seminar on benign paroxysmal positional vertigo (bppv)

1. BENIGN PAROXYSMAL
POSITIONAL
VERTIGO
(BPPV)
DR. BIBAN CHHABRA

2. INTRODUCTION
• Benign paroxysmal positional vertigo (BPPV) is the
commonest presenting cause of vertigo with an
estimated lifetime prevalence of 2.4%.
• It has a characteristic history and can easily be
diagnosed on examination.
• Treatment can be performed in the clinic with a
good outcome, making it the most rewarding
vestibular condition to manage.

3. • BPPV may, however, be associated with a reduced
quality of life, falls and depression, in which case
the term ‘benign’ may be misleading, particularly
when unrecognized and therefore untreated.

4. HISTORY
• The first clinical description of positional vertigo is
attributed to Barany in 1921 and in 1952 Dix and
Hallpike were the first to clearly describe the
provoking maneuvers.
• Dix and Hallpike coined the term ‘benign
paroxysmal positional vertigo’ in view of the
associated benign (non-cancerous) origin and
momentary (paroxysmal) bursts of intense vertigo
upon head movements (positional).

5. PATHOPHYSIOLOGY
• Otoconia are calcium carbonate crystals embedded
in the macula of the utricle and saccule.
• Otoconia have a greater density than the
surrounding endolymph thus making the macula
sensitive to changes in linear acceleration and,
importantly, gravity.
• The semicircular canals, on the other hand, are
sensitive to changes in angular acceleration.

6. • In BPPV otoconia from the utricle are thought to
collect in the semicircular canals, making them
abnormally gravity-sensitive.
• The net result is that changes in head position with
respect to gravity result in an abnormal
displacement of the cupula and stimulation of the
corresponding vestibular afferents.
• This results in the characteristically abnormal eye
movements and vertigo.

7. • There are two theories of how this might occur:
−Cupulolithiasis proposes that degenerative
otoconia stick to the cupula making it gravity-
sensitive.
−Post-mortem findings of such deposits in patients
who had suffered from BPPV add weight to this
theory.

8. −The more recent theory of Canalolithiasis gained
momentum after surgical observations of free-
floating debris in the posterior semicircular canal
during an occlusion procedure.
−This theory suggests that degenerative otoconial
debris float freely in the endolymph of the semi-
circular canal.
−When exposed to gravity, the otoconia fall to the
lowest part of the canal, causing a change in
endolymph pressure with subsequent displacement
of the cupula.

9. −The change in pressure is due to a hydrodynamic
‘plunger effect’ where the otoconial debris act like
a piston creating endolymph flow which deforms
the cupula.
−This theory explains the ‘latency’ (delay in onset) of
the nystagmus that is related to the time taken for
the otoconial debris to fall and the initial adherence
to the membranous canal.

10. • While the majority of BPPV cases seem to be more
compatible with the theory of canalolithiasis, some
cases with atypical features may be explained on
the basis of cupulolithiasis.
• Canalolithiasis may be converted to cupulolithiasis
when otoconial debris floating in the canal attach
to the cupula.

11. SYMPTOMS AND NATURAL
COURSE OF DISEASE
• BPPV most commonly arises from the posterior
semicircular canal (p-SCC).
• Much less frequently the horizontal semicircular
canal (h-SCC) is involved while the anterior canal (a-
SCC) is very rarely affected.
• BPPV may also arise from pathology of more than
one canal on one or both sides.

12. • The propensity for the accumulation of particles in
the posterior canal is postulated to be related to
anatomical factors such as the size of the common
crus of the posterior and superior semicircular
canals, its position below the utricle when supine
and its dependent position when both erect and
supine.
• Particles can become trapped in the posterior
canal; any debris that may have entered the
superior canal is more likely to fall back into the
utricle.

13. • In the upright position, the horizontal canal’s open-
ing into the utricle is undermost, thus facilitating
particle migration out of the canal, while the
posterior canal’s opening is uppermost.
• Therefore, the horizontal canal can be easily
cleared by natural head movements but the
posterior canal is a trap for any particles that have
entered it.

14. • Similarly, particles may leave the horizontal canal
just by the action of the person rolling over in bed
whereas particles in the posterior canal will only be
shifted backwards and forwards. This may explain
the infrequent presentation of h-BPPV.

15. • During manoeuvres, p-BPPV can be converted to
either a-BPPV or h-BPPV to p-BPPV and a-BPPV to
p-BPPV.
• Similarly, bilateral apogeotropic h-BPPV may
spontaneously convert to bilateral geotropic and is
attributed to debris located in the anterior part of
the canal sticking to the cupula dislodging and
shifting to the posterior part of the canal.
• Plugging of the horizontal canal presenting with
persistent spontaneous nystagmus, vertigo and
oscillopsia has also been described.

16. • The hallmark of p-BPPV is vertigo lasting seconds
with or without nausea and imbalance on lying
down, sitting up from the lying position, or rolling
in bed and when extending or flexing the neck.
• These symptoms can present in clusters with
several attacks per day.
• In between attacks or shortly after successful
treatment, patients are either symptom-free or
experience a sensation of imbalance.

