Posted by: debatbpdsociety | September 3, 2014

University paper on BPD – by someone with BPD



APRIL 2014

The American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) (2000) lists the Axis 11 (personality disorders) diagnostic criteria for Borderline Personality Disorder (BPD) as follows (p.710):
A persuasive 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
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)
5 recurrent suicidal behaviour, gestures, or threats, or self-mutilating behaviour
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

The DSM-IV manual puts the prevalence of BPD at an estimated 2% of the general population, with 20% of all psychiatric inpatients having the diagnosis. Common co-occurring Axis 1(clinical disorders) disorders listed are Mood Disorders, Substance-Related Disorders, Eating Disorders (notably Bulimia), Post Traumatic Stress Disorder, Attention-Deficit/Hyperactivity Disorder, and other personality Disorders. These disorders co-exist with BPD at a rate of 96% with depression, 64% with anxiety disorders, 65% with post traumatic stress disorder, 64% with substance abuse or substance dependency, 39% with ADHD, and 53% with eating disorders (Fleischer, Schafer, Coogan, Habler, & Thome, 2012).
The DSM-IV manual suggests that this disorder is predominately (about 75%) in females and can start in adolescence, but is most commonly noticeable in early adulthood, with a familial occurrence five times more common among first-degree biological relatives. Epidemiological studies by Torgersen, Kringlen, and Cramer (2001) though, estimate that BPD affects male and females equally (as cited in Stepp, Pilkonis, Hipwell, Loeber, and Stouthamer-Loeber, 2010).
Choudhary & Thapa, (2013) report: “Common clinical features of BPD include frequent intense mood swings, the inability to be alone nor to tolerate intimacy, fears of abandonment, extreme dependency on others alternating with the sudden hostility, perceiving others as all good or all bad (“splitting”), chronic self-mutilation (often described as relieving emotional pain, and chronic suicidality. Suicide attempts serve to punish others, escape suffering, and communicate distress. These patients are argumentative, irritable, sarcastic, quick to take offence and very hard to live with” (p. 171).

Choudhary and Thapa (2013) go on list self-mulilization as one of the most discriminating signs of BPD, and that it can be difficult to help someone with borderline personality disorder (BPD). Therapist – patient relationships are subject to the same inappropriate and unrealistic demands, that a borderline puts on all of their significant, interpersonal relationships. Therefore, treatment failures and dropouts are common, with BPD patients showing the highest rate of therapy dropout, at 67% within the first three months.
It is believed that BPD decreases through age, by a reduction of impulsivity. Yet a certain level of symptoms continue into adulthood, “which might be attributable to a sustained level of affective symptoms, potentially leading to long term impairment of social and vocational functioning” (Arens,Stopsack, Spitzer, Appel, Dudeck, Volzke, Grabe, & Barnow, 2013, p.205). A longitudinal Study by Gunderson et al. (2011) showed that more than half the group had remission of symptoms over a ten year course, yet they continued to show severe and persistent social and vocational problems (as cited in Arens et al. 2013). Evidence suggests that BPD pathology is characterized by two distinct types of symptoms. The first, called impulsivity-type includes self-mutilization, suicide gestures, and impulsive acts. This type can resolve most quickly over time and improves quite rapidly. The second type, called affectivity-type has symptoms such as chronic feelings of emptiness, dysphoric states, and negative affectivity,was shown to resolve more slowly, with longer periods of cognitive and affective therapy needed (Arens et al., 2013).
This paper will explore some of the many theories surrounding the development of Borderline Personality Disorder, while looking at some of the unique features that many borderline patients exhibit. It will also present most of the treatment options available today, and provide a glimpse of possible future treatments.

Helgeland and Torgersen (2004) suggest that the development of borderline personality disorder, is a result of traumatic experiences in childhood, such as sexual or physical abuse, with histories of prolonged separation, or loss through parental divorce or illness. They described borderlines as “having been exposed to domineering, cold, and sadistic parental attitudes, and to emotionally neglecting, overprotective, and controlling parenting” (p.138). They feel that the excessive aggression that a borderline is known to exhibit, is either inborn or caused by frustration, parental hindrance for independence, or a parental lack of empathy.
