We present the case of a 36-year-old woman assessed in our clinic. Her personal history included a diagnosis of epilepsy at the age of 15 and menstrual migraine. The first of these was due to several episodes of loss of consciousness preceded by feelings of dizziness, sweating and tinnitus, which occurred approximately every two months. She was treated with valproic acid (VPA) for two years, during which she remained asymptomatic. The menstrual migraine started at the age of 21 years, usually with a marked vegetative cortex and severe vomiting.
At the age of 24, after vomiting during migraine attacks, she began to lose consciousness again, from which she recovered spontaneously a few seconds later. However, on one occasion, while unconscious, she began to make guttural sounds and had a generalised seizure lasting one minute. She was evaluated by a neurologist, who performed an electroencephalogram (EEG) and magnetic resonance imaging (MRI) of the brain, all of which were normal. With the clinical diagnosis of epilepsy, she was started on treatment with zonisamide (ZNS) at a dose of 250 mg daily. The patient continued to suffer from episodes of loss of consciousness, although less frequently. They were usually preceded by tinnitus, sound distancing, palpitations, a feeling of faintness and weakness.
At this time he came to our clinic for the first time. A new EEG showed right temporal slow waves and a single peak wave discharge in the same location after hyperventilation, without clinical symptoms. We continued the study with a tilt table test, during which she suffered a regular episode of intense dizziness with palpitations coinciding with a complete left bundle branch block (LBBB). She was therefore diagnosed with an intraventricular conduction disorder and a subcutaneous Holter-electrocardiogram (ECG) was implanted, and the SNZ was progressively withdrawn.
In the following months she presented three new episodes of loss of consciousness, with stress as the only apparent cause. One of these occurred during sleep, awakening with vegetative cortex and, for the first time, was accompanied by urinary incontinence; another was preceded by asthenia and an ascending epigastric burning sensation, also associated with lateral tongue biting and subsequent confusion. The Holter-ECG reading of one episode showed a LBBB, but no changes were recorded in the other episodes. As the episodes continued and new clinical features were added (urinary incontinence and lateral tongue bite), we performed video-EEG monitoring and simultaneous ECG recording. The intercritical tracing showed the presence of slow waves and right temporal epileptiform discharges, sometimes in the form of prolonged bursts of rhythmic waves. During the study, she presented with an episode of self-limited dizziness, similar to those initially described, which on EEG recording corresponded to organised rhythmic theta activity in the anteromedial region of the right temporal lobe, then spreading to the ipsilateral posteromedial region. Coinciding with the clinical onset, a bundle branch block appeared on ECG. A brain MRI showed slight dilatation of the temporal horn of the right lateral ventricle, with no other alterations.

Based on the data obtained, we concluded that the episodes were compatible with focal seizures of right temporal origin, in the context of focal epilepsy of unknown cause, as we did not find a clear lesion in the brain MRI. She started treatment with levetiracetam (LEV) at a maximum dose of 2,000 mg/day, without the episodes disappearing and with side effects (mainly insomnia and irritability), so it had to be replaced by oxcarbazepine (OXC) up to a dose of 1,800 mg/day. With this drug he has been free of episodes and without side effects.