Intracranial aneurysm


Intracranial aneurysm, also known as brain aneurysm.


Aneurysms, including intracranial, are classified both by size and shape. 


Intracranial aneurysms may result from: diseases acquired during life, or from genetic conditions.


No specific gene loci has been identified to be associated with cerebral aneurysm.


Genes associated with the development of intracranial aneurysms: perlecan, elastin, collagen type 1 A2, endothelial nitric oxide synthase, endothelin receptor A and cyclin dependent kinase inhibitor. 

Mutations in interleukin 6 may be protective.

Other  genetic loci have been identified as relevant to the development of intracranial aneurysms: include genes 1, 2, 11, and 19.

Additional risk factors that contributes to the formation of aneurysm are: cigarette smoking, hypertension, female gender, alcoholism, family history of cerebral aneurysm, infection, and head trauma. 


Cocaine use may be associated with the development of intracranial aneurysms.

Genetic associations with intracranial aneurysms: 

Coarctation of the aorta is also a known risk factor.

Arteriovenous malformations

Connective tissue diseases

Autosomal dominant polycystic kidney disease.

Neurofibromatosis type I

Marfan syndrome

Multiple endocrine neoplasia type I

Pseudoxanthoma elasticum

Hereditary hemorrhagic telangiectasia.

Ehlers-Danlos syndrome types II and IV

Small aneurysms have a diameter of less than 15 mm. 

Larger aneurysms include those classified as large (15 to 25 mm), and giant (25 to 50 mm), and super-giant (over 50 mm).


For intracranial aneurysms larger than 7 mm in diameter treatment should be initiated because they are prone for rupture. 

Aneurysms less than 7 mm, however, arising from anterior and posterior communicating artery are more easily ruptured when compared to aneurysms arising from other locations.

Saccular aneurysms, are known as berry aneurysms.


Berry aneurysms appear as a round outpouching and are the most common form of cerebral aneurysm.


Charcot-Bouchard aneurysms are a common cause of intracranial hemorrhage.


Charcot-Bouchard aneurysms or aneurysms of the brain vasculature which occur in small blood vessels less than 300 mm in diameter.


Charcot-Bouchard aneurysms are most often located in the lenticulostriate vessels of the basal ganglia and are associated with chronic hypertension.

A small, unchanging aneurysm will produce few, if any, symptoms. 

Fusiform (dolichoectatic) aneurysms represent a widening of a segment of an artery around the entire blood vessel, rather than just arising from a side of an artery’s wall. 

They usually do not rupture.



The prevalence of intracranial aneurysm is about 1-5% or 10 million to 12 million persons in the United States.



The incidence of intracranial aneurysm is 1 per 10,000 persons per year in the United States, or approximately 27,000, with 30- to 60-year-olds being the age group most affected.



Intracranial aneurysms occur more in women, by a ratio of 3 to 2.


2-3% of the general population.

20-25% of patients have a misdiagnosis or delay in diagnosis of aneurysm at initial presentation.

Symptoms range from: None, severe headache, visual problems, nausea, vomiting, and confusion.


Almost all intracranial aneurysms rupture at their apex, with hemorrhage into the subarachnoid space and sometimes the brain parenchyma. 

Larger aneurysms have a greater tendency to rupture. 

The risk of a subarachnoid hemorrhage is greater with a saccular aneurysm than a fusiform aneurysm.


Saccular aneurysms are almost always the result of hereditary weakness in blood vessels.

Saccular aneurysms typically occur within the arteries of the Circle of Willis: affecting the following arteries in order of frequency 

Anterior communicating artery

Posterior communicating artery

Middle cerebral artery

Internal carotid artery

Tip of basilar artery

Saccular aneurysms tend to have a lack of tunica media and elastic lamina around its dilated location.

The wall of sac made up of thickened hyalinized intima and adventitia.

Parts of the brain vasculature are inherently weak, especially the Circle of Willis, where small communicating vessels link the main cerebral vessels. 

At these areas there is  particularly susceptibility  to saccular aneurysms.

A ruptured microaneurysm may cause an intracerebral hemorrhage, with focal neurological findings.


Minor leakage from aneurysm may cause warning headaches. 

After intracranial aneurysm rupture, about 60% of patients die.

Most ruptured aneurysms are less than 10 mm in diameter.


Before rupture, a large aneurysm may be asymptomatic or associated with symptoms:  sudden and unusually severe headache, nausea, vision impairment, vomiting, and loss of consciousness, or the individual may experience no symptoms at all.

When an intracranial aneurysm ruptures, blood leaks into the space around the brain, a subarachnoid hemorrhage. 

Aneurysm rupture onset is usually sudden without prodrome, presenting as a severe headache worse than previous headaches.

Symptoms of a subarachnoid hemorrhage differ depending on the site and size of the aneurysm.

Symptoms of a ruptured aneurysm include:

a sudden severe headache that can last from several hours to days

nausea and vomiting

drowsiness, confusion and/or loss of consciousness

visual abnormalities



Usual onset 30-60 years old.



Causes: Hypertension, infection, head trauma.



Risk factors: Smoking, old age, family history, cocaine use.


Approximately 25% of patients have multiple intracranial aneurysms, predominantly when there is familial pattern.

7% of unruptured aneurysms less than 1 cm present with aneurysmal symptoms other than rupture.

Most common cause of the non traumatic subarachnoid hemorrhage.

Commonly undetected until manifestations of subarachnoid hemorrhage, intracerebral hemorrhage or both.

Incidence of aneurysmal subarachnoid hemorrhage estimated between 16 and 30,000 per year.

Short term mortality after a subarachnoid hemorrhage can be as high as 45%.

Most deaths from aneurysmal subarachnoid hemorrhage can be due to initial hemorrhage, rebleeding, vasospasm of cerebral vessels or major medical complications.

