MRI of intracerebral haemorrhage and stroke Flashcards
what happens with the breakdown of haemoglobin over time.
<6 hrs - oxy Hb 6-72 hours - deoxy Hb 3-7 days - Met-Hb intracellular weeks-months Met-Hb extracellular months-years Haemosiderin
what happens when a clot forms and breakdown of haemoglobin. explain
when clot forms, hb still intact within red cell membranes. oxygen disassociaites forms deoxyhb. within 3 days metabolic process within red blood cells starts to fail and enzyme deteriorate - hb oxidises membrane of red blood cells intact
after weeks membrane starts to break down and hb becomes iron rich. after months/years proteins broken down and clot starts to contract. iron centre in haemo group unable to cross blood barrier taken up by macrophages. iron rich aggregates called haemoglobin which stay in the tissue for process tend to occur around the periphery of clot.
why does clot become less bright on imaging
with CT we see clot. clot is highly proteinatious, protein effective at stopping xrays - acute blood looks bright as protein gets degraded and taken up attenuation values drop so clot becomes progressively less bright
why do signals vary on MR sequences
hb breakdown has different signal at each stage, each product is unique. oxyhb on t2 hyperintense because oxyhb has no ability to cause susceptibility but on t1 hyperintense to water and isointense to brain parenchyma because of protein content within blood causes t1 shortening effects, when we have t1 shortening signal goes up we get a clot that looks isointense to brain parenchyma
what is hb signal on t2w at different times
<6hrs - hyper (high)
6-72 hrs - hypo (low)(deoxy hb has free electrons and can cause susceptibility related signal loss)
3-7 days - hypo (oxyhb being oxidised, still susceptibility effect. porphyrin ring that has ions changes. configuration that allows proton electron dipole dipole interaction. we have dual effect of protein and the dipole dipole interactions there is t1 shortening so blood products look bright on t1
weeks-months - hyper
months-years - hypo (and blooming)
what is hb signal on t1-w at different times
<6hrs - iso 6-72 hrs - iso 3-7 days - hyper weeks-months - hyper months-years - hypo (protein broken down, no more dipole interaction)
what do you see on hyperacute imaging
around periphery losing oxygen, becoming deoxyhb
what do you see on acute and early subacute on t1 and t2
t1 - iso deoxyhb bright
t2 - dark
what is late subacute
extracellular hb
what does late subacute 2 look like on t1 t2
bright on both
what does chronic look like on c1,c2
t2 cleft like area filled with CSF
clot has contracted down, protein reabsorbed. dark signal around peripheral. dark material blooming.
t1 - csf cleft surrounded by haemosidirin
what is MRI in ischaemic stroke
hyperacute, acute-stroke workup, longer term - monitoring, treatment planning
what can you assess in hyperacute stroke using imaging from MR, diffusion, perfusion and MRA
conventional structural MR - changes of ischaemia
identifying haemorrhage
diffusion - core infarct, discrimination of new lesions from old
perfusion - ischaemic penumbra
MRA - vascular stenoses, occlusions and dissections
what sequences can be used to see hyper acute stroke
t2 t1 FLAIR t2* (ge) or swi to look for blood products
what can happen at 3 hrs, 6 hrs, 5 days, 3-4 weeks
and in this timeline when can we use t2 or t1
before 3 hrs - cytotoxic oedema 3-6 - vasogenic oedema 6hr - 5days - cell breakdown 5days - liquefactive necrosis last encephalomalacia
can use CT in the beginning but then afterwards there’s low attenuation
can use t2 after 4 hours as most sensitive after onset of ishaemia get vasogenic oedema, breakdown and water in infarcted tissue 50% visible on t2 by 24 hrs
t1 use after - 50% visible infarct visible
what can dwi do, is it t1 or t2? how will normal tissue look. what signal will restricted diffusion have
measure of diffusivity of h20 through tissue
t2w
tissue with mobile h20 loses signal (normal tissue has natural barriers to diffusion)
dwi trace image gives readout image at the end so will look bright if water molecules in voxel move moderate distance then loses moderate amount of signal and on dwi trace image will look gray. if diffusion loses all signal then will look dark. normal tissue will look gray on trace.