When exploring the development of borderline personality disorder, most have come to believe that attachment issues between a child and their prominent caregiver, is at the heart of the disorder. “Attachment theory postulates that a threatened or frightened child will turn to an attachment figure for comfort, security, or reassurance. But if that attachment figure is itself the very source of the threat, the child is presented with an insoluble problem. No consistent behavioural strategy will relieve the threat” (Holmes, 2003).
British psychoanalyst John Bowlby (1969) conceptualizes attachment behaviours as those that “have a predictable outcome of maintaining proximity and contact with the other”( as cited in Baird, Veague,& Rabbitt, 2005, p. 1034). They go on to say that the bond that occurs from the proximity of the caregiver happens in the first year of life and represents safety and survival. A type of imprinting, if you will. This attachment guides the child’s behaviours, feelings and processing of social information, with a significant focus on affiliation.
Unfortunately though for the child, the caregiver that they have imprinted and relied upon, are usually also subjects of unresolved trauma or loss, which disrupts their capacity to focus on their care-giving role. They lack the capacity to provide buffering for their child’s emotional highs and lows, experiencing a type of dissociation from their immediate environment and insoluble fright or flight dilemma, which unfortunately the child is part of. This dissociation that happens not only applies to a distancing of the sufferer from their own psychological distress, but also a failure of a central integrative function associated with self, which causes the construction of a ‘false self’ based on compliance or control, in the child. And this of course leaves the child without a secure base of refuge, which is normally relied upon for life; leaving the child unable to self soothe when faced with emotional turmoil (Holmes, 2003).
Another facet considered in the development of borderline personality disorder comes from Fonagy and Luyten (2009), and concerns mentalization, which is a form of social cognition. Mentalization is defined as “the imaginative mental activity that enables us to perceive and interpret human behaviour in terms of intentional mental states (e.g., needs, desires, feelings, beliefs, and goals)” (p. 1357). Fonagy and Luyten (2009) suggest that disruptions of early attachment with later traumas, could fracture the capacity for mentalization, and in turn the development of a coherent self-structure. They postulate “that borderline personality functioning can be understood as the consequence of (a) the loss of mentalization in emotionally intense relationship contexts, (b) the reemergence at these times of modes of thinking about subjective experience that antedate full mentalization, and (c) the constant pressure for externalization of internal states (projective identification), which we conceive of as the re-externalization of disorganized intolerably painful self-states (the self-destructive alien self)” (p. 1357).
To investigate the development of borderline personality disorder, Carlson, Egeland, and Sroufe (2009) examined the development of the disorder from infancy to adulthood, using a longitudinal study with 162 participants. They confirmed that there is a significant link between borderline symptoms in adulthood, consisting of temperament, attachment disorganization, attention, emotion, behaviour, and relationships, with self-representation in middle childhood to early adolescence. They called BPD a “severe psychiatric disorder that is characterized by pervasive patterns of disturbance or instability across multiple domains of functioning” including behaviour, affect (emotion), cognition, attention, and relationship interaction (p. 1311). Manifesting as impulsivity, self destructive actions, suicide, fear of abandonment, emotional instability with inappropriate and intense anger, distorted thoughts and perceptions, dissociative experiences, and intense volatile relationships. “Specifically, the disorder and symptom spectrum have been associated with histories of prolonged childhood separations, caregiver emotional withdrawal, conflictual, distant or over-protective maternal relationships, failure of father presence, maltreatment (i.e., especially sexual abuse), ongoing family chaos and insensitivity, genetic vulnerabilities and other endogenous factors such as temperament and stress reactivity” (p. 1312). The childhood time line correlations that were discovered during the study, were cited as attachment disorganization (12 – 18 months) and maltreatment (12 – 18 months), maternal hostility and boundary dissolution (42 months), family disruption related to father presence (12 – 64 months), and family life stress (3 – 42 months).
