Developmental Profile of Borderline Personality Disorder

Bivariate Analysis of Risk Factors influential to BPD
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This chart displays a few of the significant risk factors to developing BPD to be further discussed within![4]

As depicted throughout the previous sections of this Neurowiki, Borderline Personality Disorder presents with extreme intensities in emotional states. These patients have challenges with interpersonal relationships, react impulsively, and demonstrate behaviors that are detrimental to themselves, and often times to their loved ones[1]. Crucial to finding a way to best help these patients, however, is first considering the development of this disorder. To the extent that they can, researchers have been studying adolescents who present with symptomatic resemblance to BPD, or those who have actually been recently diagnosed with BPD. Due to a wide array of conflicting evidence, a true developmental profile for the disease is difficult to depict, particularly in terms of the neuroanatomical background of this disorder. In today’s research, brain imaging techniques such as MRIs and fMRIs (fMRIs only really completed on adults)[2] among several other techniques have been extremely popular in understanding of this disorder, and have identified various volume abnormalities, several of which seem to be somewhat contradictory of one another[1]. Hyper and hypoactivity of various limbic – as well as a number of other neuroanatomical structures – structures, volume variations within structures, and much more will be discussed to depict the neuro-development of this disorder. Further, current research additionally indicates that the development of this disorder does not cease at a neurological cause. Genetic associations and environmental influences perhaps occurring throughout childhood largely contribute to the onset of this disorder[3]. The first step to finding the ideal cause, and ultimately treatment, of this disorder is to understand its development, and here will be presented a wide array of research completed to provide an accurate and detailed account of said development of BPD as recognized by researchers today.

1.1 Genetic Predisposition

The first step in identifying what may lead to the unfortunate development of borderline personality disorder is considering the fundamental genetic background. While an extensive review of the genetic basis has been completed in the previous section, in terms of the development of this disorder goes, undoubtedly there remains some sort of genetic component to this disease. As of late, none of this research has been confirmed to be a direct, unifying cause, but the evidence does clearly suggest a high correlation between a genetic counterpart to the development of BPD. Torgerson studied BPD with the use of twin studies, and set the stage for genetic development in one of his monozygotic twin studies that ultimately indicated BPD had a hereditary factor of .69, or in other words, a 69% likelihood that the person would inherit the disorder[4]. Beyond just twin studies, investigators have further identified a few potential genetic markers responsible for the development of this disorder: most prominent of these is the 5-HTT gene region[5]. Literature recognizes that BPD patients have some sort of serotonergic pathway abnormality, and in accordance with this the 5-HTT gene, which regulates a serotonin 2A receptor[5]. Ni and colleagues identified two definitive factors isolating the abnormality in the gene: repeats of the VNTR marker and obtaining the S-10 (Short Allele) form of the gene, as opposed to the L-10 (Long Allele)[5]. These genetic results have been replicated in several other studies, and are a large contributor to the development of BPD. Genetic predispositions alone, however, are not substantial in causing the true development of BPD.

1.2 Adolescence

Given that this disorder predominantly arises throughout adolescence and young adulthood[2], a focus on childhood development is crucial in gaining a full perspective on what may trigger the onset of BPD. Several researchers as such have devoted their efforts to understanding influences of childhood traumatic events, parenting styles, and particular risk factors associated with BPD development [6][7][8][9].

1.2.1 Childhood Trauma

One of the most significant common denominators among BPD patients is the occurrence of some sort of childhood traumatic event[2]. Childhood marks the point in life where a child is most plastic, and inarguably learns the most about themselves, about others, and understands the world in a way that guides them in their development through adulthood[6]. It is throughout childhood, therefore, that external factors have the largest influence on what children may believe, and how their personalities will develop –the origin of personality disorders is therefore centered around childhood, with BPD being no exception. Puberty is accompanied by a large fluctuation in hormone levels, which inevitably makes the child susceptible to more permanent negative implications should some sort of trauma occur[6]. When studying adolescents, Newnham and Janca found that should some sort of traumatic event or adversity occur throughout childhood, the patient’s risk of developing BPD dramatically increases[6]. These traumas, such as childhood sexual abuse, give rise to not as permanent symptoms such as unstable emotional regulations, increased discussion of suicides, and lack of impulse control[6]. Additionally and even more concerning to the development of BPD is the more permanent negative affect that develops, as well as a permanent detriments to social and vocational functioning[6]. Childhood trauma additionally has such a profound effect on a person’s ability to regulate their emotions that those at risk for BPD may additionally develop a very clingy personality in a need to have reassurance in their interpersonal relationships[7]. They undergo the potential of gaining substance abuse troubles, developing an eating disorder, may develop anger in their interpersonal relationships and various dissociative episodes, all characteristic and that indicate a potential development of BPD[7]. The development of these traits due to the occurrence of a traumatic childhood event had been demonstrated to increase likelihood of the onset of BPD[7].

