Dr. T. Balasubramanian M.S. D.L.O.
Definition: Vertigo is defined as the subjective
sence of imbalance. It has its root in latin word "Vertere" which
means to turn. Patient generally has difficulty describing his
Synonyms: Vertigo, Dizziness, Unsteadiness.
Types of vertigo: Vertigo can be grossly classified into two
1. Rotatory: If the sensation is rotatory it is easy to describe
2. Non rotaroty: There is obviously no sence of rotation and the
patients have difficulty in describing this sensation.
These groups can further be subdivided into episodic and continuous
according to the persistence of symptoms.
Figure showing classification of vertigo
Vertigo can be caused due to
disturbances in the inner ear or in the central nervous system.
It is important to differentiate the vertigo caused by peripheral and
||Weeks / Months
||Seconds / minutes
|Nerologic / Visual
Table showing the features of central and peripheral vertigo.
A detalied history of the disorder is
elicited from the patient with specific reference to postural
variations, severity, mode of onset etc. The patient must also be
quizzed about the associated neurologic / visual / auditory
symptoms. Left to themselves the patient may not give the
complete story, the examiner will have to take active control of
history taking. The patients will be keen to emphasise the
aspects which has impressed them the most. The patient should be
specifically asked about periods of freedom from vertigo. History
taking should be done chronologically.
A detailed history of drug intake is also a must to rule out drug
induced dizziness / vertigo. A list of possible drugs are given
1. Anti Alzeimers - Drugs used in treatment of Alzeimers disease like memantine,
rivastigmine, tacrine can cause dizziness.
2. Anti psychotics - Anti psychotic drugs like chlorpromazine,
prochlorperazine, fluphenazine,perphenazine, thioridazine,
trifluoperazine can cause dizziness.
3. Antidepressants - Can cause dizziness
4. Anxiolytics - Like diazepam, alprazolam can cause
5. Mood stabilisers - Like Gamapentin can cause dizziness
6. Anticonvulsants - Like Phenytoin can cause dizziness
Examination of a Dizzy patient:
As a first step the peripheral causes of vertigo should be ruled
out. This can be achieved by a through otological
examination. All the cranial nerves must be tested for
integrity. Cerebellar function should be assessed by past
pointing or by dysdiadokokinesis. Every dizzy patient must be
examined for the presence of nystagmus with specific reference
to its type. If the nystamus is horizontal then in all
probability the cause could be peripheral i.e. auditory. A
direction changing horizontal or vertical nystagmus could indicate a
central cause for the same.
Examination of corneal reflex: This test is sufficient to test
the integrity of the trigeminal nerve. This test is so sensitive
that it is positive even in patients with a small acoustic
Assessment if facial nerve: can be performed by just looking at the
patient when he / she attempts to close the eyes. They will have
inability to bury their eyelashes during tight closure of eyelids.
Performing a routine audiogram will assess 8th nerve function.
Cranial nerves 9th and 10th can be rapidly tested by looking for gag
reflex. 11th nerve can be tested by asking the patient to shrug
the shoulders, which is not possible if the nerve is affected.
Hypoglossal nerve can be assessed by just asking the patient to
protrude the tongue. It always tends to deviate towards the side
of paralysis, inaddition there may be wasting of tongue musculature on
the side of the lesion.
Blood flow through the carotids should also be carefully examined to
rule out carotid occlusion as a cause of giddiness. Patient's
blood pressure and blood sugar levels must also be measured.
Presence of Nystagmus along with vertigo is always organic.
Nystagmus is defined as a disturbance in ocular posture, characterised
by a more or less rhythmical oscillation of the eye ball. The
speed of the ocular movements may be the same in both directions or may
be quicker in one directior when compared to the other. The
direction of nystagmus is also important, a vertical nystagmus is more
common in central causes of vertigo.
Basics of ocular movements: The movement of eyeball is controlled
by 6 extraocular muscles i.e. 4 rectus and 2 oblique muscles.
