Status Epilepticus


Status Epilepticus

Pediatric Status Epilepticus Study Group (pSERG)

Some of our physicians participate in a national network called the Pediatric Status Epilepticus Study Group that was established to facilitate the collection, analysis and sharing of clinical specimens and data from children with recurrent Status Epilepticus (SE). The ultimate goal of pSERG is to identify better treatment strategies to reduce the mortality rate and provide better outcomes for children with Status Epilepticus (SE).

Currently, benzodiazepines are the preferred initial treatment for SE. If that does not help, it is followed by other anti-epileptic medications such as phenytoin, valproic acid, phenobarbital or ketamine. Some patients have super-refractory seizures and these drugs, either individually or in combination, are not effective in curbing their seizures.

Very few randomized drug studies have been conducted to guide treatment choices for SE patients, especially among the pediatric population. The current clinical care regimen of SE children is mostly based on limited evidence from adult literature.

To address these gaps in knowledge, the multicenter Pediatric Status Epilepticus Research Group (pSERG) was formed in 2010. Pediatric epileptologists and emergency room neurologists from many top Children’s Hospitals in the US, a few hospitals in Canada and Europe participate in this network.

Texas Children’s Hospital has been a part of this national network since its inception. TCH neurologist, Drs. James Riviello, is one of founding member of this network. Drs. Anne Anderson, epileptologist at Texas Children’s hospital and Yi Chen Lai, physician in the Critical Care department at Texas Children’s Hospital and investigators in the Gordon and Mary Cain Pediatric Neurology Research Foundation Laboratories are currently active members of pSERG.

View scholarly publications from pSERG

Other studies conducted by Dr. Anne Anderson and Dr. Yi Chen Lai have led to following important advances in our understanding of SE -

  • SE affects the normal functioning of mitochondria (‘cellular energy generators’), damaging the hippocampal neurons in rodents. This study shows hyper-activation of a mitochondrial enzyme, poly (ADP-Ribose) Polymerase-1 (abbreviated as PARP-1), is one of the molecular mechanisms that leads to SE neuropathology. Thus, PARP-1 may be a potential target to limit neuronal damage during SE. Learn More
  • Convulsive status epilepticus can adversely affect cardiovascular function in children. These findings suggest that children with epilepsy may be particularly vulnerable to seizure-induced arrhythmias. This study shows it is crucial that SE patients continue to receive cardiac surveillance during the postictal state, which is the altered state of consciousness after an epileptic seizure. Learn More
  • A particular type of voltage-gated potassium channel (Kv4.2), is reduced in hippocampal synapses of rodents following status epilepticus. This channel subunit also undergoes a post-translational modification (addition of a phosphate group) that renders it dysfunctional. Mutations in this particular potassium channel subunit have also been implicated in temporal lobe epilepsy. Learn More