1.2.2 Parental Influences

Beyond just a childhood sexual misconduct, research additionally suggests that specific types of parenting styles contribute to the development of BPD. A study that provided data over an extended duration of time indicated the correspondence between parental involvement in childhood and the development of a child[8]. This was clearly indicated in the fact that from the ages of roughly 14-17, females generally retained similar attributes and did not experience a drastic developmental alteration, likely because the child is gaining more independence at this point in time, and parents may tend to back off[8]. One study looks at the bidirectional effects of parenting, specifically at enforcing particularly harsh punishment, and not exhibiting warmth and love towards children in females[8]. Results did suggest that in addition to just having a negative influence on their personality and increasing negative affect, these poor parenting techniques did indeed promote the development of BPD in females throughout the ages of 14-17, in other words it influenced the time of onset, but not the ultimate intensity of the disorder[8]. Previous research has likewise indicated that precursors to BPD include the child’s own characteristics – if the child has a negative temperament, is high in impulsivity, and has difficulty regulating his emotions, there is a high likelihood of the onset of BPD[8]. Research supports that therefore furthering studies on parental patterns may help clarify temporal information about the development of BPD.

Multivariate Analysis of Risk Factors influential to BPD
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After completing a second round of statistical analysis, Stepp and colleagues found that two main risk factors (located above) were the most influential in causing BPD. The occurrence of either of these will increase the levels of shame in a patient 10% and 31% more than what it should be, ultimately largely impacting the onset of BPD[8]

1.2.3 Risk Factors

New research has been aimed at identifying potential risk factors of BPD, as distinguishing concrete causes of the disorder could lead to earlier treatment and prevention. As such, consider the following 16-year longitudinal study published early in March for their identification of four risk factors associated with the development of BPD[9]. This study isolated the course of the affective symptom “shame” over a series of 16 years, composed of eight 2-year follow ups, and found several peculiar results[9]. First, keep in mind that the benefits to this type of longitudinal study have been monumental as they are valuable not only for determining the type of onset of the disorder, but also in developing predictions as far as the length of recovery time for BPD[10]. Following traits and development of affective states over a long period of time reveals internalized characteristics that can help identify the course of a disorder. In looking specifically at the beginning of the disorder, however, researchers found that in shame – one of the characteristics of borderline personality disorder – there were four positively correlated risk factors to the onset of BPD: “severity of childhood sexual abuse,” “severity of childhood verbal, emotional and/or physical abuse,” “severity of childhood neglect,” and “severity of adult adversity”[9]. These were determined under a bivariate analysis, but when accounting for multiple variables, only the two following remained significant risk factors for development of BPD: “severity of childhood sexual abuse” and “severity of childhood neglect”, resulting for the patient in a 10% and 31% increase in shame respectively[9].

1.3 Neurological Development

In identifying the neuroanatomy of BPD, especially in adolescents so as to determine the onset of the disorder, most research is confined to strictly MRI neuroimaging studies; the following however presents information from an EEG recording, which demonstrates actual brain functioning, not just volumetric analysis which will be discussed further later.

1.3.1 Event Related Potential in BPD

There have been significant findings that indicate an impulsivity of actions in adults with BPD[11], but this study is monumental and sets to provide and explanation as to the neurological functioning behind an adolescent onset of this disorder [12]. The P300 ERP is a positive inflection on an electroencephalograph reading where a positive amplitude suggests the brain designating resources to interpreting a rare event[12]. Ceballos and colleagues took the EEG recordings of 123 female adolescent girls between the ages of fourteen and nineteen, some who were likely to have BPD and some who were a healthy control comparison [12]. They hypothesized that females with the BPD affective symptoms would not have the normal response of a decreased positive amplitude (level of brain functioning) over time in response to the P300 ERP, indicating a lack of brain maturation in activity corresponding to impulsivity and negative affect compared to a healthy control group[12]. This type of response could additionally be demonstrated in an antisocial personality disorder group, with which another study compared adolescents with conduct disorder and borderline personality disorder in the same type of research setting[13]. Ultimately, results yielded a maturational abnormality in adolescent females who presented with signs of Borderline Personality Disorder compared to those who did not[13]. Segmenting into the section on brain physiological abnormalities, it is important to additionally note that these deficits in maturation was found specifically in the right frontal lobe of these adolescent patients, indicating some sort of potential biological predisposition to developing [12].
A follow up study expanded on this research, still focusing on the P300 inflection, but instead included a study of both female and male adolescents in both Conduct Disorder (the developmental precursor to Antisocial Personality Disorder) and Borderline Personality disorder[13]. Within the confines of this Neurowiki, the focus shall remain on the results pertinent to the development of BPD specifically. The normal maturational pattern of response at the P300 inflection is to over time decrease in amplitude (suggesting that a patient would in time react less impulsively to rare-events); any response that does not indicate this decrease would signify an abnormal brain development, and results in this study reinforce what was found in the first study in 2005 – that there are dysfunctional responses in BPD adolescents that indicate the development of the impulsivity patterns notorious for BPD[13]. This study identifies significant differences between male and female adolescents as follows: initial analyses of the data collected from the P300 ERP in the BPD patients seemed to be quite normal, which significantly contradicted the study just previously discussed[12][13]. Given the unexpected nature of this data, the researchers removed the male participants’ responses, and found that females analysis was consistent with the results indicated one year prior to – it seems that during adolescence in the P300 ERP, there may be a gender variation in neuronal development between early BPD patients[13]. Including the males skewed the results to make it seem that BPD had normal brain maturation, but in reality, males obtained normal response patterns to P300 while females did not, seemingly making females at a higher developmental risk for BPD than males[13]. This perhaps accounts for the reasoning that most developmental studies include solely females as participants – they may be more likely to present with Borderline Personality Disorder.

