Cerebrovascular Disease - Cochran & Helms Flashcards
Review of anatomy
Where along the motor and sensory cortices correspond to the face, and lower limb?
What arteries supply these regions?
The lower limb is represented near the midline, within the central fissure. It is supplied by the ACA.
The face is represented laterally, near the sylvian fissure. It is supplied by the MCA.
Review of anatomy
What two vessels are the source of the brain’s blood supply?
From what do they arise, and how do they enter the cranium?
Vertebral artery arises from the subclavian artery, travels within the foramina transversaria and enters via the foramen magnum.
Internal carotid artery arises from the common carotid artery, enters via the carotid foramen.
Review of anatomy
What arteries comprise the circle of willis?
What arteries comprise the vertebrobasilar system?
Circle of willis: ACAs, Anterior communicating artery, MCAs, Posterior communicating arteries, PCAs. Gives off perforating branches.
Vertebrobasilar system: Vertebral arteries, PICAs, AICAs, basilar artery, SCAs, PCAs, pontine/labyrinthine/other smaller vessels.
Review of anatomy
What artery supplies the bulk of the neocortex?
What perforting branches does it also contribute?
The middle cerebral artery (MCA).
Gives off lenticulostriate arteries (supply the basal ganglia, internal capsule, etc).
Review of anatomy
What 5-6 components comprise the basal ganglia?
What tracts cross over at the pyramidal decussation?
Putamen, Caudate, Globus pallidus interna & externa, subthalamic region, and substantia nigra.
The pyramidal tracts (Corticobulbar, lateral and ventral corticospial). Distinguish from extrapyramidals (rubrospinal, reticulospinals, vestibulspinals, tectospinal)
Review of anatomy
Where does the Great vein (of Galen) drain to?
Trace the path of blood as it is drained from the anterior/superior frontal lobe.
Great vein drains posteriorly into the straight sinus.
Blood enters the superior sagittal sinus, travels posteriorly where it joins with the straight sinus. It travels along either transverse sinus into the sigmoid sinus, where it finally drains into the jugular vein.
Review the three mechanisms of hypoxia and give examples of each.
Which is worse - Ischemia or hypoxia? Why?
Low oxygen content of blood (eg respiratory arrest, drowning, anemia)
Low blood flow (eg cardiac arrest, obstruction, increased ICP)
Decreased oxygen utilization (eg metabolic poisons)
Ischemia is worse–the anoxia is compounded by accumulation of toxic metabolites.
What are the two forms of ischemia that affect the brain?
Give example etiologies for each.
Global ischemia (SBP < 50); due to cardiac arrest, shock, hypotension.
Focal ischemia (stroke); due to thrombosis, embolism, stenosis.
What are watershed regions?
What implication does this have in the context of cerebrovascular disease?
Watershed regions lie at the boundaries between two arterial beds.
They are less susceptible to focal ischemia (eg vessel occlusion), but are more susceptible to global ischemia.
What cells are most vulnerable to ischemia in the brain?
Why?
Neurons more than glia (oligodendrocytes > astrocytes).
Metabolic demands (oxygen/energy requirements) as well as glutamate receptor densities (Glu accumulates in tissue injury, is itself excitotoxic).
What regions of the neocortex are most damage under global ischemia.
How do they appear?
Hippocampus (distinctive “jelly roll” necrosis)
Cerebral cortex laminae 3/5/6 (laminar necrosis)
Purkinje cells of the cerebellum (???)
In severe global ischemia, brain function may be impaired to the point of persistent vegetative state or brain death.
Distinguish between the two.
PVS: Unconscious, but with preservation of sleep-wake cycles and some reflexes.
Brain death: Absent reflexes/responses and respiratory drive. Usually occurs with brainstem injury. A legal definition.
Describe the gross and microscopic appearance of brain tissue in the context of global ischemia.
Gross: Diffuse swelling, which may obliterate ventricles or cause herniation.
Microscopic: Pallor and vacuolation with eosinophilic, pyknotic neurons without apparent nucleoli or nissl substance.
Focal ischemia results from either thrombotic or embolic action. Which is more common?
What sites are most classically affected by thrombosis? Why do you think this is?
Embolic.
Branch points such as the carotid bifurcation, origin of the MCA, and the basilar artery. These sites have more turbulent flow.
Recall the pathophysiology of atherosclerosis.
If an ICA were to be completely occluded, what would be the resulting clinical presentation?
LDL deposition subintimally due to macrophage-driven oxidation causes intimal proliferation. This can “infarct” the tunica media in turn.
