VERTIGO CASE REPORT

Presented by : dr. Desin Pambudi Sejahtera

Moderator : Dr. dr. Cempaka Thursina Srie, Sp.S(K)
Examiners : Prof. Dr. dr. Sri Sutarni Sudarmadji, Sp.S(K)
dr. Atitya Khairani, M.Sc., Sp.S
Thursday, June 11th, 2015
At 12.30 13.30 pm
IDENTITY
Name
: Mrs. K
Age
: 66 years old
Sex
: Female
Religion
: Moslem
Occupation
: Housewife
Education
: Senior High School
Address
: Paseban, Bayat, Klaten
Marital status
: Married
Date of addmission
: May 13th 2015
MR No
: 01.72.87.xx
ANAMNESIS (May 15th 2015)
Obtained from the patient (autoanamnesis) and her husband (alloanamnesis)
Chief complaint :
Abnormal sensation of rotation/movement of patients environment
The history of present illness :
Two weeks before admission, patient suddenly felt the rotation sensation of her
environment. The intensity was moderate to severe. There was nausea but no vomitus. Patient
denied: worsening of the rotation sensation when she changed the position of the head, decreasing
rotation sensation when she closed her eyes, previous head trauma, uncounciousness, seizure,
fever, ringing sound sensation in the ear, ear infection, clogged ear, decrease in hearing, ear
discharge, skewed lips, lisp speech, limb weakness, psychososial stressor. Patient consulted to
emergency department in Soejarwadi District Hospital. She was admitted to the hospital ward,
examined with Head CT Scan dan diagnosed with vertigo. Patient given some medications which
the patient didnt remember the name. The rotation sensation did not reduced. Five days after
admitted in this hospital, patient went home but the rotational sensation was still present. The
intensity of the sensation was mild to moderate
Day of admission, the rotational sensation was still present. There was nausea without
vomitus. The intensity of the sensation was moderate to severe. Patient denied: worsening of the
rotation sensation when she changed the position of her head, decreasing of the sensation when
she closed her eyes, previous head trauma, uncounciousness, seizure, fever, ringing sound
sensation in the ear, ear infection, clogged ear, decrease in hearing, ear discharge, throbbing
headache, skewed lips, lisp speech, limb weakness, psychososial stressor. Patient went to
Sardjito Hospital Emergency Department and entered the Neurology Ward.

The history of previous illnessess

1. There were history of :
a. Hypertension, approximately 10 years, with average systolic blood pressure
approximately 150 mmHg, uncontrolled to physician
b. Diabetes melitus since 20 years ago without appropriate medication.
2. No history of :
Previous vertigo, Head trauma, Tumor, chemo and radiotherapy
Chronic cough, cough treatment for 6 months, night sweats, subfebrile fever, bloody
cough, Ear, nose, and teeth infection
Hypercholesterolemia, heart disease, stroke, smoking.
The history of family illnessess
History of stroke in father.
The Psychosocial aspect:
She was a grandmother with 4 grandchild from 2 sons and a daughter. Living with her husband,
and her family in good conditions. Economic level was middle and her insurance with BPJS Non
PBI
Systemic evaluation
Cerebrospinal system : sudden rotational sensation,
lasting for two weeks, accompanied with nausea. The
sensation did not reduced with eye closed and did not get
worse with head position changing.
Cardiovascular system
: uncontrolled hypertension
Respiratory system
: normal
Gastrointestinal system
: nausea
Urogenital system
: normal
Musculoskeletal system
: normal
Integumental system
: normal
Endocrine system
: uncontrolled diabetic
Summary of anamnesis
Female patient, 66 years old, came to Sardjito Hospital Emergency Department with the
chief complaint of rotational sensation with nausea which lasting for two weeks. The rotational
sensation was decreased after patient took medication from previous hospital but it has no got
better. The intensity was moderate to severe. The sensation did not get better with eye closing
and did not get worse with head position changing. There is a history of uncontrolled
hypertension and diabetic.

