stroke imaging Flashcards
cerebral blood flow
rate of delivery of blood and nutrient to the tissue capillary bed, is the main parameter to measure cerebral perfusion
cardiac stroke volume
70ml
average heart frequency
70/min
cardiac output
5L/min
flow in the brain is expressed as
mL/min/100g
normal cerebral blood flow
50mL/min/100g
gray matter blood flow
60-100 mL/min/100g
white matter blood flow
30-45 mL/min/100g
cerebral perfusion prressure
the difference between the mean arterial pressure (MAP) and the intracranial pressure (ICP)
MAP-ICP = CPP
normal CPP
50-150 mm Hg
if CPP is too low
the brain becomes ischaemic
if CPP is too high
the brain becomes hypereamic
autoregulation
maintains blood flow to the brain
unlike other organs, the cerebral blood low in independant of arterial pressure (in normal range)
what happens in an embolic infarct
the territoory perfused by this artery and areas with little or no collateral flow are subjected too extreme hypoxia and nectrotic cell death
in the penumbra, where there is some degree of collateral blood flow, a gradient of tissue perfusion establishes a threshold among nectrotic cell death (infarct core), apoptotic cell death (ischaemic penumbra), and tissue survival
when oxydative phoosphorylation stops
membrane pump failure influx of Na and Ca cytotxic oedema damage to endothelium vasogenic oedema (inundation of water - seen on CT, takes a few hours)
4 goals of multimodal imaging in stoke
parenchyma - rule out haemorrhage
pipes (vessels) - assess extracranlial (carotid and vertebral) and intracranial circulation for evidence of intravascular thrombus
perfusion - assess cerebral blood volume, cerebral blood flow, mean transit time and capillary permeability
penumbra - assess tissue at risk of dying brain tissue if ischaemia continues without recanalisation of intravascular thrombus
how to rule out intracranial heamorrhage
CT remains the gold standard to rule out intracranial haemorrhage
intracerebral or subarachnoid
spontaneous (non-traumatic) intracranial haemorrhage accounts for 15-20% of all acute stroke syndromes
early signs of acute stroke
non-contrast CT is not very good in showing early signs of infarction
traditional CT signs or early infarction in the distribution territory of the middle cerebral artery
- hyperdense MCA sign - a hyperdense left middle cerebral artery
- obscuration of the lentiform nucleus
- insular ribbon sign - asssymetry between the grey matter
limitations of CT in acute stroke
in most cases CT is normal within the first hours after onset of symptoms
therefore, in acute stroke, noncontrast CT is not reliable
what about MRI in acute stroke
preferred techniquue, not available in western australia
why dies diffusion restriction signal aucte stroke
in normal brain tissue there is free brownian motioon of water molecules
in cytootoxic oedema, swelling of cells with restricted movement of H2O molecules
‘mismatch’ concept
relied on perfusion imaging to show the difference between infarct core and penumbra
predicts how the stroke will evolve
CT perfusion test
IV bolus 40mL iodinated contrast
sequential time=points show contrast transversing the capillary bed at a fixed level
can CT be used for easrly detection of ischaemic brain
no
