Epileptic seizures involve intense, abnormal, synchronous neural firing in the corticothalamic system (Browne and Holmes, 2000; Coombes and Terry, 2012; Engel and Pedley, 1997; Hall and Kuhlmann, 2013; Jirsa et al., 2017; Kim et al., 2009; Kramer et al., 2012; Larter et al., 1999; Liley and Bojak, 2005; Lytton, 2008; Lytton et al., 2005; Penfield, 1933; Robinson et al., 2002; SalekHaddadi et al., 2006; Schiff, 2012; Velazquez et al., 2006; Wendling et al., 2005). Absence seizures are generalized epileptic seizures, most commonly observed in children (Crunelli and Leresche, 2002; Engel and Pedley, 1997; Proix et al., 2014; Suffczynski et al., 2004; 2005; Vercueil et al., 1998), which involve a sudden loss of consciousness, motionless stare, and cessation of ongoing activities (Browne and Holmes, 2000; Engel and Pedley, 1997; Panayiotopoulos, 1999). The majority of absence seizures last for 20 seconds or less (Panayiotopoulos, 1999). The characteristic hallmark of absence seizure is bilaterally synchronous “spike and wave” discharges (SWDs) with a frequency of 3–۴ Hz (Breakspear et al., 2006; Crunelli and Leresche, 2002; Jirsa et al., 2014; Marten et al., 2009; Panayiotopoulos, 1999; Proix et al., 2014; Lopes da Silva et al., 1997; Suffczynski et al., 2004; 2005; Vercueil et al., 1998; Zhao and Robinson, 2015). A number of authors have investigated the mechanism behind SWD generation (Breakspear et al., 2006; Crunelli and Leresche, 2002; Jirsa et al., 2014; Marten et al., 2009; Panayiotopoulos, 1999; Proix et al., 2014; Lopes da Silva et al., 1997; Suffczynski et al., 2004; 2005; Vercueil et al., 1998; Zhao and Robinson, 2015) by using both neural network (Crunelli and Leresche, 2002; Panayiotopoulos, 1999; Proix et al., 2014; Suffczynski et al., 2004; 2005; Vercueil et al., 1998) and neural field approaches (Breakspear et al., 2006; Marten et al., 2009; Zhao and Robinson, 2015). It is widely considered that the transitions from healthy states to spike-wave discharges occur upon changing corticothalamic connectivity strengths, e.g., increasing excitatory connections between the cortex and the thalamus (Breakspear, 2017; Breakspear et al., 2006; Chen et al., 2014; Destexhe, 1999; Dhamala et al., 2004; Guye et al., 2006; Kim and Robinson, 2007; Luo et al., 2012; Marten et al., 2009; Meeren et al., 2002; Roberts and Robinson, 2008; Robinson et al., 2002; Rodrigues et al., 2009; Tan et al., 2007; Ullah et al., 2015; Wallace et al., 2001; Zhao and Robinson, 2015). Thalamic involvement in the SW generation is also supported by in vivo studies (Andrew, 1991; Prevett et al., 1995; Seidenbecher et al., 1998; Steriade et al., 1998; Steriade and Contreras, 1998; Vergnes and Marescaux, 1992; Voss et al., 2009; Williams, 1953). Many modeling studies have been done to find the underlying corticothalamic mechanisms of absence seizures (Breakspear et al., 2006; Chen et al., 2014; Marten et al., 2009; Roberts and Robinson, 2008; Robinson et al., 2002; Rodrigues et al., 2009; Yang and Robinson, 2017; Zhao and Robinson, 2015), as well as oscillatory activity during the pre-ictal to ictal transition in the cortex and the thalamus (Berényi et al., 2012; Godlevsky et al., 2006; Liley et al., 1999; van Luijtelaar et al., 2016; Wendling, 2008). However, the impact of underlying parameter changes on the onset and dynamics has not been studied in detail. The possible physiological reasons behind the variation of the amplitudes of the oscillations with time (Breakspear et al., 2006), which are seen in the clinical EEGs like Breakspear et al., are also needed to be explored. In this study, we apply a widely used neural field model of the corticothalamic system (Breakspear et al., 2006; Kim and Robinson, 2007; Marten et al., 2009; Roberts and Robinson, 2008; Robinson, 2006; Robinson et al., 2002; 2004; Zhao and Robinson, 2015).