Posterior Communicating Artery Aneurysm: Progressively Enlarging, Symptomatic, and Partially Thrombosed Fusiform True Posterior Communicating Artery Aneurysm, Treated by Coil Occlusion of the Parent Artery and Disconnection of the Posterior Communicating Artery by Parallel Flow Diversion in Two Treatment Sessions; Complete Aneurysm Occlusion, Aneurysm Shrinkage, and Good Clinical Recovery

Abstract

Back in 1998, a then 44-year-old male patient presented with a left hemispheric minor ischemic stroke of undefined cause and was diagnosed by DSA with a small, right-hand asymptomatic yet partially thrombosed true posterior communicating artery (TPcomA) aneurysm. The patient failed to regularly attend the assigned follow-up clinical and cross-sectional imaging examinations. In 2016, 18 years after the first DSA examination, the patient presented with progressive left-hand hemiparesis and mild fluctuating central facial nerve palsy. Cranial non-contrast-enhanced computed tomography (NCCT) revealed the presence of a large lobulated and partially thrombosed right-hand TPcomA aneurysm. The thrombotic material in the aneurysmal sac was exerting a local mass effect on the thalamus and brainstem. Contralateral ischemic changes in the left-hand capsular region were also noted. Diagnostic angiography confirmed that the lobulated aneurysm originated from the right-hand “fetal” PcomA itself. In 1998, as well as in 2016, the patient clearly rejected all the treatment options offered. Another 2 years later, the patient presented with a worsening of his left-hand hemiparesis. A cranial MRI and the following DSA examination confirmed that the aneurysm had been progressively growing over the past two decades. Due to progressive neurological deterioration, endovascular management was now requested by the patient. A balloon test occlusion (BTO) of the fusiform TPcomA aneurysm was tolerated. The first endovascular treatment session comprised coil occlusion of the aneurysmal lumen and the middle part of the PcomA. The proximal PcomA segment between the internal carotid artery (ICA) and the fusiform aneurysm and the distal segment between the aneurysm and the PcomA/posterior cerebral artery (PCA) connection were not occluded. A p64 flow diverter was implanted into the distal right ICA across the proximal origin of the PcomA. Neither a shrinking of the aneurysm nor a complete clinical recovery was seen after this treatment. DSA showed blood flowing from the right-hand PCA toward the aneurysm via the remnant of the right-hand PcomA. During a second treatment session, a p48 low profile flow diverter was deployed across the transition of the right P1/P2 segments, fully covering the distal connection between the PcomA remnant and the PCA. This procedure was done in order to prevent retrograde aneurysm filling via the PcomA from the P1 segment. Hemodynamic isolation led to significant shrinkage of the thrombosed part of the aneurysm. The management of TPcomA aneurysms is the main topic of this chapter.