Oct10 M1,2,3-Stroke Flashcards
(136 cards)
1
Q
stroke def
A
damage to CNS caused by abnormality of vascular supply
2
Q
stroke types
A
- ischemic (something blocked arterial supply)
- hemorrhagic (artery broken or bursts and blood leaks out in brain): TWO problems –>abnormal blood supply + pressure on the brain
- venous (venous output blocked and P builds up. this leads to ischemic AND hemorrhagic stroke bc arterial supply diminishes)
3
Q
type of stroke where time is brain
A
ischemic
4
Q
main risk factor for CBVD (cerebrovascular disease) and why
A
hypertension
- the pathophysiology of ischemic stroke = atherosclerosis from increased turbulence and shear stress at BIFURCATIONS
- turbulence and shear stress caused by hypertension
5
Q
examples of bifurc areas prone to shear stress
A
- where common carotids split off brachiocephalic trunk
- where internal carotid and external carotid split off common
- etc
6
Q
4 main vessels going to the neck for supply
A
- internal carotids (2): anterior circulation
- vertebral aa (2): posterior circul.
7
Q
components of the anterior circulation
A
- each internal carotid gives 1 anterior cerebral a (ACA) and 1 middle cerebral (a).
- the internal carotid is between the two (links them)
- ACA goes forward medial (along surface of each hemisphere)
- MCA goes lateral (in the Sylvian fissure between temporal and frontal lobes)
- the two ACAs on each side are linked by a short anterior communicating artery
8
Q
components of the posterior circulation
A
- vertebral aa join to give a single basilar a
- at circle of Willis, basilar splits (at level of midbrain) into posterior cerebral arteries (PCA)
- PCA linked to origin of MCA (leaving internal carotid a) by posterior communicating artery (2 of those, one on each side)
9
Q
components of circle of Willis
A
front to back
- anterior comm a (1)
- ACA (2), one on each side
- internal carotid aa (2), one on each side
- MCA (2), one on each side)
- posterior comm aa (2), one on each side
- 2 PCAs, branching off basilar a in the very back of the circle
10
Q
where is the basilar a
A
on VENTRAL surface of the pons
11
Q
circle of Willis things to know
A
- anastomoses protect against prob in blood supply
- occlusion of one ACA = the other compensates, blood crosses
- not all people have all the components of the circle of Willis, imp bc occlusion tells you want happened
12
Q
other arteries in post circul at level of brainstem
A
bottom to tp
- posterior inferior cerebellar aa (PICA) branching off vertebral aa middle
- anterior spinal a (one artery of spinal cord on its ant. surface) first level is a branching off vertebral aa top
- anterior inferior cerebellar aa (AICA) branching off base of basilar a
- pontine aa (many) branching off middle of basilar a
- superior cerebellar aa (branching off top of basilar a before it forms the PCAs)
13
Q
course of ACA
A
on medial surface of the brain (sagittal medial cut)
- goes up between the hemispheres
- initially in the back
- passes behind the corpus callosum and cingulate gyrus (limbic lobe)
- to the front
14
Q
course of MCA
A
course observed in coronal view
- goes lat and supplies blood to outer surface of brain
- sends tiny lenticulostriate arteries going to deep structures in the brain (head of caudate, putamen, internal capsule)
15
Q
clinical imp of lenticulostriate aa
A
bc are very tiny and comme right from a big vessel (MCA), are very prone to damage from htn
16
Q
RFs for ischemic stroke other than htn (related to shear stress at bifurcations)
A
modifiable: -smoking -diabetes -lipids nonmodifiable: -CHF -age >75 -diabetes -prior stroke or thromboembolism (a thrombus (clot) forms somewhere and then embolizes = detaches and travels)
17
Q
what is the CHADS2 score
A
IN AFIB PATIENTS, sum up score assoc to diff risk factors for ischemic stroke (IN THESE PTS) and give aco above a certain score
18
Q
common ischemic stroke sx
A
- weakness
- numbness (loss of sensation, not tingling or wtv)
- aphasia (language problem: expressing, understanding language) and dysarhtria (motor problem of speech, of muscles making noises of speech)
- visual loss
- SUDDEN ONSET
- FOCAL SYMPTOMS (STROKE IS FOCAL so sx are related to part of brain affected)
- (headache) but IS NOT the main complaint, especially in ischemic stroke
19
Q
stroke type where big headache can be the main presentation
A
hemorrhagic stroke
-this happens bc of high P
20
Q
important hx component for dx of stroke
A
time course.
