Cerebrovascular diseae Flashcards
Clinical term applies to any abrupt nontraumatic brain insult- literally a blow from an unseen hand
Stroke
2/3 of infarct are from
Thrombi
Normal brain metabolism is how many ml/100g tissue/min
55 ml/100g tissue/min
Oligemia is more common in the gray matter due to
Gray matter receives 3-4x more blood flow than white matter
Why are watershed zones more prone to infarction
They are served by penetrating end arteries and have no alternate route for perfusion
Mechanism of cytotoxic edema
Failure of membrane pumps permits efflux of K+ and simultaneous influx of Ca, Na and water, causing increased water content in the affected region
Cytotoxic edema peaks at how many days post infarction, and is maximum in what brain matter
3-7 days in gray matter
Vasogenic edema primarily affects what brain matter
White matter due to lose endothelial cell integrity
A subtle but important blurring of the gray white layers of the insula due to early edema. Can be seen in CT done within 6 hours of MCA occlusion
Insular ribbon sign
Hyperintense light bulb sign signal in DWI can be seen as early as how many minutes post infarction
15 minutes
T2 hyperintense signal from infarct will develop how many hours post ictus
6-12 hours post ictus
IV t-PA is frontline therapy for patients within how many hours of symptom onset
4.5 hours
endovascular thrombectomy can be done within how many hours of symptom onset
24 hours
ASPECTS score that can be a considered a candidate for thrombolysis
7 to 10
may be useful in identifying ischemic but still salvageable tissue (ischemic penumbra) to successfully guide selection of patients for stent retriever therapy beyong 4.5 hours
perfusion sensitive CT and MR techniques
this MRI sequence reflects “pure” diffusion behavior, free of underlying T2 contributions (“shine through” or “dark through”)
ADC
peak of edema in infarct as well encephalomalacic changes occur in what days
3-7 days
“fogging effect” may be encountered on CTs done during what week after infarction as edema and mass effect are subsiding
2nd week
edema that persists beyong __ month/s effectively rules out simple ischemia and should raise the possibility of recurrent infarction or an underlying tumor
1 month
pathophysiology of hemorrhagic transformation
reperfusion into infarcted capillary beds may secondarily lead to gross or microscopic hemorrhage, microscopic leakage of RBC (diapedesis), physical disruption of the capillary endothelial cells, loss of vascular autoregulation and anticoagulation or thrombolytic use
difference of hemorrhagic infarction from hemorrhagic transformation
hemorrhagic infarction is confined to the territory of the infarcted vessel, wheras primary hemorrhage does not necessarily respect vascular boundaries
true or false: IVH is uncommonly seen with hemorrhagic transformation and should raise the posibility of another process (such as hypertensive bleed or a ruptured AVM)
true
peak time of hemorrhagic transformation
1 to 2 weeks
appearance of hemorrhagic transformation
serpiginous line of petechial blood ff the gyral contours of the infarcted cortex. the dots are often patchy and discontinuous (petechial gyral pattern)
this event underlies both hemorrhagic transformation and contrast enhancement of infarctions
blood brain barrier breakdown
CT detected enhancement of infarcted brain parenchyma typically begins at about what week and peaks at how many days
1 week and peaks at 7 to 14 days
enhancement fades in infarct when gliosis ensues and BBB is repaired, and then resolves by what month
3 months
intravascular enhancement on MR is commonly seen in the infarcted territory during what week
1st week; seen in a majority of cortical infarcts at 1 to 3 days, and resolves by 10 days
virtually all cortical infarcts enhance by MR at __ weeks
2 weeks
Elster rule of 3s in cortical infarct enhancement in MR
parenchymal enhancement peaks at 3 days to 3 weeks and resolves by 3 months
patterns of ischemic events
diffuse (hypoxic-ischemic injury), multifocal (vasculitis, emboli), or focal (single embolism or thrombus)
Minutes post infarct CT and MR findings
CT- no changes
MR- absent flow void, arterial enhancement (1 to 10 days), DWI shows high signal
2-6 hours post infarct CT and MR findings
CT- hyperdense artery sign, insular ribbon sign
MR- brain swelling (T1), subtle T2 hyperintensity
6 to 12 hours post infarct CT and MR findings
CT- sulcal effacement, +/- decreased attenuation
MR- T2 hyperintensity
