West Visayas State University – College of Medicine – Batch 2020

Block XX
Module 1 The Vestibular System and Diseases of the Inner Ear
Lecture 6
04/ 11/ 19
Dr. Florence Yul N. Saquian

TOPIC OUTLINE Our vestibular system is just one of the apparatuses.

I. Lecture Objectives Our sense of balance is composed of muscles,
II. Introduction spinal cord, eyes, and ears.
III. Vestibular System
A. Function
• Control eye movements to maintain a clear visual
B. Embryology Of The Ear (Supplementary Notes) image of the external world while the individual, the
C. Integrated Balance System environment, or both are in motion.
D. Vestibular Anatomy You won’t be able to walk straight if you are dizzy
E. Neural Pathways of the Vestibular System
F. Vestibulo-Ocular Reflex because that is part of your vestibular system.
G. Nystagmus
IV. Dizziness and Vertigo B. EMBRYOLOGY OF THE EAR
V. Common Vestibular Pathologies (SUPPLEMENTARY NOTES)
A. Benign Paroxysmal Positioning Vertigo • Inner ear begins at 3 weeks AOG as a thickening of
B. Meniere’s Disease/Endolymphatic Hydrops
C. Vestibular Neuronitis and Viral Labyrinthitis the ectoderm (Otic Placode)
VII. References • Otic placode invaginates to form the otic pit which then
Review Questions pinches off to enlarge and form otocyst
References
Appendices
• 5-6 wks AOG - otocysts elongates and partitions itself
into the 6 sensory structures (3 semicircular canals, 2
LECTURER BOOK REFERENCE OLD TRANS otolothic organs, and one cochlea) and the
endolymphatic duct and sac
• 12 wks AOG - membranous labyrinth is complete
I. LECTURE OBJECTIVES • 16 wks AOG - cartilage has formed around the
• To provide an overview of the vestibular balance system membranous labyrinth
• To review the anatomy of the vestibular system and its • 23 wks – cartilage has undergone complete
central pathways endochondral ossification
• To discuss the functions of the vestibular system
• 26 wks – human inner ear is sending auditory
• To review common vestibular pathologies and their
information to the brain
management
End of supplementary notes.

II. INTRODUCTION
C. INTEGRATED BALANCE SYSTEM
The VESTIBULAR SYSTEM, which contributes to
our balance and our sense of spatial orientation, is
the sensory system that provides the dominant input
about movement and equilibrium.

III. VESTIBULAR SYSTEM

• Phylogenetically, one of the oldest sensory organs in
the animal world.
Example: snails, insects – they have antenna to
perceive their orientation of space
• (ppt script) Even the most primitive forms of life such as
worms have statocysts, which are rudimentary forms of
vestibular receptors.
Figure 1. Integrated Balance System. (Doc’s ppt) (see appendix for a
• A key element of an integrated system that allows all larger image)
mobile life forms to move in their environment.
• (ppt script) The vestibular system clearly has a critical
A. FUNCTION role in accomplishing the function of the balance
• Provide accurate perceptions of the position of the system. But we must always remember that it is but
body in its environment, and perceptions of direction part of the integrated balance system that involves
and speed of movement. input from the visual and proprioceptive systems and
also perception of depth modulation by the central nervous system.

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 The interconnection between the ears, eyes and
skeletal muscles toward the central vestibular
pathways enables you to adapt to the surroundings.
Taking one would lead to dysfunction.
There is a control of your right and left labyrinth
going to your vestibular apparatuses and it has a
connection with your ocular pathways and your
vestibular spinal pathways. Example, if you try to
stand on one leg with eyes open, more or less you
have a good balance. But if you to try to close your
eyes, you may be out of balance but you still
maintain a position. This is because your vestibular
system and muscles (feet and spinal cord contract) Figure 3. Anatomy of Vestibulocochlear System
maintain your correct posture, you don’t fall right
away. Interactions enable you to adapt to any situation.
(between the different structures)
COMPONENTS • (ppt script) On the other hand, endolymph is contained
• Peripheral Sensory Apparatus within the membranous structure where the specialized
Bony Labyrinth sensory neuroepithelial tissue is located. The
Membranous Labyrinth vestibular sensory cells are concentrated in different
Hair Cells areas within the membranous labyrinth. Three of these
• Central Processor areas are located in the enlarged portion of each
Vestibular Nuclear Complex semicircular canal – the ampulla, and are known as the
Cerebellum cristae ampullaris. Two more are located in the macula
• Mechanism of Motor Output of the two otolithic organs, the utricle and the saccule.
Vestibulo-Ocular Reflex The arrangement and spatial orientation of the sensory
Vestibulospinal Reflex receptors within each area are unique, allowing for
differential sensitivity to different types of head
D. VESTIBULAR ANATOMY movement.

