CASE REPORT

BENIGN PAROXYSMAL POSITIONAL VERTIGO

BY :

ULLYA AISYAFITRI, S.Ked

CONSULENT:

dr. RANGGA PUTRA NUGRAHA, Sp. THT-KL

EAR NOSE THROAT STASE

TANJUNGPURA UNIVERSITY HOSPITAL

FACULTY OF MEDICINE, TANJUNGPURA UNIVERSITY

PONTIANAK

2019

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 CHAPTER I

PREFACE
a. Background
Benign paroxysmal positional vertigo (BPPV) is one of the most common
causes of vertigo. A primary complaint of dizziness accounts for 5.6 million
clinic visits in the United States per year, and between 17% and 42% of
patients with vertigo ultimately receive a diagnosis of benign paroxysmal
positional vertigo (BPPV). BPPV is a form of positional vertigo. Vertigo is
defined as an illusory sensation of motion of either the self or the
surroundings in the absence of true motion. Positional vertigo is defined as a
spinning sensation produced by changes in head position relative to gravity.1
In this context, the descriptor benign implies that BPPV was a form of
positional vertigo not due to any serious central nervous system (CNS)
disorder and that there was an overall favorable prognosis for recovery.1 This
favorable prognosis is based in part on the fact that BPPV can recover
spontaneously in approximately 20% of patients by 1 month of follow-up and
up to 50% at 3 months.2,3 The term paroxysmal in this context describes the
rapid and sudden onset of vertigo, initiated at any time by a change of
position, thus resulting in BPPV.4
Although benign paroxysmal positional vertigo can be a bothersome
problem, it's rarely serious except when it increases the chance of falls.
However, the clinical and quality-of-life impacts of undiagnosed and
untreated BPPV may be far from “benign,” as patients with BPPV are at
increased risk for falls and impairment in the performance of daily activities.
Furthermore, patients with BPPV experience effects on individual health-
related quality of life, and utility measures demonstrate that treatment of
BPPV results in improvement in quality of life.5

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 CHAPTER II
CASE REPORT

a. History Taking
Identity
Name : Mrs. TA
Age : 73
Gender : Female
Occupation : Housewife
Religion : Konghucu
Address : Jl. Hijas
Date of hospital admission : 16th September 2019

Chief complaint
The patient complains that the left ear feels rumbling and feels dizzy
spinning.

Current medical history

The patient complains that the left ear feels rumbling and feels dizzy
spinning. Complains left ear felt rumbling intermitten about 2 weeks. The
head feels dizzy spinning felt since 2 months ago, complaints arise when
changing positions from lying down to standing, and when complaints appear
accompanied by nausea, and ringing and it happens about 30 seconds.
Complaints are getting worse

Accompanying complaints
Othalgia (-), ringing (+), itching (-), nausea (+), vomiting (-), feeling full (-),
discharge (-)

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 History of previous illnesses
Hypertension about 3 years, cataracts in the right eye about 1 year, glaucoma
in the left eye about 3 months.

Family history
There’s no family history with similar complaints.

Treatment history
Hypertension treatment: amlodipine and candesartan. The patient has never
been treated for complaints of spinning dizziness

b. Physical Examination
1. Generalist Status
Awareness : compos mentis
Blood Pressure : 150/80 mmHg
Heart rate : 86 x / minute
Respiration rate : 20 x / minute
Temperature : 36.7 ° C

2. ENT Examinatiom
a. Ear

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 Examination Dekstra Sinistra
Inspection Normal ear shape, Normal ear shape,
deformity (-), scar (-), deformity (-), scar (-),
edema (-), hyperemia (-), edema (-), hyperemia (-),
discharge (-) discharge (-)
Palpation Tenderness(-), tragus pain Tenderness(-), tragus
(-) pain (-)
Otoscope CAE edema (-), CAE edema (-),
hyperemia (-), cerumen(-), hyperemia (-), cerumen (-
discharge (-), granulation ), discharge (-),
(-), intact tympanic granulation (-), intact
membrane, cone of light tympanic membrane,
(+) at 5 o'clock cone of light (+) at 7
o'clock
Tuning Fork Rinne : + Rinne : +
test (512 Hz) Weber : no lateralization Weber : no lateralization
Schwabach : same as the Schwabach : same as the
examiner examiner

