Status epilepticus(SE) can be considered as failure of regulatory inhibitory or “brake” networks in the human brain. We examined anatomic magnetic resonance (MR) correlates of neonatal status epilepticus in neonatal hypoxic ischemic encephalopathy (HIE) with an aim to discover key regions where critical nodes of such inhibitory network(s) may exist.

EEG-Video recordings of 78 encephalopathic neonates undergoing hypothermia were visually analyzed for seizures and status epilepticus. MRI brain from first two weeks of life were scored for injury in each individual regions and sub-regions including Brainstem (BS), Basal-ganglia/Thalamus (BG/T), Posterior limb of internal capsule(PLIC), white matter(WM) and grey matter(GM).

In infants with seizures, presence of any BG/T injury lead to status epilepticus in 81% of infants as compared to only 20% of those without (p=0.005). All infants with moderate-severe BG/T injury had SE. Similarly, in infants with seizures, all infants with BS injury developed SE as compared to only 33% of infants without any BS injury (p=0.006). Overall, only one infant with mild brainstem injury (isolated abnormal diffusion in BS) did not seize, rest not only had seizures but also developed SE.

The dichotomy of the seizure burden in relation to BS and BG/T complex injury raises possibility that regulatory networks with anti-ictal properties may have key nodes in these subcortical regions. Neuronal networks in neonatal EEG bursts have been shown to involve brainstem and deep nuclear complex. Role of similar networks in neonatal seizures needs to be examined further.