Research suggest that damages to the frontal and prefrontal cortexes account for the deviant characteristics and behaviours found in individuals with BPD (Burnner et al., 2010; Ruocco, 2005; Soloff et al., 2003).
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Orbitofrontal CortexThe primary role of the OFC lies in decision-making, and regulation of emotions and behaviour (Soloff et al., 2003). Hence, one’s social behaviours are influenced by the OFC (Kringelbach & Rolls, 2004). In BPD studies, both reduced activation (Minzenberg, Fan, New, Tang, & Siever, 2007) and grey matter volume has been observed in the OFC (Burnner et al., 2010). In Soloff, Meltzer, Greer, Constantine, and Kelly’s (2000) study, BPD subjects had high levels of emotional lability, thus, leading to irascibility. Lastly, reduced OFC activation accounts for exhibition of improper behaviours during social interactions in BPD (Soloff et al.
, 2000). Prefrontal cortexThe PFC provides signals to other brain structures, exhibiting top-down control on the hippocampus and amygdala (Miller & Cohen, 2001). Similar to the OFC, BPD subjects are observed to have lower activation as compared to healthy subjects (Silbersweig et al., 2007). Consequently, BPD subjects have difficulties refraining from impulsive behaviours. Another study by Ruocco et al. (2010) derived at findings that BPD subjects had dull and slower hemodynamic oxygenated response (i.
e. oxygenated blood flow to the PFC) when tasked to suppress negative emotions. This indicates that BPD subjects had troubles with controlling negative emotions. With regard to the PFC volume, Brunner at al. (2010) observed a decrease in PFC grey matter volume among BPD subjects, resulting in impaired modulation of negatively valanced emotions. Additionally, Korzekwa, Dell, and Pain (2009) posited that neural death in the PFC places the individual at greater susceptibility to stress.
Lastly, the PFC monitors amygdala activation to prevent amygdala hyperactivity (Korzekwa, Dell, & Pain, 2009; Perez et al., 2016; Mitchell, Dickens, & Picchioni, 2014). However, in BPD patients, the PFC is unable to downregulate amygdala activity due to irregularities in the neural circuitry connecting the PFC to the amygdala (New et al., 2007).
This leads to an exaggerated perception of threat to neutral or mild stimuli (Dell’Osso, Berlin, Serati, & Altamura, 2010). Next, the limbic system, specifically the amygdala, ACC, and hippocampus, is suggested to play a role in the onset of BPD (Nunes et al., 2009). Brunner et al. (2010) observed that hyperactivation in the limbic system was associated to disorganized affect. Furthermore, brain imaging scans indicate reduced white and grey matter volume in the limbic systems (Niedtfeld et al., 2013; Nunes et al.
, 2009). AmygdalaResearch suggest that the role of the amygdala entails the memory of negatively valanced emotions, particularly fear (Korfine & Hooley, 2000), modulating emotions and response towards stimuli (Perez et al., 2016). Overall, there is a growing consensus that BPD is characterised by increased amygdala activation (Cullen et al., 2011; Hazlett et al., 2012; O’Neill & Frodl, 2012).
In response to negatively valenced visual stimuli, heightened amygdala activity was recorded in BPD subjects as compared to healthy subjects (Kamphausen et al., 2013; Minzenberg et al., 2007). This hyperactivity in the amygdala leads to aberrant social-emotional processing in BPD (Mier et al., 2012). Furthermore, Korfine and Hooley’s study (2000) conducted a free-recall task using positive, neutral, and negative words.
Participants were tasked to remember or forget presented words. Results indicated that BPD subjects had better recall for negative words as compared to healthy subjects, even after receiving instructions to forget. Hence, negative stimuli are conspicuous to BPD subjects. Conversely, mixed findings were gathered with regard to volume changes in the amygdala in BPD. Several studies found a reduced amygdala volume in BPD (Nunes et al., 2009).
Driessen et al. (2000) found that the amygdala in BPD subjects were 8% smaller than in healthy subjects. Similarly, van Elst et al. (2003) found a 24% decrease in amygdala volume in comparison to healthy subjects. However, findings from Minzenberg et al. (2008) proposed that BPD subjects had larger grey matter amygdala volume in comparison to healthy subjects. On the other hand, BPD subjects in Zetzsche et al.’s study (2006) had no significant differences in amygdala volume.
Several reasons might explain the varied findings. Firstly, BPD patients often have comorbid disorders (i. e. Major Depressive Disorder (MDD), Post-Traumatic Stress Disorder (PTSD) Bipolar Disorder, and Epilepsy) which are also associated with altered amygdala volume (Nunes et al., 2009).
For instance, Zetzsche et al. (2006) found increased amygdala volumes only in BPD subjects with MDD, but not BPD subjects without MDD. Similarly, Driessen et al. (2004) observed no amygdala activation in BPD individuals without PTSD, while BPD individuals with PTSD experienced decreased amygdala activation. These results align with Nunes et al.’s stand (2009) that comorbidity illnesses may account for discrepant findings in BPD studies. In addition, discrepant findings can be attributed to the type of medication taken by each participant, subjects’ head tilts, or different image resolution of the brain scans used in studies (Lis, Greenfield, Henry, Guilé, & Dougherty, 2007).
Also, changes in brain matter is suggested to occur up to 20 years of age (O’Neill & Frodl, 2012). Next, research also indicate that aggression and anxiety in BPD surface due to the decrease functional connectivity from the amygdala to the ACC (Banks, Eddy, Angstadt, Nathan, & Phan, 2007; Cullen et al., 2011). ACC is also one of the brain structures involved in BPD.