FIRST DISCUSSION
Dizziness and vertigo are among the most common symptoms causing patients to visit a
physician (as common as back pain and headaches). The overall incidence of dizziness, vertigo,
and imbalance is 5-10%, and it reaches 40% in patients older than 40 years. The incidence of
falling is 25% in subjects older than 65 years. Falling can be a direct consequence of dizziness in
this population, and the risk is compounded in those with other neurologic deficits. A report
reviewing presentation to US emergency departments from 1995-2004 indicated that vertigo and
dizziness accounted for 2.5% of presentations (Kerber et al., 2008)
Mild hearing loss is the most common disability in the United States and worldwide. The
incidence of hearing loss is 25% in people younger than 25 years, and it reaches 40% in persons
older than 40 years. About 25% of the population report tinnitus. Vertigo, dizziness, tinnitus, and
hearing loss are typically associated with inner-ear diseases as opposed to CNS diseases.
Migraine is more prevalent (10%) than Mnire disease (< 1%). About 40% of patients with
migraine have vertigo, motion sickness, and mild hearing loss. Therefore, differentiating migraine
from primary inner-ear disorders is sometimes difficult.
The role of the primary care physician and the neurologist in treating patients with
dizziness or vertigo has increased over the last decade. Emphasis is on differentiating peripheral
from central dizziness.
The patient's history is critical in the evaluation of the patient with dizziness. Ask the
patient to describe their symptoms by using words other than "dizzy." The rationale for using
other words is that patients may use dizzy nonspecifically to describe vertigo, unsteadiness,
generalized weakness, syncope, presyncope, or falling.
Dizziness includes light-headedness, unsteadiness, motion intolerance, imbalance,
floating, or a tilting sensation. A critical distinction is differentiating vertigo, which is a subtype
of dizziness, defined as an illusion of movement caused by asymmetric input of the vestibular
system, from other types of dizziness. This dichotomy is helpful because true vertigo is often due
to inner-ear disease, whereas other symptoms of dizziness may be due to CNS, cardiovascular, or
systemic diseases.
Sudden onset and vivid memory of vertiginous episodes are often due to inner-ear
disease, especially if hearing loss, ear pressure, or tinnitus is also present. Gradual and ill-defined
symptoms are common in CNS, cardiac, and systemic diseases. The time course of vertigo is also
important. Episodic true vertigo that lasts for seconds and is associated with head or body
position changes is probably due to benign paroxysmal positional vertigo (BPPV). Vertigo that
lasts for hours or days is probably caused by Mnire disease (if associated with hydropic ear
symptoms) or vestibular neuronitis (if hydropic ear symptoms are absent). Vertigo of sudden
onset that lasts for minutes can be due to brain or vascular disease, especially if cerebrovascular
risk factors are present.
Central vertigo secondary to brainstem or cerebellar ischemia usually lasts for 20 min to
24 h and is often associated with other brainstem characteristics, including diplopia, autonomic
symptoms, nausea, dysarthria, dysphagia, or focal weakness. Patients with cerebellar disease are
frequently unable to ambulate during acute episodes of vertigo. Patients with peripheral vertigo
can usually ambulate during episodes and are consciously aware of their environment. A history
of headaches, especially migraine headaches, can be associated with migraine-related dizziness.

Previous viral illness, cold sores, or sensory changes in the cervical C2-C3 or trigeminal
distributions usually indicate vestibular neuronitis or recurrent episodes of Mnire disease.
Dysdiadochokinesis and gait ataxia during episodes are more likely due to cerebellar
diseases, especially in the elderly and in subjects with evident cardiovascular risk factors. Sensory
and motor symptoms and signs are usually associated with CNS diseases. The history should
include a review of systems (especially head trauma and ear diseases, trauma, or surgery). The
impact of dizziness on activities of daily living at work and home should be addressed. Screening
for primary or reactive anxiety and depression is important. History of prescription medicines,
over-the-counter medications, herbal medicines, and recreational drugs (including smoking and
alcohol) can help to identify pharmacologically induced syndromes. Accurate diagnosis of
dizziness or unsteadiness in the elderly may be more difficult mostly because of atypical
presentation of underlying disorders. Although dizziness in the elderly can be attributed to
weakness and fatigue at times, it may be more serious than in younger patients and should be
carefully investigated. To diagnose dizziness, physicians must use the essential tools of history,
clinical examination, and follow-up (Katsarkas , 2008).

