General information
A cerebral aneurysm is a sac-like bulge (cystic aneurysm) formed by a localized bulge in the blood vessel wall of an intracerebral artery that communicates with a blood vessel, and is classified as micro (less than 5mm), small (5-10mm), large (11-25mm), and giant (25mm or more) intracranial aneurysms. Small, microscopic intracranial aneurysms are often asymptomatic, but can cause serious symptoms and danger if they rupture and bleed.
Epidemiology
According to radiological and autopsy reports, the incidence of intracranial saccular aneurysms is about 3.2%, and the average age of prevalence is 50 years (40-60 years), with no significant differences between the sexes. However, there are some gender differences in the aneurysms seen clinically, especially in patients over 50 years of age who are about twice as likely to be female as male. 20%-30% of intracranial aneurysms are intracranial multiple aneurysms. The incidence of aneurysm rupture is estimated to be 6-16 per 100,000, and bleeding from aneurysm rupture is one of the major causes of stroke, with approximately 10% of patients dying before reaching the hospital and only about 30% having a relatively good prognosis after treatment.
Location distribution
85% of intracranial aneurysms are located in the anterior circulation (internal carotid artery system), and the willis loop of the skull base vessels is the most common site of aneurysms, specifically at the union of the anterior communicating artery and the anterior cerebral artery, the junction of the posterior communicating artery and the internal carotid artery, the bifurcation of the middle cerebral artery, and the junction of the ophthalmic artery and internal carotid artery. Posterior circulation (vertebrobasilar system) aneurysms are mainly located at the tip of the basilar artery, at the connection between the anterior inferior cerebellar artery and the main trunk of the basilar artery, and at the connection between the posterior inferior cerebellar artery and the vertebral artery.
Predisposing risk factors
Genetic factors
Genetic disorders.
Genetic disorders such as the connective tissue disease Ehlers-Danlos syndrome have been associated with the occurrence of intracranial aneurysms.
Patients with autosomal dominant disease polycystic kidney are 6.9 times more likely to develop intracranial aneurysms than the rest of the population.
Patients with familial hyperaldosteronism have an increased risk of intracranial aneurysm.
Patients with smog have an increased risk of intracranial aneurysm. Studies have found a likely genetic susceptibility to smog, which may be reflected in familial smog.
Familial aneurysms.
First-degree relatives of patients with aneurysms are significantly more likely to have an aneurysm, with some studies reporting up to a 3.6-fold increase. Familial aneurysms rupture at a younger age and with smaller aneurysms.
Other factors
Smoking: Patients who smoke are 3-4.7 times more likely to have an intracranial aneurysm rupture resulting in subarachnoid hemorrhage than those who do not smoke. Smoking predisposes to aneurysms because of the reduced potency of alpha-1 antitrypsin, which is an important elastase inhibitor.
Hypertension: Although the relationship between hypertension and aneurysm is controversial, the available data still suggest that hypertension is a factor in aneurysm susceptibility.
Estrogen deficiency: The increased incidence of aneurysms in postmenopausal women may be due to a decrease in collagen as a result of estrogen deficiency.
Aneurysm pathophysiology
Saccular aneurysm: a thin-walled bulge of an intracranial artery in which the aneurysm wall lacks an elastic lining or mesentery or is severely disrupted. Hemodynamic pressure and turbulence can lead to disruption of the vessel wall. There is evidence of a local inflammatory response of the vessel wall in relation to aneurysm formation and growth. The process of aneurysmal wall changes is roughly linear in endothelialized vessel wall smooth muscle cells, wall thickening with disorganized smooth muscle cell arrangement, intimal hyperplasia with reduced cellular components or interlaminar thrombosis, and minimal intimal cellular components with massive thrombotic component formation.
Spindle aneurysm: The lumen of the entire affected vessel is enlarged or dilated, and atherosclerosis is one of the causes.
Intercalated aneurysm: the endothelium is locally lifted under the impact of blood flow from a ruptured arterial endothelium to form an enlarged aneurysmal lumen under the endothelium.
Mycotic aneurysm: often due to infective endocarditis resulting in dislodgement of the mycotic thrombus.
