Neonatal hypoglycemia: role in infantile epilepsy.

H ypoglycemia remains a significant cause of brain injury in newborn infants(1), as highlighted by Udani, et al.(2) in this issue of Indian Pediatrics. The authors recruited 100 consecutively presenting infants with epilepsy, 83 of whom had brain imaging and/or a clear metabolic or genetic diagnosis. The majority of the 83 infants had evidence of brain injury of perinatal onset and in the largest subset of these, the injury pattern suggested hypoglycemia as a cause. Genetic, metabolic and documented postnatal causes constituted a much smaller group. Infants with acute symptomatic seizures, those without available imaging and those with uncertain age of epilepsy onset were not included; it would have been informative to know the number of children excluded to have a better understanding of how representative was the study cohort. It is somewhat surprising that only eight children had imaging evidence of acute perinatal hypoxia-ischemia; perhaps these are under-represented as their difficulties had been known from birth and the cause of seizures was already clear. Burns, et al.(3) recently reported on the spectrum of neonatal MR imaging abnormalities in term-born infants having symptomatic neonatal hypoglycemia; these included arterial territory stroke, white matter change that was not confined solely to posterior parietal and occipital lobes, focal hemorrhage and also a diffuse increase in signal on T1-weighted imaging in the globus pallidum. Of note is that the white matter findings associated with neonatal hypoglycemia can be subtle such that they might not be easily seen on imaging carried out after the neonatal period. In the present study, 9 infants with hypoglycemia were not thought to have typical imaging patterns and hence were not included in that etiological category, potentially underestimating the contribution of hypoglycemia in their cases, as also pointed out by Udani, et al.(2). On the other hand, the injury pattern typically described in hypoglycemia is not pathognomonic and it is a concern that etiology was based, for many infants, solely on the imaging characteristics without confirmatory biochemistry – this may have resulted in an overestimate of the contribution of hypoglycemia to later epilepsy in some infants. Typically, hypoglycemia does not affect the posterior putamen and ventrolateral thalamic nuclei or the main motor tracts as is seen with acute perinatal hypoxic-ischemic injury. The authors also found a striking lack of severe spasticity and dystonia in the infants with epilepsy following neonatal hypoglycemia. The more diffuse signal in the globus pallidum is …