Dr. Roezwir Azhary Sp.

S
SMF SARAF RSAM
 Definisi
Dulu (WHO)
Sindrom Klinis berupa defisit neurologis
fokal/global yang menetap lebih dari 24 jam,
atau berakhir dengan kematian tanpa
diketahui sebab lainnya, kecuali gangguan
aliran darah di otak

Sekarang
Dianggap stroke bila ditemukan patologi
(infark atau perdarahan) di jaringan otak
 Insidens stroke
Dari data WHO dikatakan ada sekitar 15
juta pasien stroke diseluruh dunia setiap
tahun nya . Dari jumlah tersebut sekitar 5
juta akan meninggal dunia ,5 juta lain nya
menderita cacat berat dan membutuhkan
perawatan khusus, sisanya bisa kembali ke
pekerjaan semula (2011).
 Anatomi

4/5 otak bagian depan diperdarahi oleh sistem

karotis dan 1/5 bagian belakang (batang otak,
bagian oksipital dan bagian dalam otak)
diperdarahi oleh sistem vertebro basiler
Normal tiap 100gr jaringan otak harus mendapat
darah 50 55 cc/menit = 1/5 dari kardiak
output
 Anatomi

Ke2 sistem arteri dihubungkan oleh sepasang

arteri komunikan posterior,
menghubungkan arteri karotis interna
dengan arteri serebri posterior dan arteri
komunikan anterior yang menghubungkan
kedua arteri serebri anterior membentuk
sirkulus arteriosus WILLISI
 Klasifikasi

1. Stroke Non Hemoragik (iskemik / infark)

2. Stroke Hemoragik (perdarahan
intraserebral dan perdarahan
subarakhnoid)
 Faktor Resiko

1. Unmodifieable
Usia, jenis kelamin, ras ,riwayat keluarga
2. Modifieable
Hipertensi, DM, kelainan jantung,
merokok, dislipedemia, hiperuricemia,
obesitas hiperhomositeinemia,
penyakit imunnulogi dan kelainan
pembuluh darah (takayasu dan moya-
moya disease) dll nya
 PATOGENESIS BRAIN INFARCTION

Metabolisme normal dan aliran darah

Otak: Sebuah organ yang sangat aktif secara metabolik

Glukosa sebagai substrat tunggal
Energi yang dihasilkan tergantung pada kehadiran oksigen
ATP sebagai energi untuk
menjaga integritas neuronal
menjaga Ca + + di luar dan K + dalam sel-sel
persyaratan otak
O2 500 mL Each minute !!
Glukosa 75-100 mg
 BRAIN INFARCTION

Normal metabolism and blood flow

Cerebral Blood Flow (CBF)

53 ml/100 otak / menit gm (kisaran 50-60)
Cerebral Metabolisme Rate untuk Oksigen (CMRO2)
Cerebral O2 Konsumsi
3,5 ml / mg / menit
Kompensasi maksimum untuk mempertahankan CMRO2
di CBF 20-25 ml/100 gm / min
 BRAIN INFARCTION

Cerebral Blood Flow (CBF) dalam 100mg/minute

Jika CBF menurun sampai 15-18 kegagalan listrik

Di bawah 15 perubahan dalam membangkitkan potensi

somato-sensorik
Pada 10-15 ml (antara kegagalan listrik dan ionik)
Neuron tidak berfungsi, tapi masih layak
 BRAIN INFARCTION

Neuron ini muncul di pinggiran, sekitar

daerah infark (area perifocal).
Keberadaan mereka ditentukan oleh sistem jaminan.
Daerah ini disebut penumbra.
Ini adalah target intervensi!.

Di bawah 10 kegagalan ionik

Ekstraseluler K + ,intraselular Ca + +
Rilis asam lemak bebas, kerusakan ATP,
asidosis intraseluler
kematian neuronal
 BRAIN INFARCTION

Faktor-faktor yang menentukan CBF

Regional Cerebral Blood Flow (rCBF)
Auto-regulasi
perubahan mikrosirkulasi
Metabolik dan neuro-kimia control
 BRAIN INFARCTION

Regional Cerebral Blood Flow (rCBF)

Hagen Poisseuille Law
p . r4 .
V=
n.l.8
V = velocity of blood flow to the brain
p = intravascular pressure
r4 = radius of the artery
n = blood viscosity
l = arterial length

Changes of these factors can lead to ischemia

tissue necrosis
 BRAIN INFARCTION

Auto-regulasi

Kapasitas sirkulasi otak untuk mempertahankan

relatif konstan CBF
meskipun tekanan berubah

CBF relatif konstan di MABP 50-150 mmHg

Hipertensi kronis: tingkat atas dan bawah

auto-regulasi dibangkitkan.
 BRAIN INFARCTION

Auto-regulation
CBF

75

50

25

MABP
50 100 150 200
 BRAIN INFARCTION

Auto-regulasi

Kemampuan auto-regulasi dan jaminan sistem

Memainkan peran penting dalam serangan stroke.

