Thrombosed brainstem developmental venous anomaly
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At the time the case was submitted for publication Andrei Tsoriev had no recorded disclosures.View Andrei Tsoriev's current disclosures
Acutely presented with "the hardest headache ever", having an allergy to iodinated contrast media. MRI performed on the 8th day from symptoms onset.
1.5T MRI 8 days after symptoms onset
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Linear low-intensity vascular structures at T2* gradient echo and high intensity at T1 images reflecting dilated and thrombosed veins. Note "caput medusae" appearance. Subarachnoid blood in basal cisterns as well as ventricles and other CSF cisterns (Fisher 4 SAH).
Low-intensity lines in the pons as well as inhomogeneous diffuse signal increase, consistent with vasogenic edema. Inhomogeneous, low and slightly high signal intensity at b=1000 DWI images in the pons. No restricted diffusion found, which is consistent with vasogenic edema and explains high signal at b=1000 as T2 shine through.
Early signs of hydrocephalus are also present: dilated 3rd ventricle, lower displacement of its bottom and dilated temporal horns.
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Some of the most representative images from the MRI and MRA series, showing linear vascular structures in the pons, as well as a thrombus in subarachnoid space just below the origin of the left superior cerebellar artery, possibly representing draining venous vessel with thrombus.
Developmental venous anomaly (DVA), also known as venous angioma, represent a dilated cerebral vein which is a collector for other smaller veins; it is considered a persistent embryonal vein.
Most authors agree than DVAs are normal veins but in an unusual location, so they are required for normal venous outflow and resection of them should be avoided, because in most cases this would lead to venous infarction.
This case represents combined subarachnoid hemorrhage (SAH) and venous infarction due to thrombosis of DVA in the hindbrain. Coexistence of SAH and venous infarction of such etiology are rare, to our knowledge, this is the first case, because we could not identify similar cases in the English literature.
Since this case demonstrates the development of venous infarction after DVA thrombosis, one may consider this a proof for the requirement of DVA patency for normal venous outflow and the need for avoiding DVA resection.
The differential diagnosis for the case is pontine arterial infarction due to vasospasm and delayed cerebral ischemia, that is frequent after 3-10 days in patients with SAH, but the lack of restricted diffusion in the brainstem lesions makes arterial stroke unlikely.
- Agarwal A, Kanekar S, Kalapos P et-al. Spontaneous thrombosis of developmental venous anomaly (DVA) with venous infarct and acute cerebellar ataxia. Emerg Radiol. 2014;21 (4): 427-30. doi:10.1007/s10140-014-1216-2 - Pubmed citation
- Kiroglu Y, Oran I, Dalbasti T et-al. Thrombosis of a drainage vein in developmental venous anomaly (DVA) leading venous infarction: a case report and review of the literature. J Neuroimaging. 2011;21 (2): 197-201. doi:10.1111/j.1552-6569.2009.00399.x - Pubmed citation
- Konan AV, Raymond J, Bourgouin P et-al. Cerebellar infarct caused by spontaneous thrombosis of a developmental venous anomaly of the posterior fossa. AJNR Am J Neuroradiol. 1999;20 (2): 256-8. AJNR Am J Neuroradiol (full text) - Pubmed citation