STROKE

Definisi Stroke

Stroke adalah gangguan fungsional otak fokal

maupun global yang terjadi secara akut, berasal dari
gangguan aliran darah otak . Termasuk di sini
perdarahan subarachnoid, perdarahan intra-
serebral, dan iskemik atau infark serebri. Tidak
termasuk di sini gangguan peredaran darah otak
sepintas, tumor otak, infeksi atau stroke sekunder
karena trauma (WHO, 1986)
 STROKE
RISK FACTOR
 Stroke: Predisposing factors
Age (risk doubles for Obesity
every decade > age 55) Smoking
Gender
(males>females) Atrial fibrillation
Family history of Sedentary lifestyle
stroke/TIA Drug abuse (e.g.
Hypertension cocaine use)
Diabetes Hormone
Hyperlipidemia replacement therapy
Hyperhomocysteinem Oral contraceptive
ia
Risk Factor for Stroke

Modifiable
Hypercholesterolemia
Cigarette smoking
Non modifiable Arterial hypertension
Age Diabetes Mellitus
Gender Hyperhomocysteinemi
Ras a
Herediter Alcohol abuse
Oral contraceptive
Menopause
Physical inactivity
Obesity
Atrial Fibrillation
Hipercoagulability
Risk Factors for First Ischemic Stroke
Modifiable, value established:
Hypertension
Cardiac disease
Atrial Fibrillation
Infective endocarditis
Mitral stenosis
Recent large myocardial infarction
Cigarette smoking
Sickle cell disease
Transient ischemic attacks
Asymptomatic carotid stenosis
Nonmodifiable Potentially
Age
modifiable
Diabetes mellitus
Gender

Hereditary/famili Hyperhomocysteine
al factors mia
Race/ethnicity
Leftventricular
Geographic hypertrophy
location
Less well-documented risk factors Potentially
modifiable
Elevated blood cholesterol and lipids
Cardiac disease
Cardiomyopathy
Segmental wall motion abnormalities
Nonbacterial endocarditis
Mitral annular calcification
Mitral valve prolapse
Valve strands
Fibrin formation and fibrinolysis
Fibrinogen
Anticardiolipin antibodies
Genetic and acquired causesSubclinical diseases
Intimal-medial thickness
Aortic atheroma, Ankle-brachial blood pressure ratio,
Infarct like lesions on MRI, Socioeconomic features, Non
modifiable : Season and climate
 Less well-documented risk factors
Potentially modifiable (cont.)
Spontaneous echocardiographic contrast
Aortic stenosis
Patent foramen ovale
Atrial septal aneurysm
Use of oral contraceptives
Consumption of alcohol
Use of illicit drugs
Physical inactivity
Obesity
Elevated hematocrit
Dietary factors
Hyperinsulinemia and insulin resistance
Acute triggers (stress)
Migraine
Hypercoagulability and inflammation

Stroke, July 1, 1997; 28(7): 1507 - 1517.

Smoking related atherosclerosis
Increased blood viscosity
Hypercoagulability
Elevated fibrinogen level
Enhanced platelet aggregation
Elevation blood pressure

Gorelick, 2002
Insidensi:
Infark : Insidensi 80% - mortalitas 40%
50% - Thrombotic atherosclerosis
Large-vessel 30% (carotid, middle cerebral)
Small vessel 20% (lacunar stroke)
30% Embolic (heart dis / atherosclerosis)
Young, rapid, extensive.

Hemorrhage: Insidensi 20% - mortalitas 80%

Intracerebral atau subarachnoid.
aneurysm, hypertension/congenital.
 Stroke: Classification
Ischemic stroke: Account for 80%. Results from
occlusion in the blood vessel supplying the brain
Thrombotic: Occlusion due to
atherothrombosis of small/large vessels
supplying the brain
Embolic: Occlusion due to embolus
arising either from heart (e.g. atrial
fibrillation, valvular disease) or blood
vessel
 Classification (contd.)
Hemorrhagic stroke: Account for 20%. Results from
rupture of blood vessels leading to bleeding in brain
Intracerebral: Bleeding within the brain
due to rupture of small blood vessels. Occurs
mainly due to high blood pressure
Subarachnoid: Bleeding around the brain;
commonest cause is rupture of aneurysm.
Other causes: Head injury
 Ischemic Stroke

Incidency : 70-85%
Classification :
1. TIA (transient ischemic attack) : < 24 hours
2. RIND (Reversible Ischemic Neurological
Deficits) normal between 24 48 hours.
Prolonge-RIND normal in max. 3 4 days.
3. Stroke in evolution : worsen stroke ( > 48 hours)
4. Stroke complete : permanent neurologic deficit
Definition of Ischemic Stroke
Almost 80% of strokes
are from an emboli or a
thrombus
Embolic & Thrombotic
strokes are ISCHEMIC
< 15% of strokes are
from hemorrhage, with
an even smaller
percentage caused by
hypoperfusion
2 process in ischemic stroke:
1. Vascular : Aterosclerotic process
2. Biochemistry change /cellular
chemist
Aterosclerotic is a normal response to arterial endotel
injury
Aterosclerotic plaque forming, start in young
Clinical manifestation : acute and tent to occur one
time because sudden plaque rupture
- Demensia - Contralateral limb weakness
- Ggn mood - Contralateral sensory loss
- Ggn perilaku - Disfasia
- Inkontinensia - Disleksia, disgrafia, diskalkulia
- disfungsi olfaktorius - Disorientasi spasial
- Disfungsi opticus

Hemianopsia
Homonim
Kontralateral

- Ggn bahasa
- Ggn memori Nistagmus
- Ggn mood Disartria
- Ggn perilaku Ataksia
- Ggn saraf kranial
- Ggn fx vital Tremor
inkoordinasi
(Wilkinson, 1997)
Komplikasi Stroke

Demensia Bronchopneumonia
Depresi Deckubitus
Kecacatan Septikemia
Epilepsi Trombosis vena
Kontraktur profunda
Peptic ulcer Emboli pulmo
Ggn keseimbangan
cairan
 KONDISI STROKE ISKEMIK AKUT STROKE HEMORAGIK

Sangat Diastolik > 140 mmHg

emergensi

Sistolik > 230 mmHg dan Sistolik > 230 mmHg

Emergensi / atau Diastolik 121 140 dan / atau Diastolik >
mmHg 140 mmHg
Sistolik 180 230 mmHg Sistolik 180 230
Urgensi dan / atau Diastolik 105 mmHg dan / atau
120 mmHg Distolik 105 140
mmHg
Sistolik < 180 mmHg dan Sistolik < 180 mmHg
Tunda Diastolik < 105 mmHg dan Diastolik < 105
mmHg

GUIDELINE STROKE, 2000

 (caspase apoptosis: programmed cell death)

(necrosis)

ISCHEMIC CORE AND ISCHEMIC PENUMBRA

(Friedlander 2003)
 Ischemic
Injury
Apoptotic
Cell Death
Necrotic
Cell Death

Dr.J.Husada 11-2003
 Faktor Risiko Aterosklerosis
Proses aterosklerosis terjadi atau dipercepat dg adanya
faktor risiko yg mempengaruhi sel endotel, shg terjadi
disfungsi endotel

Teori lama :
Hipertensi, DM, perokok, kolesterol, oksidan, obesitas,
olah raga kurang,dll

Teori baru (Braunwald) :

Defisiensi estrogen, homosistein, fibrinogen, faktor VII,
tPA-1, lipoprotein (a), C-reaktif protein, chlamydia
pneumonia, inflamasi, infeksi, genetik (HLA)
Ischemic Stroke Infarct
When a stroke occurs,
it kills brain cells in
that immediate area
This area of dead cells
is called an infarct
These cells usually die
within minutes to a
few hours after the
stroke starts
Causes of Ischaemic STROKE
Blockade of blood flow by ateroma, emboli,
and ateroscelerotic
Embolic
Once in your brain,
the embolus
eventually travels to a
blood vessel small
enough to block its
passage
The embolus lodges
there, blocking the
blood vessel and
causing a stroke
Thrombotic
A thrombotic
stroke is when a
blood clot forms
in one of the
arteries in the
brain, or
supplying the
brain, and grows
and grows until it
is large enough to
block blood flow.
ATHEROSKLEROSIS
 Definition Of Atherosclerosis

Chronic inflammatory disorder of

intima of large arteries characterised
by formation of fibrofatty plaques
called atheroma.

