Absence Seizures [ICNApedia]

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====== Absence Seizures ======
Absence seizures are short seizures with behavioural arrest and generalised 3-Hertz spike-and-wave discharges on EEG. Absence seizures occur in multiple genetic generalized epilepsies, including [[childhood absence epilepsy]] (CAE), [[juvenile absence epilepsy]] (JAE), and [[juvenile myoclonic epilepsy]] (JME).
===== Pathophysiology =====
<imgcaption absences|Thalamocortical circuitry involved in the pathogenesis of absence seizures. Thalamic relay (TR) neurons exhibit spike-wave discharges that result from activation of T-type Ca++ channels, followed by hyperpolarization mediated by GABA released from thalamic reticular (NRT) neurons.>{{ :content:absenceseizurespathophysiology.png?280x105}}</imgcaption>
  * The pathogenesis of absence seizures involves the cortico-thalamic-cortical circuit[(:cite:pmid22989853>{{pmid>long:22989853}})]
  * Glutamatergic neurons from cortical layer VI send activation signals down to the thalamus' nucleus reticularis
  * Excitatory thalamic relay neurons connect to cortical pyramidal neurons and produce rhythmic oscillatory neuronal firing between these two regions of the brain
  * The thalamic nucleus reticularis' neurons can fire rhythmically (for example, to generate sleep spindles) or constantly in single spikes
  * Spikes in thalamocortical networks and thalamic nucleus reticularis neurons influence these firing patterns
  * Inhibitory GABA-ergic projections from thalamic nucleus reticularis neurons connect with other neurons and thalamic relay neurons, but not with the cortex.
  * An aberrant oscillatory rhythm can result from T-type channel defects or enhanced GABA-B activity. T-type calcium channels act as low-threshold transient calcium channels. After depolarization, T-type channels momentarily allow calcium in before inactivating. Reactivation requires a protracted GABA-B receptor-facilitated hyperpolarization. 

Hence T-type calcium channel suppressors like ethosuximide and valproate are used for treating absence seizures. GABA-A agonists like benzodiazepines that preferentially activate thalamic nucleus reticularis neurons can also decrease absence seizures. However Vigabatrin, which increases GABA-B activity will increase absence seizures. Other medications which can worsen absence seizures are sodium channel blockers like Carbamazepine, phenytoin and gabapentin.
{{tag>childhood_absence_epilepsy}}