What is BPPV?
What is its natural history?
What causes BPPV?
How is BPPV diagnosed?
What are the treatments for BPPV?
Medical Officer, Dept. of
It is a common occurence. and one of the easiest to
diagnose and treat.
As the name BPPV indicates that it is:
Benign or not a very serious or progressive condition;
Paroxysmal, meaning sudden and unpredictable in onset;
Positional, because it comes about in specific head
“BPPV is a spinning dizziness that occurs in only one or
two of a series of head positions and each attack is
characterized by spinning vertigo, is short, usually severe
and may be accompanied by geotropic nystagmus that
occurs a few seconds after specific head movement.”
Age: It occurs most frequently in the middle-aged, in the
forties and fifties.It is rare or infrequent in childhood or
youth and old age.
Sex: It shows no sex preference other than slightly
greater representation of women in fifth decade.
The symptoms are most often experienced when the
patients lie down, which distinguishes it from Orthostatic
hypotension. Movements like rolling over in bead, bending
over, or looking upward usually initiate a attack of BPPV.
The vertigo usually lasts no more than a minute or two.
Both the vertigo and nystagmus tend to lessen in severity
with repititions of the evoking movement.
It may be accompanied by a slight feeling of nausea and
vomiting in some patients.
Vertigo persists typically for only a few days or weeks, then
declines and stops. The period of remissio that follows is
usually prolonged from months to years. In the group of
patients with reasonable antecedent cause such as head
injury the period of activity may be long, but not in the
It is not possible to quantify postural vertigo other than to
note its presence or absence, and if present, its intensity.
Positional Nystagmus however, lends readily to
Persistent forms of positional nystagmus occur from static changes of head position
relative to gravity (STATIC)
Paroxysmal forms require in addition a certain brisk speed of movement from one
position into the provocative position (DYNAMIC)
The proposed classifiction Hugh o Barber’s, divides nystagmus into two types:
Type I (STATIC PERSISTENT)
Type II (DYNAMIC PAROXYSMAL)
While Paroxysmal Postional Nystagmus (PPN) is certainly nearly always due to non
lethal (benign) inner ear abnormality, this is not always the case.
Cases of PPN due to vertebrobasilar disease, tumors of posterior fossa, cerebellum
and brain stem have been reported. However in these cases the nystagmus is
more likely to be atypical than typical.
Another name of BPPV is cupulolithiasis,
meaning “rocks in the cupula”
It has been discovered that the probable cause
of BPPV is dislodgement of small calcium
carbonate crystals that float through the inner
ear fluid (endolymph) and strike against the
sensitive nerve endings (the cupula) within the
balance apparatus at the end of each
semicircular canal (the ampulla)
Assessment of any disorder of Equilibrium must be based on
a multidisciplinary approach.
A comprehensive careful medical history is imperative and
can often indicate the direction to take in order to further
investigate the cause of the complaints.
Together with complete general medical examination, with
particular attention to CVS, Locomotor System, CNS,
Eyes and Ears.
Although exclusion of otological pathology is essential in any
balance disorder, many conditions will elude diagnosis if
balance is equated purely with a disorder of vestibular
Patient should describe in
his own words what the
complaint of “dizziness” or
“vertigo” actually involves
From this description it
becomes clear whether the
pateint means dizziness in
the medical sense of
vertigo or whether it’s a
matter of visual
headedness , orthostatic
It it really is “vertigo” then it
is necessary to ask:
What type is it
In case of attacks one has to know the frequency and
duration, or any vegetative symptoms.
Influencing circumstances if any.
Secondary Symptoms e.g., tinnitus, reduced
hearing, headache, neurologic
abnromalities(parasthesias), visual and speech
disturbances, or diminished awareness etc.
GENERAL & SYSTEMIC EXAMINATION:
Patient’s temperature, blood pressure and
Pallor, cyanosis, jaundice.
Assessment of Cardiovascular /
Neurological / Psychiatric status is important.
A simple hearing test using wispering voice can give an
estimate of Hearing loss if any.
• TUNNING FORK TESTS
• Gives a more
accurate idea of
hearing loss and
determining the type
of hearing loss.
• Following tests can be
STANCE & GAIT (Vestibulospinal
(1) Romberg (Romberg 1846)
Assess ability to stand, feet together,
hands by the side, with eyes open
and closed for 20-30 sec.If required
clasp his hands together and pull t
divert his attention.
