Case Report

VERTIGO

By:
Rizqina Putri
1408465586

Supervisor:
dr. Enny Lestari, Sp.S

DEPARTMENT OF NEUROLOGY
MEDICAL SCHOOL RIAU UNIVERSITY
RSUD ARIFIN ACHMAD
PEKANBARU
2016
KEMENTRIAN PENDIDIKAN DAN KEBUDAYAAN

FAKULTAS KEDOKTERAN UNIVERSITAS RIAU

SMF/BAGIAN SARAF
Sekretariat : Gedung Kelas 03, RSUD Arifin Achmad Lantai 04
Jl. Mustika, Telp. 0761-7894000
E-mail : saraffkur@gmail.com
PE K AN B AR U

I. PATIENTS IDENTITY
Name

Mrs. E

Age

51years

Gender

Female

Address

Pekanbaru

Religion

Moslem

Marital Status

Married

Occupation

Housewife

Date of Admission

Desember, 28th 2015

Medical Record

7117xx

II. ANAMNESIS
Autoanamnesis (December, 29th 2015)
Chief Complaint
Dizziness since three hours before admitted to the hospital
Present Illness History
Three hours before admitted to the hospital, the patient complained
dizziness, the patient describes it as a sudden and severe spinning
sensation precipitated by rolling over in bed onto her right side. Symptoms
typically last <30 seconds. She describes no precipitating event prior to
onset, nausea (+),There was no headache, no visual changes, no weakness,
no numbness, no paresthesias, no associated hearing loss, tinnitus or
vomited. Patient had history of head trauma, and no loss of consciousness.

Past Illness History

There is no history of ear infections

There is no history of hypertension

There is no history of diabetes mellitus

Family Illness History

There is no history of vertigo in family

History of hypertension is unknown

History of diabetes melitus is unknown

Socioeconomic History

She is not a smoker

She no consumed alcohol

Long Drug Consumption (-)

THE SUMMARY OF ANAMNESIS

Mrs. E, 51 years old admitted to the hospital on Desember, 28th 2015. The
patient has complained dizziness, the patient describes it as a sudden and severe
spinning sensation precipitated by rolling over in bed onto her right side.
Symptoms typically last <30 seconds. She describes no precipitating event prior
to onset, nausea (+),There was no antecedent headache, palpitations, or chest pain,
and no headache, no visual changes, no weakness, no numbness, no paresthesias
no associated hearing loss, tinnitus or vomited. There were no history of
hypertension and diabetes mellitus.
III. PHYSICAL EXAMINATION
A. General status
Blood Pressure : 130/80 mmHg
Heart Rate

: 82 bpm

Respiratory Rate: 20 times per minute

Temperature

: 36.8C

B. Neurological status
1) Consciousness

: Alertness

2) Noble Function

: Normal

3) Neck Stiffness

: Negative

GCS : 15

4) Cranial Nerves
1. Cranial nerve I (Olfactory)
Sense of Smell

Right
Normal

Left
Normal

Interpretation
Normal

2. Cranial nerve II (Optic)

Right
Normal
Normal
Normal

Visual Acuity
Visual Fields
Colour Recognition

3. Cranial nerve III (Oculomotor)

Right
Ptosis
(-)
Pupil
Shape
Round
Size
3 mm
Extraocular movements
Normal
Pupillary reactions to light
Direct
(+)
Indirect
(+)

Left
Normal
Normal
Normal

Left
(-)

Interpretation
Normal

Interpretation

Round
3 mm
Normal

Normal

(+)
(+)

4. Cranial nerve IV (Trochlear)

Right
Normal

Extraocular movements

Left
Normal

Interpretation
Normal

5. Cranial nerve V (Trigeminal)

Motor
Sensory
Corneal reflex

Right
Normal
Normal
(+)

Left
Normal
Normal
(+)

Interpretation
Normal

6. Cranial nerve VI (Abducens)

Right
Normal

Extraocular movements

Left
Normal

Interpretation
Normal

Strabismus
Deviation

7. Cranial nerve VII (Facial)

Right
Tic
(-)
Motor
Normal
Sense of Taste Normal
Chvostek Sign
(-)

