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

Mr. S

Age

51 years 10 months

Gender

Male

Address

Matoluok Village, Bangkinang

Religion

Moslem

Marital Status

Married

Occupation

Driver

Date of Admission

December, 27th 2015

Medical Record

88 93 xx

II. ANAMNESIS
Autoanamnesis and alloanamnesis with patients wife (December, 28th
2015)
Chief Complaint
The weakness on the right limbs
Present Illness History
Since 4 hours before admission, the patient has complained the weakness on
his right limbs. At first, the patient has complained weakned on the right
limbs suddenly when he woke up in the morning. He never complained the
numbness before.
Furthermore, the patients speech became nonfluent or lisp.
No history of headache, vomiting, losing of vision and decreasing of
consciousness. No history of trauma.

Past Illness History

Patient had an uncontrolled hypertension since 6 years ago

Unknown history of Diabetes mellitus and Cardiovascular disease

No history of obesity

Family Illness History

His father had a hypertension

His nephew had a stroke

No history of Diabetes mellitus

No history of Cardiovascular disease

Socioeconomic History

He is a smoker since 30 years ago

He never consumed alcohol and drugs

Dietary habit is irregular

THE SUMMARY OF ANAMNESIS

Mr. S, 51 years old admitted to the hospital on December, 27th 2015. The
patient has complained the sudden weakness on the right limbs since 4 hours
before admission. The patients speech nonfluent or lisp. Patient had an
uncontrolled hypertension since 6 years ago, his family had a history of
hypertension and stroke. He is a smoker since 30 years ago and dietary habit is
irregular.

III. PHYSICAL EXAMINATION

A. General status
Blood Pressure : 210/90 mmHg
Heart Rate
Respiratory Rate
Temperature

: 88 bpm
: 20 times per minute
: 36,5C

Weight : 70 kg Height : 165 cm

B. Neurological status
1) Consciousness

: Alertness

2) Cognitive Function

: Normal

3) Neck Stiffness

: Negative

GCS : E4M6V5

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

Left

Interpretation

Normal

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

Left

Interpretation

Extraocular movements
Strabismus
Deviation

Normal
(-)
(-)

7. Cranial nerve VII (Facial)

Right
Tic
(-)
Motor
Decrease
- corners of
the mouth
Shallow
- folds
nasolabialis
(+)
- frowning
(+)
- Raise
(+)
eyebrows
(+)
Closed eyes
(-)
Sense of Taste
Chvostek Sign

Normal
(-)
(-)

Left
(-)
Normal
(+)

Normal

Interpretation

(+)

Paresis N VII
dextra central
type

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

8. Cranial nerve VIII (Acoustic)

Right
(+)

Sense of Hearing

Left
(+)

9. Cranial nerve IX (Glossopharyngeal)

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

Interpretation
Normal

Interpretation
Normal

10. Cranial nerve X (Vagus)

Pharyngeal Arch
Dysphonia

Right

Left

Interpretation

Normal
(-)

Normal
(-)

Normal

11. Cranial nerve XI (Accessory)

Right
Motor
Normal
Trophy
Eutrophy

Left
Normal
Eutrophy

Interpretation
Normal

12. Cranial nerve XII (Hypoglossal)

Right
Motor
Tongue compelled
Trophy
Eutrophy
Tremor
(-)
Dysarthria
(+)

Left
Normal
Eutrophy
(-)
(+)

Interpretation
Parese N XII dextra

IV. MOTOR SYSTEM

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

Right

Left

Interpretation

4
4
Normal
Eutrophy
(-)
(-)

5
5
Normal
Eutrophy
(-)
(-)

4
4
Normal
Eutrophy
(-)
(-)

5
5
Normal
Eutrophy
(-)
(-)

Eutrophy
(-)
(-)

Eutrophy
(-)
(-)

Hemiparesis
dextra (UMN
Type)

Normal

V. SENSORY SYSTEM
Touch
Pain
Temperatur
Propioseptif

Right

Left

(+)

(+)

(+)

(+)

(+)

(+)

(+)

(+)

VI. REFLEX
Right

Left

Interpretation

Interpretation

Normal

Physiologic
Biceps
Triceps
Knee
Ankle
Pathologic
Babinsky
Chaddock
Hoffman Tromer
Openheim
Schaefer
Primitive Reflex
Palmomental
Snout

