Vertigo

Dr Bala Pradeep Boyidapu

Post graduate resident
Department of Neurology
GMKMCH, Salem
Vestibular system
• Function : equilibrium, coordination, orientation to space
• Monitor linear and angular acceleration
• Transduced into neuronal signals within labyrinth.

• Labyrinths:
1. Otolith organs-utricle, saccule --> macula acoustae --> linear
acceleration
2. 3 semicircular canals --> Cristal ampullaris --> angular acceleration
3 semicircular canals – oriented at right angle to each other
1. Lateral/horizontal
2. Anterior/superior
3. Posterior/inferior

• Utricle- parallel to skull base--- horizontal movements of head

• Saccule – parallel to sagittal plane--- vertical/tilting

• The canals are maximally stimulated in the lane of their anatomical axis.
• The horizontal canal best detects rotational head movement in the side to side (“no-no”) direction (with
chin tucked to bring the canal fully horizontal)
• The posterior canal best detects movement in the anterior posterior plane (“yes-yes”)
• The anterior canal best detects lateral tilting movement

• The canals on the two sides form functional pairs.

• The horizontal canals work together
• The anterior canal on side is approximately parallel to the posterior canal on the opposite side forming a
spatial pair
 Cell bodies of vestibular ganglion of scarpa

Vestibular nerve
superior aspect – input from anterior, horizontal SCC , Utricle
Inferior aspect – input from posterior SCC, saccule

Lateral brainstem-pontomedullary junction

Bifurcates into ascending and descending fascicles

Vestibular nuclei (4)

Superior-Bechtel, lateral-dieters, medial-Schwalbe, inferior/spinal-roller
Rostral medulla to caudal pons
Saccule-superior, medial nuclei
Macula-medial, inferior nuclei

4 vestibular connections
1. Oculomotor system
2. Spinal cord
3. Cerebellum
4. Cortex
MLF
-through the connections with 3,4,6,11, upper cervical nerves regulate
conjugate eye movements, head posture and neck movements.
-superior vestibular nuclei-I/L MLF, medial nuclei-C/L

Medial vestibulospinal tract-crossed

-excitatory/inhibitory effects on C/L cervical and upper thoracic cord
-medial vestibular mostly, lateral, inferior

Lateral vestibulospinal tract-uncrossed

-regulates muscle tone and posture- extensor tone of trunk
-lateral,inferior vestibular nuclei to I/L cord
Vestibulo-cerebellum
• Juxta restiform body-collection of fibres medial to inferior cerebellar peduncle
• Vestibulocerebellar fibres run throu and form art of mossy fibre input to cerebellum
• Direct/primary vestibulocerebellar tract: bypass vestibular nuclei, terminate in I/L
nodules, uvula, fastigial nucleus
• Indirect/secondary vestibulocerebellar tract: from superior, medial, inferior nuclei
terminate in flocullus bilaterally

Reticular formation

VPL nucleus and posterior group nucleus of thalamus

-B/L superior, lateral, inferior nuclei

Cortex
Post central gyrus-broadmann area 2,5; area 6 of frontal lobe, superior temporal gyrus
• Blood supply
• Membranous labyrinth- labyrinthine artery----br of AICA mostly, rarely
basilar artery
• 3 branches –
1. Anterior vestibular– anterior, lateral SCC, Utricle
2. Posterior vestibular– posterior SCC, Saccule,
3. Cochlear
Physiology
• Under normal circumstances, the neural activity in the labyrinths is equal on both sides.
• Action of each vestibular system as pushing towards opposite side.
• When two labyrinths push equally, the system is in balance and function is normal.
• When one labyrinth is under active, the opposite labyrinth pushes the eyes extremities and body towards the side
of under activity.
• Nystagmus results from corrective saccade initiated by frontal eye field in response to the deviation of gaze
towards the side of the underactive labyrinth.
• The fast component is opposite direction of underactive labyrinth.
• When both labyrinths are disease, there is no vestibular imbalance and hence no nystagmus, vertigo, or other
signs.
• Over time, either an asymmetry in the baseline firing rates resolves or the central nervous system (CNS)
compensates for it. (entire u/l peripheral vestibular system can be surgically destroyed and pts only
experience vertigo for several days to weeks, with slow-growing tumors-acoustic neuroma generally do not
experience vertigo or nystagmus]
Bedside tests of vestibular function
• Vestibulo spinal reflexes- past pointing, Romberg sign, tandem
Romberg, unterberger-Fukuda stepping test, star walking test,
tandem gait
• Vestibulo ocular reflexes- doll’s eye test, head thrust test, dynamic
visual acuity, caloric tests
• Nystagmus- spontaneous, positional, after head shaking
Past pointing
Vestibular imbalance---
• The normal more active labyrinth will push the limb to the abnormal
less active side and he miss the target.
• After a period of compensation, it disappears and may even occur in
opposite direction.