(-)
(-)

Left
(-)
Normal
Normal
(-)

(-)
(-)

Interpretation
Normal

8. Cranial nerve VIII (Acoustic)

Right
Normal

Left
Normal

Interpretation
Normal

9. Cranial nerve IX (Glossopharyngeal)

Right
Pharyngeal Arch
Normal
Sense of Taste
Normal
Gag Reflex
(+)

Left
Normal
Normal
(+)

Interpretation

Left
Normal
(-)

Interpretation

Sense of Hearing

Normal

10. Cranial nerve X (Vagus)

Right
Normal
(-)

Pharyngeal Arch
Dysphonia
11. Cranial nerve XI (Accessory)
Right
Motor
Normal
Trophy
Eutrophy

Left
Normal
Eutrophy

12. Cranial nerve XII (Hypoglossal)

Right
Motor
Normal
Trophy
Eutrophy
Tremor
(-)
Dysarthria
(-)

Normal

Interpretation
Normal

Left
Normal
Eutrophy
(-)
(-)

Interpretation
Normal

IV. MOTOR SYSTEM

Right

Left

Interpretation

Upper Extremity
Strength
Distal
Proximal
Tone
Trophy
Involuntary movements
Clonus
Lower Extremity
Strength
Distal
Proximal
Tone
Trophy
Involuntary movements
Clonus
Body
Trophy
Involuntary movements
Abdominal Reflex

5
5
Normal
Eutrophy
(-)
(-)

5
5
Normal
Eutrophy
(-)
(-)

5
5
Normal
Eutrophy
(-)
(-)

5
5
Normal
Eutrophy
(-)
(-)

Eutrophy
(-)
(-)

Eutrophy
(-)
(-)

Normal

Normal

Normal

V. SENSORY SYSTEM
Light Touch
Pain
Temperature
Proprioceptive
Position
Two point discrimination
Stereognosis
Graphestesia
Vibration

Right

Left

(+)
(+)

(+)
(+)

(+)
(+)
(+)
(+)
Not Tested

(+)
(+)
(+)
(+)
Not Tested

VI. REFLEX

Physiologic
Biceps
Triceps
Knee
Ankle
Pathologic
Babinsky
Chaddock
Hoffman Tromer
Openheim

Right

Left

(+)
(+)
(+)
(+)

(+)
(+)
(+)
(+)

(-)
(-)
(-)
(-)

(-)
(-)
(-)
(-)
5

Interpretation
Physiologic reflex
(+)

Pathologic reflex (-)

Interpretation

Normal

Schaefer
Primitive Reflex
Palmomental
Snout

(-)

(-)

(-)
(-)

(-)
(-)

VII. COORDINATION

Point to point movements

Walk heel to toe
Gait
Tandem
Romberg

Right

Left

Normal
Normal
Normal
(+)
(+)

Normal
Normal
Normal
(+)
(+)

VIII. AUTONOMY SYSTEM

Urination

: Normal

Defecation

: Normal

IX. Others Examination

a. Laseque

: Unlimited

b. Kernig

: Unlimited

c. Patrick

: Negatif

d. Kontrapatrick

: Negatif

e. Valsava test

: Negatif

f. Brudzinski

: Negatif

X. THE SUMMARY OF EXAMINATION

General Status

Blood Pressure 130/80 mmHg

Heart Rate 82 bpm
Respiratory Rate 20 times per minute
Temperature 36,8C
Noble Function

: Normal

Neck Stiffness

: Negative

Interpretation
Tandem (+),
Romberg (+)

Cranial Nerves

: Normal

Motoric

: Normal

Sensory

: Normal

Coordination

: Tandem test (+), romberg test (+)

Autonomy

: Normal

Reflex

: Physiology (+), Pathology (-)

XI. WORKING DIAGNOSIS

CLINICAL DIAGNOSIS

: Peripheral Vertigo

TOPICAL DIAGNOSIS

: Aparatus vestibular

ETIOLOGICAL DIAGNOSIS : Suspect BPPV (post head trauma)

