Surgical and Endovascular Management of Patients With Unruptured Aneurysm

Introduction

Intracranial aneurysms are abnormal focal dilations of blood vessels in the brain that result in weakening of the vessel wall making it more prone to rupture. They are common acquired lesions that are usually saccular. Rupture of an intracranial aneurysm results in subarachnoid hemorrhage (SAH), which can have devastating effects with high morbidity and mortality.

With the advances in imaging techniques, a large number of intracranial aneurysms are being detected before they rupture. There are several treatment strategies that can be employed to manage unruptured intracranial aneurysms (UIAs) to prevent the deadly outcomes associated with hemorrhage. Several factors have to be taken into consideration to decide the optimal treatment approach, including the natural history of cerebral aneurysms and risk factors for aneurysm formation, growth, and rupture. This chapter describes the different approaches in managing UIAs and the factors to consider in deciding the treatment strategy.

Epidemiology

The reported prevalence of intracranial aneurysms has varied greatly between different studies depending on the study design, the population studied, and the diagnostic tool used (angiography vs autopsy). In 2011, in a systematic review that included 68 studies, 94,912 patients from 21 countries reported the overall prevalence of UIAs to be 3.2% . Most UIAs are located in the anterior circulation, predominantly in the proximal arterial bifurcations on the circle of Willis arising from the internal carotid artery, the middle cerebral artery, and the anterior cerebral artery . Other common sites include the junction of the anterior communicating artery and the anterior cerebral artery, the junction of the posterior communicating artery and the internal carotid artery, the middle cerebral artery branch points, and the internal carotid artery bifurcation. Posterior circulation aneurysms are less common, with most aneurysms occurring on the tip of the basilar artery, the junction of the superior cerebellar and anteroinferior cerebellar arteries and the basilar artery, and the junction of the vertebral artery and the posteroinferior cerebellar artery .

The prevalence of UIAs increases with age; is higher in women than in men, especially in women older than 50 years; and increases with certain disorders including autosomal dominant polycystic kidney disease (ADPKD), coarctation of the aorta, fibromuscular dysplasia, Ehlers-Danlos syndrome type IV, Marfan syndrome, multiple endocrine neoplasia I, neurofibromatosis 1, moyamoya disease, and brain arteriovenous malformations . Prevalence of UIAs is higher in patients with a family history of SAH (two or more affected first-degree relatives), so it is recommended to screen for cerebral aneurysms in such patients. Approximately 15–30% of patients have multiple aneurysms .

Clinical Presentation

Small aneurysms (<7 mm in size) do not usually cause symptoms and are frequently detected incidentally after neuroimaging for other reasons (e.g., headache, ischemic cerebrovascular disease, or transient ischemic attack) . UIAs are often identified during evaluation of hemorrhage from another aneurysm. They may also be discovered when they present with mass effect, cranial nerve deficits (most commonly a third nerve palsy), seizures, or motor and sensory deficits . Petrous ICA segment aneurysms are uncommon but may result in abducens nerve or trigeminal nerve deficits. Cavernous ICA segment aneurysms may result in compression of cranial nerves within the cavernous sinus and can cause cavernous sinus syndrome with ophthalmoplegia, chemosis, proptosis, Horner syndrome, or trigeminal sensory loss as they grow . Expansion of clinoidal ICA segment aneurysms may result in retro-orbital headaches, facial pain, or visual loss from optic nerve compression. Ophthalmic ICA aneurysms may present with visual field defects and visual loss. Anterior communicating artery aneurysms are rarely symptomatic. Middle cerebral artery aneurysms may result in hemiparesis, hemisensory loss, visual field defect, or seizure . Posterior communicating artery or basilar artery aneurysms may result in third cranial nerve palsy. Vertebrobasilar distribution aneurysms may result in bulbar dysfunction and signs and symptoms related to compression of brainstem structures.