stroke happens suddenly, immediately, very fast
(tumor = weeks, neurodegenerative dz = months)
21
Q
rare sx of stroke
A
- LOC (rare bc need BOTH hemispheres affected = most strokes don’t do that, OR something damaged midbrain (rare)
- pain
- abnormal mvmt
- loss of memory (is a BILATERAL function)
- decreased concentration
22
Q
example of stroke presentation
A
- having dinner
- suddenly has slurred garbled speech
- couldn’t speak to his wife + understood only a few words
- could barely move left arm and leg
23
Q
left side face weakness with sparing of forehead indicates what
A
it’s a UMN problem (bc UMNs of facial nerves go to both motor nuclei of VII for inn. of FOREHEAD LMNs so one side UMNs not working = no problem)
24
Q
signs of UMN damage in stroke
A
- weakness of arms (detected with pronator drift for ex = flex arm up 90, one arm weak and pronates down)
- clumsy fingers (UMNs imp for fine mvmts)
- positive Babinski
- increased reflexes
25
UMN signs + speech prob: where to localize
region somewhere above the brainstem, probably right hemisphere bc left side sx for ex. then think stroke
26
stroke: after localizing the site of injury with the neuro exam, what is the next step
localizing which vessels are affected
27
vascular territories on the lateral surface of the brain (in sagittal lateral section)
- thin dome front to back on top = ACA
- line in bottom temporal + back occipital = PCA
- all rest of frontal, parietal, temporal = MCA (big circle in the middle)
28
vascular territories on medial surface of brain (sagittal medial section)
- ant half of region below corpus callosum = MCA
- post half of region below corpus callosum + occpital lobe = PCA
- top (frontal + parietal) = ACA
29
vascular territories in coronal cut of the brain
- ACA = superior fifth
- PCA = inferior fifth
- MCA = 3 middle fifths
* all ganglia + cortex*
30
vascular territories in axial cut of the brain
- ACA = anterior fifth
- MCA = middle 3 fifths
- PCA = posterior fifth
31
cortex charact
- diff areas control diff portions of the body
- bigger part of the body to be controlled = bigger portion of cortex dedicated to it. for ex, much more cortex for muscles of face than foot
32
regions of cortex and what they supply from superior medial to middle lateral to inferior medial (imagined in a coronal section)
- top fifth (sup medial) = foot + distal leg
- 2nd fifth = hand
- 3rd fifth (middle lat) = face, arm, proximal leg
- 4th fifth = face
- 5th fifth (inf medial) = vision
33
sx you get with ACA ischemic stroke and related to cortex fct
leg weakness (bc ACA top fifth foot and distal leg)
34
sx you get with MCA ischemic stroke and related to cortex fct
face, arm and proximal leg symptoms weakness (bc MCA to 3 middle fifths)
35
sx you get with PCA ischemic stroke and related to cortex fct
visual loss (bc inf fifth)
36
cortical vs subcortical ischemic stroke
- cortical = in large artery like MCA
| - sub-cortical = in small aa like lenticulostriate aa of MCA (causing small volume infarct)
37
lacunar lesion in ischemic stroke def
small infarct volume, implying ischemic stroke of a small vessel.
and sub-cortical is a word use to precise the location = cerebral hemispheres but not cortex
38
symptoms related to small artery ischemic stroke causing small infarct volume + are they less important
- NOT less important than major vessel occlusion.
