The topic of Borderline Personality Disorder has been researched extensively from a clinical disorder standpoint though there are clear underlying neuroanatomical, neurophysiological, and biochemical substates. The paper will present a definition of Borderline Personality Disorder and its epidemiology. Next, neuropsychological models of borderline personality disorder will be discussed. This will be followed by neuropsychological assessment and neurodiagnostic findings will be presented. Lastly, information on prognostic factors and treatment approaches will be discussed.
Definition & Epidemiology
The term ‘borderline personality’ was first proposed by Adolph Stern in 1938 of which he described as “a group of patients who fit frankly neither into the psychotic nor into the psychoneurotic group” (British Psychological Society, 2009). Later in 1975, Otto Kernberg introduced the term ‘borderline personality organization’ to indicate a pattern of behaviors best described as ‘instability’ regarding psychological functioning (British Psychological Society, 2009). According to Kernberg, borderline personality reflects a group of symptoms that manifest as variability or rapid changes in which a person experiences shifts in moods, feelings of abandonment, poor self-image, and many times, intense feelings of despair that triggers thoughts of self-harm. For many individuals that endure the personality disorder, psychotic symptoms, delusions, and hallucinatory experiences may occur (Pines, 1977). In the current psychiatric diagnostic manual (DSM 5), borderline personality disorder, is defined as a ‘pervasive pattern of instability of interpersonal relationships, self-image, and affects, and marked impulsivity, beginning by early adulthood and present in a variety of contexts, as indicated by five or more of the following:
1. Frantic efforts to avoid real or imagined abandonment. (Note: Do not include suicidal or self-mutilating behavior covered in Criterion 5.)
2. A pattern of unstable and intense interpersonal relationships characterized by alternating between extremes of idealization and devaluation.
3. Identity disturbance: markedly and persistently unstable self-image or sense of self.
4. Impulsivity in at least two areas that are potentially self-damaging (e.g., spending, sex, substance abuse, reckless driving, binge eating). (Note: Do not include suicidal or self-mutilating behavior covered in Criterion 5.)
5. Recurrent suicidal behavior, gestures, or threats, or self-mutilating behavior.
6. Affective instability due to a marked reactivity of mood (e.g., intense episodic dysphoria, irritability, or anxiety usually lasting a few hours and only rarely more than a few days).
7. Chronic feelings of emptiness.
8. Inappropriate, intense anger or difficulty controlling anger (e.g., frequent displays of temper, constant anger, recurrent physical fights).
9. Transient, stress-related paranoid ideation or severe dissociative symptoms.
While the course of borderline personality disorder fluctuates and many individuals may receive a diagnosis till much later in life, it is found that most people exhibit symptoms in late adolescence or early adult life (Álvarez-Tomás, et al., 2018). In community samples, borderline personality disorder has been found to have a 1.7% prevalence (Ten Have. Et al., 2016). Furthermore, borderline personality has a prevalence that is like other psychiatric disorders, such as schizophrenia or bipolar disorder though lower than major depressive or anxiety disorders. In contrast, its prevalence in clinical settings is much higher and ranges from 6.5%–42.7% with inpatient and between 8%-18% prevalence of all psychiatric outpatients. For clinical settings, there is a three times higher incidence in females than in males while a more even prevalence is observed in community samples.
Neuropsychological Models of Borderline Personality Disorder
There is an extensive amount of research that has been invested on borderline personality disorder as a clinical disorder, and how the condition has a direct implications with regards to environmental factors (Barnow, et al., 2010). For example, attachment theory has proposed that attachment styles are the primary or central issue with borderline personality disorder. (Lansky, 2003; Agrawal, et al., 2004). However, other research has given focus to the neuroanatomy and neuropsychological findings of the condition in an attempt to better understand how borderline personality disorder is manifested in the brain. In general, executive neurocognitive regions are implicated with borderline personality disorder. Imaging studies have consistently implicated the prefrontal and fronto-limbic regions of the brain, which are implicated in the regulation of emotion, impulsive behavior, and executive cognitive functions (Soloff, et al., 2012). The prefrontal cortex and more specifically, the anterior cingulate and orbitofrontal regions are heavily implicated in the regulation of aggression (Soloff, et al., 2012). Other prefrontal regions implicate the dorsolateral prefrontal regions and have also been associated with aggression and impulsivity (Anderson et al 1999).
