A brain aneurysm (cerebral or intracranial aneurysm) is a weakened area in an artery wall within the brain that balloons outward. A seizure is a sudden, uncontrolled electrical disturbance in the brain that causes changes in behavior, movements, or consciousness. A brain aneurysm can cause seizure activity, primarily when it ruptures and causes bleeding, or when a large unruptured aneurysm interferes with normal brain function. Understanding the processes that link this vascular abnormality to an electrical event is fundamental for proper diagnosis and treatment.
Understanding Brain Aneurysms
A cerebral aneurysm forms when the inner muscular layer of a blood vessel weakens, creating a bulge that fills with blood. The most common type is a saccular or “berry” aneurysm, often located at the base of the brain in the Circle of Willis. Aneurysms are categorized as unruptured or ruptured.
An unruptured aneurysm may remain asymptomatic for years and is often discovered incidentally during imaging. If the weak spot tears, blood rapidly leaks into the space surrounding the brain, resulting in a life-threatening subarachnoid hemorrhage (SAH). SAH is an emergency that accounts for about 90% of all ruptured aneurysm cases.
A tear in the vessel wall introduces blood, triggering a cascade of secondary complications, including seizures.
The Mechanism of Causation
An aneurysm can trigger seizure activity through two distinct pathways: mass effect and chemical irritation. Mass effect occurs when a very large unruptured aneurysm (over 2.5 cm), sometimes called a “giant” aneurysm, physically presses on adjacent brain tissue. This sustained pressure on the cerebral cortex can disrupt normal electrical signaling, potentially leading to focal seizures.
The more common trigger is the chemical irritation and inflammation following a subarachnoid hemorrhage. When the aneurysm ruptures, the blood released into the subarachnoid space irritates the meninges and underlying cortical tissue. This irritation immediately disrupts neuronal membranes, causing the uncontrolled electrical firing that defines a seizure.
The presence of blood can also lead to secondary injuries causing delayed seizures. These issues include cerebral edema (brain swelling), hydrocephalus (excess cerebrospinal fluid accumulation), and delayed cerebral ischemia due to vasospasm.
When brain tissue is damaged by lack of blood flow or prolonged inflammation, it can develop scar tissue, or gliosis. Gliosis forms a chronic focus for future seizure activity, meaning both the rupture and the subsequent injury cascade contribute to seizure risk.
Characteristics of Aneurysm-Related Seizures
Seizures related to a ruptured aneurysm are categorized by their timing relative to the hemorrhage. Immediate seizures occur within the first 12 hours of the subarachnoid hemorrhage, resulting directly from acute chemical irritation. Later seizures, known as “late epilepsy,” can emerge weeks or years after the event due to permanent brain changes like gliosis or cortical infarction.
The incidence of seizures following aneurysmal SAH ranges from 3% to 26% of patients. These seizures are often focal, meaning they begin in a specific area of the brain. This localization is tied to the region of the cortex irritated by the aneurysm or subsequent injury. Aneurysms in the middle cerebral artery (MCA) territory carry a higher risk because this area supplies the temporal and frontal lobes, which are highly epileptogenic.
Clinical Management and Prognosis
Managing aneurysm-related seizures involves treating the underlying vascular issue and controlling the abnormal electrical activity. The aneurysm is typically treated urgently to prevent re-rupture, often through surgical clipping or endovascular coiling. Endovascular coiling, which blocks blood flow by filling the aneurysm with metal coils, is associated with a lower risk of future seizures compared to surgical clipping, which requires a craniotomy.
Anti-epileptic drugs (AEDs) are administered to control acute seizures. They are sometimes used prophylactically for a short term (three to seven days) following SAH. Prolonged prophylactic use is avoided because it has not been proven to prevent late epilepsy and carries side effect risks. Long-term AED therapy is reserved for patients with recurrent, unprovoked seizures, establishing a diagnosis of post-hemorrhagic epilepsy. The prognosis for seizure control depends on the extent of the initial brain injury. Factors like large amounts of blood on imaging, severe vasospasm, and cerebral infarction increase the likelihood of developing chronic epilepsy.