Intracranial aneurysms may rebleed.



Intracranial aneurysms may lead to hydrocephalus, or vasospasm.



Vasospasm of blood vessels can occur secondary to subarachnoid hemorrhage following a ruptured aneurysm. 



Vasospasm is most likely to occur within 21 days of an intracranial aneurysm rupture, and is seen radiologically within 60% of such patients. 


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

These cells reach the subarachnoid space to phagocytose the hemorrhaged red blood cells. 

With apoptosis, there is a degranulation of vasoconstrictors, including endothelins and free radicals, that cause the vasospasm.

13.5%-60% of major aneurysm ruptures associated with unrecognized warning signs.

With subarachnoid hemorrhage affects 28,000 people per year and is associated with death or permanent disability in nearly two thirds of patients.

Most recent studies suggesting 2-4% of general population has an unruptured intracranial aneurysm.

Increasing incidence with advancing age.

Intracranial aneurysms are rarely seen in pediatric populations.



Manifests as a weakness in the wall of a cerebral artery or vein causes a localized dilation or ballooning of the blood vessel.



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



It is theorized low shear stress causes growth and rupture of large aneurysms through inflammatory response while high shear stress causes growth and rupture of small aneurysm through response from the blood vessel wall.


This causes fibrosis of the arterial wall, with reduction of number of smooth muscle cells, abnormal collagen synthesis, resulting in thinning of arterial wall and formation of aneurysm and rupture. 

Primary goal in management involves the detection and treatment before catastrophic rupture.

Treatment options for intracranial aneurysm: 


Endovascular coiling, Surgical clipping, Cerebral bypass surgery.

Cerebral angiography is the standard technique to diagnose and characterize the anatomy of a cerebral aneurysm and imaging is utilized in planning medical, endovascular, or surgical treatment.

Incidence of subarachnoid hemorrhage from intracranial aneurysm increases with age.

80-90% of all intracranial aneurysms are saccular or berry aneurysms, which appear as small, round berrylike dilatations.

Aneurysms in the posterior circulation involving the basilar artery, vertebral arteries and posterior communicating artery,have a higher risk of rupture. 



Basilar artery aneurysms represent only 3-5% of all intracranial aneurysm.



Basilar artery aneurysms, however, are the most common aneurysms in the posterior circulation.

Multiple aneurysms occur in 20-25% of patients with saccular aneurysms and approximately 20% of patients have a family history of subarachnoid hemorrhages or intracranial aneurysms.

Associated with polycystic kidney, arteriovenous malformations, aortic coarctation, Marfan’s syndrome, Ehlers-Danlos syndrome, pseudoxanthoma elasticum, fibromuscular dysplasia, and pituitary tumors.

Wide variability in growth rate of aneurysms from hours, weeks to several years.

Some aneurysms may decrease in size or spontaneous obliterate.

A large percentage of unruptured intracranial aneurysms appear to remain unchanged in size over time.

Intracranial aneurysms can be diagnosed radiologically using magnetic resonance or CT angiography.



Such  methods have limited sensitivity for diagnosis of small aneurysms.



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



CSF is analyzed  for RBC count, and presence or absence of xanthochromia.

Diagnosis by  Angiography, CT scan.

Angiographic diagnosis and treatment with coil embolization can be performed during the diagnostic procedure.

Rupture during diagnostic angiogram is extraordinarily rare.

Treatment for a ruptured cerebral aneurysm generally includes restoring deteriorating respiration and reducing intracranial pressure. 



The two treatment options for securing intracranial aneurysms: surgical clipping or endovascular coiling. 



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 rebleeding.



Meta-analysis found the outcomes and risks of surgical clipping and endovascular coiling to be statistically similar.



The International Subarachnoid Aneurysm Trial indicated a higher rate of recurrence when intracerebral aneurysms are treated using endovascular coiling. 



Endovascular coiling consists of 


the insertion of platinum coils into the aneurysm. 



With endovascular coiling a catheter is inserted into a blood vessel, typically the femoral artery, and passed through blood vessels into the cerebral circulation and the aneurysm. 



Coils are released into the blood stream ahead of the aneurysm. 



Coils expand and initiate a thrombotic reaction within the aneurysm. 



Coiling prevents further bleeding from the aneurysm.



Aneurysms can be clipped at the base of the aneurysm by craniotomy, or by endoscopic endonasal approach.



Cerebral bypass surgery may be used 


when a patient has an aneurysm involving a blood vessel at the base of the skull by replacing it with an artery from another part of the body.



Small aneurysms of less than 7 mm have a low risk of rupture of less than one percent for aneurysms of this size.



The prognosis for a ruptured cerebral aneurysm varies  with the extent and location of the aneurysm.



Other prognostic factors include age, general health, and neurological condition of the patient.



A initial ruptured cerebral aneurysm may be lethal.



In others  with cerebral aneurysm rupture recovery with little or no neurological deficit can occur.



The most important factors in determining prognosis of a cerebral aneurysm rupture are age and the 


Hunt and Hess scale.



Patients with Hunt and Hess grade I and II hemorrhage, and patients who are younger can anticipate a good outcome, without death or permanent disability. 



Older patients and those with poorer Hunt and Hess grades have a poor prognosis. 



Generally, about two-thirds of patients with an intracranial aneurysm rupture have a poor outcome, death, or permanent disability

During endovascular treatment intraprocedural aneurysm rupture can occur in as many as 8% of cases and if occurs, carries mortality rate of up to 38%.

Endovascular treatment complications are associated to guide wire perforation, microcatheter perforation or coil perforation, and less commonly to increased intraaneurysmal pressure induced by injection of contrast medium.

Leave a Reply

Your email address will not be published. Required fields are marked *