The cingulate cortex which is known to be associated with emotional regulation, attention, behavior inhibition, and motivation is located in the inner wall of each hemisphere of the brain and lies above and adjacent to the corpus callosum. In a general sense, the cingulate cortex plays an important role in the regulation of emotions. However, within the cingulate cortex, the anterior cingulate limbic channel lies in a strategic place in the brain and has connections to both the emotional limbic system and the cognitive prefrontal cortex (Rolls, 2019). It is therefore evident that it plays, an important role in the neuronal circuitry for affect regulation. However, different components within the anterior cingulate cortex (pregenual portion and subgenual portions) are activated differently. For instance, simple emotions activate the anterior cingulate cortex, with the pre-gen anterior cingulate cortex being more responsive to happiness whereas the subgenual anterior cingulate cortex being more responsive to sadness. As it pertains to borderline personality disorder, the left subgenual anterior cingulate cortex may be more implicated to emotional and conflict regulation. Fear inhibition is associated within subgenual anterior cingulate cortex. However, the pregenual portion of the anterior cingulate cortex is also implicated in emotional regulation. As previously stated, the anterior cingulate limbic channel receives information from the anterior cingulate and from the temporal cortices, and more specifically, the amygdala and hippocampus.
Within the frontal lobe, prefrontal regulatory regions are involved in borderline personality disorder. In general, the orbitofrontal cortex has been consistently found to be heavily implicated with disinhibition which may manifest as being hyperactive, intrusive, and exhibiting pressured behavior (British Psychological Society, 2009). Furthermore, the orbitofrontal lobe is also associated with poor impulse control and as it pertains to borderline personality disorder, may be visible as having poor social insight and poor social awareness. Emotional lability or poor emotional regulation, and difficulties in being able to focus attention away from certain stimuli is characteristic of the disorder is therefore correlated with orbitofrontal dysfunction.
Other prefrontal regulatory regions of the frontal lobe implicate the dorsal lateral prefrontal cortex which is associated with impulsivity though a different study found an inverse correlation with aggressiveness. Similarly, the ventrolateral prefrontal cortex is associated with response inhibition and goal-appropriate response selection has also been found to be correlated with aggression (Aron, Robbins, & Poldrack, 2004). cortex is correlated with aggression.
Neuropsychological Assessment Findings
Patients that are conflicted with the condition of borderline personality disorder exhibit highly elevated executive dysfunction. According to Ruocco (2005), the most significant deficits fall under cognitive planning. Specifically, poor self-regulation in borderline personality disorder manifests as increased impulsivity, suicidal and self-destructive behaviors (Scheichel, 2007). In one study, 60% of participants with borderline personality disorder exhibited clinically significant struggles with sustained attention (Lazzaratti, 2012). Researchers used the N-Back Test, which measures working memory, and the Conners Performance Test, used to assess attention related problems and found that subjects diagnosed with borderline personality disorder performed more poorly on the N-Back Test though not necessarily on the Conners Performance Test (Lazzaratti, 2012). It is concluded that deficits in working memory may be due to impulsivity associated to the dorsolateral prefrontal cortex. Despite inconsistencies in the research literature on the effects on sustained attention in people with borderline personality disorder, Lazzaratti (2012) found clear differences in performance with sustained attention. However, sustained attention deficits may be more closely tied to impulsivity which is linked to the dorsolateral prefrontal cortex.
In contrast, Krause-Utz (2012) found that working memory disruptions are closely associated with emotional distracting stimuli which may be due to a higher activation of the amygdala while experiencing a decrease in activation in the dorsolateral prefrontal cortex. In addition, patients diagnosed with borderline personality disorder exhibited longer reaction times with performance tasks while also exhibiting higher activation of the amygdala. Because of higher activation of limbic systems, particularly the amygdala, patients diagnosed with the condition were found to exhibit working memory deficits.