XII. SUGGESTION EXAMINATION

Blood routine

Blood chemistry

Electrolit

XIII. MANAGEMENT

IVFD RL 20 dpm

Betahistin 3 x 6 mg

Dimenhidrinat 3 x 50 mg

Ondanserton 8mg 1 x 1 iv

XIV. LABORATORY AND RADIOLOGY FINDINGS

1. Blood Routine (Desember, 28th 2015)
-

Hemoglobin

: 12,6 g/dL

Hematocrit

: 38,8 %

Leukocyte

: 18.600/mm3

Thrombocyte

: 492.000/mm3

2. Blood Chemistry (Desember, 28th 2015)

-

Glucose

: 121 mg/dL

Ureum

: 47 mg/dL

Creatinin

: 1,25 mg/dL

AST

: 18 U/L

ALT

: 18 U/L

3. Electrolit (Desember, 28th 2015)

4.

Na+: 136, 5mmol/L (135 145)

5.

K+: 3,17 mmol/L (3,5 4,5)

6. Cl : 108,3 mmol/L (97-107)

FOLLOW UP
Desember,30h 2015
S

: dizziness (), nausea (-), vomit (-)

GCS 15
Blood Pressure 130/90 mmHg
Heart Rate

86 bpm

Respiratory Rate 22 tpm

Temperature

36.8C

Noble Function

: Normal

Neck Stiffness

: Negative

Cranial Nerves

: Normal

Motoric

: Normal

Sensory

: Normal

Coordination

: Romberg test (+)

Autonomy

: Normal

Reflex

: Pathologic (-),Physiology (+)

: Peripheral vertigo + vulnus laseratum

IVFD RL 20 dpm

Betahistin 3 x 6 mg

Dimenhidrinat 3 x 50 mg

Inj ceftriaxon 2 x 1 gr

DISCUSSION
Vertigo
1.

Definition
Vertigo is the hallucination of movement of the environment around the

patient, or of the patient with respect to the environment. It is not a fear of heights.
Vertigo is not necessarily the same as dizziness. Dizziness is a non-specific term
which can be categorised into four different subtypes according to symptoms
described by the patients:Vertigo, presyncope (the sense of impending faint,
caused by a reduced total cerebral perfusion), light-headedness (often described as
giddiness or wooziness), disequilibrium (a feeling of unsteadiness or imbalance
when standing).1
2.

Epidemiology
Most patients who complain about dizziness do not have true vertigo: 5

community based studies into dizziness indicated that around 30% of patients
were found to have vertigo, rising to 56.4% in an older population. A postal
questionnaire study which examined 2064 patients, aged 18-65, 7% described true
vertigo in the

previous year. A full time GP can therefore expect between 10-

20 patients with vertigo in one year. 93% of primary care patients with vertigo
have either benign paroxysmal positional vertigo (BPPV), acute vestibular
neuronitis, or Mnire's disease.2
3.

Etiology
A wide range of conditions can cause vertigo, and identifying whether

deafness or CNS signs are present, can help narrow the differential diagnosis, as
shown in Table 11.
Vertigo with deafness

Vertigo

Mnires disease

deafness
Vestibular neuronitis

Labyrinthitis

Benign

without Vertigo with intracranial

signs
Cerebellopontine angle

tumour
positional Cerebrovascular

vertigo

disease : TIA / CVA

10

Labyrinthine trauma

Acute

vestibular Vertebro-basilar

dysfunction

insufficiency

and

thromboembolism:
lateral

medullary

syndrome-

subclavian

steal syndrome- basilar

migraine
Acoustic neuroma

Medication

induced

vertigo

e.g.

aminoglycosides

Brain

tumour:-

e.g.
ependymoma or
metastasis in the
fourth ventricle

Acute

cochleo- Cervical spondylosis

vestibular dysfunction
Syphilis (rare)

Following

Migraine

flexion- Multiple sclerosis

extension injury
Aura of epileptic attack
especially temporal
lobe epilepsy
Drugs e.g. phenytoin,
barbiturates

Syringobulbia
Tabel 1. Cause vertigo
4.