Supplementary notes.
Sensory Cells are found in the ampulla of
semicircular canal and macula of utricle and saccule.
The fluid that bathes both the vestibular and hearing
components is the same. The only difference
between the two is the function.
As our movements consist of rotations and
translations, the vestibular system components:
1. Semicircular Canal System
Detect angular rotational movements (spin around)
Contains crista ampullaris
has an ampullated end – bulge at the end of the
Figure 2. Vestibular Anatomy. (Adeos Notes)
canal
composed of:
• Bony Labyrinth – Perilymph
─ Horizontal or lateral semicircular canal
• Membranous Labyrinth – Endolymph
─ Superior semicircular canal
Membranous labyrinth is contained within
─ Posterior semicircular canal – where you can
membranous labyrinth.
see ampullated end
How are they different? In the contents of sodium
Superior and posterior semicircular canals have
and potassium
common non-ampullated end. Ampullated end
• (ppt script) The vestibular receptors are embedded
contains ampulla
within the membranous labyrinth, which is housed
The Cristae and the Maculae are specialized
within the bony labyrinth, a series of hollow channels in
neuroepithelium where the hair cells (sensory
the petrous portion of the temporal bone. This bony
receptors) are located
component is held securely by connective tissue and
Ampullae of the semicircular canals are
bathed by perilymph.
responsible for sensing head turning.
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 SCC ampulla contains the crista. Hair cells lie on
the surface of the crista
The stereocilia protrude upward off the surface
of the crista and into a gelatinous material called
cupula
2. Otolithic Organs (Urticle and Saccule)
Detect linear accelerations ( moving back and
forth, side to side)
Contains the Maculae
Crista macularis and ampulla =
neuroepithelium or sense organ of vestibular
system
End of supplementary notes.
THE BONY LABYRINTH
• Composed of 3 semicircular canals AMPULLA and
the vestibule.
• Filled with perilymphatic fluid
High Na:K ratio (high Na, low K)
It is important to know the fluid composition
because some diseases of the inner ear involve
the balance between the electrolytes inside your
perilymph and endolymph.
Endolymph: high K, low Na
• Communicates with the subarachnoid space via the
cochlear aqueduct.
Perilymph resembles CSF
─ The anterior canal is AKA the superior canal.
There is no inferior semicircular canal.
─ The lateral canal is AKA the horizontal canal.
Figure 4. Bony Labyrinth. (Doc’s ppt)
MEMBRANOUS LABYRINTH
Your sensory organs are crista ampullaris and
macula
• Contains 5 sensory organs
Membranous portions of 3 SCC (semicircular
canal: posterior, anterior, lateral or PAL) – contains
crista ampullaris
Membranous portions of 2 otolith organs: utricle
and saccule – contains macula
• Filled with endolymphatic fluid
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High K:Na ratio (high K, low Na)
Endolymph resembles intracellular fluid
• (ppt script) The vestibular sensory cells are
concentrated in different areas within the membranous
labyrinth. Three of these areas are located in the
enlarged portion of each semicircular canal – the
ampulla, and are known as the cristae ampullaris. Two
more are located in the macula of the two otolithic
organs, the utricle and the saccule. The arrangement
and spatial orientation of the sensory receptors within
each area are unique, allowing for differential
sensitivity to different types of head movement.
Figure 5. The Membranous Labyrinth. (Doc’s ppt)
VESTIBULAR BLOOD SUPPLY
The basilar artery supplies the vestibular apparatus
which divides into the anterior inferior cerebellar artery
(AICA) and the anterior vestibular artery. AICA then
divides into the labyrinthine artery, which branches
out into the common cochlear artery and anterior
vestibular artery. The anterior vestibular artery
provides blood supply to the utricle and ampullated end
of semicircular canal. Common cochlear artery
branches out into vestibulocochlear artery and the
posterior vestibular artery, which supplies part of
semicircular canal.
Figure 6. Vestibular Blood supply. (Adeos Notes)
• (ppt script) The vestibular system obtains its blood
supply from the labyrinthine artery. The basilar artery is
the supplier to the labyrinthine artery either directly, or
more commonly through the anterior inferior cerebellar
branch. The labyrinthine artery divides into the
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 common cochlear artery and the anterior vestibular
artery. The anterior vestibu9lar artery provides the
blood supply to the anterior and horizontal semicircular
canals but not to the cochlea. The vestibular apparatus
is susceptible to ischemic events because labyrinthine
arteries lack collateral anastomoses with other major
arterial branches. Isolated occlusion of the anterior
vestibular artery may therefore cause acute vestibular
syndrome without hearing loss.
Figure 7. The Semicircular Canal. (Doc’s ppt)
ANATOMIC ORIENTATION OF SSCS
Your right and left are mirror images of each other.
Horizontal Canal (HC) and utricle: plane 30 degree
anterodorsally relative to naso-occipital plane.
Person walks: head normally declines (pitched
downward) by 300 line of sight directed few meters
in front of feet (this means the HC and utricle come
to lie on a HORIZONTAL PLANE).
Figure 8. Orientation Presentation. (Doc’s ppt) (pls see appendix for a
larger image)
Anterior Canal (AC) and Posterior Canal (PC) and
saccule arranged vertically in the head, orthogonal
(or perpendicular) to HC and utricle and to each
other.
The anterior and posterior have a 90-degree
orientation to each other. In your naso-occipital
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plane, the anterior is tilted 30 degrees above the
horizon.
Horizontal semicircular canal is oriented 60
degrees.
Orthogonal = perpendicular
WHAT TO REMEMBER: 30 degrees above –
anterior, 90 degree – horizontal and posterior, and
they are co-planar mirror images of each other.
• Co-Planar Pairs:
RHC and LHC
RAC and LPC
RPC and LAC
• (ppt script) The semicircular canals are organized in
three nearly orthogonal (mutually perpendicular)
planes.
• (ppt script) The lateral canal resides in a plane that
makes a 30-degree upward angle with the horizontal
plane when the head is in a natural upright position
• (ppt script) The other two canals are roughly vertical,
