The majority of the cited risk factors associated with cerebral aneurysm relate to rupture [3, 4, 5]. A handful of risk factors have only recently been reported that relate to growth, likely as a result of the increased use and availability of noninvasive brain vascular imaging [2]. Of these, female gender and cigarette smoking have been cited overnight delivery as risk factors for cerebral aneurysm progression. As such, surveillance imaging, blood pressure control and smoking cessation currently make up the essence of any long-term management plan for patients diagnosed with a cerebral aneurysm, regardless of prior surgical treatment.

Determining the frequency of surveillance imaging is arbitrary and often spans up to twelve months between studies. In this case series and literature review, we highlight a possible relationship between carotid occlusive disease and rapid cerebral aneurysm progression. The implication of these findings is that in

patients with a previously diagnosed or treated cerebral aneurysm, this non-modifiable anatomic finding may either justify anatomic exclusion, or at the very least, warrant more frequent surveillance of brain vascular imaging. Case One A 48-year-old woman with a history of cocaine use was found unconscious by neighbors and brought to the hospital where she was found to be drowsy, but with an otherwise normal neurologic examination. A plain head CT scan demonstrated diffuse basilar cistern subarachnoid hemorrhage (Fig. 1A). A basilar terminus aneurysm was embolized and a small right 2 mm posterior communicating artery aneurysm was seen in conjunction with a right cervical internal carotid artery (ICA) occlusion (Fig. 1B). Fig. 1 A. Noncontrast head CT demonstrating diffuse basilar cistern and right Sylvian fissure subarachnoid hemorrhage. B. AP right common carotid angiography demonstrating a carotid occlusion at the bulb. C. AP left vertebral angiography showing neck recanalization … Four months later, she returned with a second episode of subarachnoid

hemorrhage and there appeared to be significant neck recanalization of her previously embolized basilar terminus aneurysm and an unchanged appearance of the laterally directed rightsided 2 mm Dacomitinib posterior communicating artery aneurysm (Fig. 1C). The basilar terminus aneurysm remnant was embolized with the adjunctive use of a horizontally placed intracranial stent from one P1 segment to the other P1 segment. She had a favorable angiographic and clinical result. Two weeks later, she developed a right oculomotor nerve palsy and evaluation showed no acute hemorrhage but remarkable growth in size and morphology of her right posterior communicating artery aneurysm, now nearly 5 mm (Fig. 1D). The previously seen oblong shape now became multilobulated. This aneurysm was embolized to satisfactory occlusion (Fig. 1E).