Seizures can be classified as those of early and those of late onset in a paradigm comparable to post-traumatic epilepsy, with an arbitrary dividing point of two weeks after the event. Most early-onset seizures occur during the first day after the stroke. Late-onset seizures occur three times more often than early-onset ones. A first late-onset epileptic event is most likely to take place between six months and two years after the stroke. However, up to 28% of patients develop their first seizure several years later.

Simple partial seizures, with or without secondary generalisation, account for about 50% of total seizures, while complex partial spells, with or without secondary generalisation, and primary generalised tonic–clonic insults account for approximately 25% each. Status epilepticus occurs in 12% of stroke patients, but the recurrence rate after an initial status epilepticus is not higher than after a single seizure.² Inhibitory seizures, mimicking transient ischaemic attacks, are observed in 7.1% of cases.

Risk Factors
Early-onset seizures in ischaemic stroke are mainly found in patients with large cortical lesions, decreased consciousness and additional haemodynamic and metabolic – mainly renal – disturbances. In haemorrhagic stroke, the products of blood metabolism, such as haemosiderin, may cause a focal cerebral irritation, leading to seizures.

In the Seizures After Stroke Study (SASS), the main predictors for late-onset seizures after an ischaemic stroke were the severity of the initial neurological deficit and the presence of a large cortical infarct.1 In our series we found that the only clinical predictor of late-onset seizures was the initial presentation of partial anterior circulation syndrome due to a territorial infarct. Patients with total anterior circulation syndrome had less chance of developing epileptic spells, not only due to their shorter life expectancy but also due to the fact that the large infarcts are sharply demarcated in these patients. Large cortical infarcts with irregular borders located in the temporal–parietal regions represent an increased risk of developing seizures. Epileptic spells can also occur after a ‘silent’ cerebral infarct triggered by alcohol or drug abuse. Finally, a late-onset seizure can be due to recurrent infarction, mainly of cardioembolic origin. Lacunar infarcts and ischaemic white-matter lesions are probably not a direct cause of seizures and epilepsy, and there is no evidence that post-stroke epilepsy occurs more frequently in patients with cardioembolic, as opposed to thromboembolic, infarcts. Arterial hypertension, coronary and valve disorders, diabetes and hypercholesterolaemia are not risk factors for seizures in stroke patients. Only chronic obstructive pulmonary disease (COPD) is more frequently found in patients with stroke-related seizures. Lobar haematomas are frequently accompanied by early-onset fits. Surgery for an intra-cerebral haemorrhage is an additional risk for the development of late-onset seizures.²