b. Nose
Examination Dekstra Sinistra
Inspection Deformity (-), secret (-), Deformity (-), secret (-),
scars (-), edema (-) scars (-), edema (-)
Palpation Crepitus (-), tenderness (-) Crepitus (-),tenderness(-)
Anterior Hyperemic mucosa (-), Hyperemic mucosa (-),
Rhinoscopy hyperemic concha (-), hyperemic concha (-),
media concha and inferior media concha and
hypertrophy (-), secret (-), inferior hypertrophy (-),
edema (-), nasal septal secret (-), edema (-),
deviation (-), mass in nasal septal deviation (-),

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 nasal cavity (-) mass in nasal cavity (-)

c. Mout and Throat

Mouth Can open mouth well
Color of buccal mucosa: pink
Edema: (-)
Chapped: (-)
Oral Mucisa Hyperemic mucosa (-)
Uvula in the middle
Oropharyngeal The surface of the tonsils is flat, the crypts don't widen
examination Tonsil’s size :T1-T1
Hyperemic tonsils (-)
Peritonsil abscess (-)
The color of mucosa is pink

d. Head-Neck
Head: normocephal
Neck: lumps, tenderness (-), edema (-)
e. Romberg Test
Closed eyes The patient lost balance and almost fell over
Open eyes The patient not lost balance
f. Tandem Gait
Patient steps deviated more than 1 meter

3. Clinical Diagnosis
Benign Paroxysmal Positional Vertigo

4. Differential Diagnosis
Central vertigo
Meniere disease

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5. Therapy
CRT which is done 20 times in 1 day, at least 2 times a week, followed by
tablet 16 mg of oral betahistine dihydrochloride 3 times daily which is
consumed for about 2 months.

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 CHAPTER III
LITERATURE REVIEW
a. Definition
Vertigo is defined as an illusory sensation of motion of either the self or
the surroundings in the absence of true motion. Positional vertigo is defined
as a spinning sensation produced by changes in head position relative to
gravity. BPPV is defined as a disorder of the inner ear characterized by
repeated episodes of positional vertigo.1

b. Pathophysiology
The vestibular part of the membranous labyrinth consists of 3
semicircular canals: the anterior, posterior, and the horizontal canals. These
canals detect turning movements of the head. The labyrinth also consists of 2
otolith structures, the utricle and saccule, that detect linear acceleration,
including detection of gravity. The macula of the utricle is the presumed
source of the calcium particles that cause BPPV. It consists of calcium
carbonate crystals (otoconia) embedded in a gelatinous matrix, into which the
stereocilia of hair cells project. BPPV is caused when otoliths originate from
the utricular macula and move within the lumen of one of the semicircular
canals. When the calcium carbonate crystals move within the semicircular
canal, they cause endolymph movement that stimulates the ampulla of the
affected canal, thereby causing vertigo. The direction of the nystagmus is
determined by ampullary nerve excitation in the affected canal by direct
connections to the extraocular muscles. Each canal affected by canalithiasis
has its own characteristic nystagmus.6
The reason for this shedding of calcium crystals from the macula is not
well understood. The calcium debris may break off following trauma or viral
infections, but in many instances it seems to occur without identifiable illness
or trauma. Primary or idiopathic BPPV is of unknown cause and by far the
more common (about 50%–70%) presentation, etio-pathological associations
of secondary benign paroxysmal positioning vertigo like head trauma,

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 vestibular neuritis,meniere disease, otitis media, otosclerosis, inner ear
surgery. It may have to do with age-related changes in the protein and
gelatinous matrix of the otolithic membrane.6

