A stroke is the sudden interruption of blood flow to the brain, causing brain cells to die and leading to a functional deficit. A seizure is a brief episode of abnormal, excessive electrical activity among groups of neurons. The two conditions are closely linked, as stroke is the most common cause of new-onset seizures and epilepsy in older adults. This severe cerebrovascular event disrupts the brain’s electrical and chemical balance. As the brain heals, resulting structural and inflammatory changes can transform the neural network into one capable of generating recurrent, unprovoked seizures.
The Neurological Mechanism: Why Brain Injury Leads to Seizures
When a stroke occurs, the area of dead or damaged brain tissue initiates a cascade of destructive processes. In the immediate aftermath, acute excitotoxicity and metabolic dysfunction develop. This involves the rapid release of excitatory neurotransmitters like glutamate and an increase in extracellular potassium ions, which lowers the threshold for neurons to fire abnormally.
Over a longer period, the damaged area undergoes gliosis, a structural repair process where glial cells, particularly astrocytes, form dense scar tissue around the lesion. This gliotic scar actively remodels the surrounding neural network. The scar tissue and persistent neuroinflammation disrupt the integrity of the blood-brain barrier (BBB) and alter ion channel function in nearby surviving neurons. This chronic damage creates an “irritable focus,” a region of hyperexcitable neurons that can spontaneously discharge.
Acute Seizures Versus Post-Stroke Epilepsy
Seizures following a stroke are categorized by the time of their occurrence, which impacts prognosis and treatment. Acute symptomatic seizures (ASyS) happen within the first seven days after the stroke event. These seizures are considered a direct, provoked consequence of the immediate brain injury, often linked to transient factors like acute brain swelling, metabolic shifts, or blood products.
The risk of these acute seizures recurring is relatively low, estimated at 30 to 33% over ten years. However, if the acute seizure manifests as status epilepticus—a prolonged seizure or a series of seizures without regaining consciousness—the risk of developing long-term epilepsy increases significantly (81 to 94%). Post-stroke epilepsy (PSE) is defined as two or more unprovoked seizures occurring more than seven days after the stroke. This late onset indicates epileptogenesis, a permanent alteration in brain circuitry resulting in a chronic tendency to generate seizures.
The long-term recurrence risk for unprovoked seizures in patients diagnosed with PSE is high, often exceeding 60 to 70%. This distinction is important because ASyS may resolve as the acute injury stabilizes, while PSE represents a lasting neurological condition requiring long-term management. The development of PSE is associated with poorer functional outcomes and increased mortality compared to stroke survivors without late seizures.
Stroke Characteristics That Increase Seizure Risk
Specific features of a stroke influence the likelihood of developing post-stroke seizures or epilepsy. The type of stroke is a major predictor: hemorrhagic strokes (bleeding into the brain) carry a higher risk than ischemic strokes (clot blocking blood flow). This increased risk is due to the cytotoxic effects of blood products, such as iron from blood breakdown, on surrounding brain tissue.
The anatomical location of the injury is also a determinant of seizure risk. Strokes that involve the cerebral cortex, the outer layer of the brain responsible for higher-level functions, are more likely to cause seizures. Damage to this superficial layer directly impacts the dense network of neurons that generate electrical activity. Strokes confined to subcortical or deeper brain structures pose a lower risk.
The overall severity and size of the stroke lesion also increase the probability of seizures. Larger strokes, often indicated by a higher score on the National Institutes of Health Stroke Scale (NIHSS), disrupt a greater volume of neural tissue, leading to more extensive gliotic scarring. Younger age in adult stroke patients is an independent factor associated with a greater risk of developing post-stroke seizures.
Treatment and Long-Term Management
The management approach for post-stroke seizures depends on whether they are acute or established post-stroke epilepsy. For acute symptomatic seizures occurring within the first week, treatment focuses on correcting the underlying acute cause, such as reducing brain swelling or addressing metabolic imbalances. Long-term use of anti-seizure medications (ASMs) is not recommended following a single acute seizure event, as they have not been shown to prevent the future development of epilepsy.
If the patient experiences status epilepticus in the acute phase, or if a high-risk pattern is seen on an electroencephalogram, a short course of ASM may be initiated but is typically tapered off as the patient recovers. Conversely, a diagnosis of post-stroke epilepsy requires long-term ASM therapy due to the high probability of seizure recurrence. The goal of this treatment is to achieve complete seizure freedom.
Physicians must carefully select ASMs, such as levetiracetam or lamotrigine, to minimize drug interactions with other medications the stroke survivor is taking, such as antiplatelet or anticoagulant drugs. These newer-generation medications are preferred because of their favorable tolerability profile and reduced interference with other vascular treatments.