Temporary diagnosis :
Clinical diagnosis
: Acute rotational sensation, nausea
Topical diagnosis
: Organon vestibular central dd perifer
Etiological diagnosis :
1. Central : Vascular (Susp. Vertebrobasilar stroke dd vertebrobasilar artery insufficiency)
2. Perifer
3. Mixed type
PHYSICAL EXAMINATION
General status
General Condition
: Moderate
Consciousness
: Compos mentis (GCS :E4,V5,M6)
BMI
: 26,66 (BB: 60Kg; TB: 150cm)
VAS/ NPS
: 2/ 0
Blood pressure
: 150/90 mm Hg
Pulse
: 84 x/minute, regular
Respiratory rate
: 16 x/minute, regular
Temperature
: 36,7 oC
: Anemic conjunctival (-), icteric of sclerae (-)
Head
: Jugular Vein pressure normal, no carotid bruit
Neck
: No sign of inflammation or enlargement of thyroid gland
within normal limit, mass (-)
Chest
Heart
: normal cor configuration, S1 and S2 regular, murmur (-), gallop
(-)
Lung
: sonor, vesicular, ronchi (-)
Abdomen
: unpalpable liver and spleen, no tenderness, normal peristaltic

Extremities

: no edema

Neurobehavioural status:
Alertness
Behavioural observations
1. History of behavioural changes
2. Mental status
General behaviour
Fluency
Mood and emotional
change
Mind state
Intelectual capasity
Sensorium
a. Consciousness
b. Attention
c. Orientation
d. Short term memory
e. Long-term memory
Calculation
Visuospatial function
Denial or neglect
Apraxia
MMSE
Neurological Examinations
Consciousness
Head & eye

Neck
Description of cranial nerves
N.I
N.II
N.III

Smelling
Visual Function
Visual Field
Colour Vision
Ptosis
Eyes motion to medial
Eyes motion to below
Eyes motion to above
Pupil
Kind of pupil
Direct of light reflex

: alert
: none
: good
: fluent
: none
: realistic
: good enough
: compos mentis
: good enough
: good enough
: good enough
: good enough
: good enough
: good enough
: (-)
: (-)
: 29/30
: fully allert, GCS E4V5M6
: mesocephal
isochoric pupil, 3mm/3mm
light reflex +/+, corneal reflex +/+,
nistagmus horizontal : +/+, vertical +/+,
pendular +/+, rotatoar +/+ slurred speech (+)
: meningeal sign (-)
Right
Wnl
>3/60
Wnl
Wnl
(-)
Wnl
Wnl
Wnl
3 mm
Round
(+)

Left
Wnl
>3/60
Wnl
Wnl
(-)
Limited
Limited
Limited
3 mm
Round
(+)

N.IV

N.V

N.VI

N.VII

N.VIII

N.IX

N.X

NXI

N.XII

Indirect of light reflex

Accomodation reflex
Strabismus divergen
Eyes motion to medial below
Strabismus konvergen
Biting
Open mouth
Sensibility of face
Corneal reflex
Trismus
Eyes motion to lateral
Strabismus konvergen
Diplopia
Blinking
Nasolabial Fold
The angle of the mouth
Wrinkling of the forehead
Eye closure
Puffing cheek
Whistle
Taste on the 2/3 anterior of the
tongue
Hearing of the whispered voice,
watch ticking
Rinne
Weber
Schwabah
Nystagmus
Arcus pharyngeal
Taste on the 1/3 posterior of the
tongue
Vomiting Reflex
Pronouncing the lingual
Retching
Pulse per minute
Arcus pharyngeal
Swallowing
Head Turning
Shoulder position
Shoulder elevation
Trophy of shoulder muscles
Tongue position
Tremor of tounge
Tounge protraction
Trophy of tounges muscle
Fasiculation of tounge

(+)
(+)
(-)
(+)
(-)
Wnl
Wnl
Wnl
Wnl
(-)
(+)
(-)

(+)
(+)
(-)
(+)
(-)
Wnl
Wnl
Wnl
Wnl
(-)
(+)
(-)
(-)

(+)

(+)
Symmetrical
Symmetrical
Symmetrical

Wnl

Wnl
Symmetrical

(-)
Wnl

(-)
Wnl

Normal

Normal

(+)

