Dr.

Aseem Mishra
Vestibular Physiology and
Approach to a patient of vertigo

Ascending Pathways
Vestibular nerve
Vestibular nuclei
Cerebellum
Oculomotor complex
CN 3, 4, and 6
Along with vestibulospinal reflexes coordinate head and
eye movements
Relay Centers
Thalamus
Connection with vestibular cortex and reticular formation
arousal and conscious awareness of body;
discrimination between self movement vs. that of the
environment
Vestibular Cortex
Junction of parietal and insular lobe
Target for afferents along with the cerebellum
Both process vestibular information with somatosensory and visual
input






Netter 1997
Neural Pathways for Equilibrium and Balance
Otolith organs
Utricle and saccule
Otolith sensory structures
Maculae
Otolithic membrane
Otoconia
Movement of gel membrane & otoconia cause a
shearing action to occur over the hair cells
sensitivity of otoliths
Otolith Function
Respond to:
Linear head motion on acceleration
Static tilt
Two organs respond to respective accelerations or
tilts in their respective planes
Saccule has vertical orientation of maculae
Utricle has horizontal orientation of maculae














Bear 1996
Striola of the Macula
Striola serves as a structural landmark
Contains otoconia arranged in narrow trenches,
dividing each otolith
Orientation of the hair cells change over the
course of the macula
Allows otoliths to have multidirectional sensitivity
Vertigo
Vertigo (from the Latin vert "a whirling or
spinning movement"
[
) is a subtype of dizziness in
which a patient inappropriately experiences
the perception of motion (usually a spinning
motion) due to dysfunction of the vestibular
system. It is often associated
with nausea and vomiting as well as a balance
disorder, causing difficulties standing or walking.
Types of vertigo
There are three types of vertigo-
objective
subjective
Pseudovertigo

Depending on the location of the dysfunction of the
vestibular pathway
Central vertigo
Peripheral vertigo

Differentiation Between Peripheral &
Central Causes of Vertigo
Peripheral Central

Nausea severe
moderate
Imbalance mild severe
Hearing Loss common rare
Oscillopsia mild severe
Neurologic Symptoms rare common
Compensation rapid slow

(Furman JM, Whitney SL. 2000)
Visual illusion of oscillating movement of
stationary objects
Can arise with lesions of peripheral or central
vestibular systems
Indicative of diminished VOR gain
motion of images on fovea
diminished visual acuity
Oscillopsia
Nystagmus
Rapid alternating movement of eyes in
response to continued rotation of the body
Primary diagnostic indicator in identifying
vestibular lesions
Physiologic nystagmus
vestibular, visual, extreme lateral gaze
Pathologic nystagmus
spontaneous, positional, gaze evoked
Labeled by the direction of the fast
component
Central vs. peripheral cause differentiated by
duration

Gaze-Evoked (Gaze-Paretic)
Nystagmus

Gaze-evoked nystagmus is elicited by the attempt to
maintain an eccentric eye position, and it is the most
common form of nystagmus encountered in clinical
practice. Patients recovering from a central gaze
palsy show a phase in which lateral gaze movement
is possible but cannot be maintained in the deviated
position; that is, the eyes drift back slowly toward
primary position.
A corrective saccade repositions the eyes
eccentrically, and repetition of this pattern produces
nystagmus, aptly designated "gaze-paretic."
Saccades: Quick, darting conjugate
movements which direct the eyes to a new
target.

Smooth pursuit: A slower conjugate
movement which allows for tracking of a moving
object, or of a stationary object while we are
moving.

Convergence: A dysconjugate movement of
both eyes toward the midline to allow for
focusing on a near object by adjusting the angle
between the eyes.
Targeting eye movements
Variety of pathways contribute to
saccadic control and smooth pursuit
Smooth Pursuit
Two types:

Voluntary (actually termed smooth pursuit)
movements - originate in the temporo-parietal
lobe

Reflexive - which are under vestibular nuclear
control alone and constitute what is called the
vestibulo-ocular reflex (VOR).

