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