Carlson et al. (2009) feels that disturbances within self-representation in early adolescence may mediate the pursuant personality disorder in adulthood, “with disturbances including self-injurious behaviour, dissociative symptoms, drug use and related relationship dysfunction, criminal activity, domestic violence, suicidal ideation, and histories of maltreatment and family disruption” (p. 1327). Stepp et al. (2010) insists that individuals exhibiting BPD features, were likely to experience poor outcomes in occupational, academic, and interpersonal situations. Baird et al. (2005) agrees by pointing out, that dealing with the borderline’s constant misunderstanding of seemingly innocuous events, rapid mood swings, and frequent cognitive distortions, makes maintaining a relationship with a borderline, a particularly daunting task.
Carlson et al. (2009) defined ‘self’ as the “inner organization of attitudes, feelings, expectations, and meanings with manifestation attention, behaviour and relationships” (p. 1313). Normal processes of organization and integration are compromised in BPD, by overwhelming traumatic and emotional experiences. Liotti (1992) suggests that when dysfunctional caregivers provide such unstable experiences, it evokes simultaneously conflicting needs, “resulting in multiple, incompatible emotional, attentional, and behavioural patterns, and expectations of self and others” (as cited in Carlson et al., 2009, p. 1314).
Herman (1992) and Putnam (1994 & 2006) insists that from having such much maltreatment at an early age, the child may come to expect important others to be unavailable or ineffective to their needs, during times of distress. Rendering the child “passive, isolated, and vulnerable to seeking sources of nurturance, regulation, and connection through external sources of stimulation, dissociative processes, and body manipulation rather than through more meaningful interpersonal interactions” (as cited in Carlson et al., 2009, p. 1314). Also making the child hyper-vigilant to the attitudes and intentions of others, which causes more problems with their own emerging self-awareness and sense of authorship to their own existence; causing a profound distortion or fragmentation in the self system. In turn, compromising emerging capacities in affect (emotion) regulation, impulse control, and arousal modulation. The child becomes hyper or hypo responsive to emotional stimuli, especially to emotions that signal threat or danger.
Lacking sufficient support from caregivers for the integration and mentalization of emotional experiences, the child learns to act rather than reflect. And unfortunately, as the child tries to illicit anyone to attend to their regulatory needs, they only end up appearing deviant, manipulative, and controlling. And with the inability to control their own behaviour, it causes their emotions to be manifested by frustration and anger, while attempting to control the feelings and behaviour of others around them. Fischer and Ayoub (1994) with Weston and Cohen (1992) suggest that for the child to preserve a semblance of safety and adult protection within the harsh care-giving relationship, the child may internalize a sense of self-criticism and hostility, and over time come to “regard the self as defective, unlovable, loathsome, or frightening” (as cited in Carlson et al., 2009, p. 1315).
Considering the negative emotions around the concept of self, it is no wonder that BPD patients have difficulty with self-regulation. A study by Bornovalova, Fishman, Strong, Kruglanski, and Lejuez (2007) hypothesizes that self-regulation plays an important role in the development, as well as the maintenance of borderline personality disorder. In their study, they examined the “relationship between the self-regulation constructs of locomotion (i.e., the ability to commit the mental and physical resources necessary for goal-directed action) and assessment (i.e., the ability to critically evaluate a given state in order to judge the quality as compared to alternatives) in BPD, at the level of diagnostic symptoms as well as the dimensional hallmark features of interpersonal sensitivity, aggression, and impulsivity” (p. 22).
The key role of self-regulation is described as the ability to govern or direct attention, resources, or actions toward a particular goal; something that is well known to be very difficult for someone with BPD. The results of their study suggest that poor self-regulation, which comes in the form of low locomotion and high assessment, could play a role in a number of the maladaptive, behavioural characteristics of BPD. Bornovalova et al. (2007) insist, “specifically, BPD may be well characterized by overly critical self-evaluation (high assessment) combined with the lack of productive goal-directed action following from this evaluation (low locomotion)” (p. 24).