- the sx for small vessel occlusion are weakness of face, arm and leg because it supplies blood to internal capsule (where descending UMNs from cortex and ascending axons to cortex pass) (internal capsule goes towards brainstem)
39
symptoms that are found in ischemic stroke with major vessel occlusion that ARE NOT FOUND in ischemic stroke with small vessel occlusion
- language problem
- spatial problem
- visual prob
* sub-cortical injury spares these cortical fcts*
40
what is a cortical homunculus
representation of cortex and the parts of body on its side, disproportional and made as big as the parts of the cortex for them
-use this map for dx what artery affected in stroke pt
41
cortical ischemic stroke (large vessel occlusion) causes what sx and presentation overall
damage to large areas of the brain causes
- language impairment
- impairment in the dominant hemisphere (usually left bc people right handed, etc.) mvmts
- visual problems in the non dominant hemisphere
42
(imp) arteries that can be affected (be the cause) in an ischemic stroke in the brainstem + THEIR LOCATION (doesn't mean what they supply)
- posterior comm aa (midbrain and pons junction)
- PCAs (midbrain and pons junction)
- superior cerebellar (comes off pons junction) (pons and medulla)
- basilar a (pons)
- pontine aa (pons)
- AICAs (medulla top)
- PICAs (medulla middle)
- anterior spinal a (medulla bottom)
43
sx of ischemic stroke to brainstem
- wide variety bc affects CN III to XIII: prob of connections to cerebellum, descending motor tracts, ascending sensory tracts
- visual fct SPARED except if ischemic stroke involving PCA (goes to occipital lobe)
44
(dnm details) midbrain blood supply
- PCAs and branches (sides)
- basilar a (middle)
- superior cerebellar aa (sides)
45
(dnm details) pons blood supply
- basilar a (post half)
| - AICA (ant half)
46
(dnm details) medulla blood supply
if split each side into 3 Ls stuck together medial to lateral (3rd L is really a circle)(small line of the L is in the back)
- PICA (most lat third)
- vertebral aa (middle third = middle L)
- anterior spinal a (medial third = medial L)
47
how MRI helps find ischemia
bright signals = areas of infarct = damage
| -small area of infarct = lacunar infarct
48
usual type of ischemic stroke in brainstem (big a occlusion or small a occlu)
small artery occlusion. (like the lenticulostriate aa of MCA)
49
pathophgy of ischemic stroke in brainstem
htn damaging the small arteries (like pathophgy of small a occl ischemic stroke of lenticulostriate aa of MCA)
50
after did neuro exam to localize sx + suspecting a specific occluded artery, what is the next step
do some tests
- CBC
- PT, PTT (make sure no coag problem)
- SMA-7 (a panel of blood tests including electrolytes, glucose, etc. to rule out other causes of these sx like renal prob or high glucose)
- CT head (rule out tumor or hemorrhage (but should be ruled out in hx) + look for infarction)
- CT angiogram (look for the vessel affected)
51
acute ischemic stroke on CT
can see
- borders of the brain regions harder to distinguish = early sign of ischemia
- can see loss of a cortical ribbon = early sign of infarct
- acute thrombus in vessel (appears bright). in MCA for ex, would call it dense MCA
- NEED TIME before see damage
52
acute ischemic stroke on CT after time elapsed
can see
- large area of infarct (called completed stroke = brain is dead)
- partial territory of infarct with sparing
53
diffusion-weighted MRI in acute ischemic stroke
- can see the changes from stroke earlier than CT
| - can see small areas of infarct or ischemia not seen on CT (after a normal CT, you do an MRI)
54
perfusion imaging (perfusion CT) in acute ischemic stroke
can detect
- contrast of areas with good blood flow (red) vs poor flow (blue)
- TELLS THE DIFFERENCE BETWEEN ISCHEMIA AND INFARCT
* is not a CT angiogram
55
ideal scenario in ischemic stroke
patient symptomatic, found to only have ischemia (no infarct) on perfusion CT, we can now improve the blood flow
(in infarct = no flow = damage = can't help)
56
CT angiogram in acute ischemic stroke
to see the blood vessel that is occluded
- uses IV radio-opaque contast
- visualize cerebral vessels
57
acute ischemic stroke tx options
- ASA (aspirin) small benefit, only give if pt can't receive tPa or thrombectomy
- IV tPa (tissue plasminogen activator) (to lyse the thrombus)
- thrombectomy
58
what tPa does
catalyzes transformation of plasminogen into plasmin, leading to lysis of thrombi
59
when tPa used
- when can be given in the first 4.5 hours
| - if given in within 4.5 hours FROM ONSET OF SYMPTOMS , better functional outcomes at 3 months (especially motor)
60
imaging sequence in acute ischemic stroke usually
1. CT
| 2. CT angiogram if it's relevant (meaning if it's not too late = there's no complete stroke on CT)
61
best way of diff ischemia vs infarction
perfusion CT
62
perfusion CT in a pt with small vessel occlusion acute ischemic stroke before and after tPa
