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CEREBROVASCULAR
DISEASE
CEREBROVASCULAR
DISEASE
“STROKE”
• Macrovascular disease
• Microvascular disease
• Emboli
• Venous thrombosis
Blood supply to the brain - or better, the
supratentorial level,
posterior fossa level and
(upper) spinal level.
Describe the “two”
vascular arterial supplies
to the intracranial
compartment, and their
distribution to the portions
of the neuraxis
Closer view of the
vertebral-basilar and
carotid arterial systems.
Know their distribution,
branches, “territories”
and syndromes
associated with the
named vessels.
Mid sagittal view of the supratentorial level and posterior fossa level
with their respective blood supplies. The vertebral-basilar vessels
supply a portion of the supratentorial level.
Angiography to demonstrate the middle cerebral
artery. The utility of a number of imaging techniques
allows for the demonstration of vascular integrity and
disease in vivo.
The blood vessels of the “base” of the brain and their
distribution.
Vessels of the supratentorial level, medial left
hemisphere.
Which is carotid, and which is vertebral-basilar?
Vessels of the supratentorial level, medial left
hemisphere.
Which is carotid, and which is vertebral-basilar?
Sometimes there appears to be less significance given
to the veins, but their location and distribution give
rise to some interesting findings, especially in
hypercoagulable states, and trauma.
Blood drains from the veins into the sinuses,
the dural sinuses.
Define and differentiate hypoxia,
ischemia and infarction
Discuss the etiology and pathogenesis
of ischemic encephalopathy
Define and differentiate hypoxia,
ischemia and infarction
STRAIGHT FROM ROBBINS
Discuss the etiology and pathogenesis
of ischemic encephalopathy
Ischemic (hypoxic) Encephalopathy
Vulnerability to ischemia
Neurons
First to die
Glial cells
Tissue necrosis
Prolonged ischemia
Mechanism of neuron cell death
Excitotoxin release
Persistent opening of NMDA receptor channels
Influx of Ca++
NO toxicity
Why is this important? NO synthase inhibitors protect
against effects of ischemia in some model systems!!!!
Treatment for ischemia?
Define and differentiate hypoxia,
ischemia and infarction
Discuss the etiology and pathogenesis
of ischemic encephalopathy
STRAIGHT FROM ROBBINS
Ischemic encephalopathy
Episodes of hypotension
Transient (if mild)
Severe global ischemia
Survivor = persistent vegetative state
Isoelectric (flat) EEG
Respirator brain
Morphology
Brain swollen
Flat surface
Poor gray-white distinction
Acute neuronal changes (12 - 24 hours)
Glial cell death
Vulnerability factor
Necrosis, macrophages, vascular
proliferation, gliosis
What is a watershed infarct,
and how does it relate to the
discussion of ischemic
encephalopathy?
Vessels of the supratentorial level, medial left
hemisphere.
Which is carotid, and which is vertebral-basilar?
Differentiate between ischemic
and hemorrhagic (white vs.
red) infarcts, and define the
most likely causes of each
A
B
A
B
Infarct, acute. Acute infarcts may be red or white, hemorrhagic or ischemic,
leaks or plugs. In A, the lesion is an acute hemorrhage. In B, on the right, the
lesion is ischemic, with secondary congestion of the tissue, but no large
hemorrhage. “A” could be caused by a ruptured aneurysm (hypertensive, for
example) whereas (B) would be caused by a thrombus. Note that in B, the
damage is confined to the territory of the middle cerebral artery,
What is the lesion on the left side of picture B?
Differentiate between thrombotic and
embolic infarction, and given a
gross or microscopic picture, be
able to recognize the difference
between the two
CEREBROVASCULAR
DISEASE
“STROKE”
• Macrovascular disease
• Microvascular disease
• Emboli
• Venous thrombosis
STROKE: EPIDEMOLOGIC
FACTORS
• 0.5 million / year
• 3 X 106 ‘survivors’
• 150,000 deaths / year
• Incidence
100 / 100,000 ages 45-54
1800 / 100,000 ages 85+
• Risk factors
• Infarction 10 X > Hemorrhage
STR0KE: RISK FACTORS
MAJOR FACTORS
• Age
• Family history
• Diabetes Mellitus
• Cigarette smoking
• Hypertension
• Lipid Metabolism
• Truncal obesity
OTHER FACTORS
• Oral contraceptives
• Hematologic
Sickle cell
Polycythemia
• Coagulation disorders
• Cardiac disease
• Vascular disease
ATHEROSCLEROSIS &
STROKE
• Documented risk factors
• TIA -- common presentation
• TIA -- high risk
• Embolization
• Occlusive thrombosis
Extracranial -- common
Intracranial -- less often
Vascular, acute thrombosis. The hemostat is positioned to show the
internal carotid artery on the right (yellow arrow) in which there is a
fresh thrombus. The patient had severe atherosclerosis; note the left
internal carotid and the patchy yellow-white plaques in the basilar and
posterior cerebral arteries (blue arrows).
