Flow Diversion for the Management of Ruptured Intracranial Arterial Infudibular Dilatation: Proof of Principle and Therapeutic Protocol

Abstract

Thought to be benign anatomical variants, cerebral infundibular dilatations (ID) are most commonly encountered at the junction of the internal carotid artery (ICA) and the posterior communicating artery (PcomA). The true nature of this entity remains controversial, as some literature reports suggest they should be considered preaneurysmal lesions and a potential source of devastating subarachnoid hemorrhage. This report describes cases of presumably ruptured IDs and their therapeutic endovascular management. We retrospectively reviewed and analyzed patients with isolated subarachnoid hemorrhage (SAH) where the only potential cause was ruptured cerebral IDs, treated or not, between January 2012 and June 2021. Morphological and radiological features, treatment and procedural considerations, clinical and angiographic outcomes were also reviewed. Natural history of the ID is poorly understood, and its relation to SAH remains controversial. Ruptured cerebral IDs can be the suspected cause of bleeding if no other vascular lesion is present during multimodal examinations. Endovascular flow diversion stenting is safe and effective for the proper treatment of ruptured IDs. Pending further validations with longitudinal data are needed to legitimate the natural course of these mysterious lesions.

Keywords: anterior choroidal artery; flow diverter; infundibular dilatation; posterior communicating arteries; subarachnoid hemorrhage.

Figure 1

Schematic representation of ID with the adjacent origin of an intracranial artery, ophthalmic artery ID (A), posterior communicating artery ID (B) and ID at anterior choroidal artery (C).

Figure 2

EVT of a ruptured PcomA ID. An initial CT scan demonstrated the presence of SAH predominantly distributed across the left basal cisterns (A; white arrow). Cranial CTA did not document any cerebrovascular findings that could have caused the SAH (B). At 6 h after onset, catheter angiography confirmed the absence of a ruptured aneurysm but revealed a typical ID at the origin of the left PcomA (C). Delayed 3DRA/DSA (D,E; white arrows) 7 days after onset identified a possible rupture bleb on the lateral side of the left PcomA ID. Endovascular coil embolization of the ruptured bleb was unsuccessful, and a p64 FD was carefully deployed across the C7 segment of the left ICA (F,G). Contrast stagnation inside the ruptured ID bleb was seen on the delayed angiographic phase (not provided).

Figure 3

EVT of ruptured OA ID in a young woman. The initial radiological work-up indicated intracranial hemorrhage, suggesting the rupture of an intracranial aneurysm (A; white arrow). Cranial CTA and initial DSA did not reveal any cerebrovascular pathologies that could be associated with the hemorrhage (B,C). Three-dimensional rotational angiography demonstrated the presence of an ID at the level of the orifice of the left ophthalmic artery (D; white arrow). Endovascular FD deployment was performed with complete coverage of the OA infundibular orifice (E–G).

Figure 4

EVT of a ruptured PcomA ID in a 60-year-old man. Non-contrast cranial CT revealed a thin hemorrhage in the chiasmatic, interpeduncular, and left crural cisterns (A; white arrow). Subsequent repeated radiological examinations did not reveal any cerebrovascular pathology but confirmed the presence of an ID at the level of the left PcomA (B,C; white arrow). The assumed rupture site was the observed ID, and the patient received EVT (D,E). Noticeable contrast stagnation was observed in the PcomA ID after stent implantation (F).