Classification
Vertigo may be classified as3:
Central - due to a brainstem or cerebellar disorder
Peripheral - due to disorders of the inner ear or the Vestibulocochlear
(VIIIth) cranial nerve
Vertigo can be defined as an illusion or hallucination of movement. The

control of balance is complicated. Vertigo can be caused by many different

pathologies, some of which are potentially life threatening. An important
11

differentiation is whether the symptoms of vertigo originate from a central or

peripheral origin. Clues to a central origin are other brainstem symptoms or signs
of acute onset such as headache, deafness and other neurological findings. These
patients warrant urgent referral and investigation. Red flags in patients with
vertigo include: headache, neurological symptoms, and neurological signs, It is
useful to categorise vertigo into acute and chronic. The former usually has a single
mechanism whereas chronic dizziness is often multifactorial.3
Vertigo of peripheral origin is conditions & causes. Condition Details
benign paroxysmal brief, position-provoked vertigo episodes caused by positional
vertigo abnormal presence of particles in semicircular canal decreasing frequency
menieres disease An excess of endolymph, causing distension of endolymphatic
system. Vestibular neuronitis Vestibular nerve inflammation, most likely due to
virus Acute labyrinthitis. Labyrinth inflammation due to viral or bacterial
infection. Labyrinthine infarct Compromises blood flow to the labyrinthine.
Labyrinthine concussion Damage to the labyrinthine after head trauma. Perilymph
fistula Typically caused by labyrinth membrane damage resulting in perilymph
leakage into the middle ear Autoimmune inner ear. Inappropriate immunological
response that attacks inner ear disease cells.3
Vertigo of central origin is conditions & causes. Condition Details
Migraine Vertigo may precede migraines or occur concurrentlyDecreasing
frequency Ischaemia or haemorrhage in vertebrobasilar system can Vascular
disease affect brainstem or cerebellum function. Demyelination disrupts nerve
impulses which can result in Multiple sclerosis vertigo. Vertigo resulting from
focal epileptic discharges in the vestibular epilepsy temporal or parietal
association cortex. Cerebellopontine tumours Benign tumours in the internal
auditory meatus.3

5.

Pathophysiological
Pathophysiological pathways endolymph movement, depending on the

direction of flow and deflection of otoliths by gravity, either stimulates or inhibits

neuronal output from the attached hair cells. Nerve impulses from the vestibular
12

system are transmitted to the vestibular nuclei in the brain stem and cerebellum
through the eighth cranial nerve From there, connections are made to the
oculomotor system, spinal cord, and cerebral cortex, which integrate the
information to produce the perception of motion Vertigo results from lesions or
disturbances along this pathway.4
Vertigo is role of neurotransmitters. Neurotransmitters that work centrally
and peripherally include the acetylcholine for functions as an excitatory
neurotransmitter in central and peripheral pathways, glutamate to maintains the
resting discharge of the central vestibular neurons, and GABA to thought to be
inhibitory for commissures of the medial vestibular nucleus.4
6.

Clinical manifestation
Vertigo may be due to central lesions or peripheral lesions. Vertigo may

also be psychogenic or occur in conditions which limit neck movement, such as

vertigo caused by cervical spondylosis, or following a whiplash flexionextension injury.5
It is essential to determine whether the patient has a peripheral or central
cause of vertigo. Information obtained from the history that can be used to make
this distinction includes5:
- The timing and duration of the vertigo
- Provoking or exacerbating factors
- Associated symptoms such as
- Pain
- Nausea
- Neurological symptoms
- Hearing loss
Central vertigo:
- The vertigo usually develops gradually
- Except in: an acute central vertigo is probably vascular in origin, e.g.
-

CVA
Central lesions usually cause neurological signs in addition to the

vertigo
Auditory features tend to be uncommon.
- Causes severe imbalance
- Nystagmus is purely vertical, horizontal, or torsional and is not
inhibited by fixation of eyes onto an object
Physical/signs6,7
1. Examination of ear drums (Otoscopy/ Pneumatic otoscopy) for:

