Summary
Dural arteriovenous malformations (dAVMs) are uncommon lesions that constitute about 12% of all the arteriovenous malformations. Depending on the location and the hemodynamics of the lesion, bruit, focal neurological deficit, and visual symptoms represent the more common presentation modalities. Although uncommon, intracranial hemorrhage can occur.
In the present study, we report six patients with dural arteriovenous malformation that presented with intracranial hemorrhage. In five cases the hemorrhage was intraparenchymal (localized to the parietooccipital area in three), while it was confined to the subarachnoid space in the remaining one. The dAVM involved the transverse sinus in three cases, was based along the tentorial incisura in two, and was at the level of the torcular Herophili in one. Leptomeningeal drainage was present in all the cases. Aneurysmal dilatation of the draining vein(s) was identified in three. Sinus stenosis/occlusion was identified in two of the four patients with a dAVM draining into a major dural sinus. Four patients underwent preoperative embolization, and all patients had surgical resection of their lesions. Anatomical cure, as defined by absence of any residual dAVM on postoperative angiogram, was achieved in all six patients.
We conclude that several findings such as leptomeningeal drainage, location outside a major venous sinus, variceal dilatation, sinus stenosis/occlusion increase the risk of bleeding and are frequently observed in those dAVMs that present with intracranial hemorrhage. Recognition of these angiographic features is critical in planning a therapeutic approach tailored to the characteristics of the individual case. When these angiographic findings are present, prompt and definitive treatment is mandatory. Death from the initial hemorrhage and, in absence of definitive treatment, rebleeding are not uncommon.
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Lanzino, G., Jensen, M.E., Kongable, G.L. et al. Angiographic characteristics of dural arteriovenous malformations that present with intracranial hemorrhage. Acta neurochir 129, 140–145 (1994). https://doi.org/10.1007/BF01406493
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DOI: https://doi.org/10.1007/BF01406493