Jika tekanan darah meningkat, pembuluh akan menyempi

dan jika tekanan darah menurun, mereka akan membesar.

Kerusakan auto-regulasi dan jaminan sistem

penurunan CBF daerah
iskemik infark
 Intracerebral Hemorrhage
Perdarahan ke dalam otak hasil dari pecahnya salah satu
pembuluh otak.
Dalam banyak kasus, berasal dari sebuah kapal
arteriosclerotic pecah.
Major penyebab - pecahnya mikroaneurisma. (end hasil
hipertensi arteri lama)
pada penetrasi arteri.
Aterosklerosis (dalam penuaan atau HTN kronis)
microaneurysms pada penetrasi arteri + 1mm:
Charcot-Bouchard aneurysm
Situs yang paling umum - ganglia basal.
 Intracerebral Hemorrhage
Otak hematoma:
Efek Kompresi Memperpanjang sistem ventrikel atau
ruang subarachnoid
 Subarachnoid Bleeding
Penyebab:
pecah aneurisma
pecah AVM
pecah angioma
dyscrasia darah

Aneurysm: ditemukan biasanya dalam lingkaran Willis dan

cabang-cabangnya
Darah aneurisma pecah mengisi subarachnoid
ruang dan otak parenkim dekat dengan itu.
 Subarachnoid Bleeding

Komplikasi Asosiasi Perdarahan subarachnoid

vasospasme:
Penyempitan arteri Tertunda kapasitansi besar di
dasar otak setelah SAH
Sering terjadi pada hari ke 2 sampai 12 setelah
onset.
hidrosefalus
Perdarahan ulang: terjadi dalam beberapa minggu
setelah onset
hiponatremia
kejang
Patogenesis & Patofisiologi
 Diagnosis
Anamnesis
Pemeriksaan fisik
Pemeriksaan penunjang
 Anamnesis
Biasanya pasien mengeluh :
1. Kelemahan lengan dan tungkai sesisi tubuh, gangguan
berjalan (ataksia)
2. Rasa kesemutan, baal sesisi tubuh
3. Gangguan saraf kranial (mulut mencong, bicara pelo,
gangguan menelan, gangguan lapangan pandang)
4. Gangguan fungsi luhur
5. Gangguan saraf otonom
6. Tanda tekanan intrakranial meninggi (sakit kepala hebat,
muntah proyektil, kesadaran menurun)
7. Faktor resiko
 Pemeriksaan Fisik
Pemeriksaan tingkat kesadaran dan TTV
Pemeriksaan saraf kranial I-XII
Pemeriksaan kekuatan motorik
Pemeriksaan refleks fisiologis dan patologis
Pemeriksaan sensorik
Pemeriksaan fungsi luhur
Pemeriksaan saraf otonom
 ss
Hasil anamnesis dan pemeriksaan fisik tergantung pada
daerah otak mana yang aliran darah terganggu.
MCA : biasanya kekuatan lengan lebih lemah dibanding
tungkai, bisa ditemukan afasia (hemisfer dominan)
ACA : biasanya kekuatan tungkai lebih lemah dibanding
lengan, bisa ditemukan gangguan miksi (cerebral
incontinencia).
Gangguan pada batang otak menyebabkan hemiparese
alternans (saraf kranial kiri motorik kanan), vertigo dan
disfagia persistent
 Pemeriksaan Penunjang
Tujuan :
1. Memastikan diagnosis
2. Mencari faktor resiko
3. Mencari penyakit penyerta (comorbidity)
Antara lain : DL, UC, AU, GD, kolesterol,
SGOT/SGPT, Pemeriksaan kekentalan darah (INR),
Pemeriksaan faktor koagulasi lainnya, EKG, Echo
kardiogravi, TCD, CT-Scan dan MRI kepala.
 Penatalaksanaan

Atasi kegawat daruratan bila ada (Resusitasi)