13

Vesicles (Ramsay Hunt syndrome)

Cholesteatoma
2. Tuning fork tests for hearing loss Rinne/Weber tests
3. Cranial nerve examination. Cranial nerves should be examined for
signs of :
- Nerve palsies
- Sensorineural hearing loss
- Nystagmus 3
4. Hennebert's sign
- Vertigo or nystagmus caused by pushing on the tragus and external
5.
-

auditory meatus of the affected side

Indicates the presence of a perilymphatic fistula.
Gait tests:
Romberg's sign (not particularly useful in the diagnosis of vertigo 1)
Heel-to- toe walking test
Unterberger's stepping test (The patient is asked to walk on the spot
with their eyes closed if the patient rotates to one side they have

labyrinth lesion on that side

6. Dix-Hallpike manoeuvre
- The most helpful test to perform on patients with vertigo
- If rotational nystagmus occurs then the test is considered positive for
BPPV. During a positive test, the fast phase of the rotatory nystagmus
is toward the affected ear, which is the ear closest to the ground.
7. Head impulse test/head thrust test
- Useful in recognizing acute vestibulopathy
8. Caloric tests
- Cold or warm water or air is irrigated into the external auditory canal
Not commonly used
Investigations/Testing to consider8:
1. Special auditory tests
- Audiometry helps establish the diagnosis of Mnire's disease
2. The history is most important and may give a quite good indication of
the cause of vertigo. General medical causes such as anaemia,
hypotension and hypoglycaemia may present with dizziness, and

7.

therefore should be investigated.

3. If features of CNS causes is suspected from the history or examination:
- CT/MRI Brain imaging as appropriate
Treatment
Treatment modalities in vertigo Pharmacological interventions9,1:
Anticholinergics
Antihistamines
Benzodiazepines
Calcium channel antagonists (especially verapamil and nimodipine)
14

 GABA modulators (like gabapentin and baclofen)

Neurotransmitter reuptake inhibitors (SSRIs, SNRIs and tricyclics)
Nootropics (piracetam)

2. The Basic of Diagnosis

2.1 Clinical diagnosis : Peripheral Vertigo
According to anamnesis and physical examination, we have found:

Dizziness, the patient describes it as a sudden and severe spinning

sensation precipitated by rolling over in bed onto her right side. Symptoms
typically last <30 seconds, nausea (+), and post head trauma.

Tandem walking test (+), romberg test (+)

The several important things above mean that there is vertigo

2.2 Topical Diagnosis : Aparatus vestibular

From anamnesis there are obtained a dizziness , it as a sudden and severe
spinning sensation precipitated by rolling over in bed onto her right side,
Symptoms typically last <30 seconds, nausea (+), post head trauma and There is
no neurological deficit then diagnosis of the topic in this case is aparatus
vestibular.
2.3 Basic of etiological diagnose
Basic etiological diagnose of this patient is suspect BPPV because Benign
positional vertigo, believed to be the most common type of peripheral vertigo, can
be seen following head injury on this patient is post head injury and the patient
complained dizziness, the patient describes it as a sudden and severe spinning
sensation precipitated by rolling over in bed onto her right side, Symptoms
typically last <30 seconds, nausea (+). So we considered to BPPV (post head
trauma).

15

2.4 Basic of supporting examination

a. Laboratory :to find the risk factor for the vertigo and general condition
of patient.

2.5 Basic of treatment

a. IVFD (30cc/kgbb/day) RL 20 gtt/i

to maintance the euvolemik

condition.
b.

Betahistin 3 x 6 mg as the anti vertigo.

c. Dimenhidrinat 3 x 50 mg to descrease nausea and spinning sensations

neurotropic.
d. Ondanserton 1 x 8 mg to descrease nausea.
e. Inj ceftriaxon 2 x 1 g iv as the antibiotic for vulnus laseratum.

16

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Diunduh tanggal 1 Januari 2016. Diunduh dari
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