12 to 24 hours post infarct CT and MR findings
CT- decreased attenuation
MR- T1 hypointensity
3 to 7 days post infarct CT and MR findings
CT- maximum swelling
MR- maximum swelling
3 to 21 days post infarct CT and MR findings
CT- gyral enhancement (peak 7 to 14 days)
MR- gyral enhancement (peak 3 to 21 days) petechial methemoglobin
30 to 90 days post infarct CT and MR findings
CT and MR- encephalomalacia, loss of enhancement, resolution of petechial blood
classically, strokes and TIAs are divided into
anterior (carotid territory) or posterior (vertebrobasilar territory)
carotid endarterectomy can be done in anterior circulation infarcts if the carotid is narrowed by at least how many percent compared to its normal diameter
70%
ischemia in this territory may cause visual changes, aphasia, or sensorimotor deficits due to retinal, cortical or subcortical damage
carotid artery
strokes in this territory more likely to cause syncope, ataxia, cranial nerve findings, homonymous visual field deficits and facial symptoms opposite those of the body
vertebrobasilar strokes
occlusion of ophthalmic branch of ICA may cause
transient monocular blindess (amaurosis fugax)
atherosclerotic disease in this carotid segment is responsible for the majority of ischemic events in ICA territory
carotid bifurcation
carotid hemodynamic effects begin to be seen when there is ___% reduction in area or ___ % decrease in diameter
> 70% stenosis, <30% narrowing
gold standard for pre procedure carotid artery evaluation, but is being replaced by noninvasive studies in many centers
common carotid angiography
terminal bifurcation of ICA is into the
Anterior and middle cerebral arteries
serves the rostral portions of the basal ganglia
medial lenticulostriates
these branches supply the corpus callosum
pericallosal branches
branches that supply the medial aspects of the frontal and parietal lobes
hemispheric branches
5% of infarcts involve the
ACA
supplies the anterior-inferior aspect of the internal capsule, putamen, globus pallidus, caudate head, and portions of hypothalamus and optic chiasm
medial lenticulostriates
largest of the medial lenticulostriates that supply the caudate head/anterior internal capsule region
recurrent artery of Heubner
infarctions in the medial lenticulostriate territory may cause
problems with speech production (motor aphasia), facial weakness, and disturbances in mood and judgement
frontal pole branches of the ACA
orbitofrontal and frontopolar arteries
ACAs terminate as a bifurcation into the _____. these arteries run parallel to the corpus callosum from front to back, giving supply to the medial cortex of the frontal and parietal lobes
lower pericallosal and upper callosomarginal branches
branches that courses around and feeds the corpus callosum
pericallosal artery
unilateral damage in the ACA hemispheric branches will cause _____ on the opposite side of the body
preferential leg weakness
bilateral ACA infarction lead to
incontinence and an awake but apathetic state known as akinetic mutism
infarction in this area can cause a variety of interhemispheric disconnections syndromes
infarction of corpus callosum
artery that is host to almost 2/3 of infarcts
MCA
supplies most of the basal ganglia
lateral lenticulostriates
supplies the lateral cerebral surface
hemispheric branches
arise from the proximal MCA as numerous small perforating end-arteries distributed to the putamen, lateral globus pallidus, superior half of the internal capsule and adjacent corona radiata
lateral lenticulostriates
infarcts in these regions are commonly asymptomatic or may affect contralateral muscle tone and motor control
isolated vascular lesions of the globus pallidus or putamen
interruption of visual connections to the lateral geniculate nucleus results in
subtle type of contralateral homonymous hemianopsia
conduction aphasia or the inability to repeat, read aloud, despite preserved comprehension and fluency is due to infarction in the
arcuate fasciculus pathway from Wenicke to Broca speech areas
insula is supplied by
hemispheric branches
early presence of insular ribbon sign is due to
insular region is the farthest from any potential collateral supply when proximal MCA is occluded
supplies the anterolateral tip of the temporal lobe
anterior temporal artery
supplies the frontal lobe
operculofrontal arteries
supplies the motor and sensory strips
central sulcus arteries
supplies the parietal lobe behind the senosry strips
posterior parietal artery from posterior hemispheric branches of MCA
