Introduction. Seizures are a known complication of stroke. They may increase the cerebral lesions and induce epileptic status or encephalopathy. The correlation between brain structural damage, epileptic foci, antiepileptic drugs and clinical outcome is unknown. Late o nset seizures are thought to be caused by gliosis and the development of a meningocerebral cicatrix. Changes in membrane properties, deafferentation, selective neuronal loss, and collateral sprouting may result in hyperexcitability and neuronal synchrony s trong enough to cause seizures. Can we consider as Epilepsy one grand mal seizure after a massive ischemic stroke? Case report. A 41 year old woman with a history of thrombosis of the right coronary artery, myocardial infarction at the age of 35, was co nfirmed with primary antiphospholipid syndrome. After two years, she developed cerebral infarction in MCA territory, and with mild left hemiparesis she was hospitalized at the Neurological Institute. The 3T cerebral MRT was performed on Siemens Magnetom Sk yra 3T, and confirmed a large cerebral infarction in the right hemisphere with a density of 12 UH, dimensions 9.0 x 5.0 x 6.0 cm without mass effect. She continued anticoagulation therapy warfarin under the INR (2.0 2.5) control. At the age of 39 the patient developed a single generalized tonic clonic epileptic seizure. Routine EEG, prolonged EEG (2 hours) at the Nicolet EEG Wireless Amplifier System were performed. EEG data showed focalized slow spike wave: theta waves right F C T and T poste rior spike. Hyperventilation has induced F bilateral extension, without secondary generalization. Photic stimulation test maintains focalized epileptic activity. Lamotrigine was initiated in increasing doses reaching the therapeutic dose 200 mg/24 hours. Epileptic seizures have not recurred. Free period of seizures 3 years with antiepileptic treatment. EEG and cerebral MRI monitoring were performed regularly, once a year over the last 3 years. Cerebral MRI did not reveal adjacent lesions. EEG showed the disappearance of sharp waves and the persistence of slow F C right waves. Conclusions. According to the literature data, the seizures could repeat at any time, i.e. over 5 years or 10 after the stroke. In the 3 year period without seizures probably the re was no transformation of a structurally damaged brain into an epileptic one. The last definition of epilepsy by R. Fisher confirmed that one epileptic seizure cannot be epilepsy. The severity and location of the infarction advocates a vascular epilepsy, not epileptogenic foci.