A brain bleed, medically known as an intracranial hemorrhage, can cause seizures. This bleeding is defined as the rupture of a blood vessel within the skull, allowing blood to pool and compress or irritate brain tissue. Seizures are episodes of abnormal, uncontrolled electrical activity in the brain that temporarily disrupt normal function. The presence of blood acts as a powerful irritant, dramatically increasing the risk of abnormal electrical discharges. This complication is a significant concern following any type of bleeding inside the head.
The Mechanism Linking Bleeding and Seizures
The core reason a brain bleed triggers seizures lies in the neurotoxic properties of blood components when they are outside of a vessel. Blood is highly irritating to brain cells, which are normally shielded by the blood-brain barrier. The breakdown of red blood cells releases hemoglobin, which is metabolized into free iron.
This free iron is a potent neurotoxin that disrupts normal neuronal signaling and promotes oxidative stress. Iron generates harmful free radicals, damaging the cell membranes and DNA of surrounding neurons. This chemical irritation lowers the seizure threshold of the affected brain region, making neurons hyperexcitable.
Inflammation and swelling, known as edema, also contribute by increasing pressure on the surrounding brain tissue. This pressure further irritates neurons and exacerbates the risk of abnormal electrical activity. Over time, specialized glial cells form scar tissue, a process called gliosis, as the brain attempts to heal.
This gliotic scar tissue is often highly epileptogenic, creating an unstable electrical environment that promotes chronic, recurrent seizures. The chemical toxicity from iron and the long-term structural changes from gliosis are the main drivers of both immediate and long-term seizure risk.
Specific Brain Bleeds and Associated Seizure Risk
The risk of seizure is not uniform across all types of brain bleeds, but is determined by the injury’s location and proximity to the cerebral cortex. Hemorrhages that directly involve the cortex have the highest seizure risk because this area contains the most electrically excitable neurons.
An Intracerebral Hemorrhage (ICH), bleeding directly into the brain tissue, carries a high risk, especially when located in the cortex (lobar hemorrhage). Patients with lobar ICH have a risk of developing late seizures that is approximately three times higher than those with deeper bleeds. A larger hematoma volume also contributes, as it increases the amount of neurotoxic blood products released.
Subarachnoid Hemorrhage (SAH), bleeding into the space surrounding the brain, also presents a moderate to high risk. In SAH, blood spreads across the surface of the brain, causing widespread cortical irritation. Seizures occur in a significant percentage of SAH patients in the acute phase.
A Subdural Hematoma (SDH) or an Epidural Hematoma (EDH) generally presents a lower risk. These bleeds are located outside of the brain tissue itself, meaning irritating blood products are less directly exposed to the neurons. However, a large SDH or EDH that severely compresses the brain can still cause focal irritation and seizures.
Acute Versus Delayed Seizures and Treatment
Seizures following a brain bleed are categorized based on their timing relative to the initial event, which influences their underlying cause and management. Acute symptomatic seizures occur within the first week of the hemorrhage and are primarily caused by the immediate irritation from the hematoma and surrounding swelling. Most of these early seizures happen within the first 72 hours.
Delayed seizures, or post-hemorrhagic epilepsy, occur more than a week after the bleed and are linked to long-term changes in the brain tissue. These late seizures are a consequence of epileptogenesis, where the initial injury leads to permanent scar formation (gliosis). This scar tissue creates a focus for abnormal electrical activity.
The medical management of post-hemorrhagic seizures involves the use of anti-epileptic drugs (AEDs). Once a patient experiences a seizure, treatment with AEDs is standard to prevent recurrence. However, using AEDs preventatively—known as prophylactic treatment—in patients who have not yet seized is debated and not routinely recommended for all brain bleeds.
Prophylactic AED use is typically considered only for patients with a very high risk of acute seizures, such as those with a cortical intracerebral hemorrhage. This caution exists because AEDs can have side effects, and studies have not consistently shown that early preventative use improves long-term functional outcome. For most patients, careful monitoring during the acute phase and treatment only after a seizure occurs remains the standard approach.