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

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

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

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

(-)
(-)

(-)
(-)

Physiologic reflex
(+)

Pathologic reflex (-)

Primitive Reflex (-)

VII. COORDINATION

Point to point movements

Walk heel to toe
Gait
Tandem
Romberg

Right
Normal
Normal
Normal
Normal
Normal

Left
Normal
Normal
Normal
Normal
Normal

Interpretation
Normal

VIII. AUTONOMY SYSTEM

Urination

: Normal

Defecation

: Normal

IX. Others Examination

a. Laseque

: Unlimited

b. Kernig

: Unlimited

c. Patrick

: -/-

d. Kontrapatrick

: -/-

e. Valsava test

: -

f. Brudzinski

: -

GAJAH MADA ALGORITHM

Loss of consciousness (-), headache (-), pathology reflex (-)
Hemorrhagic stroke

Non-

SIRIRAJ SCORE
(2.5 x level of consciousness (0)) + (2 x Vomit (0)) + (2 x headache (0)) + (0.1 x
diastolic (100)) (3x atheroma factor (1)) 12 = - 5 Non-Hemorrhagic stroke
X. THE SUMMARY OF EXAMINATION
General Status

: Hypertension (210/90 mmHg)

Cognitive Function : Normal

Neck Stiffness

: Negative

Cranial Nerves
Motoric

: Parese N VII dextra central type

Parese N XII dextra
: Hemiparesis dextra (UMN Type)

Sensory

: Normal

Coordination

: Normal

Autonomy

: Normal

Reflex

: Normal

Gajah Mada Algorithm: Non-hemorrhagic stroke

Siriraj Score

: Non-hemorrhagic stroke

XI. WORKING DIAGNOSIS

CLINICAL DIAGNOSIS

: Stroke

TOPICAL DIAGNOSIS

: Carotid system

ETIOLOGICAL DIAGNOSIS : Ischemic stroke

DIFFERENTIAL DIAGNOSIS : Hemorrhagic stroke
XII. SUGGESTION EXAMINATION

Blood routine

Blood chemistry

Electrocardiography

Chest X-ray

Head CT Scan

XIII. SUGGESTION FOR MANAGEMENT THERAPY

General
-

Immobilization and head up 20-30

Monitoring of vital sign

Medical rehabilitation

IVFD (30ml/kgBB/day) Ringer Lactate 20 dpm

Special
-

Citicoline 3 x 500 mg per IV

Aspilet 2 x 80 mg per oral

Folic acid 2 x 400 g tab per oral

XIV. LABORATORY AND RADIOLOGY FINDINGS

1. Blood Routine (December, 27th 2015)
-

Hemoglobin

: 14,1 g/dL

Hematocrit

: 42,9 %

Leukocyte

: 6.700/mm3

Thrombocyte

: 280.000/mm3

Interpretation: Normal
2. Blood Chemistry
(December, 29th 2015)
-

Glucose

: 112 mg/dL

Choresterol

: 295 mg/dL

HDL

: 70,9 mg/dL

Triglyceride

: 107 mg/dL

Uric acid

: 7,6 mg/dL

LDL Cholesterol

: 203 mg/dL

Ureum

: 32 mg/dL

Creatinin

: 1,50 mg/dL

AST

: 23 U/L

ALT

: 17 U/L

Albumin

: 4,07 g/dL

3. Electrocardiography

Interpretation : synus rithm, no abnormal morphology waves.

4. Head CT Scan without contrast

Interpretation: ischemic on the left paraventricel hemisphere cerebri

XV. FINAL DIAGNOSIS

-

Ischemic stroke

Hypertension

Hyperlipidemia

FOLLOW UP
December, 29th 2015
S

: weakness of the right limbs, lisp.