Hardening of arteries - Arteriosclerosis

Definition Of Atherothrombosis
Atherothrombosis is characterized by a sudden
(unpredictable) atherosclerotic plaque disruption
(rupture or erosion) leading to platelet activation and
thrombus formation
Atherothrombosis is the underlying condition that
results in events leading to myocardial infarction,
ischemic stroke, and vascular death

Plaque rupture1 Plaque erosion2

1. Falk E et al. Circulation 1995; 92: 65771. 2. Arbustini E et al. Heart 1999; 82: 26972.
 Faktor Risiko Aterosklerosis
Proses aterosklerosis terjadi atau dipercepat dengan adanya faktor risiko
yg mempengaruhi sel endotel, sehingga terjadi disfungsi endotel

Teori lama :

Hipertensi, DM, perokok, kolesterol, oksidan, obesitas, olah raga

kurang,dll

Teori baru (Braunwald) :

Defisiensi estrogen, homosistein, fibrinogen, faktor VII, tPA-1, lipoprotein

(a), C-reaktif protein, chlamydia pneumonia, inflamasi, infeksi, genetik
(HLA)
Microvascular Macrovascular

Coronary artery disease

Peripheral vascular disease
Cerebrovascular disease
Cholesterol related
atherosclerosis
Oxidazed LDL is toxic effects (activates inflamatory
process) and cell/vessel wall dysfunctions (include
impaired endothelium dependent dilatation and
paradoxical vasoconstriction)
Inactivation of nitric oxide by the excess
production of free radicals (consequences include a
procoagulant milieu and enhanced platelet
thrombus formation)
Reduced transcription of nitric oxide synthase
messenger RNA
Posttranscriptional destabilizationof mRNA
Progressive lipid accumulation and the migration
an
proliferation of smooth muscle cells, resulting in
fibrous plaque.

Activated platelet (produce to several growth factor,

thrombin, angiotensin II), macrophag, dysfunction
endothelial cells that characterize early
atherogenesis.
At sites of endothelial disruption have
vascular
inflammation and platelet rich trombosis

Deficiency of endothelium derived nitric

oxide
potentiate proliferative stage of plaque
maturation.
 Etiologi Aterosklerosis
Sumbatan aliran darah oleh ateroma, emboli, trombus
(Aterosklerosis)
 Proses Aterosklerosis

Mediate area are insuficiently supplied with blood, and they die

Dimulai luka sel endotel - permukaan tidak mulus lagi

produksi molekul adesi (ICAM) peningkatan NO -
terjadi ketidak seimbangan (Depolarisasi) - ggn tonus
vaskuler - aktivasi monosit menjadi makrofag yg
mengambil LDL - foam cell
Foam Cell (sel busa) merupakan komponen penting
pembentuk struktur masa plak
 Pembentukan Plak Aterosklerotik

1. Akumulasi lipoprotein pd tunika 2. Stres oksidatif

intima
3. Aktivasi Citokine 4. Penetrasi Monocyte
5. Migrasi makrofag foam cell 6. Muscle Cell Smooth
7. Akumulasi matriks ekstraseluler 8. Kalsifikasi dan fibrosis
 Faktor Risiko Ruptur Plak
Faktor Lokal Faktor Sistemik
Kelelahan Smoking

Cholesterol
Atheromatous Core
(size/consistency)
Diabetes
Mellitus Fibrinogen
Ketebalan /
konsistensi
Homocysteine
Inflamasi Impaired
Fibrinolysis

Plaque
Rupture
Fuster V, et al. N Engl J Med. 1992;326:310-318.
Falk E, et al. Circulation. 1995:92:657-671.
 Multiple faktor risiko Aterotrombosis
Generalized Lifestyle
Disorders Smoking
Age Diet
Obesity Lack of exercise

Systemic
Conditions
Atherothrombotic Hypertension
Genetic Traits Hyperlipidemia
Gender Manifestations
Diabetes
PlA2 (MI, stroke, Hypercoagulable
vascular death) states
Homocysteinemia

Inflammation
Local Factors
Elevated CRP
Blood flow patterns
CD40 Ligand, IL-6
Shear stress
Prothrombotic factors (F I and II) Vessel diameter
Fibrinogen Arterial wall structure
% arterial stenosis
MI, myocardial infarction.
Adapted from Yusuf S, et al. Circulation. 2001;104:2746-2753.
Drouet L. Cerebrovasc Dis. 2002;13(suppl 1):1-6.
Progression of atherosclerosis
to arterial thrombosis

Plaque
Athero- Rupture/
Myocardial
Fatty Fibrous sclerotic Fissure & Infarction
Normal Streak Plaque Plaque Thrombosis

Ischemic
Stroke

Critical Leg
Ischemia

Clinically Silent Angina

Transient Ischemic Attack
Claudication/PAD Cardiovascular Death

Increasing Age
Atherosclerosis and Thrombus Formation
 Risk of a second vascular event
Increased risk vs general population (%)

Original event Myocardial infarction Stroke

Myocardial infarction 57 x greater risk1 34 x greater risk2

(includes death) (includes TIA)

Stroke 23 x greater risk2 9 x greater risk3

(includes angina and
sudden death*)
Peripheral arterial disease 4 x greater risk4 23 x greater risk3
(includes only fatal MI (includes TIA)
and other CHD death)

*Sudden death defined as death documented within 1 hour and attributed to coronary heart disease (CHD)
Includes only fatal MI and other CHD death; does not include non-fatal MI

1. Adult Treatment Panel II. Circulation 1994; 89:133363. 2. Kannel WB. J Cardiovasc Risk 1994; 1: 3339.
3. Wilterdink JI, Easton JD. Arch Neurol1992; 49: 85763. 4. Criqui MH et al. N Engl J Med 1992; 326: 3816.
 Major clinical manifestations
of atherothrombosis
Ischemic Transient ischemic
stroke attack

Myocardial Angina:
infarction Stable
Unstable

Peripheral arterial
disease:
Intermittent claudication
Rest Pain
Gangrene
Necrosis

Adapted from: Drouet L. Cerebrovasc Dis 2002; 13(suppl 1): 16.