Cerebellar ---
I/L limbs has ataxia, incoordination, past pointing occurs only with the
involved arm, to the side of the lesion.
Romberg test
U/L vestibulopathy
• If balance lost with eyes closed, then patient tend to fall towards the side of lesion
• If the patient has spontaneous nystagmus due to vestibular pathology, fall will be
in the direction of slow phase.
Direction of fall can be affected by changing head position
• In Right vestibulopathy,
• facing straight ahead, tend to fall to right
• Looking over right shoulder, fall backwards
• Looking over left shoulder, fall forwards.
• Sharpened Romberg or tandem Romberg ---pt stand tandem with eyes closed
• Tandem gait – tend to fall towards the side of lesion
Unterberger-Fukuda stepping test
Oculocephalic reflex doll’s eye test
• In comatose pts
• Turning head in one direction causes eyes to turn in opposite
direction
• Vestibular nuclei in medulla to extraocular nuclei in pons,midbrain are
intact functioning –brainstem intact
Head thrust test
Dynamic visual acuity
Caloric test COWS
NYSTAGMUS
spontaneous
• The slow phase of spontaneous vestibular nystagmus is in the
direction of lesion,
• fast phase away– due to normal labyrinth pushing eyes towards the
diseased side with cortex generating corrective saccade away from
the abnormal side.
• Torsional component suggests peripheral origin
Alexander’s law: Amplitude increases with gaze in the direction of fast phase

• First degree- when nystagmus is only present with gaze in the direction of fast
phase.
• Second degree- nystagmus present in the primary gaze
• Third degree- nystagmus occurs when fast component opposite to direction of
gaze.

• Peripheral nystagmus is markedly inhibited by visual fixation

• Spontaneous nystagmus due to central is pure horizontal or pure vertical
• Inhibiting fixation with Fresnel lenses will make the nystagmus more obvious
both by blocking fixation and magnifying eyes
• Torsional nystagmus is more prominent bcoz vertical/horizontal are easily
suppressed by fixation
• Head shaking nystagmus – turing head back and forth with eyes
closed for 30sec
• No nystagmus occurs is normal, with vestibular – brief spontaneous
nystagmus away from the abnormal side
• Can be seen by tapping on the head or low frequency vibration on
mastoid.
Positional nystagmus
• Placing head to particular position
Dix hallpike / nylen-barany maneuver:
• If vertigo or nystagmus occurs, the patient is held in provoking
position until symptoms subside and movement is repeated to assess
recurrence.
Side lying test:
• Head is turned 45 degree in one direction and patient lies on his
opposite shoulder.
• In BPPV,
• Nystagmus begins after a latency of 3-10sec to 40sec persist for 20-
30sec to 1min
• Commonly torsional with fast component towards the geotropic ear
(dependent)
• BPPV involving other than posterior canal, D H test is negative
• Roll test – rolling the head of supine patient to one side provoke
response with horizontal canal BPPV
Positional nystagmus

Paroxysmal Static
• Fleeting, fatiguable, • No fatigue
• Difficult to reproduce • Present as long as head is in
• Vertigo prominent provoking position
• Vertigo less prominent
• Centre or peripheral vertigo
Quantitative tests
Electronystagmography(ENG)
• Electrooculography (EOG) –method of recording direction,amplitude, velocity
of eye movements by measuring changes in corneoretinal potentials with
electrodes, EOG during stimulation of labyrinth to cause nystagmus is ENG.

Rotatory chair testing

Posturography
• Measures the compensatory movements of the patient’s feet while visual,
somatosensory and vestibular perceptions are manipulated.
HINTS
Central vertigo
• Typically less severe
• Imbalance is more severe
• Facial weakness, numbness
• Nystagmus changes direction, not
affected by visual fixation
• Nystagmus persists for weeks to months
• in the direction of nystagmus slow phase.
• Nystagmus – lack of latency, adaptable,
fatiguability.
Peripheral vertigo
• More severe
• Nausea, vomiting, autonomic symptoms more
• Aural symptoms
• Nystagmus does not change direction, suppressed
by visual fixation
• For 12-24hrs
• Patient will past pointing, fall on Romberg, turn
on stepping test, drift while walking eyes closed---
• Nystagmus is positional, latency, adaptable,
fatiguability. Have rotatory component
Thank you