(+)
No lateralization
Normal
Normal
(-)
(-)
Wnl
Wnl
Wnl
Wnl
(+)
(+)
(+)
84x/mnt
Wnl

84x/mnt
Wnl
Wnl

Wnl
Wnl
(+)
Eutrophy

Wnl
Wnl
(+)
Eutrophy
Wnl

(-)

(-)
Wnl

Eutrophy
(-)

Eutrophy
(-)

Extremity
Movement

Free

Free

Free

Free

RP

Streng

5/5/5
5/5/5

Tn

5/5/5

RF

5/5/5
Tr

2+ 2+
2+ 2+

Cl -/ -

Sensibility
Protophatic
wnl
pain
wnl
temperature
Propioceptive
wnl
pressure
wnl
vibration
wnl
position
wnl
discrimination
Disdiadokokinesis
:(+)
Rebound phenomenon : (+)
Slurred speech
: (+)
Romberg test (opened) : (+)
Tandem gait
: (+)
Fukuda
: (+)
Ataxia
: (+)
Fungsi Vegetatif
: micturition, defecation wnl
Supporting examination:
Laboratory findings
13-05-2015
14-05-2015

Hb (g/dL)
Hct (%)
RBC (106/mm3)
WBC(103/mm3)
PLT (103/mm3)
Neut (%)
Lymph
Mono
Eos
Baso
KED (mm/jam)
Na (mmol/L)
K (mmol/L)
Cl (mmol/L)
GDN (mg/dL)
GD2JPP (mg/dL)

14,5
44,2
5,10
9,46
366
82,6
13,2
1,8
1,0
0,3

Nistagmus
horizontal : +/+
Nistagmus
vertical
: +/+
Nistagmus
rotatoar
: +/+
Dismetri
:(+)

18-05-2015

13,3
45,2
5,90
11,6
286
72,6
23,2
1,5
1,0
0,6
8 (0-15)

137
3,4
98
227

136
3,2
103
259
312

HbA1C (%)
Chol total (mg/dl)
HDL (mg/dL)
LDL (mg/dL)
TG (mg/dL)
BUN (mg/dL)
Cre (mg/dL)
Uric (mg/dL)
SGOT
SGPT
Urinalisis
Glu
Pro
Bil
Uro
pH
SG
Bld
Ket
Nit
Leu
Color
Sediment
LP
LG
Eritrosit
Epitel

6,4
189
35
45
125
16
0,9
50
21
Normal
6,0
>1.030
Light yellow
0
0
0
0

Electrocardiography
Result : normal sinus rythm, HR 90 x/minute
Radiologic findings
Chest X ray : Normal
Head CT Scan

Lesion on pons and left cerebelli hemisfer, may fokal edema caused by infection process
BERA
Lesion of left N. VIII tract at the level of mesencepalon and lesion at level of right cochlea
Supporting mixed lesion of vertigo

10

Consult to others department:

Internal Department:
Diagnose:
- DM2O
- Hipertension
- Observasi vertigo
Therapy:
- Novorapid 8-8-8
- Amlodipin 10mg/ 24jam
- Valsartan 80mg/ 24 jam
NeuroImaging:
Hypodence lesion at border of mesencephalon and left pons.
Hypodence lesion on left cerebellum.
Suspecsious of infarction on both area.

RESUME OF EXAMINATION

11

General status : moderate,compos mentis

Vital sign : blood pressure 150/90 mmHg, pulse : 84x/minute, respiratory rate 16
x/minute, temperature 36,7 C
VAS : 2, NPS: 0
Neurobehavior status is within normal limit
Neurological status :
Cranial nerve examination parese of left 3rd Cranial Nerve
Nistagmus horizontal : +/+
Nistagmus vertical
: +/+
Nistagmus rotatoar : +/+
Dismetri
: (+)
Disdiadokokinesis
: (+)
Rebound phenomenon : (+)
Slurred speech
: (+)
Romberg test
: (+)
Tandem gait
: (+)
Fukuda
: (+)
Ataxia
: (+)
Head CT Scan : Hypodence lesion at border of mesencephalon and left pons. Hypodence
lesion on left cerebellum. Susp of infarction on both area.
Chest X ray : Normal
ECG : normal sinus rythm, HR 90 bpm.
BERA: Lesion of left N. VIII tract at the level of mesncepalon and lesion at level of right
cochlea. Supporting mixed lesion of vertigo