restricted diffusion is bright (no diff - no signal loss)
apply 2 separate diffusion gradients
dwi then determines how far the water molecules within each voxel have moved between those 2 diffusion gradients
now if water molecules within that voxel have moved a long way that voxel will lose a lot of its potential signal
so amount of signal that voxel is losing is proportional to the distance water molecules are diffusing
so if water molecule diffuses long way then loses signal
if hasn’t moved any distance at all then has the potential signal that it had at the start of the sequence
what can happen in cytotoxic oedema
oxygen dependent process fail membrane pumps cell swell
water molcuecl diffuse between cells
swelling, water moluecule difffisuvity restricted so dwi picks up pathological bright signal can occur within minutes of ischaemia
what is the problem with using dwi and how to solve it.
t2 shines through as its high. tissue bright signal on t2, even though water molecules can diffuse unable to lose all of that signal between the two diffusion gradients can stilll look bright on dwtrace image don’t kno whether effect of t2 or diffusion.
can use adc map. untangles t2 and dwi and will measure diffusivity only and makes restricted diffusion dark
what can a graph about the adc map show
adc map looks at rate of fall of signal between diffusion gradients. slope depicted with adc map
is aderived parameter
low adc value - gradient is shallow- water molecule restricted not losing signal is dark
high adc - gradient steep - bright.
first image we acquire low resolution t2 map
how strong diffusion gradient are
b value can show how strong diffusion gradient is
how do the voxels look on adc maps if the slope on the graphs are the same
voxels look same
what does bright dwi and dark adc map mean
restricted diffusion
what does bright dwi and normal/bright adc map mean
t2 shine through
what is a pitfall of dwi with the adc map how many weeks after does it happen
explain
pseudonormalisation -occurs at 2 weeks. after 2 weeks adc map not reliable.
diffusivity drops, adc goes dark
at some point as cell breaks down
diffusivity got to go hthrough point
got to have same diffusivity as normal tissue
degree of ceeluar breakdown offsets restricted diffusion bfecause of cytotoxic edema because that tissue will look like it has the same diffusivity eve though tossue abnormal effects balance each other out called pseudonorm
point at which edema because of the infarct is balanced out by the loss of restricted diffusion due to cellular breakdown
mature infarct - all cytoachitectuere broke down, everything that was a barrier to normal diffusion of water molecules is now disappeared
diffusivity of mature infarcts is very free
at what time is t2 normal
at 4 hours
what time is t1 normal
at 12 hours
how is mr perfusion done
what are some characteristics of it
dynamic susceptibility contrast imaging. t2* effect of Gd bolus passage.
measures of mean transit time, relative CBV, rCBF
not quantitative
ischaemic penumbra - physiological basis for thrombolysis of time driven
monitoring precarious perfusion over time
exam of cerebrovascular reserve
what can mr perfusion look at in ischaemic penumbra
look at the difference between core infarct tissue which is irretrievable or hypoperfused
what can mra look at
stroke workup intracranial occlusion/stenosis extracranial circulation - carotid bifurcation stenosis vertebral origin stenosis dissection - fat sat axial sequences
what imaging is good to see haemorrhage and what happens in it
t2* and SWI sensitive to many Hb states
Haemoglobin broken down
what imaging can be used on acute stroke
dwi - for infarct
t2*/SWI - haemorrhage
PWI - ischameic penumbra
MRA/fat sats - intra and extra cranial vessels
what are magnetic/cellular/molecular properties, of iron according to the timeline of the breakdown of Hb
<6hrs: dia magnetic, intra, Fe in plane
> 6 - para magnetic, intra, Fe out of plane
> 3 days - para magnetic, intra, Fe in plane
weeks-months - para magnetic, extra, Fe in plane
months-years - superpara magnetic, intra, porphyrin degraded
what is impacted on MR signal
susceptibility
proton electron dipole dipole interaction
protein
what is impacted on susceptibility
para/superparamagnetic molecules compartmentalised local field inhomogeneities spin dephasing --> signal loss positive on GE makes t2 signal go down
what is impacted on proton-electron dipole dipole
h20 protons close to fe2, fe3
t1 down , only in hb if Fe is accessible in plane
where are the proteins and what is the spin
large macromolecules precess close to lamor Hz of h20 prootns
spin down then spin up so t1 down
