Abstracts

RATIONALE: Conflicting views exist between laboratory and clinic on whether seizures (szs) in newborns (NBs) are injurious to the immature brain. Most neuroscientists[ssquote] research concludes that they are, and may be epileptogenetic. Most clinical investigations conclude that NBs szs, if systemic complications are controlled, are not injurious and that there is no evidence for their epileptogenicity. Pertinent to such conflict, I summarize here data obtained from a prolonged follow-up of a large cohort of seizing NBs.
METHODS: The neurological status, of 190 unselected full-term (FT) NBs, after a time span of 8 to 20 years, comprise the nucleus of this investigation. Thirty-two died before 2 years (16%). Of the surviving 158 NBs reliable data could be obtained in ninety five (60%) when adolescent or adult. Data on their motor, developmental status and on the occurrence of epilepsy at any time of their life, were obtained by direct contacts or by questionnaires sent to them, their families and, for many, schools or work places.
RESULTS: Forty-three (46%) did not have szs since neonates, and were free of neurodevelopmental deficits. Fifty-two (48%) had either motor, or neurodevelopmental abnormalities. Twenty-three (25%) persisted having szs or had developed ex-novo epileptic syndromes, the majority being those with worst phenotypes. Almost all with epilepsy had motor and/or developmental deficits, but the converse was uncommon.
Review of early biographies: of the 23 with epilepsy revealed that the etiological factors inducing NB szs were the most severe in twenty (88%), only three (12%) were cryptogenic or had transient metabolic disorders (p.[lt]0.01). In contrast, of the 43 free of sequelae, in 34 (80%), their szs had been triggered by benign etiologies. Only nine were shown or suspected to harbor CNS pathologies (p.[lt] 0.03)
CONCLUSIONS: To my knowledge this is the first very prolonged study of outcomes in a large cohort of NBs with szs. Main conclusions are: 1. Long-term sequelae of NBs szs correlate best with etiologies, characteristic for this age. 2. The majority of NBs szs are either symptomatic markers of preexisting CNS pathologies or reactive to metabolic derangements. 3. There is no clinical evidence to support laboratory conclusions that NBs szs are, per-se, epileptogenetic, though many of their etiologies are. 4. Prolonged antiepileptic therapies fail to prevent or ameliorate sequelae, even when the NBs szs stop early.
Hence the results of these clinical studies appear to be in conflict with the conclusions arising from much experimental research. Whether or not an [dsquote]inevitable energy failure[dsquote], or the [dsquote]excitotoxic effects[dsquote], or the [dsquote]aberrant circuitries following neurogenesis[dsquote] described in the laboratory also occur in human NBs, their long-term functional effects are still obscure.
From the optics of a clinician further research could be focused more on the [dsquote]protective[dsquote], compensatory751002 mechanisms existing in the CNS that prevent or ameliorate the putative injurious consequences of ictal phenomenology in the immature brains.
[Supported by: Self Supported]