Cerebrovascular Disease ANTERIOR CIRCULATION/CAROTID SYSTEM Global Hypoxic-Ischemic Encephalopathy

Anterior Cerebral Cortical branches: medial surface of orbital,
Types
Generally divided into 3 major categories:
1. Global Hypoxic-Ischemic Encephalopathy
2. Infarcts / Ischaemic Stroke (most common cause of stroke– 80%)
3. Intracranial Hemorrhage : Intraparenchymal hemorrhage
(Hemorrhagic Stroke) & subarachnoid hemorrhage
Anatomy Revision
Cerebral hemispheres are supplied by 3 paired major arteries:
a) Anterior cerebral a. arise from internal carotid artery
b) Middle cerebral a. carry the anterior circulation
c) Posterior cerebral a. arise from basilar artery & carry post.
Circulation
Ischemia: ↓tissue perfusion
Artery frontal and parietal lobe
Medial lenticulostriate branches: caudate
head, globus pallidus, anterior limb of internal
capsule
Middle Cerebral Cortical branches: lateral frontal and parietal
Artery lobes lateral and anterior temporal lobe
Lateral lenticulostriate branches: globus
pallidus and putamen, internal capsule
Anterior Choroidal Optic tracts, medial temporal lobe,
Artery ventrolateral thalamus, corona radiata,
posterior limb of the internal capsule
Hypoxia: ↓oxygen availability to tissues
Definition
characterized by clinical and laboratory evidence of acute or subacute
brain injury due to asphyxia (ie, hypoxia, acidosis)
Etiology:
Any circumstances that results in a global ↓ in amount of oxygenated
blood to the brain (e.g. shock, cardiac dysrhythmias or large ICP↑ )
Modifying Factors
a) Age : young patients tolerate better
b) Duration of circulatory disturbances
c) Temperature: hypothermia ↑ resistance to hypoxic-ischemic injury
d) Susceptibility of certain regions & types & subpopulation of cells:
 Types: neurons are more vulnerable than glial cell
 Subpopulation: pyramidal cell of hippocampus, Purkinje cells of
cerebellum, neurons of globus pallidus
 Regions: areas at junction of arterial territories ( arterial
border zone/watershed area) are the 1st area to be deprived of
blood during hypotensive period.
(e.g: superior cerebral convexity: junction of MCA & ACA)

Pathogenesis
Asphyxia event (hypoxia & hypercapnia)
↓
Sympathetic & R-A-A system activated
↓
Shunting of blood to vital organ (e.g: brain, heart, adrenal)
↓
↑ B.P & cerebral blood flow (CBF): Compensated
POSTERIOR CIRCULATION / VERTEBROBASILAR SYSTEM
↓
Posterior Cerebral Artery Cortical branches: occipital lobes,
Eventually decompensation occur & CBF autoregulation also fails
medial and posterior temporal and
↓
parietal lobes
Perforating branches: brainstem, Ischemic Brain Injury:
posterior thalamus and midbrain Reduce reuptake of neurotransmitter Glutamate which is excitatory in
nature  overstimulation of neurons  neuronal loss (excitotoxicity)
Posterior Inferior Inferior vermis; posterior and inferior
Cerebellar Artery cerebellar hemispheres
Anterior Inferior Anterolateral cerebellum Pathology (within 24-48 hours)
Cerebellar Artery  Softened & edematous
Superior Cerebellar Superior vermis; superior cerebellum  Demarcation of white & gray matter blurred d/t edema
Artery  Band of Laminar necrosis: vulnerability of midcortical layers of cells

Autoregulation:
 Brain receives 15% of cardiac output & it’s dependent on the
steady supply of O2
 So autoregulation mechanism maintain blood flow over a wide
range of perfusion pressure:
a) ↑pressure: constriction  Histology:
b) ↓pressure: dilation  Widened perivascular space: d/t edema
 However the mechanism will fail when systolic B.P is <50mmHg  Neuronal changes: shrinkage, cytoplasmic eosinophilia, nuclear
pyknosis
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Stroke 2. Anterior Cerebral Artery b) Thalamic syndromes: chorea/hemiballismus with hemisensory