Tabel 1. Etio-pathological associations of secondary benign paroxysmal positioning

vertigo6

BPPV may affect the posterior, horizontal, or anterior semi-circular canal,

and in some cases it may even involve more than one canal at a time. Due to
its gravity-dependent position, the most commonly affected semicircular
canal is the posterior canal. The anterior canal and polycanalicular forms are
the least common.6

c. Diagnosis
The diagnosis of BPPV can be made based on the history and
examination. Patients usually report episodes of spinning evoked by certain
movements, such as lying back or getting out of bed, turning in bed, looking
up, or straightening after bending over. The episodes of vertigo last 10–30 s
and are not accompanied by any additional symptoms other than nausea in
some patients.6
The diagnosis of BPPV of the posterior canal is confirmed by observing
paroxysmal positional nystagmus with the Dix–Hallpike maneuver. The Dix–
Hallpike maneuver is performed by rapidly moving the head from an upright
to head hanging position with one ear 45 degrees to the side. The Dix–
Hallpike maneuver results in torsional upbeating nystagmus corresponding in
duration to the patient's subjective vertigo, and occurring only after Dix–
Hallpike positioning on the affected side. 6

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 Figure 1. Dix-Hallpike positioning maneuver

The most reliable way to diagnose horizontal BPPV is by a supine head

turn maneuver. The patient's head is turned to one side, then is turned back to
the supine face-up position. Then the head is turned to the other side. The
nystagmus of horizontal canal BPPV, unlike that of posterior canal BPPV, is
distinctly horizontal and changes direction with changes in the head position.
The paroxysmal direction changing nystagmus may be either geotropic or
apogeotropic.7

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 Figure 2. Supine head turn maneuver to determine the presence and affected side of
horizontal canal benign paroxysmal positional vertigo

The anterior canal form of BPPV is associated with paroxysmal

downbeating nystagmus, sometimes with a minor torsional component
following Dix–Hallpike positioning.Polycanalicular BPPV is uncommon, but
indicates that 2 or more canals are simultaneously affected at the same time.
The most common circumstance is posterior canal BPPV combined with
horizontal canal BPPV.7

d. Treatment
The treatment of posterior canal and anterior canal BPPV is the canalith
repositioning maneuver, sometimes referred to as the “Epley maneuver.” The
most commonly used treatment for horizontal canal BPPV is the roll
maneuver.8
Evidence is lacking to recommend postmaneuver restrictions in patients
treated with canalith repositioning therapies, although there is generally no
associated harm with these instructions.8

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 Occasionally, freely mobile otoconia moving within the lumen of one
semicircular canal can be moved during the course of treatment; not back to
the vestibule as intended, but to one of the adjacent canals, as the canals all
directly communicate with one another. The most common canal switch is
from the posterior to the horizontal and posterior to the anterior canals.8
Brandt and Daroff developed an Epley manuever for the treatment of
otolith disease : the patient starts in a sitting position, changes rapidly to a
right supine position with the head rotated at a 45° angle to the left. Thirty
seconds following the resolution of the resultant vertigo, the patient would sit
rapidly and stare forward for another 30 sec, then change rapidly to a left
supine position with the head rotated at a 45° angle to the right. This would
be repeated 20 times, twice daily, 1–2 times per week, and could be gradually
stopped after symptom remission. 9
Patients with limited cervical spine motion could use the modified Semont
procedure: i) the patient wears a cervical gear while sitting on the front of the
bed, then while maintaining head and neck position, rotates the body 45° to
the left in order to treat the right posterior semicircular canal, ii) the patient
changes rapidly to a right supine position (the same with the modified lateral
supine position), the back of the head contacts the bed, and the apex nasi
faces upward, iii) after resolution of vertigo and nystagmus, the patient
changes from a right supine to a left supine position with the rear arm as the
pivot point, the forehead and apex nasi contacting the bed, and the back of the
head facing upward and iv) the patient sits up. The treatment for the left
posterior semicircular canal was the same as that for the right posterior
semicircular canal, except for reversed directions.10
The most classical treatment for PC-BPPV is the Epley reduction, which
was developed by Epley based on the hypothesis of otolith in the semicircular
canal: i) the patient starts in a sitting position with their head tilted to the
affected side at a 45° angle, ii) the patient changes from a sitting to a supine
position with the head beneath the bed at an angle of 45°, iii) while
maintaining the positioning of the body, the head was then rotated to the