Complete occlusion may not have symptoms! This is due to robust collateral circulation. However, these plaques may throw small emboli.
Name four or more potential sources of emboli that can cause focal ischemia.
Where do they most commonly enlodge?
Mural thrombi, endocarditis, atheroma, fat/neoplasm/air.
Generally in the MCA (this is intuitive; flow is greater there than in any other cerebral vessel).
Thrombotic infarcts are generally (hemorrhagic/pale), while embolic infarcts are generally (hemorrhagic/pale).
Why is this?
Thrombotic infarcts are generally pale, while embolic infarcts are generally hemorrhagic.
Emboli may resolve slightly, allowing flow of blood into the infarcted tissue. Note that this is not the same as a hematoma!
Describe the pathophysiology of a lacunar infarct.
Vascular disease such as diabetes mellitus or hypertension causes hyaline arteriolosclerosis of small penetrating arteries (classic: Lenticulostriate). These may occlude or rupture.
What are the classic locations for lacunar infarcts?
Subcortical brain structures: Basal ganglia, internal capsule, thalamus, pons, white matter in general/
Either! Note that they may either involute fully or rupture.
Describe the changes seen in infarcted tissue over the course of hours to months.
What pattern of necrosis is this?
Initially, eosinophilia is seen. Leukocytes enter (first neutrophils, then microglia/macrophages) to clear debris and eventually reactive astroctes form a glial scar (gliosis).
Liquefactive necrosis.
What is primary angiitis?
How does it appear on histology?
Occlusion of small/medium sized vessels by inflammatory processes
Lymphocytes, fibrinoid necrosis, and giant multi-nucleated cells (as well as an occluded lumen will all be seen on histology)
Describe what is seen in the brain grossly and histologically during:
Acute Infarct
Subacute Infarct
Chronic Infarct
Acute Infarct
Grossly: swollen tissue with a lack of distinction between grey/white matter
Histologically: eosinophilic neurons on a pale background, neutrophils may be seen
Subacute Infarct
Grossly: liquefactive necrosis
Histologically: macrophages, reactive astrocytes, vascular proliferation, necrosis
Chronic Infarct
Grossly: Cavitated with glial scarring
Histologically: Cavitated with glial scarring
What will show up on a CT during an acute infarct?
What will show up on a conventional MRI?
What will show up on a diffusion MRI?
CT
Mildly swollen looking tissue, with less distinct grey/white matter
Conventional MRI
Nothing
Diffusion MRI
Bright areas where the infarct is occuring (lack of water movement shows up bright)
What can be seen on imaging for a subacute infarct?
What can be seen on imaging for a chronic infarct?
Subacute infarcts will look significantly darker on CT than the surrounding area
Chronic infarcts will show cavitation of the hollow area on both MRI and CT
What is vascular dementia?
What patterns of damage can be seen?
A generalized term for dementia that progresses slowly, but is vascular in nature (IE the mechanism of a stroke, but the progression of alzheimer’s)
Multiple Lacunar Infarcts
Diffuse White Matter disease
Infarcts in areas necessary for memory, cognition
Where are cerebral venous thromboses most likely to occur?
What are some causes/risk factors?
Superior sagittal sinus or lateral sinus
Infection, injury, neoplasm, surgery, pregnancy, oral contraceptives, hematologic abnormalities, dehydration
IE EVERYTHING
What are the three main causes of intracerebral hemorrhage?
Hypertension
Vascular Malformations
Amyloid angiopathy
What are the two most common vascular malformations that might causes intracerebral hemorrhage?
Arteriovenous malformation- agenesis of the capillaries, leading to increased blood pressure in the veins
Cavernous Angioma- large capillaries with little surrounding brain (possibly means lack of diffusion potential?)
What is amyloid angiopathy?
What other diseases is it related to?
Accumulation of amyloid proteins in the walls of blood vessels, making them fragile and likely to bleed.
Related to alzheimer’s but not to any other amyloid condition
What are the two largest causes of subarachnoid hemorrhages?
Trauma
Aneurysms
What are berry anuerysms?
Where are they most likely to occur?
What is seen on histology?
A congenital defect in the artery compounded by stress which causes a ballooning
Most likely to occur at branch points
Defects in the vessel wall will be seen on histology
How do patients with berry aneurysms typically present?
What risk factors are there for berry aneurysms?
“the worst headache I’ve ever had”
Anything that would raise the blood pressure and stress the already weakened
Hypertension
smoking
arteriovenous malformation
Etc.
