Takumi Otake, Masahiro Nishihori, Shunsaku Goto, Issei Takeuchi, Takashi Izumi, Yusuke Sakamoto, Ryuta Saito
When a hypoplastic PcomA arising from the aneurysm dome functions as a dominant terminal feeder of the anterior thalamoperforating artery, progressive intra-aneurysmal thrombosis after flow diversion may cause thalamic infarction-a risk incompletely addressed by antiplatelet optimization alone. An adequate P1 segment does not guarantee perfusion of such a dome-originating perforator. Preoperative functional assessment of collateral supply and branch-preserving alternatives merit consideration in this configuration.
BACKGROUND: Flow diverter stents are widely used for internal carotid-posterior communicating artery (IC-PC) aneurysms, and covered branches such as the posterior communicating artery (PcomA) generally remain patent. Branches arising directly from the aneurysm dome, however, occupy a distinct anatomical position and may behave differently.
CASE DESCRIPTION: A woman in her 50s underwent Pipeline Flex with Shield Technology placement (5.0 × 16 mm) for a 9.2-mm wide-necked right IC-PC aneurysm. A thin branch arising directly from the aneurysm dome was preoperatively interpreted as a hypoplastic PcomA, with anticipated collateral support from an adequate ipsilateral P1 segment. Preoperative platelet function testing revealed clopidogrel non-response (adenosine diphosphate inhibition, 7.6%). On postoperative day 4, the patient developed left hemiparesis. Diffusion-weighted imaging demonstrated acute infarction in the right anterolateral thalamus, while digital subtraction angiography confirmed complete aneurysm thrombosis with disappearance of the branch and a fully patent stent. Vertebral artery angiography showed no retrograde filling of the PcomA. The hemiparesis resolved rapidly, but visuospatial and attentional-executive deficits persisted; the modified Rankin Scale score remained 2 at 18 months.
CONCLUSION: When a hypoplastic PcomA arising from the aneurysm dome functions as a dominant terminal feeder of the anterior thalamoperforating artery, progressive intra-aneurysmal thrombosis after flow diversion may cause thalamic infarction-a risk incompletely addressed by antiplatelet optimization alone. An adequate P1 segment does not guarantee perfusion of such a dome-originating perforator. Preoperative functional assessment of collateral supply and branch-preserving alternatives merit consideration in this configuration.