It is apparent that memory impairment is characteristic of borderline personality disorder and such deficits are apparent in neuropsychological. Verbal and visual memory are found to be a part of general executive dysfunction characteristic of the condition. Regarding verbal memory, Kurtz, and Morey (1999) studied patients with major depressive disorder and borderline personality disorder. The study found that patients with borderline personality disorder performed worse when assessing recall and recognition memory when compared to control subjects. Even when compared to patients with major depressive disorder, patients with borderline personality disorder were less accurate with recognition verbal memory when compared to patients with the depressive disorder. However, the findings are inconsistent with other studies that were not able to find convincing evidence of verbal memory deficits in neuropsychological findings. For instance, there is evidence of executive functions deficits in the domains of nonverbal executive function and nonverbal memory though found minimal evidence of deficits in the areas of verbal fluency and verbal working memory. A separate study by Seres et al.,( 2009) corroborated with these findings. Studies confirming deficits in visual memory have been found to be somewhat more consistent than verbal memory. A reason for the differences between the findings may rest on the well-established understanding that borderline personality disorder is a condition that implicates the right hemisphere (Seres et al., 2009). In fact, a meta-analysis study found that 71% of the studies that were reviewed found a higher incidence of right hemispheric visual memory impairments (Gvirts, 2012). Such deficits uncovered with neuropsychological tasks used to assess visual memory, are also present in visuospatial abilities tasks, and visual tasks used to assess executive functions. (Beblo, et al., 2014). In a different study designed to predict treatment outcomes using neuropsychological performance for patients with borderline personality disorder, it was found that patients that performed better with visual memory tasks engaged the longest in treatment (Fertuck, et al., 2006).
Neurodiagnostic Findings
Borderline personality disorder is associated with structural abnormalities across various brain regions, with major neuropathological differences within the prefrontal and fronto-limbic regions (Gan, 2016). Such regions are involved in the regulation of emotion, impulsivity, executive functions, and episodic memory.
Within the fronto-limbic region, imaging findings have consistently found decreased gray matter volumes in the middle-inferior orbital frontal cortex, in addition to decreased dorsolateral and ventrolateral prefrontal cortex gray matter volumes. Other regions not part of the prefrontal cortex though connected, include the anterior and posterior cingulate cortex, amygdala, hippocampus, and insula.
While borderline personality disorder is attributed to right hemispheric deficits and implicate frontal and temporal lobe dysfunctions (Seres et al., 2009), reductions in gray matter are found to be bilateral gray matter concentrations are apparent in the ventral cingulate gyrus, and other regions of the medial temporal lobe that include the hippocampus, amygdala, parahippocampal gyrus, and uncus Soloff, 2012), with the amygdala and hippocampus been the most consistent with magnetic resonance imaging studies.
The amygdala, which can be seen as a primary mediator of emotional information processing (Gan, et al., 2016), in addition to the hippocampus which plays a role in cognition, have been found to have decreased gray mater volumes. Furthermore, the insular cortex which is a component of the limbic area and has connections to various brain regions that include the prefrontal and orbital cortex, and limbic structures and is found to playing an important role in emotional functioning and cognitive functions such as decision-making has been found to have diminished grey matter (LeGris, et al., 2006). However, the structural differences are more visible in patients with borderline personality disorder that have been found to be more susceptible to suicidality when compared to patients with the condition that are not prone to suicidality (Soloff, et al., 2012).
Imaging studies have found neuropathological differences in the left orbitofrontal cortex. Specifically, reduced volumes in this region are closely associated to impulsivity dysregulation, irritability, and emotional instability, and mood disorders, as it relates to borderline personality disorder (Schmahl and Bremner, 2006).
