| III. Histopathologic correlation (con't)
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69 yr old patient presented with loss of consciousness.
A) CT demonstrates hypodensity consistent with infarction of
basilar artery distribution in the left cerebellar lobe,vermis and medial
portion of the right cerebellar lobe.
B,C) MRI FLAIR and MRI T2WI demonstrate vasogenic edema in the
same distribution.
D) ADC map (b=1000) demonstrates diffusion restriction due to
cytotoxic edema in the same distribution.
E,F) DWI (b=500, b=1000) also demonstrates diffusion
restriction due to cytotoxic edema.
| This case demonstrates acute infarction in the left
and right cerebellar lobes and the vermis in a stage of intermixed
vasogenic and cytotoxic edema. |
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60 yr old patient presented with loss of consciousness.
A) CT of the posterior fossa demonstrates normal brain
parenchyma, but dense basilar artery due to luminal thrombus.
B) MRI axial T1WI demonstrates loss of signal void of the
basilar artery due to luminal thrombus.
C) MRI axial FLAIR demonstrates loss of signal void in the
basilar artery and minimally increased T2 signal in the right
cerebellar hemisphere and right middle cerebellar peduncle. This is due
to early mild vasogenic edema.
D) 3D Time of flight MR angiogram demonstrates occlusion of the
basilar artery (arrow).
E,F) MRI DWI (b=1000), G,H) ADC map (b=1000) demonstrate bright
DWI signal and dark ADC signal in the right cerebellar lobe extending
to the right middle and inferior cerebellar peduncles and pons due to
diffusion restriction of cytotoxic edema as consequence of acute
infarction.
| This case demonstrates the early development
of cytotoxic edema in the hyperacute stage of infarction with normal CT
and minimal vasogenic edema which is starting to occur. |
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72 yr old patient who had left MCA posterior branch infarction.
A,B) MRI DWI (b=500, 1000) demonstrates increased SI in the left
MCA territory on b=500 DWI while normal SI on b=1000 DWI related to T2
shine through effect that is more prominent on low gradient strength.
C) ADC map (b=1000) demonstrates increased intensity due to
increased diffusion excluding the presence of any diffusion restriction.
This increased diffusion is due to vasogenic edema in the subacute stage
of infarction.
D,E) MRI FLAIR and T2WI demonstrate bright signal from vasogenic
edema.
F) MRI T1WI demonstrates early gliosis (cortical laminar
necrosis).
T2 Shine Through
DWI SI is influenced by T2 signal as concluded from its SI formula
while ADC map is a pure diffusion effect.
The DWI SI is influenced by the b value. The higher the b value, the
stronger the diffusion SI and the lesser the influence from T2 SI.
58 yr old patient who had right MCA infarct.
A) CT image demonstrates subacute right MCA infarct.
B,C,D) Axial and coronal MRI FLAIR and axial T2WI demonstrate
vasogenic edema in the right MCA territory associated with gliosis and
focal encephalomalacia causing widening of the lateral fissure (arrow).
E,F,G) ADC map with fluid attenuation inversion recovery (b=1000)
demonstrates dark CSF in the widened right lateral fissure not related to
diffusion restriction. The surrounding brain tissue demonstrates no
evidence diffusion abnormality. H,I,J) MRI DWI (b=1000) demonstrates
increased SI in the right MCA territory around the lateral fissure likely
related to T2 shine through since the ADC revealed no diffusion
abnormality.
| This case demonstrates a possible source of
false positive diffusion imaging. |
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57 yr patient who presented with loss of consciousness.
A) Axial DWI (b=1000) image demonstrates diffusion restriction
in the left side of the pons secondary to acute infarction.
B,C) Conventional T2WI and T2 FLAIR MRI demonstrate very faint
signal in the pons related to minimal vasogenic edema.
D,E,F) Repeat DWI, T2WI and T2 FLAIR one week later demonstrate
progression of infarction as seen in the DWI (increased infarct size and
signal brightness). T2 images demonstrate interval increase in vasogenic
edema since the last exam.
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