Post-stroke epilepsy is a common and easily overlooked complication of acute cerebrovascular disease. Long-term seizures can seriously affect the prognosis and quality of life of patients. Electroencephalogram (EEG) is the simplest way to diagnose epilepsy, and plays an important role in predicting seizures and guiding medication.

To explore the EEG characteristics of patients with post-stroke epilepsy and improve the detection rate of inter-seizure epileptiform discharges.

From January 2017 to June 2020, 10 patients with post-stroke epilepsy in our hospital were included. The clinical, imaging, and EEG characteristics were collected. The stroke location, seizure type, and ictal and interictal EEG manifestations of the patients with post-stroke epilepsy were then retrospectively analyzed.

In all 10 patients, epileptiform waves occurred in the side opposite to the stroke lesion during the interictal stage; these manifested as sharp wave, sharp-wave complex, or spike discharges in the anterior head lead of the side opposite to the lesion.

In EEG, epileptiform waves can occur in the side opposite to the stroke lesion in patients with post-stroke epilepsy.

Post-stroke epilepsy (PSE) refers to seizures that occur within a certain time after stroke in patients without a prior history of epilepsy or brain and systemic diseases. The epileptic discharges detected by electroencephalogram (EEG) are generally consistent with the lesion site of the stroke[1].

PSE can be divided into two categories based on the time between the stroke and the first seizure. Seizures that occur within 1 week after stroke are called “early-onset” seizures, also known as “acute symptomatic epilepsy.” Epileptic seizures that occur 1 wk or more after stroke are known as “late-onset” seizures, and are most common 6-12 mo after stroke. A later onset is associated with an increased risk of recurrent stroke, also known as “stroke-related epilepsy”[2]. The most common seizure types in PSE are focal seizures or tonic-clonic seizures that progress to bilateral focal seizures. Although generalized convulsive status epilepticus is very rare in PSE, nonconvulsive status epilepticus occurs in 4%-19% of patients with acute stroke[3,4]. Focal status epilepticus occurs occasionally, and epileptic seizures may be the first or only manifestation of acute stroke; they thus require prompt recognition and active management[4].

PSE is a common complication after acute cerebrovascular events, and is a common etiology in older patients with epilepsy. It can prolong the hospitalization time of patients with cerebrovascular diseases, increase disability and mortality rates, and affect the long-term prognosis and quality of life of patients[1,5]. EEG is the most objective auxiliary examination method for the diagnosis of PSE, and plays a very important role in epileptic seizure prediction, disease monitoring, drug selection, and prognosis evaluation[6]. In the present study, the special EEG findings of 10 PSE patients were retrospectively reviewed and are briefly reported.

Brain tissue damage caused by stroke is the main cause of PSE. Acute stroke results in local brain tissue hypoxia, abnormal brain metabolism, whole-brain low/high perfusion, glutamate excitotoxicity, ion channel dysfunction, and blood–brain barrier damage; these changes can lead to early-onset PSE. By contrast, glial scarring, chronic inflammation, angiogenesis, neurodegeneration, neurogenesis, selective neuronal loss, and synaptic plasticity secondary to stroke are closely related to late-onset PSE[3,7]. The occurrence of PSE can also have a negative impact on stroke; PSE can lead to decreased intracranial blood flow and increased intracranial pressure, aggravate secondary damage of neurological function, and worsen patient prognosis. Simultaneously, the risk of recurrent stroke increases[8,9].

The most common EEG findings in acute stroke are focal slow waves and diffuse slow waves on the infarct or hemorrhage side[10]. The presence of focal spikes, sharp waves, or unilateral periodic epileptiform discharges suggests an increased risk of PSE[11]. For patients with symptomatic epilepsy who have structural lesions in the brain, bioelectrical activity decreases as a result of damage at the stroke site and in surrounding neurons, and scalp EEG asymmetries—such as focal slow waves or low voltage—can occur. These background abnormalities are generally consistent with the structural lesions[2,12]. However, in some cases, such as those of cerebral trauma or cerebral perforation deformity, the focal or unilateral epileptiform discharges are inconsistent with the structural lesions, and the discharge sites are located distant from the structural lesions, or even in the contralateral hemisphere[13].

In the 10 PSE patients in the present study, symptom onset was consistent with the structural abnormal lesions that were observed on imaging; however, the interictal epileptic waves were located contralaterally to the lesions. The underlying mechanisms of this phenomenon may be as follows: (1) Local or unilateral pathological changes and abnormal sites of background EEG mean that EEG activity is almost lost; there is therefore no structural and functional basis for producing epileptiform discharges, and the discharges thus come from the relatively normal lobes or hemispheres. For example, it has been reported that when most of one hemisphere is damaged and necrotic, EEG shows generalized low voltage in this hemisphere, and discharges often come from the relatively normal hemisphere (i.e., on the same side of the hemiplegia)[14]; and (2) A local structural or functional brain injury affects distant sites via specific known or unknown intermediate links, thus producing epileptoid discharges[13].

PSE can lead to an important increase in the disability and mortality rates of stroke patients. However, compared with other types of symptomatic epilepsy, the refractory rate of PSE drugs is relatively low, and overall prognosis is better[5]. Together, the current findings indicate that the use of long-range video EEG monitoring should be refined in patients with severe cerebrovascular disease, to identify atypical seizures and unexplained disturbances of consciousness as soon as possible and to improve the detection rate of interictal epileptiform discharges[6]. For patients with PSE presenting with a first seizure (especially a focal nonmotor seizure), if scalp EEG discharges are on the side contralateral to the lesion during seizure intervals, the following steps should be taken: (1) Carefully examine the patient’s medical history; (2) analyze whether the clinical manifestations of seizure onset correspond to the softening lesions of stroke; and (3) capture the ictal EEG (if possible). A diagnosis of epilepsy should be considered for such focal seizures, and the possible etiology should first be presumed to be stroke.

In EEG, epileptiform waves can occur in the side opposite to the stroke lesion in patients with post-stroke epilepsy.