Spike-and-wave
Antiepileptic drugs (AEDs) are commonly prescribed to treat epileptic seizures, and new ones are being discovered with fewer adverse effects.
He continued to refine his technique and increase the sensitivity to the galvanometer, in which he accumulated many EEGs of individuals with and without a brain malfunction or disorder.
[4] Hans Berger published his findings in 1933, however his results did not give a definitive characterization of the general EEG pattern seen during an epileptic seizure.
[6] The spike-and-wave pattern seen during an absence seizure is the result of a bilateral synchronous firing of neurons ranging from the neocortex (part of the cerebral cortex) to the thalamus, along the thalamocortical network.
[7] Metabotropic glutamate receptors (mGluRs) in the thalamocortical network have also shown to display some role in the generation of spike-and-wave discharges (SWDs) associated with absence epilepsy.
[11] In one study, knockout mice lacking mGlu4 receptors showed a disruption of glutamate and GABA release in the thalamocortical network and were resistant to absence seizures induced by low doses of pentylenetetrazole.
[12] Another study showed that bilateral injection of a mGlu4 receptor antagonist into the nRT (thalamic reticular nucleus) of normal mice protected against pentylenetetrazole induced seizures.
The rats from these two strains show spontaneously occurring absence seizures that consist of typical spike-and-wave activity seen on an EEG.
[1] Rat genetic models have given data showing that the expression of absence seizures involves both the thalamic and cortical networks.
In this study, relay and reticular thalamic neurons of epileptic and non-epileptic rats were dual extracellularly recorded and juxtacellularly labeled.
[3] Medium oscillations (5–9 Hz) in both types of rats were noted to occur randomly in an unsynchronized pattern in relay and reticular neurons.
However, spontaneous spike-and-wave discharges were observed in epileptic rats when the medium oscillations became synchronized, suggesting a dependence of the two.
[17] The activity of the primary and secondary cortical regions, as well as the adjacent insular cortex were recorded using an EEG and where applied with electrical stimulation.
[17] Elongator Protein Complex 4 (ELP4) has been identified as a key component in the transcription of genes known to regulate the actin cytoskeleton, cell motility and migration of neurons.
Similar to the insulin effect, overnight fasting, where blood glucose levels were reduced by 35% also showed this double in occurrence.
This model concludes that low glucose levels could be a potential trigger for absence seizures, and could be an environmental risk factor for humans.
Lennox-Gastaut syndrome (LGS) is a childhood epileptic encephalopathy characterized with generalized seizures and slow spike-wave activity while awake.
LGS is a combination of atonic absences, tonic seizures, cognitive deterioration, and slow spike-wave activity in the EEG.
This syndrome is characterized on an EEG by high voltage bursts and slow waves mixed with multifocal spikes alternating with almost flat suppression phases.
This rare disorder is also called encephalopathy with status epilepticus during sleep (ESES) and found in 0.2–0.5% of all child epilepsy cases.
However, what is hypothesized is that corticothalamic neuronal network that is involved in oscillating sleep patterns may begin to function as a pathologic discharging source.
Some of the adverse effects, such as serious cutaneous, haematological and hepatic events, usually require withdrawal in children and place a heavy burden on the costs of healthcare.
[27] Despite these major advances, there is always room for improvement, especially regarding the tailored treatment of individuals who have suffered adverse effects from older AEDs.