supplies the posterolateral parietal and lateral occipital lobes
angular artery
supplies majority of the temporal lobe
posterior temporal artery
occlusion of the rostral MCA branches of the dominant hemisphere will cause
motor/Broca aphasia
supplies the Wernick area
posterior branches of MCA in the dominant hemisphere
occlusion to this MCA branch may interrupt visual radiations, causing contralateral homonymous field defects
posterior temporal branch occlusion
infarction of these areas will produce contralateral weakness which affects face and arm more than leg
either hemispheres’s precentral gyrus
contralateral cortical sensory loss occurs when these areas are affected
the primary or association sensory cortex behind the central sulcus is affected
infarct in this area causes confusional states, bizarre impairment in visuospatial abilities and sometimes neglect (nonrecognition) of the left body
nondominant right hemisphere posterior MCA infarcts
complete occlusion of this artery cause these combination of deficits contralateral face and arm hemiparesis, field defect, either neglect or global aphasia, depending on which hemisphere is affected
MCA
If MCA stem is occluded because of internal capsule involvement, this symptom is apparent
leg weakness
VA originate from
subclavian arteries
VA ascend upward in the transverse foramina of what cervical level and turns sharply at what level
C6-C3, turns at C2-C1 foramen magnum levels
VA unites at what level to form Basilar artery
anterior to the low medulla
narrowing of cervical portions of the VA may be due to
compressive uncovertebral osteophytes
remains mainstay of tx for VB ischemia
anticoagulation and antiplatelet agents
leg weakness can be seen in what region of insult
either hemispheric ACA branch
incontinence, akinetic mutism may be seen in what arterial branch
both hemispheric ACA branches
facial weakness may be seen in what arterial branch
either medial lenticulostriates of ACA
dysarthria, with or without motor aphasia may be seen in what arterial branch
left medial lenticulostriates of ACA
face and arm > leg weakness may be seen in what arterial branch
either hemispheric branch of MCA
motor aphasia, receptive aphasia, global aphasia may be seen in what arterial branch
left hemispheric branch of MCA
neglect syndrome, visuospatial dysfunction may be seen in what arterial branch
right hemispheric MCA branch
variable lacunar syndromes may be seen in what arterial branch
either lateral lenticulostriates of MCA
hemianopsia may be seen in what arterial branch
eithr hemispheric PCA
cortical blindness, memory deficits may be seen in what arterial branch
both hemispheric PCA
somnolence and sensory disturbances may be seen in what arterial branch
either thalamoperforators of PCA
ataxia, vertigo, vomiting, coma if mass effect with or without brainstem deficits may be seen in what arterial branch
either PICA, AICA or SCA of cerebellar arteries
man in barrel syndrome may be seen in what arterial branch
wither ACA/MCA/PCA (watershed)
severe memory problems may be seen in what arterial branch
bilateral ACA/MCA/PCA (watershed)
sends large branches to the cerebellum and smaller perforating vessels to the brainstem
basilar artery
occlusion of this artery is usually rapidly fatal, due to infarction of respiratory and cardiac centers in the medulla
basilar artery
occlusion of perforating end arteries of BA causes focal brainstem infarction, usually manifest as ____. these lesions often extends to the ventral surface
cranial nerve dysfunction, ataxia, somnolence, and crossd motor or sensory deficits
metabolic disturbances and hypertensive hemorrhages most commonly in the pns tend to be more located where
centrally and diffusely located
locked in state is associated with large or multiple lesions in the
pons
BA ends at its bifurcation into ___ at the midbrain level, just above the tentorial hiatus
PCA
major branches of PCA
midbrain and thalamic perforating vessels, posterior choroidal arteries, cortical branches to the medial temporal and occipital lobes
10 to 15% of infarcts occur at what vessel
PCA
infarction in this part of brainstem leads to loss of pupillary light responses, impaired gaxe and somnolence
midbrain, due to the damage of the quadrigeminal plate, third cranial nerve nuclei, RAS formation
most common problem in thalamic infarction
contralateral sensory loss
supply the choroid plexus of third and lateral ventricles, pineal gland, regions contiguous with the third ventricle
