CASE REPORT

SENIOR CLINICAL CLERKSHIP

Period of May 10th June 7th, 2010

Semester

JUL
: Fifi Yuniarti
Hero Akbar
: 04080505060
04080505062
: XII

Date

: June 19th, 2010

Advisor

: Dr. H. A. Rachman Toyo, SpS(K)

Name
NIM

DEPARTMENT OF NEUROLOGY
FACULTY OF MEDICINE SRIWIJAYA UNIVERSITY/ RSMH
PALEMBANG
2010

ENDORSEMENT PAGE
Case Report

Benign Positional Vertigo

Presented by:
Fifi Yuniarti

04080505060

Hero Akbar

04080505062

Has been accepted as one of requirements in undergoing senior clinical clerkship

period of June 7th July 5th, 2010 in Department of Neurology Faculty of
Medicine Sriwijaya University / RSMH Palembang.
Palembang, June 2010
Advisor

Dr. H. A. Rachman Toyo, SpS(K)

NEUROLOGY MEDICAL RECORD

IDENTIFICATION
Name

: Mrs. N

Age

: 52 years old

Gender

: female

Marital Status : married

Religion

: Moslem

Address

: stay in town

Admission Date : June 8th 2010

ANAMNESIS (Auto Anamnesis)
The patient was hospitalized in neurology ward of RSMH Palembang
because of the dizziness with the sensation of spinning.
About 5 days before admitted to the hospital, the patient felt dizziness
accompanied by the sensation of spinning. The patient described the complaint
happened and worsen when he changed the position upon rising from a lying or
sitting to a standing position and turned the head while lying, lasted a few seconds
to a few minutes and intermittent. The complaint would be subside when she
moved her head to the previous position. Besides nausea and vomiting, she is also
complained about tinnitus in the left ear. There was no difficulty in doing skillful
movement and no complain about difficulty to speak. The patient didnt complain
about double vision and weakness with her eyes. About 2 hours before admitted,
patient felt the dizziness more severe and increasing of nausea and vomiting.
Patient suffered from Hypertension, controlled about 1 years ago. No
history of getting fever. No hitory of getting fever. No history of secreted the
smelly fluid from the ear. No history of ringing sound in the ear, sensation of
fullness in the ear that accompanied by intermittent hearing loss before. No
history of getting head injury. No history of diabetes mellitus. No history of longterm using streptomycin, gentamycin, quinine and antineoplastics agent.
This illness was the first time for her.

PHYSICAL EXAMINATION

PRESENT STATE
Internal State
Sense

: E4M6V5

Lungs

: no abnormality

Nutrition

: sufficient

Liver

: no abnormality

Pulse

: 88 beats/min

Spleen

: no abnormality

Respiratory rate

: 22 times/min

Extremities

: no edema

Blood pressure

: 160/90 mmHg

Genital

: no abnormality

Attention

: cooperative

Facial Expression

: natural

Attention

: normal

Psyche contact

: natural

Shape

: brachiocephaly

Deformity

: no

Size

: normal

Fracture

: no

Symetric

: yes

Fracture pain

: no

Hematome

: no

Vessel

: no widening

Tumor

: no

Pulsation

: no disorder

Position

: straight

Deformity

: no

Torticolis

: no

Tumor

: no

Nape of neck stiffness : no

Vessels

Psychiatric state

Neurological state
Head

Neck

: no widening

CRANIAL NERVES
Olfaktorius nerve

Right

Left

Smelling

No disorder

No disorder

Anosmia

No

No

Hyposmia

No

No

Parosmia

No

No

Right

Left

Opticus nerve
Visual acuity

6/6 PH (-)

6/6 PH (-)

