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 : [email protected]
PEKANBARU

I. PATIENT’S 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.

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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

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Respiratory Rate: 20 times per minute
Temperature : 36.8°C

B. Neurological status
1) Consciousness : Alertness GCS : 15
2) Noble Function : Normal
3) Neck Stiffness : Negative
4) Cranial Nerves
1. Cranial nerve I (Olfactory)
Right Left Interpretation
Sense of Smell Normal Normal Normal

2. Cranial nerve II (Optic)

Right Left Interpretation
Visual Acuity Normal Normal
Visual Fields Normal Normal Normal
Colour Recognition Normal Normal

3. Cranial nerve III (Oculomotor)

Right Left Interpretation
Ptosis (-) (-)
Pupil
Shape Round Round
Size Φ3 mm Φ3 mm Normal
Extraocular movements Normal Normal
Pupillary reactions to light
Direct (+) (+)
Indirect (+) (+)

4. Cranial nerve IV (Trochlear)

Right Left Interpretation
Extraocular movements Normal Normal Normal

5. Cranial nerve V (Trigeminal)

Right Left Interpretation
Motor Normal Normal
Sensory Normal Normal Normal
Corneal reflex (+) (+)

6. Cranial nerve VI (Abducens)

Right Left Interpretation
Extraocular movements Normal Normal Normal

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 Strabismus (-) (-)
Deviation (-) (-)

7. Cranial nerve VII (Facial)

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

8. Cranial nerve VIII (Acoustic)

Right Left Interpretation
Sense of Hearing Normal Normal Normal

9. Cranial nerve IX (Glossopharyngeal)

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

10. Cranial nerve X (Vagus)

Right Left Interpretation
Pharyngeal Arch Normal Normal
Normal
Dysphonia (-) (-)

11. Cranial nerve XI (Accessory)

Right Left Interpretation
Motor Normal Normal
Normal
Trophy Eutrophy Eutrophy

12. Cranial nerve XII (Hypoglossal)

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

IV. MOTOR SYSTEM

Right Left Interpretation

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 Upper Extremity
Strength
Distal 5 5
Proximal 5 5 Normal
Tone Normal Normal
Trophy Eutrophy Eutrophy
Involuntary movements (-) (-)
Clonus (-) (-)
Lower Extremity
Strength
Distal 5 5
Proximal 5 5
Tone Normal Normal
Trophy Eutrophy Eutrophy Normal
Involuntary movements (-) (-)
Clonus (-) (-)
Body
Trophy Eutrophy Eutrophy
Involuntary movements (-) (-) Normal
Abdominal Reflex (-) (-)

V. SENSORY SYSTEM
Right Left Interpretation
Light Touch
(+) (+)
Pain
(+) (+)
Temperature
Proprioceptive
 Position (+) (+) Normal
 Two point discrimination (+) (+)
 Stereognosis (+) (+)
 Graphestesia (+) (+)
 Vibration Not Tested Not Tested

VI. REFLEX
Right Left Interpretation
Physiologic
Biceps (+) (+)
Triceps (+) (+) Physiologic reflex (+)
Knee (+) (+)
Ankle (+) (+)
Pathologic
Babinsky (-) (-)
Chaddock (-) (-)
Hoffman Tromer (-) (-) Pathologic reflex (-)
Openheim (-) (-)
Schaefer (-) (-)

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 Primitive Reflex
Palmomental (-) (-)
Snout (-) (-)

VII. COORDINATION
Right Left Interpretation

Point to point movements Normal Normal

Walk heel to toe Normal Normal Tandem (+),
Gait Normal Normal Romberg (+)
Tandem (+) (+)
Romberg (+) (+)

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 36,8°C
Noble Function : Normal
Neck Stiffness : Negative
Cranial Nerves : Normal
Motoric : Normal

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Sensory : Normal
Coordination : Tandem test (+), romberg test (+)
Autonomy : Normal
Reflex : Physiology (+), Pathology (-)

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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)

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FOLLOW UP
Desember,30h 2015
S : dizziness (↓), nausea (-), vomit (-)
O :
GCS 15
Blood Pressure 130/90 mmHg
Heart Rate 86 bpm
Respiratory Rate 22 tpm
Temperature 36.8°C
Noble Function : Normal
Neck Stiffness : Negative
Cranial Nerves : Normal
Motoric : Normal
Sensory : Normal
Coordination : Romberg test (+)
Autonomy : Normal
Reflex : Pathologic (-),Physiology (+)
A : Peripheral vertigo + vulnus laseratum
P :
 IVFD RL 20 dpm
 Betahistin 3 x 6 mg
 Dimenhidrinat 3 x 50 mg
 Inj ceftriaxon 2 x 1 gr

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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 Ménière'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 without Vertigo with intracranial
deafness signs
Ménière’s disease Vestibular neuronitis Cerebellopontine angle
tumour
Labyrinthitis Benign positional Cerebrovascular disease
vertigo : TIA / CVA

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Labyrinthine trauma Acute vestibular Vertebro-basilar
dysfunction insufficiency and
thromboembolism:
lateral medullary
syndrome- subclavian
steal syndrome- basilar
migraine

Acoustic neuroma Medication induced Brain tumour:-

vertigo e.g. e.g.
aminoglycosides ependymoma or
metastasis in the
fourth ventricle

Acute cochleo- Cervical spondylosis Migraine

vestibular dysfunction
Syphilis (rare) Following 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

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 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
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
meniere’s 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

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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
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” flexion-
extension 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:

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- 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:
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
auditory meatus of the affected side
- Indicates the presence of a perilymphatic fistula.
5. 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

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 - 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 Ménière'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
therefore should be investigated.
3. If features of CNS causes is suspected from the history or examination:
- CT/MRI Brain imaging as appropriate
7. Treatment
Treatment modalities in vertigo Pharmacological interventions9,1:
• Anticholinergics
• Antihistamines
• Benzodiazepines
• Calcium channel antagonists (especially verapamil and nimodipine)
• GABA modulators (like gabapentin and baclofen)
• Neurotransmitter reuptake inhibitors (SSRIs, SNRIs and tricyclics) •
Nootropics (piracetam)

2. The Basic of Diagnosis

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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).

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

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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.

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