:
GCS E4M6V5
Blood Pressure 180/90 mmHg
Heart Rate 80 bpm
Respiratory Rate 20 tpm
Temperature 36,8C
Cognitive Function

: Normal

Neck Stiffness

: Negative

Cranial Nerves

: Paresis N VII dextra central type

Paresis N XII dextra

Motoric

: Right extremity hemiparesis

Sensory

: Normal

Coordination : Normal
Autonomy

: Normal

Reflex

: Normal limit

: Ischemic stroke + Hypertension

IVFD RL 20 dpm

Citicolin 3 x 500 mg per IV

Aspilet 2 x 80 mg per oral

Folic acid 2 x 400 g per oral

December, 30st 2015

10

: weakness of the right extremity, lisp.

:
GCS E4M6V5
Blood Pressure 170/100 mmHg
Heart Rate 76 bpm
Respiratory Rate 20 tpm
Temperature 36,5C
Cognitive Function: Normal
Neck Stiffness

: Negative

Cranial Nerves

: Paresis N VII dextra central type

Paresis N XII dextra

Motoric

: Right extremity hemiparesis

Sensory

: Normal

Coordination

: Normal

Autonomy

: Normal

Reflex

: Normal

: Ischemic stroke + Hypertension + Hyperlipidemia

IVFD RL 20 dpm

Citicolin 3 x 500 mg per IV

Aspilet 2 x 80 mg tab per oral

Folic acid 2 x 400 g tab per oral

Amlodipine 1 x 10 mg per oral

Simvastatin 1 x 10 mg per oral

11

Discussion
ISCHEMIC STROKE
1. Definition
Stroke is applied to a sudden focal neurologic syndrome, specifically the
type due to cerebrovascular disease. The term cerebrovascular disease designates
any abnormality of the brain resulting from a pathologic process of the blood
vessels. Pathologic process is given an inclusive meaning namely, occlusion of
the lumen by embolus or thrombus, rupture of a vessel, an altered permeability of
the vessel wall, or increased viscosity or other change in the quality of the blood
flowing through the cerebral vessels. The vascular pathologic process may be
considered not only in its grosser aspects embolism, thrombosis, dissection, or
rupture of a vessel but also in terms of the more basic or primary disorder, i.e.,
atherosclerosis, hypertensive arteriosclerotic change, arteritis, aneurysmal
dilation, and developmental malformation. Equal importance attaches to the
secondary parenchymal changes in the brain resulting from the vascular lesion.
These are of two main types ischemia, with or without infarction, and hemorrhage
and unless one or the other occurs, the vascular lesion usually remains silent. The
only exceptions to this statement are the local pressure effects of an aneurysm,
vascular headache (migraine, hypertension, temporal arteritis), multiple small
vessel disease with progressive encephalopathy (as in malignant hypertension or
cerebral arteritis), and increased intracranial pressure (as occurs in hypertensive
encephalopathy and venous sinus thrombosis). Also, persistent acute hypotension
may cause ischemic necrosis in regions of brain between the vascular territories of
cortical vessels, even without vascular occlusion.1
More than any other organ, the brain depends from moment to moment on
an adequate supply of oxygenated blood. Constancy of the cerebral circulation is

12

assured by a series of baroreceptors and vasomotor reflexes under the control of

centers in the lower brainstem. Obstruction of an artery by thrombus or embolus is
the usual cause of focal ischemic damage, but failure of the circulation and
hypotension from cardiac decompensation or shock, if severe and prolonged
enough, can produce focal as well as diffuse ischemic changes.1
Focal cerebral ischemia differs fundamentally from global ischemia. In the
latter state, if absolute, there is no cerebral blood flow of the entire brain and
irreversible destruction of neurons occurs within 4 to 8 min at normal body
temperature. In focal ischemia, there is nearly always some degree of circulation
(via collateral vessels), permitting to a varying extent the delivery of oxygenated
blood and glucose.
The effects of a focal arterial occlusion on brain tissue also vary depending
on the location of the occlusion in relation to available collateral and anastomotic
channels. If the obstruction lies proximal to the circle of Willis (toward the heart),
the anterior and posterior communicating arteries of the circle are often adequate
to prevent infarction. In occlusion of the internal carotid artery in the neck, there
may be anastomotic flow from the external carotid artery through the ophthalmic
artery or via other smaller externalinternal connections. With blockage of the
vertebral artery, the anastomotic flow may be via the deep cervical, thyrocervical,
or occipital arteries or retrograde from the other vertebral artery. If the occlusion
is in the stem portion of one of the cerebral arteries, i.e., distal to the circle of
Willis, a series of meningeal interarterial anastomoses may carry sufficient blood
into the compromised territory to lessen (rarely to prevent) ischemic damage.
There is also a capillary anastomotic system between adjacent arterial branches,
and although it may reduce the size of the ischemic field, particularly of the
penetrating arteries, it is usually not significant in preventing infarction. Thus,
in the event of occlusion of a major arterial trunk, the extent of infarction ranges
from none at all to the entire vascular territory of that vessel. Between these two
extremes are all degrees of variation in the extent of infarction and its degree of
completeness.1
Additional ischemia-modifying factors determine the extent of necrosis.
The speed of occlusion assumes importance; gradual narrowing of a vessel allows