Campus visi

V.O.D

V.O.S

Anopsia

No

No

Hemianopsia

No

No

Oculi fundus

Edema papil

No

No

Atrophy papil

No

No

Retina bleeding

No

No

Right

Left

No

No

No

No

No

No

No

No

No

No

No

No

No

No

no abnormality

no abnormality

Occulomotorius,

Trochlearis

and Abducens nerves

Diplopia
Eyes gap
Ptosis
Eyes position

Strabismus

Exophtalmus

Enophtalmus

Deviation conjugae

Eyes movement
5

Accessorius Nerve

Right

Left

Shoulder Raising

No disorder

No disorder

Head Twisting

No disorder

No disorder

Hypoglossus Nerve
Tounge Showing

Right

Left

No deviation

No deviation

Fasciculation

no

no

Papil Athrophy

no

no

Dysarthria

no

no

Right

Left

Motion

Sufficient

Sufficient

Power

Tones

Normal

Normal

MOTORIC
Arms

Physiological Reflex

Biceps

Normal

Normal

Triceps

Normal

Normal

Radius

Normal

Normal

Ulna

Normal

Normal

None

None

None

None

None

None

None

None

Right

Left

Sufficient

Sufficient

normal

Normal

Negative

Negative

Pathological Reflex

Hoffman Tromner

Leri

Meyer

Trofik

LEG
Motion
Power
Tones
Clonus

Tigh

Foot

Negative

Negative

Physiological reflex

KPR

Normal

Normal

APR

Normal

Normal

Negative

Negative

Negative

Negative

Negative

Negative

Negative

Negative

Negative

Negative

Negative

Negative

Negative

Negative

Abdominal skin reflex

Negative

Negative

Upper

Negative

Negative

Middle

Negative

Negative

Lower

Negative

Negative

Pathological reflex

Babinsky

Chaddock

Oppenheim

Gordon

Schaeffer

Rossolimo

Mendel Bechterew

Tropik
SENSORY
No abnormality.
PICTURE

VEGETATIVE FUNCTION
Micturition

: No abnormality

Defecation

: No abnormality

VERTEBRAL COLUMN
Kyphosis

: no

Tumor

: no

Lordosis

: no

Meningocele

: no

Gibbus

: no

Hematome

: no

Deformity

: no

Tenderness

: no

SYMPTOMS OF MENINGEAL IRRITATION

Right

Left

Nape of neck stiffness

Negative

Negative

Kerniq

Negative

Negative

Lasseque

Negative

Negative

Brudzinsky

Neck

Negative

Negative

Cheek

Negative

Negative

Symphisis

Negative

Negative

Leg I

Negative

Negative

Leg II

Negative

Negative

GAIT AND EQUILIBIRIUM

Gait Equilibirium and Coordination
Ataxia

: negative

Romberg

: positive

Hemiplegic

: negative

Dysmetri

Scissor

: negative

finger finger

: normal

Propulsion

: negative

finger nose

: normal

Histeric

: negative

heel - heel

: normal

Limping

: negative

Reboundphenomenon : negative

Steppage

: negative

Dysdiadochokinesis : negative

Astasia-Abasia

: negative

Trunk Ataxia

: negative

Limb Ataxia

: negative

MOTION ABNORMAL
Tremor

: no

Chorea

: no

Athetosis

: no

Ballismus

: no

Dystoni

: no

Myoclonus

: no

LIMBIC FUNCTION
Motoric aphasia

: no

Sensoric aphasia

: no

Apraksia

: no

Agraphia

: no

Alexia

: no

Nominal aphasia

: no

LABORATORY FINDINGS
BLOOD
Hb

: 13,8 gr/dl

Ureum

: 27 mg/dl (15-39 mg/dl)

Leucocyte

: 9500/mm3

Creatinin

: 1,9 mg/dl (0,6-1,0 mg/dl)

Hematocrit

: 40 vol%

HDL

: 33 mg/dl

Diff Count

: 0/3/0/65/25/7

LDL

: 226 mg/dl

Trigliseride

: 214 mg/dl (<150)

Thrombocyte : 350.000/mm3

Kolesterol tot : 302 mg/dl (<200)

LED

: 74

Na

: 133 mmol/l (135-155)

: 4,4 mmol/l (3,5-5,5)