each oriented at an approximate 45-degree angle with
respect to the sagittal plane that bisects the head.
• (ppt script) Each semicircular canal is synergistically
paired with a canal in the opposite ear such that they
reside in approximately parallel planes. The three pairs
are the (a) two horizontal canals, (b) right anterior and
left posterior canals, and © right posterior and left
anterior canals.
HAIR CELL STRUCTURE
Figure 9, 10, 11. The Hair Cells. (Doc’s ppt)
• Hair cells transducer mechanical energy to neural
activity
• Neurotransmitter release changes firing rate of
vestibular neurons
• 70 stereocilia
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• Single kinocilium
Otolithic organs (from utricle and saccule) contain the
hair cells – main sensory organs of the vestibular
apparatus.
• (ppt script) The vestibular sensory receptor, the hair
cell, is a specialized cell that transduces
hydromechanical energy to neural activities.
Microscopic displacement of the hair cells subsequent
to the applied forces causes the chemical reaction that
releases neurotransmitter substance and changes the
neural firing rate of the primary vestibular neurons. The
vestibular hair cell contain approximately 70 short hairs
called stereocilia and a single, thicker longer hair called
a kinocilium.
VESTIBULAR HAIR CELLS
• AMPULLAE
rest on the crista ampullaris
overlaid with by the cupula
Otolithic membranes contain otoconia ( “little stones
of the inner ear)
• MACULAE
Located on medial wall of the saccule
Located on the floor of utricle
Excited when bent towards kinocilium
Figure 12. Vestibular Hair Cells. (Doc’s ppt)
Supplementary notes. You may proceed to Hair Cell Function
• Hair cells are the sensory receptor cells of hearing and
balance. They are specialized mechanoreceptors that
convert the mechanical stimuli associated with hearing
and balance into neural information for transmission to
the brain.
• Most important cells in the inner ear
• 100 stereocilia at their apical end
• Stereocilia are packed with a filamentous actin
cytoskeleton. Arrangement is asymmetrical and
polarized. They are arranged in rows of short,
intermediate and tall stereocilia.
• Single kinocilium is located adjacent to the tallest row.
• Kinocilium is thought to establish the morphologic
polarization of the stereocilia bundle.
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• The deflection of the stereocilia toward the tallest row
toward the tallest row causes shearing between the
stereocilia, which causes the tip links to pull on the
transduction channels, opening them. This leads to
entry of K and Ca ions causing depolarization.
• Deflection in the other direction releases tension of the
tip link, causing the transduction channels to close.
This leads to channel closure and results in hair cell
hyperpolarization.
• Hair cells have a mechanism for adjusting their set
point and this is called adaptation.
End of supplementary notes
Hair Cell Function
Kinocilium moves away from the stereocilia =
excitatory
Kinocilium moves towards the stereocilia = inhibitory
When the stereocilia moves toward the kinocilium =
EXCITATION or depolarization
When the stereocilia moves away the kinocilium =
INHIBITION or hyperpolarization
• (ppt script) The majority of the hair cells generate
spontaneous neural firing at rest. The steady release of
neurotransmitters across the junction of the hair cells
and its afferent neurons appears to be the mechanism
that provokes this tonic neural activity in the absence
of any external stimuli. A key characteristic of
vestibular hair cells is its directional polarization. When
the stereocilia bundle is bent toward the kinocilium, the
firing rate of the afferent nerve fiber connected to that
cell increases. Bending of the stereocilia away from the
kinocilium causes a decrease in the firing rate. In
general, the change in the firing rate of the afferent
neuron is proportional to the displacement of the
stereocilia. However, there is an inherent asymmetry
between the excitatory and inhibitory responses. The
firing rate of neurons can increase to approximately
400 spikes per second during the excitatory phase.
However, the inhibitory response is limited to cessation
of neural activity and therefore cannot exceed the
spontaneous firing rate.
Figure 13. The Hair Cell Function. (Doc’s ppt)
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STRUCTURE OF THE MACULA
• (ppt script) The cilia of the macular hair cells likewise
project into a gelatinous membrane called the otolithic
membrane.
• (ppt script) However, unlike that in the crista, the
otolithic membrane is topped by deposits of calcium
carbonate called otoconia or otoliths, and this
increases the specific gravity of the otolithic membrane
to three times that of the endolymph.
• (ppt script) The mechanism of stimulation for the otolith
organs is any force that displaces the otolith
membrane with respect to the macula, and as can be Figure 16. Different Layers of the Macule. (Adeos Notes)
seen from the diagram, would consist of a force
parallel to the macula that would cause a shearing • The gelatinous layer, located on top of the otoliths, makes
it possible for the kinocilium and stereocilia to move
force that can displace the hair cells and generate
gently.
neural activity. Thus, the maculae are responsive to
• Also provides cushion for the hair cells.
linear acceleration, such as the force of gravity.
• The maculae are responsible for sensing gravity (linear
acceleration).
• Maculae are flat, ovoid structures that are covered with
hair cells across their surface,
• The stereocilia protrude upward and are embedded in the
gelatinous otolithic membrane, which contains calcium
carbonate crystals called otoconia.
• Otoconia have a density greater than water, so when
head is tilted from side to side, gravity causes a shearing
force between the otolithic membrane and the surface of
the maculae. This results in bending of stereocilia.
• Deflection towards the kinocilium causes depolarization
while deflection away causes hyperpolarization
Figure 14. Structure of Macula. (Doc’s ppt) • Utricle and saccule have hair cells oriented bidirectionally.
A single macule can produce both excitatory and
Supplementary notes. You may proceed to Otoliths
inhibitory signals with a change in the head position.
ORIENTATION OF THE MACULE
End of supplementary notes

