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Clinical Case: A 50-year-old man experienced sudden onset of vertigo. Neurologic • vertebral arteries enter the cranium through – foramen magnum
examination showed dysarthria, difficulty with swallowing, left Horner syndrome, • at the junction between medulla and pons, the 2 vertebral arteries
left palatal weakness, and loss of pain sensibility over the left face and right limbs unite to form a single basilar artery
and trunk. He had coarse ataxia and incoordination of his left arm. • at the junction between pons and midbrain, the basilar divides into
right and left Posterior Cerebral Artery
A. Where is the location of the lesion?
Infratentorial Area affecting the brainstem & cerebellum
B. What is the vascular supply of this region? Posterior Inferior Cerebellar Artery • All arteries that supply the supratentorial (cerebral cortex) and
C. What is the most likely etiology? Diagnosis? Ischemic Stroke infratentorial / posterior fossa arise from the aortic arch.
I. ANATOMY OF THE VASCULAR SYSTEM • The aortic arch will form the brachiocephalic, left common
rd
carotid, and left subclavian artery (3 branch)
• Anterior Circulation • Posterior Circulation st
o The brachiocephalic artery (1 branch of aortic arch) which
o From carotid system o From vertebral system forms the right common carotid artery and right subclavian
o Supplies 80% of brain o Supplies 20% of brain artery, will supply the right side of the neck, arm and head.
nd
o Left CCA (2 branch) is the direct branch of aortic arch.
• The vertebral artery originates from the subclavian artery.
• Vertebral artery has four parts namely:
o V1 preforaminal – before it enters the transverse foramen
o V2 foraminal – where it inserts at the transverse foramen of
the cervical arteries starting from C6 going to C2
o V3 extradural – arises from C2 before it pierces the dura
o V4 intracranial – the only intracranial segment; placed
st
between the hypoglossal nerve and anterior nerve of the 1
cervical nerve.
• All arteries that supply the supratentorial and posterior fossa arise
from the aortic arch The Vertebral Arteries in Relation to the Cervical Vertebrae
o Anterior circulation = internal carotid artery • V1 – preforaminal part, located behind the
o Posterior circulation = vertebrobasilar system internal jugular vein then it will run in the
transverse foramen of C2-C6 and surrounded
by the branches of the inferior cervical
sympathetic chain.
• V2 – foraminal part, where it inserts at the
transverse foramen of the cervical arteries
• V3 – extradural or the Atlantic part, located
at the C2/atlas transverse foramen
transversarium at the medial side of rectus
capitis lateralis then it will pierce the dura to
become the V4
• V4 – intracranial part (pierce the dura to
become Basilar artery)
Circle of Willis
• A heptagon composed of:
o 2 anterior cerebral arteries
o 1 anterior communicating artery
o 2 posterior cerebral arteries
o 2 posterior communicating arteries
Right common carotid artery originates from brachiocephalic artery. MIDDLE CEREBRAL ARTERY IS NOT PART OF THE CIRCLE OF WILLIS.
Common carotid artery will give branch to external and internal carotid Posterior cerebral artery connects to internal carotid artery by inferior
artery. The one that goes to the brain is the Internal carotid artery communicating artery
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Blood Supply to the Cerebral Hemispheres
Anastomoses and Collateral Circulation
• Circle of Willis
• Corticomeningeal anastomoses
o communication of the 3 major cerebral vessels on the surface of
the hemispheres at the junctional zones of the areas supplied by
these vessels
• Anastomoses between Extracranial and Intracranial arteries
o The ophthalmic artery communicates with the superficial
temporal and facial branches of the external carotid artery
Functional Anatomy of the Cerebral Vasculature
• Clinically, the distribution of a presumed arterial lesion can be
inferred by relating the observed signs and symptoms to the
anatomy of the cerebral vessels.
