Migralepsy; a controversial entity.

The term migralepsy was used for the first time in 1960 to describe a case of ophthalmic migraine followed by typical symptoms of epileptic seizure. 1 But it is not until 2004 that migraine-triggered epilepsy or migralepsy was included (under point 1.5.5) in the 2nd edition of the International Classification of Headache Disorders (ICHDII) 2 where it is defined as an epileptic seizure occurring during or within 1 hour after a migraine aura. We report here the case of a 15-year-old female with a family history of migraine with aura (father and grandmother). From the age of 10 years, the patient had presented paroxysmal seizures with a visual aura in the form of flashes of light and zigzagging lines in the centre of her field of vision, moving slowly and crossing over each other. After 20 or 30 minutes, she presented clonic movements on the right hand side of her body, occasionally extending into generalized seizures in which she lost consciousness, with tonic-clonic jerking in all four limbs. These seizures continued with intense left hemicranial cephalea accompanied by photophonophobia and nausea. She was initially diagnosed as having migraine with aura and treatment was begun with gabapentin at a dose of 300 mg every 12 h. Subsequently, an electroencephalogram (EEG) was performed while she was awake and this revealed an acute left temporal focus; she was then diagnosed as having complex focal epilepsy and treatment was begun with levetiracetam 2,000 mg/day. At age 15, she was once more admitted to our department following a new episode. Magnetic resonance (MR) scan of the brain presented no alterations. The EEG in vigil revealed persistent acute activity in the left temporal region figure 1. The patient and her family reported 1 to 2 episodes per month despite good compliance with medication. In view of the diagnosis of migraine-induced epilepsy, it was decided to replace her treatment with 600 mg per day of valproic acid; after 8 months of follow-up, total remission of her clinical symptoms has been achieved, with a slight asymmetry in the checkup EEG in vigil. The theory most commonly accepted with respect to the pathophysiological substrate of migraine aura is the phenomenon of propagated cortical depression. This phenomenon consists in a wave of neuronal and glial depolarization extending from the visual area throughout the occipital pole (visual aura) and, less frequently, to the parietal sensory cortex (sensory aura) and the motor …