Page 241 - ILAE_Lectures_2015

The onset of perinatal seizures and timing of the cerebral insult are broadly as follows:

In utero Day l Day 2 Day 3 Day 4 Day 5 Day 6 (and beyond)

Cerebral malformation/dysgenesis ------------------------------------------>
Intrauterine (congenital) infection ------------------------------------------->
Pyridoxine/pyridoxamine dependency/deficiency --------------------------------------------->

Perinatal asphyxia
Sepsis
Hypoglycaemia
Maternal drug withdrawal
Periventricular haemorrhage

Hypocalcaemia
Benign familial neonatal convulsions

Aminoacidopathies
Galactosaemia
Ketotic and non-ketotic hyperglycinaemia
Early infantile epileptic encephalopathy
Folinic acid-responsive neonatal seizures
Glucose transport protein deficiency

Migrating partial seizures (epilepsy) of infancy

Perinatal and neonatal seizures are both over- and under-diagnosed. Generalised tonic-clonic
seizures do not occur in neonates, and most seizures are myoclonic or clonic and localised
(focal or partial including Jacksonian) and fragmentary, again reflecting an immature brain.
Even though almost two decades old, the classification of neonatal seizures remains a
pragmatic classification2:

Seizure type Relative frequency

_________________________________________________________________________

Subtle (fragmentary) 33%
bicycling or boxing; oral-buccal-lingual
(chewing, swallowing or tongue-thrusting);
tonic eye deviation; apnoea (cessation of breathing);
complex, purposeless movements

Clonic 27%

Tonic 20%

Myoclonic 20%
focal; multifocal; generalised

(Note: subtle seizures are more common in premature infants, i.e. before 37 completed weeks of gestation)