Case Report - Ischemia Stroke - Iklima Asiah-1

KEMENTRIAN PENDIDIKAN DAN KEBUDAYAANFAKULTAS KEDOKTERAN UNIVERSITAS RIAU

SMF/BAGIAN SARAFSekretariat : Gedung Kelas 03, RSUD Arifin Achmad Lantai 04

Jl. Mustika, Telp. 0761-7894000E-mail : [email protected]

P E K A N B A R U

I. PATIENT’S 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 patient’s 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 patient’s speech became nonfluent or lisp.

No history of headache, vomiting, losing of vision and decreasing of

consciousness. No history of trauma.

Past Illness History

1

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 patient’s 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 : 88 bpm

Respiratory Rate : 20 times per minute

Temperature : 36,5°C

Weight : 70 kg Height : 165 cm

2

B. Neurological status

1) Consciousness : Alertness GCS : E4M6V5

2) Cognitive 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

NormalVisual Fields Normal NormalColour Recognition Normal Normal

3. Cranial nerve III (Oculomotor)Right Left Interpretation

PtosisPupil Shape SizeExtraocular movementsPupillary reactions to light Direct Indirect

(-)

RoundΦ3 mmNormal

(+)(+)

(-)

RoundΦ3 mmNormal

(+)(+)

Normal

4. Cranial nerve IV (Trochlear)Right Left Interpretation

Extraocular movements Normal Normal Normal

5. Cranial nerve V (Trigeminal)Right Left Interpretation

MotorSensoryCorneal reflex

NormalNormal

(+)

NormalNormal

(+)Normal

6. Cranial nerve VI (Abducens)Right Left Interpretation

Extraocular movements

Normal(-)

Normal(-)

Normal

3

StrabismusDeviation (-) (-)

7. Cranial nerve VII (Facial)Right Left Interpretation

TicMotor- corners of

the mouth- folds

nasolabialis- frowning- Raise

eyebrows- Closed eyes

Sense of TasteChvostek Sign

(-)

Decrease

Shallow

(+)(+)

(+)(+)(-)

(-)Normal

(+)

(+)

(+)(+)

(+)(+)(-)

Paresis N VII dextra central type

8. Cranial nerve VIII (Acoustic)Right Left Interpretation

Sense of Hearing (+) (+) Normal

9. Cranial nerve IX (Glossopharyngeal)Right Left Interpretation

Pharyngeal ArchSense of TasteGag Reflex

Normal Normal

(+)

NormalNormal

(+)Normal

10. Cranial nerve X (Vagus)Right Left Interpretation

Pharyngeal ArchDysphonia

Normal (-)

Normal

(-)Normal

11. Cranial nerve XI (Accessory)Right Left Interpretation

MotorTrophy

NormalEutrophy

NormalEutrophy Normal

4

12. Cranial nerve XII (Hypoglossal)Right Left Interpretation

MotorTrophyTremorDysarthria

Tongue compelledEutrophy

(-)(+)

NormalEutrophy

(-)(+)

Parese N XII dextra

IV. MOTOR SYSTEM

Right Left Interpretation

Upper Extremity Strength

DistalProximal

Tone Trophy Involuntary movements Clonus

44

Normal Eutrophy

(-)(-)

55

NormalEutrophy

(-)(-)

Lower Extremity Strength

DistalProximal

Tone Trophy Involuntary movements Clonus

44

Normal Eutrophy

(-)(-)

55

NormalEutrophy

(-)(-)

Hemiparesis dextra (UMN

Type)

Body Trophy Involuntary movements Abdominal Reflex

Eutrophy(-)(-)

Eutrophy(-)(-)

Normal

V. SENSORY SYSTEMRight Left Interpretation

Touch

Pain

Temperatur

Propioseptif

(+)

(+)

(+)

(+)

(+)

(+)

(+)

(+)

Normal

VI. REFLEX

Right Left Interpretation

5

PhysiologicBicepsTricepsKneeAnkle

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

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

Physiologic reflex (+)

Pathologic Babinsky Chaddock Hoffman Tromer Openheim SchaeferPrimitive Reflex Palmomental Snout

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

(-)(-)

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

(-)(-)

Pathologic reflex (-)

Primitive Reflex (-)

VII. COORDINATION

Right Left InterpretationPoint to point movementsWalk heel to toeGaitTandemRomberg

NormalNormalNormalNormalNormal

NormalNormalNormalNormalNormal

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 (-) Non-

Hemorrhagic stroke

6

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 : Parese N VII dextra central typeParese N XII dextra

Motoric : 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

7

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 µg 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

8

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

9

- Ischemic stroke

- Hypertension

- Hyperlipidemia

FOLLOW UP

December, 29th 2015

S : weakness of the right limbs, lisp.

O :

GCS E4M6V5

Blood Pressure180/90 mmHg

Heart Rate 80 bpm

Respiratory Rate 20 tpm

Temperature 36,8°C

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

A : Ischemic stroke + Hypertension

P :

IVFD RL 20 dpm

Citicolin 3 x 500 mg per IV

Aspilet 2 x 80 mg per oral

Folic acid 2 x 400 µg per oral

December, 30st 2015

S : weakness of the right extremity, lisp.

10

O :

GCS E4M6V5

Blood Pressure170/100 mmHg

Heart Rate 76 bpm

Respiratory Rate 20 tpm

Temperature 36,5°C

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

A : Ischemic stroke + Hypertension + Hyperlipidemia

P :

IVFD RL 20 dpm

Citicolin 3 x 500 mg per IV

Aspilet 2 x 80 mg tab per oral

Folic acid 2 x 400 µg 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

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

12

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

time for collateral channels to open. The level of blood pressure may influence the

13

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 Modifable

1. Age

2. Gender

3. Genetic

4. Ethnic

1. Stroke history 10. Smoking

2. Hypertension 11. Alcohol

3. Heart disease 12. Drug abuse

4. Diabetes melitus 13. Hyperhomosisteinemia

5. Carotid stenosis 14. Antibody anti fosfolipid

6. TIA 15. Hyperurisemia

14

7. Hypercholesterolemia 16. Elevation of hematocrit

8. Oral contraception 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

15

Place the patient’s head in 30o positions, head an chest in a field, change

the sleep position every 2 hours. Mobilization began gradually when

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 doesn’t 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

16

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

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

17

trauma. It is consistent with the WHO’s 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

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 patient’s <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

18

cholesterol total increased (295 mg/dL) and LDL cholesterol is 203 mg/dL this

appropriate with Hyperlipidemia.

6. Basic of final diagnosis

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 300 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

19

REFFERENCE

1. Ropper AH, Brown RH. Adams and Victor’s 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.

20

21