From Child Abuse to Developing Borderline Personality Disorder Into Adulthood: Exploring the Neuromorphological and Epigenetic Pathway

Borderline personality disorder (BPD) is one of the most common personality disorders seen in the general population. Among multiple identified risk factors, one of the most influential elements is exposure to an adverse childhood experience in terms of emotional, physical, or sexual abuse. A cascade of neuromorphological and epigenetic changes occurs in response to these childhood stressors, which may have a strong link to the development of BPD. PubMed and Google Scholar were searched for articles relevant to child abuse and the development of BPD. The search was not restricted to any time frame or geographic location. Significant epigenetic and neuromorphological changes are seen with child abuse, contributing to the development of BPD. Chronic stressors lead to hypothalamic-pituitary axis (HPA) activation, releasing cortisol that acts on the prefrontal cortex, amygdala, and hippocampus, producing the behavioral patterns seen in BPD. Overstimulation of gray matter leads to permanent neuromorphological changes, which can be visualized in functional MRI/brain scans. Hypermethylation of messenger ribonucleic acid in various sites suggests the impact of child abuse on the genetic level. Interestingly, the prevalence of BPD is seen equally in both genders but is diagnosed more frequently in females because they tend to be more likely to seek help. Understanding the impact of early age life stressors into adulthood calls for serious focus on early diagnosis and intervention. This implies the need for more studies in patients with BPD with or without any childhood traumatic experience and a better understanding of the changes that occur biopsychologically and genetically in response to trauma.