OTOLITHS
• Respond to linear head motion and static tilt with
respect to gravitational axis.
• The saccule is vertically oriented
Occipital Axis
Anterior-Posterior Axis
• The utricle is horizontally oriented
Interaural Axis
Anterior-Posterior Axis

Figure 15. Orientation of the Macule. (Adeos Notes)

• The sensory epithelium (macula) of the Saccule is

oriented vertically senses vertical acceleration
• The sensory epithelium (macula) of the Utricle is oriented
horizontally senses horizontal acceleration

Figure 17. Otoliths. (Doc’s ppt)

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 E. NEURAL PATHWAYS
Once your neurons detect the movement, whether
inhibition or excitation, it [signal] goes into your
vestibular nerve and vestibular nuclei. The vestibular
nuclei are found in the brainstem. So from the
vestibular nuclei, there are descending tracts to the
muscles in your spinal column which control
movements of muscles and joint. There is lateral
innervations and contralateral connection
(decussation.)
• Afferent nerve projections from bipolar neurons of the
vestibular ganglion
• Enters brainstem at the pontomedullary junction
Figure 18. Neural Pathways. (Adeos Notes)
VESTIBULAR NERVE
Figure 19. Vestibular Nerve. (Doc’s ppt)
• (ppt script) The afferent nerve fibers from the
semicircular canals and the otolith organs merge to
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form the vestibular nerves, which are branches of the
combined vestibulocochlear nerve – the 8th cranial
nerve.
• (ppt script) Vestibular nerve fibers are bipolar neurons
with their cell bodies in Scarpa’s ganglion, their
peripheral synapses on the hair cells, and their central
synapses on the central vestibular structures. Scarpa’s
ganglion consists of a superior portion, which receives
fibers from the horizontal and superior SSC and the
utricular maculae, as well as a branch of the saccular
nerve; and an inferior portion, which comprises fibers
from the crista of the posterior canal and the saccular
macula.
VESTIBULAR NEURAL PATHWAYS
• Vestibular nerve fibers
Innervate vestibular nuclei located in the pons and
medulla primarily
Some innervate the cerebellum directly
• Vestibular nuclei
Receive afferent innervation from numerous
sources
─ Cerebellum
─ Reticular formation
─ Spinal cord and cervical areas
─ Interconnection from contralateral nuclei
Figure 20. Peripheral Connections of the Vestibular System. (Doc’s
ppt) (pls see appendix for larger image)
• (ppt script) Vestibular nerve fibers are bipolar neurons
with their cell bodies in Scarpa’s ganglion, their
peripheral synapses on the hair cells, and their central
synapses on the central vestibular structures.
• (ppt script) Scarpa’s ganglion consists of a superior
portion, which receives fibers from the horizontal and
superior SSC and the utricular maculae, as well as a
branch of the saccular nerve; and an inferior portion,
which comprises fibers from the crista of the posterior
canal and the saccular macula.
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Figure 21. Major Central Connections of the Vestibular System. (Doc’s
ppt) (pls see appendix for larger image)
Figure 22. Vestibular Neural Pathways. (Doc’s ppt)
(Adeos) From your vestibular nerve, it goes to the
vestibular ganglion (which is located in the
cerebellopontine angle), then it goes to the
brainstem, which has connection to the cerebellum
(involve in the maintenance of balance), goes to the
thalamus and then finally to the cortex (central control
of vestibular system)
CEREBELLUM: ADDAPTIVE PROCESSOR
• A major recipient of outflow from/source of inhibitory
input to the vestibular nucleus
• Flocculus: adjusts and maintains the gain of the VOR
• Nodulus: adjusts the duration of VOR responses and
involved with processing of otolith input
• Anterior-superior vermis: Vestibulospinal Reflex
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Figure 23. Cerebellum. (Doc’s ppt)
BRAINSTEM: NEURAL INEGRATOR
• For the oculomotor system:
Nucleus prepositus hypoglossi
Just below the medial vestibular nucleus
• For the vestibulospinal system:
Presently unknown
F. VESTIBULO- OCULAR REFLEX (VOR)
(Adeos) It is composed of the afferent and efferent
sensory organs of your eyes and vestibular apparatus.
• Mechanism by which the vestibular system participates
in the task of providing clear vision during head
movement.
• It maintains a steady retinal image by generating
compensatory eye movements in response to head
motion.
(Adeos) When you jiggle a pen in front of you, you get
a blurred image of the pen. But, when you shake your
head left and right, you see a clear image of the pen
instead. This is the function of VOR. The movement of
your head has a connection with the movement of your
eyes. The VOR maintains as steady focus on a certain
position.
(Adeos) Your labyrinth has a connection to your
vestibular nuclei. The vestibular nuclei have a
contralateral connection to the nuclei of the sixth nerve
(Abducens) which controls the lateral rectus of the
contralateral eye. It also has a connection to the nuclei
of the third nerve (Oculomotor) which controls the
medial rectus. When you move your head to one side,
the medial rectus of the contralateral eye and the
lateral rectus of the ipsilateral eye contract (inhibit) to
fix the eye movement. There is compensatory eye
movement in response to head movement. When you
move to the left, your eyes tend to remain focus.
(Adeos) In Doll’s eye maneuver, the eyes are not
steady. They follow the movement of the head.
Probably, one of the components of the VOR [is
abnormal].
• Generates eye movements that enable clear vision
while the head is in motion
• Example, right head rotation:
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 Activation of right (ipsilateral) medial rectus and left
(contralateral) lateral rectus
Inhibitory impulses to antagonists
Result: compensatory eye movements toward the
left