Pemeriksaan laboratorium (DL, Fungsi Ginjal,
Gula darah, asam urat, lipid profile, fungsi liver,
analisa gas darah, elektrolit, dan pemeriksaan
lainnya sesuai indikasi)
Pemeriksaan Radiologi
Pemeriksaan Jantung (EKG dan echo cardiografi
sesuai indikasi)
 Jaga jalan nafas tetap baik bila perlu
berikan oksigen (nasal, sungkup,
endotrakeal)
Jaga keseimbangan cairan dan elektrolit
Nutrisi : jaga jangan sampai terjadi under
nutrisi (katabolisme)
Penatalaksanaan hipertensi pada stroke
Fase akut
Tekanan darah tidak diturunkan pada stroke non
hemoragik apabila TD sistemik tidak melewati
MABP yg ditetapkan kecuali ada gangguan pada
target organ
Penurunan TD tidak boleh >20-25% terutama pada
jam jam pertama pasca onset stroke
Tekanan darah diturunkan pada stroke hemoragik
apabila TD sistemik >180/105 mmhg
 Penatalaksanaan hiperglikemi
Gula darah harus diturunkan apabila >180 mg
%
Hati hati dengan hiperglikemi reaktif
Ada bermacam cara menurunkan kadar gula
darah
 Anti platelat agregasi
Aspirin dosis rendah 325 mg/hari pada hari
pertama dan kedua, selanjutnya 80 mg/hari
Cilostazol, clopidogrel, dipiridamol, dll
Neuroprotektan (kontroversi)
Antibiotik bila ada infeksi
Trombolisis (3 jam pasca onset)
 Rehabilitasi
Dilakukan sedini mungkin
Pasif
Melakukan latihan lingkup gerak sendi
(ROM), mobilisasi bertahap
Aktif
Dilakukan apabila cardiovaskular stabil, dan
setelah fase akut terlewati pada stroke
hemoragik

Tujuannya : mencegah kontraktur dan

trombosis vena dalam
 Pencegahan Stroke
Primer
Ditujukan pada orang yang belum kena stroke tapi
mempunyai faktor resiko
Sekunder
Pada Orang yang pernah mengalami TIA dan
stroke
Carotid stenting
pemasangan balon pada pembuluh karotis yang
mengalami stenosis >60% (asimptomatik)
 TIA
Traditional
Ischemic event lasting under 24 hours
Proposed (probably more accurate)
Ischemic event lasting under 1 hour, AND
No visible infarct by CT/MRI
Equivalent to stroke
TIAs should be thought of and treated as a stroke that
just recovered quickly
These patients are at very high risk of stroke over the
subsequent 30 days
 Epidemiology in USA
750,000 new or recurrent strokes per year in the United
States
Every 45 seconds, someone in America has a stroke.
Every 3.1 minutes, someone in America dies of a stroke.
283,000 stroke deaths in 2000 in the US (1 in 14 deaths)
22% of men and 25% of women who have an initial stroke
die within one year
4,700,000 stroke survivors alive today in the US
28% of people who suffer a stroke within a given year are
under 65
 Brain Physiology
Neural tissue has no reserve of glucose or
oxygen
Neurons are therefore dependent on a
constant flow of blood to supply nutrients
In the absence of blood flow, neurons will
die within minutes
 Definitions
CBF (Cerebral blood flow)
The volume of blood flowing into the brain
tissue each minute
CPP (Cerebral perfusion pressure)
The difference between mean arterial pressure
and intracerebral pressure
 Definitions
OEF (Oxygen extraction fraction)
The amount of oxygen taken from the blood into
the tissue
CMRO2 (Cerebral metabolic rate of O2 )
The amount of oxygen used by brain
Measure of health of cells
A drop in CMRO2 signifies
Reduced metabolic demand
Failure of metabolism
 Autoregulation
According to the laws of physics, the
volume of fluid that flows through a vessel
is proportional to its pressure
The blood vessels in the brain have the
unique ability to maintain a constant blood
flow despite changes in perfusion pressure
 Autoregulation
Constant flow maintained with cerebral
perfusion pressure of 70-150 mmHg
When autoregulation fails, the brain can
increase OEF to maintain enough tissue
oxygen
Mediated by dilation and contraction of
arterioles
 Autoregulation
Edema or
CBF hemorrhage

