Last updated date: 09-Feb-2023

Medically Reviewed By

Medically reviewed by

Dr. Lavrinenko Oleg

Originally Written in English

Brain (Cerebral) Aneurysm: Causes, Symptoms and Treatment

    Brain (Cerebral) Aneurysm


    A brain aneurysm is a berry-shaped swelling in a cerebral artery. Normally, arteries, like hoses, are strong and elastic. An aneurysm occurs when a section of an arterial wall weakens, expands outward, and bulges.

    Aneurysms can form in a variety of locations throughout the body, such as the biggest artery in the abdomen (abdominal aortic aneurysm) or an artery in the head (brain aneurysm). Brain aneurysms frequently occur as the arteries that feed blood to the brain break and branch off.

    Many people who have a brain aneurysm are unaware of it. Others, on the other hand, feel symptoms or their aneurysm is more prone to rupture (burst) and cause life-threatening bleeding in the brain. Treatment is occasionally recommended to prevent such ruptures and ease symptoms.


    What is Brain Aneurysm?

    Cerebral aneurysms are dilations that form at weak spots in the cerebral artery circulation. They can range in size (small less than 0.5 mm, medium 6 to 25 mm, and large greater than 25 mm). The majority are saccular (berries), with a thin or missing tunica medium and an absent or badly fragmented internal elastic lamina. Fusiform (circumferential) and mycotic (infectious) aneurysms, on the other hand, are seen in a tiny number of instances.

    An intracranial aneurysm can affect up to 5% of the population, and many of these people are unaware of it. The majority of cerebral aneurysms are asymptomatic, but a tiny percentage of them can burst and bleed, resulting in life-threatening consequences.

    Dolichoectatic, fusiform, or arteriosclerotic aneurysms are elongated proximal artery outpouchings that account for 7% of all cerebral aneurysms. Infectious or mycotic aneurysms are located in the periphery of the brain and account for 0.5 percent of all cerebral aneurysms.

    Neoplastic aneurysms, uncommon sequelae of embolized tumor pieces, and traumatic aneurysms are examples of peripheral lesions. Traumatic damage can also cause dissecting aneurysms in the proximal arteries. Hypertension can cause microaneurysms of tiny perforating arteries.

    In 85-95 percent of patients, saccular aneurysms are located in the anterior circulation, whereas dolichoectatic aneurysms mostly impact the vertebrobasilar system. The frequency of saccular aneurysms at certain artery segments varies due to variations in reported research populations. In 20-30% of individuals with cerebral aneurysms, multiple saccular aneurysms are seen.



    The global prevalence of cerebral aneurysms is around 3.2 percent, with a mean age of 50 and a gender ratio of 1:1. After the age of 50, this ratio changes dramatically, with a rising female predominance reaching 2:1, which is considered to be due to decreasing circulating estrogen, which causes a decrease in the collagen composition of the vascular tissue.

    Aneurysmal SAH is a devastating disease that affects 30,000 people in the United States each year. The majority of these people (60 percent) die or are permanently disabled; 50 percent of those who survive with positive results have significant cognitive impairment. Cerebral vasospasm (narrowing of the proximal arterial segments) worsens 20-50% of cases and is the leading cause of mortality and disability in aneurysmal SAH.

    The rate of rupture resulting in SAH is around 10 per 100,000. This is more prevalent among some groups, such as the Finnish and Japanese. This is not because these populations have a higher rate of aneurysms.

    Overall mortality from aneurysmal SAH is estimated to be 0.4 to 0.6 percent of all-cause fatalities, with an estimated 20% mortality and an additional 30% to 40% morbidity in patients with known rupture.


    Brain aneurysm causes

    The majority of cerebral aneurysms are acquired lesions, having a higher frequency in individuals with risk factors such as advanced age, hypertension, smoking, alcohol misuse, and atherosclerosis. Cocaine use, tumors, trauma, and some embolic-forming diseases, such as endocarditis, are other causes.

    There is also a substantial hereditary component, with the incidence being much higher in people with a strong family history of aneurysms. Aneurysms are occasionally produced by hereditary disorders such as autosomal dominant polycystic kidney disease, Ehlers-Danlos syndrome, fibromuscular dysplasia, tuberous sclerosis, arteriovenous malformations (AVM), and aortic coarctation.


    Risk factors

    Brain Aneurysm chart

    Because of the increased familial occurrence and association with hereditary conditions (e.g., autosomal dominant polycystic kidney disease), a genetic predisposition to develop a brain aneurysm must be assumed, but a specific candidate gene linked to the development of cerebral aneurysms has not yet been identified.

    People who smoke and have high blood pressure are more prone to develop brain aneurysms. Women are more likely than males to have a brain aneurysm, as do those who have a parent or sibling with a brain aneurysm. The danger rises with age as well.