Gratz, Tull, & Gunderson (2007) agrees with the general consensus that BPD is best understood through a diathesis-stress model, which presents itself as a combination of temperamental vulnerabilities, with the addition of distressing childhood experiences. They postulate though, that there is another temperamental risk factor that would increase the risk of developing BPD; namely anxiety sensitivity (AS). Which is not to be confused with trait anxiety, which deals with frequency and intensity of anxiety. Anxiety sensitivity (AS) is one’s own characteristic way of evaluating and responding to the experience of anxiety, a main trait of BPD. AS’s relationship to BPD is thought to be mediated by the vulnerability factor such as experiential avoidance, which includes attempts to avoid unwanted internal experiences, such as emotions, thoughts, and bodily sensations. AS sufferers attempt to avoid anxiety-related symptoms, which is similar to the heightened experiential avoidance tendencies of BPD. Grantz et al. (2007) believes this temperamental, emotional vulnerability of AS increases the risk of developing BPD, through its association with the increased use of avoidant emotion regulation strategies commonly used in BPD. It is the unwillingness to remain in contact with stressful situations while tolerating anxiety-related symptoms, that heightens the risk of developing BPD. “This tendency to try to reduce anxiety-related symptoms perceived as threatening by avoiding them entirely, is likely to be exacerbated by a lack of access to affective emotion regulation strategies – a characteristic thought to be central to BPD” (Grantz et al., 2007, p. 556).

Nigg, Silk, Stavro, and Miller (2005) proposed an alternative developmental route to borderline personality disorder, which they termed Primary Impulsivity. This route would “emanate from weakness in the executive response inhibition mechanisms, leading to extremes of impulsivity, inappropriate interpersonal relations, and a cascade of negative socialization experiences leading to personality disturbance” (p. 1145). It was thought that this route could originate in vulnerable genotypes, inadequate socialization, early perinatal or prenatal injury, or a combination of any of the above. Insufficient behavioural inhibition in BPD would be manifest by excessive fearlessness, and from failing to learn from punishment cues, “thus going on to carry out impulsive actions that are counter productive to them” (Nigg et al., 2005, p. 1137). This impulsive behaviour would be described as hasty, ill-considered responses in a context where careful responding would have been appropriate. Moeller et al. (2001) defines impulsivity as “a predisposition toward rapid, unplanned reactions to internal or external stimuli without regard to the negative consequences of these reactions to the impulsive individual or to others” (as cited in Svaldi, Philipsen, & Matthies, 2012, p. 114). Svaldi et al. (2012) adds to this concept by saying that as a consequence of impulsivity, patients with BPD would repeatedly engage in risky behaviour, primarily due to an altered feedback processing in their executive functions. From their study, Svaldi et al. (2012) found that the higher the frequency of risky decision making, the higher the levels of impulsivity, and the severity of the BPD symptoms. And even though the BPD sufferer usually knows the deleterious long-term consequences of their impulsive behaviours, they will still engage in them. This is now thought to be connected to the properties of readily available rewards (e.g., a reduction of immediate tension), and the borderline’s well known difficulties in delayed gratification.
Nigg et al. (2005) believes there would be a break down in various kinds of inhibition processes that help regulate behaviour. They point out that most etiological studies on impulsivity or disinhibition in BPD have emphasized the neurotransmitter level of analysis, putting an importance on serotonin. Posner et al. (2002, as cited in Nigg et al., 2005) is even more specific, when suggesting BPD is related to the breakdown of the anterior executive neural network, which is the same network involved in executive response inhibition. Mayes (2000, 2006) goes on to explain “that regulation of stress is a differential balance of excitation and inhibition involving multiple, interactive neural systems with different neurochemical substrates regulating specific and different aspects of prefrontal, posterior cortical, and subcortical functions” (as cited in Fonagy & Luyten, 2009, p. 1367). Fonagy and Luyten (2009) clarifies by adding that a neurochemical switch is associated with high levels of stress, and that patterns of brain functioning could shift from flexibility to automaticity, where slow executive functions are mediated by the prefrontal cortex to faster, habitual and instinctual behaviours mediated by the posterior cortical (e.g., parietal) and subcortical structures (e.g.,amygdala, hippocampus, and striatum). Amounting to an abnormal pattern of frontal deactivation with an associated hyper-responsiveness of the limbic system. BPD patients that have trauma history, show a reduction in pituitary size, elevated cerebrospinal levels of corticotropin releasing hormone, dysfunctions of cortisol responsivity, and disturbed dexamethasone suppression test response (Fonagy et al., 2009).
