A brain bleed (cerebral or intracranial hemorrhage) occurs when a blood vessel ruptures, causing blood to leak into the surrounding brain tissue or spaces. This collection of blood creates an abnormal mass and introduces foreign chemicals into the sensitive neurological environment. A seizure is a transient event caused by abnormal, excessive electrical activity in the brain’s nerve cells. Brain bleeds are a recognized cause of seizures because the spilled blood directly irritates and injures brain cells, disrupting their normal electrical signaling. This article explains the biological mechanisms behind this connection, identifies high-risk hemorrhage types, and outlines the medical approach to management.
The Neurological Connection: How Bleeding Disrupts Brain Activity
The brain is highly sensitive to blood outside its vascular network, as this material is toxic to neural tissue. This toxicity is a primary mechanism initiating abnormal electrical discharges. Blood contains iron-rich hemoglobin, and as the hemorrhage breaks down, the released iron chemically irritates adjacent neurons, triggering the hyperexcitability that characterizes a seizure.
The physical presence of the hematoma (blood clot) also creates a mass effect, exerting pressure on surrounding brain structures. This compression and distortion of neural networks mechanically disrupt normal communication pathways. The resulting pressure and inflammation lower the seizure threshold of the tissue, making it prone to sudden, uncontrolled electrical bursts.
Over time, this initial injury leads to gliosis, a form of scarring. Specialized glial cells proliferate to wall off the damaged area and absorb blood products. This scar tissue is often less functional and can become an isolated focus of electrical instability, leading to a chronic predisposition for seizures long after the bleeding has stopped.
Different Types of Brain Hemorrhage and Seizure Risk
The risk of developing a seizure depends largely on the location of the hemorrhage. Bleeds close to the brain’s surface (the cortex) carry a significantly higher risk than those in deeper structures. This is because the cortex contains the dense network of neurons responsible for generating and propagating electrical activity.
Intracerebral Hemorrhage (ICH)
Intracerebral Hemorrhage (ICH), bleeding directly into the brain tissue, is a common cause of post-hemorrhagic seizures. When an ICH is located in a lobar area involving the cortex, the risk of a late seizure is approximately three times higher than in deeper, non-cortical regions. A larger volume of the hematoma also increases the likelihood of seizure development due to greater mass effect and tissue destruction.
Surface Hemorrhages
Subarachnoid Hemorrhage (SAH), bleeding into the space surrounding the brain, carries a seizure risk, especially if the blood involves the cortex. Subdural Hematoma (SDH) and Epidural Hematoma (EDH) are collections of blood that form on the surface, often after trauma. Because these hematomas directly compress or irritate the underlying cortical surface, they are associated with an elevated risk of seizures. The proximity of the blood to the highly excitable cortical gray matter is the most important anatomical predictor of seizure risk.
Acute Seizures Versus Post-Hemorrhagic Epilepsy
Seizures following a brain bleed are classified based on the time elapsed since the initial injury. Acute symptomatic seizures occur within the first seven days following the hemorrhage. These early seizures are a direct consequence of the immediate insult, driven by transient irritation from fresh blood and pressure from swelling.
Acute events can be non-convulsive, meaning they lack noticeable jerking movements, and may only be detectable through continuous electroencephalogram (EEG) monitoring. While acute seizures can worsen the patient’s outcome, they do not always lead to a chronic seizure disorder. The risk of recurrence is lower once the initial swelling and blood products are cleared from the brain.
In contrast, post-hemorrhagic epilepsy (PHE) is a chronic condition defined by two or more unprovoked seizures occurring more than one week after the initial bleeding event. PHE results from permanent structural changes, specifically the development of gliosis or scar tissue. This scarred region acts as a permanent focus of abnormal electrical activity, and patients who experience a single late seizure have a high likelihood of meeting the criteria for an epilepsy diagnosis.
Medical Management of Post-Hemorrhagic Seizures
The medical approach begins with accurate diagnosis, often involving continuous EEG monitoring in the acute phase. This testing is necessary because subclinical seizures (seizures without outward physical signs) can occur frequently. Imaging studies, such as computed tomography (CT) or magnetic resonance imaging (MRI), are also used to track the size and location of the hematoma and any structural damage.
Treatment protocols differ between acute seizure prevention and long-term epilepsy management. For acute seizures, anti-epileptic drugs (AEDs) are administered immediately to stop the activity. For high-risk patients, such as those with cortical bleeds, a short course of prophylactic AEDs may be considered during the first week. Common AEDs include levetiracetam, often preferred over older medications due to fewer side effects and drug interactions.
For patients diagnosed with established post-hemorrhagic epilepsy, long-term AED therapy is the standard of care to control recurrent, unprovoked seizures. The decision to start long-term medication is typically made after the first unprovoked seizure occurring outside the acute period. The decision to continue or stop medication requires balancing seizure risk against the potential side effects of the drugs.