Figure 24. Sample Output for Vestibulo- ocular Reflex. (Doc’s ppt)

Supplementary notes.
• The neural signals coming from the semicircular canals
start the Vestibulo-ocular reflex
• VOR is critical to the ability to visually fixate on an
object while one’s head is turning.
• In contrast, keeping one’s head still while trying to
follow a moving target with the eyes is predominantly
under cortical and cerebellar control.
• An excitatory response from one semicircular canal
results in an excitatory signal that crosses the midline
of the brainstem via a second neuron to the
contralateral Abducens nucleus. This nucleus then
sends signals via the 6th CN to the lateral rectus
muscle in the contralateral eye. In addition, the
Abducens nucleus sends an excitatory input via the
medial longitudinal fasciculus to the ipsilateral ocular
motor nucleus which controls the ipsilateral medial
rectus muscle.
End of supplementary notes
G. NYSTAGMUS
• A rhythmic to-and-fro eye movement typically identified
by a slow drift (physiologic nystagmus) of the eyes in
one direction followed by a fast reset in the opposite
direction.
Supplementary notes.
• In vestibular nystagmus
VOR - causes slow component
Saccadic movement – causes compensatory fast
component
• Gaze Nystagmus – very fine movements elicited by
moving an object
Figure 25. Classification of Nystagmus. (Adeos Notes)
End of supplementary notes
IV. DIZZINESS VS VERTIGO
• Dizzy (“hilo”, “liyo”, “tiyug palibot”, “lignin ulo”)
Used to describe various sensations with different
causes.
Important to distinguish dizziness from true vertigo;
differential diagnosis and management are totally
different
• Dizziness: light headed, syncopal, “passing-out”
sensation (as on standing up abruptly); replicated by
hyperventilating.
• Vertigo: sensation of spinning, whirling or falling, either
of self (I’m spinning) or of the environment (the room is
spinning); replicated by spinning like a top.
A. VERTIGO
• A symptom rather than a disease.
• Can have various causes
• May occur suddenly and be accompanied by nausea,
vomiting and disequilibrium.
• Mild episodes: a rocking sensation or mere light-
headedness and confused with dizziness.
Guided adequately, the patient usually able to
describe the symptoms (what actually felt in their
own words) for the physician to decide whether the
patient is experiencing true vertigo.
How to ask the correction questions in differentiating
dizziness from vertigo? It is done by taking a good
history.

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 HISTORY
• History taking should provide information about:
Pattern of vertigo: onset, duration, relation to
position, triggering and alleviating factors.
Accompanying symptoms: hearing loss, tinnitus,
ear fullness (otologic).
Drug (including alcohol) ingestion and trauma.
Other systemic, neurologic, neck, ophthalmologic,
otologic, and psychiatric problems
Pneumatic otoscopy – otoscope with attachment
which introduces air to tympanic membrane to
create vertigo
Fistula test – When pressure is applied in the ears,
patient gets dizzy because there is a hole which
causes a movement in the labyrinthine or
semicircular canal.
• Dix-Hallpike maneuvers (for positioning vertigo)

Table 1. SNNOOP Tool. (Doc’s ppt)

PHYSICAL
SNNOOP WHAT TO LOOK FOR
EXAMINATION
Vital Signs, Chest and Hypo/hypertension or
SYSTEMIC Heart Findings postural hypotension,
Arrhythmias
Cranial Nerve Exam, Neurologic deficits that
Motor Sensory Exam, might point out a
Cerebellar Exam cerebrovascular
accident (CVA) e.g. Figure 26. Pneumatoscopy and Tuning Fork Test. (Doc’s ppt)
NEUROLOGIC
Unilateral weakness,
paresthesias, cerebellar Supplementary notes.
dysfunctions Dix- Hallpike Maneuver
Auscultation for Bruits, Neck Positions that to detect benign positional vertigo (peripheral or
NECK Range of Motion might induce dizziness, central proble,); movement of otoconia (calcium
Carotid Bruits
carbonate) in relation to semicircular canal;
Visual Errors of Refraction, nystagmus is positive
Acuity/Refraction, Limitation of EOMs,
OPHTHALMOLOGIC Extraocular Muscles Papilledema, Retinal
To determine whether vertigo is peripheral or central.
(EOMs), Fundoscopy Abnormalities
Otoscopy, Pneumatic Otologic diseases e.g.
Otoscopy, Tuning Fork AOM, CSOM,
Tests, Vestibular nystagmus, Hearing
Function Tests, Dix- deficits, Vestibular
OTOLOGIC Hallpike, Head Shaking dysfunction
Nystagmus, Head
Trust Test,
Unterberger/ Fukuda
Marching Test
Mental Status Exam Abnormalities in
memory, concentration,
PSYCHIATRIC Figure 27A. Dix- Hallpike Test. The examiner stands at the patient’s
aphasias
head, 45o to the right, to align the right posterior semicircular canal with
the sagittal plane of the body.