17. • This sensation of imbalance can be described as
‘walking on pillows’ and may be attributed to the
underlying damage of the otolith organs.
• However, some patients may report atypical
symptoms, and it is worth- while conducting the
positional tests in all patients presenting with
episodic vertigo.
• In the majority of cases the BPPV symptoms will
subside within a few weeks, but in up to 30% the
symptoms may persist for months.

18. ETIOLOGY
• Hallpike described ear disease in 66 out of 100
BPPV patients, although in only 28 ears was it on
the side with the BPPV. No cause has been found in
34–86% of patients. These cases have been termed
‘primary’ or idiopathic BPPV.

19. • However, there may also be an association with
other pathologies:
• BPPV occurred in 9.8–15.3% of cases following
vestibular neuritis.
• Otosclerosis may be associated with BPPV in upto
51% of patients and may also occur following
stapedectomy.

20. • Studies have suggested that Ménière’s disease may
be found in up to 2% of cases but it has been
reported to occur in up to 30% of cases. It has been
postulated that hydropically induced damage to the
maculae or partial obstruction may be responsible.

21. • Head trauma is one of the most common causes of
BPPV in 14.5–18% and can involve more than one
canal. The force of the injury may cause the release
of otoconia into the endolymph.
• BPPV can also result following traumatic spinal
cord injury in up to 14.5% of cases.

22. • Patients with positional vertigo may have
migrainous vertigo. Migrainous symptoms during
the positional episodes, atypical features of
positional nystagmus and frequent recurrence of
symptoms may differentiate between BPPV and the
central positional syndrome due to migraine.
• Otosclerosis and osteopenia are found with greater
frequency in females with BPPV, particularly older
post- menopausal women.

23. • BPPV also is associated with progressive cochlear
or vestibular failure, vertebrobasilar ischaemia
and other vestibular disorders.
• The common feature of these conditions is that
they may lead to dislodgement of otoconia from
the utricle, which may invade one or several
semicircular canals after days, weeks or months.
• In idiopathic BPPV, which becomes more prevalent
with advancing age, release of otoconia is probably
related to degeneration of the otolith organs.

24. • Risk factors that may initiate an acute episode of
BPPV include :
prolonged bed-rest, bending forward with the
head down, and general anaesthesia, because the
supine, head-down and head- reclined position
(e.g. during intubation) lower the opening of the
posterior canal, thus promoting the penetration
of particles.

25. DIAGNOSIS
• Diagnosis of BPPV is made on the basis of typical
signs (nystagmus) and symptoms (vertigo and
nausea) provoked by specific positional tests.
• Understanding the characteristic eye movements
during these tests will help in making the diagnosis.

26. • Our understanding of vestibular eye movements is
based on fundamental principles described by
Ewald:
−The direction of eye movement is in the plane of
the canal or canals that are stimulated.
−In the horizontal canal, endolymph flow towards
the ampulla (ampullopetal) results in an excitatory
and stronger response than flow away from the
ampulla (ampullofugal), which is inhibitory. The
opposite holds true for the vertical canals.

27. −For example, the posterior canal and anterior canal
pairs are stimulated when performing the Dix–
Hallpike test.
−The patient is seated along the couch, feet up, and
the head is turned 45 degrees towards the side
being tested, aligning the vertical canals with the
sagittal plane.
−The head is brought down briskly over the end of
the couch to lie 30 degrees below the horizontal
while maintaining a position 45 degrees to the side
being tested.

28. −Patients should be counselled prior to the test
about dizziness but that they are to try and
maintain their eyes open for examination.

29. • The Left Anterior and Right Posterior canals (LARP)
are stimulated during the right Dix–Hallpike and the
Right Anterior and Left Posterior (RALP) in the left
Dix–Hallpike.
• During the right Dix–Hallpike there is ampullofugal
(excitatory) flow in the right posterior canal and
ampullopetal (inhibitory) flow in the left anterior.
Normally this balances out and there is no
nystagmus.

30. • However, if there were particles in the posterior
canal, the ampullofugal forces would be greater,
resulting in a net excitatory effect and eye
movement consistent with the plane of the canal.

31. • The slow-phase eye movements when excitatory
would be towards the right ear or downwards and
inwards via the ipsilateral superior oblique muscle
and the contralateral inferior rectus muscle.
• The fast phase would be upwards and outwards or
upbeating geotropic-torsional nystagmus. This is
best seen by closely watching the scleral vessels.
• The nystagmus typically reverses when sitting up. A
cupulolithiasis type BPPV can also rarely occur and
is characterized by nystagmus that occurs without
latency and does not fatigue.

32. • The side-lying test is an alternative and has been
shown to produce similar results to the Dix–
Hallpike.
• In contrast to the Dix–Hallpike, the head is turned
45 degrees away from the side being tested such
that the vertical canals are in the frontal plane.
• The patient is quickly moved to a supine-lying
position with the neck hyperextended 20 degrees.
The typical torsional nystagmus is seen beating
towards the lowermost ear.

