Cavernous Internal Carotid Artery Aneurysm

• A 7-year retrospective single-center study on treatment strategy and clinical outcome of giant intracranial aneurysm
• A Case of thrombosed intracavernous carotid giant aneurysm with ipsilateral carotid thrombosis: Imaging, and management challenges
• A 15-year follow-up of permanent intraoperative internal carotid artery occlusion for hemostasis in a giant cavernous sinus hemangioma: a case report
• Adjunctive Coiling in Flow Diverter Treatment Does Not Prevent Delayed Rupture: A Nationwide Survey
• Spontaneous carotid-cavernous sinus fistula with fibromuscular dysplasia: illustrative case
• Unexpected internal carotid artery injury during endoscopic transsphenoidal surgery
• Trigeminal nerve palsy associated with intracranial aneurysms: Scoping review
• Challenges in the treatment of giant cavernous carotid aneurysm associated with hemophilia A: illustrative case

Cavernous carotid aneurysms (CCA) represent 2-9% of all intracranial aneurysms. For long considered benign lesions, these entities are unique when it comes to clinical presentation and management. Usually asymptomatic, CCAs can grow and rupture causing different manifestations. The lack of a long-term assessment of both treated and untreated CCAs' natural history justifies why there is no consensus regarding what are the recommended therapeutic measures. While some advocate that an intervention is always necessary, others consider that patients deserve an individualized evaluation ¹⁾.

Extradural place and the skull base location make this type of an aneurysm different in clinical features .

Most cavernous carotid aneurysms (CCAs) are considered benign lesions, most often asymptomatic, and to have a natural history with a low risk of life-threatening complications.

Aneurysms involving the cavernous segment of the internal carotid artery may produce cranial nerve dysfunction by compression, and occasionally rupture or ischemic event ^{2) 3)}.

Most present with symptoms of the third, fourth, fifth and sixth cranial nerves. Medially projecting cavernous carotid aneurysm can produce optic nerve dysfunction.

Giant aneurysms may cause more symptoms than their smaller counterparts ⁴⁾.

Raeder described the paratrigeminal syndrome that consists of Horner’s syndrome and sixth nerve palsy ⁵⁾.

Cavernous Internal Carotid Artery Aneurysm treatment

Junior et al. from São Paulo described a single-institution experience in diagnosis, follow-up, and management of 201 CCAs. In addition, they evaluate the association of giant CCAs with aneurysms in other locations using a Chi-square test.

201 patients had 245 CCAs. 92% of the patients were women. The mean age at diagnosis was 61 years. Concomitant aneurysms were observed in 53.2% of the patients, and the middle cerebral artery was the most affected artery. 66 (30.6%) CCAs were considered “giant”, and the follow-up period ranged from 1 to 23 years.The presence of a giant CCA seemed to hinder other aneurysms' formation - RR 0.47 (IC 95% 0.31-0.67), p < 0.0001.

CCAs should be individually assessed. A conservative approach ought to be adopted for asymptomatic and oligosymptomatic lesions. Finally, a multidisciplinary team must evaluate the other situations, in order to define whether the microsurgical or the endovascular treatment is better option. Presence of a giant lesion within the cavernous sinus is associated with less occurrence of other aneurysms ⁶⁾.

A rare instance of rupture of a CCA that had been previously treated with a flow diverter, which resulted in the development of a carotid-cavernous fistula, requiring venous access endovascular treatment. The patient experienced persistent neurological deficits following treatment, specifically paralysis of the IV cranial nerve and palpebral ptosis, underscoring the complex nature of such cases and the potential for lasting complications despite intervention ⁷⁾.

This case report highlights an important complication of endovascular treatment for CCAs, contributing valuable insights into its management. However, its potential impact is limited by a lack of technical and contextual depth, as well as insufficient focus on mechanisms and follow-up. Enhancing these aspects would significantly elevate its educational and clinical utility.

Cavernous internal carotid artery (ICA) aneurysm complicated by simultaneous and spontaneous formation of thromboses in the aneurysm and the parent artery is a rare clinical condition. Although the majority of patients have good outcomes, some patients experience severe ischemic stroke. Here, we report a case of symptomatic large cavernous ICA aneurysm complicated by rapid growth of an intra-aneurysmal thrombosis with simultaneous parent artery thrombosis. A 68-year-old female presented with sudden-onset diplopia, right ptosis, right conjunctival hyperemia, and paresthesia of the right face. Magnetic resonance imaging (MRI) and digital subtract angiography (DSA) revealed the presence of a large partially thrombosed aneurysm in the cavernous portion of the right ICA. We planned endovascular embolization using a flow-diverting (FD) stent. Dual-antiplatelet therapy (DAPT) with aspirin and clopidogrel was started 2 weeks prior to treatment. Although the neurological state was stable, DSA conducted on the day of the endovascular treatment showed rapid growth of an intra-aneurysmal thrombosis and de novo thrombosis in the parent artery. Direct aspiration was performed via a distal support catheter with proximal blood flow arrest using a balloon-guide catheter, and the FD stent was successfully deployed. The patient's symptoms improved postoperatively and DSA obtained 12 months after the procedure confirmed complete occlusion of the aneurysm. Although the exact mechanism of simultaneous thrombosis formation of the aneurysm and its parent artery remains unclear, it is important to recognize that rapid growth of the thrombosis increases the risk of ischemic stroke ⁸⁾.