With this tool, diagnosis will be clear.

PHYSICAL EXAMINATION
• may provide information leading to diagnosis
• may be normal (unless patient is vertiginous at the time
of examination)
corroborated by nystagmus
• Blood pressure recorded in supine, sitting & standing
positions Figure 27B. The examiner moves the patient, whose eyes are open,
from the seated to the supine, right-ear down position and then
to rule out orthostatic hypotension extends the patient’s neck slightly so the chin is pointed slightly
upward. The latency, duration, and direction of nystagmus (if present)
OTOLOGIC EXAMINATION should be noted. Inset: the arrows over the eyes depit the direction of
nystagmus in patients with typical BBPV. The presumed location in the
• Bedside hearing evaluation (tuning fork). labyrinth of the free-floating debrs thought to cause the disorder is also
• Pneumatic otoscopy and fistula test (vertigo and shown. (Adeos Noes)
End of supplementary notes.
observed nystagmus from alternating position and
negative ear canal pressure).

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 Figure 30 and 31. Head Shake Nystagmus (Adeos Notes)

Romberg’s test

Figure 28. Dix-Hallpike Test. (Doc’s ppt)

NEURO- OTOLOGIC TESTS

• Oculomotor evaluation for various forms of nystagmus,
oscillopsia & vestibulo-ocular-reflex cancellation
• Caloric testing (bithermal or ice)
• Postural tests
Figure 32. Rhomberg’s Test. (Doc’s ppt)
Romberg’s (standard & sharpened)
Jendrassik’s maneuver Also known as Romberg's sign or the Romberg
Unterberger or Fukuda (marching) maneuver is a test used in an exam of neurological
Babinski-Weill (walking) test function for balance, and also as a test for driving
under the influence of an intoxicant.
Supplementary notes. The exam is based on the premise that a person
Caloric Test requires at least two of the three following senses to
• also called vestibular caloric stimulation maintain balance while standing: proprioception (the
• test of the vestibulo-ocular reflex that involves irrigating ability to know one's body position in space);
cold or warm water or air into the external auditory vestibular function (the ability to know one's head
canal position in space); and vision (which can be used to
monitor and adjust for changes in body position).

Unterberger’s Stepping Test/ Fukuda Marching

patient marches in place; pathologic if patient turns
≥45 degrees from original position; patient drift
towards the lesion; there is a central component to
the vertigo

Figure 29. Caloric Test. (Adeos Notes)

End of supplementary notes.

Head Shake Nystagmus

Oscillopsia and Vestibulo- Ocular reflex cancellation

Figure 33. Unterberer’s Stepping Test/Fukuda. (Adeos Notes)

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 ─ (+) nystagmus with eyes shut (easily
observed beneath closed eyelids)
CENTRAL
─ spontaneous nystagmus with eyes open
─ disappears when eyes are shut

Table 2. Peripheral VS Central Vertigo. (Doc’s ppt)

PERIPHERAL
• EAC Foreign Body
• Otitis Media: Effusion,
Acute, Chronic &
Figure 34 and 35. Unterberer’s Stepping Test/Fukuda. (Doc’s ppt) Cholesteatoma
• Acute Labyrinthitis
Supplementary notes.
• Meniere’s Disease
Jendrassik’s Maneuver
• Benign Paroxysmal
• A modified Romberg Test Positioning Vertigo
• Patient stands with eyes closed and hands clasped (as • Perilymphatic Fistula
if singing in an opera) • Labyrinthine Insufficiency
• Vertigo has a central component • Trauma
• Ototoxicity
• Ramsay-Hunt Syndrome
• Vestibular Neuronitis
CENTRAL
• Acoustic Neuroma
• Meningitis, Encephalitis,
Brain Abscess
• Brainstem Cerebellar
Infarct or Hemorrhage
• Vestibular Insufficiency
• Vertebrobasilar
Insufficiency
• Subclavian Steal Syndrome
• Temporal Lobe Infarct
• Temporal Bone Fracture
• Drugs
• Multiple Sclerosis
• Tumor

A. BENIGN PAROXYSMAL POSITIONING VERTIGO

(Adeos) Most common cause of peripheral vertigo
• Sudden onset
• Brief episode (seconds to minutes)
• Associated with certain head positions, particularly
when involved ear positioned dependently.
• Dix-Hallpike maneuver
Figure 36. Jendrassik’s Maneuver; (Adeos Notes)
crescendo-decrescendo nystagmus pattern
Babinski- Weil test
following 10-15 secs latency after affected ear
• patient will be asked to walk in a straight line
positioned dependently
• positive if patient cannot maintain walking in a straight
Geotropic (horizontal or rotator) nystagmus about
line.
30 secs
(For labyrinthine disease) the patient, with eyes
Increasingly difficult to replicate (fatigability)
shut, walks forward and backward ten times; with
• Pure tone audiometry and caloric testing are normal.
labyrinthine disease there will be deviation from the
• Caused by free-floating calcium carbonate crystals in
straight path, bending to one side when walking
the posterior semicircular canal, maybe a one-off in
forward and to the other when walking backward.
many people.
End of supplementary notes.

