Brain Tumors & Aneurysms

Brain tumors and intracranial aneurysms are two distinct types of conditions that affect structures inside the skull — the brain's tissue in one case and its blood vessels in the other. Both fall under the broader category of neurovascular and neuro-oncologic disorders of the brain. While they are separate conditions with different causes and treatments, they can share some symptoms and both require specialized neurosurgical or neuro-oncologic care.

A brain tumor is an abnormal mass of cells that grows within or around the brain. Tumors can arise from the brain's own cells — these are called primary brain tumors — or from cancer cells that have traveled to the brain from another part of the body, such as the lung, breast, or skin. These are called secondary or metastatic tumors. Primary brain tumors are further classified by the type of cell they come from, their molecular characteristics, and their grade — a measure of how aggressive they are likely to behave. More than 100 distinct types of brain tumors exist. Not all are cancerous: about 73 percent of primary brain tumors are classified as non-malignant (benign or slow-growing), while about 27 percent are malignant. In the United States, approximately 89,158 new primary brain and central nervous system tumor cases are diagnosed each year. Brain tumors are responsible for about 16,853 deaths annually. They are the most common solid tumor diagnosis in children between the ages of 5 and 19, accounting for 30 percent of all new cancer diagnoses in that group.

An intracranial aneurysm — also called a cerebral aneurysm — is a bulge or blister that forms on the wall of a blood vessel in the brain where the vessel wall has become weakened. Most aneurysms never cause any symptoms and are discovered incidentally. However, if an aneurysm ruptures, it causes a life-threatening bleed around the brain called a subarachnoid hemorrhage (SAH). Approximately 3.6 to 6 percent of the general population carries an unruptured intracranial aneurysm, most without knowing it. Rupture is rare — occurring in roughly 0.01 percent of the population annually — but catastrophic when it occurs. About 25 percent of people who have a ruptured aneurysm die within the first 24 hours, and an additional 25 percent die within six months from complications of the bleed.

Aneurysms are classified by their shape, cause, size, and location. The type influences both the risk of rupture and the preferred treatment approach.

• Saccular (berry) aneurysm: By far the most common type, accounting for about 90 percent of all cerebral aneurysms. It appears as a rounded, grape-like bulge at the point where an artery branches. Most are located in the Circle of Willis — the ring of arteries at the base of the brain. Aneurysms at the anterior communicating artery account for about 35 percent of all ruptured saccular aneurysms.
• Fusiform aneurysm: Accounts for 3 to 13 percent of aneurysms. Instead of a focal bulge, the entire vessel wall in a segment balloons out circumferentially. It is most commonly found in the vertebrobasilar arteries at the back of the brain and is usually caused by atherosclerosis (hardening of the arteries) or vessel wall dissection.
• Dissecting aneurysm: Occurs when a tear develops in the inner layer of an arterial wall, allowing blood to enter and separate the layers. It can cause either ischemic stroke (if blood flow is blocked) or subarachnoid hemorrhage (if the outer wall ruptures).
• Mycotic aneurysm: A rare infected aneurysm caused when bacteria from the bloodstream — most commonly from infective endocarditis — invade and weaken the wall of a cerebral artery. These aneurysms form in more peripheral locations than typical saccular aneurysms.
• Blister aneurysm: A small but extremely fragile blister-like outpouching that forms on the wall of an artery at a non-branching point. Though rare (less than 1 percent of aneurysms), they carry a high rupture risk and are technically challenging to treat.
• Giant aneurysm: Any aneurysm 25 mm or larger in diameter. Giant aneurysms carry an annual rupture risk of 40 to 50 percent and often cause symptoms through direct compression of surrounding brain tissue even before rupture.

Most primary brain tumors arise from accumulated mutations errors in the DNA of brain cells  that disable the normal controls on cell growth and division. Modern molecular diagnostics have identified specific driver mutations that define and classify many tumor types. The cause of most sporadic brain tumors, including the most common and most deadly type (GBM), is not known. No confirmed dietary, cellphone, or occupational environmental cause has been established in large prospective studies. The only firmly validated environmental cause is prior therapeutic radiation to the head.