Among these muscles the superior oblique muscle is innervated by
trochlear nerve, and lateral rectus by abducens nerve. All the
other muscles are innervated by oculomotor nerves. There is
something unique in the oculomotor supply, i.e. it innervates the
ipsilateral ocular muscles except for superior rectus which receives it
supply from the contralateral side.
The superior oblique muscles are supplied by the
contralateral trochlear nerve. The abducens nerve have two types
1. Motor neurons innervating the ipsilateral lateral rectus muscle
2. Internuclear neurons supplying the contralateral medial rectus
Axes and planes of ocular movements: The axes
and plane of ocular movements should be clearly defined before an
assessment could be made. Three axes have been referred:
1. X axis : Also known as parasagittal or naso occipital
2. Y axis : Also known as transverse or interaural
3. Z axis : Also known as vertical axis
Movement along these axis are described as:
Torsional - Roll or rotation about X axis.
Vertical - Pitch or rotation about Y axis
Horizontal - Yaw or rotation about Z axis
Primary position of the eye: is the postion of the eye in which there
is pure horizontal or vertical rotation is associated with zero
torsion. Clinically this position refers to the position of the
eye when looking straight ahead with the body and head held straight
Secondary position of the eye: is reached by pure horizontal or
vertical rotation of the eye.
Tertiary position of the eye: is reached when there is a combination of
horizontal and vertical rotation from the primary position
Torsional eye movements: These are rotatory movements of the eye
ball. When the eye ball rotates in such a way that the upper pole
of the eye tilts towards the right of the subject it is known as clock
wise rotation (always in the subject's point of view). When the
upper pole of the eye tilts towards the left of the subject it is known
as counter clock rotation.
The position of the eye ball is dependent on two sets of impulses, the
visual and vestibular. The visual impulses are concerned with
maintenance of position of eye in relation to the object of
interest. The vestibular impulses help in maintainance of the
position of eye ball in relation to that of the head.
Pendular nystagmus: is a horizontal to and fro movement of the eye
ball. The to and fro movements are almost equal in
velocity. This is commonly seen in patients with blindness.
The eye ball is attempting to focus the image at the fovea of the
retina. Since the patient is blind the eye ball keeps searching
for visual object to focus hence this nystagmus. It is also known
as the Blind Man's nystagmus.
Horizontal nystagmus: This is characterised by rhythmic
oscillations in which the movement in one direction is significantly
faster than the other. The slow movement is the pathological one
while the faster one is the corrective component. The direction
of the corrective faster movement is used to denote the direction of
the nystagmus. The position in which the nystagmus is least
marked is known as the Null point.
Figure showing horizontal nystagmus
Spontaneous nystagmus: is said to occur when the
rhythmic movements are present on the forward gaze.
Induced nystagmus: is said to occur when the rhythmic movements of the
eye are brought about by some specific test.
Gaze nystagmus: or intermediate nystagmus is said to occur during
extremes of lateral or vertical gaze positions.
Procedure for examining for nystagmus:
1. The patient should be positioned in good light.
2. The object of focus should be at infinity
3. While looking for lateral gaze nystagmus care must be taken to
ensure that the nose does not block the field of vision.
Causes for spontaneous nystagmus:
Labyrinthine: Labyrinthine nystagmus is usually biphasic.
Its features are:
a. It is usually associated with a sensation of vertigo
b. It is always unidirectional.
c. It is more marked when looking at the direction of the fast phase
d. It is enhanced on removal of optic fixation or on eye
closure. Frenzels glasses can be used to remove optic
fixation. It is actually a 10 diopter glasses worn by the
patient. It removes optic fixation there by enhancing
labyrinthine nystagmus. These glasses makes the eye look larger
when viewed by the observer. Even small degrees of nystagmus will
e. The nystagmus produced is fatiguable
Central nervous system lesions causing spontaneous nystagmus:
Nystagmus caused by lesions involving the central nervous system has
the following features:
a. Nystagmus is bidirectional (direction changing)
b. Nystagmus could be commonly vertical
c. Nystagmus usually is non fatiguing in nature
d. Nystagmus is not enhanced on removal of optic fixation
Nystagmus caused due to drugs and toxins:
Drugs and toxins cause nystagmus by their effect on the central nervous
system. The nystagmus induced by toxins and drugs more or less
resembles that of central nervous system nystagmus
Ocular nystagmus: Any lesion affecting the macula, especially
when the peripheral vision is still maintained may cause nystagmus
which is pendular in nature. This nystagmus commonly occur in
ambylopia. Miner's nystagmus also fall into this category.