- before tPa = small area of infarct (very dark blue) with big area of ischemia around (blue) called THE PENUMBRA
- after tPa = small area of infarct (very dark blue) and SAVED the big area of ischemia
63
two ways tPa helps in acute ischemic stroke
- opens the occluded vessel (main thrombus)
| - sometimes, improvement with thrombus still there bc tPa helped improve collateral blood flow
64
why time is brain
odds ratio of a good functional outcome is good if thrombolysis is done <90 min and diminishes after that to become low above 3 hours (odds of good fctal outcome are low)
65
major risk of giving tPa
hemorrhage at the site of the stroke (happens bc vessels initially damaged and fragile)
66
do you give tPa in hemorrhagic stroke
no. only for acute ischemic stroke
67
when is thrombectomy done
- in pts with proximal occlusion of vessel (we can reach it)
- if can be done 6 hours or less after sx onset
- done by interv radiologist, like angiogram of angiography and stenting but now go up in cerebral aa
- pull clot out
68
tPa contraindications
- active aco
- very recent surgery
- recent heart attack
- hx of intercranial bleeding
- hemorrhagic stroke
- >4.5 hrs
69
thrombectomy contraindications
- distal vessels
| - >6 hrs
70
first step of managing acute ischemic stroke
treat etiology and risk factors
71
how to find etiology of managing acute ischemic stroke
is inferred from the investigations. if an investigation leads to a possible cause, you assume this is what caused the stroke
72
investigations done to find etiology of acute ischemic stroke
- investigate cardiac source: EKG, Holter, echocardiogram -> find if afib or other -> if + for cardiac source = give aco (AFIB IS THE ONLY INDICATION for aco, rest is antiplatelet)
- investigate large artery source: doppler, CT and MRI angiography -> find if carotid or vertebral a source -> if + (meaning there was a thromboembolism), antiplatelet + surgery (cardiac endarterectomy)
- investigate intracerebral source: CTI and MRI angiography -> if +, antiplatelet
73
aside from aco or antiplatelet (cardiac source), antiplatelet + surgery (large a), antiplatelet (intracerebral), what do you always do in these 3 cases for acute ischemic stroke
treat the RFs
- ***HTN***
- smoking
- diabetes
- cholesterol
74
after management of etiology and RF, what do you do
aid adaptation and recovery
- interprofessionalism
- nurses help prevent complications
- think of where to discharge the patient (note: stroke more common with older age)
75
how recovery happens after an acute ischemic stroke, for the following 3-6 months
2 ways
1. brain plasticity (but less as you get older)
2. restored blood supply to ischemic area
3. pt adapts to the DEFICIT that remains (physio, etc.)
76
what is cardiac endarterectomy
procedure to remove the ats plaque and widen the artery lumen
- surgeon ties artery
- slices it open
- expose lumen
- scoop out the plaque
- sew back up the artery
77
who benefits from cardiac endarterectomy in acute ischemic stroke
pts with SYMPTOMATIC internal carotid artery stenosis of 70-99%
* symptomatic means you had an artery occlusion acute ischemic stroke on the same side (like MCA occlusion)
* want to remove this big thrombus which can embolize*
78
in a pt with an ats plaque in the internal carotid a, how do you deduce the % of stenosis
analyze velocity of blood flowing in that area. can deduce stenosis from it. higher flow = more stenosis
79
important thing about rehab hospitals
not just somewhere to send the patient. goals are
- maximize experience-dependent neural plasticity (if pt uses their damaged arm more = enhanced plasticity in the brain)
- develop compensatory strategies to improve fct
80
after tx of etiology and RFs (which can include surgery) + sent to rehab hospital, what do you do
F-U one month later
- check QOL
- BP monitoring
- RFs (smoking, exercise, diet)
- meds compliance
* explain you want to reduce the ats risk*
81
TIA def
transient neurological deficit caused by ischemia with full resolution between 5 min and 1 hour (textbooks = up to 24 hours but probably infarction by then)
82
pathophgy of TIA
- same as stroke, something occluding an a (ats or thromboembolism from ICA or vertebral a)
- fortunately, blood supply is restored naturally fast enough that the person recovers completely
83
sx of TIA
same as stroke but recover
| -loss of vision for ex
84
what is the ABCD2 score (age, BP, clinica = weakness and language, duration = less or more than 1 hour) in TIA
score when you give each of these things some pts, greater score = greater risk of having a STROKE
*STROKES are very likely to occur in the 1-2 years after a TIA*
85
TIA management
*very serous problem, have to tx it*
-treat the RFs (smoking, exercise, diet, htn)
-tx the cause (like for stroke). find it by inferring it and treating appropriately (cardiac, stenosis in big artery, etc.
so same as initial management of stroke but bc TIA no rehab hospital, etc.