< 20 : aktifitas listrik hilang
< 10 : Gangguan homeostasis
Konsep penumbra
Kebutuhan Glukosa & Oksigen
CBF: 50 ml / 100 gr jar otak permenit.
Oksigen: 6 ml / 100 gr jar otak per menit
untuk substansia grisea dan 2 ml / 100 gr
jar otak per menit untuk substansia alba.
Kebutuhan oksigen: 19-23 ml / 100 gr jar
otak per menit.
Kebutuhan glukosa: 4.5 - 7 mg / 100 gr jar
otak per menit.
Otak: 20% dari seluruh output jantung,
yaitu sekitar 800 ml / menit
Proses Iskemi

Sumbatan
Aliran darah Penurunan CBF

Iskemia
Nekrosis
neuron

ATP, merubah
permeabilitas membran
Kerusakan
membran
Influks Ca+
berlebihan
Oleh karena ruptur aneurisma, angioma, lesi
aterosklerotik
Definition:
Intracerebral
hemorrhage (ICH)
results from the rupture
of an intracerebral vessel
leading to the
development of a
hematoma in the
substance of the brain.
Subarachnoid Hemorrhage: Intraventricular Hemorrhage:
 Vasospasme Process on Haemorrhage
vasoconstrictor agens & blood componen release

Vasospasme

Influks Ca+ smooth muscle

vasculer

Lumen stronge
vasculer Vasospasme

Ischemic + deficit neurologic

 Hasil optimal terapi Stroke perdarahan sampai 96
jam setelah onset
Puncak vasospasme antara hari ke 5-10)
 Etiology %
Ruptured AVM 29,1%
Arterial hypertension 15,3%
Sympathomimetic drug abuse 9,7%
Tumor* 6,9%
Acute EtOH intoxication 4,2%
Pre-eclampsia/eclampsia 2,8%
Superior sagittal sinus thrombosis 1,4%
Moyamoya 1,4%
Cryoglobulinemia 1,4%
Undetermined 23,6%
ruptur aneurisma, angioma, lesi aterosklerotik
 Perdarahan
Pelepasan agen
Efek toksik Peningkatan vasokonstriktor
darah TIK
Serotonin, Prostaglandin, darah

Iskemia
Influks Ca+
global

Influks Ca+ Vasospasme

Nekrosis
Iskemia Fokal
Neuron
 (Zauner, 2002)

Hipoksia / Iskemia / Trauma

Pelepasan neurotransmiter Penurunan ATP

Depolarisasi sel Kegagalan pompa

Ca intrasel naik Nekrosis

Pembentukan Ca mitokondria naik

Reactive
Oxygen Species
Fx apoptogenik lepas Tranduksi signal abnormal

Apoptosis
 Sitotoksik
Vasogenik
EDEMA SEREBRI
Interstisial
Cerebral edema
Blood Vessels in the Brain
CONTROL CENTER OF BRAIN
Anterior Cerebral
Artery
Much rarer
The classic
presentation is
proximal arm/
leg weakness
with present of
distal strength,
the so-called
man in a barrel
CEREBRI MEDIA ARTERIES
 Characterized by
Middle weakness of the
contralateral face with
Cerebral Artery hemianopsia and a
preference of the eyes and
head toward the side of the
involved hemispere
Aphasia in dominant
hemisphere injury
Hemineglect
Involvement restricted to
branches of the MCA may
produces fragment of this
syndrome sparing of leg
strengh
 Involves the brainstem,
cerebellum, thalamus &
occipital lobes
Present with bilateral limb
weakness or sensory
Posterior Cerebral Artery disturbances, cranial nerve
defisit, ataxia, nausea, and
vomiting or coma
occlusion of the basilar
artery trunk : Present with
hemianopia, memory
disturbance, mild
personality disturbance
Rarely; bilateral thalamus
: a state of decreased
responsiveness and apathy
without motor, sensory or
visual impairment
LENTICULOSTRIATE ARTERIES
Anatomy Stroke.
Functional Areas of the Brain

Back
 Mungkin sulit dipercaya bahwa di dalam otak tersimpan
informasi mengenai segala hal yang mengatur kelangsungan
hidup manusia
Brain Stem Stroke: Common Pattern
Pure Motor - Weakness of face and limbs on one side
of the body without abnormalities of higher brain
function, sensation, or vision (MCA/ACA)
Pure Sensory - Decreased sensation of face and limbs
on one side of the body without abnormalities of
higher brain function, motor function, or
vision (PCA).
Brain Stem / Cerebellum / Post Hemisp.
Patterns.

Motor or sensory loss in all four limbs

Crossed signs
Limb or gait ataxia
Dysarthria
Dysconjugate gaze
Nystagmus
Amnesia
Bilateral visual field defects
 Clinical Large Vessel Syndromes:

Carotid Territory
Internal Carotid Artery
proximal MCA
proximal ACA

Vertebrobaciliar Territory
Vertebral Artery
Basilar Artery
Proximal PCA
A.Carotis interna
A.Coroidea anterior a.Komunikans posterior
Talamus dan ganglia basalis
Non Neurological:
Infection : Respiratory, Urinary, Septicaemia
Metabolic : Dehydration, Electrolyte Disturbance,
Hypoglycaemia
Drugs : Major and Minor Tranquillizers, Baclofen,
Lithium Toxicity, Antiemetics
Hypoxia : Pulmonary Embolism, Chronic Pulmonary
Disease, Pulmonary Oedema
Hypercapnoea: Chronic Pulmonary Disease
Others : Limb or Bowel Ischaemia in Patients with a
Cardiac or Aortic Arch Source of Embolism
Neurological:
Progression/completion of the stroke
Extension/early recurrence
Haemorrhagic transformation of an infarct
Development of oedema around the infarct or haemorrhage
Obstructive hydrocephalus in patients with stroke in the
posterior fossa, or after subarachnoid haemorrhage
Epileptic seizures
Delayed ischaemia (in subarachnoid haemorrhage)
Incorrect diagnosis :
Cerebral Tumour - Cerebral abscess
Encephalitis - Chronic Subdural Haematoma
Subdural empyema
A.Carotis interna
A.Cerebri anterior
Talamus dan ganglia basalis
a.Cerebri media
Bagian terbesar dari korteks
lateral(frontal,temporal dan
parietal)
A.basilaris
A . Cerebri posterior D/S
Sisi medial lobus temporal
Bag.belakang sisi bawah
lobus temporal
Bag.medial &bag.terbesar
dari lobus occipital
 Large Vessel Stroke

Diagnostic Criteria: Differential Dx:

Clinical Large Vessel syndrom : Infarction due Embolik

to low flow or artery-to-artery embolism in the Lacuner
presence of disease in the ipsilateral arterial tree Other Mechanism
(extracranial or intracranial segments of carotid or
vertebrobasilar arteries, or proximal MCA)
Brain imaging with infarction in the territory of a
large vessel

Features suggestive of artery-to-artery

Features suggestive of low flow infarction
Stereotyped TIAs
Borderzone infarction
Evidence of hemodynamically significant
stenosis by imaging or BP-dependent
clinical symptoms
embolism
Repetitive, non-stereotyped TIAs
referable to the large vessel stenosis
Amaurosis fugax (transient monocular
blindness)
Mulitfocal or peripheral cortical or
subcortical infarction
Absence of hemodynamic symptom
threshold
- Demensia - Contralateral limb weakness
- Ggn mood - Contralateral sensory loss
- Ggn perilaku
- Disfasia
- Inkontinensia
- disfungsi olfaktorius
- Disleksia, disgrafia, diskalkulia
- Disfungsi opticus - Disorientasi spasial

Hemianopsia
Homonim
Kontralateral

- Ggn bahasa
- Ggn memori Nistagmus
- Ggn mood Disartria
- Ggn perilaku Ataksia
- Ggn saraf kranial
- Ggn fx vital Tremor
inkoordinasi
(Wilkinson, 1997)
Komplikasi Stroke

Demensia Bronchopneumonia
Depresi Deckubitus
Kecacatan Septikemia
Epilepsi Trombosis vena
Kontraktur profunda
Peptic ulcer Emboli pulmo
Ggn keseimbangan
cairan
 KONDISI STROKE ISKEMIK AKUT STROKE HEMORAGIK