• A1 – proximal portion, arises from the internal carotid artery and • It is essential to be able to determine whether a lesion lies in the
extends in the anterior communicating artery which supplies distribution of either the carotid (anterior circulation) or
caudate and anterior limb of the internal capsule vertebrobasilar (posterior circulation) arterial systems.
o posterior limb is in the corticospinal tract (supplied by MCA)
• A2 – extends from the anterior communicating artery to the Carotid System Vertebrobasilar System
bifurcation it is where the recurrent artery of Heubner arises. Hemiparesis (contralateral) Hemiparesis (crossed)
o It is affected in syphilitic vasculitis Hemisensory loss (contralateral) Hemisensory loss (crossed)
• A3 – Pericalosal artery. One of the main branches of ACA gives rise
Homonymous hemianopsia Diplopia (double vision)
to calosomarginal and pericalosal which supplies corpus callosum
Monocular Vision Loss Dysphagia
Aphasia Dysarthria
Clinical Correlations
Dysequilibrium and or
MCA and the Motor Homunculus incoordination
• The MCA supplies the lateral surface of the cerebral hemisphere,
including the representations of the face and arm of homunculus Blood Supply to the Spinal Cord
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• The deep white matter and deep nuclei of the brain drain into the
deep venous system, which includes the great cerebral vein of
Galen, inferior sagittal sinus, and straight sinus.
Blue arrow – ASA | Green arrow – PSA
• The largest of these radicular • From these venous channels, blood empties into the transverse
arteries is located in the low sinuses, sigmoid sinuses, and ultimately the jugular veins.
thoracic or upper lumbar region
(Artery of Adamkiewicz)
• Because of this uneven blood supply,
the spinal cord is most vulnerable to
ischemia at the midthoracic and
upper lumbar levels (black areas →)
• Veins on the inferior surfaces of the cerebral hemisphere end
directly or indirectly in the Cavernous Sinus.
Venous Drainage of the Nervous
Venous Drainage of the Nervous System System
o located on either side of the pituitary fossa and contains the
Superior sagittal carotid artery; CN III, IV, and VI; and branches of CN V
sinus Great cerebral
vein of Galen
Inferior sagittal
sinus Straight
sinus
Intercavernous Transverse
sinus sinus
Sigmoid
sinus
Inferior petrosal
sinus
• Cerebral veins drain into dural venous sinuses. II. PHYSIOLOGY OF THE VASCULAR SYSTEM
• Important sinuses to remember include the:
o inferior sagittal sinus • Normal CBF = 750 ml/min (50-55 ml/100 gm brain tissue/min)
o transverse sinus • Oxygen consumption = 50 ml/min (3.7 ml/100 gm brain tissue/min)
o sigmoid sinus • Weight of adult brain = 1,500 gm or 2% of the body weight
o cavernous sinus • Brain receives 15% of the cardiac output
• The venous drainage of the brain is divided into: • Brain utilizes 20% of the O2 consumed in the basal state (CMRO2)
o Superficial system and Deep system
• The cortical gray matter, because of its increased metabolic
• The cerebral cortex and outer half of the white matter drain in to demand, has about 6x the blood flow of white matter.
the superficial system of veins located over the convexity of the • CBF is directly proportional to the perfusion pressures (mean
brain in the subarachnoid space arterial pressure – central venous pressure); and is inversely
o The superficial veins of the superior half of the brain drain into proportional to the cerebrovascular resistance
the superior sagittal sinus, and those from the inferior half
OR
Sample Problem:
• Compute for the MAP of an individual with BP of 70/40 mm Hg
• A: 40 + [(70 – 40) ÷ 3] = 53 or [70 + 2(40)] ÷ 3 = 50
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• Several factors can modify cerebral blood flow by altering different Chemical Factors
elements in this equation. • Carbon dioxide – most potent physiologic and pharmacologic agent
• These have been divided arbitrarily into two groups: that influences cerebral blood flow.
o Extracerebral factors – factors outside the cranial cavity that • Cerebral blood vessels react rapidly to any change in local carbon
modifies or regulates cerebral blood flow dioxide tension (PaCO2).
§ Systemic BP • Any increase in PaCO2 produces vasodilatation and increases
§ Efficiency of Cardiac Function cerebral blood flow.