SECOND DISCUSSION
In patients with dizziness, general examination should emphasize vital signs, supine and
standing blood-pressure measurement, and evaluation of the cardiovascular and neurologic
systems. Examine the ears for visible infection or inflammation of the external or middle ear. Test
hearing and discrimination by using a tuning fork and by whispering and asking the patient to
repeat heard words. Examine the neck for range of motion and flexibility. Focused neurologic
examination of the cranial nerves, motor and sensory modalities, gait, and stance is important in
initial visit. Cerebellar tests, especially failure of fixation suppression of vestibular eye
movements, are important for checking the vestibulocerebellum. Failure of fixation suppression
can be tested by asking the patient to stretch his arms and look at his thumb while being passively
rotated (manual rotation of examination chair). A visible nystagmus (right or left) indicates failure
of fixation suppression that is always central in origin.
Central vertigo is vertigo due to a disease originating from the central nervous system
(CNS). In clinical practice, it often includes lesions of cranial nerve VIII as well. Individuals with
vertigo experience hallucinations of motion of their surroundings. Central vertigo may be caused
by hemorrhagic or ischemic insults to the cerebellum, the vestibular nuclei, and their connections
within the brain stem. Other causes include CNS tumors, infection, trauma, and multiple
sclerosis. Vertigo due to acoustic neuroma is also included in the broader category of central
vertigo. An acoustic neuroma develops within the eighth cranial nerve, usually within the course

12

of the internal auditory canal, yet it often expands into the posterior fossa with secondary effects
on other cranial nerves and the brain stem.
Pathophysiology
The brainstem, cerebellum, and peripheral labyrinths are all supplied by the
vertebrobasilar arterial system. Thus, the central and peripheral ischemic vertigo syndromes
overlap.
Vertebrobasilar arterial system
The basilar artery is formed from the 2 vertebral arteries within the cranium at the level
of the medulla. The artery has 3 branches on each side that supply the cerebellum. The posterior
inferior cerebellar artery branches from the vertebral artery, while the anterior inferior cerebellar
artery and the superior cerebellar artery branch from the basilar artery. All 3 of the cerebellar
arteries may have branches that supply brainstem tissue. A labyrinthine artery on each side
branches from the basilar artery and supplies the labyrinth and associated structures via the
internal auditory canal. In approximately two thirds of people, the basilar artery ends by
bifurcating into the posterior cerebral arteries, with small posterior communicating arteries
connecting to the internal carotid system in the circle of Willis.
Arterial occlusion and ischemic infarction
Arterial occlusion and ischemic infarction can result from cardioembolism, embolism of
plaque from a vertebral artery, or local arterial thrombosis. One or both vertebral arteries, the
basilar artery, or any of the smaller branches may be occluded. Even complete occlusion of a
large artery may not result in death because of anastomotic retrograde flow via the circle of Willis
and posterior communicating arteries. Temporary vertebrobasilar ischemia may present as
migraine syndrome or transient ischemic attacks (TIAs). While less common than cerebellar
infarction, spontaneous cerebellar hemorrhage is an important life-threatening cause of vertigo
associated with hypertensive vascular disease and anticoagulation (St. Louis et al., 1998)
Laboratory Studies

Laboratory studies may be useful for patients who do not complain strictly of vertigo.

Rule out anemia, pregnancy, and derangement of serum glucose, if relevant, in patients
who complain of lightheadedness or disequilibrium.

Imaging Studies

Imaging of the posterior fossa is necessary if the clinician suspects a central lesion.
o

Magnetic resonance imaging (MRI) is the preferred modality to detect infarction

(Simmons et al., 1986) , hemorrhage, tumor, and the white matter lesions of
multiple sclerosis.

13

If MRI is unavailable, computed tomography (CT) scan with fine cuts through
the posterior fossa may be used. Unfortunately, CT scan is limited by poorer
resolution than MRI and bony artifact.

