![]() Proximal vessel sacrifice would ordinarily preserve PICA flow through retrograde flow from the left vertebral system but would perpetuate flow to the dissecting aneurysm and thus maintain the risk of rerupture. An occipital artery to PICA bypass or PICA-PICA bypass could achieve the latter objective however, the presence of significant medical comorbidities disfavored a surgical approach. Due to the improvement in the patient’s neurological status, surgical and endovascular options were considered to (1) control the aneurysm and prevent imminent rebleeding and (2) avoid ischemia of the right PICA territory in light of lack of clear collateral perfusion. He exhibited clinical improvement with ventricular drainage to the point where he was speaking, following commands, and moving all extremities, though he was somnolent and confused. The patient was intubated and an external ventricular drain (EVD) was placed, before initiation of antiplatelet therapy. There was a normal variant short segment partial duplication of the right VA at the V2-V3 junction that was not involved by the dissection. Injection of the left VA did not demonstrate any appreciable collateral flow to the right PICA territory, although a balloon occlusion test was not performed. The right posterior communicating artery (posterior communicating artery (PCOM)) was not visualized. There is also a proximal normal variant partial duplication of the vessel.ĭigital subtraction angiography further revealed a dissection of the distal aspect of the vessel and a broad-based, 5 mm aneurysm that involved the origin of a large PICA. ![]() (b) Three-dimensional volume rendered image of the distal vertebral artery during initial catheter angiography, showing vessel wall irregularity and a broad-based fusiform lesion consistent with a dissecting aneurysm (arrow) that involves a dominant posterior inferior cerebellar artery. The left vertebral artery (LVA) is labeled. (a) Computed tomography angiography in the coronal plane revealed an aneurysmal lesion arising from the distal right vertebral artery (arrow) that is surrounded by high-density subarachnoid hemorrhage. Treatment options and considerations for treatment of this condition were reviewed. The patient was ultimately treated with a flow-diverting stent. Here, we report an illustrative case of a patient with VADA involving the origin of PICA, with anatomically poor collateral flow to PICA demonstrated on angiography. However, the risks associated with these treatment options are not clearly understood in the context of VADA involving PICA, and there are other variables (e.g., arterial configuration, presence of collaterals, operator skill, and potential bleeding events from antiplatelet therapy following endovascular treatment) that may factor into favorable treatment outcomes. Many endovascular and surgical treatment options for VADA have been proposed, and new developments such as flow-diverting stents continue to expand the armamentarium. Involvement of branch vessels of the VA, for example, PICA, further complicates matters due to the need to preserve brainstem and cerebellar perfusion, limiting treatment options and resulting in worse outcomes. VADA is usually not amenable to treatment with standard clipping or coil embolization due to the morphology of the lesion. Therefore, ruptured VADA is treated emergently to prevent mortality and severe disability. In patients with rebleeding, the mortality rate is high and has been estimated near 50%. However, ruptured VADA presents a precarious situation with a high propensity for subsequent rebleeding, estimated at 30–70% and typically occurring within hours to days of the initial event. Due to its uncertain natural history, the management of unruptured lesions is controversial. Alongside surgical and endovascular treatment options, conservative management may be considered. Unruptured VADA may present with headache, ischemic symptoms (e.g., lateral medullary syndrome), or mass effect, and remain stable or even improve without treatment. The hematoma may be eccentric to the adventitia or intima subadventitial dissection preferentially occurs in the VA alone and presents as aneurysmal enlargement and SAH whereas subintimal dissection preferentially involves the basilar artery and presents with luminal narrowing and brainstem ischemia. Intracranial VADA results from a tear in the intima, degeneration of the media, or disruption of the internal elastic lamina, which lead to the formation of an intramural hematoma. Vertebral artery dissecting aneurysms (VADA) cause 3–5% of cases of subarachnoid hemorrhage (SAH), particularly in middle-aged men, and can occasionally involve the posterior inferior cerebellar artery (PICA).
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