Term
| two general categories of stroke |
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Definition
STROKE = disruption of blood supply to focal area of the brain
ischemic stroke
hemorrhagic stroke |
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Term
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Definition
may be arterial or venous
arterial: acute, focal, conforms to a vascular territory
venous: acute, focal or multifocal, variable distribution |
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Term
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Definition
| acute, focal, may mimic vascular territory, mass effect |
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Term
| arterial supply to the brain |
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Definition
-carotids come off aorta and brachiocephalic and brancch into MCA and ACA (middle and anterior cerebral artery)
-verterbral arteries come off subclavian
and join to form basilar
-final branches off basilar is PCA (posterior cerebral artery)
-PCA and ACA connected via communicating branches
ABOVE = Circle of Willis |
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Term
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Definition
the MCA is a branch off of the carotids; supplies the biggest territory of cortex
it splits into superior and inferior divisions
sup: up middle, over top of cortex
inf: out to temporal lobe |
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Term
territorial syndrome - MCA
body regions affected |
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Definition
the MCA covers a majority of the lateral aspect of the cortex
going my the homunculus, this area is correlated with the head and upper limbs so the face and arms show preferential s/sx with damage in this area |
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Term
territorial syndrome - MCA
weakness & numbness |
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Definition
weakness occurs first in FACE>ARMS>LEGS
numbness occurs first in FACE>ARMS>LEGS
contralaterally affected |
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Term
territorial syndrome - MCA
vision |
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Definition
visual field cut on contralateral side
gaze preference toward ipsilateral side
(even though occipital cortex is supplied by PCA, the optic fibers/radiations much run through the parietal and temporal lobes to get there) |
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Term
territorial syndrome - MCA
cognition |
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Definition
when on dominant hemisphere(usually L) - aphasia
non-dominant side (usually R) - L/contralateral neglect and anosognosia |
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Term
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Definition
| inability to recognize that you have a problem |
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Term
territorial syndrome - ACA
body areas affected |
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Definition
the ACA supplies the medial surface of each hemisphere and just over the top of the brain
impairment to ACA manifests as worse in the legs that arms or face |
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Term
territorial syndrome - ACA
weakness & numbness |
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Definition
weakness: contralateral LEGS>ARMS
numbness: contralateral LEGS>ARMS |
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Term
| territorial syndrome - internal carotid artery |
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Definition
blockage is proximal to the branching off of ACA and MCA, so get a combo of both
also get ophthalmic artery manifestations - monocular blindness |
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Term
| territorial syndrome - PCA |
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Definition
supplied occipital cortex, damage leads to contralateral vision field cut
if damaged in the dominant hemisphere - alexia without agraphia |
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Term
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Definition
| territory between the major arteries ACA and MCA |
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Term
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Definition
these zones are at risk of hypoperfusion in the setting of internal carotid stenosis
these distal territories receive less blood because the proximal parts of the MCA and ACA zones take what they need first and there is not enough left
can result in transcortical aphasia |
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Term
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Definition
occurs when watershed infarcts disconnects the primary language circuit from the brain (Broca and Wernicke areas sit just inside)
patient is still able to repeat things |
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Term
| in what pathological condition is the watershed area likely to be spared? |
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Definition
| with specific infarct of PCA, MCA, or ACA because of collateral flow |
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Term
lacunar infarct
definition |
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Definition
| a small (<1.5 cm) subcortical infarct from occlusion of a single penetrating artery to the brain |
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Term
lacunar infarct
common sites |
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Definition
basal ganglia
thalamus
pons
internal capsule
cerebellum |
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Term
lacunar infarct
classic syndromes |
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Definition
pure motor (hemiparesis with no sensory deficit; IC)
pure sensory (numbness on one whole side but normal strength; thalamus)
ataxic hemiparesis (ataxia and mild weakness on one side)