Intra-arterial angiography is used traditionally to diagnose occlusions in the

vertebrobasilar system. CT angiography (CTA), noninvasive magnetic resonance
angiography (MRA), and Doppler ultrasonography are steadily supplanting it.
This may be particularly important as early thrombolysis becomes more
established as a therapy.

Other Tests

Electrocardiography (ECG) is necessary to assess for atrial fibrillation, other

dysrhythmias, or evidence of acute myocardial infarction (AMI).

AMI, particularly involving the anterior wall of the left ventricle, can lead to a stiffened
ventricle with poor wall movement and secondary stasis. This may serve as a
cardioembolic source for cerebral thromboembolism.

The consulting neurologist may perform caloric testing and electronystagmography

(ENG) to help localize the lesion in the vestibular apparatus or vestibular nerve nuclei;
audiometry and brainstem auditory evoked potentials (BAER) also may be performed.

FINAL DIAGNOSIS
Clinical diagnosis
Topical diagnosis
Etiological diagnosis
Other diagnosis

: Acute rotational sensation, nausea, parese of left 3rd Cranial Nerve

: Organon vestibular central (pons and cerebellum) and perifer (cochlea)
: Central: Vascular (Brainstem and Cerebellum infarction)
: HT stage II, diabetic

Management
Emergency Department Care
First, distinguish true vertigo from disequilibrium and other forms of dizziness. Ascertaining this
history from patients sometimes requires patience and persistence. Once the presence of vertigo
or disequilibrium has been confirmed, consider a central cause. Evaluate on the basis of a careful
history and physical examination and liberal use of imaging studies of the posterior fossa.

Therapy usually targets the etiology of the symptoms. However, a variety of medications
may be used to reduce symptoms of central vertigo, including antihistamines and
benzodiazepines.

Regardless of the vertigo's etiology, attempt to alleviate the patient's suffering.

o

Place intravenous lines to rehydrate patients.

14

Allow patients to lie still in bed as desired.

Administer parenteral medicines for symptomatic relief.

If clinical and radiologic evaluation suggest an acute ischemic stroke, consider

thrombolytic therapy after thorough evaluation and consultation.
o

Thrombolytic therapy is administered with an intra-arterial catheter close to the

clot , or intravenously, if within 3 hours of the onset of symptoms and no other
contraindications exist (The National Institute of Neurological Disorders, 1995).

Prior to using thrombolytic therapy, consider several issues, especially the risk of
intracerebral bleeding. Emergency physicians should be familiar with
contraindications such as major surgery within the previous 10 days, severe
hypertension, evidence of acute bleed or edema on CT scan, and rapidly
improving symptoms.

The decision to administer thrombolytic therapy preferably is made with direct

neurologic consultation and only after the patient has received a thorough
explanation of the procedure and given informed consent. This therapy is
discussed further in other articles (see Stroke, Ischemic and Thrombolytic
Therapy).

Lethargic patients or those with altered level of consciousness require vigilance and close
supervision, including direct visual, ECG, and pulse oximetry monitoring.

Do not administer anticoagulant medicine, including aspirin, until intracranial

hemorrhage has been ruled out by imaging.

Imaging studies should be performed expeditiously, and the patient never should be left
unattended by clinical personnel in the imaging suite.

Patients with altered consciousness and a deteriorating course in the ED may require
emergent interventions to minimize edema and brainstem compression.
o

As the posterior fossa is a relatively small and nonexpandable space, hemorrhage

or edema can lead to rapid compression and compromise of vital medullary
functions, obstructive hydrocephalus, or herniation of the medullary tonsils.

Invasive actions may include endotracheal intubation to protect the airway,

control breathing, and allow therapeutic hyperventilation.

Consider elevating the head of the bed, performing diuresis with mannitol or
furosemide, and administering dexamethasone.

15

Preliminary evidence suggests that recombinant activated factor VII may be useful for
acute hemorrhagic stroke when administered within 4 hours of symptom onset (Mayer et
al., 2005). The data supporting the use of this therapy for hemorrhagic cerebellar stroke is
too limited thus far to make a therapeutic recommendation, but further results are
expected to clarify its utility and adverse effect profile.