Transcranial magnetic stimulation tests of patients with BPD, reveal a significant reduction in cortical silent period in the right cortex, which is believed to be mediated by GABA receptors, the main inhibitory neurotransmitter. Additionally, higher activity in response to negative stimuli, was found in the amygdala, which also has high levels of GABA receptors. All being interpreted as a “neurodevelopmental deficit in the right hemisphere, that may have been caused by several traumatic life events” (Barnow, Volker, Moller, Freyberger, Spitzer, Grabe, & Daskalakis, 2008, p. 317).
Friedel (2004) backed up these findings through his study on dopamine dysfunction in BPD, when he found that stress induces release of dopamine in the nucleus accumbens, but more strongly in the medial prefrontal cortex. Resulting in increased activation of local GABA transmission in the prefrontal cortex, that ultimately inhibits the dopamine response of the nucleus accumbens, to stress. “Dopamine dysregulation in these neural circuits could result in an inappropriate balance of amygdala and prefrontal cortical activity in response to affect-inducing stimuli. A specific example of how this could operate in BPD is the conditioned fear response” (p. 1032). One could also expect affect-driven memory formation and recall.
MRI tests found two unique features in subjects with BPD. A decreased volume of the amygdala and hippocampus, and enhanced responses to emotionally charged visual stimuli in the medial and lateral orbital prefrontal cortex, as well as the amygdala. All while finding facial expressions to be eliciting greater activation in the left side of the amygdala. Neuroimaging proved that in BPD brain regions critical to cognitive activity, structural and functional changes could be seen, such as decreases in frontal lobe and hippocampal volumes, with additional changes in frontal lobe glucose metabolism (Friedel, 2004).
A study by De La Fuente, Goldman, Stanus, Vizuete, Morlan, Bobes, and Mendlewicz (1996) offered evidence for glucose metabolism dysfunction, finding metabolic cortical and subcortical disturbances in a sample of non medicated BPD patients. “Relative hypometabolism was found in the dorsolateral part of the frontal cortex, in the anterior congulate cortex, the basal ganglia, and the thalamus” (p. 536), confirming low glucose metabolism in brain tissue. This frontal hypometabolism might be a correlate of the characteristic reality distortion often presented by BPD patients, in the form of chronic feelings of de-personalization, unreality and impulsiveness. The writers go on to say, “moreover, the frontal cortex is the main source of input to midbrain serotoninergic neurons of the dorsal raphe nucleus (Mayberg et al., 1990), and serotonin system dysfunction is thought to be involved in the production of impulsiveness in BPD (Brown et al., 1982; Coccaro et al., 1989; Hollander et al., 1994). A diminished frontal metabolism could parallel impaired serotoninergic function and be therefore related to the impulsiveness” (as cited in De La Fuente et al., 1996, p. 537).
One more related issue with the limbic system lies in the anterior part of the cingulate gyrus, which has also been found to be hypometabolic in BPD patients. This area receives projections from higher-order sensory areas in order to project to other cortical areas, including the prefrontal cortex, which influences impulsiveness, as well. More importantly though, the anterior cingulate has been associated with pain representation, which is important in BPD, since the automutilation experienced may be related to a distinctive relationship to pain. It is postulated that the hypometabolic state in BPD is due in part by the altered endogenous opiate system, even though the anterior cingulate is rich in opiate receptors (De La Fuente, 1996).
Baird et al. (2005) report “anatomical investigations of patients with BPD have found relative reductions in gray matter volume in both the limbic and frontal systems of the brain”, with “reduced amygdalar and hippocamal volume” (p. 1043).
