CEREBROVASCULAR DISEASE

Neurologic deficit due to cerebrovascular

compromise
Due to ischemia (85%) or hemorrhage
(15%).

Regional ischemia that results in focal

neurologic deficits for >24 hrs
Symptoms <24 hrs is termed TIA

Causes:
Global cerebral ischemia
Low perfusion (atherosclerosis)
Acute decrease in blood flow (shock)
Chronic hypoxia (anemia)
Repeated episodes of hypoglycemia
(insulinoma)
Clinical features
Mild global ischemia: transient confusion
with complete recovery (insulinoma)
Severe global ischemia: Diffuse necrosis of
brain, no survival or vegetative state
Moderate global ischemia: Infarcts in
watershed areas (regions at the end of
circulation), we can get damage to highly
vulnerable regions (pyramidal neurons of
cortex → 3,5,6 → creates line of necrosis →
corticolaminar necrosis; also pyramidal
neurons of hippocampus (in temporal lobe,
convert info into long term memory),
Purkinje layer of cerebellum)
Ischemic stroke
a) Thrombotic stroke: Rupture of
atherosclerotic plaque; usually
develops at cranch points
Results in pale infarct at the
periphery of the cortex. Why pale?
Even though the body lyses the
thrombus, bc the atherotic plaque is
present and ruptures, the thrombus
is reformed quickly, so blood isn’t
sent to the region.
b) Embolic stroke: Due to
thromboemboli; most common
source is left side of heart (due to A-
fib). Usually involves the middle
cerebral artery. Results in a
hemorrhagic infarct at the periphery
of the cortex. Why? Bc the embolus
is easily lysed.
c) Lacunar stroke: Involves small blood
vessels of the brain (lenticulo-striate
vessels, branches of middle cerebral
artery). Secondary to hyaline
arteriolosclerosis (benign hypertension,
diabetes). → small zone of necrosis →
resorbed forming a small cystic region
(small circular areas like lakes).
 Img.: lenticulostriate vessels
(secondary to hyaline
arteriosclerosis)

Img.: red neurons

Img.: lacunar strokes in deep brain

structures.

Ischemic stroke leads to liquefactive

necrosis
- Red neurons are early finding
(WITHIN 12 HRS)
- Then...Inflammation (neutrophils,
Img.: Liquefactive necrosis
microglial cells)
underwent cyst formation with area
- After 1 week… Granulation- like
of gliosis around it.
tissue
- At the end… results in fluid- filled
HEMORRHAGE
cystic space surrounded by gliosis
(reactive astrocytes that surround
cystic space with gliotic connective
tissue).
 2 types of cerebral hemorrhage: Img.: Affects basal ganglia
a) Intracerebral hemorrhage:
into the brain parenchima Subarachnoid hemorrhage
b) Subaracnoid hemorrhage: Bleeding into subarachnoid space
into subaracnoid space Presents as sudden headache (worst
headache of my life) with nuchal rigidity
Intracerebral hemorrhage: LP shows xanthochromia (bc of bilirrubin
Bleeding into the brain parenchyma breakdown products)
Due to rupture of Charcot- Bouchard
microaneurysms (wall thinning)
Complication of HTN
Basal ganglia is most common site
(perforating arteries: lenticulostriate blood
vessels)
Presents as headache, nausea, vomiting,
and eventual coma

Img.: bleeding on the bottom of the brain

(it’s the only thing that gives you bleeding in
the bottom)

Most frequently due to rupture of berry

aneurysm
Berry aneurism: thin- walled saccular
outpouching; lacks a media layer
Img.: hyaline arteriosclerosis can result in
lacunar strokes or aneurisms
Img.: medial layer doesn’t form in the
branching point

Most frequently located in anterior circle of

Willis (branch points of anterior
communicating artery)
Associated with Marfan and ADPKD
(autosomic dominant polichistic kidney
disease/ adult form).