BSS

: 95 mg/dl

URINE
Epithel

: not performed

Protein

: not performed

Leucocyte

: not performed

Glucose

: not performed

Eritocyte

: not performed

FECES
Consistency

: not performed

Erytrocyte

: not performed

Slime

: not performed

Leucocyte

: not performed

Blood

: not performed

Worm egg

: not performed

Amoeba coli/ : not performed

Hystolitica

: not performed

CEREBRO SPINAL FLUID

Colour

: not performed

Protein

: not performed

Clarity

: not performed

Glucose

: not performed

Pressure

: not performed

NaCl

: not performed

Cell

: not performed

Queckensted

: not performed

Nonne

: not performed

Celloidal

: not performed

Pandy

: not performed

Culture

: not performed

SPECIFIC EXAMINATION
Cranium X- Ray

: not performed

Chest X- Ray

: not performed

Vertebral column X- Ray

: not performed

Ro Cervical

: Spondyloarthrosis cervicalis & calcification of

lig. Nuchae and normal of for. intervertebralis.

Electroencephalography

: not performed

Electroneuromyography

: not performed

Electrocardiography

: normal

Arteriography

: not performed

Pneumography

: not performed

CT-Scan

: not performed

RESUME
IDENTIFICATION
Mrs. N/ 52 years old/ female/ married/ Moslem/ stay in town/ June 8th
2010
ANAMNESIS (Auto Anamnesis,)
The patient was hospitalized in neurology ward of RSMH Palembang
because of the dizziness with the sensation of spinning.
About 5 days before admitted to the hospital, the patient felt dizziness
accompanied by the sensation of spinning. The patient described the complaint
happened and worsen when he changed the position upon rising from a lying or
sitting to a standing position and turned the head while lying, lasted a few seconds
to a few minutes and intermittent. The complaint would be subside when she
moved her head to the previous position. Besides nausea and vomiting, she is also
complained about tinnitus in the left ear. There was no difficulty in doing skillful
movement and no complain about difficulty to speak. The patient didnt complain
about double vision and weakness with her eyes. About 2 hours before admitted,
patient felt the dizziness more severe and increasing of nausea and vomiting.
Patient suffered from Hypertension, controlled about 1 years ago. No
history of getting fever. No history of secreted the smelly fluid from the ear. No
history of ringing sound in the ear, sensation of fullness in the ear that
accompanied by intermittent hearing loss before. No history of getting head
injury. No history of diabetes mellitus. No history of long-term using
streptomycin, gentamycin, quinine and antineoplastics agent.
This illness was the first time for her.
EXAMINATION
Present State
Sense

: compos mentis (GCS 15: E4M6V5)

Blood pressure

: 160 / 90 mmHg

Pulse

: 88x/minute

Respiratory rate

: 22x/minute

11

Temperature

: 36,8o C

Nutrition

: sufficient

Neurological state
Nn. Craniales
Vestibular nerve

: Nystagmus (+) one way and lateral, Vertigo (+).

Motoric function
Motoric function

Arm

Right
Left
Motion
Sufficient
Sufficient
Power
5
5
Tones
Normal
Normal
Clonus
Physiological reflex
Normal
Normal
Pathological reflex
Sensory function
: No abnormality
Vegetative function

: No abnormality

Limbic function

: No abnormality

Leg
Right
Sufficient
5
Normal
Normal
-

Left
Sufficient
5
Normal
Normal
-

Abnormal Movement : (-)

Gait & Stability

: Romberg Test (+)

Meningeal Irritation : (-)

Ro Cervical

: Spondyloarthrosis cervicalis and calcification of lig.

Nuchae and normal of foramen intervertebralis.

LABORATORY FINDINGS
BLOOD
Trigliseride

: 214 mg/dl (<150)

Cholesterol total : 302 mg/dl (<200)

DIAGNOSIS
Clinical Diagnostic

: Benign Positional Vertigo + Hypertension stage 1 +

Hypercholesterolemia + Spondyloarthrosis cervicalis

Topical Diagnostic

: Labirinth (peripheral lession)

Etiological Diagnostic: Idiopathic

MANAGEMENT
Non Medication :
Give information about this disease and how to treat this disease by
physical exercise.
Medication

:
Betahistine mesylate 3 x 6 mg
Dimenhydrinat 3 x 1 tablet
Vitamin B1, B6, B12 3 x 1 tablet
Simvastatin 1 x 20 mg
Captopril 2 x 12,5 mg
Bed rest
Rice diet
Consult to ENT and Internal medicine Department