clumsy hand |
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Term
| cerebral venous thrombosis |
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Definition
can get a clot in the venous drainage of the brain-->lead to backup-->can lead to hemorrhage or ischemia
usually occur in people with a pre-existing clotting disorder
(not as well understood) |
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Term
gross pathology
very recent infarct |
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Definition
at one day out, get discoloration at the junction of gray and white matter
blurring of boundary |
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Term
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Definition
at 2-4 days:
add in edema to blurring of gray/white junction and dusky discoloration |
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Term
gross pathology
chronic infarction |
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Definition
| infarct undergoes liquefaction necrosis as the edema resolves, leading to an eventual cavitation |
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Term
microscopic pathology
acute infarct |
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Definition
normal appearance for first 0-12 hours
ischemic change appears after 6-12 hours |
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Term
microscopic pathology
ischemic change in acute infarct |
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Definition
cytoplasm becomes eosinophilic
shrunken nucleus
nucleolus no longer visible
Nissle substance dispersed
vacuolation of neuropil
capillary endothelium swells
some extravasation of RBC
myelinated fibers begin to disintegrate |
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Term
microscopic pathology
acute infarct : 12-48 hours |
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Definition
neutrophils migrate into the infarct region around day 1-2
NFs are replaced by lymphocytes and macrophages after 48 hours |
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Term
microscopic pathology
chronic infarct |
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Definition
macrophages clean things up
reactive astrocytes transform and lay down connective tissue; organize damaged area
result in a cystic cavity with a few residual astrocytes |
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Term
| most common disease process related to stroke |
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Definition
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Term
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Definition
plaques (may be hemorrhagic plaques) in carotid arteries
compromise of blood flow
same disease process as with peripheral artery disease |
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Term
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Definition
the small(est) penetrating arteries in the brain fall victim to a different pathology process than the carotids (though same risk factors apply)
thickening of the wall of tiny blood vessels until ultimately the vessels are occluded
these penetrating areas feed the common locations for lacunar stokes: basal ganglia, cerebellum, brainstem, thalamus, internal capsule |
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Term
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Definition
mechanism by which local blood vessels constrict and dilate to maintain constant blood flow to the brain over the range of BPs it typically sees
if pressure gets too high or too low, cerebral blood flow will end up increasing or decreasing, respectively |
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Term
| shift in autoregulation curve |
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Definition
at consistently high blood pressure, the autoregulation curve can shift to the right
habitually high HTN
need to be careful when lowering BP of this patient in the setting of a stroke because the brain is used to a higher pressure and lowering it too much or too fast could cause new areas of stroke in another part of the brain |
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Term
| autoregulation in the setting of stroke |
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Definition
in an area of ischemia in the brain, the mechanisms of autoregulation break down
brain becomes very sensitive to even small changes in BP |
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Term
| thresholds of ischemic damage |
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Definition
the effects of local cerebral ischemia depend on how much the cerebral blood flow is reduced. Range:
normal range (maintained by autoregualtion)
oligemia
mild ischemia
moderate ischemia
severe ischemia |
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Term
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Definition
CBF 30-40 ml/100gm/min
increased oxygen extraction from the blood can maintain normal function
brain continues to function, but has little if any reserve, at great risk of damage in setting on further BP reduction/increased metabolic stress |
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Term
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Definition
CBF 20-30- ml/100gm/min
increase in anaerobic glycolysis and lactate; acidosis
suppression of protein regulation/translation in general, however UPregualtion of immediate early genes (some protective, some deleterious effects)
brain continues to function, but has little if any reserve, at great risk of damage in setting on further BP reduction/increased metabolic stress |
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Term
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Definition
CBF 10-20 ml/100gm/min
decrease in electrical excitability of neurons (2ndary to decreased pH for lactic acidosis)
triggers "ischemic cascade" (increased intracellular calcium, cellular edema) |
