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)
 Age (risk doubles for Obesity
every decade > age Smoking
55)
Atrial fibrillation
Gender
(males>females) Sedentary lifestyle
Family history of Drug abuse (e.g.
stroke/TIA cocaine use)
Hypertension Hormone
Diabetes replacement
Hyperlipidemia therapy
Hyperhomocysteinem Oral contraceptive
ia
 Modifiable
Hypercholesterole
mia
Cigarette smoking
Non modifiable Arterial
Age hypertension
Gender Diabetes Mellitus
Ras Hyperhomocystei
Herediter nemia
Alcohol abuse
Oral
contraceptive
Menopause
Physical inactivity
Obesity
Atrial Fibrillation
Hipercoagulability
 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/fami
Hyperhomocystei
lial factors nemia
Race/ethnicity
Leftventricular
Geographic hypertrophy
location
 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, July1,1997; 28(7): 1507 - 1517.

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

Gorelick, 2002
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.
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
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
 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
Aterosclerotic is a normal response to arterial
chemist
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)
 Demensia Bronchopneumonia
Depresi
Deckubitus
Septikemia
Kecacatan
Trombosis vena
Epilepsi profunda
Kontraktur Emboli pulmo
Peptic ulcer Ggn keseimbangan
cairan
 KONDISI STROKE ISKEMIK AKUT STROKE HEMORAGIK

Sangat Diastolik > 140 mmHg

emergensi

Sistolik > 230 mmHg Sistolik > 230 mmHg

Emergensi dan / atau Diastolik 121 dan / atau Diastolik >
140 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 dea

(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)
 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
Blockade of blood flow by ateroma,
emboli,
and ateroscelerotic
 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
 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
 Chronic inflammatory disorder of
intima of large arteries
characterised by formation of
fibrofatty plaques called atheroma.

Hardening of arteries -
Arteriosclerosis
 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
 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.
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 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.
 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.
 Plaque Myocardial
Athero- Rupture/
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
 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.
 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
 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
 Sumbatan
Aliran darah Penurunan CBF

Iskemia
Nekrosis
neuron

ATP, merubah
permeabilitas membran
Kerusakan
membran
Influks Ca+
berlebihan
Oleh karena ruptur aneurisma, angioma, lesi
aterosklerotik
 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:
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)
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
Interstisial
Cerebral edema
CONTROL CENTER OF BRAIN
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
weakness of the
contralateral face with
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
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
Functional Areas of the Brain

Back
 Mungkin sulit dipercaya bahwa di dalam otak
tersimpan informasi mengenai segala hal yang
mengatur kelangsungan hidup manusia
 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).
 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
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.CEREBRI ANTERIOR A.CEREBRI MEDIA

Talamus dan ganglia Bagian terbesar dari

basalis korteks
lateral(frontal,tempor
al dan parietal)
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
- Ggn mood weakness
- Ggn perilaku
- Inkontinensia
- Contralateral sensory
- disfungsi olfaktorius
loss
- Disfungsi opticus - Disfasia
- Disleksia, disgrafia,
diskalkulia
- 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)
 Demensia Bronchopneumoni
a
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 Sistolik > 230 mmHg

Emergensi dan / atau Diastolik 121 dan / atau Diastolik >
140 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
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)
 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
 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
 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
CSF Mas
Bones

Copied from: Rogers (1996) Textbook of Pediatric

 Aneurysma 70-75%
AVM 5%
Bleeding diathesis
Anticoagulant <5%
Tumor
Vasculitis
Undefined 15%
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
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
 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)
 CT Scan : 95 % (dalam 48 jam)
Lumbar Puncture : >6 jam
- Uniformly blood stained
- Xanthochromic
MRI : kurang sensitif 24-48 jam
Cerebral angiogram : gold standard
 CT Scan : 95 % (dalam 48 jam)
Lumbar Puncture : >6 jam
- Uniformly blood stained
- Xanthochromic
MRI : kurang sensitif 24-48 jam
Cerebral angiogram : gold standard
 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
 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
 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
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)

 Left (Dominant) Hemisphere Stroke
Aphasia
Right hemiparesis
Right-sided sensory loss
Right visual field defect
Apraxia
Dysarthria
Difficulty reading, writing, or calculating
 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
 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)
 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)
 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)
 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)

 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)

 Visual loss - homonymous hemianopia (C)
Visual loss - upper quadrant anopsia (C)
Constructional apraxia (ND)
Aphasia receptive (D)

( AHA Stroke center, 2004)

 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
 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
 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)
 Medical Management
Surgical 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
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
 Medical Management
Surgical 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
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
 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.

 Vasogenic :
kerusakan vaskuler endotel kapiler, gangguan
tight junction, permeabilitas meningkat
Cytotoxic :
gangguan pompa Na, K, ATP ase, Na intrasel
meningkat
Interstisial :
Transudasi
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)
 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
 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 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
 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)
 Mechanism (neuronal)
Repair cell membran fluidity
Repair neurotransmission
Stimulation adenylate kinase
Mechanism (vascular)
Increase eritrocyte deformability
Decrease platelet hyperagregation
Repir microcirculation

(Perdossi, 2004)
 PCCT
Hidrolisa
Cytidine Otak
Citicholine
diabsorbsi Citicholine
Choline Sintesa

1-2 DAG
Asetilasi Phosphatidilserin
Vaskularisasi
Lokal Acetylcholin Phosphatidiletanolami Phosphatidilkolin
n
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 :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
 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
 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)
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
 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
 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)
To reduce the worth consequence of pro
long in activity as contracture, ulcus
decubitus, muscle weakness, deep end
thrombosis, cardiopulmonar
complication, depression.
 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)