PROGNOSIS :

Quo ad vitam

: bonam

Quo ad functionam

: bonam

LITERATURE
BACKGROUND
Benign paroxysmal positional vertigo (BPPV) is probably the most
common single cause of vertigo in the United States. Estimates indicate that at
least 20% of all patients who present to the physician complaining of vertigo have
benign paroxysmal positional vertigo. However, because benign paroxysmal
positional vertigo is misdiagnosed frequently, this figure may not be completely
accurate and is probably an underestimation. As benign paroxysmal positional
vertigo can occur concomitantly with other inner ear diseases (eg, a patient may
have Mnire disease and BPPV concurrently), statistical analysis may be skewed
toward lower numbers.
Benign paroxysmal positional vertigo was described first by Mnire in
1921. The characteristic nystagmus and vertigo associated with positioning
changes were at that time attributed to the otolithic organs. Dix and Hallpike in
1952 became the namesakes for the provocative positional test still used today to
identify benign paroxysmal positional vertigo. They further defined the classic
nystagmus and went on to localize the pathology to the affected ear during
provocation.1

DEFINITION
Defining benign paroxysmal positional vertigo is complex because, as our
understanding of its pathophysiology has evolved, so has its definition. As more
interest is focused on benign paroxysmal positional vertigo, new types of
positional vertigo have been discovered. What was previously lumped together as
benign paroxysmal positional vertigo is now subclassified on the basis of the
offending semicircular canal (posterior semicircular canal vs lateral semicircular
canal). These groups are divided further into canalithiasis and cupulolithiasis
depending on pathophysiology. Benign paroxysmal positional vertigo is defined
as an abnormal sensation of motion that is elicited by certain critical provocative
positions. The provocative positions usually trigger specific eye movements (eg,
nystagmus). The character and direction of the nystagmus is specific to the part of
the inner ear af fected and the underlying pathophysiology.

Although some controversy exists regarding the 2 pathophysiologic

mechanisms, canalithiasis and cupulolithiasis, agreement is growing that the 2
entities actually coexist and account for different subtypes of benign paroxysmal
positional vertigo. However, classic benign paroxysmal positional vertigo is best
explained by canalithiasis. In canalithiasis (literally, canal rocks) the particles
reside in the canal portion of the semicircular canals (in contradistinction to the
ampullary portion). These densities are considered to be free-floating and mobile,
and to cause vertigo by exerting a force. Cupulolithiasis (literally, cupula rocks),
on the other hand, refers to densities adhering to the cupula of the crista
ampullaris. Cupulolith particles reside in the ampulla of the semicircular canals
and are not free-floating.
Classic benign paroxysmal positional vertigo is the most common variety
of benign paroxysmal positional vertigo. It involves the posterior semicircular
canal and is characterized by the following: geotropic nystagmus with the
problem ear down, predominantly rotatory, fast phase toward undermost ear,
latency (ie, a few seconds), and limited duration.

EPIDEMIOLOGY
Benign paroxysmal positional vertigo (BPPV) is the most common form
of positional vertigo, accounting for nearly one-half of patients with peripheral
vestibular dysfunction. Approximately 18 percent of patients seen in dizziness
clinics2 and 25 percent of patients sent for vestibular testing have BPPV.3 BPPV
also accounts for about 20 percent of pediatric referrals.4
In a population-based survey study, the lifetime prevalence of BPPV was
2.4 percent.5 The one-year prevalence of BPPV increased with age and was seven
times higher in those older than age 60 years, compared with those aged 18 to 39
years. BPPV was more common in women than men in all age groups.