As a result of this brain dysfunction, a social storm is created manifesting as constant impulsive actions, cognitive sensitivity, hostility, an untrusting paranoid world view, and friend exclusivity, while leaving the patient with a painful intolerance to being alone, hypersensitive to their social environment, expecting hostility from others, having greatly reduced positive memories, and having a lower threshold for activation of the flight or fight systems (Fonagy et al., 2009).
Another significant predictor of the affective component of BPD has to do with hormones; particularly the weaker perinatal androgen action. Evardone, Alexander, and Morey’s (2007) study examined the hypothesis that prenatal hormones may influence the development of BPD traits, by measuring a marker of perinatal androgen action , the 2D:4D ratio (a phenotypic trait that appears sensitive to the degree of perinatal androgen action), and the salivary hormone levels in 58 men and 52 women. Their findings concluded that “weaker perinatal androgen action was associated with greater borderline symptoms overall, and greater affective instability” (p. 278). They also found that the greater the change in salivary estrodiol in women, the greater the affective instability. Suggesting that the ‘measures of hormonal change’ was much more significant to symptom ratings in women, rather than the absolute levels of circulating hormones. They speculate that the responsiveness of the hypothalamic-pituatary-axis to stress may be exaggerated in women with affective instability, and that they would experience more variability in gonadal steroid secretion in response to life’s stressors; with it ultimately causing greater disruption in reproductive function, as measured by cycle irregularity, abnormal luteal phase, and infertility (Evardone et al., 2007).
The last developmental consideration this paper will address, is the single genetic factor which is considered to underlie most of the variance in BPD symptoms. A multinational, large scale twin study implicated genetic influence on BPD features, while having a hereditary estimation of 42%. In this linkage analysis study, genotype and phenotype data from 1,032 offspring, and genoptype data from 561 parents were used. Distel, Hottenga, Trull, & Boomsma (2008) discovered that evidence for linkage was found on chromosomes 1, 4, 9, and 18, “with significant linkage “found on chromosome 9 near marker D9S286, with a LOD (logarithm of odds) score of 3.548 and a genome-wide empirical P value of 0.0001” (p.305). They have hopes that as we move forward, the knowledge of this genetic etiology of BPD, will have important implications in the future treatments.

Normal cognitive development is considered a progression from diffuse and undifferentiated states to those of more organized complexity, based on a “ transactional approach in which genetic, biological, and environmental forces influence each other and make reciprocal contributions to developmental outcomes (Judd, 2005, p. 1173). Within the matrix of attachment, developmental accomplishments continue to be shaped by environmental forces throughout one’s life. And these accomplishments are combined with new accomplishments to cause successive adaptations. Unfortunately for the child with borderline personality disorder, this development would be disrupted in infancy and persist throughout childhood and adolescence, if no modifying intervention prevailed. Through a cohort study of girls aged 6 – 12, Stepp et al. (2010) found that the core dimensions of BPD features, which are impulsivity, negative affectivity, and interpersonal aggression, could be reliably measured during those ages, which gave hope of early identification and progressive prevention.
As early as 1969, Anna Freud (1969) proposed that children exhibiting borderline symptoms would have massive developmental arrests, poor reality testing, and difficulty synthesizing information (as sited in Judd, 2005). Bemporad, Smith, Hanson,and Cicchetti (1982) identified organic impairment with social awkwardness, neurological soft signs and general unevenness in development, in these children (as cited in Judd, 2005), while having an impaired ability to process and integrate emotional and sensory-motor information, into adequate interpersonal memory systems. Leading to “various manifestations of cognitive issues, including denial, splitting, unusual beliefs, all or nothing (black / white) thinking, paranoia, transient psychoses, and illusory phenomena” (Judd, 2005, p. 1174). Leading to cognitive dysfunction in adulthood , characterized by having “unusual beliefs (e.g., superstitious, magical thinking, belief in a sixth sense, clairvoyance, or telepathy)”, dichotomous (black / white) thinking, overvalued ideas, unusual perceptions, severe dissociation, paranoia, and transient psychotic thought (Judd, 2005, p. 1190). In fact, the dysphoric, cognitive thought patterns that are uniquely associated to borderline personality disorder, reflect themes of paranoia and being tortured or abused (Baird et al., 2005).

