Absence Seizures: A Case Study

1. Introduction

Absence Seizures have been a medical concern for a long time, and were first described in medical literature back in 1705 by Poupart (Temkin, 1971). According to The World Health Organization (WHO) at least 40 forms of epilepsy have been identified, and they are characterized by an abrupt and transitory synchronization of neuron activities, whose causes are not always well known.

2. Overview and Clinical Presentation of Absence Seizures

2.1 Overview

According to the American Epilepsy Society, (2014), Absence Seizures (AS), which in the past were called ‘petit mal’, are a type of generalized seizure. In 1935, Gibbs, Davis, and Lennox described a typical pattern of AS, consisting of a correlation between the episodes of diminished consciousness and 3-4 Hz spike-wave discharges (SWD) on electroencephalograms (EEGs), which is a valid association to date (Blumenfield,

Moreover, typical absences usually last 9–12 s (Hooge, & De Deyn, 2001). Indeed, mutations of genes coding for GABA A receptors and T-type calcium channels have been linked to AS. More recent studies have found that Glucose transporters might also be linked to AS, however data is limited in this respect and offers further room for exploration.

The pathophysiological theories hypothesized to date, have clearly always recognised the contribution of two forebrain structures, the thalamus and the cerebral cortex, and their fundamental roles in the generation of seizures. However, many recent findings state that even when focusing on a particular network (e.g. the thalamus), different cellular (e.g. channels) as well as molecular dysfunctions can occur, which may lead to irregular brain rhythms and associated cognitive difficulties (Avoli,