Specific molecular mechanisms that have been identified in brain tumor development include:

• IDH1/IDH2 mutation: Found in astrocytomas and oligodendrogliomas. This mutation causes the cell to produce an abnormal metabolite called 2-hydroxyglutarate, which disrupts the normal epigenetic (gene expression) controls in the cell, driving tumor growth. IDH-mutant tumors tend to affect younger adults and carry a better prognosis than IDH-wildtype tumors.

• EGFR amplification and chromosome gains and losses: The molecular fingerprint of glioblastoma, IDH-wildtype. Combined gain of chromosome 7, loss of chromosome 10, amplification of the EGFR gene, and TERT promoter mutation define the most aggressive adult brain tumor.

• H3 K27M mutation: The defining mutation of diffuse midline glioma, a pediatric brainstem tumor. This histone mutation disrupts the way genes are turned on and off in the cell.

• 1p/19q codeletion: The simultaneous loss of specific parts of chromosomes 1 and 19. This defines oligodendroglioma and makes the tumor respond unusually well to chemotherapy.

• MGMT promoter methylation: Silences the DNA repair gene MGMT in glioblastoma cells. This epigenetic change predicts a better response to the chemotherapy drug temozolomide. About 40 to 50 percent of GBM cases carry this methylation.

• BRAF V600E and MAPK pathway alterations: Drive many pediatric low-grade gliomas, including pilocytic astrocytoma. These mutations are potentially targetable with specific molecular therapies.

• Inherited genetic syndromes: Several hereditary conditions significantly increase brain tumor risk. Neurofibromatosis type 1 (NF1) predisposes to optic pathway gliomas and low-grade brain tumors. Neurofibromatosis type 2 (NF2) causes bilateral vestibular schwannomas, meningiomas, and ependymomas. Tuberous sclerosis complex (TSC) is associated with subependymal giant cell astrocytoma. Li-Fraumeni syndrome (caused by inherited TP53 mutation) increases the risk of high-grade gliomas. Von Hippel-Lindau syndrome (VHL) predisposes to hemangioblastomas — highly vascular cerebellar tumors.

• Therapeutic ionizing radiation: The only well-established environmental risk factor. Prior radiation treatment to the head or neck — for example, in childhood leukemia or other cancers — significantly increases the risk of developing a secondary brain tumor, often decades later.

Intracranial aneurysms develop when the wall of a cerebral artery weakens enough to bulge outward under the force of blood pressure. The specific mechanisms depend on the type of aneurysm.

Saccular aneurysms — the most common type — typically form at the points where arteries divide and branch. At these bifurcation points, blood flow is turbulent, and the shear forces against the inner vessel wall are highest. Over time, this hemodynamic stress damages the inner elastic layer of the artery wall. Inflammatory cells are recruited, and enzymes called matrix metalloproteinases further degrade the vessel wall, allowing it to progressively bulge. Atherosclerosis (plaque buildup inside arteries) weakens the vessel wall through a similar degradative mechanism and is the primary driver of fusiform aneurysms. When bacteria enter the bloodstream — most commonly from an infected heart valve in infective endocarditis — they can seed the walls of cerebral arteries, causing localized vessel wall destruction and the formation of mycotic aneurysms. Additional causes include:

• Connective tissue disorders: Autosomal dominant polycystic kidney disease (ADPKD) is associated with intracranial aneurysm in approximately 12 percent of patients. Ehlers-Danlos syndrome type IV weakens arterial walls through defective collagen production. Marfan syndrome affects the connective tissue scaffolding of vessel walls. Fibromuscular dysplasia causes non-inflammatory arterial wall abnormalities that predispose to both aneurysm and dissection.

• Family history: Intracranial aneurysms cluster in families. Having a first-degree relative with an aneurysm approximately doubles individual risk. Genome-wide association studies have identified multiple genetic loci associated with aneurysm susceptibility.

• Hypertension: Chronically elevated blood pressure increases the mechanical stress on arterial walls and accelerates the degenerative changes that lead to aneurysm formation.

• Smoking: A well-established risk factor for both aneurysm formation and rupture. Smoking promotes vascular inflammation and directly damages arterial wall integrity.

• Arterial wall dissection: A spontaneous or trauma-related tear in the inner layer of an arterial wall creates a false passage for blood, weakening the wall and forming a dissecting or fusiform aneurysm.

Brain tumors affect people across all age groups, but the type of tumor and the risk profile differ substantially by age.

