in the cristae and maculae
– Absorbed in endolymphatic sac which
connected by endolymphatic, utricular and
saccular ducts
Sensory structures



Ampulla of the semicircular canals
Dilated end of canal
Contains sensory neuroepithelium, cupula,
supporting cells



Cupula is gelatinous
mass extending across
at right angle
Extends completely
across, not responsive
to gravity
Crista ampullaris is
made up of sensory
hair cells and
supporting cells




Sensory cells are either
Type I or Type II
Type I cells are flask
shaped and have chalice
shaped calyx ending
One chalice may synapse
with 2-4 Type I cells
Type II cells – cylinder
shaped, multiple efferent
and afferent boutons
Hair cells have 50-100 stereocilia and a single
kinocilium.
stereocilia are not true cilia, they are graded in height with tallest
nearest the kinocilium.
Otolithic organs

Utricle and saccule sense linear acceleration
 Cilia from hair cells are embedded in gelatinous
layer
 Otoliths or otoconia are on upper surface

Calcium carbonate or
calcite
 0.5-30um
 Specific gravity of
otolithic membrane is
2.71-2.94
 Central region of
otolithic membrane is
called the striola



Saccule has hair cells
oriented away from
the striola
Utricle has hair cells
oriented towards the
striola
Striola is curved so
otolithic organs are
sensitive to linear
motion in multiple
trajectories



Senses and controls
motion
Information is
combined with that
from visual system
and proprioceptive
system
Maintains balance and
compensates for
effects of head motion
DEFINITION &
TERMINOLOGIES
DEFINITION &
TERMINOLOGIES

VERTIGO (illusion of rotational, linear or
tilting movement such as “spinning”,
“whirling” or “turning” of the patient or the
surrounding . DISEQUILBRIUM sensation
of instability of the body positions, walking
or standing described as “off balanced” or
“imbalanced”.
DEFINITION &
TERMINOLOGIES

OSCILLOPSIA (inability to focus on
objects with motion, such as reading a sign
while walking , seen with bilateral or central
vestibular loss).
DEFINITION &
TERMINOLOGIES


LIGHTHEADEDNESS (sense of impending
faint, presyncope).
PHYSIOLOGIC DIZZINESS (motion
sickness, height vertigo),
EVALUATION OF THE DIZZY
PATIENT
History
 Dizziness is a term used to describe any of a
variety of sensation that produce spatial
disorientation.
 Onset and Duration of Symptoms:
EVALUATION OF THE DIZZY
PATIENT
History



Character of Dizziness:
Contributing Factors:
Associated Symptoms:
PHYSICAL EXAMINATION

H & N and General Physical Exam:
 Otoscopy:
 Vestibular Testing:
 Neurological Exam:
General Characteristics of
Peripheral and Central Causes of
Vertigo
Characteristic
Intensity
Fatigability
Associated
Peripheral Central
severe
fatigues,
adaptation fatigue
mild
does not
General Characteristics of
Peripheral and Central Causes of
Vertigo
Characteristic
Peripheral
Symptoms
nausea,
hearing loss,
sweating
Eye closed
symptom,
worse with
eyes closed
Central
weakness,
numbness
falls more
likely
symptoms
better with
eyes closed
General Characteristics of
Peripheral and Central Causes of
Vertigo
Characteristic
Peripheral
Nystagmus
horizontal, may
be unilateral
rotary
suppresses
nystagmus (may
not suppress
during acute
phase )
Ocular
Fixation
Central
vertical
bilateral
no effect
or enhances
nystagmus
CAUSES OF VERTIGO
PERIPHERAL VERTIGO:
 Benign Paroxysmal Positional Vertigo
 Meniere Disease
 Vestibular Neuronitis
 Perilymphatic Fistulas
CAUSES OF VERTIGO
CENTRL CAUSES
 Cerebellospontine Angle Tumuors
 Traumatic Vestibular Dysfunction
CENTRAL AND SYSTEMIC CAUSES
OF VERTIGO



Multiple Sclerosis
Other Neurological Disorder (stroke,
seizures, middle cerebellar lesions,
parkinsonism, psudobulbar palsy)
Metabolic Disorders (hypo/hyperthyroidism, diabetes)
CENTRAL AND SYSTEMIC CAUSES
OF VERTIGO


Medications and Intoxicants (psychotropic
drugs, alcohol, analgesics, anesthetics,
antihypertensives, anti-arrhythmics,
chemotherapeutics)
Vascular Causes (vertebrobasilar
insufficiency, basilar migraine syndrome,
vascular loop compression syndrome)
VESTIBULAR TESTING
HALLPIKE TEST
ELECTRONYSTAGMOGRAPHY
ROTATION TEST
OCULOMOTOR TESTING
POSTUGRAPHY
CALORIC TESTING



Only test that evaluates vestibular function
in each ear independently, determines
unilateral versus bilateral weakness
Technique:
Theoretical Normal Response:
CALORIC TESTING