Sangat Diastolik > 140 mmHg

emergensi

Sistolik > 230 mmHg dan Sistolik > 230 mmHg

Emergensi / atau Diastolik 121 140 dan / atau Diastolik >
mmHg 140 mmHg
Sistolik 180 230 mmHg Sistolik 180 230
Urgensi dan / atau Diastolik 105 mmHg dan / atau
120 mmHg Distolik 105 140
mmHg
Sistolik < 180 mmHg dan Sistolik < 180 mmHg
Tunda Diastolik < 105 mmHg dan Diastolik < 105
mmHg

GUIDELINE STROKE, 2000

ARTERI VENOSE MALFORMATION

AVM :
Kelainan kongenital, yaitu adanya pola embrionik
pembuluh darah yang menetap (tidak berkembang),
bukan suatu neoplasma yang terdiri dari pembuluh
darah yang melebar dan kacau (anyaman pembuluh
darah) yang terbentuk dari hubungan eksternal
antara sistem arteri dan sistem vena, karena tidak
terbentuknya sistem kapiler yang
menghubungkannya
(Adam, et.al, 1997)
(Gilroy, 1992)
(Selman & Ratcheson, 1991)
 Kebutuhan Glukosa & Oksigen
CBF: 50 ml / 100 gr jar otak permenit.
Oksigen: 6 ml / 100 gr jar otak per menit untuk
substansia grisea dan 2 ml / 100 gr jar otak per menit
untuk substansia alba.
Kebutuhan oksigen: 19-23 ml / 100 gr jar otak per menit.
Kebutuhan glukosa: 4.5 - 7 mg / 100 gr jar otak per menit.
Otak: 20% dari seluruh output jantung, yaitu sekitar 800
ml / menit
 A-V Malformation
Cause : anomali vascular intracranial
AVM : Aneurysma = 1:5.3 (US)
Gejala : haemorrhage, epilepsy, headache,
neurological deficit, cranial bruit,mass effect
Penunjang : CT scan, MRI,Angiography
Indikasi intervensi :
Expending haematoma
Risiko perdarahan
Defisit neurologic progresif
SAH - Anatomy
 Gadjah Mada Stroke Algorithm
Patient admitted with sudden onset of stroke
with
Decreasing consciousness +, headache +, Babinskis reflex + yes HS
No
Decreasing consciousness +, headache +, Babinskis reflex - yes HS
No
Decreasing consciousness +, headache -, Babinskis reflex - yes HS
No
Decreasing consciousness +, headache -, Babinskis reflex + yes HS
No
Decreasing consciousness -, headache +, Babinskis reflex + yes HS
No
Decreasing consciousness -, headache +, Babinskis reflex - yes HS
No
Decreasing consciousness -, headache -, Babinskis reflex + yes AIS
No
Decreasing consciousness -, headache -, Babinskis reflex - yes AIS
 Brain Blood
Monroe- Kellie Principle
CSF Mas
Bones

Copied from: Rogers (1996) Textbook of Pediatric

Intensive Care p. 646
Penyebab SAH
Aneurysma 70-75%
AVM 5%
Bleeding diathesis
Anticoagulant <5%
Tumor
Vasculitis
Undefined 15%
CLINICAL SIGNS OF INTRACEREBRAL HEMORRHAGE (1)
(Caplan 1988)
Lesion Pupils/eye movement Motor & Other
sensory
deficits
Caudate Sometimes ipsilaterally Contralateral Headache, confusion
nucleus constricted/ conjugate hemiparesis, often
deviation to side of lesion transient

Putamen Normal/conjugate deviation to Contralateral Aphasia (if lesion on

(small) side of lesion hemiparesis & left side)
hemisensory loss

Putamen With herniation, pupil dilated Contralateral Decreased

(large) on side of lesion/conjugate hemiparesis & consciousness
deviation to side of lesion hemisensory loss

Thalamus Constricted poorly reactive to Slight contralateral Aphasia (if lesion on

light bilaterally/lids retracted. hemiparesis but left side)
Eyes down and in. Cannot greater hemisensory
look up. loss
CLINICAL SIGNS OF INTRACEREBRAL HEMORRHAGE
(2) (Caplan 1988)
Lesion Pupils/eye movement Motor & sensory Other
deficits

Occipital lobar Normal Mild, transient Contralateral

white matter hemiparesis hemianopsia

Pons Constricted reactive to Quadriplegia Coma

light/no horizontal
movements. Vertical
movements preserved

Cerebellum Constriction on side of Ipsilateral limb ataxia. Gait ataxia,

lesion/slight deviation No hemiparesis vomiting
to opposite side.
Movements to side of
lesion impaired or 6th
cranial nerve palsy
Tanda & gejala SAH
Nyeri kepala berat, acut
Penurunan kesadaran sementara/lama
Kejang
Nausea & vomitus
Defisit neurologic focal (hemiparese,disfasia)
Funduscopi : papiledema/vitreous haemorrhage
Reactive hypertension
Pyrexia
Meningismus
(Lindsay,1997)
Pemeriksaan penunjang SAH

CT Scan : 95 % (dalam 48 jam)

Lumbar Puncture : >6 jam
- Uniformly blood stained
- Xanthochromic
MRI : kurang sensitif 24-48 jam
Cerebral angiogram : gold standard
Pemeriksaan penunjang SAH

CT Scan : 95 % (dalam 48 jam)

Lumbar Puncture : >6 jam
- Uniformly blood stained
- Xanthochromic
MRI : kurang sensitif 24-48 jam
Cerebral angiogram : gold standard
Common Stroke Patterns
Left (Dominant) Hemisphere Stroke
Aphasia
Right hemiparesis
Right-sided sensory loss
Right visual field defect
Apraxia
Dysarthria
Difficulty reading, writing, or calculating
 Skor iskhemik Hachinski

Gambaran skor
Awitan sangat mendadak 2
Perubahan bertahap 1
Perjalanan klinis berfluktuasi 2
Bingung malam hari 1
Kepribadian relatif baik 1
Adanya depresi 1
Keluhan somatik 1
Gangguan emosional 1
Riwayat hipertensi 1
Riwayat adanya stroke 2
Bukti adanya atherosklerosis 1
Adanya gejala neurologik fokal 2
Adanya tanda neurologik fokal 2
Common Stroke Patterns
Right (Non-dominant) Hemisphere Stroke
Extinction of left-sided stimuli
Left hemiparesis
Left-sided sensory loss
Left visual field defect
Poor left conjugate gaze
Spatial disorientation
Aneurysma
Ruptur aneurysma : 6-12 per 100000/th
Wanita : pria = 3:2
Umur : sering 40-60 th, jarang anak
> 40 th, wanita > pria
< 40 th, pria > wanita
Penyebab : congenital (defect T.media),
atherosclerotik/hipertensi,emboli,infeksi,trauma, dll
Tempat : 20-25% A.cerebri media
10% sirkulasi posterior
35-40% A.cerebri anterior
30% A.carotid interna
Aneurysma
Gejala :
Ruptur (90%) : NK(+),muntah,KK(+),penurunan
kesadaran,focal sign,kejang
Compression (7%) : visual defect, hipopituitarism,
parese anggota gerak, optalmoplegi, facial pain
Incidental finding (3%)
 (21 67 %) (Adams, et.al, 1997)
(Listiono, 1998)
(Selman & Ratcheson, 1991)
(Toole, 1990)
Ti : - letak di frontal & temporal
- Lesi besar & melibatkan struktur kortikal (Litriono, 1998)
 Sudden weakness, paralysis, or numbness of the face,
arm and the leg on one or both sides of the body