• Older age: The overall rate of brain tumor diagnosis rises sharply with age, from 5.79 per 100,000 in children under 14 to 76.85 per 100,000 in adults 65 and over. Glioblastoma is predominantly a disease of adults over 40 and becomes more common with each passing decade.
• Male sex: Although overall brain tumor incidence is higher in women (because meningioma predominates and is far more common in women), malignant brain tumor incidence is higher in men (8.24 vs. 5.94 per 100,000). GBM affects men significantly more often than women.
• Female sex: Women are at substantially higher risk than men for meningioma (nearly 2.5 times the rate), which is the most common primary brain tumor overall.
• Prior ionizing radiation to the brain: The strongest confirmed environmental risk factor. Children treated with cranial radiation for leukemia or other childhood cancers have significantly elevated lifetime risk of secondary brain tumors.
• Inherited genetic syndromes: Neurofibromatosis type 1 and 2, tuberous sclerosis complex, Li-Fraumeni syndrome, von Hippel-Lindau syndrome, Gorlin syndrome, and Lynch syndrome each carry substantially elevated brain tumor risk.
• Family history of brain tumors: A small but real increase in risk is associated with having a first-degree relative with a primary brain tumor, even in the absence of a known hereditary syndrome.
• Immunosuppression: People with weakened immune systems — including those living with HIV/AIDS or those taking immunosuppressive medications after organ transplant — have a substantially higher rate of primary CNS lymphoma.
• White race: Malignant brain tumor incidence is highest in White Americans compared to other racial and ethnic groups, based on CBTRUS data.

• Female sex: Women are more likely than men to develop intracranial aneurysms, particularly saccular aneurysms, and account for a larger proportion of rupture cases.
• Older age: Aneurysm prevalence increases with age. The risk of rupture for any given aneurysm also increases with age.
• Hypertension: High blood pressure is one of the most important modifiable risk factors for both formation and rupture of intracranial aneurysms.
• Smoking: A well-established risk factor for aneurysm formation and a major modifiable contributor to rupture risk.
• Family history: Having two or more first-degree relatives with intracranial aneurysms significantly elevates personal risk and is an indication for screening.
• Autosomal dominant polycystic kidney disease (ADPKD): Carries a 12 percent or higher prevalence of intracranial aneurysms and is a standard indication for screening.
• Connective tissue disorders: Ehlers-Danlos syndrome type IV, Marfan syndrome, and fibromuscular dysplasia all weaken arterial walls and increase aneurysm risk.
• Prior aneurysm: Having had one intracranial aneurysm increases the likelihood of harboring additional aneurysms. Multiple aneurysms are present in approximately 20 percent of cases.
• Heavy alcohol use: Excessive alcohol consumption is associated with increased aneurysm rupture risk.

There is no population-wide screening program for primary brain tumors in people without symptoms. Most brain tumors are discovered when a person develops neurological symptoms and undergoes imaging. For individuals with a known hereditary syndrome that increases brain tumor risk — such as NF1, NF2, tuberous sclerosis, or Li-Fraumeni syndrome — regular surveillance imaging (typically MRI of the brain) is recommended, with the frequency determined by the specific syndrome and the patient's history. Individuals who received cranial radiation therapy during childhood should also be monitored long-term for secondary tumors. There is no confirmed way to prevent primary brain tumors, as most arise from sporadic mutations without a clearly identifiable external cause. Avoiding unnecessary exposure to ionizing radiation — such as not performing CT scans of the head without a clinical indication — is a reasonable precaution.

Screening for unruptured intracranial aneurysms is recommended for specific high-risk groups. Current guidelines support screening with MR angiography (MRA) or CT angiography (CTA) for individuals with two or more first-degree relatives with intracranial aneurysms, for all patients with autosomal dominant polycystic kidney disease (ADPKD), and for those with certain connective tissue disorders such as Ehlers-Danlos syndrome type IV. The decision to screen in other high-risk individuals — such as those with a single affected first-degree relative or those with hypertension and a strong family history — involves a discussion of individual risk and the patient's preferences regarding treatment if an aneurysm is found. For aneurysms that are found incidentally and are not treated immediately, regular imaging follow-up (typically MRA or CTA at 6 to 12 months after discovery and then annually or biannually depending on stability) is recommended to monitor for growth, which increases rupture risk.