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healthy side at a 45° angle, iv) both the body and the head then rotated to the
healthy side at 90° angles, v) the body was then shifted to a supine position
towards the healthy side, with an angle of 135° between the head and the bed
and vi) the patient then sat and tilted their head forward at a 20° angle. Each
position was maintained for 1 min. Rotation was stopped upon vertigo and
continued 30 sec after resolution of nystagmus .11

Figure 3. Procedures of Epley reduction for treatment of PC-BPPV. PC-BPPV,

posterior canal benign paroxysmal positional vertigo.11

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Figure 2. Lempert 360- (Barbeque) degree roll maneuver to treat horizontal canal BPPV.

Prior to the application of manual reduction, drugs that improve

microcirculation and inhibit the vestibule have been used as first line drugs
for BPPV, and have been shown to improve efficacy. For refractory BPPV
patients, manual reduction alone could not achieve good efficacy, so two
surgeries could be considered: i) single neurectomy could improve the
clinical symptoms of BPPV patients. In fact, this surgery can achieve good
efficacy, yet some patients may be subjected to high risk of hearing loss. ii)
Semicircular canal occlusion can be used to occlude the space in the crest
with special material to reduce the stimulation of the hair cell sensory
receptors in the ampulla. This procedure has low risk. However, surgeries
may cause severe hearing loss, and thus should be considered carefully and
should only be used when the efficacy of manual reduction and medical
treatment was unsatisfactory.12,13

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 There is Comparative Study between Epleys Manouvre and Betahistine.
Patients in Group A were treated with Epleys manoeuvre alone, in Group B
were treated with Epleys Manouvre followed by oral Betahistine and patients
in Group C were treated with Betahistine alone. All the patients were
followed up after 1 week and 4 weeks following treatment. In our study we
found that patients responded better when they were treated with Epleys
Manouvre with Betahistine with less relapse and recurrence. Treatment with
Epleys manouvre resulted in early improvement of symptoms. It was found in
our study that Betahistine as a sole modality of treatment of vertigo in BPPV
can be preferred in patients who are unfit to undergo canal repositioning
manouvres.14

e. Complication
The most common complications include nausea, vomiting, fainting, and
conversion to lateral canal BPPV during the course of treatment due to “canal
switch.15

f. Prognosis
At present, the generally accepted recurrence rate of BPPV after successful
treatment is 40%–50% at 5 years of average follow-up. There does appear to
be a subset of individuals prone to multiple recurrences.11

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 CHAPTER IV
DISCUSSION

In the history of the patient's complaint, the ear feels rumbling and head
spinning. complaints are felt intermitten, suddenly,especially when changing
positions from sleep to standing or vice versa, the patient feels nauseous when
dizziness recurs, the patient does not complain of hearing loss. Compaint is
getting worse This complaint is a characteristic of vertigo specifically BPPV.
Vertigo is defined as an illusory sensation of motion of either the self or the
surroundings in the absence of true motion. Positional vertigo is defined as a
spinning sensation produced by changes in head position relative to gravity.
BPPV is defined as a disorder of the inner ear characterized by repeated episodes
of positional vertigo .
In patients not found hearing loss, which if a complaint exists then the
diagnosis will be Meniere's disease, hearing loss will subside when the dizziness
has disappeared. And we can difference it with central vertigo because patient’s
complain that has a suddenly onset and getting worse with change of head
position. At the patient are not found another clinical feature like ataxia, diplopia,
hemiplegia that can be a sign of central vertigo.