    The aneurysm is more prone to rupture due to the same reasons. However, this risk is dependent on factors such as the aneurysm's specific position and size.

    Dolichoectatic aneurysms of the proximal arteries are most likely arteriosclerotic in nature. These convoluted, elongated dilatations, which lack a genuine aneurysmal neck, usually include layered thrombus. Although aneurysmal SAH can occur, these lesions generally cause mass effects on the surrounding parenchyma, resulting in brainstem compression and cranial neuropathies, or obstructing CSF outflow or causing distant thromboembolic consequences.

    Infectious aneurysms are frequently seen in distal branches of the middle cerebral artery (MCA; 75-80% of cases), indicating an embolic origin for these lesions. Septic material cardioembolism complicates the course of 4% of patients with subacute bacterial endocarditis and may impact other individuals with congenital heart disease and right-to-left shunts.

    Direct extension of septic emboli harboring Streptococcus viridans or Staphylococcus aureus (the most prevalent pathogens) from lumen to adventitia may result in deterioration and aneurysm development. In the case of meningitis, widespread infiltration from the periphery to the lumen may occur, as evidenced by aneurysms of the basal circulation associated with fungal infections.

    Traumatic aneurysms can develop in the peripheral cortical branches as a result of contact with the falcine edge or skull fractures caused by a penetrating or closed head injury. Traumatic dissecting aneurysms caused by intramural hematoma growth are most often found at the skull base.

    False aneurysms, which lack complete layers of the artery wall, can compress cranial nerves and cause distant embolization. A carotid-cavernous fistula can result from a rupture of the internal carotid artery (ICA).



    Under normal conditions, cerebral arteries have three layers (from inside to outside):

    1. The intima with the basal membrane and endothelial cells 
    2. The media, consisting of smooth muscles cells, embedded into a dense network of collagen and elastin fibers and
    3. The adventitia, which mainly consists of collagen, providing the structural integrity of the vessel wall.


    Importantly, the intima and media are separated by the internal elastic lamina, which is thought to be the essential component that should degenerate in order for aneurysm development to occur on a structural level.

    Intracranial blood vessels vary from extracranial blood vessels in that they have a thicker internal elastic lamina, a lower number of elastin fibers and smooth muscle cells in the media, and a thinner adventitia. This, along with the smaller quantity of connective tissue inside the subarachnoid space, may make cerebral arteries more prone to aneurysm development.

    The following processes are proposed by current hypotheses on cerebral aneurysm development. First, there occurs apoptosis of vascular smooth muscle cells within the artery wall, followed by a breakdown of the internal elastic lamina. Second, collagen fiber reconstitution as a result of the resultant change in tensile stresses causes collagen and/or elastin degradation and break-down, resulting in vessel wall remodeling.

    The degree of aneurysm wall inflammation, hemodynamic stress due to cardiovascular risk factors (e.g., hypertension or nicotine consumption), and remodeling/turnover of tissue and collagen in the aneurysm wall are thought to influence whether this remodeling results in aneurysm sack stabilization, progression, or even rupture.

    In recent research, the importance of the inflammatory component in the pathophysiology of aneurysm development and rupture has become clear.

    Saccular aneurysms are thought to arise as a result of a multifactorial mechanism. Over time, hemodynamic stress on the internal elastic lamina produces disintegration. This is combined with vibrations caused by turbulent blood flow, resulting in structural fatigue.

    T-cell and macrophage-mediated inflammation has also been linked to histologic alterations inside the arterial wall, which contribute to aneurysmal development and expansion. The process is accelerated and exacerbated in individuals who have specific risk factors, as previously reported.

    Fusiform aneurysms, on the other hand, are mostly produced by atherosclerosis, while mycotic aneurysms are formed by septic emboli found in infected endocarditis.


    Brain aneurysm symptoms and signs

    Unruptured cerebral aneurysms are asymptomatic and hence cannot be identified based only on history and physical exam. When they burst, however, they frequently manifest with a rapid onset, severe headache. This is commonly referred to as a "thunderclap headache" or the "worst headache of my life."

    The discomfort is lateralized to the side of the aneurysm in 30% of individuals. A headache may be followed by a temporary loss of consciousness, meningismus, nausea and vomiting, or other symptoms. Seizures are uncommon, occurring in fewer than 10% of patients. In 10 to 15% of patients, sudden death may occur.

    The most frequent consequence of aneurysms is bleeding. The chance of brain aneurysms rupturing and causing bleeding is determined by the risk factors listed above, particularly the size of the aneurysm.


    Surprisingly, 30 to 50% of individuals with significant SAH describe a sudden and intense headache 6 to 20 days before the event. This is known as a "sentinel headache," because it indicates a small hemorrhage or "warning leak." Elevated blood pressure, dilated pupils, visual field and/or cranial nerve deficits, mental state changes such as drowsiness, photophobia, motor or sensory deficits, neck stiffness, and lower back discomfort with neck flexion are all possible physical exam results.