13

time for collateral channels to open. The level of blood pressure may influence the
result; hypotension at a critical moment may render anastomotic channels
ineffective. Hypoxia and hypercapnia are presumed to have deleterious effects.
Altered viscosity and osmolality of the blood and hyperglycemia are potentially
important factors but difficult to evaluate. Finally, anomalies of vascular
arrangement (of neck vessels, circle of Willis, and surface arteries) and the
existence of previous vascular occlusions must influence the outcome.1
The specific neurologic deficit obviously relates to the location and size of
the infarct or focus of ischemia. The territory of any artery, large or small, deep or
superficial, may be involved. When an infarct lies in the territory of a carotid
artery, as would be expected, unilateral signs predominate: hemiplegia,
hemianesthesia, hemianopia, aphasia, and agnosias are the usual consequences. In
the territory of the basilar artery, the signs of infarction are frequently bilateral and
occur in conjunction with cranial nerve palsies and other segmental brainstem and
cerebellar signs; quadriparesis, hemiparesis, and/or unilateral or bilateral sensory
impairment are typical, coupled with diplopia, dysarthria, and vertigo in various
combinations.1
2. Risk factor
According to the American Heart Association (AHA), the risk factors of
stroke are divided into two, that are not modifiable risks factors and modifiable
risk factors. Not modifable risk factors include: age, sex, low birth weight, race or
ethnicity, and genetic factors. Modifiable risk factors include: hypertension,
smoking, diabetes, nutritional imbalance, lack of physical activity, alcohol
consumption, and drug abuse. Incidence of stroke can occur with one or more risk
factors (multifactor).1-3
Table 3. Stroke risk factors1-3
Not Modifable
1 Age
2 Gender
3 Genetic
4 Ethnic

Modifable
1. Stroke history
2. Hypertension
3. Heart disease
4. Diabetes melitus
5. Carotid stenosis
6. TIA
7. Hypercholesterolemia
8. Oral contraception

14

10. Smoking
11. Alcohol
12. Drug abuse
13. Hyperhomosisteinemia
14. Antibody anti fosfolipid
15. Hyperurisemia
16. Elevation of hematocrit
17. Elevation of fibrinogen

9. Obesity

3. Clinical Manifestation
The specific neurologic deficit obviously relates to the location and size of
the infarct or focus of ischemia. The territory of any artery, large or small, deep or
superficial, may be involved. When an infarct lies in the territory of a carotid
artery, as would be expected, unilateral signs predominate: hemiplegia,
hemianesthesia, hemianopia, aphasia, and agnosias are the usual consequences. In
the territory of the basilar artery, the signs of infarction are frequently bilateral and
occur in conjunction with cranial nerve palsies and other segmental brainstem and
cerebellar signs; quadriparesis, hemiparesis, and/or unilateral or bilateral sensory
impairment are typical, coupled with diplopia, dysarthria, and vertigo in various
combinations.1,2
4.

Management
Stroke patients should be handled by a multidisciplinary team.