86
most important thing for acute ischemic stroke primary prevention
hypertension
87
most imp things in acute ischemic stroke tx
time is brain
- 4.5 hrs for tPa
- 6 hrs for thrombectomy (or more if only ischemia on imaging)
- ID etiology and RFs
- TIA = tx as stroke, high risk of stroke occurence
88
4 types of hemorrhagic strokes
- epidural (dura attached to skull tightly at multiple pts)
- subdural (between dura and arachnoid, no strong attachment)
- sub-arachnoid (between arachnoid and pia) *cerebral arteries and circle of Willis are in subarachnoid space*
- intra-parenchymal (intra-cerebral) within the brain itself
89
epidural vs subdural hemorrhagic stroke
- epidural = strong attachment of dura to skull so hematoma can't spread around external surface of dura
- subdural = less strong attachment so blood can spread easily in hemisphere + to another one
90
anatomy of each type of hemorrhagic stroke
- epidural = biconvex (bc restricted)
- subdural = crescent (bc can spread along convexity)
- sub-arachnoid = follows contour of brain bc pia does so. + follows the sulci
- intraparenchymal = oval, round
91
how will know it's a hemorrhagic stroke
on CT. hematoma = bright white appearance (ischemia was more subtle on CT)
92
why epidural hematoma is very serious (life-threatening surgical emergency)
1. dura attached to skull = large volume in a restricted space = increased P. brain can get pushed, can get herniation under tentorium or down foramen magnum compressing brainstem (can be fatal)
2. is often from a damage to the middle meningeal A so high P arterial blood accum rapidly in this restricted space
93
epidular hematoma management
- remove the blood
| - repair the arterial injury and the skull fracture if that was the cause
94
subdural hematoma: why is it less serious
1. blood can spread along convexity of hemisphere so less pressure
2. often from damage of fragile veins draining in the venous dural sinuses
3. bc is venous blood, accum less quickly
95
why subdural hematoma happens more in elderly
- brain atrophy = more space for venous blood to circulate
- falls
- antiplatelets and acos
96
tx of subdural hematoma
either surgical or conservative depending on mass effect (clinical, radiological), age, comorbidity, aco
-conservative bc blood products can get proken down sometimes + when large volume of blood
97
primary vs secondary prevention in stroke
- primary = tx RFs and never had TIA or stroke (so TIA included) if tx RFs after TIA = secondary prevention
- secondary = already had stroke or TIA + tx the stroke or the TIA AND tx the RFs
98
are all strokes sx
not all. some called subclinical
- especially small aa in deep areas of brain supplying areas for subtle fcts
- this is detected with imaging
99
middle meningeal a supplies blood where
meninges (so not brain)
100
pathologies of middle meningeal a
hemorrhage
| NOT ischemia to the brain, doesn't supply the brain
101
what is the Monroe-Kelley hypothesis for ICP
increased ICP is either due to increased
- normal components (CSF, brain, blood)
- new components (tumor, pus, extravascular blood)
102
why is increased ICP harmful
- direct damage to neural tissue
- displacement of the brain (herniation)
- drop in the cerebral perfusion pressure (CPP). CPP = BP - ICP (bc of this gradient where BP > ICP, blood flows to brain). if ICP higher, less blood to brain
103
in what types of hemorrhagic strokes do we worry about increased ICP
- epidural hematoma
| - subdural hematoma
104
sx and signs of increased ICP (seen in subdural hematoma and epidural hematoma)
- headaches bc CN V inn. meninges
- nausea
- false localizing sign (damage of VI easily)
- papilledema (P in back of eye)
- cerebral dysfct (some fcts not working, more sx from that)
- decreased level of consciousness (ONLY when both hemispheres affected, as in sub-falcine herniation)
105
diff kinds of herniations that increased ICP (seen in epidural and subdural hematoma) can cause
first to last one to happen:
- sub-falcine (one hemisphere pushed across falx cerebri)
- central herniation (brain going downwards)
- trans-tentorial herniation
- brain going downwards (tonsillar herniation)
106
importance of sub-falcine herniation (1st one) in subdural or epidural hematoma
- initially, hematoma causes increased P in one hemisphere, only one hemisphere affected = no decreased consciousness
