What are febrile seizures?
Febrile seizures usually occur in children and are associated with a rise in the body temperature. In most cases, febrile seizures are relatively harmless. However, a subset of children has febrile seizures that last 30 min or longer; this is called febrile status epilepticus (FSE). FSE has been shown to be a risk factor for temporal lobe epilepsy (TLE) later in life (as long as 10 years after the FSE episode). Unfortunately, at this point we have no way of saying definitively whether a child that has FSE will go on to develop TLE later in life. Finding a biomarker that predicts this has obvious benefits; children who test positive could get necessary treatment long before spontaneous seizures start.
Can febrile status epilepticus (FSE) be replicated in rodents?
The scientists in a recent study set out to discover if such a marker exists in a rat model of FSE. Rodents are very important in epilepsy research because they simulate the human condition quite well, and various manipulations can be tested. In this study, once the rat pups underwent an experimental model of FSE, they were subjected to scans on a MRI scanner. In addition, rats also underwent video-EEG monitoring, and were tested again on the MRI scanner 10 months after FSE. The readout of MRI scanning is T2 intensity; reduction in T2 intensity signifies reduced tissue oxygenation (presumably because that part of the brain is consuming more energy).
Can we find a marker that can predict whether there will be spontaneous seizures later on in life?
All rat pups exhibited a decrease in T2 intensity right after the FSE episode. However, when checked 10 months later, only the rats that developed spontaneous seizures as observed by EEG recordings had a reduced T2 intensity. Interestingly, this effect was specific for a part of the brain called the amygdala. This exciting finding was paired with work that showed that there was more inflammation in the amygdala, perhaps causing the decreased T2 intensity. The magnet of the MRI scanner used in this study was very powerful; hence it is worthwhile to know whether similar differences would be picked up by a more conventional MRI scanner. Indeed, even a more conventional low-power magnet scanner was capable of picking up these differences in the amygdala as well.
What do these results mean?
Until now, there has been no way to predict who will go on to develop TLE later in life after experiencing FSE in childhood. One advantage of MRI is that it is repeatable; hence, one could envision a scenario where all children who experience FSE are subject to MRI scanner. Only the ones that show a decrease in T2 intensity in the amygdala go on to receive therapy that could presumably halt epileptogenesis (the process that makes the brain susceptible to seizures) in its tracks.