Spontaneous Thrombosis of a DVA with Subsequent Intracranial Hemorrhage

Abstract

A 24-year-old man was admitted to the emergency room (er) with impaired consciousness and left-sided hemiplegia. He had suffered from progressive headache and emesis since the day before and had been treated with Acetylsalicylic acid (AsA). The previous medical history was otherwise unremarkable. on admission, a computed tomography (CT) scan demonstrated intraparenchymal hemorrhage in the right temporal and parietal lobe with very marked surrounding hypoattenuation and mass effect (Fig. 1). digital subtraction angiography (dsA) revealed the typical caput medusae aspect of the draining vein in the territory affected by hemorrhage with signs of venous outflow obstruction such as prolonged transition, venous stasis, and a missing central venous collector as a sign for thrombosis of the latter (Fig. 2). The patient was transferred to the neurosurgical or and the hematoma was evacuated via a temporoparietal craniotomy. During the operation, an enlarged superficial vein with obvious signs of thrombosis was found. disproportionate perioperative hemorrhage from the subcortical parenchyma was encountered, but could be controlled by means of resecting a subcortical distended vascular structure, reminiscent of an angioma and connected to the thrombosedcollecting vein (Fig. 3). Histopathological examination revealed a vascular malformation with extensively dilated and thin-walled blood vessels consisting of fibrous tissue; however, lacking a lamina elastica interna. A lamina elastica interna as part of the arterial component would be expected in an arteriovenous malformation (AVM). In this case, the malformated vessels showed only venous characteristics. Its vascular nature was confirmed by immunohistochemical expression of smooth muscle actin, Cd31, and Cd34. Blood vessels were located within a hematoma mainly located in the leptomeninges without evidence for previous hemorrhage. In addition, leptomeningeal blood vessels were attached to fragments of neocortex with reactive astrocytes, fibrillary gliosis, and prominent microglial activation. There was no evidence for an associated cavernoma.