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Repeated paroxysmal oropharyngeal fits consisting of sialorrhea and speech arrest are described in a 5 year-4-month old patient. Investigations were initially oriented towards a laryngeal or a gastrointestinal disease. Electroencephalographic tracings showed repeated bilateral centrotemporal spikes-waves discharges which sometimes were associated with bilateral facial clonic contractions synchronous with anarthria and sialorrhea. Consciousness was preserved. Attacks were related with a cluster of fits of a partial epilepsy. Transient pseudo-bulbar palsy (anterior opercular syndrome) resulted from seizures: loss of identifiable speech, drooling with difficulties in swallowing, absence of palatal movements and of the gag reflex. Intellectual functions remained normal. Other investigations were all normal (CT scan, MRI, cytologic and immunological CSF studies). With common anticonvulsant drugs (Valproate and Carbamazepine) seizures resolved within a few weeks. These findings suggest that this particular epilepsy is an unusual type of benign partial epilepsy with centrotemporal (or Rolandic) spikes.

A historical cohort study was undertaken to determine the risk of epilepsy in a population of 18 newborns with neonatal hypoglycemia due to insulin excess. Follow-up was 3 years 8 months (range 7 years-1 year 3 months). Insulin excess was associated with maternal diabetes in 13 infants, with an isolated macrosomia in 2 infants, in one case with probable Langerhans hyperplasia, and in 2 newborns only prolonged beta-sympathomimetic therapy was the possible cause of insulin excess. Newborns with anoxia, brain malformation or small for date were excluded. Two newborns had hypoglycemia with epileptic clonic seizures, but only one was later epileptic. In this case, hypoglycemia was severe and persistent (16 hours). Hyperinsulinism was related to Langerhans hyperplasia. CT scan made at ages one and 6 months showed large hypodensity of the frontal and occipital white matter. Visual evoked responses were also abnormal. Visual evoked responses and CT scan normalized at 1 year. In other children, asymptomatic hypoglycemia (n = 11) or symptomatic hypoglycemia without epileptic seizures (n = 5) did not increase the epileptic risk as none of them had epileptic seizure later on. Thus, seizures associated with neonatal hypoglycemia alone seem to increase the epileptic risk with duration and severity of hypoglycemia being also essential prognostic factors.

A 15 years-old girl with no previous history of epilepsy or neurological disease presented three types of epileptic symptoms the same day: 1) clusters of rhythmic myoclonus of the left hemiface; 2) episodes of painful paresthesias of the left arm followed by secondary generalised seizures; 3) episodes of elementary visual hallucinations of the right hemifield. She had several seizures each hour and some were recorded. There were no EEG abnormalities during the facial myoclonus but rapid rhythms were seen during the sensory and visual partial seizures on the right parietal and left occipital lobes. There was no fever and no drowsiness. The CSF tap showed pleocytosis. Serological studies indicated recent mumps. The drugs were initially inefficient. The seizures disappeared after a month. The drugs were stopped after three months and the seizures had not relapsed after a one year's follow-up. Though there were no other sign of encephalitis, we believe that episode of multifocal seizures was due to mumps encephalitis.