posterior choroidal artery from proximal PCA
supplies the inferomedial temporal lobe
inferior temporal arteries from PCA cortical branches
superior occipital gyrus is supplied by
parieto-occipital artery from PCA cortical branches
visual cortex of the occipital lobes is supplied by
calcarine artery from PCA cortical branches
bilateral inferomedial infarction may cause
memory deficits
loss of the primary visual cortex causes
complete loss of vision in the opposite visual field (homonymous hemianopsia)
condition found in 20% if patients, in which one or both of the proximal P1 PCA segments may be hypoplastic or absent. in these cases, flow is derived from the ICA system via a prominent posterior communicating artery. this is commonly referred to as
fetal origin of PCA, since embryologiclly, the PCA develops with the ICA
headache, vertigo, nausea, vomiting and ipsilateral ataxia are hallmarks of what region of infarct
cerebellar infarct
management of cerebellar infarction or hemorrhage
posterior fossa decompression
upper parts of cerebellum are supplied by
superior cerebellar arteries
SCA territory includes
superior vermis, middle and superior cerebellar peduncles and superolateral aspects of the cerebellar hemisphere
these arteries arise from proximal BA to supply the anteromedial cerebellum and sometimes part of the middle cerebellar peduncle
AICA
usually the smallest of the 3 major cerebellar hemisphere branches
AICA
occlusion of this cerebellar artery causes ipsilateral limb ataxia, nausea, vomiting, dizziness and headache
AICA
bottom of the cerebellum is supplied by
PICA
it is the first major intracranial branche of the VB system, usually arising from the distal vertebral artery, 1 to 2 cm below the basilar origin
PICA
PICA territory includes
dorsolateral medulla, inferior vermis, and posterolateral cerebellar hemisphere
AICA-PICA loop means
PICA maintains a reciprocal relation with AICA above it. if PICA is large, then the ipsilateral AICA is usually small, and vice versa
usually the largest cerebellar hemispheric branch and is the most commonly infarcted cerebellar artery
PICA
Wallenberg syndrome, including ataxia, facial numbness, Horner syndrome , dysphagia and dysarthria are seen in what region of brain and artery
medulla, PICA
an episode of transient global hypoperfusion may result in infarctions at what regions
watershed regions between arterial territories
typical triggering events in watershed infarcts
cardiac arrest, massive bleeding, anaphylaxis, surgery under general anesthesia
these are regions perfused by terminal branches of 2 adjacent arterial territories
watershed zones
imaging shows a string of small deep white matter lesions (“rosary bead sign”) or damage extending out from the “corners: of the lateral ventricles on higher sections in these infacted regions
watershed infarcts
characteristic clinical findings include weakness isolated to the upper arms (man in a barrel syndrome) , cortical blindness and memory loss
watershed infarcts
these are small subcortical infarcts that may occur in any territory. accounts for 15 to 20% of strokes
lacunes
size of lacunes
2-5 mm3 cavities
lacunar infarcts result from unfarction of
penetrating arteries
pure motor or sensory syndromes may occur with these infarcts
lacunar infarct
these infarcts are common in patients with history of long standing hypertension, leading to lipohyalinosis of the vessels and eventual thrombosis
lacunar infarcts
characteristic locations of lacunar infarcts
lenticular nucleus 37%, pons 16%, thalamus 14%, caudate 10%, IC/corona radiata 10%
isolated lesions in the anterior limb of IC interrupt connections to the
anterior frontal lobe
begining at the genu of IC and posterior IC, it carries the
corticobulbar, head,arm, and then leg fibers in somatotopically organized fashion
lesions in what part of IC are clinically most important since they may cause severe sensory, motor or mixed deficits
posterior limb of IC
lesions at this part of the IC may disrupt speech production or swallowing, but generally become apparent only when bilateral
genu
refers to state of multiple lacunar infarcts
etat lacunaire
refers to enlarged perivascular spaces (Virchow-robin spaces) that may develop around perforating vessels
etat crible
Virchow-robin spaces should follow these features
follow CSF intensity in all sequences, have no associated mass effects, occur along the path of a penetrating vessel
common locations for Virchow-robin spaces
