Vol. 2, Issue 2, Article 1 Neurographics logo Radaideh, et al.

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III. Histopathologic correlation (con't)

 

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.
 

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.

 

 

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.

 

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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