Title: CEREBROVASCULAR
1CEREBROVASCULAR DISEASE
2CEREBROVASCULAR DISEASE
- STROKE
- Macrovascular disease
- Microvascular disease
- Emboli
- Venous thrombosis
3Blood 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
4Closer view of the vertebral-basilar and carotid
arterial systems. Know their distribution,
branches, territories and syndromes associated
with the named vessels.
5Mid 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.
6Angiography 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.
7The blood vessels of the base of the brain and
their distribution.
8Vessels of the supratentorial level, medial left
hemisphere. Which is carotid, and which is
vertebral-basilar?
9Vessels of the supratentorial level, medial left
hemisphere. Which is carotid, and which is
vertebral-basilar?
10Sometimes 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.
11Blood drains from the veins into the sinuses, the
dural sinuses.
12Define and differentiate hypoxia, ischemia and
infarction Discuss the etiology and pathogenesis
of ischemic encephalopathy
13Define and differentiate hypoxia, ischemia and
infarction STRAIGHT FROM ROBBINS Discuss the
etiology and pathogenesis of ischemic
encephalopathy
14Ischemic (hypoxic) Encephalopathy Vulnerability
to ischemia Neurons Glial cells Tissue necrosis
First to die Prolonged ischemia
15Mechanism 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?
16Define and differentiate hypoxia, ischemia and
infarction Discuss the etiology and pathogenesis
of ischemic encephalopathy STRAIGHT FROM ROBBINS
17Ischemic encephalopathy Episodes of
hypotension Transient (if mild) Severe global
ischemia Survivor persistent vegetative
state Isoelectric (flat) EEG Respirator brain
18Morphology Brain swollen Flat surface Poor
gray-white distinction Acute neuronal changes
(12 - 24 hours) Glial cell death Vulnerability
factor Necrosis, macrophages, vascular
proliferation, gliosis
19What is a watershed infarct, and how does it
relate to the discussion of ischemic
encephalopathy?
20Vessels of the supratentorial level, medial left
hemisphere. Which is carotid, and which is
vertebral-basilar?
21Differentiate between ischemic and hemorrhagic
(white vs. red) infarcts, and define the most
likely causes of each
22B
A
23B
A
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?
24Differentiate between thrombotic and embolic
infarction, and given a gross or microscopic
picture, be able to recognize the difference
between the two
25CEREBROVASCULAR DISEASE
- STROKE
- Macrovascular disease
- Microvascular disease
- Emboli
- Venous thrombosis
26STROKE 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 gt Hemorrhage
27STR0KE 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
28ATHEROSCLEROSIS STROKE
- Documented risk factors
- TIA -- common presentation
- TIA -- high risk
- Embolization
- Occlusive thrombosis
- Extracranial -- common
- Intracranial -- less often
29Vascular, 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).
30COAGULATION DEFECTS BRAIN INFARCTS
- Protein C deficiency
- Factor V Leiden mutation
- (Arg506Gln)
- Protein S deficiency
- Antithrombin III abnormalities
- Carbohydrate-deficient
- glycoprotein synthase type I
31MICROANGIOPATHY
- Angitis and vasculitis
- Primary angitis of CNS
- Vasculitides
- Polyarteritis nodosa
- Allergic angitis and granulomatosis
- Wegeners granulomatosis
- Lymphomatoid granulomatosis
- Microvasculopathy associated with dementia
- Binswangers
- Autosomal dominant arteriopathy
32BINSWANGERS SUBCORTICAL ARTERIOSCLEROTIC
LEUKOENCEPHALOPATHY
- Slowly progressive, but stairstep
- 6th to 7th decade
- Memory, mood, cognition
- Pseudobulbar gait and sphincter control
33EMBOLIC 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
34SOURCES OF BRAIN SPINAL CORD EMBOLI
- Atheroma
- Cardiogenic
- Fat
- Neoplasms and parasites
- Iatrogenic
- Miscellaneous
35SOURCES OF BRAIN SPINAL CORD EMBOLI
- Atheroma
- Complicated atherosclerosis
- Cardiogenic
- Left atrium (noncontractile)
- Mural thrombi
- Endocarditis
- Valve lesions
36CNS 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
37ACA
MCA
B
A
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.
38CNS 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
39CORTICAL DYSFUNCTION TERRITORIAL
MCA hemipariesis aphasia hemisensory
deficit ACA hemipariesis transcortical
aphasia abulia
PCA thalamic syndrome hemianopia alexia
40B
A
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
41Infarcts, microscopic. What vessel? What
section of the brainstem? What is the syndrome?
42INTRACRANIAL HEMORRHAGE
- Extradural
- Subdural
- Subarachnoid
- Parenchymal
- Cerebral
- Cerebellar
- Brain stem
43Define the etiology and pathogenesis of
hypertensive vascular disease including
hemorrhage and lacunar infarcts
44HYPERTENSIVE PARENCHYMAL HEMORRHAGES
Pathogenesis rupture of weakened arterioles
replacement of muscle by fibrous tissue
fragmentation of elastic tissue focal
microaneurysms Associated systemic hypertension
45PARENCHYMAL HEMORRHAGES
- Hypertension
- Trauma
- Cerebral amyloid angiopathy
- Saccular aneurysms
- Vascular malformations
- Bleeding diathesis (anticoagulants)
- Vasculitis
- Neoplasms
- Infections
46HYPERTENSIVE HEMORRHAGES
Symptoms and Signs
- Putamen
- hemiparesis
- hemisensory loss
- visual field defects
- Thalamus
- hemiparesis
- hemisensory loss
- gaze abnormalities
- Cerebellum
- vomiting headache
- ataxia
- cranial nerve abnormalities
- Large pontine
- coma
- quadriparesis or quadraplegia
- small reactive pupils
- Small pontine
- gaze paresis
- ataxia
- sensorimotor deficit
47HYPERTENSIVE HEMORRHAGES
- Gross findings
- acute hematoma
- intraventricular extension
- swelling, herniation
- resorb, cavitation
- does not respect vascular territory
- secondary Wallerian degeneration
48HYPERTENSIVE HEMORRHAGES
Microscopic features fresh blood inflammatory
cells, macrophages hemosiderin, hematoidin
Small vessels onion-skinning lipohyalinosis m
icroaneurysms fibrinoid necrosis
49HYPERTENSIVE HEMORRHAGES
ARTERIOSCLEROTIC CHANGE
Thickening of the media Adventitial
fibrosis Fragmentation / reduplication of
elastica Intimal thickening Accumulation of
macrophages
Charcot - Bouchard microaneurysm
50MICROVASCULAR DEMENTIA
Cerebral Autosomal Dominant Arteriopathy
With Subcortical Infarcts Leukoencephalopathy (C
ADASIL) BinswangerS Subcortical Arteriosclerotic
Leukoencephalopathy Cerebral Amyloid Angiopathy