A stroke, an interruption of blood flow to the brain, can cause a seizure as a complication. The stroke starves brain tissue of oxygen and nutrients, leading to cell damage or death. This injury disrupts the brain’s normal electrical signaling, which is the basis for a seizure—a sudden, abnormal burst of electrical activity. Post-stroke seizures represent a significant risk for survivors.
Defining Post-Stroke Seizures
The term Post-Stroke Seizures (PSS) refers to seizures that occur after a stroke event, distinct from pre-existing epilepsy. Approximately 5% to 15% of all stroke survivors will experience at least one seizure within a few years. PSS is the most common cause of new-onset seizures and epilepsy in older adults. PSS can manifest in various ways, not always as dramatic, full-body convulsions. Many post-stroke seizures are focal, meaning the abnormal electrical activity begins in one area of the brain, leading to localized symptoms like twitching, sensory changes, or confusion.
The Distinction Between Acute and Late Seizures
Post-stroke seizures are categorized into two temporal groups, which is important for understanding prognosis and treatment.
Acute Seizures
Acute symptomatic seizures occur within the first seven days following the stroke event. These seizures are generally considered a reaction to the immediate physiological and metabolic disturbances caused by the acute brain injury. Most acute seizures happen within the first 24 hours when brain swelling (edema) and metabolic disruption are at their peak. Although they indicate severe brain injury, acute seizures carry a lower risk of recurrence, with about 30% of patients experiencing another seizure.
Late Seizures and Epilepsy Risk
If a seizure occurs after the initial seven-day period, it is classified as a late seizure (or remote symptomatic seizure). Late seizures indicate a higher risk of developing chronic Post-Stroke Epilepsy (PSE). PSE is defined as having two or more unprovoked seizures more than 24 hours apart. A single late seizure places the survivor at a greater than 60% risk of recurrence over the next decade, often sufficient for an epilepsy diagnosis. The type of stroke also influences risk: hemorrhagic strokes and strokes affecting the cerebral cortex carry a higher risk for both acute and late seizures than non-cortical ischemic strokes.
Biological Mechanisms Driving Seizure Activity
The physical damage from a stroke initiates a cascade of cellular events that fundamentally alter the brain’s electrical stability, a process known as epileptogenesis. One major mechanism is the immediate disruption of neurotransmitter balance within the brain’s circuitry. Lack of blood flow and oxygen triggers an excessive release of the excitatory neurotransmitter glutamate, which overstimulates neurons. This overstimulation, combined with reduced inhibitory signals from the neurotransmitter GABA, lowers the seizure threshold and can provoke acute seizures.
In the weeks and months following the stroke, permanent structural changes begin to drive the risk of late seizures. Damaged neural tissue is replaced by a glial scar, primarily formed by reactive astrocytes, in a process called gliosis. This scar tissue physically disrupts the normal, finely tuned synaptic connections between neurons, creating an area of hyperexcitability that can act as a focus for abnormal electrical discharge. Chronic inflammation also makes the brain susceptible to seizures. The stroke triggers an inflammatory response involving immune cells and the release of pro-inflammatory molecules like cytokines, which persist long after the acute event, further lowering the seizure threshold.
Clinical Diagnosis and Treatment Approaches
The clinical identification of PSS begins with a detailed neurological evaluation and brain imaging, typically a Computed Tomography (CT) scan or Magnetic Resonance Imaging (MRI), to precisely locate the stroke injury. Since seizures can be non-convulsive, the Electroencephalogram (EEG) is used to confirm the diagnosis by recording the brain’s electrical activity. Continuous EEG monitoring may be used in the acute phase to detect subtle seizure activity.
The therapeutic strategy depends directly on the seizure’s timing relative to the stroke. Acute seizures generally do not require long-term treatment. They are often managed with short-term courses of anti-seizure medications (ASMs) only if they are severe or recurrent. The goal in this acute phase is to stabilize the patient and allow the brain to recover from the immediate injury. Conversely, if a patient experiences a late seizure, long-term ASM therapy is usually recommended due to the high risk of recurrence and chronic epilepsy development. Common ASMs used include levetiracetam, lamotrigine, and carbamazepine, chosen based on the patient’s profile and potential for drug interactions.