SYMPTOMS
Patients complain of recurrent episodes of vertigo lasting one minute or
less. Although individual episodes are brief, these typically recur periodically for
weeks to months without therapy.6 In one study, the median duration of BPPV was

two weeks.5 Episodes are provoked by specific types of head movements, such as
looking up while standing or sitting, lying down or getting up from bed, and
rolling over in bed. The spells may wax and wane over time; patients often have
sudden spontaneous remissions, only to have the episodes recur at a later date.
The vertigo may be associated with nausea and vomiting.
Patients with BPPV typically have no other neurologic complaints, in
contrast to those with central causes of vertigo. Some patients have evidence of
prior inner ear damage. Approximately half of patients complain of imbalance
between attacks, even after successful treatment.5

PATHOPHYSIOLOGY
Benign positional vertigo (BPV) is caused by calcium carbonate particles
called otoliths (or otoconia) that are inappropriately displaced into the
semicircular canals of the vestibular labyrinth of the inner ear. These otoliths are
normally attached to hair cells on a membrane inside the utricle and saccule.
Because the otoliths are denser than the surrounding endolymph, changes in head
movement vertically causes the otoliths to tilt the hair cells, which triggers a nerve
that send a signal to the brain letting the brain know that the head is tilting up or
down.
The utricle is connected to the 3 semicircular canals. The otoliths may
become displaced from the utricle by aging, head trauma, or labyrinthine disease.
When this occurs, the otoliths have the potential to enter the semicircular canals.
When they do, they almost always enter the posterior semicircular canal because
this is the most dependent (inferior) of the 3 canals. (Figure 1)
According to the canalolithiasis theory (the most widely accepted theory
of the pathophysiology of benign positional vertigo), the otoliths are free-floating
within the canal. Changing head position causes the otoliths to move through the
canal. Endolymph is dragged along with the movement of the otoliths, and this
stimulates the hair cells of the cupula of the affected semicircular canal, causing
vertigo. When the otoliths stop moving, the endolymph also stops moving and the
hair cells return to their baseline position, thus terminating the vertigo and
nystagmus. Reversing the head maneuver causes the particles to move in the

opposite direction, producing nystagmus in the same axis but reversed in direction
of rotation. The patient may describe that the room is now spinning in the opposite
direction. When repeating the head maneuvers, the otoliths tend to become
dispersed and thus are progressively less effective in producing the vertigo and
nystagmus (hence, the concept of fatigability).

Figure 1. Anatomy of the semicircular canals

HISTORY
Benign paroxysmal positional vertigo typically has a sudden onset. Many
patients wake up with it, noticing the vertigo while trying to sit up suddenly.
Thereafter, propensity for positional vertigo may extend for days to weeks and
occasionally to months or years. In many, the symptoms periodically clear and
then recur.
The severity covers a wide spectrum. In extreme cases, the slightest head
movement may be associated with nausea and vomiting. In other cases, despite

significant nystagmus, the patient seems relatively unfazed. People who have
benign paroxysmal positional vertigo do not usually feel dizzy all the time. Severe
dizziness occurs when head movements trigger the attack. At rest and between
episodes, patients usually have few or no symptoms.
However, some patients complain of an incessant foggy or cloudy
sensorium. Classic benign paroxysmal positional vertigo usually is triggered by
the sudden action of moving from the erect position to the supine position while
angling the head 45 degrees toward the side of the affected ear. Merely being in
the provocative position is not enough to trigger an attack. The head must actually
move to the offending position. After reaching the provocative position, the
person experiences a lag period of a few seconds before the vertigo strikes again.
When benign paroxysmal positional vertigo is triggered, patients feel as
though they are suddenly thrown into a rolling spin, toppling toward the side of
the affected ear. The symptoms start very suddenly and usually dissipate within
20-30 seconds. This sensation is triggered again upon sitting erect; however, the
direction of the nystagmus is reversed.

EXAMINATION
Observing nystagmus during a provoking maneuver solidifies the
diagnosis of BPPV in patients with a typical history. Nystagmus is optimally
provoked by the Dix-Hallpike (show figure 2).6 With the patient sitting, the neck
is extended and turned to one side. The patient is then placed supine rapidly, so
that the head hangs over the edge of the bed. The patient is kept in this position
until 30 seconds has passed if no nystagmus occurs. The patient is then returned to
upright, observed for another 30 seconds for nystagmus, and the maneuver is
repeated with the head turned to the other side.