V. COMMON VESTIBULAR PATHOLOGIES

COMMON CAUSES OF VERTIGO
• Can be grouped into peripheral or central causes:
Many peripheral causes of vertigo are not life-
threatening, though debilitating
─ Less urgent
─ Cause severe discomfort, nausea, and vomiting
─ Merit admission for supportive therapy
Many central causes of vertigo merit urgent
admission and evaluation
• Presence/Absence of spontaneous nystagmus with
eyes open or shut
PERIPHERAL
─ (-) nystagmus with eyes open
Figure 37. Benign Paroxysmal Positioning Vertigo. (Doc’s ppt)

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 Special canalith positioning techniques (Epley
Maneuver) can relieve symptoms when recurrent
and not self-limiting (Froehing et al 2000; Soto 2001;
Cohen 1999; Ruckentein 2001)
TREATMENT
• Canalith Repositioning Techniques (Epley
maneuver)
Supplementary Notes
A. First a Dix-Hallpike Test is performed with the
patient's head rotated 45' towards the right ear and the
neck slightly extended with the chin pointed slightly
upward. The position results in the patient's head
hanging to the right.
Figure 38. (Adeos Notes)
B. Once the vertigo and nystagmus provoked by the Dix-
Hallpike test cease, the patient's head is rotated about
rostral-caudal body axis until the left ear is down
Figure 39. (Adeos Notes)
C. Then the head and body are further rotated until the
head is face down
Figure 40. (Adeos Notes)
D. The vertex of the head is kept tilted downward
throughout the rotation. The maneuver usually provokes
brief vertigo. The patient should be kept in the final, face-
down position for about 10-15 seconds. With the head
kept turned toward the left shoulder, the patient is
brought into the seated position.
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Figure 41. (Adeos Notes)
End of supplementary Notes.
• Vestibular suppressions should be administered
selectively only for severe attacks as they prevent
habituation
• Surgery when severe BPPV-related vertigo does not
respond to canalith repositioning procedure, as
vestibular suppressants only lessen symptoms in the
short-term. (Foster & Belch 1996)
Supplementary notes. You may proceed to Meniere’s
Disease
• Benign Paroxysmal Positioning Vertigo is one of the most
common types of peripheral vertigo
• Lasting seconds with no associated hearing loss
• Average age of presentation is at the 50s with no gender bias
• BPPV occurs because a semicircular canal has debris either
attached to the cupula or free floating in the endolymph.
• Majority is due to debris in the posterior canal
• Signs and Symptoms:
Sudden onset of vertigo that lasts 20-30 seconds with
certain head positions
Triggering positions include rolling over in bed into a
lateral position, getting out of bed, looking up and back,
and bending over
Normal hearing
No spontaneous nystagmus
Normal Neurological evaluation
• BPPV is diagnosed by observing a characteristic nystagmus
when performing the Dix-Hallpike test
• Treatment:
Nonsurgical
─ Maneuvers, Epley (particle or canalith repositioning
procedure), and Semont (liberatory maneuver)
─ Epley – most widely used
─ 80% of patients are cured with repositioning
maneuvers
• Surgery – if repositioning maneuvers are not effective and
patients have no intracranial pathology
Posterior semicircular canal occlusion – primary surgical
option
13 of 17
 ─ A standard mastoidectomy is performed and the
posterior semicircular canal is fenestrated. The
membranous canal is occluded with muscle, fascia,
or bone pate, or collapsed with a laser
End of supplementary notes
B. MENIERE’S DISEASE/ ENDOLYMPHATIC
HYDROPS
• Increased pressure or endolymphatic hydrops
• Increased production and decreased reabsorption of
endolymph
(Adeos) When there is too much production, it may
burst. The endolymph will be admixed with the
perilymph, thus ear fullness.
• Subjective sensation of aural fullness or pressure
• diagnostic triad of:
progressive sensorineural hearing loss
tinnitus
vertigo (minutes to hours)
• Dizziness usually accompanied by ear fullness and
ringing in the ears.
• Diagnostic triad:
Progressive sensorineural hearing loss
Tinnitus
Vertigo
• Vertigo builds in intensity over 30 minutes to <24 hours
• May be accompanied by nausea and vomiting.
• Symptom-free intervals may last several days to
months.
(Adeos) Sac ruptures so there is admixture of the
perilymph and endolymph. With too much production
of endolymph  burst  mixing with perilymph,
causing sensation of vertigo, hearing loss, tinnitus.
Healing of the sac  symptom free interval
• Physical examination findings may be normal
• Pure tone audiometry may reveal low frequency
sensorineural hearing loss early on
• Progressive course until hearing loss becomes total,
vertigo begins to wane till it disappears
Figure 42. Meniere’s disease. (Adeos Notes)
TREATMENT
• Supportive therapy:
reducing pressure through dietary sodium
restriction and diuresis (“maize tea”)
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(Adeos) When there is less absorption of endolymph,
diuretics such as hydrochlorothiazide can be used.
• Severe attacks: vestibular suppressants
dimenhydrinate or diazepam
• Betahistine HCl, 16mg BID for 2-3 months may reduce
frequency and severity of vertiginous attacks
• Surgery: intractable cases unresponsive to medications
(-) Dix-Hallpike
Figure 43. Meniere’s disease. (Doc’s ppt)