Table 2. Clinical and differential features of benign paroxysmal positional vertigo

(BPPV) versus central paroxysmal positional vertigo (CPPV)20

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 BPPV is caused when otoliths originate from the utricular macula and move
within the lumen of one of the semicircular canals. When the calcium carbonate
crystals move within the semicircular canal, they cause endolymph movement that
stimulates the ampulla of the affected canal, thereby causing vertigo.
Therapy for this case is with Epleys Manouvre followed by oral Betahistine.
There is Comparative Study between Epleys Manouvre and Betahistine. Patients
in Group A were treated with Epleys manoeuvre alone, in Group B were treated
with Epleys Manouvre followed by oral Betahistine and patients in Group C were
treated with Betahistine alone, treatment with Epleys manouvre resulted in early
improvement of symptoms than the others.
At this case is treated with oral betahistine. Dosage of betahistine at this case
is 16mg tablet taken 3 times a day. The clinical efficacy of betahistine could be
explained both by the histaminergic-like effect of vasodilation of the cerebral
microcirculation and inner ear and by the action at the level of the central
histaminergic system as a weak H1 agonist and H3 antagonist enhancing the
process of vestibular compensation and reducing the spontaneous activity of
peripheral vestibular receptors.
Moreover, the reduction in the number of attacks of positional paroxysmal
vertigo, in the case of cupulo-canalolithiasis, is probably associated both with the
improvement in the labyrinthine blood flow, with a relative safeguard of macular
trophism, and to a modulation of the neuronal activity with a relative reduction of
any eccessive vestibular reflectivity of a peripheral or central nature.
Drugs with an antivertiginous effect modulate the activity of neuromediators
involved in the control of the vestibular system (GABA, acetylcholine,
histamine). In general, they induce a decrease in the nervous activity
(vestibuloplegic drugs). Among these, betahistine plays a significant role in the
therapeutic approach to the vertiginous patient on account of its mode of action on
the histaminergic system. Betahistine causes not only a specific inhibition of the
neurons of the lateral vestibular nucleus, but also involves, centrally, the
histaminergic neurotransmission and peripherally the microcirculation of the
cochleo-vestibular system as well as the activity of the ampullary ciliated cells.

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 At this case, patient take 16 mg of oral tablet betahistine dihydrochloride 3
times daily. Maximum efficacy of betahistine is obtained with long periods of
treatment of 3-8 weeks and with daily doses of 32 to 36 mg. High doses, up to 48
mg/day, or treatment periods prolonged up to 4 months do not seem to induce, on
average, further benefits. 16,17 The molecular weight of betahistine
dihydrochloride is 209g/mol, while that of betahistine mesilate is 328g/mol; the
molecular weight of betahistine is 136g/mol, the dihydrochloride group is
73g/mol and the mesilate group is 192g/mol. Therefore, each tablet of betahistine
dihydrochloride 16 mg contains betahistine 10.4mg, equivalent to two tablets of
betahistine mesilate 12 mg, each containing 4.9 mg betahistine. It may be noted
that betahistine mesilate is currently not available in higher strength tablets, which
may be a potential disadvantage with respect to the pill burden on the patient.18
The choice for surgery between singular nerve section (SNS) and semicircular
canal occlusion (SCO) for the few patients with intractable BPPV is based on the
success rate and risk for hearing loss. This review would seem to indicate a
slightly lower success rate for SNS, perhaps due to the difficulty in locating the
singular nerve near the base of the round window. When performing a SCO, there
are no problems in locating the semicircular canals for any otologic surgeon, and
the result in hearing preservation depends mostly on how carefully the canal is
opened and manipulated. In our experience, SCO is a very straightforward
technique and it avoids the anatomical difficulty of locating the singular nerve.
Thus, we consider SCO as the technique of choice for those rare patients who
require surgery for intractable positional vertigo.19

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 CHAPTER V
CONCLUSION

Based on the results of examination of the patient's diagnosis is BPPV.

Therapy for patients is CRT which is done 20 times in 1 day, at least 2 times a
week, followed by 16 mg of oral tablet betahistine dihydrochloride 3 times daily
which is consumed for about 2 months.

