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Neurology:

The Vascular System


Lecturer: Ma. Regina Victoria Reyes, MD


Transcriber: Patrick Angelo R. Bautista August 2019

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

Anterior Cerebral Artery (ACA) supplies the medial surface of the


cerebrum
Middle Cerebral Artery (MCA) supplies the dorsolateral surface of
the cerebrum
Posterior Cerebral Artery (PCA) supplies the entire occipital lobe
inferior and medial portions of
temporal lobe
Lenticulostriate Arteries supplies the Deeper structures of the
cerebral hemispheres
arise from penetrating branches of
larger arteries



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

ACA and the Motor Homunculus • Longitudinal


• The ACA supplies the medial surface including the representation of o 1 Anterior Spinal Artery (ASA) – arises from the vertebral artery;
the leg of the homunculus. supplies the anterior 1/3 of the spinal cord
o 2 Posterior Spinal Arteries (PSA) – 25% arises from the vertebral
Blood Supply to the Posterior Fossa artery but most (75%) arises from posterior inferior cerebellar

artery; supplies the posterior 2/3 of the spinal cord
Branches of Vertebral and supplies the Brainstem & Cerebellum
• Horizontal
Basilar Arteries
o 6 – 8 Radicular Arteries
• At each level of the brainstem, short median and paramedian § ventrally located; that arise from intercostal, lumbar and
perforating branches arise and supply a zone on either side sacral arteries; these radicular arteries connect with the ASA
• The lateral areas of brainstem and cerebellum are supplied by 3 at various levels
pairs of long circumferential arteries (PICA, AICA, SCA)

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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

Superior petrosal Confluence


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:

F E U – N R M F Department of M E D I C I N E Section of N E U R O L O G Y Cerebral Blood Flow


o superior sagittal sinus

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

drain into the transverse sinuses



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

• Compute for the MAP of an individual with BP of 210/120 mm Hg


• A: 120 + [(210 – 120) ÷ 3] = 150 or [210 + 2(120)] ÷ 3 = 150

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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

Systemic BP MAP <50 – 70 mmHg


CV Function Arrhythmias, Orthostatic
hypotension, loss of
carotid sinus and aortic
arch reflexes
Blood viscosity Anemia Polycythemia
Intrinsic
State of cerebral Arteriovenous Atherosclerosis
BV malformation
ICP Increased ICP
Cerebral auto regulatory mechanism
Myogenic factors ↓ intraluminal pressure ↑ intraluminal pressure
Neurogenic Parasympathetic Sympathetic
Cerebral Metabolism
factors
• High metabolic activity and high oxygen consumption characterize
Biochem – ↓ pH (Acidosis) ↑ pH (Alkalosis)
cerebral metabolism.
Metabolic Lactic Acid
• A constant supply of energy is necessary for the support of neuronal

and neurologic functions (establishment of membrane potentials,
Regulation of Cerebral Blood Flow
maintenance of transmembrane ionic gradients, membrane
Autoregulation transport, and the synthesis of cellular constituents such as proteins,
• The normal brain is able to regulate its own blood supply, nucleic acids, lipids, and neurotransmitters).
autoregulation, in response to changes in arterial blood pressure • The energy needed is supplied in the form of high energy phosphate
and metabolic demand. bonds from ATP, which is synthesized in the brain, as in other organ
systems, through: Glycolytic pathway, the Krebs (Citric Acid) Cycle,
• Autoregulation is defined as the ability of an organ (e.g., the brain) and the Respiratory (Electron Transport) Chain.
to maintain blood flow constant for all but the widest extremes in
perfusion pressure. • Aerobic Conditions
• Autoregulation of cerebral blood flow occurs when the mean arterial o Glucose is metabolized through the glycolytic pathway, citric
Cerebral Blood Flow Cerebral Blood Flow
blood pressure is between 60 and 150 mm Hg. acid cycle (Krebs’), and respiratory chain.