Congenital nystagmus: is often familial, usually horizontal and
pendular. The null point in this type of nystagmus is close to
the position of forward gaze. Closure of the eyes results in
reduction of nystagmus.
Causes of induced nystagmus:
Nystagmus may be induced by clinical testing
or by certain investigations. The most common clinical test
inducing nystagmus is the positional test (Dix Hallpike
manoeuver). This is useful in diagnosing BPPV. This
procedure is explained in detail under the topic BPPV.
Another way of inducing nystagmus is by performing a fistula
test. This test is positive in the presence of labyrinthine
fistula. In this test nystagmus and giddiness is induced by
altering the pressure of air in the external canal.
Exposure to loud sounds in these patients also can cause nystagmus and
giddiness. This is known as Tullio phenomenon.
In clinical setting nystagmus can be induced by performing caloric
tests / cold caloric tests or by the use of optokinetic drum which can
stimualte optokinetic nystagmus.
Oscillopsia: is the term used to describe the illusion of motion
of environment due to an inadequate vestibulo ocular reflex.
During head and body movements images are held steady on the retina by
the presence of vestibulo ocular reflex. Patients with reduced
peripheral vestibular function often have oscillopsia. One method
for testing for oscillopsia is to test the patients visual acuity with
a Snellen eye chart with the head held still, and repeating the same
test during passive high frequency head movements produced by the
examiner. The patient will have reduction in acuity if
oscillopsia is present.
2. Caloric tests
3. Electric nystagmography
4. CT scan / MRI scan to rule out acoustic neuromas / CNS lesions
Figure showing the causes of vertigo
Alternobaric vertigo is caused due to sudden change in
altitude. This occurs in fighter pilots due to sudden altitude
changes which occur during flying military jet fighter planes.
Episodic vertigo can also occur due to metabolic failure of labyrinth
as seen in:
1. Menier's disease
2. Syphilitic labyrinthitis
3. Delayed endolymphatic hydrops
4. Following middle ear surgery.
Destructive lesions of labyrinth: Can cause prolonged rotatory
vertigo lasting for more than 24 hours, usually less than 3-4
weeks. These include:
1. Vestibular neuronitis
2. Trauma: Head injury, Ear surgery, Labyrinthectomy, and vestibular
3. Labyrinthitis: Bacterial / viral
4. Vascular lesions
5. Metastatic deposits in CP angle
Unsteadiness: Patients who are unsteady may have problems
describing their symptoms. Commonly it could be due to:
Physiological overload: Unsteadiness caused due to physiological
overload of the vestibule or the central processing systems may
cause unsteadiness. This could occur due to:
a. Excessive input as can happen in a normal person with very rapid
b. May also occur as a result of abnormal input, especially from visual
c. It may result from minor inadequacies in visual, proprioceptive or
Unsteadiness lasting for hours / days may be due to temporary
impairment of central vestibular connections or decompensation of
vestibular system. Drugs are the most common cause for this
temporary unsteadiness. Other causes include travels sickness,
perilymph fistula, Active chronic suppurative otitis media,
Vestibular inadequacy may cause unsteadiness lasting for weeks or
months. This is often seen in elderly. Vestibulo toxic
drugs like gentamycin can cause unsteadiness.
Vertigo following head injury may be due to:
a. Post concussional syndrome
c. Perilymph fistula
d. Delayed hydrops
Treatment of vertigo:
Vestibular system can be suppressed by using labyrinthine sedatives
Wait for compensation to occur: In all peripheral causes of
vertigo central compensation eventually occur in 6 weeks time.
Patient should be encouraged to performed labyrinthine exercises.
As a last resort the offending labyrinth can be eliminated by using
intra tympanic drugs like streptomycin or surgical labyrinthectomy.
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