An intracranial aneurysm refers to a localized abnormal dilation of an intracranial artery, resulting in a saccular outpouching of the arterial wall. It accounts for 75%–80% of cases of subarachnoid hemorrhage (SAH). The condition is most commonly observed in middle-aged and elderly individuals between the ages of 40 and 60.
Etiology
The exact cause of intracranial aneurysms remains unclear. The congenital defect hypothesis suggests that the arterial walls, particularly at bifurcation points in the circle of Willis, lack smooth muscle layers from birth. The acquired degeneration theory postulates that intracranial atherosclerosis and hypertension progressively damage the internal elastic lamina, eventually leading to the formation of saccular aneurysms. Inflammatory processes and the associated increase in proteolytic enzyme activity may also play a role in aneurysm formation, but further research is needed to elucidate these mechanisms. Infectious foci, such as bacterial endocarditis or pulmonary infections, may lead to the development of infectious aneurysms through emboli that erode the walls of cerebral arteries. Traumatic aneurysms may also occur following head injury, but both infectious and traumatic aneurysms are less commonly encountered in clinical practice. Hereditary factors might also contribute to aneurysm formation.
Pathology and Classification
Most intracranial aneurysms are saccular, taking a spherical or berry-like shape. Externally, they appear purplish-red, with very thin walls, and the apex of the sac is the weakest point, often serving as the site of rupture. Ruptured aneurysms are commonly surrounded by clots, with the aneurysmal dome adhering to nearby tissues. Histological examination reveals that the aneurysmal wall consists solely of the intimal layer, with the absence of smooth muscle in the medial layer and disruption or loss of elastic fibers.
Dissecting aneurysm occurs when a tear in the arterial intima allows blood to dissect into the arterial wall, a condition typically caused by trauma.
Classification by Location:
- Internal carotid artery system aneurysms: These account for about 90% of intracranial aneurysms and include aneurysms at the internal carotid artery-posterior communicating artery junction, anterior cerebral artery-anterior communicating artery junction, and middle cerebral artery.
- Vertebrobasilar artery system aneurysms: These account for about 10% of intracranial aneurysms and include aneurysms at locations such as the vertebral artery-posterior inferior cerebellar artery junction, basilar artery, and posterior cerebral artery.
Clinical Manifestations
Unruptured Small- to Medium-sized Aneurysms
Most patients exhibit no symptoms, and the aneurysms are often discovered incidentally. When an aneurysm ruptures, it manifests as SAH. In some cases, triggers such as physical exertion or emotional stress precede the rupture, though the event can also occur without a clear precipitant, even during sleep.
In many cases, the ruptured aneurysm is temporarily sealed by clots, stabilizing the condition. However, as the clots dissolve, the aneurysm may rupture again, typically within two weeks of the initial bleeding event.
Following SAH, red blood cell breakdown in the cerebrospinal fluid releases vasoactive substances such as serotonin and catecholamines, leading to cerebral vasospasm. This typically occurs between 3 and 15 days post-hemorrhage. Local vasospasms usually result in no significant symptoms and appear as narrowed arteries near the aneurysm on cerebral angiography. Extensive vasospasms, however, may cause cerebral infarction, worsening neurological deficits, hemiplegia, or death.
Focal Symptoms
The clinical presentation depends on the location of the aneurysm, its relationship to neighboring anatomical structures, and its size. Oculomotor nerve palsy frequently occurs with aneurysms of the internal carotid artery-posterior communicating artery and posterior cerebral artery. Sometimes, focal symptoms, such as headaches or orbital pain followed by oculomotor nerve palsy, arise before the aneurysm rupture, signaling an impending rupture. Aneurysms of the middle cerebral artery may cause hematomas leading to hemiplegia and/or aphasia. Visual field deficits and impaired vision may occur if the aneurysm compresses the optic nerve.
Diagnosis
Diagnosis During the Acute Phase of Hemorrhage
The diagnostic approach follows the protocols described for spontaneous subarachnoid hemorrhage in the prior section.
Complete Cerebral Angiography via Femoral Artery Catheterization
This technique is critical in determining the location, number, morphology, and size of aneurysms, as well as the degree of vasospasm. It is also essential for formulating surgical strategies. For patients with Hunt-Hess grades below 3, early cerebral angiography is recommended. For those at grade 3 or above, angiography is typically delayed until the patient's condition stabilizes.
Early angiographic diagnosis allows for prompt interventions, such as microsurgical clipping or endovascular embolization, to prevent re-rupture of the aneurysm. In cases where the initial angiography fails to visualize an aneurysm (potentially due to vasospasm), repeat angiography one month later may be necessary.
Treatment
Time to Surgery
Prompt surgical intervention is recommended for ruptured aneurysms, either through microsurgical clipping or endovascular embolization, to prevent rebleeding. For patients with a Hunt-Hess grade of ≤3, early surgery (within 3 days post-hemorrhage) is favored. For patients with a Hunt-Hess grade >3, the presence of cerebral vasospasm and hydrocephalus tends to increase the risks associated with urgent surgery. In such cases, surgery is typically delayed until the patient's condition stabilizes.
Perioperative Management
Absolute bed rest is advised, with appropriate sedation to reduce adverse stimuli such as noise and light. Blood pressure is maintained within normal limits. For patients with constipation, laxatives are administered.
To alleviate cerebral vasospasm following subarachnoid hemorrhage, nimodipine is used. Antifibrinolytic agents, such as ε-aminocaproic acid, are administered to prevent rebleeding from the aneurysm.
Surgical Techniques
Aneurysmal neck clipping is considered effective for completely eliminating the aneurysm. In elderly or critically ill patients, or in cases where surgical clipping is not feasible, endovascular treatment may be an option, particularly for vertebrobasilar aneurysms. Hybrid operations, combining interventional techniques with aneurysmal clipping, may be performed in complex cases within a hybrid operating suite. Postoperative cerebral angiography is conducted to confirm the obliteration of the aneurysm.
Unruptured Aneurysms
There are no high-level clinical guidelines for the treatment of unruptured aneurysms identified by CTA or MRA. Treatment strategies for unruptured aneurysms currently take into account factors such as patient age, aneurysm morphology, size, and location. Treatment is recommended for giant and/or symptomatic aneurysms, as well as for aneurysms that exhibit growth or morphological changes, especially in younger patients.
For incidental aneurysms that are untreated, follow-up imaging with MRA or CTA every six months is advised. If the aneurysm shows evidence of growth, treatment is recommended. Aneurysms that remain stable in size may continue to be monitored.