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Term
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Definition
-decreased neuronal excitability from low pH leads to fewer APs being generated
-AP necessary for regulating intracellular Ca
-release of excitatory amino acids: glutamate and aspartate; their reuptake is suppressed
-high levels of AA can further increase intracellular Ca
-high Ca affects protein phosphorylation
-alterations in gene expression and protein synthesis
-ionic changes create an osmotic gradient allowing water to passively flow into cells
-cellular EDEMA |
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Term
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Definition
CBF <10 ml/100gm/min
deterioration of transmembrane ionic gradients leads to deterioration of transmembrane electric potential
worsening acidosis
glycolysis stops
accumulation of free radicals --> damage proteins, DNA, fatty acids in cell membrane } --> all contributes to more changes in permeability
MORE increase in intracellular Ca |
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Term
| ultimate result of ongoing ischemic cascade |
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Definition
at a certain point, cascade becomes irreversible - even if blood flow to the tissue is restored, unable to recover (brain tissue cannot survive CBF <7 for more than 1 hour)
APOPTOSIS from altered gene expression and DNA damage
CELL NECROSIS from accumulation of intracellular Ca and free radicals (as result of membrane damage and cytoskeleton breakdown)
INFLAMMATORY RESPONSE from substances produced during ischemia
HEMORRHAGE can result from abnormalities of vascular wall in infarcted vessels |
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Term
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Definition
goal of acute stroke therapy is to prevent cell death in this region
zones of tissue outside/around the center of ischemia, which has more access to collateral blood flow than the central zone (which is most dependent on the affected artery) and thus has a longer time window during which restoration of blood flow may salvage the tissue |
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Term
| main goals in the management of ischemic stroke |
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Definition
I. restoration of blood flow (keep penumbra alive!)
II. limitation of deficits
III. primary vs. secondary prevention
IV. secondary prevention
V. primary prevention |
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Term
| considerations in the restoration of blood flow in ischemic stroke |
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Definition
must accomplish before ischemic cascade is irreversible (at least in the penumbra)
carries a risk of hemorrhage due to high pressure in damaged blood vessels
thrombolytics carry additional risk of hemorrhage |
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Term
| consequences/time frame of restoration of blood flow in ischemia stroke |
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Definition
GOAL: keep penumbra alive
HOW: open blocked artery
IV TPA within 4.5 hours of symptom onset (3hr preferred)
intra-arterial TPA within 6 hours
endovascular clot retrieval up to 8 hours |
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Term
| considerations to take to try and limit the damage of stroke |
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Definition
AVOID: hypotension, hyperthermia, hypoxia, hyperglycemia
PROPHYLAX FOR: DVTs, decubitus ulcers (because immobile)
POSS: induce hypothermia, hemicraniectomy if massive edema that is pushing on neighboring brain
WATCH FOR: seizures, SIADH (hyponatremia), depression
REHAB |
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Term
| ways to minimize the risk of future stroke |
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Definition
primary and secondary prevention
1: reduce risk in those who have never had TIA/stroke (but has RFs)
2: reduce risk in those who have had at least one TIA or stroke |
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Term
| risk of stroke in symptomatic vs. asymptomatic carotid disease |
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Definition
people with carotid disease who have had a stroke of TIA previously are at a much higher risk of having a a repeat event than people with asymptomatic carotid disease having a first event
annual probability of 16% vs. 1.3% |
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Term
| endarterectomy for ischemic stroke prevention? |
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Definition
evidence suggests a clear benefit to endarterectomy to patients with >70% carotid blockage who are SYMPTOMATIC, that is, who have already had a previous TIA or stroke
Asymptomatic individuals saw only a 1%/year decrease in risk with endarterectomy |
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Term
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Definition
all-cause AE outcomes (MI, stroke or death) the same for both
MI only - more with endarterectomy
stoke only - more with stent
older patients seem to fare better with endarterectomy |
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Term
| antiplatelet agents in secondary prevention of ischemic stroke |
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Definition
aspirin, clopidogrel, aspirin.ER dipyridamole combo
low and high dose aspirin reduces risk of subsequent stroke by ~13%
other agents seem to have slightly greater benefit |
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Term
primary prevention of ischemic stroke
cerebrovascular risk factors |
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Definition
non modifiable: age, race, sex, ethnicity
modifiable:
HTN
hyperlipidemia
DB
a-fib
smoking
carotid stenosis |
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Term
| HTN and ischemic stroke prevention |
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Definition