Inflection Amplitude (Y Axis) at P300 ERP (X Axis) Readings over time in BPD Adolescent (Male and Female)
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This chart is the graph of what was discussed in the subsection. Ceballos and colleagues completed a follow up study, recording P300 ERP amplitudes in male and female adolescents throughout their early life years. The bold line is the first recording, and the dotted line represents a recording taken years later throughout the end of adolescence. The data shown is what would be expected for any normally functioning young adult: The response to P300 should indeed decrease over time. The reason this graph is therefore so puzzling is that it did not reflect results they found from a study they completed on just female adolescents alone the year before. Female adolescents of the same age and demographic background one year prior to this study exhibited an abnormal maturation of brain functioning, and demonstrated no change in P300 amplitude throughout adulthood. The variation in results was attributed to the fact that there were male adolescents included in this sample - it seems they obtained a normal brain maturation in response to P300, while females did not. This reinforces genetic influences, and suggests specifically that there is a gender influence in BPD development [13]

1.3.2 Neuroanatomy in Adolescence

The neuroanatomical precursors responsible for the development of BPD are as of now still incredibly controversial[2]. Several neuroimaging studies have been completed employing various programs of analysis, and still there are many controversies as to which results are true and ultimately the most significant, because many studies seem to indicate different results. The reason adolescent neuroimagining is so invaluable is because it reveals the disorder, or symptoms leading to developing disorder, in terms of a neurological interpretation without any influence of treatment (whether that be a form of psychotherapy or pharmacotherapy)[14]. At this point in time, it is difficult to establish one unique profile of the neuroanatomy responsibly for BPD given the wide varying results obtained by different research groups, but here is provided a summary of some of the abnormalities observed.
In a 2008 study using MRI neuroimagine techniques employed the ANALYZE paradigm for data analysis in looking at part of the cortex and limbic system. They found in comparing just diagnosed BPD patients to healthy control patients no changes in the amygdala or hippocampus – which may seem slightly odd given the limbic system is associated with emotion, and BPD is characterized by a dysfunctional emotional regulation – but found a reduction of grey matter of the orbitofrontal cortex[15]. Alterations to the OFC seem to make sense because this is a brain region that does indeed help regulate emotion, some of the impulsivity challenges, sensitivity, etc[16]. However, the other key region to emotion seemed puzzling: they did find some volumetric differences in the limbic system counterparts, but did not find it to be a significant variation[15]. A more recent study found contrasting results. Still using MRI as the neuroimagining module, Richter and colleagues studies on the earliest presentations of borderline personality disorders in adolescent females, of clinical control groups (other psychologically impaired patients who did not have BPD), as well as in healthy controls (no mental health related deficiencies)[14]. They employed an analysis paradigm of FreeSurfer – which is said to be one of the most accurate programs of use this date compared to some older modules such as Voxel Based Morphometry (VBM) or Statistical Parameter Mapping 5 (SPM5) – and found that there was no significant in cortical thickness between BPD patients and others, but found a statistically significant increased size of the right amygdala in BPD, differences in the right and left hippocampus, and reductions in the right middle frontal gyrus, the orbital inferior frontal gyrus bilaterally, and the superior parietal gyrus bilaterally[14]. VBM was shown to previously confirm the 2008 revelation that there is a reduction in size of the left OFC, and even in the dorsolateral prefrontal cortex, but in this case did not show any limbic changes[14]. Other studies have additionally identified differences (again different studies revealing opposing volumetric findings) in the Anterior Cingulate Cortex of BPD patients compared to normal controls, and additionally have identified an abnormality within the natural Hypothalamic-Pituitary-Axis release of cortisol that could result in a maladaptive stress pattern to contribute to the onset of the disorder[2].
While there are many neurological conflicts, the results to these studies clearly indicate two significant findings: it seems the BPD is caused not by one unique brain region or function, but rather by abnormalities found widespread throughout various brain regions. These adolescent studies help provide an explanation of what the brain is like at the onset of the disorder, and as of now it still remains entirely unclear if these neurological abnormalities were present all throughout a child’s life from birth, or if because of various environmental influences such as a childhood trauma, perhaps combined with the genetic influence of the 5-HTT region, that could result in the brain regions malfunctions, and then the development of BPD. Regardless, these regions are highly correlated to the onset of BPD in adolescent patients, and help complete the developmental profile thus far.

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