Prevention of aneurysm formation and rupture centers on modifying known vascular risk factors:

• Control blood pressure: Hypertension is the most important modifiable risk factor for aneurysm formation and rupture. Keeping blood pressure well-controlled reduces the mechanical stress on artery walls.
• Quit smoking: Smoking is a major risk factor for both aneurysm formation and rupture. Cessation at any age reduces risk.
• Avoid heavy alcohol use: Excessive alcohol is associated with elevated rupture risk and should be reduced or eliminated.
• Seek genetic counseling if high-risk: Families with multiple members affected by aneurysm, or those with ADPKD or connective tissue disorders, should discuss screening and risk management with a vascular neurologist or neurosurgeon.

The symptoms of a brain tumor depend primarily on where it is located in the brain and how quickly it is growing. Tumors cause symptoms by pressing on or infiltrating nearby brain tissue, by increasing pressure inside the skull (raised intracranial pressure), or by irritating brain tissue and triggering seizures. Benign, slow-growing tumors may be present for years before causing any symptoms. Rapidly growing malignant tumors can produce dramatic symptoms within weeks. The hallmark symptom that should always prompt evaluation is a new, progressive neurological change — any new weakness, vision change, speech difficulty, seizure, or personality change in an adult or child warrants medical attention.

• Headaches: A new pattern of headaches, particularly ones that are worse in the morning, wake a person from sleep, or are accompanied by nausea or vomiting, should be evaluated. Brain-tumor headaches result from increased intracranial pressure and tend to be positional and progressive.

• Seizures: New-onset seizures in an adult with no prior seizure history are one of the most common presenting features of a primary brain tumor, particularly low-grade gliomas. Seizures may be convulsive or may cause subtle changes in awareness, sensation, or behavior.

• Progressive weakness on one side of the body: Tumors in the motor cortex or its connections cause arm or leg weakness, clumsiness, or difficulty walking that worsens gradually over days to weeks.

• Speech and language difficulties: Tumors in or near the language-dominant hemisphere (usually the left hemisphere) can cause difficulty finding words, speaking clearly, or understanding spoken or written language.

• Vision changes: Double vision, visual field loss, or blurred vision can result from tumors pressing on the optic nerves, visual pathways, or the cranial nerves controlling eye movement.

• Cognitive and personality changes: Frontal lobe tumors can cause changes in judgment, mood, behavior, and personality that may be noticed by family members before the patient is aware.

• Nausea and vomiting: Often related to elevated intracranial pressure; the vomiting associated with raised ICP is characteristically sudden and forceful, sometimes without preceding nausea.

• Balance and coordination problems: Tumors in the cerebellum or brainstem can cause unsteady gait, clumsiness, and difficulty with fine motor tasks.

• Hormonal symptoms: Pituitary tumors and craniopharyngiomas can cause menstrual irregularities, infertility, excessive milk production, abnormal growth, or cortisol and thyroid disturbances.

The vast majority of unruptured aneurysms cause no symptoms and are discovered incidentally during imaging for an unrelated reason. When symptoms do occur, they signal either rupture or a large aneurysm pressing on nearby structures.

• Sudden, severe headache: The most critical warning symptom of aneurysm rupture. Patients and their families describe this as the worst headache of their life — a thunderclap headache that reaches maximum intensity within seconds. Any headache fitting this description requires emergency evaluation, even if the person feels better afterward. This represents a medical emergency.
• Neck stiffness and light sensitivity: Accompanying a severe sudden headache, these are signs of blood in the subarachnoid space (the fluid surrounding the brain) after rupture.
• Loss of consciousness or altered mental status: May occur at the moment of rupture from a sudden spike in intracranial pressure.
• Drooping eyelid and a large, unreactive pupil: A specific warning sign of an enlarging posterior communicating artery aneurysm pressing on the third cranial nerve, producing ptosis (lid droop) and pupil dilation on one side. This combination is a pre-rupture emergency requiring immediate imaging and treatment.
• Double vision: An unruptured aneurysm pressing on the cranial nerves controlling eye movement can cause diplopia.
• Facial pain or numbness: Compression of the trigeminal nerve by an aneurysm can produce facial sensory symptoms.
• Pulsatile tinnitus: A rhythmic whooshing or pounding sound in the ear can occasionally be caused by a large or turbulent intracranial aneurysm near the skull base.
• Warning or sentinel headache: Some patients experience a milder headache in the days or weeks before a major subarachnoid hemorrhage, caused by a small leak from the aneurysm. This warning should never be dismissed.
   

