ACC is important in response suppression, emotional and cognitive modulation (Perez et al., 2016; Wingenfeld et al., 2010). Inhibition of ACC activity, as indicated by low blood flow, was commonly seen in BPD subjects as compared to healthy subjects (Goodman et al., 2011; Juengling et al., 2003). Reduced activation was observed when processing facial expressions of fear (Minzenberg et al., 2007) or when responding to negative emotional words in a Stroop task (Wingenfeld et al., 2009). Additionally, studies also found reduction in the grey and white matter in ACC among BPD subjects (Goodman et al., 2011; Whittle et al., 2009). Aberrance in the ACC was associated to impulsive behaviours (Whittle et al., 2009) and suicidal tendencies (Goodman et al., 2011).
Lastly, Rüsch et al. (2010) observed disrupted interhemispheric connectivity between both dorsal ACCs among BPD subjects. This accounts for the compromised cognitive and emotion processing in BPD.
The central role of the hippocampus involves memory, that is required to encode, consolidate, and retrieve information (Perez et al., 2016). Hence, the hippocampus plays a role in the construction of new memories, also known as learning (Haaland, Esperaas, & Landrø, 2009). Next, neural death in the hippocampus is associated to enhanced susceptibility to stress (Korzekwa et al., 2009; O’Neill & Frodl, 2012), and aggression (Perez et al., 2016). A 14% and 23% decrease in hippocampal volume was found in studies by Schmahl, Vermetten, Elzinga, and Bremner (2003) and Brambilla et al. (2004) respectively.
On the contrary, Haaland et al. (2009) found that BPD patients did not suffer any verbal learning and memory impairments, in which, these functions involve the hippocampus. Hence, they questioned the involvement of hippocampus in BPD as found in other studies.
In summary, there have been extensive literature suggesting fronto-limbic involvement in the onset of BPD. Abnormalities in brain structures have been examined to gain a better understanding of the brain structures involved in the onset of BPD. Overall, BPD subjects are observed to exhibit decreased activation in the OFC, PFC, amygdala, and ACC. Furthermore, reduced volume were observed in the OFC, PFC, and ACC. On the other hand, mixed findings were found with regard to volume alterations in the amygdala and hippocampus. This paper is limited to its focus on the neuropsychology aspect of BPD, hence, it is essential to not overlook the importance of neurochemistry, and environment in the development of BPD.