 Sudden loss of blood circulation to an area of brain resulting in a  Severity depends on site of occlusion: disturbances
corresponding loss of neurologic function > 24hours  Proximal to anterior  Cortical branches: homonymous hemianopia, posterior cortical
 Previously called cerebrovascular accident / stroke syndrome communicating a. is well tolerated infarction (dominant hemisphere) will gives nominal aphasia
 Broadly classified as hemorrhagic or ischemic stroke (70-80%) as blood is received from the
contralateral side 5. Basilar Artery
Ischemic Stroke  Distal to ant. Communicating a. :
Weakness & sensory loss in
Subtypes contralateral lower limbs ++ urinary
a) Large artery Infarction: internal carotid a., vertebrobasillar a. , incontinence
cerebral arteries (proximal to major branches)
b) Small vessel / Lacunar Infarction: perforating vessels  Bilateral frontal lobe infarction  akinetic mutism (appears alert
c) Cardioembolic Infarction intermittently but is not responsive)

Etiology 3. Middle Cerebral Artery

1. Thrombosis of Atherosclerotic arterial segment:
most commonly seen in carotid bifurcation & basilar artery
2. Embolus:
a) Artery to artery: intracranial a., carotid bifurcation, aortic arch
b) Cardioembolic: valvular heart disease, arrhythmias, endocarditis,  Supplies Brainstem (from medulla upwards)
myocardial infarction, dilated cardiomyopathy  Eventually divides into:
3. Hypercoagulable disorders (uncommon): a) post. Cerebral artery b) post. Communicating artery
sickle cell anemia, protein C & S deficiency, antithrombin III  Branches can be classified into:
deficiency a) Posterior Cerebral Artery (see no.4)
4. Vasculitis (uncommon) b) Long Circumflex branches (see Branch Occlusion)
5. Venous Sinus thrombosis: c) Paramedian branches (see Branch Occlusion)
may be associated with hypercoagulable state  Complete basilar syndrome:
 Course: largest branch of ICA  gives off deep branches  Impaired consciousnesscoma
Large Vessels Occlusion (lenticulostriate)  pass thru insula  to the lateral surface at  Bilateral motor & sensory dysfunction
lateral sulcus  gives off cortical branches:(2) temporal, (3) frontal,  Cerebellar signs
1. Internal Carotid Artery (4) parietal  CN signs: indicative of level of occlusion
 If all cortical branches are involved:
 Severity depends on presence of collaterals
 Contralateral hemiplegia (legs are  Unilateral Neglect / 6. Vertebral Artery
 may be asymptomatic
relatively spared) hemiagnosia/hemispatial  Only posterior inferior cerebellar artery (PICA) depends solely on
 In severe cases:
 Contralateral sensory loss neglect flow of vertebral artery
 ↓Conscious level  Aphasia (if dominant hemisphere)  Dressing difficulty
 Homonymous hemianopia contralateral side  Therefore vertebral artery occlusion  PICA syndrome
 If cortical branches are involved individually  less severe
 Contralateral hemiplegia & hemisensory
 Occlusion of deep branches will be discussed later Branch Occlusion
disturbance
 Gaze palsy to opposite side away from
4. Posterior Cerebral Artery 1. Long Circumflex Occlusion (arteries of cerebellum)
hemiplegic limbs
 Global aphasia if dominant hemisphere
 Partial Horner Syndrome on side of occlusion

GAZE
 Cortical descending pathways from 1 side
activate : ipsilateral CN III nuclei &
contralateral CN VI nuclei
 CN III: medial rectus  medial movement
 CN VI: lateral rectus  lateral movement
 Cerebellum are supplied by 3 paired blood vessels:
 Thus giving conjugate gaze
 Deep branches: a) Superior cerebellar artery arise from basilar artery
a) Midbrain syndrome: III nerve palsy + contralateral hemiplegia b) Ant. Inferior cerebellar a.