Autoregulation of
o Yields 38 moles of ATP / mole of glucose
Hypertensive
normotensive individuals
individuals
• Anaerobic Conditions
o The Krebs’ cycle and respiratory chain cannot be activated;
Shift to the right o the pyruvate derived from glycolysis is metabolized to lactate
and yields only 2 moles ATP / mole of glucose

• Glucose is the basic substrate for brain metabolism.
o The astrocytes store glycogen and are the source of lactate,
• When it is less than 60 mm Hg, blood flow decreases, and when it is
FEU–NRMF MEDICINE N E U RFOELUO–GNYR M F
which can be used by neurons to produce glucose.
Department of Section of MEDICINE
Department of NEUROLOGY Section of

more than 150 mm Hg, blood flow increases.


• Autoregulation is achieved with myogenic, neurogenic, and • Creatine phosphate
chemical-metabolic mechanisms. o Another source of high-energy phosphate bonds
o More abundant than ATP in the brain, used to regenerate ATP
• Autoregulation occurs in both large and small arterioles. from ADP, thus important for maintaining level of tissue ATP
• It is a major homeostatic and protective mechanism.
If there is reversible alteration in the cerebral function, like lack of
• Cerebral vessels, like other hollow organs that contain smooth oxygen will result to ischemia and becomes irreversible causing
muscle, can change diameter in response to intraluminal pressure. infarction (ischemia – not totally blockage of flow; infarction – necrotic
• This effect, called the Bayliss effect, results in vasoconstriction with tissue) so after the vessel occlusion and deprivation of blood flow to the
increased intraluminal pressure and vasodilatation with decreased brain, a series of events and ischemic cascade can lead to neuronal
intraluminal pressure. dysfunction and neuronal death.

• Therefore, autoregulation is primarily a pressure- controlled
myogenic mechanism that operates independently but synergistically
with other neurogenic and chemical-metabolic factors.

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Pathophysiology III. PATHOLOGY OF THE VASCULAR SYSTEM
• Reversible alteration in cell function from the lack of oxygen results

in ischemia, and irreversible alteration results in infarction. Normal Arterial Histology


• After vessel occlusion and deprivation of blood flow to the brain, a • Intima – layer of endothelial cells surrounding the vessel lumen with
series of events unfold, the ischemic cascade that lead ultimately to a small amount of extracellular connective tissue, the internal elastic
neuronal dysfunction and death. lamina

• Media – diagonally-oriented smooth muscle cells surrounded by
collagen and mucopolysaccharides
• Adventitia – fibroblasts and smooth muscle cells with collagen and
MPS

Intracranial Arterial Aneurysm


• An abnormal, localized dilatation of the arterial lumen
• Most commonly encountered type is a round or oval- shaped,
• Decreased cerebral blood flow (CBF) produces a gradient of severity berry-like structure, arising at the bifurcation of the cerebral vessels
of deprivation of oxygen and glucose in brain tissue. • Due to a defect in the media and internal elastic lamina
• Ischemic Penumbra – area of jeopardized brain tissue between the

area of infarction and normal tissue


o Neurons in this region have potentially reversible
electrophysiologic failure due to energy deprivation but have not
experienced the cascade leading to neuronal death.
o The ischemic penumbra is the target of neuroprotective
treatment in ischemic stroke

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

Unstable Plaque – has tendency to dislodged and will travel to brain to


become embolus that will produce stroke (EMBOLIC STROKE)


• Severe atheromatosis of basal arteries.
• Confluent yellow atheromatous plaques
occur in the arterial walls.
• The basilar artery is elongated and stiff, and
the lumen is distended.

Hemorrhagic Strokes
• Atheromatous plaque in the wall of the Intracerebral Hemorrhage
basilar artery shows focal subintimal
cholesterol clefts, disruption of the
elastic lamina, and marked intimal
proliferation severely reducing the
lumen.

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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