The etiology of borderline personality disorder is complex and there tends to be a high correlation with childhood sexual or physical abuse with many patients. Long term exposure to neglect or over strict parenting styles have also been found to be characteristic of the disorder. Studies on borderline personality disorder, particularly with childhood abuse found reduced right hippocampal volumes when compared to control subjects (Sala, et al., 2011). The structural differences were found to be inversely correlated with aggressiveness. Such inverse correlations were also found between a reduction in the dorsolateral prefrontal cortex and impulsivity (Sala, et al., 2011). The right ventrolateral prefrontal cortex has been found to be remarkably decreased in gray matter and more particularly in patients with borderline personality with a history of childhood trauma. The same study also found the ventrolateral prefrontal cortex to be with implicated with aggression. Imaging of patients with high susceptibility to committing suicide were also found to exhibit diminished gray matter in the left and right insula. Those most prone to self-harm further exhibited notable decreased gray matter in the right mid-superior temporal gyrus, right mid-inferior, orbitofrontal gyrus, left fusiform gyrus, left lingual gyrus, and right hippocampal gyrus when compared to patients with the disorder less susceptible to suicidality (Soloff, et al., 2012).
White matter changes have also been identified in intralimbic regions, such as the fornix and interhemispheric connectivity such as the corpus callosum in (Rolls, 2019). The findings may suggest a reduction in fiber density and low directional coherence. The fornix is of significance due to the connectivity within the limbic system and therefore plays a fundamental role in the coordination of emotional processing and is also implicated with impulse control (Gan, et al., 2016). It can then be concluded that such white matter decreases may be related to the impulsivity component of borderline personality disorder due to the deficits in interhemispheric connectivity, in combination with prefrontal deficits.
In addition to the structural differences observed with MRI imaging studies, positron emission tomography (PET) studies reveal consistent decreases in metabolic functions in the prefrontal cortex. Specific areas include the orbital frontal and the ventromedial cortex. Metabolic decreases have also been found in the cingulate gyrus and in the temporal lobe (Schmahl & Bremner, 2006).
Prognostic factors
Borderline personality disorder is a debilitating condition that is difficult to treat due to the elevated emotional dysregulation that is characteristic of the disorder. Unfortunately, many patients fail to become fully committed to therapeutic treatment, both psychotherapy and medication management. In addition to this, mental health professionals eventually become frustrated with the minimal progress with patients with the condition (Dixon-Gordon, 2011). It is found that short to medium term treatment outcomes for borderline personality disorder have a poor prognosis (Stoffers, et al., 2011).
However, recent studies indicate that the long-term prognosis in borderline personality disorder has improved and is overall better, further suggesting that most patients do improve over time (Álvarez-Tomás, et al., 2018). In an older study found that 53 percent of patients that were followed up for a span of seven years no longer met the diagnostic criteria for the condition. Researchers also found that two thirds of patients treated in a psychiatric hospital were clinically well. In another long term 5-year study outside of the United States found that patients diagnosed with borderline personality disorder exhibited significant symptom improvement (Álvarez-Tomás, et al., 2018). However, it is noteworthy to state that various predictors of long-term prognosis have been identified to influence the outcomes. Such factors include demographic characteristics, childhood trauma, life stressors, treatment compliance, severity of comorbidities, personality traits, and psychosocial functioning.
Treatment Factors
It is well established in the literature and in clinical settings that pharmacotherapeutic interventions are beneficial in the treatment of borderline personality disorder (Stoffers, et al., 2010). However, treatment outcomes with regards to this intervention approach are variable as many factors come into play and include the severity of the disorder, the prominent symptoms for each patient, or each patient’s body/metabolic response to medication. Such factors have a direct influence over the effectiveness of treatment. As previously stated, borderline personality disorder is characterized by the symptoms, avoidance of abandonment, interpersonal problems, identity disturbance, impulsivity, suicidal ideation, suicidal behavior, self-mutilating behavior, affective instability, anger, psychotic symptoms, dissociation, and secondary symptoms that include depression and anxiety. A study of several clinical trials found that first and second-generation antipsychotics are beneficial to address the severity of the disorder. However, no benefits were uncovered with such medication treatments for other characteristics such as avoidance of abandonment. Antidepressants and first-generation antipsychotics offer benefits for impulsivity while first generation antipsychotics helped to address suicidal behavior. It is evident that while pharmacotherapy is beneficial to address the different dimensions of the disorder, the disorder is highly complex and certain characteristics such as a sense of abandonment, feelings of emptiness, identity issues, and dissociation, are not significantly improved with medication. Such findings only confirm that not all symptoms are treatable with medication, and thus concluding that other treatments such as psychotherapy can render good treatment outcomes (Stoffers, et al., 2010).
