Post on 31-Aug-2019
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
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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
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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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