Brain tumors are typically diagnosed by a neurologist or neuro-oncologist, often after a patient presents with neurological symptoms and undergoes imaging. MRI of the brain with gadolinium contrast is the primary diagnostic tool. A final diagnosis, however, always requires tissue — a biopsy or surgical specimen examined by a neuropathologist. In the modern era, diagnosis goes beyond histology alone: molecular and genetic testing of the tumor tissue is now required for accurate classification and grading under the 2021 WHO CNS tumor classification.

• MRI of the brain with gadolinium contrast: The most sensitive and specific imaging test for detecting brain tumors. Different MRI sequences reveal tumor size, location, degree of contrast enhancement (reflecting blood-brain barrier breakdown), surrounding edema, and involvement of critical structures. Functional MRI (fMRI) and MR spectroscopy may be added to assess proximity to eloquent brain areas and tumor metabolic characteristics.
• CT scan of the head: Faster than MRI and used in emergency settings, particularly when acute hemorrhage is suspected. CT is less sensitive than MRI for detecting small tumors and lower-grade lesions.
• Surgical biopsy or resection with neuropathology: The definitive diagnostic step. A neuropathologist examines the tumor tissue under a microscope to identify the cell type, grade, and key histological features. In most cases, molecular testing is performed on the same tissue sample.
• Molecular and genetic testing: Identification of IDH mutation status, 1p/19q codeletion, MGMT promoter methylation, EGFR amplification, TERT promoter mutation, H3 histone mutations, and other markers is now standard of care and essential for accurate diagnosis, prognosis estimation, and treatment planning.
• Neurological examination: A comprehensive assessment of cognitive function, cranial nerve function, motor and sensory function, coordination, and reflexes establishes baseline function and identifies deficits that guide surgical planning.
• Lumbar puncture (spinal tap): Used when CNS lymphoma, leptomeningeal metastasis (cancer spreading along the brain and spinal cord lining), or infectious cause is suspected. CSF is examined for malignant cells, inflammatory markers, and tumor-specific proteins.
• PET scan: Used in select cases to distinguish tumor recurrence from treatment-related changes (radiation necrosis), to identify the highest-grade area within a tumor for targeted biopsy, or to stage systemic cancer when a metastatic brain tumor is suspected.

Unruptured aneurysms are most commonly identified during MRI or CT imaging performed for an unrelated reason. Ruptured aneurysms typically present as a neurological emergency and require immediate imaging.

• Non-contrast CT scan of the head: The first test performed when subarachnoid hemorrhage is suspected. Blood appears bright white on CT. Sensitivity is approximately 98 percent within six hours of onset but drops over subsequent days as blood breaks down.
• Lumbar puncture: If CT is negative but subarachnoid hemorrhage is still clinically suspected (for example, in a patient with a thunderclap headache and a CT performed more than six hours after onset), a lumbar puncture is performed to look for blood or its breakdown products (xanthochromia) in the CSF.
• CT angiography (CTA): A rapid, high-resolution imaging technique that injects iodine-based contrast into the bloodstream and takes detailed CT images of the cerebral arteries. It can detect aneurysms 3 mm or larger with high sensitivity and is the most commonly used emergency imaging test for suspected aneurysm.
• MR angiography (MRA): A non-invasive MRI-based technique that images cerebral arteries without radiation. It is used for screening high-risk individuals, for follow-up of known unruptured aneurysms, and when CT contrast is contraindicated.
• Digital subtraction angiography (DSA): The gold standard test for cerebrovascular imaging. A catheter is placed through an artery in the groin and guided to the cerebral vessels, where contrast is injected and real-time X-ray images are taken. DSA provides the most detailed visualization of aneurysm morphology, neck width, and relationship to surrounding vessels — information critical for treatment planning.