    Physical examination findings may include prominent scalp veins, indications of congestive heart failure (for example, vein of Galen aneurysms), or orbital bruits (eg, cavernous carotid aneurysms).

    Because of variations in aneurysm features, neurologic findings vary greatly. Among the findings are the following:

    • Aneurysmal SAH is characterized by nuchal stiffness, a reduced degree of awareness, subhyaloid hemorrhages, pupillary abnormalities (usually dilated), ophthalmoplegia, cranial neuropathies, and other localized impairments.
    • Giant aneurysms, also known as dolichoectatic aneurysms, can produce mass effects and distal thromboembolism, as well as significant localized impairments; large aneurysms can also cause optic atrophy or other cranial neuropathies, as well as brainstem compression.

    Certain disorders have been linked to specific aneurysmal sites. Aneurysms in the anterior communicating artery, for example, the most prevalent location of aneurysmal SAH (34%), exhibit the following characteristics:

    • These aneurysms are usually silent until they rupture
    • Suprachiasmatic pressure may cause altitudinal visual field deficits, abulia or akinetic mutism, amnestic syndromes, or hypothalamic dysfunction.
    • Neurologic deficits in aneurysmal rupture may reflect intraventricular hemorrhage (79%), intraparenchymal hemorrhage (63%), acute hydrocephalus (25%), or frontal lobe strokes (20%)


    Clinicians can utilize the Hunt and Hess grading system to predict outcomes based on baseline neurologic state. There are five classes based on the severity of symptoms, which correspond with the total fatality rate.

    • Grade 1 includes a mild headache with slight nuchal rigidity. 
    • Grade 2 is given for a severe headache with a stiff neck but without a neurologic deficit other than cranial nerve palsy. 
    • For grade 3, the patient is drowsy or confused with a mild focal deficit.
    • In grade 4, the patient is stuporous with moderate to severe hemiparesis. Finally,
    • Grade 5 includes a coma with decerebrate posturing.



    Brain aneurysm symptoms

    Most unruptured cerebral aneurysms are discovered by chance when a patient undergoes neuroimaging for another reason. Individuals at high risk, on the other hand, may be tested using magnetic resonance imaging (MRI), computed tomographic angiography (CTA), or traditional angiography.

    A non-contrast CT of the brain, with or without a lumbar puncture, is typically used to make the diagnosis of a suspected rupture producing SAH (LP). When the patient appears early, CT alone is regarded extremely sensitive for SAH, although sensitivity diminishes over time. According to some research, CT is 100 percent sensitive if conducted within 6 hours after the beginning of symptoms, but declines to 92 percent after 24 hours and 58 percent after 5 days (14 to 18)

    Aneurysms are particularly visible utilizing a method known as digital subtraction angiography (DSA), which involves taking an x-ray with and without the injection of a contrast material. After that, a computer generates a picture that only displays blood vessels — other structures, such as bones, are no longer visible.

    If the CT scan is negative but there is still a clinical suspicion of SAH, an LP should be performed. The standard LP findings include an increased opening pressure and an increased red blood cell count that does not decrease from tube 1 to tube 4. The presence of xanthochromia, a pink or yellow tinge to the cerebrospinal fluid (CSF) caused by hemoglobin breakdown products, strongly suggests SAH.

    Lab studies used in the diagnosis and assessment of cerebral aneurysms include the following:

    • Complete blood count (CBC):

     Monitor for infection, evaluate anemia, and identify bleeding risk

    • Prothrombin time (PT)/activated partial thromboplastin time (aPTT):

     Identify a coagulopathy that increases bleeding risk

    • Serum chemistries, including electrolytes and osmolarity:

    Obtain baseline studies to monitor hyponatremia, address arrhythmogenic abnormalities, assess blood glucose, and monitor hyperosmolar therapy for elevated intracranial pressure

    • Liver function tests:

     Identify hepatic dysfunction that may complicate clinical course

    • Arterial blood gases:

     Assess blood oxygenation


    Xanthochromia can be detected visually or by spectrophotometry, which is more than 95% sensitive when conducted at least 12 hours following the beginning of the bleed.

    Once SAH has been diagnosed, the cause of the bleeding should be determined. This can be accomplished with the use of CTA, MRA, or digital subtraction angiography (DSA). DSA entails introducing a catheter into the arterial circulation and injecting contrast under fluoroscopic guidance. This is regarded as the "gold standard" for detecting aneurysmal SAH.


    Management of Brain Aneurysm

    The choice to treat is complex and is influenced by the patient's size, location, age, and comorbidities, as well as the presence or absence of a rupture. There are two types of treatment: surgical and endovascular.