(WEBER’S Syndrome) c) Post. Inferior cerebellar a. - arise from vertebral artery
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Lacunar Stroke
 Produces subcortical infarction characterized by preservation of
 80% of infarct occur in periventricular white matter & basal ganglia
 Some common syndromes are:
 Generally vascular lesions in territory of these vessels will
produce cerebellar signs & also Brainstem signs (as discussed
above which includes (A) SCA syndrome, (B) AICA syndrome & (C)
PICA syndrome/lateral medullary syndrome
2. Paramedian Branch Occlusion
 Produced by occlusion of penetrating midline branches of basilar
artery
MIDBRAIN
 red nucleus (outflow of opposite
hemisphere)  contralateral tremor
 Complete/partial III nerve paralysis
PONS
 VI nerve palsy + ipsilateral facial (VII)
weakness
 Medial lemniscus: contralateral
sensory loss (light touch &
proprioception)
MEDULLA
 At this level, bilateral damage
are common resulting in
 LOCKED-IN SYNDROME: pt is
paralysed but some facial/eye
movement are preserved
 Medial lemniscus: loss of
‘discriminatory sensation’
cortical function (language, other cognitive & visual functions)
Pure motor hemiplegia:  Lenticulostriate artery (MCA)
 Equal weakness of contralateral
face, arm, & leg + dysarthria
Pure sensory stroke  Thalamogeniculate artery (PCA)
 Numbness & tingling of
contralateral face & limbs
Dysarthria-clumsy hand  Perforating branch of basilar
syndrome artery
*lesion of dorsal pons  Dysarthria d/t weakness of
ipsilateral face & tongue
Ataxic Hemiparesis  Perforating branch of basilar a.
 Mild hemiparesis with more
marked ipsilateral limb ataxia
Severe dysarthria + facial  Lenticulostriate artery
weakness  Dysarthria, dysphagia, mutism
Lesion of anterior limb  No / mild limb weakness
Pathogenesis (ISCHEMIC Cascade)
ATP depleted  failure of pump  influx of Ca2+ (depolarization)
↓  Antiplatelet: aspirin is the only drug approved
1. Release of neurotransmitter including glutamate  excitoxicity
 further Ca2+amplify initial ischemic insult
2. ↑Ca2+ also activates various degradative enzyme 
destruction of cell membrane & other structures
3. Production of free radicals, nitric oxide, A.A  damages cell
Pathology
 4-12 hours: gross & histology of brain is normal
 36-48 hours: necrotic tissue become swollen & softer, demarcation
of white & gray matter become poor (edema)
 3rd day: macrophage infiltrate & phagocytose necrotic tissue 
better demarcation
 1month: softening & liquefaction  irregular cavities
 6 month: completely liquefied
Investigation
1. Confirmation of Diagnosis
a) CT scan:
 Infarction : low density lesion which conforms to a vascular
territory
 Hemorrhage : High density lesion even without contrast
 Identify site & size of infarct  prognostic value
b) MRI
2. Demonstrate Site of Primary Lesion
a) Cerebral angiography:
 “gold standard” to identify atherosclerotic stenosis
 Also identify other pathologies e.g. vasculitis, aneurysm,
intraluminal thrombi
b) Ultrasound:
 Doppler / Duplex scanning: assess the flow velocity
Management for Acute Ischemic Stroke
1. Medical support: (optimize perfusion to ischemic penumbra(viable))
 Mild hypertension is preferred : ↑collaterals
 ↓B.P only if : malignant HPT, MI or > 185/110 mmHg
 Edema (peaks 2nd/3rd day): water restriction & IV mannitol to ↑
reduce osmolarity but hypovolemia is avoided to prevent
hypotension
2. Intravenous thrombolysis:
 Administration of rt-PA within 3hour of onset showed benefits
 Rapid recanalization of occluded vessels
 Risk of hemorrhage ↑in ↑infarct, longer time from onset,↑dose
 Use of Streptokinase shows ↑risk of intracranial hemorrhage &
have been suspended
3. Endovascular techniques:
 Mechanical thrombectomy as an alternative to patients who are
ineligible for thrombolytics
 Restoration of patency within 8hr of onset of symptoms
4. Antithrombotic treatment
 Anticoagulants
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Transient Ischemic Attack Pathology
 Sudden loss of neurologic function usually within seconds, & lasts for 1. Common site (in decreasing order): c) branches of MCA
minutes to hours ( but <24hours) Basal ganglia(putamen & ext. capsule)  thalamus  white matter
 Consciousness is usually preserved, complete recovery  pons  cerebellum  1/3 of cases rupture during acute ↑ICP: straining at stool / orgasm
 Causes: *in hypertensive patient: up to 70% in basal
a) microemboli b) ↓cerebral perfusion ganglia & thalamus
 May herald thromboembolic stroke 2. Brain midline structures are asymmetrically
 Findings: distorted
Anterior circulation Posterior circulation 3. Various patterns of herniation can be seen
Amaurosis fugax, aphasia, Diplopia, vertigo, vomiting, 4. Haematoma may expand for several hours
hemiparesis, hemisensory loss, choking, ataxia, hemianopia, following initial hemorrhage
hemianopia tetraparesis, dysarthria 5. Hematoma may dissect into:
Ventricles & Subarachnoid space
 Amaurosis Fugax: sudden transient loss of vision of an eye.
