Académique Documents
Professionnel Documents
Culture Documents
Semester
JUL
: Fifi Yuniarti
Hero Akbar
: 04080505060
04080505062
: XII
Date
Advisor
Name
NIM
DEPARTMENT OF NEUROLOGY
FACULTY OF MEDICINE SRIWIJAYA UNIVERSITY/ RSMH
PALEMBANG
2010
ENDORSEMENT PAGE
Case Report
Presented by:
Fifi Yuniarti
04080505060
Hero Akbar
04080505062
: Mrs. N
Age
: 52 years old
Gender
: female
: Moslem
Address
: stay in town
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
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
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
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
Left
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
: 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
Leucocyte
: 9500/mm3
Creatinin
Hematocrit
: 40 vol%
HDL
: 33 mg/dl
Diff Count
: 0/3/0/65/25/7
LDL
: 226 mg/dl
Trigliseride
Thrombocyte : 350.000/mm3
: 74
Na
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
: not performed
: 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
: not performed
Ro Cervical
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
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
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
-
LABORATORY FINDINGS
BLOOD
Trigliseride
Topical Diagnostic
:
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.
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).
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.
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).
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).
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 5. Modified Epley's maneuver for self-treatment of benign positional vertigo (left)
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.
CASE ANALYSIS
Differential Diagnosis by Topical lesion:
1. Central lesion
2. Peripheral lesion
1. Central Lesion
- Dizziness accompanied by sensation
of
spinning
usually
develops
(permanent)
Mild attack
Severe attack
and
fatigue
(-),
latency
(-),
habituation (-).
-
direction
-
diplopia,
disartria,
symptoms
of
brainstem
disorder
-
disphagia, disphonia.
-
No
No
symptoms
of
cerebellum
disorder
skillfull movement.
The possibility of central lesion can be rejected.
2. Peripheral Lesion
- Dizziness accompanied by vertigo,
moving
the
head.
Changing
Severe attack
Nystagmus
(+)
with
horizontal
Severe attack
Nystagmus
(+)
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
affected ear.
fullness in ears.
sensation of -
recovered
medication.
constant
or
recovered
after
take
some
without
medication.
The possibility of menieres disease can be rejected.
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Tinnitus J. 2008;14(2):159-67.
2. Hughes, CA, Proctor, L. Benign paroxysmal positional vertigo.
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3. Wiener-Vacher, SR. Vestibular disorders in children. Int J Audiol 2008;
47:578.
4. von Brevern, M, Radtke, A, Lezius, F, et al. Epidemiology of benign
paroxysmal positional vertigo: a population based study. J Neurol
Neurosurg Psychiatry 2007; 78:710.
5. Brandt, T, Daroff, RB. Physical therapy for benign paroxysmal positional
vertigo. Arch Otolaryngol 1980; 106:484
6. Dix, MR, Hallpike, CS. The pathology, symptomatology and diagnosis of
certain common disorders of the vestibular system. Ann Otol Rhinol
Laryngol 1952; 61:987.
7. Furman, JM, Cass, SP. Benign paroxysmal positional vertigo. N Engl J
Med 1999; 341:1590.
8. Hoffman, RM, Einstadter, D, Kroenke, K. Evaluating dizziness. Am J Med
1999; 107:468.
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findings and possible underlying mechanisms. Int J Audiol 2008; 47:276.
10. Brandt, T, Steddin, S, Daroff, RB. Therapy for benign paroxysmal
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of
benign
paroxysmal
positioning
nystagmus.
ORL J