- when reach point of sub-falcine herniation, P now on both hemispheres so can get decreased of consciousness
107
charact of uncal trans-tentorial herniation (3rd one) in subdural or epidural hematoma
- tentorium cerebelli between cerebellum and temporal lobe
- opening medially where the brainstem sits
- the medial part of the temporal labe is called the uncus
- you can get an uncal trans-tentorial herniation
108
charact of tonsillar herniation (4th one) in epidural and subdural hematoma
- tonsils can herniate in the foramen magnum where the spinal cord is
- this is caused by step wise process from something increasing ICP in skull
109
anatomy relating to uncus of the temporal lobe
- one uncus on each side
- midbrain middle
- optic nn and chiasm on top of midbrain
110
uncal (trans-tentorial) herniation: what happens exactly
- one uncus swollen bc something increasing ICP above on its side
- swollen uncus herniates medially
- swollen uncus pushes midbrain to contralat side
- herniation of MIDBRAIN causes CN III (coming off on both sides, fragile) damage
- also, midbrain herniating more and more and pushed against hard edge of contralateral tentorium so is damaged too (part containing UMNs of cerebral peduncles)
111
consequences of uncal trans-tentorial herniation
- ipsilateral hemiparesis (ipsi to swollen uncus) = weakness in body on ipsilateral side (of swollen uncus), contralat to where mdibrain damaged by tentorium
- blown pupil (dilates) bc of CN III dysfct = no more control
112
what problems if stroke rather than uncal trans-tentorial herniation
- stroke = contralateral hemiparesis and ispilateral CN III dysfct
- uncal trans-tentorial herniation on midbrain injuring midbrain = ipsilateral hemiparesis + contralateral CN III dysfct
* in both cases hemiparesis from UMN injury*
113
bloody tap after difficult LP (lumbar puncture) and not sure if blood in subarachnoid space (CSF) or just badly done LP: should you do an angiogram?
no. angiogram only tells if there is non ruptured aneurysms present at the moment and not if any aneurysms already ruptured causing blood leak in CSF (remember aa in subarachnoid space)
114
causes of subarachnoid hemorrhage (SAH)
- aneurysmal (MOST COMMON): ''berry aneurysm'' and circle of Willis
- traumatic
- idiopathic (peri-mesencephalic)
* aneurysms are ACQUIRED (developmental) not congenital and are asx until they rupture and bleed*
* DON'T usually cause sx by exerting P*
115
two common clinical pres for ANEURYSMAL SAH
1. sentinel bleed with headache
- sudden onset, maximal at onset
- worst headache of my life
- constant for many hours then fades away
2. full rupture
- bigger volume leaked in subarachnoid space
- LOC
- focal neuro deficits
- seizure
116
pathophgy of full rupture aneurysmal SAH
- initially, the brain damage giving the bad sx is bc of toxicity lot of accum blood with cells proteins and cytokines, irritating surface of the brain
- it is only LATER that this causes damage by ischemia or raised ICP
117
steps of diagnosis of SAH
- clinical suspicion from complaint or severity (LOC) leads to you doing a CT brain
- if the CT is negative, an LP is done (even though negative CT makes SAH very unlikely)
- if there was no SAH, the CSF is normal
- if there was a SAH recently (few hours ago) = blood in CSF
- if there was a SAH about 12 hours ago or more = xanthochromia of CSF (yellowish discoloration of CSF from breakdown of cells)
- (CAN do an angiography CT vs MRA vs conventional) but will only show present aneurysms and won't tell if there was an SAH
118
2 tx for aneurysms related to circle of Willis
- surgical clip put around the neck of the aneurysm on its outside (risky surgery)
- with interventional radiology, a catheter stuffs the aneurysms with coils to cause clotting INSIDE it. the clot will never leave. problem is if neck of aneurysm too big, the coils can slip out
119
long term prognosis for someone who's had an aneurysmal SAH
- grade severity
- depends a lot on volume and extent of blood
- comatose pt + large volume of blood = poor prognosis
- pts who recover LOC do physically well
- subtle cognitive deficits can remain and be disabling, but hard to see on exam
120
should we tx an incidental (asymptomatic) aneurysm (meaning you find it by accident and didn't know it was there) ?