6. For patient who survive hemorrhagic stroke:
ICA stenosis  embolization  pass thru retinal artery  AF
resorption of hematoma  cystic(fluid) cavity lined by gial neuropil
Hemorrhagic Stroke / Intraparenchymal stroke Pathogenesis
Investigation Weak tunica media at branch point chronic hemodynamic injury
1. CT scan: determine the exact site & size of hematoma
Epidemiology:
2. CT angiography Saccular aneurysm enlargement
Peak incidence at age 60
↓
Prognosis ↑risk of rupture if 6-10mm:
Etiology
 Overall mortality : 25-60% “Thunderclap” headache, vomiting, loss of consciousness (COMA)
1. Hypertension : most common
 Poor prognosis: large & deep lesion, intraventricular blood, LOC Neck stiffness & Kernig’s sign
2. Cerebral amyloid angiopathy
 Good prognosis: small & superficial lesion, conscious patient CSF: bloody  xantochromic(yellow)
3. Aneurysm
4. Atriovenous malformation ↓
5. Coagulation disorder Management If it doesn’t rupture & reach >25mm: ↓risk of rupture
6. Others: vasculitis, drug abuse, trauma 1. Medical: **signs & symptoms more on mass effects
Hypertension should be controlled to prevent enlargement of
hematoma Complication
Pathogenesis
2. Supratentorial hematoma: conservative approach is applied as  Organization of blood in arachnoid granulation  hydrocephalus
Hypertension
operative evacuation showed no difference in outcome  Brain parenchyma infarction: d/t arterial spasm
3. Cerebellar hematoma:  Rebleeding tendency
Abnormalities in Vessels wall Development of Charcot-
 Small hematoma (<1cm): conservative
1. accelerated atherosclerosis Bouchard microaneurysm
 Large hematoma (>3cm): surgical decompression Morphology
(e.g. hyaline arteriosclerosis in Minute aneurysm in small
small vessels: weak) arterioles most commonly in  >1cm & <3cm: put under careful observation for deterioration  Small (<3mm) rounded bulges usually at arterial bifurcation
2. Necrosis of arterioles in severe BASAL GANGLIA 4. Pontine hematoma: ↑ mortality, conservative approach  Depending on its location, it might bleed in subarachnoid space
cases
Subarachnoid Hemorrhage Investigation
Vulnerable to rupture Spontaneous arterial bleeding into subarachnoid space of dramatic 1. CT scan: investigation of choice where subarachnoid &
↓ onset & accounts for 5% of stroke interventricular blood can be seen
Intracranial Hemorrhage 2. Lumbar puncture & CSF analysis: uniformly blood stained or
Etiology: ‘xantochromic’(d/t breakdown products of Hb >6 hrs after onset)
Haematoma & edema ↑Intracranial P Localizing sign may 1. Rupture of saccular/berry aneurysm ( most common): 3. CT/MR angiography: non-invasive techniques to demonstrate the
↓ ↓ be present but are  ↑Incidence in shape & size of the neck
Mass effect Severe headache difficult to detect Genetic: Polycystic Kidney Disease, fibromuscular dysplasia,
↓ vomiting in the presence of fibromatosis type 1, coarctation of aorta Management
Brain Herniation & brain stem Rapid loss of Coma & massive Social: hypertension, smoking 1. Bed Rest & supportive measures: to prevent rebleeding
compression consciousness ↑ICP 2. AV malformation 2. Medical: control hypertension to ↓ pressure
↓ ↓ 3. Uncommon: Tumor,Bleeding Diathesis, Vasculitis 3. Operative techniques:
Deep coma Int. capsule: a) direct clipping of aneurysm neck without compromising proximal
spasticity hemiparesis Saccular/Berry aneurysm: or distal vessels
Cheyne-Stokes respiration  Common sites are: b) coil embolization: helical platinum coils are packed into aneurysm
Dilated , non-responsive pupils a) Junction of ACA & ant. Communicating a fundus
b) Junction of ICA & post. Communicating artery Joen