33. • Similarly, the anterior canal during a right Dix–
Hallpike or side-lying tests will be inhibited, i.e. flow
will be ampullopetal. If particles are present, they
will cause an inhibitory effect which will
predominate causing the opposite nystagmus to
the posterior canal – beating downwards and
intorsional in the ipsilateral eye.
• The straight head-hanging manoeuvre has also
been shown to be useful to diagnose a-BPPV where
the head is extended backwards to a head-hanging
position of the end off the bed from seated to
supine.

34. • Horizontal canal BPPV is assessed using the roll
test.
• The head is flexed 30 degrees, bringing the
horizontal canal into the axial plane, and is then
briskly rolled to one side.
• The same is repeated to the opposite side.
• In the majority of cases the nystagmus will be
horizontal and geotropic and towards the ear being
tested.

35. • When turned to the opposite side, the nystagmus
will reverse and beat towards the undermost ear
again.
• When a canal is stimulated with an ampullopetal
force, the nystagmic response is greater (Ewald’s
second law), therefore the ear containing the loose
particles would generally present with the brisker
nystagmus hence helping to make the diagnosis.

36. • An apogeotropic nystagmus is also described and is
thought to be related to cupulolithiasis.
• In this situation, when the head is turned to the
affected side, the force is ampullofugal hence the
nystagmus will beat away (apo- geotropic) from the
affected ear.

37. • Frenzel glasses can be used to better observe the
nystagmus or it can be recorded with electro- or
video-oculography.
• As BPPV can sometimes coexist with other
vestibular disorders and the history can sometimes
be atypical, many would perform a Dix–Hallpike
routinely as part of a vestibular assessment.

38. • Treatment consists of repositioning maneuvers.
• There is no role of any medicine.
• The following maneuvers are effective in majority
of the BPPV patients.
TREATMENT

39. Repositioning Maneuvers
• After the maneuver, patients are told to sleep with
45°elevated head and avoid bending.
• En bloc movement of the head and body is
preferred during these maneuvers.
• Mastoid vibrator gives slightly better results.

40. • During these maneuvers, posterior canal BPPV
can be converted to lateral canal BPPV (resolves in
several days), superior canal BPPV (vertigo
worsens when the affected ear is up) or canalith
obstructs common crus and simultaneously excite
both superior and posterior canals.
• Thus, the opposing vertical components are
cancelled and the torsional components are
added.

41. For Posterior SCC
 Epley maneuver :
• It is effective in 90% cases of posterior canal BPPV.
Meclizine or benzodiazepine 1 hour before may be
given in anxious patients.
• First two positions (upright and supine position
with extended neck turned 45°) are similar to Dix-
Hallpike maneuver.

42. • Then head is rolled 180° in two 90° increments so
that the offending ear is up.
• From this position, patient is brought to the sitting
position.
• The repositioning maneuver is repeated again and
again until no nystagmus is produced.
• Head remains in that particular position until any
nystagmus resolves.

43. Canalith repositioning for right posterior canal BPPV. (A) Patient sitting with head turned right and debris
near ampulla (inset); (B) Patient in supine position with extended neck and debris move away from the
ampulla in the posterior canal (inset); (C) Head moved 90° to left and debris comes near the common crus
(inset); (D) Patient rolled onto left and head faces down and debris starts entering into the utricle from the
common crus (inset); (E) Patient in upright position and debris collects in utricle (inset).

44.  Semont maneuver :
• The patient is turned rapidly into the position that
provokes vertigo and kept in that position for 4
minutes.
• Then patient is moved quickly to opposite position
with normal ear down.
• After some time, patient is asked to sit slowly in
upright position.

45. Photo from MB
Semont maneuver for right posterior canal BPPV. (A) Upright sitting position; (B)
Patient is turned rapidly into the position that provokes vertigo and kept in that
position for 4 minutes; (C) Then patient is moved quickly to opposite position with
normal ear down; (D) After some time, patient is asked to sit slowly in upright position.

46. For Lateral SCC
• Geotropic nystagmus: Lying on the normal side
with affected ear up for 12 hours—effective in
92% cases.
• Modified Epley : Patient lies on the affected side
with normal ear up. Then, patient is moved in 90°
increments to supine, affected ear up, prone and
at last affected ear down

47. Modified Epley’s maneuver for right lateral canal BPPV. side with normal
ear up. Then patient is moved in 90° increments to (B) supine; (C)
affected ear up; (D) prone; and at last (E) affected ear down

48. For Superior SCC
• The head is positioned into a dependent position
so that ampulla of superior canal is superior, then
turned by 180°, and finally brought back to the
original position.
• The patient initially lies on the normal side, then
head is turned downwards 45°, then horizontally,
upwards 45° and at last patient sits upright.
• The patient remains in each position for 30
seconds.

49. Surgical Treatment
• The following surgical procedures are considered in
cases that are refractory to the above mentioned
maneuvers and the symptoms are disabling to the
patient:
 Occlusion of posterior semi-circular canal (PSCC):
Plugging of PSCC prevents free-floating particles.

50. Vestibular neurectomy: Rarely done in BPPV
Singular neurectomy: It cuts the innervation of
PSCC ampulla. It is technically difficult and risk of
hearing loss (HL) is high.

51. THANK
YOU