Figure 2. Dix hallpike maneuver

In addition to the prototype of posterior canal BPPV, there are three
variants: anterior canal, horizontal canal, and pure torsional.
Posterior canal BPPV The Dix-Hallpike maneuver will usually provoke
paroxysmal vertigo and nystagmus if posterior canal dysfunction is present in the
ear that is turned downward during the exercise.

Diagnostic criteria employing the Dix-Hallpike maneuver have been

proposed for posterior canal BPPV (show figure 2)7: Nystagmus and vertigo
usually appear with a latency of a few seconds and last less than 30 seconds. It has
a typical trajectory, beating upward and torsionally, with the upper poles of the
eyes beating toward the ground. After it stops and the patient sits up, the
nystagmus will recur but in the opposite direction. The patient should then have
the maneuver repeated to the same side; with each repetition, the intensity and
duration of nystagmus will diminish.
The latency, transience, and fatiguability, coupled with the typical mixed
upbeat/torsional direction, establish this as a peripheral vertigo. Variation in these
features may occur with peripheral disease but may also indicate a central lesion
(show table 1). Overall, the sensitivity of the Dix-Hallpike maneuver in patients
with BPPV ranges from 50 to 88 percent.8

Tabel 1. Dix Hallpike maneuver for positional nystagmus

Anterior canal BPPV Anterior canal BPPV (also known as the superior
canal BPPV) has similar provoking factors as classic posterior canal BPPV, but
the nystagmus is downbeat and torsional, with the top of the eye torting away
from the lower ear, ie, ageotropic9. The latency, duration, and fatiguability are
similar.10, 11
Horizontal canal BPPV Horizontal canal BPPV is provoked by turning
the head while lying down, sometimes by head turns while upright, but not by
getting in or out of bed or extending the neck. The nystagmus is elicited by a

lateral head turn in the supine position. Horizontal nystagmus beating toward the
floor begins after one to eight seconds of turning the affected ear down; it lasts
approximately one minute, and after a few seconds of inactivity is followed by a
reversal of the nystagmus, which also lasts up to one minute. A milder nystagmus
is seen with the normal ear down, again beating toward the ground.
Approximately 25 percent of patients also have posterior canalithiasis.12
Recognizing horizontal canal BPPV is important because it requires a
different therapeutic maneuver. (See "Particle repositioning maneuvers" below).

Figure 3. Particle repositioning manuvers

Pure torsional BPPV About one-half of patients with a history of BPPV
have a pure torsional nystagmus by the Dix-Hallpike maneuver 13. This type of
BPPV may be due to canalithiasis that involves both the anterior and posterior
canals14. Time to remission with repeated repositioning maneuvers is prolonged
for pure torsional BPPV compared with posterior BPPV (mean 25 versus 2.5 days,
respectively)13.

DIFFERENTIAL DIAGNOSIS
There are four major disorders in the differential diagnosis of BPPV:
postural hypotension, chronic unilateral vestibular hypofunction, migrainous
vertigo, and central positional vertigo with downbeat nystagmus.
Postural hypotension Postural (orthostatic) hypotension can be confused with
BPPV since both cause dizziness that is provoked by a positional change.
However, orthostatic presyncope is not induced by rolling over in bed or lying
down, while 90 percent of patients with BPPV complain that these maneuvers
cause dizziness.
Chronic unilateral vestibular hypofunction Chronic unilateral vestibular
hypofunction is associated with transient dizziness after rapid head turns, but
these are fleeting, lasting only one to two seconds. In contrast, vertigo from BPPV
does not require rapid head turns, and it typically lasts 30 to 60 seconds.
Furthermore, vertigo in posterior canal BPPV is provoked by looking up or down,
whereas these maneuvers are not necessarily problematic for patients with chronic
unilateral hypofunction.
Migrainous vertigo Migraine is a frequent cause of episodic vertigo, and
migrainous vertigo (MV) can present as an isolated positional vertigo mimicking
BPPV (pseudo BPPV).
Central positional vertigo and nystagmus Central positional vertigo may
occur with lesions of the vestibulocerebellum. The classic ocular motor sign of
central positional vertigo is downbeat nystagmus. In some patients, the downbeat
nystagmus is present or increased only when lying down, more so when prone
than supine.15
Static positional vertigo Patients with positional vertigo may have nystagmus
that persists as long as the provocative position is maintained, termed static
positional vertigo. This can occur with either central or peripheral vestibular
lesions.
The direction of nystagmus is helpful in distinguishing between central
and peripheral causes of vertigo. Pure downbeat nystagmus from cerebellar
disease can be accentuated in the reclining position and occasionally occurs only
in this position. The lack of a torsional component to the nystagmus differentiates