Psychotherapy has been found to be an effective therapeutic approach in the treatment of borderline personality disorder. Among different personality disorders, the cluster B personality disorders have been researched the most extensive and may be due to the highly elevated emotional dysregulation and impulsiveness that is found within this cluster (Winston, 2000). Five treatment approaches have been found to be effective and classified as evidence-based treatment approaches for the treatment of the disorder. The therapeutic approach that has been found to be the most used in psychotherapy for the condition is dialectical behavior therapy. The therapeutic approach is a form of cognitive behavior therapy and emphasizes a balance of validation and acceptance of the patient, while implementing behavioral changes. Tranference-focused psychotherapy gives emphasis to improving a patient’s ability to properly perceive and respond to interpersonal relationships through the use of the therapeutic relationship. Mentalization based therapy has also been found to be an effective tool in the treatment of borderline personality disorder. The approach has a component of attachment theory and gives focus to the patient’s difficulties with fully understanding how their thought processes and emotions have a direct impact on their behaviors. Lastly, schema focused therapy addresses maladaptive cognitive schemas that have been formed, primarily, during early development, with the use of cognitive behavior therapy approaches.
Conclusion
Borderline Personality Disorder is a complex condition that is characterized by several symptoms that include, avoidance of abandonment, interpersonal problems, identity disturbance, impulsivity, suicidal ideation, suicidal behavior, self-mutilating behavior, affective instability, anger, psychotic symptoms, dissociation, and secondary symptoms of depression and anxiety. There is extensive research that establishes the direct correlation of specific brain regions, primarily in the prefrontal cortex and limbic system are highly implicated to the disorder. There is a significant decrease of gray and white matter in various brain structures and such deficits are implicated with the main characteristics of the disorder that include aggression, impulsivity, and depression. Furthermore, neurodiagnostic findings reveal notable cognitive deficits in the form of executive dysfunction, memory deficits, and disinhibition. While the condition is complex and highly impairing for many patients, the prognosis can be favorable for long term treatment that is composed of pharmacotherapy and psychotherapy.
References:
Agrawal, H. R., Gunderson, J., Holmes, B. M., & Lyons-Ruth, K. (2004). Attachment studies with borderline patients: A Review. Harvard Review of Psychiatry, 12(2), 94–104.
Álvarez-Tomás, I., Ruiz, J., Guilera, G., & Bados, A. (2018). Long-term clinical and functional course of borderline personality disorder: A meta-analysis of prospective studies. European Psychiatry, 56(1), 75–83.
Aron, A. R., Robbins, T. W., & Poldrack, R. A. (2004). Inhibition and the right inferior frontal cortex. Trends in Cognitive Sciences, 8(4), 170–177.
Barnow, S., Arens, E. A., Sieswerda, S., Dinu-Biringer, R., Spitzer, C., & Lang, S. (2010). Borderline personality disorder and psychosis: A Review. Current Psychiatry Reports, 12(3), 186–195.
Beblo, T., Mensebach, C., Wingenfeld, K., Rullkoetter, N., Schlosser, N., & Driessen, M. (2014). Subjective memory complaints and memory performance in patients with borderline personality disorder. BMC Psychiatry, 14(1).
British Psychological Society. (2009). Borderline personality disorder: Treatment and management.
Dixon-Gordon, Katherine L., et al. “Psychotherapy for Personality Disorders.” International Review of Psychiatry, vol. 23, no. 3, 2011, pp. 282–302.
Fertuck, E. A., Lenzenweger, M. F., Clarkin, J. F., Hoermann, S., & Stanley, B. (2006). Executive neurocognition, memory systems, and borderline personality disorder. Clinical Psychology Review, 26(3), 346–375.
Gan, J., Yi, J., Zhong, M., Cao, X., Jin, X., Liu, W., & Zhu, X. (2016). Abnormal white matter structural connectivity in treatment-naïve young adults with borderline personality disorder. Acta Psychiatrica Scandinavica, 134(6), 494–503.
Gvirts, H. Z., Harari, H., Braw, Y., Shefet, D., Shamay-Tsoory, S. G., & Levkovitz, Y. (2012). Executive functioning among patients with borderline personality disorder (BPD) and their relatives. Journal of Affective Disorders, 143(1-3), 261–264.
