Cerebral Vascular Diseases

Nabila Hamdi

MD, PhD

Outline

I. Stroke statistics

II. Cerebral circulation

III. Clinical symptoms of stroke

IV. Pathogenesis of cerebral infarcts (Stroke)

1. Ischemic

- Thrombotic

- Embolic

- Lacunar/small vessel disease

2. Hemorrhagic

- Primary brain parenchymal hemorrhage

- Subarachnoid hemorrhage & saccular aneurysm

V. Traumatic brain vascular injury

- Epidural hematoma

- Subdural hematoma

2

ILOs

1. To distinguish ischemic stroke from hemorrhagic stroke in terms of etiology

and pathology

2. To know the most common causes of ischemic infarcts

3. Explain “small vessel disease”, mention 2 conditions that cause it and

know its effects on the brain

4. Know 4 different causes of intracerebral hemorrhage

5. Understand the role of hypertension in the pathogenesis of hemorrhagic

strokes

6. Explain the subarachnoid hemorrhage resulting from the rupture of

saccular aneurysms

7. Distinguish intracerebral hemorrhage from traumatic brain hemorrhages

8. Differentiate between epidural and subdural hematoma

3

Stroke Statistics • About 795,000 Americans each year suffer a new or recurrent

stroke. That means, on average, a stroke occurs every 40 seconds.

• No. 3 cause of death after cardiovascular diseases and cancer

• About 1 of every 18 deaths.

• On average, every 4 minutes someone dies of stroke.

• Of all strokes, 87% are ischemic, 10% are intracerebral

hemorrhages, and 3% are subarachnoid hemorrhages

• The estimated direct and indirect cost of stroke for 2009 is $68.9

billion (inpatient care, rehabilitation and follow-up care necessary

for lasting deficits) 4

Cerebral Circulation

5

http://mauryillustrates.com/anatomical.html Neuro4Students, Cerebrovascular attack

Cerebral Circulation

Circle of Willis: major

source of collateral flow

little if any collateral flow for

the deep penetrating vessels

(thalamus, basal ganglia, and

deep white matter)

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Stroke

Ischemic (Clots) 87%

Hemorrhagic (Bleeds) 13%

Ischemic injury/infarction

of specific regions of the

brain, depending on the

vessel involved.

Hemorrhage leads to direct

tissue damage as well as

secondary ischemic injury

“Stroke”

3% subarachnoid hemorrhage

10% intracerebral hemorrhage

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Stroke

Focal neurological deficit

Longer than 24 hours Less than 24 hours

(minutes)

Stroke Transient ischemic attacks (TIAs)

No permanent tissue damage Permanent tissue damage

1/3 of patients with TIA develop clinically

significant infarcts within 5 years

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Signs & Symptoms of Stroke

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Signs & Symptoms of Stroke • Hemiplegia: Sudden paralysis of a leg, arm or one side of the face

• Hemiparesis: Sudden numbness or weakness of arm, leg or face

• Consciousness: +/- loss of consciousness

• Aphasia: loss/impairment of the power to use or comprehend words.

• Dysarthria: affects the mechanics of speech.

• Amaurosis fugas sudden loss of vision in one or both eyes: “gray or black

shade coming down over their eye”

• Hemianopsia: loss of half of the visual field.

• Ataxia: Sudden trouble walking, dizziness, loss of balance or coordination,

leading to difficulty in walking normally

• Vertigo (spinning form of feeling dizzy)

• Sudden severe headache with no known cause

• Memory, emotions, orientation,

• Incontinence

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Warning Symptoms of Stroke

Does one side

of the face

droop or is it

numb? Ask the

person to smile.

Is the person's

smile uneven?

Is one arm

weak or

numb? Ask the

person to raise

both arms.

Does one arm

drift

downward?

Is speech slurred? Is

the person unable to

speak or hard to

understand? Ask the

person to repeat a

simple sentence. Is the

sentence repeated

correctly?

even if the symptoms

go away, call

emergency and get the

person to the hospital

immediately. Check the

time so you'll know

when the first

symptoms appeared

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Ischemic Stroke

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Modifiable Non modifiable

Hypertension Age >55

Diabetes Male gender

Atrial fibrillation Black race

Smoking Family history of stroke

Hyperlipidemia Personal history of stroke

Carotid stenosis Sickle Cell Disease

Lack of physical activity

Definition:

Ischemic stroke or cerebral infarct is a focal brain necrosis due to complete and

prolonged ischemia that affects all tissue elements, neurons, glia and vessels.

Risk factors:

Major Causes:

1. Atherosclerosis

2. Embolisms

3. Small vessel disease

4. Vascular spasm (following hemorrhagic stroke)

5. Other: Vasculitis, hypercoagulability, dissection of a vessel wall, sickel cell disease….

Ischemic Stroke

Neuro4Students

Cerebrovascular attack

1. Atherosclerosis (most common cause)

Kindly refer to CVS lecture

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Left MCA Right ACA

Left PCA

Neuroradiology Unit, S P Institute of Neurosciences,Solapur,Maharashtra, INDIA

Radiology department of the Rijnland Hospital in Leiderdorp, the Netherlands

14 Lacunar infarct

Ischemic Stroke

Cerebrovascular anatomy and common sites of atherosclerosis

Risk factors !

Atheromatous plaques can cause narrowing or

occlusion of the vascular lumen by themselves

or after rupture and thrombosis

Bifurcation points of large arteries & major

cervical and intracranial arteries (blood flow!)