COAGULATION DEFECTS &
BRAIN INFARCTS
• Protein C deficiency
• Factor V Leiden mutation
(Arg506Gln)
• Protein S deficiency
• Antithrombin III abnormalities
• Carbohydrate-deficient
glycoprotein synthase type I
MICROANGIOPATHY
• Angitis and vasculitis
• Primary angitis of CNS
• Vasculitides
Polyarteritis nodosa
Allergic angitis and granulomatosis
Wegener’s granulomatosis
Lymphomatoid granulomatosis
• Microvasculopathy associated with dementia
Binswanger’s
Autosomal dominant arteriopathy
BINSWANGER’S SUBCORTICAL
ARTERIOSCLEROTIC
LEUKOENCEPHALOPATHY
• Slowly progressive, but “stairstep”
• 6th to 7th decade
• Memory, mood, cognition
• Pseudobulbar: gait and sphincter control
EMBOLIC DISEASES
Embolic stroke results when solid material:
forms in the arterial circulation
is introduced into arterial circulation
shifts from venous to arterial circulation
Resultant infarct is:
abrupt
hemorrhagic (reperfusion
Differential diagnosis is:
ischemic infarct
cerebral hemorrhage
SOURCES OF BRAIN &
SPINAL CORD EMBOLI
• Atheroma
•
•
•
•
•
Cardiogenic
Fat
Neoplasms and parasites
Iatrogenic
Miscellaneous
SOURCES OF BRAIN &
SPINAL CORD EMBOLI
• Atheroma
Complicated atherosclerosis
• Cardiogenic
Left atrium (noncontractile)
Mural thrombi
Endocarditis
Valve lesions
CNS INFARCTION
• Acute
5-8 hours undetectable
12-36 hours blurring gray/white
interface, dusky, softening
territorial
• Subacute
2-4 days softening, blurring, dusky, EDEMA
• Chronic
Stage I: liquefactive necrosis to cavitation
Stage II: (months) cavitary
ACA
MCA
A
B
Infarcts, recent (A) and old (B).
A. The infarct is in the distribution of the middle cerebral artery on the right. It
began as an ischemic infarct, there is no large mass of hemorrhage. What is present
now is the soft, necrotic resorbing tissue (inflammatory process at work).
B. An example of ischemia of the internal carotid distribution on the right. The
territories of both the anterior and middle cerebral arteries is involved. Again, it was
an ischemic, there is no large mass of blood as in a ruptured aneurysm. Vessel
territories are demonstrated on the left of B.
CNS INFARCTION
• Acute (hours)
eosinophilia with pyknosis
vacuolation of neurophil
• Subacute (days)
PMN infiltration
necrotic microvessels
foamy macrophages
• Chronic (weeks to months)
foamy macrophages, hemosiderin
reactive astrocytes
CORTICAL DYSFUNCTION:
TERRITORIAL
MCA
hemipariesis
aphasia
hemisensory deficit
ACA
hemipariesis
transcortical aphasia
abulia
PCA
thalamic syndrome
hemianopia
alexia
A
B
Infarct, remote. In the healing
process of the brain, cavitation is
the end result. There are several
examples of old infarcts, none of
which was initially fatal. They are
all in the distribution of the
____________ artery?
C
Infarcts, microscopic. What vessel?
What section of the brainstem?
What is the syndrome?
INTRACRANIAL HEMORRHAGE
• Extradural
• Subdural
• Subarachnoid
• Parenchymal
Cerebral
Cerebellar
Brain stem
Define the etiology and pathogenesis of
hypertensive vascular disease
including hemorrhage and lacunar
infarcts
HYPERTENSIVE PARENCHYMAL
HEMORRHAGES
Pathogenesis
rupture of weakened arterioles
replacement of muscle by fibrous tissue
fragmentation of elastic tissue
focal microaneurysms
Associated systemic hypertension
PARENCHYMAL HEMORRHAGES
• Hypertension
•
•
•
•
•
•
•
•
Trauma
Cerebral amyloid angiopathy
Saccular aneurysms
Vascular malformations
Bleeding diathesis (anticoagulants)
Vasculitis
Neoplasms
Infections
HYPERTENSIVE HEMORRHAGES
Symptoms and Signs
• Putamen
• Cerebellum
hemiparesis
hemisensory loss
visual field defects
• Thalamus
hemiparesis
hemisensory loss
gaze abnormalities
vomiting & headache
ataxia
cranial nerve abnormalities
• Large pontine
coma
quadriparesis or quadraplegia
small reactive pupils
• Small pontine
gaze paresis
ataxia
sensorimotor deficit
HYPERTENSIVE HEMORRHAGES
• Gross findings
acute hematoma
intraventricular extension
swelling, herniation
resorb, cavitation
does not respect vascular territory
secondary Wallerian degeneration
HYPERTENSIVE HEMORRHAGES
Microscopic features
fresh blood
inflammatory cells, macrophages
hemosiderin, hematoidin
Small vessels
“onion-skinning”
lipohyalinosis
microaneurysms
fibrinoid necrosis
HYPERTENSIVE HEMORRHAGES
ARTERIOSCLEROTIC CHANGE
Thickening of the media
Adventitial fibrosis
Fragmentation / reduplication
of elastica
Intimal thickening
Accumulation of macrophages
Charcot - Bouchard microaneurysm
MICROVASCULAR DEMENTIA
Cerebral Autosomal Dominant
Arteriopathy With
Subcortical Infarcts &
Leukoencephalopathy
(CADASIL)
Binswanger’S Subcortical
Arteriosclerotic
Leukoencephalopathy
Cerebral Amyloid Angiopathy

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