Krause-Utz, A., Oei, N. Y., Niedtfeld, I., Bohus, M., Spinhoven, P., Schmahl, C., & Elzinga, B. M. (2012).
Kurtz, J. E., & Morey, L. C. (1999). Journal of Psychopathology and Behavioral Assessment, 21(2), 141–156.
Lansky, M. R. (2003). Discussion of Peter Fonagy et al.'s “the developmental roots of borderline personality disorder in early attachment relationships: A theory and some evidence.” Psychoanalytic Inquiry, 23(3), 460–472.
LeGris, J., & van Reekum, R. (2006). The neuropsychological correlates of borderline personality disorder and suicidal behaviour. The Canadian Journal of Psychiatry, 51(3), 131–142.
Levy, K. N., Yeomans, F. E., Denning, F., & Fertuck, E. A. (2010). UK National Institute for Clinical Excellence Guidelines for the treatment of borderline personality disorder. Personality and Mental Health, 4(1), 54–58.
Lazzaretti, M., Morandotti, N., Sala, M., Isola, M., Frangou, S., De Vidovich, G., Marraffini, E., Gambini, F., Barale, F., Zappoli, F., Caverzasi, E., & Brambilla, P. (2012). Impaired working memory and normal sustained attention in borderline personality disorder. Acta Neuropsychiatrica, 24(6), 349–355.
Mak, A. D. P., & Lam, L. C. W. (2013). Neurocognitive profiles of people with borderline personality disorder. Current Opinion in Psychiatry, 26(1), 90–96.
Pines, M. (1977). Borderline conditions and pathological narcissism. by Otto Kernberg. New York: Jason Aronson. 1975. PP 361. British Journal of Psychiatry, 131(2), 212–213.
Rolls, E. T. (2019). The cingulate cortex and limbic systems for action, emotion, and memory. Cingulate Cortex, 23–37.
Ruocco, A. C. (2005). The neuropsychology of borderline personality disorder: A meta-analysis and Review. Psychiatry Research, 137(3), 191–202.
Sala, M., Caverzasi, E., Lazzaretti, M., Morandotti, N., De Vidovich, G., Marraffini, E., Gambini, F., Isola, M., De Bona, M., Rambaldelli, G., d'Allio, G., Barale, F., Zappoli, F., & Brambilla, P. (2011). Dorsolateral prefrontal cortex and hippocampus sustain impulsivity and aggressiveness in borderline personality disorder. Journal of Affective Disorders, 131(1-3), 417–421.
Schmahl & Bremner. (2006). Neuroimaging in borderline personality disorder. Journal of Psychiatric Research, 40(5), 419–427.
Schmeichel, B. J. (2007). Attention control, memory updating, and emotion regulation temporarily reduce the capacity for executive control. Journal of Experimental Psychology: General, 136(2), 241–255.
Seres, I., Unoka, Z., Bódi, N., Áspán, N., & Kéri, S. (2009). The neuropsychology of borderline personality disorder: Relationship with clinical dimensions and comparison with other personality disorders. Journal of Personality Disorders, 23(6), 555–562.
Soloff, P. H., Pruitt, P., Sharma, M., Radwan, J., White, R., & Diwadkar, V. A. (2012). Structural brain abnormalities and suicidal behavior in borderline personality disorder. Journal of Psychiatric Research, 46(4), 516–525.
Stoffers, J., Völlm, B. A., Rücker, G., Timmer, A., Huband, N., & Lieb, K. (2010). Pharmacological interventions for borderline personality disorder. Cochrane Database of Systematic Reviews.
ten Have, M., Verheul, R., Kaasenbrood, A., van Dorsselaer, S., Tuithof, M., Kleinjan, M., & de Graaf, R. (2016). Prevalence rates of borderline personality disorder symptoms: A study based on the Netherlands Mental Health Survey and incidence study 2. BMC Psychiatry, 16(1).
Winston, A. P. (2000). Recent developments in borderline personality disorder. Advances in Psychiatric Treatment, 6(3), 211–217.
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