Aa. Raymond et al., CORTICAL DYSGENESIS - SERIAL EEG FINDINGS IN CHILDREN AND ADULTS, Electroencephalography and clinical neurophysiology, 94(6), 1995, pp. 389-397
Cortical dysgenesis (CD) is becoming increasingly recognised as a caus
e of epilepsy in otherwise cryptogenic cases. We describe the serial E
EG findings in 22 patients with focal/localised CD. The EEGs covered a
minimum period of 5 years in each case (median = 13 years, range: 5-3
0 years), beginning in childhood. Median age at seizure onset was 3 ye
ars (range: 3 weeks-10 years, n = 21). The EEG was normal in the one p
atient, a 6 year old, who did not have epilepsy. Background rhythms ap
propriate for age were preserved in the majority of patients (18/22).
Slow activity localised to the area of CD was seen in 11 patients; in
3 patients, this did not appear until the second decade of life. Epile
ptiform discharges were seen in at least one EEG in 20 patients: these
were continuous or near-continuous (6 patients) or occurred recurrent
ly in short runs (6 patients). In 6-patients, these discharges appeare
d only after the second decade of life and in 11 patients, they became
more widespread over time. In the remaining patients, the EEG changes
did not evolve. Sleep failed to produce new abnormalities (n = 15). N
one of the patients showed EEG features characteristic of lissencephal
y. or evolution to the Lennox-Gastaut syndrome. Even in this selected
cohort of patients who had undergone serial clinical EEGs, the EEG abn
ormalities in focal/localised CD appeared relatively stable and showed
only moderate changes over time, CD must be included in the different
ial diagnosis of any patient who presents with localised slow activity
on EEG.