medial temporal lobes, inferior 1/3 of the putamen and thalamus, sometimes seen aong the course of small medullary veins near the vertex
most perivascular spaces seen on MR are between how many mm
1 and 3 mm, some up to 5 mm or larger
DWI in acute infacrt may remain hyperintense for about how many months
1 month
these are commonly associated with patchy or diffuse T2 hyperintensities in the centrum semiovale
small vessel ischemic changes (UBOs)
small vessel ischemic changes are also called
white matter hyperintensities, small vessel ischemic disease, senescent change, Binswanger disease, multi-infarct dementia and leukoariosis
these conditions have been linked to reversible cerebral vasoconstrction syndrome, which can mimic vasculitis
Drug exposure (heroin, amphetamines, serotonin reuptake inhibitors), migraine and post ictal states
this syndrome causes irregular beading of vessels but usually without the inflammatory infiltration of the vessel wall characteristic of vasculitis
reversible cerebral vasoconstrction syndrome
vasculitis may be trigerred by
autoimmune disorders, polyarteritis nodosa, idiopathic processes
management of vasculitis
steroids or cytotoxic drugs, RCVS is manged with vasodilators and removal of underlying trigger
these infarcts occur in younger patients who present with headache, sudden focal deficits, and often seizures
venous infarcts
predisposing factors in venous infarcts
hypercoagulable states, pregnancy, infection (spread from contiguous scalp, face, middle ear or sinus), dehydration, meningitis, and direct invasion by tumor
common sinuses affected in venous infarcts
superior sagittal, transverse, straight sinus and cavernous sinus, either alone or in combination
pattern of hemorrhagic infarction in venous versus arterial
venous- deep cortical or subcortical regions, they tend to be rounded and may spare some overlying cortex
arterial- classic wedge-shaped which grow larger toward the surface
empty delta sign in venous clot is usually seen at what weeks
1 to 4 weeks after sinus occlusion
empty delta sign may be confused if CT scanning is delayed for more than 30 min after contrast infusion due to
differential blood pool clearance and dural absorption of contrast, effectively highlighting the dural margins of a normal venous sinus
best imaging evaluation for venous clots
spin-echo MR and MR venography
MR sequence used for SAH
FLAIR
MR sequence used in parenchymal hemorrhage
GRE
better imaging modality for detection of subacute or chronic hemorrhage
MR
MR signal generated by blood depends on a complex interplay of
hematocrit, oxygen content, type of hemogobin and chemical state of its iron-containing moieties, tissue pH, protein content of any clot formed, and integrity of RBC membranes
oxygenated hemoglobin is sequentially converted to ____ over time
deoxyhemoglobin, methemoglobin and hemosiderin
a small halo of surrounding edema is common in what phase of parenchymal bleeds
subacute
iron within hemorrhage breakdown products changes the effective local magnetic field, a process known as
magnetic susceptibility
key to the diagnosis of amyloid angiopathy is
identification of numerous additional punctate old hemorrhages on GRE, distributed peripherally, in the cortex, and near the gray-white junction
hypertensive hemorrhage typically involves the
deep gray structures, especially thalami and BG
oxyhemoglobin appears as high SI on T2 because
it is diamagnetic, containing ferrous ions
deoxyhemoglobin causes accelerated dephasing of spins on T2 and GRE which results in signal loss because
it is paramagnetic, but it also containes ferrous ions
oxyhemoglobin conversion to deoxyhemoglobin occurs over how many hours and is dependent on
local pH and oxygen tension
in parenchymal or extraaxial hemaotma, further oxidation of deoxyhemoglobin leads to formation of
methemoglobin
methemoglobin is what type of magnetism
ferric paramagnetic substance
methemoglobin transformation occurs when
several days or longer, parallel in time course to lysis of RBCS
this type of hemoglobin causes a makred acceleration of T1 relaxation, leading to bright signal on T1
methemoglobin
this type of hemoglobin contained within intact RBC is able to set up local field gradients between the cell and the protons outside, leading to signal loss on T2
methemoglobin
helpful indicator of subacute blood products
bright T1 signal
methemoglobin is in early intracellular if it appears what on T2
low SI
methemoglobin is extracellular if it appears what on T2