Management stroke be done by improving the general state of the patient, treat the
risk factors, and prevent complications.3-6
4.1 Hyperacute stadium
Action at this stadium is done at the Emergency Room, the aim is to
prevent the widespread of brain tissue damaging. At this stage, patients were
given oxygen 2 L / min and crystalloid/colloid fluid, avoid administration of
dextrose. Brain CT scan examination, electrocardiography, chest X-ray, complete
peripheral blood and platelet count, prothrombin time / INR, APTT, blood
glucose, blood chemistry (including electrolytes), and if hypoxia, do the blood gas
analysis. Other actions in the Emergency Room are providing mental support to
patients and provide an explanation to the family to remain calm.3-6
4.2 Acute stadium
4.2.1 General treatment
Place the patients head in 30o positions, head an chest in a field, change
the sleep position every 2 hours. Mobilization began gradually when

15

hemodynamically stable. Furthermore, free the airway, give oxygen 1-2 liters /
min. If necessary, intubation. Fever overcome with compresses and antipyretic,
then look for the cause, when the bladder is full, emptied (preferably with
intermittent catheters).3-6
Fluid nutrition with 1500-2000 isotonic cristalloid or colloid and
electrolyte as needed, avoid fluids containing glucose or isotonic saline. Nutrition
orally only if swallowing function well, if there is swallowing disorders or
decreased consciousness, nasogastric tube is recommended. 3-6
Blood glucose levels > 150 mg% should be corrected with continuous
intravenous drip insulin during 2-3 days. Hipoglikemia (blood glucose < 60 mg%
or < 80mg% with symptoms) should be corrected immediatelywith dextrose 40%
iv until return to normal and the cause must be sought. 3-6
Headache, nausea, and vomiting treated according to the symptoms. Blood
preassure doesnt need taken down immediately, except when the systolic pressure
220 mmHg and diastolic pressure 120 mmHg, Mean Arterial Blood Pressure
(MAP) 130 mmHg (the two measurements with an interval of 30 minutes), or
obtained acute myocardial infarction, congestive heart failure as well as kidney
failure. Maximal blood pressure reduction was 20%, and the recommended drugs
are sodium nitroprusside, alpha-beta receptor blockers, ACE blockers, or
antagonists calsium. 3-6
If hypotension occurs, the systolic pressure 90 mmHg, diastolic 70 mm
Hg, the patient should be given 250 mL of 0.9% NaCl for 1 hour, followed by 500
mL for 4 hours and 500 mL for 8 hours or until hypotension treated. If not
corrected, that is systolic blood pressure still <90 mmHg, dopamine 2-20 mcg / kg
/ minute can be given until the systolic blood pressure 110 mmHg. 3-6
If there is seizure, give diazepam 5-20 mg iv slowly for 3 minutes, the
maximum dosage is 100 mg per day, followed by oral administration of
anticonvulsants such as phenytoin, carbamazepine. If the seizure appeared after 2
weeks, given orally long-term anticonvulsant. 3-6
If there is an increased of intracranial pressure, bolus mannitol were given
an of 0.25 to 1 g / kg per 30 minutes intravenously, and if rebound phenomenon
suspected, or general condition deteriorated, followed by 0,25g / kg per 30

16

minutes every 6 hours for 3-5 days. Monitoring of the osmolarity should be
performed (<320 mmol), alternatively can be administered hypertonic solutions
(NaCl 3%) or furosemid. 3-6
4.2.2

Special treatment
The goal is to reperfusion by administration of antiplatelet agent such as
aspirin and anticoagulant, or with trombolytic

rt-PA (combinant tissue

Plasminogen Activator), and neuroprotective agent, such as citicoline or

piracetam. 3-6
4.3 Subacute Stadium
Medical measures may include cognitive therapy, behavior, swallowing,
speech therapy, and bladder training (including physical therapy). Given the long
course of the disease, it takes a special intensive treatment of post-stroke in the
hospital with the goal of independence of the patient, understand, comprehend and
implement primary and secondary prevention programs.6
Subacute phase treatment:6
-

Continuing the appropriate treatment of acute conditions before

The management of complications
Restoration / rehabilitation (as needed of patients), which is
physiotherapy, speech therapy, cognitive therapy, and occupational

therapy
Secondary Prevention
Family education and discharge planning
THE BASIC OF DIAGNOSIS

1. Basic of clinical diagnosis

From the history taking, a 51 years old man had a sudden weakness on the
right arm and leg (Hemiparesis). And his speech became nonfluent. No history of
trauma. It is consistent with the WHOs definition that clinical symptoms of
stroke is cerebral disorders, either focal or global attack in 24 hours or more, no
illness is found other than vascular disorders. And elderly is a risk factor of stroke.
2. Basic of topical diagnosis
17