Directional Preponderance:
 Unilateral Caloric Weakness:
 Bilateral Weakness:
DIAGNOSIS

Based on clinical history, physical
examination and audiological findings
(initial low-frequency SNHL) with exclusion
of other causes of hearing loss and vertigo is
adequate for diagnosis and initiating
empirical therapy.
Meniere’s Disease
(Endolymphatic
Hydrops)
Signs and Symptoms
 Episodic Vertigo lasting minutes to hours
 Episodic fluctuating SNHL (usually unilateral),
recovery between episodes may be incomplete
resulting in a progressive SNHL (initially at lower
frequencies)
 Tinnitus and episodic fullness associated with or
without the hearing loss
Meniere’s Disease
(Endolymphatic
Hydrops)
Signs and Symptoms
 Classic Menieres Disease presents with all of the
above symptoms (vertigo, hearing loss, tinnitus,
and aural fullness), however Meniere Disease
may also present as any combination of the above
symptoms
Meniere’s Disease
(Endolymphatic
Hydrops)
DIAGNOSIS
 Vestibular testing may reveal unilateral
weakness on affected side.
 Electrocochleography:
MEDICAL MANAGEMENT
OF MENIERE DISEASE

Dietary Restrictions:
 Diuretics:
 Vestibular Suppressants:
 Corticosteroids:
 Allergy Management:
 Stress Reduction
BENIGN PAROXYSMAL
POSITIONAL VERTIGO
(BPPV, Cupulolithiasis)
BPPV

Frequency- 50% of peripheral vertigo, 20% of pts over 80
have BPPV

Clinical history: sudden onset, brief vertigo, brought on
by changes in head position, particularly turning in bed,
or tilting head back, may have prior history of vestibular
neuritis or head trauma

Exam: + Dix-Hallpike (don’t forget 5-10% have
horizontal variant)

Pathophysiology: loose calcium crystals in posterior
semicircular canal

Treatment: Epley manuever
MANAGEMENT





Education, reassurance and observation
Particle Repositioning Maneuver (Epley’s
Maneuver):
Home vestibular positional exercises
Antivertiginous medications
Singular Neurectomy:
Vestibular Neuritis

Frequency: 15% of peripheral vertigo

Clinical history: sudden onset severe vertigo c N/V, sx’s improve
in days to weeks secondary to central compensation, can have
chronic effects for months to years.

Exam: unilateral nystagmus c fast phase away from affected ear,
amplitude of nystagmus decreases when looking towards affected
ear, +/- hearing loss or tinnitus

Pathophysiology: probably secondary to viral infection &
inflammation of vestibular nerve or labyrinth

Treatment: steroids- 3 week tapering course, starting at 100 mg.
– Strupp et al. (2004). Methylprednisolone, Valacyclovir, or the
Combination for Vestibular Neuritis. NEJM 351, pp. 354-361.
PERILYMPH FISTULA

Pathophysiology:
 Causes:
 SSx:
 Diagnosis:
 Treatment:
VERTEBRONBASILAR
INSUFFICIENCY (VBI)

Pathophysiology:
 SSx:
 Diagnosis:
 Treatment
OTHER VESTIBULAR
DISORDERS

Basilar Migraine Syndrome:
 Vestibular Epilepsy:
 Multiple Sclerosis (MS):
 Labyrinthine Apoplexy:
 Subclavian Steal Syndrome:
 Hyperrinsulinemia/Diabetes:
Etiology Recur Onset
BPPV
+
Duration Associated features
sudden
<1 min
elderly, induced by
position change
hours
ear fullness, tinnitus,
low freq hearing loss
days-weeks 50% c preceding viral
illness, +/- hearing loss
sec-days
young F, HA, positive
visual phenomenon
mins CN, long-tract sx’s/
signs
days-months
hearing
loss +/- tinnitus
Meniere’s
+
gradual
Vestibular
neuritis
Migraine
+
gradual
or sudden
gradual
VB TIA
+
sudden
Labryinth
stroke
-
sudden
Brainstem
stroke
-
sudden
days-months
CN, long-tract
sx’s/ signs
Cerebellar
stroke
-
sudden
days-months
unil dysmetria,
“central” nystagmus
MANAGEMENT CONCEPT

Safety:
 Acute Vestibular Suppression:
 Vestibular Rehabilitation:
 Surgical Management:
SURGICAL MANAGEMENT
OF VERTIGO
SURGICAL MANAGEMENT
OF VERTIGO

Endolymphatic Sac Surgery:
 Vestibular Nerve Section:
 Transtympanic Or Intratympanic
Aminoglycoside Injections:
 Labyrinthectomy
Conclusion
1. Is this vertigo?
2. Is this central or peripheral?
3. History- focus on age, PMH, duration
4. Exam- focus on CN and coordination,
focal neurological findings, Dix-Hallpike