§ Blood viscosity
o Intracerebral factors Neurogenic Control
• Neurogenic factors do not seem to have as great a role in the
Factors Increased CBF Decreased CBF
regulation of cerebral blood flow as chemical and metabolic factors
Extrinsic
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Pathophysiology III. PATHOLOGY OF THE VASCULAR SYSTEM
• Reversible alteration in cell function from the lack of oxygen results
Picture (lower left): Conventional angiogram, AP view, showing a 7-mm left MCA
bifurcation aneurysm (arrow) after a left ICA injection
Picture (lower right): The same aneurysm (arrow) seen after three-dimensional
rotational angiography
• 📋 Hypoxia or ischemic event will result to mitochondrial failure
leading to ATP-dependent pumps failure, so once there’s failure of
pumps, it will lead to calcium accumulation and this intraneuronal
calcium accumulation will result to neuronal injury and damage in
Na-K pump will cause increase Na inside the cell that follows water
which causes cell swelling causing cytotoxic edema.
• And since there’s deprivation of glucose metabolism, it will undergo
anaerobic metabolism that will cause lactic accumulation causing
intracellular acidosis that will add up to your neuronal injury. Arteriovenous Malformation
• Developmental abnormalities often seen in
Calcium-triggered cascade young adults
• Resulted from defective communication
• large accumulation of glutamate in the extracellular space is exerted
between arteries, capillaries, and veins, with
through activation of N-methyl-D-aspartate (NMDA) and α-amino-3-
dilatation of one or more of the vascular
hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptors
elements, forming a variable-sized meshwork of
• massive entry of Ca2+ into the postsynaptic neuron
tortuous blood vessels “bag of worms”
• additional calcium-induced release of excitatory neurotransmitters
• The walls may be thin and predisposed to
during the ischemic process heightens neuronal necrosis
rupture, or may be hypertrophic.
• the increase in intracellular Ca2+ activates phospholipases,
• Rapid shunting of blood
proteases, and endonucleases and generates oxygen free radicals
may produce a chronic
and nitric oxide. This leads to membrane, mitochondrial DNA, and
ischemic state in the
microtubular damage and, eventually, cell destruction.
neighboring brain (steal)
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Atherosclerosis Stroke Subtypes
• The most important pathologic lesion responsible for cerebral
infarction
• Basic pathologic lesion – atherosclerotic plaque
• The intima is the layer that is principally involved (injury to arterial
wall causes focal desquamation of the endothelial cells exposing the
subendothelial connective tissue to the circulating platelets)
• Affects large-caliber blood vessels
From Left to Right:
1. Monocyte Adhesion
2. Monocyte Migration
3. Foam cell formation Ischemic Strokes
4. Proliferation of Smooth Muscle Cells
Large Vessel Infarcts
5. Platelet Adhesion, Activation and Aggregation
• The area of infarction is localized to the
distribution of a diseased blood vessel
• With the passage of time, the necrotic tissue
in an infarcted area is removed by phagocytes
and replaced by a cavity containing cystic
fluid surrounded by an area of glial tissue
• In patient presented with hemiparesis,
hemianesthesia, and hemianopia- the
occlusion will be in the MCA
Lacunar Infarcts
Fibrinoid Necrosis
• A segmental, non-atherosclerotic
arteriopathy
• aka lipohyalinosis, arteriolar sclerosis
• Affects primarily smaller intraparenchymal Subarachnoid Hemorrhage
blood vessels
• Found almost exclusively in the brains of
hypertensive patients
• Pathology: fibrinoid material and lipid-laden
macrophages in the subintimal layer
• Some of these lesions show progressive
luminal obliteration and eventually result in
small areas of infarction called lacunae
• Others produce progressive weakening of the vessel wall and
microaneurysm formation and eventually rupture, producing an
intracerebral hemorrhage
Reference: PPT by FEU-NRMF Department of Medicine; 3C Batch 2020 Trans
No Proofreading done; Use at your own risk.
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