Treatment for both brain tumors and intracranial aneurysms requires the expertise of specialized teams at comprehensive neuroscience centers. The specific approach depends on the type, location, size, and grade of the tumor or aneurysm, as well as the patient's overall health and preferences. Your care team will discuss all options with you and help determine the best path forward.

Treatment for brain tumors is highly individualized based on tumor type, grade, molecular markers, location, and patient factors. Most treatment plans involve combinations of surgery, radiation, and chemotherapy, and for some types, targeted molecular therapies or immunotherapy. The overarching goal for high-grade malignant tumors is to extend life and preserve quality of life; for low-grade or benign tumors, the goal is often cure or long-term control.

Surgery is the first step in management for most accessible brain tumors. The goals of surgery are to remove as much tumor as possible (maximal safe resection) — which improves survival in high-grade gliomas and immediately relieves raised intracranial pressure — and to obtain tissue for diagnosis. Modern neurosurgery uses intraoperative MRI, fluorescence-guided resection (using a dye called 5-ALA that makes glioma cells glow pink under blue light), functional brain mapping (awake craniotomy with cortical stimulation to preserve speech and motor function), and neuronavigation systems to maximize tumor removal while protecting critical brain areas. For tumors in locations that cannot be safely accessed surgically — such as deep thalamic tumors or eloquent cortex involvement — stereotactic biopsy (a needle biopsy guided by imaging) obtains tissue for diagnosis without open surgery. For some small, well-defined benign tumors such as vestibular schwannomas and certain meningiomas, radiosurgery — a non-surgical method of delivering a precisely focused, high dose of radiation in a single session using tools like the Gamma Knife or CyberKnife — can treat the tumor without opening the skull.

Radiation therapy plays a central role in treating most high-grade brain tumors and many low-grade ones after surgery. Standard-of-care treatment for glioblastoma (established by the Stupp Protocol) is maximal surgical resection followed by concurrent chemoradiation — external beam radiation therapy (typically 60 Gy in 30 fractions over six weeks) delivered simultaneously with the oral chemotherapy drug temozolomide (Temodar), followed by six months of adjuvant temozolomide. This protocol improved median survival from about 12 months with radiation alone to approximately 15 months. Patients whose tumors have MGMT promoter methylation respond better to temozolomide and have longer overall survival. For lower-grade gliomas (Grade 2 and Grade 3 IDH-mutant tumors), radiation combined with the PCV chemotherapy regimen (procarbazine, CCNU/lomustine, and vincristine) or temozolomide is standard treatment after surgery. Medulloblastoma is treated with surgery followed by craniospinal irradiation (radiation to the entire brain and spine to prevent spread) and chemotherapy — the specific protocol depends on the molecular subtype and risk classification. Bevacizumab (Avastin) — a monoclonal antibody that blocks the VEGF protein that promotes tumor blood vessel growth — is FDA-approved for recurrent GBM. Tumor treating fields (TTFields/Optune) is an FDA-approved wearable device that delivers alternating electrical fields to the brain through arrays worn on the scalp, disrupting cancer cell division. Adding TTFields to maintenance temozolomide after concurrent chemoradiation improved median overall survival in GBM patients compared to temozolomide alone. The implantable carmustine wafer (Gliadel) allows chemotherapy to be placed directly in the surgical cavity at the time of resection. For IDH-mutant gliomas, the oral IDH inhibitors ivosidenib (Tibsovo, for IDH1-mutant) and olutasidenib (Rezlidhia, for IDH1-mutant) and vorasidenib (Voranigo, FDA-approved 2024 for IDH-mutant Grade 2 glioma) represent the first targeted molecular therapies specifically approved for these tumors. For BRAF V600E-mutant low-grade gliomas — common in pediatric patients — the BRAF inhibitor dabrafenib combined with the MEK inhibitor trametinib is FDA-approved and has produced durable responses. Pituitary adenomas are typically treated with transsphenoidal surgery — an approach through the nose and sphenoid sinus — or with dopamine agonists (cabergoline, bromocriptine) for prolactin-secreting tumors, which are highly medication-responsive.

Treatment decisions for intracranial aneurysms involve careful weighing of the risk of rupture (or re-rupture, if rupture has already occurred) against the risks of intervention. For ruptured aneurysms, treatment to secure the aneurysm is generally urgent. For unruptured aneurysms found incidentally, the decision involves factors including aneurysm size, location, shape, growth on follow-up imaging, and the patient's age and overall health. Two principal treatment strategies are used: surgical clipping and endovascular coiling.