Loss of speech, or difficulty speaking or understanding

speech

Dimness or loss of vision, particularly in only one eye

Unexplained dizziness (especially when associated with

other neurologic symptoms) unsteadiness, or sudden falls

Sudden severe headache and/or loss of consciousness

NIH Stroke Scale
 Barthel Index

Modified Rankin Scale

Feeding
Bathing
Grooming
Dressing
Bowels
Bladder
Toilet Use
Transfers
(bed to chair
and back)
Mobility (on
level surfaces)
Stairs
Early CT Changes in
Ischemic Stroke
Oxford (Bamford) Stroke Classification

PAC Partial Anterior

Circulation Infarction

TAC Total Anterior Circulation

Infarction

POC Posterior Circulation

Infarction

LAC Lacunar Infarction

 Stroke Syndromes
Arranged by Vascular Territory
Physiologic Subtypes of Thrombosis-
Related Ischemic Stroke
 Evaluation & Diagnosis

Differential Diagnosis of Stroke

Ischemic stroke Hemorrhage stroke
Craniocerebral / cervical trauma
Meningitis/encephalitis
Intracranial mass
Tumor
Subdural hematoma
Seizure with persistent neurological signs
Migraine with persistent neurological signs
Metabolic
Hyperglycemia (nonketotic hyperosmolar coma)
Hypoglycemia
Post-cardiac arrest ischemia
Drug/narcotic overdose
DISTINGUISHING FEATURES HEMORRHAGIC
STROKE VS ISCHEMIC STROKE :

FEATURES SUGGESTING HEMORRHAGIC S. :

early and prolonged loss of consciousness
prominent headache, nausea and vomiting
retinal hemorrhages
nuchal rigidity
focal sign do not fit the anatomic pattern of a single blood vessel

FEATURES SUGGESTING ISCHEMIC STROKE :

stepwise deterioration or progressive worsening
waxing and waning of findings
focal neurologic impairments in the pattern of single blood vessel
signs point to a focal cortical or subcortical lession

(Adams Jr. et al., 2002)

Common Stroke Patterns
Left (Dominant) Hemisphere Stroke
Aphasia
Right hemiparesis
Right-sided sensory loss
Right visual field defect
Apraxia
Dysarthria
Difficulty reading, writing, or calculating
Common Stroke Patterns
Right (Non-dominant) Hemisphere Stroke
Extinction of left-sided stimuli
Left hemiparesis
Left-sided sensory loss
Left visual field defect
Poor left conjugate gaze
Spatial disorientation
 LACUNAR STROKE
Lacuna is used to describe a small infarct or a small cavity in
the brain tissue that develops after the necrotic tissue of a deep
infarct is resorbed.
Lacunes may be defined as small subcortical infarcts (<15 mm
in diameter) in the territory of the deep penetrating arteries
and may present with specific lacunar syndromes or may be
asymptomatic
Pathogenesis : Lipohyalinosis , microatheroma, stenosis small
artery
(Wong, 2004; Papamitsakis,
2005)
 LACUNAR STROKE
Clinical syndrome
Pure motor stroke/hemiparesis
The lacune is usually in the posterior limb of the internal
capsule or the basis pontis
Ataxic hemiparesis
Sites of infarction are the posterior limb of the internal
capsule, basis pontis, and corona radiata.
Dysarthria/clumsy hand
The main symptoms are dysarthria and clumsiness (ie,
weakness) of the hand, which often is most prominent
when the patient is writing
(Wong, 2004; Papamitsakis,
2005)
 LACUNAR STROKE
Pure sensory stroke
Persistent or transient numbness and/or tingling on one side
of the body (eg, face, arm, leg, trunk).
The infarct is usually in the thalamus.
Mixed sensorimotor stroke
Hemiparesis or hemiplegia is noted with ipsilateral sensory
impairment.
The infarct is usually in the thalamus and adjacent posterior
internal capsule (seemingly, in both the carotid and
vertebrobasilar territories).
(Wong, 2004; Papamitsakis,
2005)
 Stroke Syndromes
Middle cerebral artery - complete
Weakness - upper and lower extremity (C)
Weakness - face - lower half (C)
Hemisensory loss - upper and lower extremity (C)
Sensory loss - face - all modalities (C)
Aphasia receptive (D)
Aphasia expressive (D)
Hemineglect (ND)
Lateral gaze weakness (C)
Gaze preference (C)
Visual loss - homonymous hemianopia (C)
(AHA Stroke Center, 2004)
 Stroke Syndromes
Middle cerebral artery superior division
Weakness - upper and lower extremity (C)
Weakness - face - lower half (C)
Hemisensory loss - upper and lower extremity (C)
Sensory loss - face - all modalities (C)
Hemineglect (ND)
Aphasia expressive (D)

(AHA Stroke Center, 2004)

 Stroke Syndromes
Middle cerebral artery inferior division
Visual loss - homonymous hemianopia (C)
Visual loss - upper quadrant anopsia (C)
Constructional apraxia (ND)
Aphasia receptive (D)

( AHA Stroke center, 2004)

Common Stroke Patterns
Brain Stem / Cerebellum / Posterior
Hemisphere Stroke:
Motor or sensory loss in all four limbs
Limb or gait ataxia
Dysarthria
Dysconjugate gaze
Nystagmus
Amnesia
Bilateral visual field defects
Common Stroke Patterns
Small Subcortical Hemisphere or Brain Stem (Pure
Motor) Stroke: Common Pattern
Weakness of face and limbs on one side of the body without
abnormalities of higher brain function, sensation, or vision

Small Subcortical Hemisphere or Brain Stem (Pure

Sensory) Stroke: Common Pattern
Decreased sensation of face and limbs on one side of the body
without abnormalities of higher brain function, motor
function, or vision
 HEMORRHAGIC TRANSFORMATION OF A INFARCTION
Berhubungan dengan terapi trombolitik
The clinical correlates of the varying degrees of early
hemorrhagic transformation of a cerebral infarc are
unclear (Fiorelli, M, 2003)
Pada kejadian yang jarang intracranial hemoragik dapat terjadi pada
trombosis vena (Adams, 2002)
Trombosis disebabkan oleh :
- kehamilan
- dehidrasi
- pembedahan
- sepsis
- khemoterapi
- kelainan hiperkoagulasi
Perdarahan terjadi akibat ruptur kapiler, sekunder akibat stagnasi dari
vena( sinus sagtila superior/vena superfisial)
Management
Medical Management
Surgical Management
Management
In emergency Room
ABC rules
BP continuous monitoring
Continuous ECG monitoring
O2 pulse oxymetry
2 IV lines (norma saline only)
Blood (CBC, SMAC, RBS, PTT, INR)
Save 6 ml of blood
Facilitate transfer to the operating room or ICU
Mannitol
1. Lowering ICP : Immediate plasma expansion : reduce the
hematocrit and blood viscosity (improved rheology) which
increases CBF and O2 delivery. Osmotic effect : increased
serum tonicity draws edema fluid from cerebral
parenchyma.
2. Supports the microcirculation by improving blood rheology
3. Possible free scavenging
(Greenberg,2000)

Dose : 0,5 1,0 g/kg body weight (Adam,et al., 2001)

