Benign epilepsy of childhood with centrotemporal spikes (BECT) was studied in Malaysian children, and was observed in Chinese, Malay and Indian children in the ratio 10:6:5. There were 12 boys and 9 girls. Fit frequency varied from almost daily to a single fit. The age of onset ranged from 2-13 years and BECT was not noted in any child over 13 years old. There was a strong circadian rhythm and fits occurred mainly in sleep. Generalised seizures were more common than partial seizures. During the 3-year study from April 1989 to April 1992, 21 children with BECT were identified from the EEG records done at the University Hospital and it was found that this genetic epilepsy which is autosomal dominant with age dependent penetrance occurs in approximately 4.8% of our epileptic children. In addition there were 3 children in whom petit mal co-existed with a BECT EEG trait.
Hearing loss has been reported with valproic acid (VPA) use. However, this is the first case of VPA-induced hearing loss that was tested and confirmed with a VPA rechallenge, supported by serial audiometry and pharmacokinetic modelling. A 39-year-old truck driver with temporal lobe epilepsy was treated with VPA at 400 mg, twice daily, and developed hearing loss after each dose, but recovered within three hours. Hearing loss fully resolved after VPA discontinuation. Audiometry performed five hours after VPA rechallenge showed significant improvement in hearing thresholds. Pharmacokinetic modelling during the VPA rechallenge showed that hearing loss occurred at a level below the therapeutic range. Brainstem auditory evoked potential at three months after VPA discontinuation showed bilateral conduction defect between the cochlear and superior olivary nucleus, supporting a pre-existing auditory deficit. VPA may cause temporary hearing threshold shift. Pre-existing auditory defect may be a risk factor for VPA-induced hearing loss. Caution should be taken while prescribing VPA to patients with pre-existing auditory deficit.