Ischemia

0
70 150

CPP
 Autoregulation

CBF

Chronic
Hypertension
0
70 150

CPP
 Stroke
When a blood vessel becomes blocked, the
perfusion pressure to the area of brain supplied
by that vessel drops
If it drops below 70 mmHg, autoregulation
fails and flow is again dependent on pressure
Initially, the brains OEF increases to maintain
CMRO2 (misery perfusion)
If this does not suffice, there is not enough
oxygen to supply metabolic demands and
CMRO2 falls
 Cerebral Blood Flow
Normal
50-60ml/100g/min
Ischemic
20ml/100g/min
Protein synthesis is impaired but membrane integrity
preserved
Risk of apoptosis
Infarcted
<= 10ml/100g/min
Loss of structural integrity and cell death (necrosis)
Collateral Flow

Adjacent
normal vessel

Blocked vessel
Collateral Flow

Penumbra

Ischemic Core
Penumbra
Infarction
Ischemia
Misery Perfusion
Normal
Penumbra
Ischemic Core

Penumbra

Normal
 Cell Death
Necrosis Apoptosis
Abnormal cell death Programmed cell death
Seen in ischemic core Seen in penumbra
Results from severe Occurs when cell
drop in blood flow senses damage and
Does not require commits suicide
energy Requires energy
 Necrosis
Exhaustion Failure of Release of
Depolarization
of ATP Ion pumps Glutamate

Entry of Activation of
Disruption of
Entry of water Calcium and Calcium
Cell membrane
sodium Channels

Lack of oxygen and

Cell Death glucose result in depletion
of ATP
This takes 1-3 minutes
 Necrosis
Exhaustion Failure of Release of
Depolarization
of ATP Ion pumps Glutamate

Entry of Activation of
Disruption of
Entry of water Calcium and Calcium
Cell membrane
sodium Channels

Failure of energy dependent ion

Cell Death pumps (Na-K ATPase)
 Necrosis
Exhaustion Failure of Release of
Depolarization
of ATP Ion pumps Glutamate

Entry of Activation of
Disruption of
Entry of water Calcium and Calcium
Cell membrane
sodium Channels

The neurons lose their ionic

Cell Death gradients and depolarize
 Necrosis
Exhaustion Failure of Release of
Depolarization
of ATP Ion pumps Glutamate

Entry of Activation of
Disruption of
Entry of water Calcium and Calcium
Cell membrane
sodium Channels

Release of glutamate, an excitotoxic

Cell Death neurotransmitter
 Necrosis
Exhaustion Failure of Release of
Depolarization
of ATP Ion pumps Glutamate

Entry of Activation of
Disruption of
Entry of water Calcium and Calcium
Cell membrane
sodium Channels

Activation of voltage gated calcium

Cell Death channels
NMDA, AMPA, Kainate
 Necrosis
Exhaustion Failure of Release of
Depolarization
of ATP Ion pumps Glutamate

Entry of Activation of
Disruption of
Entry of water Calcium and Calcium
Cell membrane
sodium Channels

These open channels allow calcium

Cell Death and sodium to enter the cells
 Necrosis
Exhaustion Failure of Release of
Depolarization
of ATP Ion pumps Glutamate

Entry of Activation of
Disruption of
Entry of water Calcium and Calcium
Cell membrane
sodium Channels

Water follows the salts along

Cell Death osmotic gradients
 Necrosis
Exhaustion Failure of Release of
Depolarization
of ATP Ion pumps Glutamate

Entry of Activation of
Disruption of
Entry of water Calcium and Calcium
Cell membrane
sodium Channels

The cells swells from the excess

Cell Death water causing the membrane to
rupture
 Necrosis
Exhaustion Failure of Release of
Depolarization
of ATP Ion pumps Glutamate

Entry of Activation of
Disruption of
Entry of water Calcium and Calcium
Cell membrane
sodium Channels

Cell Death
 Necrosis
Exhaustion Failure of Release of
Depolarization
of ATP Ion pumps Glutamate

Entry of Activation of
Disruption of
Entry of water Calcium and Calcium
Cell membrane
sodium Channels

Activation of Production of Activation of

Cell Death
Proteases Free radicals NO synthase
 Necrosis
Exhaustion Failure of Release of
Depolarization
of ATP Ion pumps Glutamate

Entry of Activation of
Disruption of
Entry of water Calcium and Calcium
Cell membrane
sodium Channels

Activation of Production of Activation of

Cell Death
Proteases Free radicals NO synthase
 Necrosis
Exhaustion Failure of Release of
Depolarization
of ATP Ion pumps Glutamate