Iv bolus 100 ml of 20 % mannitol over 15 minutes (Lindsay, et al.,
1997)
Table 4. scoring system for the ICH criteria. The ICH score is calculated by
adding the six criteria. ICH score=a+b+c+d+e+f
ICH criteria Score
a.Age
Younger than 61 0
Older than 60 1
b.Limb Paresis
None to moderate (0/5-3/5) 0
Severe(2/5-0/5) 1
c.Level of consciousness:
Alert 0
Drowsy or comatose 1
d.Mass effect
no midline shift present on CT scan 0
midline shift present on CT scan 1
e.Size of hematoma
Large 1
Small or medium 0
f. Intraventricular extension
present 1
absent 0
 Outcome of ICH influenced of :
1. Therapeutic window
2. size/volume of haemorrhage
3. location
4. Risk factor : controlable/uncontrolable
(DM, HT)
5. Previous of stroke : ischaemic>haemorh
6. Deficit neurol occur : global >
focal <
 Surgery vs Non surgery, depend on :
1. superficial location vol >30 cc
2. intraventriculler haemorrhg hidroceph
3. cerebellar haemorhage
Surgery :
1. evacuation of blood-- aspiration
2. craniotomy decompresi
3. shunt
Management
Medical Management
Surgical Management
Management
In emergency Room
ABC rules
BP continuous monitoring
Continuous ECG monitoring
O2 pulse oxymetry
2 IV lines (norma saline only)
Blood (CBC, SMAC, RBS, PTT, INR)
Save 6 ml of blood
Facilitate transfer to the operating room or ICU
Mannitol
1. Lowering ICP : Immediate plasma expansion : reduce the
hematocrit and blood viscosity (improved rheology) which
increases CBF and O2 delivery. Osmotic effect : increased
serum tonicity draws edema fluid from cerebral
parenchyma.
2. Supports the microcirculation by improving blood rheology
3. Possible free scavenging
(Greenberg,2000)

Dose : 0,5 1,0 g/kg body weight (Adam,et al., 2001)

Iv bolus 100 ml of 20 % mannitol over 15 minutes (Lindsay, et al.,
1997)
Table 4. scoring system for the ICH criteria. The ICH score is calculated by
adding the six criteria. ICH score=a+b+c+d+e+f
ICH criteria Score
a.Age
Younger than 61 0
Older than 60 1
b.Limb Paresis
None to moderate (0/5-3/5) 0
Severe(2/5-0/5) 1
c.Level of consciousness:
Alert 0
Drowsy or comatose 1
d.Mass effect
no midline shift present on CT scan 0
midline shift present on CT scan 1
e.Size of hematoma
Large 1
Small or medium 0
f. Intraventricular extension
present 1
absent 0
 Outcome of ICH influenced of :
1. Therapeutic window
2. size/volume of haemorrhage
3. location
4. Risk factor : controlable/uncontrolable
(DM, HT)
5. Previous of stroke : ischaemic>haemorh
6. Deficit neurol occur : global >
focal <
 Surgery vs Non surgery, depend on :
1. superficial location vol >30 cc
2. intraventriculler haemorrhg hidroceph
3. cerebellar haemorhage
Surgery :
1. evacuation of blood-- aspiration
2. craniotomy decompresi
3. shunt
 ICH ---worsen by
1. mass effect global ischemica influx
2. release of vasoconstrict mediator
( tbx, pgd, sertn )
3. hemosiderin fe deposit
4. injury endothelium
- accumulating mast cell
- release of substance P -- pain
 Matrix metalloproteinase-9 in cerebral-amyloid-
Angiopathy-related hemorrhage

Cerebral amyloid angipathy (CAA) is defined

by the accumulation of amyloid in the walls
of small and medium-sized arteries

Although less common in nondemented

individuals, the frequency of CAA increase
dramatically with age
 Frequently, affected vessels demonstrate
double-barrel lumen, suggestive of a
weakned vascular extracellular matrix
(ECM) resulting in the separation of intima
from media during tissue preparation

One class of molecules which is involved in

the regulation of vascular integrity is the matrix
metalloproteinases (MMPs), a family of 23
zine-dependent endopeptidases capable of
degrading virtually all proteins in the
basement membrane
 Lekosit terutama pmn dan monosit berinteraksi dg endotel
dan ekstravaskuler untuk merubah fungsi dan morfolofi
sel2 endotel, sbb fungsi terpenting endotel adl
mempertahankan tonus pembuluh darah dan reaktivasi
Pelepasan lekosit terutama pmn pd vasa darah otak
menyebabkan terlepasnya ET1 (endotelin-1) dan
mengurangi keluarnya endothelium dependent vascular
relaxation (EDRF). Sedangkan ET1 meningkatkan produksi
superoksid yg tjd pd kerusakan endotel. ET! Meningkat
setelah trauma otak, perdarahan otak dan stl trauma
parenkim medulla spinalis
Adanya reaksi lekositosis pd PIS kemungkinan
menggambarkan stress induced respons dari pada sekedar
reaksi inflamasi lokal pd otak (Harsono,1992)
 Rerata kumulatif survival 80+/-9 jam pd ICH dg
AL 12,5+/-0,5 dan rerata kumulatif survival 620+/-
186 jam pd AL 9,5+/-0,5
(suzuki et al.,1995)
AL terutama lekosit pmn yang tinggi berhub dg
luasnya kerusakan endotel serta luasnya
kerusakan jar otak
Makin luas kerusakan endotel dan jar otak maka
mkn bsr hematom, edema cerebri, mkn besar
kemungkinan perluasan perdarahan ke ventrikel
serta makin luas kerusakan jar otak
Tekanan darah sistolik ACE inhibitor menurunkan lebih
banyak dibanding AIIRA (2,0 mmHg), beda bermakna
dengan losartan dan valsartan, tapi tidak berbeda
bermakna dengan irbesartan dan candesartan

Efek samping AIIRA

Rendah, sama dengan plasebo, batuk kering rendah
(1,0%) dibanding ACE Inhibitor (5,5%) putus obat
rendah (4,8%), sementara pada ACE Inhibitor 7,9%.
Efek samping serius yang jarang terdapat:
hepatotoksisitas, angioneurotic edema dan
simtom neuropsikiatrik
 NIKARDIPIN.

Sediaan intravena dari preparat Dihydropyridine

yg merupakan Ca channel blockers (CCBs) yg
diberikan mll infus kontinyu.Efek hemodinamik
promer adalah menimbulkan vasodilatasi perifer
dg mempertahankan /meningkatkan aktivitas
pompa jantung.
Dari beberapa studi telah dibuktikan bhw
nikardipin dg pemberian infus langsung
menurunkan tekanan darah sistemik dan
selanjutnya dpt dipertahankan pd leveltekanan
darah yg diinginkan.
Potential Stroke Risk Reduction for Individuals
AHA Guidelines

Factor Risk reduction with treatment

Hypertensio 30% - 40%

n
Smoking 50% within 1 year, baseline after 5 years

Diabetes 44% reduction in hypertensive diabetics with

tight blood pressure control

Hyperlipidemia 20-30% with statins in patients with known

coronary heart disease

Atrial fibrillation 68% (warfarin)

(non-valvular) 21% (aspirin)

Adapted from Goldstein, et al. Circulation 2001;103:163-182.

