Cerebral Aneurysm: Symptoms, Causes & Treatment

A cerebral (intracranial) aneurysm is a focal pathological dilatation or outpouching of a cerebral artery wall, most commonly a berry (saccular) aneurysm at vessel bifurcations — predominantly on the arteries of the Circle of Willis (anterior communicating, posterior communicating, middle cerebral artery). Cerebral aneurysms are prevalent in approximately 2–5% of the general population; most are discovered incidentally, remain asymptomatic, and never rupture.

Aneurysm rupture causes subarachnoid hemorrhage (SAH): arterial blood under systemic pressure floods the subarachnoid space. SAH is heralded by the characteristic sudden-onset thunderclap headache — described as the worst headache of the patient's life — often followed by neck stiffness (meningismus), nausea, vomiting, photophobia, and loss of consciousness. SAH is a neurological catastrophe: 10–15% of patients die before reaching hospital; in-hospital mortality is 25–40%; among survivors, 30–40% have significant neurological disability. Major complications include rebleeding (highest risk within 24 hours), cerebral vasospasm (peaks at 4–14 days causing delayed cerebral ischemia), hydrocephalus, and hyponatremia (SIADH or cerebral salt wasting).

Unruptured incidental aneurysms require individualized risk-benefit assessment. Small aneurysms (<7 mm in low-risk locations) have an annual rupture risk of ~0.05–1%; larger, posterior circulation, or growing aneurysms carry higher risk. Treatment options — microsurgical clipping or endovascular coiling — carry procedural risk that must be weighed against natural history. Expert neurovascular team management is essential.

• Most small unruptured aneurysms: completely asymptomatic — incidental finding on brain imaging
• Ruptured aneurysm (SAH): sudden-onset thunderclap headache reaching maximal intensity within seconds — the 'worst headache of my life'; this is a medical emergency
• Meningismus: neck stiffness, Kernig's and Brudzinski's signs from blood in CSF
• Nausea, vomiting, photophobia, phonophobia
• Loss of consciousness or coma in severe SAH (Hunt-Hess grade IV–V)
• Large unruptured aneurysm (mass effect): localized headache, cranial nerve palsies (CN III palsy — ptosis, fixed dilated pupil from posterior communicating artery aneurysm), visual field defects

• Congenital deficiency in the arterial wall media at bifurcations — the primary predisposing factor for saccular aneurysms
• Chronic uncontrolled hypertension — increases wall stress and aneurysm growth/rupture risk
• Cigarette smoking — the strongest modifiable risk factor for both aneurysm formation and rupture
• Genetic predisposition: positive family history (2+ first-degree relatives with cerebral aneurysm), autosomal dominant polycystic kidney disease (ADPKD — 10% have cerebral aneurysms), Marfan syndrome, Ehlers-Danlos syndrome type IV
• Atherosclerosis (fusiform aneurysms), arteriovenous malformations, post-traumatic pseudoaneurysms

Suspected SAH is a neurological emergency: non-contrast CT head — highly sensitive (95–98%) within 12 hours of onset. If CT negative but clinical suspicion remains high: lumbar puncture to detect xanthochromia (CSF bilirubin from blood breakdown) — essential to exclude SAH. Aneurysm localization: CT angiography (CTA) for rapid assessment; digital subtraction angiography (DSA) remains the gold standard for treatment planning. Incidental aneurysm characterization: MRI/MRA for size, shape, and growth monitoring over time.

Ruptured aneurysm/SAH: urgent aneurysm occlusion — endovascular coiling (preferred when technically feasible; lower procedural morbidity) or microsurgical clipping. Timing: as early as possible to prevent rebleeding. Supportive ICU care: nimodipine (calcium channel blocker) 60 mg every 4 hours for 21 days — reduces vasospasm-related delayed cerebral ischemia; blood pressure management; euvolemia; treat hydrocephalus (EVD placement). Unruptured incidental aneurysm: risk-benefit decision based on aneurysm size (>7 mm warrants stronger consideration for treatment), location (posterior circulation higher risk), patient age, smoking status, and family history. Options: endovascular coiling or microsurgical clipping vs. conservative observation with serial imaging.

• Early rebleeding: 15–20% within 24 hours — 70% of rebleeds are fatal; early aneurysm occlusion is critical
• Cerebral vasospasm and delayed cerebral ischemia (DCI): peaks days 4–14; causes secondary brain injury and worsens outcome
• Acute hydrocephalus from CSF obstruction (30%); communicating hydrocephalus requiring VP shunt (20%)
• Hyponatremia (SIADH or cerebral salt wasting) — must be distinguished as treatments differ
• Death in 25–40% of SAH patients; permanent neurological disability in 30–40% of survivors

• Smoking cessation — the single most impactful modifiable risk factor for aneurysm formation and rupture
• Blood pressure control — reduces hemodynamic stress on the aneurysm wall
• Screening MRA for high-risk individuals: ≥2 first-degree relatives with cerebral aneurysms, ADPKD patients, and patients with a prior aneurysm (10% risk of additional aneurysms)
• Avoid cocaine and amphetamines — associated with aneurysm rupture