Entry of Activation of
Disruption of
Entry of water Calcium and Calcium
Cell membrane
sodium Channels

Activation of Production of Activation of

Cell Death
Proteases Free radicals NO synthase
 Necrosis
Exhaustion Failure of Release of
Depolarization
of ATP Ion pumps Glutamate

Entry of Activation of
Disruption of
Entry of water Calcium and Calcium
Cell membrane
sodium Channels

Activation of Production of Activation of

Cell Death
Proteases Free radicals NO synthase
 Necrosis
Process takes 6-12 hours
Process is irreversible earlier
Triggers inflammation and edema
Inflammation leads to introduction of
neutrophils, lymphocytes, and monocytes
into the brain
These cells release toxic cytokines and also
contribute to the formation of free radicals
 Apoptosis
Cell senses prolonged ischemia
Prolonged failure to synthesize proteins
It decides that it is diseased and commits
suicide to save the rest of the organism
Useful as natural limit to growth of
malignancies
Also used whenever a cell has outlived its
usefulness
 Apoptosis
Glutamate is released, but at lower
concentration than in necrosis
Promotes free radical production
Leads to lesser elevation of intracellular
calcium
 Apoptosis
Promotes pro-death genes
Caspase 1,2,3
Forkhead family
REST/NRSF
Bcl-2 family
Inhibits pro-survival genes
CREB (cAMP response binding element protein)
NFKB (nuclear factor KB)
 Apoptosis
These pro-death proteins lead to orderly and
energy dependent breakdown of
mitochondria and nuclear DNA
This is a slow process and can be prevented
 Global Hypoperfusion
CPP = MAP ICP
If the MAP drops, so does the cerebral perfusion
pressure
If this is severe enough, it will cause global
ischemia
Milder drops in MAP may cause preferential
ischemia in territories supplied by stenotic
vessels.
 Causes of Focal Infarction
Atherosclerotic plaque
Thrombosis
Plaque itself occludes vessel
Hemorrhage into plaque
Embolism
From atherosclerotic plaque
From thrombus
From heart
Other- bone marrow embolus, air embolus
Arteriosclerosis
usually due to hypertension
Watershed infarction
focal infarction that results from global drop in perfusion pressure
Hemorrhage -
Come to my Lecture on Monday on Intracerebral Hemorrhage
 Causes of Focal Infarction
Atherosclerotic plaque
Thrombosis
Plaque itself occludes vessel
Hemorrhage into plaque
Embolism
From atherosclerotic plaque
From thrombus
From heart
Other- bone marrow embolus, air embolus
Arteriosclerosis
usually due to hypertension
Watershed infarction
focal infarction that results from global drop in perfusion pressure
Hemorrhage -
Come to my Lecture on Monday on Intracerebral Hemorrhage
 Thrombosis
Refers to progressive decrease in diameter
(stenosis) of a large to medium sized blood
vessel due to plaque (atheroma) within the
wall of the vessel
Most common etiology (in the elderly) is
atherosclerosis
Progressive deposition of fatty material and
fibrous tissue into the subintimal layer
(atheroma)
 Thrombosis
Methods of expansion of atheroma
Intraatheroma hemorrhage
Subintimal necrosis
Calcium deposition
Progressive stenosis may cause infarct
Common in small vessels
Rare in large/medium vessels
 Thrombosis
Atheroma rupture
Usual final common pathway of stroke (& MI)
Platelet aggregation
Fibrin deposition
Endothelium heals further lumen narrowing
Red cells become enmeshed
Occlude lumen
Embolize
 Thrombosis - Risk Factors
Modifiable Non-modifiable
Hypertension Age (increases with)
Diabetes Gender (male)
Hyperlipidemia Family history
Ethnicity
Smoking
Intracranial more
Elevated homocysteine common in Asian,
African-American, and
Chronic Hispanic
infection/inflammation Extracranial more
common in Caucasian
 Thrombosis Other Causes
All of these are more common in the young
Dissection
Tearing of the vessel wall itself
Blood accumulates in the wall, usually between intima
and media
Can occlude vessel or embolize
Usually seen in extracranial ICA or vertebral artery
Often traumatic but can be seen connective tissue
disorders
 Thrombosis Other Causes
Inflammatory process affects blood vessel wall
Primary angiitis restricted to CNS
Secondary to other systemic or CNS diseases
PAN
Temporal Arteritis
Takayasus Arteritis
Connective tissue diseases: SLE, scleroderma, Sjogren
syndrome, rheumatoid arthritis
CNS infection: Lyme, bacterial meningitis, meningovascular
syphilis, Herpes, TB