Surgical clipping is a microsurgical procedure performed under general anesthesia through an opening in the skull (craniotomy). The neurosurgeon dissects to the aneurysm and places a small titanium clip across the neck of the aneurysm, closing it off from the circulation permanently. The aneurysm is excluded from blood flow and cannot rupture or re-rupture. Clipping has a long track record and durable long-term results, and it allows the surgeon to simultaneously relieve any blood clot compressing the brain. It is generally preferred for younger patients, for aneurysms with a wide neck that would make coiling technically difficult, and for certain locations such as the middle cerebral artery bifurcation.

Endovascular coiling — also called endovascular embolization — is a minimally invasive procedure performed by an interventional neuroradiologist or endovascular neurosurgeon. A catheter is guided through the arteries from the groin to the aneurysm. Soft platinum coils are deployed through the catheter into the aneurysm dome, filling it with metal and triggering clot formation that seals the aneurysm from the inside. Coiling avoids open surgery and generally has a shorter recovery time. The landmark ISAT trial (International Subarachnoid Aneurysm Trial) demonstrated that in patients with ruptured saccular aneurysms suitable for both techniques, coiling resulted in lower rates of disability and death at one year compared to clipping. However, coiled aneurysms have a higher rate of recurrence over time and require angiographic follow-up. For aneurysms with an unfavorable wide neck, stent-assisted coiling — placing a stent across the aneurysm neck to hold coils in place — or flow diversion with the Pipeline Embolization Device (PED) can be used. The Pipeline device is a dense metallic stent placed across the aneurysm neck that redirects blood flow and causes the aneurysm to gradually clot off. It is FDA-approved and particularly effective for large and giant aneurysms of the internal carotid artery. For ruptured aneurysms causing subarachnoid hemorrhage, additional intensive care management is critical: preventing and treating vasospasm (dangerous narrowing of brain arteries that can occur 4 to 14 days after SAH, causing delayed stroke), managing hydrocephalus (fluid buildup from blood blocking CSF drainage), controlling blood pressure, and preventing complications of prolonged critical illness. The calcium channel blocker nimodipine (Nymalize) is given to all SAH patients to reduce the risk and severity of vasospasm and is the only medication FDA-approved specifically for this indication. For small, asymptomatic unruptured aneurysms in older patients with multiple medical conditions, close imaging surveillance without immediate intervention is often the safest approach.

A diagnosis of a brain tumor or intracranial aneurysm affects every aspect of a person's life — from immediate medical decisions to long-term questions about work, driving, family, and independence. The path forward depends enormously on the specific diagnosis. Many meningiomas and low-grade tumors are observed or treated with minimal disruption to daily life, while aggressive malignancies like glioblastoma require intensive, ongoing treatment. Survivors of subarachnoid hemorrhage from aneurysm rupture may face a long rehabilitation journey, but many achieve meaningful functional recovery. For all these conditions, receiving care at a comprehensive brain tumor center or cerebrovascular center of excellence — with neurosurgeons, neuro-oncologists, radiation oncologists, neuroradiologists, neuropsychologists, social workers, and rehabilitation specialists working as a coordinated team — is strongly associated with better outcomes. Connecting with patient support organizations such as the National Brain Tumor Society and the Brain Aneurysm Foundation provide community, advocacy resources, and information on clinical trials.

To further your understanding of your diagnosis and to contribute to cutting-edge research, consider participating in a clinical trial so clinicians and scientists can learn more about causes, symptoms, treatment and prevention of brain tumors, aneurysms, and related disorders. Clinical research uses human volunteers to help researchers learn more about a disorder and perhaps find better ways to safely detect, treat or prevent disease.
All types of volunteers are needed — those who are healthy or may have an illness or disease — of all different ages, sexes, races and ethnicities to ensure that study results apply to as many people as possible, and that treatments will be safe and effective for everyone who will use them.

To learn more about clinical trials and find studies that may be right for you, visit NIH Clinical Research Trials and You at www.nih.gov/health-information/nih-clinical-research-trials-you and ClinicalTrials.gov at www.clinicaltrials.gov to search active studies by condition, location, and age group.