In presence of a uncompensated
unilateral, peripheral vest. Lesion ,
lesion of posterior white column
orunilat. Cerebellar lesion patient
tends to sway towards the affected
Quantitative assessment of body sway
may be achieved by using a balance
(2) Gait Testing:
May provide information about many systems which give
rise to imbalance. Although vestibular, visual and
proprioceptive activity are all vital for maintenance of
perfect balance, spatial orientation can be controlled by
any two of these mechanisms (Joughees 1953). This
physiological principle is admirably demonstrated on gait
testing of a patient with bilateral vestibular failure.
Unilateral cerebellar hemisphere pathology like unilateral
vestibular pathology cause a tendenmcy to veer to affected
Medline cerebellar dysfunction tends to give broad based
Loss of proprioception results in high stepping foot slapping
Patient has to walk with knees
raised high, on a spot for 1
minute with his eyes closed and
his arms stretched out
horizontally in front. Turning to
one side by more than 45 deg.
In the course of 50 steps is
pathological and points to a
Patient is made to walk five paces
forward and five paces backward
with eyes shut for 30 seconds.
In a unilateral vestibular lesion
patient walks in a star shape.
EYE MOVEMENT TESTS:
Careful examination of eye movements and nystagmus provides a
wealth of information regarding vestibular disorders.(Bedside
assessment may provide much information, but quantitative data may
be more accurately interpreted by using precise visual targets and
recording the eye movt.s by electronystagmography.
(1) NYSTAGMUS TESTS:
• Involves carefully observing and interpreting involuntary eye
• Nystagmus has a slow (vestibular) phase and a fast (central) recovery
phase. Because this fast recovery phase can be seen best, the type of
nystagmus is named after the direction of this phase. Nystagmus
towards the right generally indicates pathology on the left hand side.
• Nystagmus can be divided in a number of ways:
•Spontaneous Nystagmus: Nystagmus which occurs With head in
normal upright postion. This is not necessarily pathological
•Induced Nystagmus: Nystagmus which occurs when
•Head is held in a certain position – positional nys.
•Head is brought into a certain position – Positioning nystagmus
Positional/ positioning nystagmus
When head is in a position other than a normal upright position
Wait for 10 seconds in a particular head position to give any
positioning nystagmus a chance to die away.
Any nystagmus which persists as long as patient is lying in a
particular position is permanent postional nystagmus Central
Nystagmus which occurs both when the patient islying on his left
and right side is known as symmetrical nystagmus Central Cause.
The nystagmus occurs when there is a change of head position and
provided it is of short duration has no significance.
In case of BPPV, a specific positioning nystagmus can be elicited
which is pathological.
Dix & hallpike used the term “benign postural
vertigo” to denote the symptoms & “postional
nystagmus of benign paroxysmal type” to
denote the nystagmus.
They also considered the lesion was peripheral
and located in the utricle of the ear, which, when
undermost released the nystagmus.
nystagmus is diagnostic of
It occurs when the head is
moved into a provocative
position (head hanging Rt.
Or Lt. or head hanging
sagittal) quickly but not
slowly. Latent period of 1-
10 sec. When nystagmus
appears , it quickly reaches
peak then declines more
slowly and stops within 30
seconds, and on repeating
the test the nystagmus and
vertigo can be exhausted.
Have the patient look at a point 30 deg away from
midline to the right and left in succession.
Latent nystagmus becoming stronger when looking in
one direction and not dying away Cause is peripheral
Nystagmus appearing exclusively when looking to one
side: Unilateral gaze nystagmus. Cause is central.
Bilateral gaze nystagmus points to a central CNS
(2) EYE MOVEMENT TESTS:
(1) Saccadic Eye Movements: Assessed by asking the patient to look back and
forth, between two targets directly in front of him and note (latency, velocity and
• No abnormality – Peripheral labyrinthine disorders
• Prolonged Latecny – Damage to the supranuclear control of the brain stem
saccade-generating centres eg., basal ganglion disorders.
• Impaired saccadic accuray (over and undershooting) – Cerebellar
• Slowing of saccadic movts. – lesion at any level from pretectal and
parapontine saccade-generating centres to the extraocular muscles.
(2) Smooth Pursuit System:
Smooth pursuit system may be examined
clinically by moving a finger slowly backwards
and forwards in front of the patient’s eyes.
Bilateral impaired persuit – Tired or inattentive patient,
psychotropic medication, alcohol etc.
Unilateral derangement – Organic disease of
cerebellar hemispheres, the brainstem or parieto-
Compensation from a Vestibular
The rate at which a patient compensates
depends upon four factors:
Age: The younger the patient the faster the
Patient compensates quicker from a peripheral lesion
e.g.,labyrinthitis, than from a central one, e.g., brain
stem vascular thrombosis.