 Thrombosis Other Causes
Drugs
Amphetamines, cocaine, heroin
Combination of vasoconstriction and vasculitis
Hypercoagulable states
Disorders of the blood that predispose to clotting
Polycythemia vera
Thrombocytosis (platelet ct > 1,000,000/dL)
Anti-phospholipid antibody syndrome
Lupus anticoagulant
Sickle Cell Disease
Antithrombin III
Protein C/S
Mutation in genes for Factor V or II
 Clinical Presentation
Thrombosis can cause strokes by lack of
blood flow due to progressive stenosis (Can
also cause embolism (artery to artery)
Symptoms vary based on location of infarct
 Progressive Stenosis
More likely to be preceded by TIAs than
embolic
Symptoms are acute in onset but may
worsen over brief period
Tend to be smaller than embolic infarcts
Symptoms tend to vary with blood pressure
 Internal Carotid Artery
Disease of the Internal Carotid Artery (ICA) can
cause stroke via 2 mechanisms

Thrombosis / Hypoperfusion
Embolism
We are focusing on Thrombosis right now
 Internal Carotid Artery
Patients with ICA disease frequently have TIAs
prior to actual infarct
Hemodynamic
Stereotyped symptoms
Varies with blood pressure
Preferentially affects border zones
(Well come back to this when we get to Watershed Infarcts)
 Causes of Focal Infarction
Atherosclerotic plaque
Thrombosis
Plaque itself occludes vessel
Hemorrhage into plaque
Embolism
From atherosclerotic plaque
From thrombus
From heart
Other- bone marrow embolus, air embolus
Arteriosclerosis
usually due to hypertension
Watershed infarction
focal infarction that results from global drop in perfusion pressure
Hemorrhage -
Come to my Lecture on Monday on Intracerebral Hemorrhage
 Embolism
Occlusion of a cerebral blood vessel by a
small piece of blood clot, tumor, fat, air, or
clump of bacteria
Emboli may partially or totally occlude a
cerebral vessel
Emboli to brain are frequently multiple
Can be associated with infarcts in lungs,
spleen, kidneys
 Embolic Sources
Carotid Artery plaque, dissection
Vertebral Artery plaque, dissection
Aorta plaque, dissection
Cardiac Atrial Fibrillation, PFO
Paradoxical Embolus
 Cardiac Sources of Emboli
Valvular vegetations
or calcifications
Cardiomyopathy
MI
Acute
Especially anterior wall
Chronic
Ventricular aneurysm
Focal hypokinesis
Tumor (myxoma)
Patent foramen
ovale(PFO) & atrial
septal aneurysm(ASA)
Paradoxical embolism
Thrombus within ASA
Arrhythmias
Sick sinus syndrome
Atrial fibrillation
 Cardiac Sources of Emboli
15-20% of all ischemic strokes
(23-36% in patients < 45 years old)
Cerebral circulation absorbs 10-15% of cardiac
output
Most common sites for lodgment of cardiac
emboli main trunk and branches of MCA
10% of cerebral emboli enter the vertebro-basilar
circulation lodge mainly at the top of the basilar,
or main trunk or branch of the PCA
 Clinical Features
Abrupt onset of maximum defect in an awake,
active person
Deficits depend on location of embolism
Headache
Diminished level of consciousness at onset
Rapid improvement
History of systemic emboli
Predisposing heart condition
Involvement of larger vascular area
Middle
Cerebral
Artery
Infarct

&

Dense
MCA
Sign
 Middle Cerebral Artery
Contralateral gaze palsy
Contralateral hemiplegia (arm+face>leg)
Contralateral hemisensory loss
Aphasia (dominant side only (D))
Can be global, expressive, receptive, or
transcortical depending on which branches
involved
 Anterior Cerebral Artery
Contralateral hemiplegia (leg>arm+face)
Abulia
Depression
Anterior Cerebral Artery
Anterior Cerebral Artery