Voluntary
Smooth Pursuit
originates near the
angular gyrus - Area 39 at
the temporal parietal
occipital junction

cells in this region are
able to compute the
speed and direction of a
moving object

results in ipsilateral
smooth pursuit
IPSI
Saccades
Under the control of three different areas in
the brain:

voluntary saccades - frontal eye fields
(Brodmanns area 8)

reflexive saccades to complex stimuli - parietal
lobes (Brodmanns area 7)

reflexive saccades to elementary stimuli -
superior colliculi
Saccades
Pause cells inhibit
Burst Neurons
which stimulate:
III & VI (horizontal)



or
III & IV (vertical)
CEREBRAL
HEMISPHERE
MIDBRAIN
PONS
PPRF
PPRF
VI
VI
FEF FEF
III
III
Voluntary Horizontal Saccades

Reflexive Saccades

- to complex stimuli
originates in area 7 of
the parietal lobe

- to elementary stimuli
originates in superior
colliculi



dorsolateral prefrontal
cortex involved in
planning of eye
movements
Optokinetic Reflex
Combination of saccades and
smooth pursuit that allow
tracking of targets in turn (e.g.
counting sheep as they jump
over a fence).

smoothly pursue one target,
then saccade in the opposite
direction to pick up the next
target

parieto-temporal junction
(smooth pursuit area) projects
down to ipsilateral vestibular
nucleus, inhibits it allowing
ipsilateral smooth pursuit

then, the FEF of the same
hemisphere generates a
saccade back (contralateral) to
the next target


Vestibular-Ocular Reflex
(VOR)
Causes eyes to move in the opposite direction to head
movement
Speed of the eye movement equals that of the head
movement
Allows objects to remain in focus during head
movements
Reflexive Smooth Pursuit -
VOR
maintains gaze on a
target despite head
movement

reflex arc
semicircular canal
opposite the head
turn detects motion
and activates the ipsi
vestibular n. which
deactivates its
inhibitory input on the
ipsilateral VI

results in eyes
turning opposite to
the head turn
VIII
p339 Medical Neuroscience, Nadeau et
al
Head impulse test
Peripheral Vestibular Disorders
Vestibular Neuronitis
Labyrinthitis
Menieres
Migranous Vertigo
Motion Sickness/ mal de Debarquement
Syndrome
Fistula
Benign Paroxysmal Positional Vertigo (BPPV)
Central Vestibular Disorders
Vascular
Wallenbergs Syndrome
Head Injury
Cerebellar Infarct
Postconcussive Syndrome
Demyelinating Disease
Congenital
Risk Factors

4 risk factors, 78% chance of falling in an older adult
Sedatives
Cognitive impairment
LE disability
Foot problems
Balance abnormalities
Dizziness
dependence on visual
cues
Fear of falling
Orthostatic hypotension

(Tideiksaar R 1998)
Objective of Clinical Exam
Establish location & severity of lesion (central or
peripheral)
Typical examination
- history (hearing status)
- cranial nerves
- vestibular
spontaneous nystagmus (imbalance in tone)
postural instability (abnormal tone & gain; proprioceptive loss)
VOR gain (maintained fixation, dynamic visual acuity)
head shaking (compensated UVL; not necessarily PVL)
calorics
pressure sensitivity (fistula)
positional nystagmus (Hallpike-Dix test)
hyperventilation (anxiety; acoustic neuroma)

History
Site of lesion Symptom Commen
t
Peripheral ( Labyrinth
or VIII nerve )
Tinnitus
Special cases :
Labyrinthine Ear fullness Menire's
disease
CP angle V , VI, VII
VII + VIII neuritis EAC vesicles + VII Ramsay Hunt
Brainstem
Diplopia(III, IV, VI or skew
deviation)
Facial numbness ( V )
Difficulty in swallowing,
choking
(IX, X )
Slurred speech ( XII and
cerebellum )
Uni bilateral numbness,
weakness, ataxia ( long tracts,
cerebellum )
Hemisphere Unilateral numbness,
weakness
Hemianopia (parieto-occipital
lobe)
Blindness ( both occipital
lobes )
Loss of consciousness :
Syncope, cardiac arrhythmia
epilepsy

