Seizures are most common in the neonatal period (defined as the first 28 days of life or up to 44 weeks conceptional age) compared to any other period in life with an incidence of 1.5–3.5 per 1000 live births.1,2,3 The incidence may vary according to birth weight, gestational age, and both antenatal and intranatal factors;3,4,5 most notably, there is an increase risk for seizures in premature compared to full-term infants.
The time of seizure onset is usually within the first few days of life, with 80% of all neonatal seizures presenting within the first week of life.1,4 Seizures in the neonatal period are also the most common neurological emergency and are associated with high potential mortality and morbidity.6,7,8,9,10
In contrast to seizures in infancy and childhood, most neonatal seizures are acute and symptomatic with suspected specific causes; relatively few seizures are idiopathic or symptomatic of a clearly defined epilepsy syndrome. Although neonatal seizures have many causes, a limited number account for most seizures (Table 9–111,12,13,14,15). In term newborns, hypoxic–ischemic encephalopathy (HIE) is the most common underlying factor, typically beginning in the first 2 days of life. In preterm infants, intracranial hemorrhage (ICH) is the most common associated risk factor, although a direct relationship to seizure generation is unclear. Meningitis, focal cerebral infarction, transient metabolic disorders, and congenital abnormalities of the brain may cause seizures at any conceptional age.
TABLE 9–1.COMMON CAUSES OF NEONATAL SEIZURES ||Download (.pdf) TABLE 9–1. COMMON CAUSES OF NEONATAL SEIZURES
| Hypocalcemia, hypomagnesemia
|Inborn errors of metabolism
|Maternal drug withdrawal
|Neonatal epileptic syndromes
| Early epileptic encephalopathy with suppression-burst (Ohtahara syndrome)
| Early myoclonic encephalopathy
| Benign familial neonatal convulsions
| Benign idiopathic neonatal convulsions (fifth day fits)
The developing brain is particularly susceptible to developing seizures in response to injury; several mechanisms are likely to be involved. Overall the hyperexcitable state of the immature brain is based upon enhanced excitatory neurotransmission, paucity of inhibitory mechanisms, developmental expression of neuronal ion channels, age-dependent modulation of neuropeptides, and age-dependent early microglial activation.16,17 An ...