 Edema Serebri
Vasogenic :
kerusakan vaskuler endotel kapiler, gangguan tight
junction, permeabilitas meningkat
Cytotoxic :
gangguan pompa Na, K, ATP ase, Na intrasel meningkat
Interstisial :
Transudasi
Mannitol
1. Lowering ICP : Immediate plasma expansion :
reduce the hematocrit and blood viscosity
(improved rheology) which increases CBF and O2
delivery. Osmotic effect : increased serum tonicity
draws edema fluid from cerebral parenchyma.
2. Supports the microcirculation by improving
blood rheology
3. Possible free scavenging
(Greenberg,2000)

Dose : 0,5 1,0 g/kg body weight (Adam,et al., 2001)

Iv bolus 100 ml of 20 % mannitol over 15 minutes
(Lindsay, et al., 1997)
 PENATALAKSANAAN HIPERTENSI PADA STROKE
AKUT

STROKE AKUT

Sistolik > 230 mmHg Sistolik 180-230 mmHg

Sistolik > 230 mmHg
Diastolik > 121-140 mmHg Diastolik 105-120 mmHg
Diastolik > 140 mmHg
Sistolik < 180 mmHg
Ulangi 15'
Diastolik < 105 mmHg

Sistolik > 230 mmHg Perdarahan intraserebral

Diastolik 121-140 mmHg Atau
Ggn end organ

Positif Negatif

(Guidelines Stroke,2004) Observasi

Obat antihipertensi Obat antihipertensi oral
parenteral Diberikan stl hr ke 7-10
 Penurunan Tekanan Darah
Pada stroke iskemik akut,
terdapat salah satu dari:
1. Tekanan sistolik > 220 mmHg
2. Tekanan diastolik > 120 mmHg
3. MAP > 130-140 mmHg
4. Disertai infark miokard akut / gagal jantung atau
ginjal akut / aorta torakalis

Stroke Penurunan lebih cepat

perdarahan penurunan tekanan darah:
maksimal 20%
 Angiotensin II Reseptor Blokers
Losartan, Valsartan, Irbersartan,
Candesartan

Messenger aktif terakhir lintasan renin-angotensin:

Angiotensin II
Angiotensin II terikat pada reseptor AT1 vasokonstriksi
dan retsnsi cairan tekanan darah naik.
Angotensin II reseptor blokers menurunkan tekanan darah
dengan memblok reseptor AT1.
(ACE inhibitors: menghambat sintesis angiotensin II
dengan ACE)
 Angiotensin Receptor Antagonist
(AIIRA)
Memblok aksi angiotensin II
angiotensinogen
renin
bradikinin angiotensin I
ACE NON ACE

Inactive peptide angiotensin II

Candesartan
AT I -RECEPTOR
Tekanan darah sistolik ACE inhibitor menurunkan lebih
banyak dibanding AIIRA (2,0 mmHg), beda bermakna
dengan losartan dan valsartan, tapi tidak berbeda
bermakna dengan irbesartan dan candesartan

Efek samping AIIRA

Rendah, sama dengan plasebo, batuk kering rendah
(1,0%) dibanding ACE Inhibitor (5,5%) putus obat
rendah (4,8%), sementara pada ACE Inhibitor 7,9%.
Efek samping serius yang jarang terdapat:
hepatotoksisitas, angioneurotic edema dan
simtom neuropsikiatrik
 NIKARDIPIN.

Sediaan intravena dari preparat Dihydropyridine

yg merupakan Ca channel blockers (CCBs) yg
diberikan mll infus kontinyu.Efek hemodinamik
promer adalah menimbulkan vasodilatasi perifer
dg mempertahankan /meningkatkan aktivitas
pompa jantung.
Dari beberapa studi telah dibuktikan bhw
nikardipin dg pemberian infus langsung
menurunkan tekanan darah sistemik dan
selanjutnya dpt dipertahankan pd leveltekanan
darah yg diinginkan.
 Edema Serebri
Vasogenic :
kerusakan vaskuler endotel kapiler, gangguan tight
junction, permeabilitas meningkat
Cytotoxic :
gangguan pompa Na, K, ATP ase, Na intrasel meningkat
Interstisial :
Transudasi
Mannitol
1. Lowering ICP : Immediate plasma expansion :
reduce the hematocrit and blood viscosity
(improved rheology) which increases CBF and O2
delivery. Osmotic effect : increased serum tonicity
draws edema fluid from cerebral parenchyma.
2. Supports the microcirculation by improving
blood rheology
3. Possible free scavenging
(Greenberg,2000)

Dose : 0,5 1,0 g/kg body weight (Adam,et al., 2001)

Iv bolus 100 ml of 20 % mannitol over 15 minutes
(Lindsay, et al., 1997)
 PENATALAKSANAAN HIPERTENSI PADA STROKE
AKUT
STROKE AKUT

Sistolik > 230 mmHg Sistolik 180-230 mmHg

Sistolik > 230 mmHg
Diastolik > 121-140 mmHg Diastolik 105-120 mmHg
Diastolik > 140 mmHg
Sistolik < 180 mmHg
Ulangi 15'
Diastolik < 105 mmHg

Sistolik > 230 mmHg Perdarahan intraserebral

Diastolik 121-140 mmHg Atau
Ggn end organ

Positif Negatif

(Guidelines Stroke,2004) Observasi

Obat antihipertensi Obat antihipertensi oral
parenteral Diberikan stl hr ke 7-10
 Penurunan Tekanan Darah
Pada stroke iskemik akut,
terdapat salah satu dari:
1. Tekanan sistolik > 220 mmHg
2. Tekanan diastolik > 120 mmHg
3. MAP > 130-140 mmHg
4. Disertai infark miokard akut / gagal jantung atau
ginjal akut / aorta torakalis

Stroke Penurunan lebih cepat

perdarahan penurunan tekanan darah:
maksimal 20%
 Angiotensin II Reseptor Blokers
Losartan, Valsartan, Irbersartan,
Candesartan

Messenger aktif terakhir lintasan renin-angotensin:

Angiotensin II
Angiotensin II terikat pada reseptor AT1 vasokonstriksi
dan retsnsi cairan tekanan darah naik.
Angotensin II reseptor blokers menurunkan tekanan darah
dengan memblok reseptor AT1.
(ACE inhibitors: menghambat sintesis angiotensin II
dengan ACE)
Tekanan darah sistolik ACE inhibitor menurunkan lebih
banyak dibanding AIIRA (2,0 mmHg), beda bermakna
dengan losartan dan valsartan, tapi tidak berbeda
bermakna dengan irbesartan dan candesartan

Efek samping AIIRA

Rendah, sama dengan plasebo, batuk kering rendah
(1,0%) dibanding ACE Inhibitor (5,5%) putus obat
rendah (4,8%), sementara pada ACE Inhibitor 7,9%.
Efek samping serius yang jarang terdapat:
hepatotoksisitas, angioneurotic edema dan
simtom neuropsikiatrik
 NIKARDIPIN.

Sediaan intravena dari preparat Dihydropyridine

yg merupakan Ca channel blockers (CCBs) yg
diberikan mll infus kontinyu.Efek hemodinamik
promer adalah menimbulkan vasodilatasi perifer
dg mempertahankan /meningkatkan aktivitas
pompa jantung.
Dari beberapa studi telah dibuktikan bhw
nikardipin dg pemberian infus langsung
menurunkan tekanan darah sistemik dan
selanjutnya dpt dipertahankan pd leveltekanan
darah yg diinginkan.
DILTIAZEM

Diltiazem adalah penyekat saluran kalsium, obat ini

sebaiknya digunakan melalui infus kontinyu 5-40
mg/kg/mnt daripada suntikan bolus (10 mg dilarutkan
dalam 10 ml salin disuntikan dlm waktu 3-5 mnt).
Penurunan tekanan darah 27,3% dg infus kontinyu
dan 7,5 % dg suntikan bolus. Kecepatan denyut nadi
tdk berubah dg infus kontinyu,sedangkan pada
suntikan bolus kecepatan nadiberkurang sedikit dari
88 sampai 82 per mnt. Obat ini tdk boleh diberikan pd
blok sino-atrial, blok AV derajat 2 atau 3 dan wanita
hamil. Sediaan injeksi sdh ada di Indonesia.
 CANDESARTAN