MCA\PCA
Both PCAs

Common
Rare
Non vestibular causes of
dizziness
Causes
Endocrine Hypoglycemia
Adrenal failure
Pheochromocytoma
Cardiovascular Vasovagal syncope
Orthostatic hypertension
Embolic disease
Cardiac dysrhythmias
Hematological Hyperviscosity syndromes
Anemia
Psychological Anxiety
Phobias
Panic attacks
Drugs
Alcohol
Aminoglycosides
Anticonvulsants
Antidepressants
Diuretics
Marijuana
Methadone
Quinine/choloroquine
Salicylates
Sedatives
VESTIBULAR SUPPRESANTS
Rombergs Test
Sharpened Rombergs Test
Dysdiadochokinesia
Fukuda Marching/Unterbergers Test
Fukuda Writing Test
Tandem Gait test
Gaze Paretic nystagmus
Dynamic Visual Acuity
Screening for Hyperventilation Syndrome
Testing for Orthostatic Hypotension
Rombergs Test
Benign Paroxysmal Positional
Vertigo (BPPV)
Signs & symptoms
attacks of vertigo precipitated by certain head
positions & movements
e.g., rolling over, neck extension, bending forward
lightheadedness; nausea
anxiety
avoids movement
direction & duration of nystagmus differentiates
between BPPV & a central vestibular lesion (CVL)
Benign Paroxysmal Positional
Vertigo (BPPV)
5 criteria crucial in diagnosis (Hallpike-Dix Test):
torsional/linear-rotary nystagmus; reproduced by
provocative positioning with affected ear down
nystagmus of 1-5 sec. latency
nystagmus of brief duration (5-30 sec.)
reversal of nystagmus direction on returning to upright
position
response diminishes with repetition of maneuver
(fatigability)
(Massoud 96)


BPPV
Cupulolithiasis
Debris, probably fragments of otoconia from the utricle,
adhere to the cupula
Treatment
Semont, liberatory maneuver
BPPV
Most commonly posterior SCC 65-70%
Horizontal SCC in 15-20%

Diagnosis
Dix Hallpike Test
Postererior and Anterior canal
Roll Test
Horizontal canal

The test to be repeated 3 times on 2 separate visits
Hyperventilation
Hallpike-Dix Maneuver
Gold standard used to check for the presence of
benign paroxysmal positional vertigo (BPPV)
Nystagmus induced by this test is an objective
measurement from which we can determine SSC
dysfunction and assess a response to treatment
Canalolith Repositioning
Epleys Maneuvre
Semonts repositioning maneuvre
Semonts Liberatory maneuvre
270 barbecue Roll
360 Yaw Roll
Guffonis Maneuvre
Forced Prolonged positioning
Brandt Daroff Exercise
Epleys Repositioning maneuvre
360 Yaw Roll
When not to prescribe a Vestibular
Suppresants
BPPV (Canalolithiaisis/Cupulolithiasis)
Chronic Menieres
Chronic vestibular disorder


There is inhibition of the central compensation
mechanism.
Interferes with clinical interpretation of diagnostic
tests.
Medications
Anti cholinergics
Anti Histamines
Calcium channel antagonist


Other Medications
Diuretics
Anxiolytics
Vestibular neuritis
Sudden Spontaneous vertigo
Aggravated by head movement
Horizontal torsional Nystagmus
Positive head Impulse Test
Subjective Visual Horizontal Test
Short course of Steroids
Bilateral Vestibulopathy
Bilateral vestibular or labyrinthine damage
Ototoxictity
Postural imbalance most marked while walkinng
No Spontaneous Nystagmus
Head Impulse Test
Vestibular Rehabilitation
Vestibular Migraine
Episodic headache with vertigo
Recurrent attacks with positional vertigo
Aura
Phonophobia/photophobia
Anti migranous treatment
Vestibular Exercise Program
Objectives
Complement CNS natural compensation
diminish dizziness & vertigo
enhance gaze stabilization
enhance postural stability in static & dynamic
situations
Increase overall functional activities
Patient education
nature of pathology
episodic nature, prognosis
control of exacerbations
Factors affecting Compensation
Visual Impairment
Impaired Propricoception
Hyperventilation
Somatization
Autonomic Symptoms
Vestibular Supressant Drugs
Head Injury
Cerebellar degeneration