We report the case of a 36-year-old woman evaluated in our clinic.
Personal history included epilepsy at 15 years of age and menstrual migraine.
The first was due to several episodes of loss of consciousness preceded by dizziness, sweating and tinnitus, which occurred approximately every two months.
He continued treatment with valproic acid (VPA) for two years in asymptomatic patients.
Menstrual migraine began at 21 years of age, usually with a marked vegetative process and intense vomiting.
At 24 years of age, after vomiting during migraine attacks, she began to present again loss of consciousness, which recovered spontaneously a few seconds later.
However, on one occasion, while unconscious mindset, it began to perform sinus sounds and presented a generalized seizure lasting one minute.
He was evaluated by a specialist in neurology, who studied him using an electroencephalogram (EEG) and a brain magnetic resonance imaging (MRI), all with normal results.
With the clinical diagnosis of epilepsy, treatment with zonisamide (ZNS) was initiated at a dose of 250 mg daily.
The patient continued to suffer episodes of loss of consciousness, although less frequently.
Generally, they were preceded by tinnitus, sound distancing, seizures, fainting and weakness.
At this moment she comes for the first time to our consultation.
A new EEG shows right temporal slow waves and a single point-wave discharge in the same location after hyperventilation, without clinical monitoring.
We followed the study with a basic table test, during which he suffered a habitual episode of intense dizziness with overlapping episodes with a complete left bundle branch block (LBBB).
For this reason she was diagnosed with intraventricular conduction disorder and a subcutaneous Holter-electrocardiogram (ECG) was implanted, removing the NSZ progressively.
In the following months she presented three new episodes of loss of consciousness, with stress as the only apparent cause.
One of them occurred during sleep, woke up with a vegetative cut and, for the first time, presented with urinary incontinence; another was preceded by asthenia and a sensation of confusing ascending epigastric burning.
The Holter-ECG reading of one episode showed a LBBB, but in the rest there were no changes.
As the episodes were maintained and added new clinical elements (urinary incontinence and lateral bite of the tongue), video-EEG monitoring was performed and ECG recording was performed.
The intercritical tracing highlighted the presence of slow waves and right temporal epileptiform discharges, sometimes as prolonged sprouts of rhotic waves.
During the study, the patient experienced an episode of self-limiting dizziness, similar to those initially described, which in the EEG recording corresponded to the mental retardation organized in the ipsilateral anteromedial region of the right temporal lobe.
Coinciding with the clinical onset, a branch block appeared on the ECG.
Brain MRI showed slight dilation of the temporal horn of the right lateral ventricle, with no other alterations.
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With the data obtained we conclude that the episodes were compatible with focal crisis of right temporal origin, in the context of a focal epilepsy of unknown cause, since we did not find a clear lesion in the brain MRI.
Levetiracetam (LEV) was started at maximum doses of 2,000 mg/day, with no disappearance of the episodes and side effects (mainly insomnia and irritability), so there was a need to replace it with oOX.
This drug has been free of episodes and without side effects.