Medical Treatment Overview

Acute dizziness and vertigo is usually managed with vestibular suppressants, antiviral
medication, and antiemetic medications. Steroids are useful in selected patients. Vestibular
suppressants should be used for a few days at most because they delay the brain's natural
compensatory mechanism for peripheral vertigo. Vestibular rehabilitation is very useful in
boosting central vestibular compensation.
Central Dizziness
Migraine
Migraine is a common disorder, affecting 10% of men and 30% of women. About 25% of
migraineurs have motion intolerance/sickness as opposed to true vertigo. The pathophysiology of
migraine-associated vestibulopathy is not completely understood. [4] Vestibular symptoms usually
are dissociated from headaches but sometimes can occur as an aura or as part of a headache.
Treatment of migraine-associated vestibulopathy is the same as the treatment of migraine.
Trigger factors should be eliminated and patients are encouraged to follow common sense diet
and lifestyle.[4] Prophylactic and abortive medications commonly used in treating migraine should
be tailored to patients with vestibular migraine. [3] In the authors experience, topiramate
(Topamax) and rizatriptan benzoate (Maxalt) are associated with excellent control of vestibular
migraine.
Transient ischemic attacks (TIAs)
TIAs are episodes of focal neurological symptoms of isolated or combined brainstem
symptoms such as dizziness, diplopia, or weakness. These attacks are of sudden onset and resolve
within 24 hours without residual subjective symptoms or objective signs (on examination). TIAs
are usually due to either reduced blood flow (hemodynamic theory; eg, cardiac dysrhythmia) or
blood flow obstruction (embolic theory; eg, plaques from the heart).
TIAs are commonly (75% of cases) due to posterior circulation (vertebrobasilar territory).
The differential diagnosis of TIAs includes migraine, partial seizures, hypoglycemia, syncope,
and hyperventilation.
Cerebrovascular disease
Stroke is the third most common cause of death or disability in adults. The
vertebrobasilar circulation supplies the brainstem, cerebellum, and the inner-ear auditory and
vestibular structures. Infarction of the cerebellar midline can cause acute vertigo without auditory

16

or other neurologic features (eg, isolated vertigo). This potentially life-threatening occurrence
must be differentiated from vestibular neuronitis. A key difference between these 2 entities is the
inability to ambulate without support during the acute vertigo phase with cerebellar strokes.
About one half of patients have other features of bulbar or long tract involvement, which make
the diagnosis of stroke clear.
Evaluation of the patient with stroke is directed at identifying correctable vascular risk
factors (hypertension, diabetes, hyperlipidemia, and smoking) and at determining the mechanism
of stroke (small vessel, large vessel, cardioembolic, dissection, hypercoagulability, vacuities).
Secondary prophylactic therapy and rehabilitation are individualized. Both hearing loss and
vertigo can occur in the setting of stroke due to either central and/or peripheral injury.

The patient had given therapies:

Non pharmacologic :
- Head up 30 degree
- Education
- Diet of diabetic
- Rehabilitation
Pharmacologic :
- O2 3 lpm
- IVFD NaCl 0,9% 16 dpm
- Inj. Citicholin 500 mg/12 h
- Clopidogrel 1 x 75 mg
- Flunarizin 2 x 5 mg
- Betahistine 6mg/ 8hour
- Amlodipin 10mg/ 24h
- Valsartan 80 mg/ 24h
- Novorapid injection s.c. 8-8-8 after meal
Planning :
- TCD
- DSA
Prognosis

Prognosis for patients with central vertigo depends on the underlying disease and is
highly variable.

Neurosurgical advancements have improved the prognosis for many serious conditions.
This magnifies the importance of identifying these patients in the emergency setting.

The prognosis of infarction of the basilar or vertebral arteries is poor. In one series, 45%
of patients presented in coma. Importantly, half of the patients in this series had
prodromal symptoms, including vertigo, which cleared completely in the 6 months prior
to the stroke (Ferbert et al., 1990)

17

The prognosis for this patient are:

Death
: dubia ad malam
Disease
: dubia ad malam
Discomfort
: dubia ad malam
Disability
: dubia ad malam
Dissatisfaction
: dubia ad malam
Destitution
: dubia ad malam

REFERENCES
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