this from anterior canal benign paroxysmal positional vertigo (BPPV). Other
features that indicate central disease are a lack of latency, lack of fatiguability, and
the inability to suppress nystagmus with vision (show table 1 and show table 2).

Table 2 Clinical distinction between peripheral vertigo and central vertigo

The main consideration in the differential diagnosis of positional downbeat
nystagmus is the anterior canal form of BPPV.

TREATMENT
MEDICATION
Drug use to this symptoms are Antihistamin (dimenhidrinat, promethazin),
Betahitin mesilat (mertigo , vertex), Flunarizin (frego , sibelium) and Cinnarizin
(stugeron)
SELF-TREATMENT13-19
Based on the same principles, exercises for home, self-treatment use have
been developed: the Brandt-Daroff exercises (show figure 4), a modified Epley's

maneuver (show figure 5A-5B), and the modified Semont maneuver (show figure
6).
One study of 54 patients found that vertigo resolved in 18 of 28 patients
(64 percent) using the modified Epley maneuver compared with 6 of 26 patients
(23 percent) using the Brandt-Daroff exercises. Another study of 70 patients by
the same group found that self-treatment with the modified Epley maneuver was
more effective in abolishing vertigo than self-treatment with the modified Semont
maneuver (response rate 95 versus 58 percent, respectively), likely because
patients had more difficulty performing the latter. A randomized trial in 80
patients treated with the Epley procedure alone versus the Epley procedure
supplemented by self-treatment with the modified Epley maneuver found that
combined therapy resulted in a higher rate of symptom resolution (88 versus 77
percent).
In general, Brandt-Daroff exercises are less effective than particle
repositioning maneuvers; self-treatment with either modified Epley's or Semont
maneuver has not been well-studied in comparison to more standard particle
repositioning maneuvers. Self-treatment with the modified Epley maneuver may
serve a complementary role for patients who do not respond immediately to the
single treatment maneuvers listed above, and it may become part of the routine
management of BPPV for those with frequent recurrences.
The maneuvers are well tolerated by most patients. However,
approximately 6 percent have the debris migrate into the anterior or horizontal
canals, causing other variants of positional vertigo

Figure 4. Brandt-Daroff maneuver

Figure 5. Modified Epley's maneuver for self-treatment of benign positional vertigo (left)

Figure 6. Modified semont maneuver

SUMMARY
Positional vertigo is a common problem. Both central (eg, brainstem or
cerebellum) and peripheral (eg, canalithiasis) vestibular lesions can cause
positional nystagmus and vertigo. The distinction between these two entities is
important. Central positional nystagmus is usually static, in that the nystagmus
persists as long as the head is kept in the provoking position. Positional vertigo
due to peripheral vestibular pathology is always transient.
Benign paroxysmal positional vertigo (BPPV) is the most common form
of positional vertigo, accounting for nearly one-half of patients with peripheral
vestibular dysfunction.
BPPV is characterized by recurrent episodes of vertigo lasting one minute
or less. BPPV episodes are provoked by specific types of head movements.
Although individual episodes are brief, these typically recur periodically for
weeks to months without therapy.
BPPV is most commonly attributed to calcium debris within the posterior
semicircular canal. Classic posterior canal BPPV is idiopathic in 35 percent of
cases. There are three BPPV variants: anterior canal, horizontal canal, and pure
torsional.