bright
T2 of subacute hematomas show _____, in which a dependent later of intact cells exhibits dark signal and a plasma supernatant showing bright signal
hematocrit effect
RBC and hemoglobin state in <1 day
intact RBC, oxyhemoglobin
oxyhemoglobin appearance on T1 and T2
iso or dark T1, Bright T2
RBC and hemoglobin state in 0-2 days
intact, deoxyhemoglobin
deoxyhemoglobin appearance on T1 and T2
iso or dark T1, dark T2
RBC and hemoglobin state in 2- 14 days
intact, methemoglobin (intracellular)
intracellular methemoglobin appearance on T1 and T2
T1 bright, T2 dark
RBC and hemoglobin state in 10-21 days
lysed, methemoglobin (extracellular)
extracellular methemoglobin appearance on T1 and T2
T1 bright, T2 bright
RBC and hemoglobin state in > 21 days
lysed, hemosiderin/ferritin
appearance of hemosiderin in T1 and T2
T1 iso/dark, T2 dark
hemosiderin is what type of magnetism
paramagentic ferric that is insoluble in water
occasionally, large or recurrent SAHs will lead to diffuse hemosiderin deposition on the brain surface, a condition known as
superficial hemosiderosis or superficial siderosis
CSF-lined compartment which surrounds the blood vessels and communicates with the ventricular system
Subarachnoid space
unruptured pcom aneurysm may present as
unilateral 3rd nerve palsy
unruptured ICA/parasellar aneurysm may present as
cavernous sinus syndrome
unruptured acom aneurysm may present as
optic chiasmal syndrome (bitemporal field defect)
berry aneurysms often occur where
near branch points of circle of Willis, 85% from anterior part of circle of Willis, while 15% arise in vertebrobasilar territory. branch points near acom (33%), MCA (30%), pcom (25%) and basilar (10%)
when distal aneurysm is seen, what must be considered
prior history of trauma, systemic infection
most sensitive places to look for SAh on CT
dependent portions of the subarachnoid spaces– interpeduncular fossa, posterior sylvian fissure, far posterior aspects of occipital horns
if SAH cannot be detected due to patient;s low hematocrit, or the amount of hemorrhage is small or with delayed scanning, this procedure can confirm a suspected SAh
detection of RBCs or xanthocromia by lumbar puncture
how to know the ruptured aneurysm if there are multiple aneurysms
one that is largest or more irregular, has focal mass effect, intra-aneurysmal clost, or shows change on serial examinations
much feared complication in early clipping or coiling of aneurysm
vasospasm
true or false: parenchymal bleeds generally have a higher initial mortality than infarcts, but on recovery show fewer deficits than a similar-sized infarct
true
hypertensive hemorrhage are common in these areas
putamen (35 to 50%), subcortical white matter (30%), cerebellum (15%), thalamus (10 to 15%), pons (5 to 10%)
primary predisposing factor to hypertensive hemorrhage
lipohyalinosis of vessels
four main subtypes of vascular malformations
AVMs, cavernous malformations, telangiectasias and venous malformations
these are high flow lesions and the most common type of brain vascular malformation
AVM
common location of AVMs
supratentorial
dilated capillary-sized vessels usually diagnosed at autopsy
telangiectasias
telangiectasias are mostly seen in the
pons
true or false: telangiectasias require no tx
true
classic appearance include of an enlarged enhancing stellate venous complex extending to the ventricular or cortical surace
venous malformations
thin-walled sinusoidal vessels (neither arteries nor vein) which may present with seizures or small parenchymal hemorrhages
cavernous malformations
drugs that have been commonly associated with brain hemorrhage
amphetamines and cocaine
cerebral amyloid angiopathy or congophilic angiopathy is associated with ____ 30% of cases
dementia
evolution of blood products in benign IC hemorrhage
peripheral to central
evolution of blood products in malignant IC hemorrhage
irregular and complex
hemosiderin rim in benign IC hemorrhage
complete
hemosiderin rim in malignant IC hemorrhage
delayed, incomplete
surrounding edema appearance in benign IC hemorrhage
minimal/mild
surrounding edema appearance in malignant IC hemorrhage
moderate/severe
acute enhancement patterns in benign IC hemorrhage
minimal (unless AVM)
acute enhancement patterns in malignant IC hemorrhage
moderate/severe
most common brain tumors to hemorrhage
glioblastomas
metastatic brain lesions prone to hemorrhage
bronchogenic CA, thyroid, melanoma, choriocarcinoma and renal cell carcinoma
