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Cerebrovascular Disease

Cerebrovascular Disease

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Published by Diana Hylton
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Published by: Diana Hylton on Jul 19, 2013
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Cerebrovascular Disease
Week 7 Newell
Cerebral Ischemia
Neurons must have oxygen to liveTotal loss of oxygen >
5-6 minutes
 = irreversible cell changesOther CNS cells may tolerate the same stress
 
Selective Vulnerability of Neurons
 
Hypoxic Ischemic Injury Patterns
1.
 
Global Ischemia (entire brain is affected, like heart stops, shock, hypotension)2.
 
Focal Ischemia
Global Ischemia
Selective Vulnerability
Some neurons are more susceptible than othersNote that there are differences in susceptibility between adults and infantsInfants diencephalon is much more susceptible than adults
o
 
CA1 of Hippocampal Formation
(both adults and infants)
o
 
Purkinje cells
of Cerebellum
o
 
Pyramidal neurons:
 
III, V, VI
of Cerebral Cortex
Watershed (Borderzone) Infarcts
Sustained shock/ low blood pressureFirst to suffer with global ischemia
o
 
 ACA/MCA endzone
o
 
Hypotension can play a role in this
 
Case #1: Acute Global Ischemia
A 47 year-old man is found pulseless in a parking lot. A passerby performs CPR until paramedics arrive. Apulse is returned within
8-9 minutes
 of the witnessed collapse. After 24 hours of hospitalization, he hasa fatal dysrhythmia and dies.
Timeline = Acute Within 12-24 hours
 
Red neurons
 (hypoxia, ischemic injury)
loss of Nissl, Lost nucleolusMicrovacuolization (bubbly look 
cells/ BV leaking)Nuclear pyknosis
CA1 of HF, Purkinje cells, pyramidal neurons
Case #2: Subacute Global Ischemia
A 47 year-old man is found pulseless in a parking lot. A passerby performs CPRuntil paramedics arrive. A pulse is returned within
8-9 minutes
 of thewitnessed collapse. After
5 days of hospitalization
, he has a fatal dysrhythmiaand dies.
Timeline = Subacute 24 hours to 2 weeks
 Necrosis
Macrophages (clean up dead and dying neurons) within 48hr Vascular proliferation: like granulation tissue healing in skin
Gliosis (astrocytosis, proliferation of astrocytes)
 
Focal Ischemia (Infarcts)
o
 
Thrombosis:
 occluded BV at the site of the injury
o
 
Embolism:
traveling blood clot that began somewhere else
o
 
Vasculitis:
inflammatory BV disease
o
 
CADASIL:
Cerebral AD Arteriopathy with Subcortical Infarcts and Leukoencephalopathy
Infarcts: Thombosis
In situ blood clot (blood clot at site of injury)Majority: atherosclerosis
Common site:
o
 
Carotid Bifurcation
o
 
Middle Cerebral Artery origin
o
 
Top/bottom of the Basilar Artery (Posterior circulation)
 
Case #3: Acute Infarct 
A 68 year-old man awakens with left sided weakness and speech difficulties. Ahead CT scan reveals an area of signal change in the right frontotemporal lobes.He dies 5 days later.See demarcation, swelling, shifting, blood at site
Case #4: Old Infarct 
A 66 year old woman awakens with left sided weakness. A head CT scan reveals an areaof signal change in the right frontal cortex. She recovers and dies 1 year after infarct.Note the remodeling that has taken place.As the tissue was taken away, a cystic cavity was left. The meningothelial cells that arecovering the brain are resistant to all this infarct and they will tend to stay intact. Whitematter and cortex will discolor and atrophy.
CADASIL: Cerebral Autosomal-Dominant Arteriopathy with SubcorticalInfarcts and Leukoencephalopathy
o
 
Hereditary Vascular Dementia
o
 
Notch3 gene mutation (Chromosome 19)
 Affects mainly the arterioles and leads to infarcts deeper in the brain (white matter) and willcause chronic damage/ischemia to the white matter (leukoencephalopathy)
may mimic MS!!Features of CADASIL:
1.
 
Migraine with aura (20-30 year olds)2.
 
Psychiatric illness: depression3.
 
Recurrent infarcts
: TIAs or completed infarcts4.
 
Cognitive decline, often dementia (>80% of those 65+)
Periventricular white matter changeWhite matter change also seen at the temporal poles
See reduction of myelin in white matterChanges in blood vessel staining
deposits are characteristic (seen thru body)
Granular deposits
that may be related to Notch3
 
Hypertensive CV Disease
 Arteriolar Sclerosis
Deep nuclei, white matter, and brainstem
Lacunes
(15 mm or <)
 
Putamen, globus pallidus
 
Thalamus
 
Internal capsule
 
Deep white matter
 
Caudate nucleus
 
Pons
Multiple infarcts in deep nuclei but without granular deposits (CADASIL), smaller vessel disease
Intracranial Hemorrhage Overview
Sites:
intraparenchymal, subarachnoid, epidural, subdural
Intraparenchymal Hemorrhage
Most common cause: hypertension
Pathogenesis:
o
 
Accelerated atherosclerosis
o
 
Hyaline arteriolosclerosis
increased fragility
o
 
Charcot Bouchard aneurysms (debated)
Hypertensive Hemorrhage Sites
1.
 
Putamen2.
 
Thalamus
 
Hemorrhage shows LOTS of 
 3.
 
Pons
blood, unlike ischemia.
 4.
 
Cerebellum
Cerebral Amyloid Angiopathy
Abnormal material in the blood vessel wallAmyloid materialBV are not all equal in which ones acquire this material
small vessels aremore likely to acquire it.
Small vessels in the subarachnoid spaceSmall vessels in the cortex
Not a process that affects white matter blood vesselsWhen they break open, bleeding occurs, and the blood goes deeper into thebrain
Lobar HemorrhageBlood vessel disease that is associated with aging
Same amyloid as seen with Alzheimer’s disease
Hereditary forms

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