Observing nystagmus during the Dix-Hallpike maneuver solidifies the

diagnosis of BPPV in patients with a typical history (see "Examination" above).
The diagnosis of BPPV is uncertain if no nystagmus is seen on examination.
However, empiric treatment with liberatory maneuvers in this setting is often
effective, if the history is highly suggestive of BPPV.
Further testing is not indicated with typical posterior canal BPPV. Patients
who have nystagmus with atypical features or nystagmus of undetermined origin
should be examined for neurologic signs and investigated.
The four major disorders in the differential diagnosis of BPPV are postural
hypotension, chronic unilateral vestibular hypofunction, migrainous vertigo, and
central positional vertigo with downbeat nystagmus.
Liberatory (particle repositioning) maneuvers such as the Brandt-Daroff
exercises, Semont maneuver, and Epley maneuver are effective treatments for
patients with BPPV. (See "Particle repositioning maneuvers" above).
Recurrences of BPPV are fairly common. Most respond to repeated
treatments with one of the liberatory maneuvers such as the Epley.
Drugs are not useful for the brief episodes of vertigo associated with
BPPV, except when the frequency of spells is very high. However, vestibular
suppressants can be used as premedication with liberatory maneuvers.
BPPV is intractable in a very small number of patients

CASE ANALYSIS
Differential Diagnosis by Topical lesion:
1. Central lesion
2. Peripheral lesion
1. Central Lesion
- Dizziness accompanied by sensation
of

spinning

usually

develops

Symptoms of the patient were:

-

Sudden onset, last a few seconds

gradually and last days to weeks

to a few minutes and intermittent

(permanent)

(come and go).

Dizziness is independent of changing

position and moving the head.

Depend on changing position and

moving the head.

Mild attack

Severe attack

Nystagmus (+) with vertical direction

Nystagmus (+) but not vertica

and

fatigue

(-),

latency

(-),

habituation (-).
-

direction
-

Accompanied by brainstem disorder

symptoms:

diplopia,

disartria,

symptoms

of

brainstem

disorder
-

disphagia, disphonia.
-

No
No

symptoms

of

cerebellum

disorder

Accompanied by cerebellum disorder

symptoms: coordination disorders,
difficultiy and trembling in doing

skillfull movement.
The possibility of central lesion can be rejected.
2. Peripheral Lesion
- Dizziness accompanied by vertigo,

Symptoms of the patient were:

Sudden onset, last a few seconds

vomiting develop suddenly, lasted a

to a few minutes and intermittent

few days to a few weeks

(come and go), with vomiting

Patient usually feel relieved but not

Depend on changing position and

purely free from the symptomps

moving

the

head.

Changing

Dizziness is depend on changing

position and moving the head

position and moving the head.

-

Severe attack

Nystagmus

(+)

with

worsen the dizziness

horizontal

Severe attack

Nystagmus

direction and fatigue(+), latency (+),

(+)

with

lateral

direction

habituation (+)
The possibility of Peripheral lesion can not be rejected.
Differential Diagnosis by Etiology:
1. Medication
2. Ear infection
3. Head injury
4. Menier disease
5. Idiophatic

1.Medication (ototoxicity)
- History of long-term
streptomycin,

quinine

use
and

of

anti

Symptoms of the patient were:

History of long-term use of
streptomycin, quinine and anti

neoplastic agent (+).

neoplastic agent (-).
The possibility of medications can be rejected.
2. Ear infection (otitis media)
- History of secreted the smelly fluid -

Symptoms of the patient were:

History of secreted the smelly fluid

from ear (+).

-

History of a sensation of fullness in

from ear (-).

-

History of a sensation of fullness in

the ear (+).

the ear (-).
The possibility of ear infections can be rejected.
3. Head injury
-

History of head injury (+)

Symptoms of the patient were:

-

History of head injury (-)

- Sensation of spinning (+)

- Sensation of spinning (+)
The possibility of head injury can be rejected.
4. Meniere Diease

Symptoms of the patient were:

Episodic rotational vertigo, hearing -

The patient felt dizziness with

loss, ringing sound in ear (tinnitus)

tinnitus but without accompanied

and a sensation of fullness in the

by hearing loss and sensation of

affected ear.

fullness in ears.

Vertigo, tinnitus and

sensation of -

Vertigo attack is severe and will be

fullness in ear may come and go with

recovered

the fluctuating of hearing loss, be

medication.

constant

or

recovered

after

take

some

without

medication.
The possibility of menieres disease can be rejected.

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