ideal is 120/80
goal SBP < 140 (130 if DB or chronic renal failure)
goal DBP < 90 (80 if DB or chronic renal failure)
thiazide diuetic as first-line therapy |
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Term
| hyperlipidemia and ischemic stroke prevention |
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Definition
goal of LDL < 70 mg/dl for high risk patients
statins as drug of choice (may have other protective effects) |
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Term
| diabetes and ischemic stroke prevention |
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Definition
goal od fasting blood glucose < 126 mg/dl
Hgb A1C < 6.1 |
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Term
| physical activity and ischemic stroke prevention |
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Definition
| goal of 30-60 minutes of exercise at least 3 times a week |
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Term
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Definition
epidural
> more common with head trauma
subdural
subarachnoid
parenchymal |
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Term
| causes of subarachnoid hemorrhage |
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Definition
aneurysms
vascular malformations |
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Term
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Definition
| blood layered under the arachnoid layer of the meninges |
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Term
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Definition
outpouching of one of the cerebral arteries
common cause of subarachnoid hemorrhage |
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Term
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Definition
around the circle of Willis
near branch points
need to image blood vessel to localize cause - currently with angiography but increasing use of MR/CT angiography |
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Term
| goals of treatment of subarachnoid hemorrhage |
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Definition
1. prevent and treat complications
2. prevent rebleeding |
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Term
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Definition
another cause of subarachnoid hemorrhage; 4 types:
ateriovenous malformations (AMVs)
cavernous angiomas (cavernomas)
venous angiomas (deep venous anomalies)
capillary telangiectases |
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Term
arteriovenous malformations
AMVs |
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Definition
most dangerous type of vascular malformation; most likely to produce intracranial hemorrhage
veins exposed to pressures much higher than typically occur in venous circulation
direct communication between arteries and veins; moderate sized artery feeds into moderately sized vein with no intervening capillary bed
this "nidus" (core of tangles of blood vessel channels) are separated by brain tissue
usually gliotic |
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Term
cavernous angiomas
(cavernomas) |
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Definition
small collections of closely packed, distending bloo vessels of varying wall thickness without any intervening brain parenchyma
low pressure systems
often clinically silent; only treat if they show a tendency to bleed |
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Term
venous angiomas
(deep venous anomalies) |
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Definition
one or more dilated veins with no arterial component, within normal brain
very low pressure systems
generally no clinical manifestations |
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Term
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Definition
multiple small caliber, very thin-walled vessels within normal brain
hardly ever hemorrhagic |
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Term
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Definition
want to treat right away
surgical resection is small enough (<3 cm diameter)
if too large to resect, endovascular gluing to help shrink, then resect |
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Term
| management of cavernous angiomas |
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Definition
asymptomatic = NO treatment
if symptomatic:
-progressive neurologic symptoms
-intractable epilepsy
-recurrent hemorrhage
-...SURGICAL RESECTION |
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Term
| venous angiomas, capillary telanigectases treatment |
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Definition
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Term
| types of parenchymal hemorrhage |
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Definition
parenchymal hemorrhage:
-hypertensive
-amyloidosis |
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Term
| hypertensive changes leading to parenchymal hemorrhage |
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Definition
HTN can lead to parenchymal hemorrhage int he same areas of brain that lacunar strokes are commonly found (smallest vessels)
-basal ganglia
-cerebellum
-brainstem
-thalamus |
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Term
| amyloidosis and parenchymal hemorrhage |
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Definition
amyloid depositions in the wall of blood vessels can predispose the area to hemorrhage
tends to occur in the cerebral hemispheres ("lobar hemorrhage") |
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Term
| management of parenchymal hemorrhage |
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Definition
acute management similar as for ischemic stroke - prevent and treat complications
unclear if resection of the hematoma improves outcome
-may do so when in cerebellum to reduce risk of brainstem compression |
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