Absence (petit mal) seizures are usually seen in children and are characterized by abrupt impairment in consciousness and a stereotypical EEG pattern occurring in the 2-4Hz frequency range, known as a ”spike-and-wave” discharge.
In some cases, such seizures can lead to cognitive difficulties and generalized tonic-clonic seizures later in life.
Disruptions in the corticothalamic network have been shown to underlie absence seizures. In the thalamus (a part of the brain present along the midline), there are two groups of neurons known as nuclei – the reticular thalamic nucleus (RTN) and the ventral posterior (VP) complex that are thought to be involved in generation of absence seizures. The degree that the neurons communicate in unison – known as synchrony—is important because abnormal synchrony (hypersynchrony) is believed to underlie the spike-and-wave discharges characteristic of absence seizures.
A study was recently conducted to understand the neurobiological mechanism behind this abnormal synchrony. The researchers focused the GABAergic system – the principal brain chemicals that help to calm neuron function.
By using special mice in the lab, it was revealed that GABAA receptors with the subunit α1 and β2 are predominant in the VP group of cells; whereas those expressing α3 and β3 subunits are predominant in the RTN. In the epileptic stargazer mice, Western blot analysis showed that that the levels of α1 and β2 subunit containing GABAA receptor in the VP were increased as compared to nonepileptic mice, while the levels of α3 and β3 subunit containing GABAA receptor in the RTN were unchanged.
More studies are required to understand what these results mean for the human condition, but it could be that alterations in GABAA receptor subunits in the VP contribute to the abnormal synchrony causing absence seizures. If true, this could help develop new treatments for this seizure type.