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Brain CT & MRI
Transcript of Brain CT & MRI
Attenuation is measured in Hounsfield units
- Scale -1000 to 1000
-1000 is air
0 is water
1000 is cortical bone
What we can see
-The brain is grey
White matter is usually dark grey (40)
Grey matter is usually light grey (45)
CSF is black (0)
Things that are brite on CT
Bone or calcification (>300)
Hemorrhage (Acute ~ 70)
Metallic foreign bodies
Normal Enhanced CT
55 yo female with sudden onset of worst headache of life
Most common cause is trauma
Generally a younger age group
82 yo male with mental status change after a fall
Venous bleeding from bridging veins
Older age group
Mental status change after fall
50% have no trauma history
44 yo female with right sided weakness and inability to speak
Acute ischemic left MCA stroke
50 yo male post head trauma.
Pt was initially conscious but now 3 hours post trauma has had a sudden decrease in his neurological function.
Typical history is a patient with head trauma who has a period of lucidity after trauma but then deteriorates rapidly.
Hemorrhage is a result of a tear through a meningeal artery.
71 yo male who initially complained of incoordination of his left hand and subsequently collapsed
62 yo female acute onset headache
Hemiplegic on the right and unable to speak
Clinically looks like a large MCA stroke
Generally younger than amyloid angiopathy patients
Chronic Ischemic change =
6 hours ICA territory
24 hours basilar territory
CT head plain shows no established stroke nor hemorrhage
CT perfusion shows a salvagable penumbra
53 y.o. male
Sudden onset of ataxia loss of consciousness proceeding rapidly to coma
Probable basilar occlusion with cerebellar and brainstem infarction
52 yo male with right sided weakness
Acute lacunar infarction
Cannot reliably differentiate this finding on CT from remote lacune without clinical correlation.
MRI with diffusion is the GOLD STANDARD
A word on TIA
42 yo male found in coma
Angiographic Brain Death
Cerebellar Function Test
Gait by asking you to walk in a straight line
Diffusion weighted imaging is commonly performed in MRI imaging for evaluation of an acuteischaemic stroke, and is excellent at detecting small and early infarcts. Conventional (T1 / T2) MRI sequences may not demonstrate an infarct for 6 hours, and small infarcts may be hard to appreciate on CT for days, especially without the benefit of prior imaging.
For a general discussion of pathogenesis and radiographic features please refer to ischaemic stroke.
Decreased diffusion in ischaemic brain tissue is observed within a few minutes after arterial occlusion and progresses through a stereotypic sequence of ADC reduction, followed by subsequent increase, pseudo normalisation and, finally, permanent elevation.
Reported sensitivity ranges from 88 - 100% and specificity ranges from 86 - 100%
The appearance of DWI / ADC depends on the timing.
DWI MRI in acute stroke
Acute (0 - 7 days)
ADC value decreases with maximal signal reduction at 1 to 4 days
marked hyperintensity on DWI (a combination of T2 and diffusion weighting), less hyperintensity on exponential images, and hypo-intensity on ADC images.
subsequently, release of inflammatory mediators from ischaemic brain tissue leads to vasogenic oedema with extravasation of water molecules from blood vessels to expand the interstitial space, where water molecule diffusion is highly unrestricted.
Subacute (1 - 3 weeks)
ADC pseudonormalisation occurs in the second week (7 - 15 days)
ADC values to rise and return to near baseline
irreversible tissue necrosis is present despite normal ADC values
DWI remains hyperintense due to T2 shine through
after 2 weeks ADC values continue to rise above normal parenchyma and the region appears hyperintense
Chronic (>3 weeks)
ADC signal high
DWI signal low (as T2 hyperintensity and thus T2 shine through resolve).