Supplementary notes. You may proceed to Vestibular
Neuronitis and Viral Labyrinthis
• Meniere’s disease or endolymphatic hydrops – an idiopathic
inner ear disorder characterized by attacks of vertigo,
fluctuating hearing loss, tinnitus, and aural fullness
• No gender bias
• No right or left predilection
• Pathogenesis
Anatomic, infectious, immunologic, and allergic factors
The basic premise is that there is increased
endolymphatic fluid owing to impaired reabsorption of
endolymphatic fluid
• Signs and Symptoms
Episodic attacks lasting for hours
Unilateral, fluctuating sensorineural hearing loss
(frequently low frequencies)
Vertigo lasting minutes to hours
Constant or intermittent tinnitus typically increasing in
intensity
Aural fullness
• Meniere’s is a clinical diagnosis. Diagnostic evaluation
primarily includes audiometry and FTA-BAS
• Treatment
Non-surgical
─ Dietary modifications and vestibular suppressants
Na restricted diet (<2g/d)
Diuretics
Acute attacks are managed with vestibular
suppressants (meclizine and diazepam) and
antiemetic medications
Aminoglycoside therapy
─ Intratympanitic gentamicin therapy – for medically
refractory patients with or without serviceable
hearing loss
Steroid Therapy
• Surgical
Endolymphatic sac surgery
Vestibular nerve section - provides a definitive treatment
for unilateral Meniere’s
Labyrinthectomy
End of supplementary notes
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 C. VESTIBULAR NEURONITIS & VIRAL b. Anterior Inferior Cerebellar Artery
LABYRINTHITIS c. Anterior Vestibular Artery
• Sudden onset sever vertigo and imbalance d. All of the above
• nausea and vomiting 3. Which sensory receptor is most sensitive to
• usually following non-specific viral illnesses angular acceleration.
• Vertigo persist days to weeks a. Utricle
(Adeos) Patient will just want to close eyes and little b. Crista
amount of movement will cause vertigo. c. Saccule
• Patient preferentially lie still in a dark, quiet room. d. Organ of Corti
• Spontaneous nystagmus to contralateral (unaffected) 4. The following describes Meniere’s disease,
ear except?
• Caloric responses reduced or absent in affected ear. a. Symptom free intervals usually lasts for several
• Pure tone audiometry is normal. days to months
b. Dizziness accompanied by ear fullness and
TREATMENT ringing ears
• Supportive therapy c. (+) in Dix- Hallpike test
• vestibular suppressants (central compensation delayed d. It has no right or left predilection
by prolonged administration) 5. The following tests can be used to detect if the
• Early Vestibular rehabilitation to improve balance vertigo has a central component:
function. a. Dix- Hallpike Test
Relaxant such as diazepam. b. Jendrassik’s Maneuver
• Don’t do Dix-Hallpike! c. Fukuda Marching
d. Only B and C are correct
Supplementary notes
• Vestibular neuritis is the third most common cause of For nos. 6-10: Differentiate between Peripheral and
peripheral vestibular vertigo Central causes of Vertigo. Write A if Peripheral and
• No gender bias B if Central.
• Half of the patients have an antecedent or concurrent 6. Trauma
viral illness 7. Tumor
• Propose etiologies include viral infection, vascular 8. Temporal Bone Infarct/ Fracture
occlusion, and immunologic mechanisms 9. Labyrinthine Insufficiency
• Most likely cause is reactivation of latent herpes 10. Ototoxicity
simplex virus type 1
• Injury is often seen in the superior vestibular nerve For 11-15: Classifying Nystagmus. Choose from the
• Signs and symptoms following choices the type of Nystagmus described in
Sudden onset of vertigo with nausea and vomiting the ff statements.
Normal hearing and normal neuro exam A. Convergence- Retraction Nystagmus
Postural instability towards the injured ear but is B. Downbeat Nystagmus
still able to walk without falling C. Seesaw Nystagmus
Spontaneous nystagmus D. Pendular Nystagmus
• Treatment E. Vestibular Nystagmus
Primary management includes symptomatic and
supportive care 11. Horizontal or rotary movement of the eyes which
Patients are also given vestibular suppressants may suggest cochlear dysfunction.
and antiemetic 12. Refers to irregular downward jerking of the eyes
End of supplementary notes.
during downward gaze. It can signal lower medullary
damage.
REVIEW QUESTIONS
13. Irregular jerking of the eyes back into the orbit during
1. At what week does the membranous labyrinth is
upward gaze. It can indicate midbrain tegmental
completely formed?
damage.
a. 11th Week AOG
14. Rapid movement of the eyes, one eye appears to
b. 12th Week AOG
rise while the other eye appears to fall. It can suggest
c. 16th Week AOG
an optic chiasm lesion.
d. 23rd Week AOG
2. What supplies the whole vestibular apparatus?
a. Basilar Artery

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15. Oscillations of equal velocity around a center point. It REFERENCES
can indicate congenital loss of visual acuity or as a • Upclass notes
complication of multiple sclerosis. • Doctor’s lecture

Answers: 1.B 2.A 3.B 4.C 5.D 6.A 7.B 8.B 9.A 10.A 11.E 12.B
13.A 14.C 15.D

APPENDICES

FIGURE 1. Integrated Balance System

FIGURE 3. Anatomy of Vestibular System

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 FIGURE 20. Peripheral Connections of the Vestibular System

FIGURE 21. Major Central Connections of the Vestibular System

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