    Both treatments can prevent blood from flowing into the aneurysm indefinitely. They are linked with dangers despite the fact that they prevent the aneurysm from exploding. It might benefit to have an in-depth consultation with specialists who specialize in the treatment of brain aneurysms, such as neurologists or neurosurgeons, to determine which option would be best for you.

    Under general anesthesia in the operating room, a small metal clip is placed across the neck of an aneurysm, stopping blood from entering the aneurysmal sac and therefore eliminating the danger of bleeding.

    However, whereas early surgical therapy is associated with greater operative morbidity and death rates, patients who have surgery have reduced overall morbidity and mortality rates. The combined morbidity and death rate for intraoperative aneurysmal rupture is 30-35 percent.

    Using a microscope, the aneurysm is accessible by temporarily removing a tiny piece of the skull, dissecting the dura, and separating it from other blood arteries. After carefully applying the clip, the skull is fastened in place with tiny metal plates and screws, and the incision is closed. The aneurysm will diminish and scar with time, but the clip will typically stay for life.


    Brain Aneurysm Coiling

    Endovascular coiling is a less invasive procedure that can be utilized in some cases. Thromboembolism and intraprocedural aneurysm rupture are also potential risks. The operation is carried out by putting a catheter into the femoral artery and up into the artery harboring the aneurysm. Following that, a second microcatheter with the platinum coil is placed via the first catheter.

    To remove the coil from the catheter within the aneurysm lumen, an electric current is utilized. This stimulates the development of local clots and the obliteration of the aneurysmal sac.

    In the case of a rupture, care also involves the treatment of SAH consequences. This is generally done in an intensive care unit (ICU) to look for symptoms of clinical worsening such as rebleeding, symptomatic vasospasm, hydrocephalus, seizures, and hyponatremia. Nimodipine, a calcium channel blocker, is commonly used to avoid cerebral ischemia after SAH due to vasospasm.


    Differential Diagnosis

    • Arteriovenous malformations
    • Cavernous sinus syndromes
    • Carotid/vertebral artery dissection
    • Cerebral venous thrombosis
    • Fibromuscular dysplasia
    • Migraine and cluster headaches
    • Pituitary apoplexy
    • Stroke - ischemic or hemorrhagic


    Brain Aneurysm vs Stroke

    A stroke happens when a blood vessel in the brain ruptures or the blood supply to the brain is cut off. An aneurysm is caused by a weakened arterial wall. Aneurysms produce bulges in your body, which can burst and cause bleeding. They have the potential to harm any area of the body, including the brain and heart.



    Morbidity and mortality are quite high when a brain aneurysm ruptures. Almost a quarter die within the first 24 hours, and half die within the following three months. Even with the following therapy, there is a roughly 40% death rate. The following factors also influence the prognosis:

    • Age
    • Location of an aneurysm
    • Degree of vasospasm
    • Presence of hypertension and other comorbidities
    • Neurological status on admission
    • Degree of SAH
    • The extent of intraventricular hemorrhage


    Outcome evaluations after aneurysmal SAH may not be adequately evaluated using a single scale or metric. Cognitive impairment and subjective recovery experiences should also be examined.



    • Recurrent bleeding
    • Seizures
    • Hydrocephalus
    • Arrhythmias
    • Congestive cardiac failure
    • Gastrointestinal bleeding
    • Deep vein thrombosis
    • Neurogenic pulmonary edema



    Cerebral aneurysms are dilations that form at weak points in the cerebral artery circulation. The majority of brain aneurysms are quiet and may be discovered by chance on neuroimaging or at autopsy.

    Approximately 85 percent of aneurysms are found in the anterior circulation, primarily at junctions or bifurcations in the Willis circle. Subarachnoid hemorrhage (SAH) is generally caused by a rupture and is linked with a significant morbidity and death rate. This exercise emphasizes the importance of the interprofessional team in the care of patients with cerebral aneurysms.

    The etiology of cerebral aneurysm development is a complex and poorly understood process. At the moment, it is unknown what causes the initial rupture of the elastic internal lamina in the arterial artery wall and if this process starts early or late in the patient's life.

    However, current information on the growth of aneurysms and remodeling of aneurysm tissue shows that aneurysm progression and remodeling of aneurysm tissue is a discontinuous but continuing process, and therefore cerebral aneurysms cannot be considered to be stable lesions in general.

    Unruptured cerebral aneurysms are being identified more often than ever before, owing largely to the increased use of sophisticated imaging techniques. The most serious danger of a cerebral aneurysm is rupture and catastrophic consequences. The vast majority of patients are unaware that they have an intracranial aneurysm and frequently appear with a brain hemorrhage. Because of the extraordinarily high mortality rate, it is critical to treat these aneurysms in a systematic manner once they are discovered.