berry aneurysm

**Pathophysiology:** Berry aneurysms form at bifurcations of the cerebral arteries, where hemodynamic stress is greatest and the internal elastic lamina and tunica media are deficient or absent. Defective or absent media at these branch points, plus turbulent flow and hypertension, leads to progressive outpouching. They are saccular, with a neck and a dome. The wall is thin, so rupture risk rises with size (especially >7 mm), posterior circulation location, and symptomatic or growing lesions.

**Location (high-yield):** - Anterior communicating artery (ACom)/anterior cerebral artery junction: most common (~30–40%). Rupture can cause bitemporal hemianopia from compression of the optic chiasm. - Posterior communicating artery (PCom)/internal carotid junction: compresses CN III, causing a "blown pupil" (down-and-out eye with mydriasis and ptosis). - Middle cerebral artery bifurcation: the most common site of rupture in some series, and the third most common site overall. - Basilar tip and posterior inferior cerebellar artery (PICA) are less common.

**Risk factors/associations:** - Autosomal dominant polycystic kidney disease (ADPKD): the classic association. - Ehlers-Danlos syndrome (especially vascular type IV) and Marfan syndrome. - Coarctation of the aorta, and fibromuscular dysplasia. - Hypertension, smoking, and female sex (postmenopausal). - Family history, and age >40 (typically presents ages 40–60). - Prior history of aneurysm, and bicuspid aortic valve.

**Clinical presentation:** - Most are asymptomatic and found incidentally. - Unruptured, large lesions can cause mass effect: CN III palsy (PCom), visual field defects, and headache. - Rupture causes subarachnoid hemorrhage (SAH): sudden, severe "thunderclap" headache ("worst headache of my life"), nausea/vomiting, neck stiffness (meningismus), photophobia, and loss of consciousness or seizure. - A "sentinel headache" from a minor leak may precede major rupture.

**Diagnosis:** - Noncontrast head CT is the first test (most sensitive within 6 hours of onset; shows hyperdensity in the basal cisterns). - If CT is negative but suspicion remains, perform lumbar puncture: xanthochromia (bilirubin from RBC breakdown, appears ~6–12 hours after the bleed) and elevated RBC count that does not clear across tubes. - CT angiography or digital subtraction angiography (gold standard) to localize the aneurysm.

**Complications of SAH:** - Rebleeding (highest risk in the first 24 hours). - Vasospasm and delayed cerebral ischemia (days 3–14 post-bleed). - Hydrocephalus (impaired CSF resorption by arachnoid granulations). - Hyponatremia (SIADH or cerebral salt wasting), seizures, and neurogenic pulmonary edema or cardiac stunning (ECG changes).

**Management:** - Stabilize the airway, and control blood pressure. - Secure the aneurysm early: endovascular coiling or neurosurgical clipping. - Nimodipine (a calcium channel blocker) to reduce vasospasm-related ischemic outcomes. - Manage hydrocephalus with an external ventricular drain, and give seizure prophylaxis as needed. - Screen high-risk patients (e.g., ADPKD with a family history of aneurysm or SAH) with MRA or CTA.

**Boards pearls:** - Berry aneurysm is the most common cause of nontraumatic SAH. - Differentiate from Charcot-Bouchard microaneurysms (lenticulostriate vessels, chronic hypertension, intracerebral hemorrhage in the basal ganglia) and from fusiform aneurysms (atherosclerosis, basilar artery). - Epidural hematoma (middle meningeal artery, lucid interval, lens-shaped) and subdural hematoma (bridging veins, crescent-shaped) are distinct causes of intracranial bleeding.