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 REFERENCE

1. Bhattacharyya N, Samuel PG, Seth RS, Jonathan AE, Hussam EK,Terry F,

Clinical Practice Guideline: Benign Paroxysmal Positional Vertigo
(Update). Otolaryngology– Head and Neck Surg. 2017, Vol. 156(3S) S1–
S47
2. Lynn S, Pool A, Rose D, Brey R, Suman V. Randomized trialnof the
canalith repositioning procedure. Otolaryngol Head Neck Surg.
1995;113:712-720.
3. Burton MJ, Eby TL, Rosenfeld RM. Extracts from the Cochrane Library:
modifications of the Epley (canalith repositioning) maneuver for posterior
canal benign paroxysmal positional vertigo. Otolaryngol Head Neck Surg.
2012;147:407-411.
4. Lopez-Escamez JA, Gamiz MJ, Fernandez-Perez A, et al. Long-term
outcome and health-related quality of life in benign paroxysmal positional
vertigo. Eur Arch Otorhinolaryngol. 2005;262:507-511.
5. Roberts RA, Abrams H, Sembach MK, Lister JJ, Gans RE, Chisolm TH.
Utility measures of health-related quality of life in patients treated for
benign paroxysmal positional vertigo. Ear Hear. 2009;30:369-376.
6. Xiang-Dong,Guo. Benign paroxysmal positional vertigo. J Neurosci Rural
Pract. 2011 Jan-Jun; 2(1): 109–110.
7. Prokopakis EP, Chimona T, Tsagournisakis M, Christodoulou P, Hirsch
BE, Lachanas VA, et al. Benign paroxysmal positional vertigo: 10-year
experience in treating 592 patients with canalith repositioning procedure.
Laryngoscope. 2005;115:1667–71.
8. Radtke A, von Brevern M, Tiel-Wilck K, Mainz-Perchalla A, Neuhauser
H, Lempert T. Selftreatment of benign paroxysmal positional vertigo:
Semont maneuver vs Epley procedure. Neurology. 2004;63:150–2.
9. Brandt T and Daroff RB: Physical therapy for benign paroxysmal
positional vertigo. Arch Otolaryngol 106: 484-485, 1980.
10. Semont A, Freyss G and Vitte E: Curing the BPPV with a liberatory
maneuver. Adv Otorhinolaryngol 42: 290-293, 1988.
11. Epley JM: The canalith repositioning procedure: for treatment of benign
paroxysmal positional vertigo. Otolaryngol Head Neck Surg 107: 399-404,
1992.
12. Pan J: Clinical observation of combined manual reduction in the treatment
of HBBP. Clin Ration Drug Use 7: 108, 2014.
13. Guneri EA and Kustutan O: The effects of betahistine in addition to epley
maneuver in posterior canal benign paroxysmal positional vertigo.
Otolaryngol Head Neck Surg 146: 104-108, 2012.

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14. Kaur J, Shamanna K. Management of Benign Paroxysmal Positional
Vertigo: A Comparative Study between Epleys Manouvre and Betahistine.
Int Tinnitus J. 2017 Jun 1;21(1):30-34.
15. Yimtae K, Srirompotong S, Srirompotong S, Sae-Seaw P. A randomized
trial of the canalith repositioning procedure. Laryngoscope.
2003;113:828–32.
16. Lacour M, Sterkers O. Histamine and betahistine in the treatment of
vertigo. Elucidation of mechanisms of action. CNS Drugs 2001;15:853-70
17. The mechanism of action of betahistine: towards a consensus. IMN
(International Medical News) 1999;99:1-6.
18. Hazra,A, Niteeka M. Betahistine dihydrochloride or betahistine mesilate:
two sides of the same coin or two different coins. Int J Basic Clin
Pharmacol. 2017 Aug;6(8):1833-1840
19. Behar,GC and Miguel AG. Surgical Treatment for Recurrent Benign
Paroxysmal Positional Vertigo. Int Arch Otorhinolaryngol. 2017 Apr;
21(2): 191–194.
20. Kattah JC, Talkad AV, Wang DZ, Hsieh YH, Newman-Toker DE. HINTS
to diagnose stroke in the acute vestibular syndrome: three-step bedside
oculomotor examination more sensitive than early MRI diffusion-
weighted imaging. Stroke. 2009;40:3504–3510

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