AN INTEGRATED APPROACH TO VESTIBULAR

PHYSIOLOGY AND EVERYDAY CLINICAL PRACTICE

I: VESTIBULAR ANATOMY AND PHYSIOLOGY

II. TIPS ON THE BEDSIDE EXAM OF THE DIZZY PATIENT

MUMBAI, 2017
davidsamuelzee@gmail.com
 Dynamic Visual Acuity (DVA)

Normal subjects lose only 1 line of acuity with head shaking. Patients with
no vestibular function lose about 5 lines with horizontal or vertical
rotation but not with rotation in ‘roll’ (ear to shoulder) since the image is
still on the fovea. Patients who lose same amount of DVA in ‘roll’ are
malingering!
 LOCALIZATION OF VESTIBULAR NYSTAGMUS
– Peripheral lesions
– Nystagmus is increased or brought out by
removal of fixation (Romberg sign of VOR)
– Mixed horizontal-torsional nystagmus is
characteristic for complete loss of function
on one side
– Intensifies when looking in the direction of
the quick phase (Alexander’s Law)
– Central lesions
– Fixation suppression of nystagmus may be
impaired
– Pure vertical or pure torsional nystagmus
– Nystagmus may intensify or diminish when
looking in the direction of the quick phase. If
diminishes (anti-Alexander’s law) the cause is
central
VIII Nerve lesion NYSTAGMUS WHICH
causing an CHANGES DIRECTION
ipsilateral slow-
phase vestibular ON CHANGING
bias DIRECTION OF GAZE,
i.e., GAZE-EVOKED, IS
Cerebellar lesion ALWAYS CENTRAL
causing an
ipsilateral gaze-
holding deficit
with
contralateral
slow phases
 Wernicke’s Disease (lesions in the medial vestibular nuclei)

Clinical points
• Wernicke’s syndrome can present with ophthalmoplegia, nystagmus
of virtually any type, gaze palsies and internuclear ophthalmoplegia
• B1 deficiency occurs in the setting of malnutrition due to alcoholism,
chemotherapy, eating disorders, post gastric diversion procedures
• Bilateral horizontal vestibular loss is often associated.
• Treat with IV 500mg B1
Ocular Tilt Reaction (OTR) –
acute tone imbalance of static Counterroll
utricular righting reflexes
(analogous to spontaneous
nystagmus from a semicircular
canal imbalance Skew

Head Tilt

Michael Ann Neuro 1979

Halmagyi
Why this peculiar pattern? There is a lateral-eyed rabbit in us all

SS
Wallenberg’s Syndrome – Posterior Inferior
Cerebellar Artery distribution infarct
involving the dorsolateral medulla

Caudal vestibular nuclei

Skew with lower eye on the side of the lesion occurs

because of involvement of the caudal vestibular nuclei
(VN) to which project mostly otolith inputs. Skew is
part of the OTR (ocular tilt reaction) with a skew, head
tilt and ocular counterroll.
 WE ALL HAVE RABBITS INSIDE OUR “HUMAN” BRAINS
In the lateral-eyed rabbit, a lateral tilt (one ear up and the other
down) leads to the eyes rotating around the roll axis with one eye
rotating down and the other eye rotating up (a physiological skew)

Top View
Right ear down

RE
must
move LE
up must
move
down

This is reflected in the Ocular Tilt Reaction (OTR)

– which (the rabbit) emerges when there is
imbalance in otolith (utricular) responses
 Mechanism of abnormal perception of upright in OTR
In normal, frontal-eyed, foveate animals the normal response to a
lateral head tilt is pure ocular counterroll or torsion without a skew
In pathology, in frontal-eyed, foveate animals the abnormal
response to a perceived shift of the sense of vertical
becomes a “compensatory” head tilt, counterroll and a
skew that produces vertical diplopia
Bucket technique for Subjective Visual Vertical (SVV)
(ocular counterroll)

After Zwergal, Neurology,

09, and Frisen, Neuro-
ophthalmology, 2000
 Physiological principles for testing
the angular (rotational) VOR

1. Normally with the head still, the left and right vestibular nerves and the vestibular
nucleus neurons to which they project have equal resting discharge rates (vestibular
tone so they can work in “push-pull”; when one side is excited (by rotation to that
side) the other is inhibited).

This puts the brain in good stead as even with just one labyrinth the brain can still
detect rotations in either direction based on the change in activity above and below
the tonic firing discharge from just one labyrinth.

1. But because of Ewald’s second law, there will still be an enduring deficit for rotations
toward the affected side since excitation is a more effective stimulus than inhibition
for high velocity rotations (since tonic firing rate cannot go below zero) and for high
acceleration, high frequency rotations, which can never be transduced perfectly using
just one labyrinth.
Middle cerebellar peduncle lesion in
AICA infarct
REMEMBER
A majority of AICA
infarcts cause hearing
loss.
AICA infarcts usually
lead to mixed central
(brainstem and
cerebellum) and
peripheral (labyrinthine)
involvement.
The key clinical tests in the evaluation of vertigo

Pattern of Spontaneous Nystagmus

Ocular Alignment

HIT and DVA

Head-shaking Nystagmus

Positional Nystagmus
 Some ancillary tests in the evaluation of vertigo

Valsalva

Vibration

Sound
Pursuit and VOR
cancellation

Tragal-compression

Hyperventilation