- > 1 cm or in anterior circulation = higher chance of rupturing
- risk of rupture is less than a symptomatic aneurysm
- risk of rupture depends on size, location, expected lifespan of pt (longer life remaining to live = more chance of it breaking eventually)
- depends on risks to intervention: patient factors + aneurysm anatomy
- depends on pt preference
- aneurysms with narrow neck are easy to tx (clipping or endovascular coiling)
121
what is the dilemma with doing an angiogram (MRI or CT or conventional) after SAH ?
if do the angiogram and find an aneurysm, you still don't know if the pt had a SAH and so you still don't know if the aneurysm is symptomatic or not
- take good hx (TIME FRAME IS IMPORTANT = SUDDEN ONSET LOT OF PAIN)
- tell pt we're not sure and it's fine
122
causes of intraparenchymal hemorrhage
- hypertensive (common)
- cerebral amyloid angiopathy (common)
- aco
- arterio-venous malformation
- drug use (like cocaine)
- bleeding disorder
123
hypertensive intraparenchymal hemorrhage is what
pathophysiology similar to ischemic stroke. it's just that now, the ats vessel (ats caused by htn) ruptured
124
cerebral amyloid angiopathy as cause of intraparenchymal hemorrhage is what
deposition of something on the vessel causes it to be fragile and break
125
clinical features of intraparenchymal hemorrhage
- similar to ischemic stroke
- more sudden and severe at onset
- more likely to have headache, mass effect and altered level of consciousness (remember these weren't common in ischemic stroke)
- doesn't always respect vascular territories
126
when not sure about the stroke type (hemorrhagic vs ischemic vs specifically hemorrhagic intraparenchymal)
do a CT to diff ischemic vs hemorrhagic
127
how CT helps diff the type of intraparenchymal hemorrhage
- hypertensive type is deep in the brain (more central on axial cut) and affects small arteries going there
- amyloid is more superficial and peripheral bc in superficial cerebral vessels
128
important RF in stroke overall
htn can damage vessels and increase the risk of both ischemic and hemorrhagic stroke
129
does it help to diff on CT if the intraparenchymal hemorrhage is hypertensive or cerebral amyloid angiopathy
no because both = no tx. supportive tx
- pt improves as blood resorbed
- hypertensive intraparenchymal hemorrhage = will do better long term BP control
- amyloid hemorrhage = high risk of recurrence in 1-2 yrs but nothing you can do
130
why still do CT if suspect intraparenchymal hemorrhage
helps you diff hemorrhage (very bright bc blood hypercellular) from tumor (can be mixed meaning bit bright with surrounding darker edema)
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anatomy of venous stroke
- veins in substance of brain drain to venous sinuses (between two layers of dura): the cortical veins drain in sup sagitt sinus. the deep veins drain in the inferior sagitt sinus
- superior sagittal sinus drains in trigone (where all meet in back)
- inf sagitt sinus drains in straight sinus which drains in trigone
- the two (straight and sup sagitt sinus) meet at trigone to form the two transverse sinuses
- these become the sigmoid sinuses (lat) and then these become the internal jugular vv
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when to suspect venous stroke (venous infarct)
have combination of ischemia and hemorrhage on both sides of the brain
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Virchow's triad of cerebral venous sinus thrombosis (venous stroke)
- hypercoagulability (caused by birth control pill = BCP or pregnancy up to 3 months post-partum)
- vessel injury caused by smoking
- possibly stasis
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pathophgy of venous stroke
- reduced venous outflow due to thrombosis in dural venous sinus
- increased cerebral blood volume
- increased ICP causing papilledema and ischemic stroke (bc of the high ICP damage)
- also, venous sinus can break bc of high ICP and get hemorrhagic stroke
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typical presentation of venous stroke
headache and papilledema
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main diff between venous stroke vs ischemic and hemorrhagic strokes on imaging
- venous = BILATERAL hemorrhagic and ischemic strokes
- ischemic and intraparenchymal hemorrhagic strokes = usually FOCAL and UNILATERAL
* see bilat findings = think venous sinus thrombosis*