Candesartan

O CH3 N N

N NH
HN N

COOH

Candesartan diabsorbsi kurang baik pad pemberian peroral,candesartan

cilexetil sbg esrer prodrug memperbaiki bioavailabilitasnya.
Antagonis poten yg bekerja lama dan berikatan kuat serta dissosiasi lambat dg
reseptor AT1
Half life kira-kira 9 jam (pd orang tua sampai 12 jam)
Diekskresi oleh ginjal (60%) dan empedu (40%)
Dosis 8-32 mg/hari TS :8-12 mmHg;TD :4-8 mmHg
 Citicholine
Mechanism (neuronal)
Increase choline formationnd alter degradation phosphatydilcholine
Increase glucose uptake, asetilkholine, prevention lipid radical
Increase glutation
Decrease lipid peroxida
Na/K ATPase modulation
Mechanism (vascular)
Increase CBF
Increase O2 consumtion
Decrease vasculer resistance

(Perdossi, 2004)
 Piracetam
Mechanism (neuronal)
Repair cell membran fluidity
Repair neurotransmission
Stimulation adenylate kinase
Mechanism (vascular)
Increase eritrocyte deformability
Decrease platelet hyperagregation
Repir microcirculation

(Perdossi, 2004)
 METABOLISME CITICHOLIN & PERANANNYA DLM MEMPERBAIKI FUNGSI OTAK
PCCT
Hidrolisa
Cytidine Otak
Citicholine
diabsorbsi Citicholine
Choline Sintesa

1-2 DAG
Asetilasi Phosphatidilserin
Vaskularisasi
Lokal Acetylcholin Phosphatidiletanolamin Phosphatidilkolin
Ado Me
Betaine M
Methionin Phospolipid E
M
S-Adenosyl-L-homocystein B
Antioksidan
Glutation Cystein Homocystein R
A
N

R
E
1-2 DAG : 1-2 Diasil Gliserol P
A
I
PCCT : Cytidine triphosphat phosphocholine cytidylyl transferase
R
 Melindungi Sel Memperbaiki Fungsi

Jaringan Neuron

Piracetam

Jaringan Serebrovaskuler

Meningkatkan Aliran Efek Sitoprotektif Dalam

Darah Otak Pembuluh Darah Otak

Piracetam mengurangi alir masuk Kalsium yang tidak normal ke dalam neuron & sel otot polos
pembuluh darah. Oleh karena itu, Piracetam mempengaruhi sistem saraf dan sistem
serebrovaskuler, dimana Piracetam memiliki efek sitoprotektif dan fungsional
CDP-cholin, pirasetam,
nimodipin, piritinol
CDP-cholin :meningkatkan neurotransmiter
dopaminergik, mengurangi asam radikal bebas,
memperbaiki kerusakan metab lipid mitokondria di
serebral akibat hipoksia
Pirasetam : meningkatkan cholinergik dan
neurotransmiter eksitatori amin (glutamat dan aspartat)
dlm jumlah dan fungsi, mengurangi radikal bebas,
memproteksi metab neuron.
Objective Stroke Rehabilitation

Stroke rehabilitation is an effort to help stroke

patients to optimize their ability in order to return
to their active and productive way of life.
(Ghresham et al., 1997)

Rehabilitation covers efforts to prevent deterioration

and treatment to stop damage, spasticity and
contractus and also to prevent complication as a
result of decubitus
(Gloag, 1985)
Objective :

Rehabilitation is aimed to form new connection

pathways and to reactivate neurons which
previously passive. His is conducted by
maximizing neuron capacity of healthy neurons.

This effort is achieved by exercise which is actually a

relearning process, and at the same time
stimulating functional recovery in the brain and
preventing disused athrophy and other
complication as a result of paralysis.
Rehabilitation Program :
Physical therapy :
Mobilization
Walking
Major motor or sensory impairment of the limbs
Prescription of devices, such as a cane or walker

Occupational Therapy :
Fine movements of the hand
Arm function
Utilization of tools
Assistive devices
Ability to function independently
Speech Therapy :

Disorders of language
Disorders of articulation
Disorders of swallowing
Factors that Influence the Successfully
of Rehabilitation
Cause of stroke
Severity of stroke
Location
Age
Self motivation
Premorbide personality and mood
Family
Social economy
Specific deficit neurology
Onset, duration and intensity
Rehabilitation team
 Rehabilitation Started
Stroke rehabilitation more effective when it started in first
day in hospital and the latest of 2-3 days after
onset.(Feigenson)
Stroke patients result emboli/trombosis without
complication need to mobilization within 2-3 days, but
stroke patients result subarahnoid hemorrhage have to stable
previously during 10-14 days before mobilization.(Swenson)
Stroke patients with intracerebral hemorrhage have to lie
down during 3 weeks.(Toole JF)
Purpose of Rehabilitation

To reduce the worth consequence of pro long in

activity as contracture, ulcus decubitus, muscle
weakness, deep end thrombosis, cardiopulmonar
complication, depression.
Objective Stroke Rehabilitation

Stroke rehabilitation is an effort to help stroke

patients to optimize their ability in order to return
to their active and productive way of life.
(Ghresham et al., 1997)

Rehabilitation covers efforts to prevent deterioration

and treatment to stop damage, spasticity and
contractus and also to prevent complication as a
result of decubitus
(Gloag, 1985)
Objective :

Rehabilitation is aimed to form new connection

pathways and to reactivate neurons which
previously passive. His is conducted by
maximizing neuron capacity of healthy neurons.

This effort is achieved by exercise which is actually a

relearning process, and at the same time
stimulating functional recovery in the brain and
preventing disused athrophy and other
complication as a result of paralysis.
Rehabilitation Program :
Physical therapy :
Mobilization
Walking
Major motor or sensory impairment of the limbs
Prescription of devices, such as a cane or walker

Occupational Therapy :
Fine movements of the hand
Arm function
Utilization of tools
Assistive devices
Ability to function independently
Speech Therapy :

Disorders of language
Disorders of articulation
Disorders of swallowing
Factors that Influence the Successfully
of Rehabilitation
Cause of stroke
Severity of stroke
Location
Age
Self motivation
Premorbide personality and mood
Family
Social economy
Specific deficit neurology
Onset, duration and intensity
Rehabilitation team
 Rehabilitation Started
Stroke rehabilitation more effective when it started in first
day in hospital and the latest of 2-3 days after
onset.(Feigenson)
Stroke patients result emboli/trombosis without
complication need to mobilization within 2-3 days, but
stroke patients result subarahnoid hemorrhage have to stable
previously during 10-14 days before mobilization.(Swenson)
Stroke patients with intracerebral hemorrhage have to lie
down during 3 weeks.(Toole JF)
Purpose of Rehabilitation

To reduce the worth consequence of pro long in

activity as contracture, ulcus decubitus, muscle
weakness, deep end thrombosis, cardiopulmonar
complication, depression.
 HEMORRHAGIC TRANSFORMATION OF A INFARCTION
Berhubungan dengan terapi trombolitik
The clinical correlates of the varying degrees of early
hemorrhagic transformation of a cerebral infarc are
unclear (Fiorelli, M, 2003)
Pada kejadian yang jarang intracranial hemoragik dapat terjadi pada
trombosis vena (Adams, 2002)
Trombosis disebabkan oleh :
- kehamilan
- dehidrasi
- pembedahan
- sepsis
- khemoterapi
- kelainan hiperkoagulasi
Perdarahan terjadi akibat ruptur kapiler, sekunder akibat stagnasi dari
vena( sinus sagtila superior/vena superfisial)
NATIONAL INSTITUTES OF HEALTH
STROKE SCALE (NIHSS)
CONFIDENTIAL 200
CONFIDENTIAL 201
Interpretasi NIHSS:
Nilai > 15 : defisit berat
Nilai 4-15: defisit sedang
Nilai <4 : defisit ringan