Compensates quicker from unilateral than from
Compensates from a static lesion, e.g.,
labyrinthectomy, than from a variable one eg.,
Spontaneous Resolution:In most cases
In others symptoms persist ( It is found that these latter
individuals have studiously avoided head positions that
precipitate their symptoms – Hugh.O.Barber).
Medications: Most patients who report to physicians/
surgeons are prescribed medications such as
Meclizine or Diazepam
(There is no good evidence that medications are of value
A variety of types of physical therapy have been recommended
How do these exercises work?
One possibility is that habituation of the abnormal vestibular signals
is enhanced when the patient is repeatedly put in the offending
An alternative hypothesis (Brandt and Daroff) is that exercises
shake free otlithic debris from the cupula and entered them into a
Whatever the mechanism, these exercises or similar protocols
are almost always successful provided patient adheres to them
When symptoms donot respond to the exercises, it is worthwhile
reconsidering the diagnosis and carrying out CT scanning.
THE EPLEY OR SEMONT
crystals(otoconia) away from
the nerve endings using gravity
and moving them into an area
of the inner ear that won’t cause
To achieve this, the patient’s
head is moved into various
positions of the apley
maneuver, the posterior
semicircular canal is rotated in
such a way as to deposit the
displaced otoconia back into the
Turn the patient’s head 45
degees to the side with most
prominent symptoms during
With both hands
holding the patient’s
head, gently lay the
patient down in the
supine position with the
head hanging over the
edge of the couch, by
45 deg. Keep the
postiion for at least 30
sec. or until nystagmus
Examiner now comes
to the head end of the
bed so as to be able to
rotate patient’s head
•Turn the patients head
90 deg. In the opposite
direction and observe for
observe till the nystagmus
disappears or for at least
•Ask patient to turn onto
•Guide the patient’s head down
so that he is looking at the
ground and wait for at least 30
•The patient’s head is regripped
and patient is made to sit up
with the legs hanging over the
side of the couch.
•The patient is now in sitting
• Move the patient’s head
•This completes the
Rarely required, when medical treatment and otolith
repositioning techniques have failed.
Procedures which may be considered:
Singular Neurectomy (or Posterior Ampullar Nerve Section):
This tiny branch of the balance (vestibular)nerve travels through a
bony canal before it reaches the nerve endings of the balance canal.
In experienced hands it is a safe surgery and relieves the symptoms
permanently. In a small percentage of cases the nerve is
unreachable. In a few cases hearing loss, dizziness , tinnitus can
result from surgery.
Posterior Canal Plugging Procedure:
This recently developed procedure has nearly replaced singular
neurectomy due to its ease and effectiveness. In this procedure, a
mastoidectom,y is performed and posterior semicircular canal is
opened, exposing the delicate membranous channel and is firmly
packed, so that the otolith can no longer move.
The acute vertigo of BPPV is cured in most cases. The exact
percentage of patients with some permanent hearing loss has not
Vestibular Nerve Section :
In some cases, when positional vertigo is quite severe and hearing
normal, testing reveals that this is not due to crystalline debris
floating in the canal, but due to a damaged nerve. In such ases ,
the balance nerve is cut to stop its distorted information. In
successful cases, after an initial period of several weeks,
dizziness gradually disappears.
In this operation neurosurgeon exposes the nerve as it crosses from
the ear to the brain and sections it under direct vision using a
In some cases, high frequency hearing loss can occur because the
balance nerve fibres and hearing fibres mix together along the
borders of the nerves.
Risks include hearing loss, tinnitus, facial nerve weakness, spinal
fluid leakage, and meningitis.
Overview of Vertigo Treatment
Journal of Audiological Medicine - 2000
Almost half a century has passed since Dix and Hallpike
published their landmark paper describing the clinical profile of
the three most common causes of peripheral vertigo:Benign
paroxysmal postional , Meniere’s disease and Vestibular
Cupulo-canalolithiasis is by far the most frequent cause of
rotatory vertigo; although the diagnosis can be easily carried out
at the bedside and a ‘liberatory’ manoeuvre effected in a few
minutes is curative, it is being performed only by a minority of
A sstandard pharmacological cure for Meniere’s disease has yet
to be found, since its pathogenesis is multifactorial. Salt
restriction diet and diuretics are sometimes effective, and
chemical labyrinthectomy by intratympanic delivery of
vestibulotoxic drugs or selective vestibular nerve section can
stop the vertigo attacks but do not solve the underlying
An isolated viral infection of the Scarpa’s ganglion and vestibular
nerve are thought to be the cause of vestibular neuronitis.