Atherothrombotic infarcts evolve within hours

or days

The most severe atherosclerotic lesions are

typically encountered within large vessels

However, Some patients have an

asymptomatic occlusion of a cervical internal

carotid artery ?!

1. Atherosclerosis

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Ischemic Stroke 2. Embolism

UCSF Department of Surgery , The University of California, San Francisco

Most emboli are fragments of blood clot

that originate in the heart or major vessels

MI, atrial fibrillation and other

arythmias, endocarditis…

Rarer causes are fat, air and tumor

emboli

Embolic infarcts have an abrupt onset

Assumed if:

- source of embolism is present

- multiple infarcts in the brain

- infarcts in other organs

- absence of atherosclerosis

- absence of other vascular disease 16

Ischemic Stroke 3. Lacunar Infarcts

Occlusion of deep penetrating branches of

major cerebral arteries

Deeper parts of the brain (basal ganglia,

thalamus, deep white matter) and brain stem.

The infarcts are generally from 2-20 mm in

diameter

Typically, no impairments in cognition,

memory, speech, or level of consciousness

(cortex not affected)

Atherosclerosis of small arteries

Small vessel disease; hyaline

arteriosclerosis in hypertension and

diabetes, but occurs in old age w/o these

predisposing conditions.

Lacunar stroke

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Intracranial Hemorrhages

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Primary Brain Parenchymal

Hemorrhage

Subarachnoid Hemorrhage

(Saccular Aneurysms)

Epidural Hematoma Subdural Hematoma Traumatic

Non-

Traumatic

Primary Brain Parenchymal Hemorrhage

Spontaneous, nontraumatic intraparenchymal

hemorrhages

Rupture of small penetrating arteries (basal

ganglia & thalamus)

Accounts for 15% of deaths among patients

with chronic hypertension

Hypertension is the most underlying cause

Small vessel disease: arteriolar walls affected

by hyaline change are weaker than normal

vessels and are therefore more vulnerable to

rupture.

Other causes: aging, smoking, oral

contraceptives, drug abuse, excessive alcohol

intake

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Primary Brain Parenchymal Hemorrhage

Massive hypertensive hemorrhage

rupturing into a lateral ventricle

Brain is asymmetrically distorted (mass

effect + associated edema)

Hematoma may dissect into the ventricles

Onset is always abrupt with evidence of

increased intracranial pressure: severe

headache, vomiting, seizures, rapid loss of

consciousness, papilledema (swelling of

optic disc)

Risk of herniation of cerebellum and

brain stem compression deep

coma, irregular respirations, dilated non-

responsive pupils and spasticity

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Cerebellar tonsils are pushed through

the foramen magnum into the spinal canal Normal cerebellar tonsils

Cerebellar Herniation

Mayfield Clinic, University of Cincinnati Department of Neurosurgery

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Subarachnoid Hemorrhage

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Subarachnoid Hemorrhage

Relative frequency of common sites of saccular (berry) aneurysms

in the circle of Willis

Rupture of saccular aneurysms is the most

common cause of nontraumatic SAH

Saccular (berry) aneurysms are present in

1% of the general population

Arise most commonly at arterial bifurcations

in the territories of ICA

To a less extent in posterior (vertebrobasilar)

circulation

Enlarge with time and are at greatest risk

for rupture once they reach 6-10 mm in

diameter

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Subarachnoid Hemorrhage

SAH resulting from rupture of saccular aneurysm is less common than primary cerebral

hemorrhage, with women being more affected than males with most cases before age of

50

Abrupt onset with severe headache, often described as the "worst headache of my

life”, vomiting and loss of consciousness (increased ICP)

Meningeal signs are usually present (neck rigidity and pain, back pain, and bilateral leg

pain).

Seizures during the acute phase of SAH occur in 10-25% of patients. They result from the

sudden rise in ICP or direct cortical irritation by blood.

Blood in CSF(lumbar punction)

50% dye within several days of onset of symptoms

Might be acutely complicated by cerebral infarcts (arterial spasm), acute hydrocephalus

(increased accumulation of CSF in ventricles) and herniation . 24

Traumatic Vascular Injury

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Traumatic Vascular Injury

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C. Large organizing subdural

hematoma attached to the dura

B. Epidural hematoma covering

a portion of the dura

Epidural Hematoma Neurosurgical emergency

Rupture of a meningeal artery

Middle meningeal artery, fracture of

temporal bone

Compression of subjacent dura

Risks: herniation, brain stem compression

and death

“Lucid interval” is typical: time in which

the conditions of the patients improve after a

head trauma before deteriorating (loss of

consciousness)

Neurosurgical emergency requiring prompt

drainage

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Rescuers say that he maintained

consciousness when they first reached

him, but his health quickly deteriorated

http://www.thedailybeast.com

Subdural Hematoma

Tearing of bridging veins that extend from brain surface to dural sinuses

Rapid change in head velocity: head blows, violent shaking in infants

In elderly, even after minor trauma: brain atrophy, veins are stretched out

(more space for movement)

Size vary from small to massive hemorrhage with mass effect

Sudden and progressive worsening of symptoms

No “lucid interval”!!

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References

• ROBBINS Basic Pathology 8th Edition

• Cerebrovascular diseases, Clinical aspects. Dr. Michael

P. Merchut

• FERNE: Foundation for Education and Research in

Neurological Emergencies, Stroke Pathophysiology, Sid

Shah, MD

•

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