Developmental venous anomaly - atypical

Case contributed by Oana Harsan


Migraines without aura, lateralized to the right

Patient Data

Age: 45
Gender: Female

Fourth study - one year and a half after presentation


Performed on a 1.5 T MRI.

Non-enhancing T2 FLAIR hyper-intensity located in the right corona radiata and centrum semiovale, without mass effect. No true increased diffusion restriction. No other significant white matter changes.

Small superficial draining right frontal developmental venous anomaly corresponding to the signal intensity changes, visible on the SWI and post-contrast T1 images. Possible draining vein stenosis at cortical level (key image). 

Study otherwise unremarkable.

Slightly increased corrected relative cerebral blood volume in the area seen on DSC perfusion.

MR monovoxel spectroscopy demonstrates an increased choline peak on both short and long TE, with a Cho/Cr ratio at 1.26 (short TE) and at 1.5 (long TE) respectively. No NAA decrease, no lipid or lactate increase.

First study


Performed on a 3T MRI.

T2 FLAIR hyper intensity located in the right frontal lobe deep white matter, without true increased diffusion restriction nor enhancement. No other significant white matter changes.

Small superficial tubular venous structure draining multiple converging medullary veins, located at the periphery of the signal changes, best seen on SWI and post contrast T1, draining towards a cortical frontal vein.

Study otherwise unremarkable.

Relative cerebral blood volume increase in the region when compared to the contralateral side.

Short TE MRS demonstrates a choline peak. No NAA decrease. 

Case Discussion

The presented case illustrates a non evolving deep white matter T2 FLAIR hyper intensity associated with a developmental venous anomaly (DVA).

DVAs are common vascular malformations, mainly without clinical relevance, and thus are discovered incidentally. Aproximately 10% are associated with signal intensity (SI) changes on T2/ FLAIR sequences. These changes are attributed to venous congestion with subsequent edema, hypoxia or gliosis. In this case, there was no objective evidence of thrombosis.

Some of the signal intensity changes associated increased perfusion parameters as is shown in this case, representing alterations in blood flow, such as congestion. 

The MR spectroscopic findings do not demonstrate hypoxic process (no NAA decrease) nor gliosis (mINS undetectable). There is a persistent Choline peak that could be attributed to inflammation secondary to a blood brain barrier breakdown due to persistent venous congestion and edema. 

The transient lactate and lipid peaks seen on the first study (3 T MRI) could be in keeping with a thrombotic event in the DVA with subsequent hypoxia but spontaneous recanalization, as they are no longer visible on the follow up studies.

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