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Introduction: Flow diverters such as the pipeline embolization device (PED) cause hemodynamic changes of the treated vessel segment. In posterior communicating artery (PcomA), aneurysms’ unique anatomic consideration have to be taken in account due to the connection between the anterior and posterior circulation. We hypothesize that in conjunction with PcomA remodeling, there will also be remodeling of the ipsilateral P1 segment of the posterior cerebral artery (PCA) after PED treatment for PcomA aneurysms. Methods: We retrospectively collected radiological as well as clinical data of PcomA aneurysm patients treated with PED including PcomA and P1 vessel diameters before and after treatment as well as patient and aneurysm characteristics. Results: Overall, 14 PcomA aneurysm patients were included for analysis and PED treatment was performed without complications in all patients. In 10 out of 14 patients (71%), a decrease in PcomA diameter was observed and there was a significant mean decrease of 0.78 mm in PcomA diameter on angiographic last follow-up (LFU) (p = 0.003). In the same patient population (10 out of 14 patients), there was meanwhile a significant mean increase of 0.43 mm in the ipsilateral P1 segment diameter observed (p = 0.015). These vessel remodeling effects were in direct correlation with aneurysm occlusion since all of these patients showed aneurysm occlusion at LFU while 29% showed only partial occlusion without vessel remodeling effects. A decrease in PcomA diameter was directly associated with aneurysm occlusion (p = 0.042). There were no neurologic complications on LFU. Conclusion: In the treatment of PcomA aneurysms with PED, the P1 segment of the PCA increases in diameter while the PcomA diameter decreases. Our results suggest that this remodeling effect is associated with aneurysm occlusion and decrease of PcomA is hemodynamically compensated for by an increase in the ipsilateral P1 diameter.

Background The role of arteriovenous shunts such as dural fistulas, arterial steno‐occlusive states, anatomic variants, and hypervascular tumors in the genesis of pulsatile tinnitus (PT) has long been recognized. On the venous side, diverticula, high‐riding jugular bulb, and sinus wall dehiscence have also been implicated. However, the overall most common cause—venous sinus stenosis (VSS)—continues to be underrecognized. Its clinical importance, separate from venous stenosis association with intracranial hypertension, also requires emphasis. Methods A retrospective review of the last consecutive 208 cases of PT seen at our institution was performed and cause determined, when possible, based on clinical and radiographic data. Results VSS was the common cause of PT (34% of overall cohort). Over 90% are women. Typical clinical presentation was a unilateral whoosh‐like sound in sync with heartbeat that could be completely or nearly completely abolished by ipsilateral jugular compression. This clinical scenario virtually guaranteed the presence of VSS, with very high sensitivity, specificity, positive, and negative predictive values. About two thirds of patients with VSS also harbored other venous anatomic variations such as a high‐riding jugular bulb or sinus diverticulum, that should not be misinterpreted as the primary cause of PT. Most did not have signs or symptoms of intracranial hypertension, even though cerebrospinal fluid and venous pressures are frequently elevated. Conclusions VSS appears to be the most common identifiable cause of PT. Judicious attention to this finding can be immensely helpful in prompt and accurate diagnosis.