Neuro 70: Pathology of cerebral vasc disease Flashcards
How does the healing of a cerebral infarct differ from an infarct that occurs elsewhere in the body?
- cerebral infacts do not result in collagenous scars
- instead the necrotic issue is removed –> cavity is left behind
- the cavity is surrounded by gliosis
What is the most common dirrect cause of death following a stroke?
- herniation of the brainstem
- during the first several days after an infarct there is swelling due to edema that can cause compression or herniation of important structures
- *so initial tx of stroke is to reduce this swelling!
What are 4 factors that can contribute to a pt having an infarction?
- decreased oxygen of the blood - Hbopathy, hypoxia
- decreased perfusion - hypotension, stasis, increased intracranial P
- could also be from carotid stenosis –> dont need total occlusion to get and infarct! - hypercoaguable state - pregnancy, oral contraceptives, antiphospholipid antibody syndrome
- HTN
Histology of an acute cerebral infarct
- nuclei will have ground glass appearence
- cytoplasm shrinks
- cell becomes esinophilic
- nackground becomes vacuole-ated & fluffy looking = edema
Histology of the early organization following an acute infarct
- see lots of macrophages that come in from the peripheral blood
- see endothelial cells begin to grow in the damaged areas
What is seen 4 days after a cerebellar infarct
- the affected area is well demarcated
- the defective area is swollen and fragile –> begins to fall appart and crack
What is see 2-3 weeks histologically after an acute cerebellar infarct
- sea of macriohages that fill up the area where the brain tissue was previously
- see neovascularization and capillaries
What is seen in the early cavitation stage of healing from an acute infarct?
- about 2 mnths after the infarct
- macrophages begin to leave
- the infarcted area begins to collapse, leaving behind the neovascularzation –> see lots of tiny vessels
What is left 3 weeks after an acute infarct has been healing?
- there is a cavity with thin-walled blood vessels within it
- trabecular looking
3 most common locations for primary thrombosic occlusions to occur?
- Basilar a.
- Vertebral a.
- Internal carotid a.
3 most common locations for embolic occlusions?
- Middle cerebral artery –> sort of like a continuation of the internal carotid, so thats why a lot of emboli will end up here!
- Anterior cerebral artery
- Posterior cerebral artery
What makes the lenticulostriate arteries more vulnerabel to infarcts?
-b/c they are skinny vessels that come off at right angles !
Lacunar infarcts
- typcially seen in pts with HTN
- the compensation to normotension will cause distal areas to become ischemic –> causes tiny infarcts
- there can be early swelling around these lesions that causes the compression and dysfunction of the surrounding tissue –> so the sx can be more severe than expeted
- recovery is uaully good and the sx often go away after 3mnths when the swelling reduces
Granular atrophy
- secondary to multiple small infarcts that are the result of poor profusion to distal vasculature
- seen in pts with poor control of their HTN
Leukoaraiosis
- areas in the white matter of decreased density
- shows up on CT as an UBO (unidentified bright object)
- associated HTN
- can cause cognitive impairment