From Dr Seidmans talk

 Posterior Cerebral Artery
Contralateral homonymous hemianopsia
Contralateral hemisensory loss
Neglect
Prosopagnosia (N)
Alexia without agraphia (D)
Anomic or transcortical sensory aphasia (D)
Almost always embolic
Posterior Cerebral Artery
Posterior Cerebral Artery
Alexia Without Agraphia
 Vertebral Artery
Rarely causes hypoperfusion stroke unless there is
a problem with the other VA
Posterior inferior cerebellar artery
Vertigo
Nausea/emesis
Gait ataxia
Lateral medullary artery
Wallenberg syndrome
Ipsilateral limb ataxia
Ipsilateral Horners syndrome
Contralateral hemisensory loss
Vertigo
Dysphagia
Hoarse voice
 Basilar Artery
Brainstem signs
Cranial neuropathies
Ataxia
Cerebellar signs
Nausea, emesis
Change in level of consciousness
Crossed signs
 Causes of Focal Infarction
Atherosclerotic plaque
Thrombosis
Plaque itself occludes vessel
Hemorrhage into plaque
Embolism
From atherosclerotic plaque
From thrombus
From heart
Other- bone marrow embolus, air embolus
Arteriosclerosis
usually due to hypertension
Watershed infarction
focal infarction that results from global drop in perfusion pressure
Hemorrhage -
Come to my Lecture on Monday on Intracerebral Hemorrhage
 Arteriosclerosis
a.k.a. small vessel disease
Process whereby you develop thrombosis of
small vessels (e.g. thalamic perforators)
Analogous to atherosclerosis of large/medium
arteries
Primary process is lipohyalinosis
More to come in ICH lecture on Monday
 Perforators
Small vessel disease leads to lacunar strokes
Can worsen over 1-2 days (stuttering lacune)
Pure motor
Internal capsule, pons
Pure sensory
Thalamus
Clumsy hand dysarthria
Pons
Ataxic hemiparesis
Internal capsule
 Causes of Focal Infarction
Atherosclerotic plaque
Thrombosis
Plaque itself occludes vessel
Hemorrhage into plaque
Embolism
From atherosclerotic plaque
From thrombus
From heart
Other- bone marrow embolus, air embolus
Arteriosclerosis
usually due to hypertension
Watershed infarction
focal infarction that results from global drop in perfusion pressure
Hemorrhage -
Come to my Lecture on Monday on Intracerebral Hemorrhage
 Border Zone
Areas of anastomosis between the most
distal branches of major cerebral vessels
Areas get poor supply from both arteries
Most susceptible to hypoperfusion
Border Zone
 Border Zone = Watershed Infarct
Symptoms/Signs mimic the nearby territories
Anterior Border Zone
Between MCA and ACA
Contralateral weakness
May see (motor) aphasia
May see neglect

Posterior Border Zone

Between MCA and PCA
Contralateral homonymous hemianopsia
May see (sensory) aphasia
Mood disturbance (non-dominant)
May see Anosognosia or neglect
 Special Kinds of Strokes
Venous
Spinal
Are all strokes due to arterial obstruction?
 Venous Infarcts - Anatomy
Cerebral veins contain ~70% of the total cerebral
blood volume.
Highly variable.
Can be divided into a superficial and deep system.
The superficial system drains the outer 2 cm of
brain and drains into the sinuses.
The deep system drains the deep white matter,
basal ganglia, and diencephalon and drains into
the Galenic system.
Pathophysiology of Venous Thrombosis

Cerebral blood flow depends upon the difference

in the arterial and venous pressures.
As the venous pressure rises, perfusion pressure
drops. Autoregulation will cause arterial dilation,
thus increasing arterial flow and pressure to
maintain CBF.
Only when the autoregulation limit is exceeded
will the CPP and CBF drop, leading to ischemia.
Pathophysiology of Venous Thrombosis

The outcome of venous occlusion depends

on the availability of pre-existing channels,
the extent of propagation of clot, and the
creation of new collateral channels.
Neo-vascularization cannot occur unless the
occlusion develops slowly (i.e. due to
tumor).
Pathophysiology of Venous Thrombosis

