Cerebral aneurysms are classified by size into small, large, giant, and super-giant, and by shape into saccular (berry), fusiform, and microaneurysms.

Saccular aneurysms are the most common type and can result from various risk factors, including genetic conditions, hypertension, smoking, and drug abuse.

Treatment options include surgical clipping and endovascular coiling, both aimed at preventing further bleeding.

Diagnosis typically involves imaging techniques such as CT or MR angiography and lumbar puncture to detect subarachnoid hemorrhage.

Advances in medical imaging have led to increased detection of unruptured aneurysms, prompting ongoing research into their management and the development of predictive tools for rupture risk.

[3][4] Causes include connective tissue disorders, polycystic kidney disease, arteriovenous malformations, untreated hypertension, tobacco smoking, cocaine and amphetamines, intravenous drug abuse (can cause infectious mycotic aneurysms), alcoholism, heavy caffeine intake, head trauma, and infection in the arterial wall from bacteremia (mycotic aneurysms).

[12] Rebleeding, hydrocephalus (the excessive accumulation of cerebrospinal fluid), vasospasm (spasm, or narrowing, of the blood vessels), or multiple aneurysms may also occur.

[15] Vasospasm, referring to blood vessel constriction, can occur secondary to subarachnoid hemorrhage following a ruptured aneurysm.

The vasospasm is thought to be secondary to the apoptosis of inflammatory cells such as macrophages and neutrophils that become trapped in the subarachnoid space.

Following apoptosis, it is thought there is a massive degranulation of vasoconstrictors, including endothelins and free radicals, that cause the vasospasm.

[11] This includes:[18] Specific genes have also had reported association with the development of intracranial aneurysms, including perlecan, elastin, collagen type 1 A2, endothelial nitric oxide synthase, endothelin receptor A and cyclin dependent kinase inhibitor.

The repeated trauma of blood flow against the vessel wall presses against the point of weakness and causes the aneurysm to enlarge.

[21][22][23] In addition, a combination of computational fluid dynamics and morphological indices have been proposed as reliable predictors of cerebral aneurysm rupture.

[24] Both high and low wall shear stress of flowing blood can cause aneurysm and rupture.

[25] Saccular aneurysms are almost always the result of hereditary weaknesses in blood vessels and typically occur within the arteries of the circle of Willis,[20][26] in order of frequency affecting the following arteries:[27] Saccular aneurysms tend to have a lack of tunica media and elastic lamina around their dilated locations (congenital), with a wall of sac made up of thickened hyalinized intima and adventitia.

[28] But these methods have limited sensitivity for diagnosis of small aneurysms, and often cannot be used to specifically distinguish them from infundibular dilations without performing a formal angiogram.

Lumbar puncture (LP) is the gold standard technique for determining aneurysm rupture (subarachnoid hemorrhage).

[30] Emergency treatment for individuals with a ruptured cerebral aneurysm generally includes restoring deteriorating respiration and reducing intracranial pressure.

If possible, either surgical clipping or endovascular coiling is typically performed within the first 24 hours after bleeding to occlude the ruptured aneurysm and reduce the risk of recurrent hemorrhage.

[31] While a large meta-analysis found the outcomes and risks of surgical clipping and endovascular coiling to be statistically similar, no consensus has been reached.

[41] In the case of broad-based aneurysms, a stent may be passed first into the parent artery to serve as a scaffold for the coils.