Carotid system had been considered in this patient because there is

hemiparesis, paresis N. VII dextra central type, and paresis N. XII dextra.
Hemiparesi, and paresis N. VII dextra central type and paresis N. XII dextra is
symptoms of middle cerebral artery occlusion. Middle cerebral artery is the
greatest branch of internal carotid artery. From the physical examination there is
right hemiparesis, so the lesion is on the left hemisphere because a lesion in one
side of carotid system will lead to contralateral neurological deficit. and there is
parese N.XII dextra, so the lession thought in the left hemisphere.
3. Basic of etiological diagnosis
Basic etiological diagnosis of this patient has been leaded to ischemic
stroke, because on this patient there are no losing of consciousness, no projectil
vomiting, no headache, no increasing of diastolic blood pressure and hemiparesis.
It is also supported by Siriraj score and Gajah Mada Algorithm that give the
impression of the non-hemorrhage stroke.
4. Basic of differential diagnosis
The gold standard examination for diagnosing the non hemorrhagic or
hemorrhagic stroke is CT Scan. The consideration of the hemorrhagic stroke
because of it almost has the same manifestation, like the immediate onset, the
patient was not in severe activity, and there is neurological deficit.
5. Basic of secondary diagnosis
From history taking, this patient had uncontrolled hypertension since 6
years ago and from the physical examintaion the blood pressure is 210/90 mmHg.
This is appropriate with JNC 8 criteria that in patients <60 years old the diagnose
of hypertension is when the sistolic blood pressure 140 mmHg or the diastolic
blood pressure 90 mmHg. Hyperlipidemia refers to increased levels of lipids
(fats) in the blood, including an triglycerides. And from history sosioeconomic
patient had dietary habit irregular, overweight, and from laboratory finding
cholesterol total increased (295 mg/dL) and LDL cholesterol is 203 mg/dL this
appropriate with Hyperlipidemia.

6. Basic of final diagnosis

18

The final diagnosis of this patient is ischemic stroke. This diagnosis is

based on history taking, physical examination and supporting examination.
7. Basic of supporting examination
1. Laboratory to find the risk factor for stroke and general condition of
patient.
2. Head CT-scan to know the final diagnose from the location and the wide
of the lesion.
8. Basic of treatment
a. The aim of Bed rest with head position elevated 30 0 is to maintain the
adequate circulation to the brain.
b. The aim of IVFD (30ml/kgbb/day) Ringer Lactate 20 dpm is to
maintain the euvolemic condition and glucose level needed.
c. The aim of Inj aspilet 2 x 80 mg is to prevent from recurrent stroke attack
d. The aim of Inj citicoline 2 x 500 mg is as the neuroprotector
e. The aim of amlodipine 1 x 10 mg is for control hypertension
f. The aim of simvastatin 1 x 10 mg is for control cholesterol

REFFERENCE

19

1. Ropper AH, Brown RH. Adams and Victors Principles of Neurology. 8th Ed.
New York: McGraw-Hill Companies, Inc. 2005. Chapter 34, Cerebrovascular
Disease; p.660-770.
2. Rumantir CU. Gangguan Peredaran Darah Otak. Pekanbaru: SMF Saraf
RSUD Arifin Achmad/FK UNRI. Pekanbaru. 2007.
3. Warlow C, van Gijn J, Dennis M, Wardlaw J, Bamford J, Hankey G. Stroke
Practical Management. 3th Ed. 2008. Blackwell Publishing. p.39-40.
4. Guideline Stroke Tahun 2011. Pokdi Stroke. Perhimpunan Dokter Spesialis
Saraf Indonesia (PERDOSSI). Jakarta. 2011.
5. Powers WJ. AHA/ASA Guideline 2015 AHA/ASA Focused Update of the
2013 Guidelines for the Early Management of Patients With Acute Ischemic
Stroke Regarding Endovascular Treatment. AHA journals. 2015;46:000-000.
6. Setyopranoto I. Stroke: Gejala dan Penatalaksanaan. CDK 185/Vol.38
no.4/Mei-Juni 2011; hal.247-250.

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