Normally present anastomotic channels are

sufficient to prevent infarction unless also
occluded by propagating clot.
 Case

24 year-old woman on birth control pills has

progressively worsening severe headache.
She becomes lethargic and then develops
diplopia. On exam, she is sleepy and
slightly confused. She has bilateral 6 th
nerve palsies (more on this in Dr Harths
Oncology lecture). As you are writing up
your consult note she has a seizure.
Sagittal Sinus Thrombosis
 Pathology of Venous Infarct
When infarction does occur, it is frequently
associated with petechial and gross hemorrhages
in the parenchyma as well as perivenous
subarachnoid and subdural hemorrhage.
Pathology shows neuronal loss. Oligodendrocytes
show cytoplasmic swelling. Venules show
congestion with numerous hemorrhages and
hypertrophy of the endothelial cells.
Surrounding regions also show neuronal loss
associated with microglial and astrocytic
proliferation.
 Clinical Features of
Cerebral Venous Thrombosis
Prior to CT and MR, when Dx was by autopsy
only, CVT was described as a syndrome of
alternating deficits, seizures, and coma.
Now that non-fatal cases are diagnosed, we
realized that the clinical presentation is highly
variable.
Mode of onset:
Acute (less than 2 days) 30%.
Subacute (2 days 1 month) 50%.
Chronic (over 1 month) 20%.
 Clinical Features
Headache
Diffuse, worse on recumbency, present on
awakening
Papilledema
Increased pressure on the eye, may lead to
blindness
Seizures
Loss of consciousness
Stroke/focal deficits
 Clinical Features of
Cerebral Venous Thrombosis
Rarer complaints include:
Multiple cranial nerve palsies
Cerebellar signs
Nystagmus
Hearing loss
Bilateral or alternating signs
Thunderclap headache
 Case

69 year-old-man who awoke following an

abdominal aortic aneurysm repair unable to move
his lower extremities. On exam, there is
significant weakness of both legs. He is not able
to perceive light touch or pinprick on his legs, but
he is able to feel a vibrating tuning fork on his
legs.
 Spinal Stroke
Anatomy
The spinal cord is supplied by a single anterior
spinal artery and paired posterior spinal arteries
The posterior arteries supply the dorsal
columns only
Cervical
All arise from the vertebral arteries
 Spinal Stroke
Thoracic
Posterior arteries arise from aorta at each level
There is a single branch off the aorta (artery of
Adamkiewicz) which supplies the anterior
segments
Etiology
Dissection
Atherosclerosis
Complication of surgery
Rarely vasculitis or embolic
 Spinal Stroke - Clinical
Motor
Cervical quadriplegia
Thoracic paraplegia
Sensory
Loss of sensation, sparing vibration and
position sense, below the level of the lesion
Bladder dysfunction
 Treatment of Stroke
Acute
Minimize damage from the current event
Chronic
Reduce risk of future events
 Treatment - Acute
Promotion of blood flow
Interference with cellular mechanisms of
necrosis and apoptosis
Reduction of metabolic stress
 Blood Flow
Restoration of flow through blocked artery
Increase cerebral perfusion pressure
 Restoration of Blood Flow
Recombinant tissue plasminogen activator
Attempts to dissolve the clot
Only FDA approved treatment for acute stroke
Carries high risk of hemorrhage
Must be administered in first 3 - 4.5 hours
 Restoration of Blood Flow
Intra-arterial treatment
Perform cerebral angiogram to locate clot
Infuse small doses of tPA directly into the clot
Mechanically remove the clot
 Interference
Can we intervene to prevent the cascade of
necrosis and apoptosis?
Neuroprotectants
Dozens of compounds have been tried
All have failed
 Aspirin
Acts to reduce thrombosis
Also reduces inflammation
Has been proven to slightly reduce
mortality from acute strokes
Should be given to all patients within the
first 24-48 hours
 Reduction of Metabolic Stress
The necrosis pathway begins with depletion
of ATP
If we reduce the usage of ATP, we can delay
the onset of necrosis
 Glucose
Reduced blood glucose causes starvation of
neurons
Elevated blood glucose in the setting of ischemia
lead to lactic acid production by glial cells
Lactic acid is toxic to ischemic cells and promotes
necrosis
Glucose should be maintained in narrow range
 Temperature
Metabolic demand varies proportionally
with temperature
Drowning victims
Induction of hypothermia is under
investigation
Already shown to be useful in cardiac arrest
At least, we must aggressively treat fever
 Oxygen
There needs to be enough oxygen in the
blood to support metabolism
Excess oxygen has not been shown to be
helpful
Use oxygen as needed to keep oxygen
saturation >= 95%
 Treatment - Chronic
Depends on underlying etiology
Most commonly antiplatelet agents [e.g.
aspirin, Plavix (clopidogrel), Aggrenox
(dipyridamole)]
Interferes with platelet aggregation in the
event of endothelial rupture over an
atheroma
Reduces growth of atheroma and likelihood
of embolism
 Treatment - Chronic
Anticoagulants (Coumadin)
Used in the presence of some hypercoagulable
states and atrial fibrillation
Control of risk factors
Treat diabetes, hypertension, hyperlipidemia
Stop smoking
The End