Clinical symptoms
Unruptured: Small microminiature intracranial aneurysms usually have no obvious clinical symptoms, while large giant intracranial aneurysms may develop neurological symptoms due to the occupying effect. Common symptoms include headache, dizziness, ptosis, visual acuity, visual field loss, cone bundle sign, facial pain or numbness, etc.
Rupture: Once an aneurysm ruptures, whether large or small, the condition is very aggressive. Symptoms include severe headache, nausea and vomiting, neck stiffness, limb paralysis or even unconsciousness.
Diagnosis.
The diagnosis of hemorrhage can be clarified by cranial CT after aneurysm rupture causing subarachnoid hemorrhage, and cranial CTA can detect aneurysms of 5mm or more in diameter. Cranial MRI can detect aneurysms of 3 mm in diameter, but the gold standard for intracranial aneurysm diagnosis is still whole brain angiography (DSA), which is the most important tool to guide treatment. Both cranial CTA/MRA are subject to artifacts caused by skull or brain tissue, and the diagnosis needs to be confirmed by an experienced radiologist and neurologist.
Risk of Aneurysm Rupture
Both the ISUIA study and the UCAS study suggest that the size and location of intracranial aneurysms are associated with the risk of rupture. Aneurysm growth is more common in large intracranial aneurysms.
Some studies have proposed the hypothesis that intracranial cystic aneurysms are acquired and not congenital; most aneurysms develop and stabilize in a short period of time, either hours, days or weeks, and their size is related to the elastic limit of the aneurysm wall, at which point they either rupture and bleed beyond the limit or stabilize and become firm. This could explain why small aneurysms rupture.
The risk of rupture is lowest for spongy sinus aneurysms; the posterior circulation includes the vertebrobasilar artery, anterior inferior cerebellar artery, posterior inferior cerebellar artery, and the anterior circulation aneurysms include anterior communicating artery aneurysms, anterior cerebral artery, internal carotid artery, and middle cerebral artery; the risk of rupture is highest for posterior communicating artery and other arteries.
Treatment
Because all data are population-based studies, it is not possible to determine how high the risk of bleeding is for each individual patient. Therefore, treatment of asymptomatic unruptured aneurysms requires a comprehensive analysis by physicians based on the size, shape, and location of the aneurysm, as well as consultation with the patient and his or her family. Surgical management should be actively recommended for symptomatic intradural aneurysms. Due to the risk of re-rupture and bleeding, aggressive management (craniotomy clamping or interventional embolization) of ruptured aneurysms is strongly recommended to prevent re-bleeding.
Craniotomy clamping is the use of metal aneurysm clamps to hold the aneurysm neck and block the communication between the aneurysm lumen and the aneurysm-carrying vessels, thus reducing the possibility of aneurysm hemorrhage.
Interventional embolization is performed by inserting a miniature spring coil into the aneurysm cavity through a special catheter to promote the formation of a thrombus in the aneurysm cavity and thereby close the aneurysm cavity.
In the literature, the mortality rate of open surgery for unruptured aneurysms is 1.7%, and the poor prognosis is 6.7%. ISUIA suggests that the incidence of poor prognosis for open surgery and interventional embolization is 12.6% and 9.8%, respectively, and the factors associated with poor prognosis include advanced age, large size, and posterior circulation.
Clinical studies suggest that endovascular interventional embolization has a relatively low mortality and complication rate compared with open surgical clamping of aneurysms.
New embolization devices such as blood flow steering devices and pipeline dense mesh treatment system have improved the cure rate of aneurysms to some extent, offering new possibilities for aneurysms previously thought to be untreatable.
China is the first to apply pipeline embolization device to treat intracranial aneurysm with satisfactory results and accumulated certain experience.
Both craniotomy and interventional embolization carry certain risks, so the decision of intracranial aneurysm treatment needs to be determined based on a comprehensive analysis of multiple factors such as the size, location, morphology, and family history of the patient’s aneurysm, combined with the opinions of the patient and family, and formulated and implemented by an experienced neurointerventional physician.