Elias Atallah1, Edison Valle-Giler2, Turki Elarjani3, Nohra Chalouhi1, Stavropoula Tjoumakaris1, Robert H Rosenwasser1, Nabeel Herial1, Michael Reid Gooch1, Hekmat Zarzour1, Pascal Jabbour4. 1. Department of Neurological Surgery, Thomas Jefferson University Hospitals and Jefferson Hospital for Neurosciences, Philadelphia, Pennsylvania, USA. 2. Department of Neurological Surgery, Ochsner Medical Center, New Orleans, Louisiana, USA. 3. Department of Neurological Surgery, University of Washington, Seattle, Washington, USA. 4. Department of Neurological Surgery, Thomas Jefferson University Hospitals and Jefferson Hospital for Neurosciences, Philadelphia, Pennsylvania, USA. Electronic address: pascal.jabbour@jefferson.edu.
Abstract
BACKGROUND: Thrombosed large intracranial aneurysms (TLIAs) are not continuously contemplated as stable lesions. Spontaneous recanalization of completely occluded large intracranial aneurysms has been described previously. CASE DESCRIPTION: We report a middle-aged patient presenting with agitation, acute headache, visual field defects, and left hemiparesis. A large thrombosed posterior communicating (PCom) artery aneurysm was identified with an infarct at the same arterial territory on neuroimaging studies. Digital subtraction angiography (DSA) performed 1 week later demonstrated complete recanalization of the TLIA. It was treated endovascularly with coils. The patient returned several days later with augmenting headaches due to quadrigeminal system subarachnoid hemorrhage. Repeat DSA showed filling of the coiled aneurysm from the internal carotid artery injection. The PCom artery was catheterized and deconstructed. The patient was discharged to home with no additional neurologic deficits. CONCLUSIONS: TLIAs are insidious vascular lesions. They can cause nerve or vessel damage by a mass effect or through ischemic stroke by emitting emboli into distal vasculature. We advise close periodic radiologic follow-up for TLIAs.
BACKGROUND: Thrombosed large intracranial aneurysms (TLIAs) are not continuously contemplated as stable lesions. Spontaneous recanalization of completely occluded large intracranial aneurysms has been described previously. CASE DESCRIPTION: We report a middle-aged patient presenting with agitation, acute headache, visual field defects, and left hemiparesis. A large thrombosed posterior communicating (PCom) artery aneurysm was identified with an infarct at the same arterial territory on neuroimaging studies. Digital subtraction angiography (DSA) performed 1 week later demonstrated complete recanalization of the TLIA. It was treated endovascularly with coils. The patient returned several days later with augmenting headaches due to quadrigeminal system subarachnoid hemorrhage. Repeat DSA showed filling of the coiled aneurysm from the internal carotid artery injection. The PCom artery was catheterized and deconstructed. The patient was discharged to home with no additional neurologic deficits. CONCLUSIONS: TLIAs are insidious vascular lesions. They can cause nerve or vessel damage by a mass effect or through ischemic stroke by emitting emboli into distal vasculature. We advise close periodic radiologic follow-up for TLIAs.