Patients with borderline personality disorder often report suffering from subjective sleep disorders; especially insomnia, nightmares, and dream anxiety. Fleischer et al. (2012) believes that sleep disturbances, by way of an abnormal circadian rhythm, plays an critical role in the physiological path of BPD. The characteristics of circadian rhythm presents as an endogenously driven, circa 24 hour cycle in metabolic, endocrine and behavioural processes, such as the sleep – wake cycle. In BPD, it is believed that this circadian system may have an impact on a person’s affect (emotion). When analyzing the diurnal profile of salivary cortisol in female BPD patients, elevated cortisol response to waking was revealed, as well as an upregulation of cortisol levels. Furthermore, a study by Wingenfeld et al. (2007) indicates that the level of nocturnal cortisol is associated with the severity of the BPD psychopathology (as cited in Fleischer, 2012). In a cross-sectional study with 76 participants, the relationship between subjective sleep quality and borderline personality symptoms were examined. It was found that individuals with more severe borderline symptoms, have more difficulties with their sleep structure than people with less pronounced borderline symptoms. Furthermore, patients with BPD had more non-REM stage 4 sleep, with REM density being significantly higher in the first REM period. Notable was that through many awakenings, REM latency was shorter while sleep latency and time spent awake after sleep onset, was longer. Fleischer et al. (2012) concluded from their study that “the whole BPD group exhibited lower waking after sleep onset, lower total sleep time, lower percent sleep, and less stage 1 and stage 4 of total sleep” (p. 1107). And they suggest that there might be clinical merit in using light therapy and chronobiologically based interventions such as melatonin and agomelatine, to relieve these sleep disturbances in BPD.

Lynch, Rosenthal, Kosson, Cheavens, Lejuez, and Blair (2006) define facial expressions as “nonverbal communication cues that convey messages about emotional feelings, behavioural intentions, and action requests” (p. 647). As mentioned earlier, BPD patients show greater left amygdala activation to neutral, sad, fearful, and happy facial expressions, with some patients interpreting neutral expressions as negative or threatening. Lynch et al. (2006) discovered in their study on emotional expression sensitivity, that those with BPD were more accurate in correctly classifying emotional faces, even though they were presenting less affective information. They found that those with BPD were consistent in correctly identifying facial affect, earlier then the control group. In addition, the BPD group were found to be more sensitive to specific emotions, regardless of the valence of the expressed emotion. And more importantly they found contrary to the accepted belief, that those in the BPD group did not over identify anger in non anger trials, or identify more happiness in the non happiness trials. They concluded their study, by acknowledging that those with BPD were significantly more likely to correctly identify facial affect at an earlier stage, than the normal population. And that observing subtle changes in emotional expression could substantially contribute to the emotional volatility of these individuals. They go as far as to suggest that “emotional sensitivity in BPD individuals may be a core feature of the disorder” (p. 653).

Psychoanalyst Alan Krohn (1974) was first to identify that BPD individuals appear to possess an uncanny sensitivity to other people’s subconscious mental content” (as cited in Dinsdale & Crespi, 2013, p. 172). In the past, psychoanalytic accounts attributed borderline empathy to environmental causes. It was felt that as a result of neglectful parenting, the borderline’s empathy was developed to enhance sensitivity to subtle cues of the parent. And that social dysfunction would result from the disrupted ability to develop enduring and stable experiences, in response to perceiving and responding to subconscious drives, combined with a learned distrust of conscious behaviour. “Park et al. (1992) also attributed borderline empathy and its role in BPD development, to interacting biological and environmental factors. These researchers though, emphasized the positive aspects of enhanced empathic skills and referred to them as cognitive “gifts” involving the desire and ability to understand the the thoughts and feelings of others” (as cited in Dinsdale & Crespi, p. 187 – 188).
Dinsdale and Crespi reviewed 28 studies to “propose a new model for explaining the borderline empathic paradox: a combination of increased attention to social stimuli and dysfunctional social information processing, may account in part for the specific empathic enhancements and reduced overall social functioning in BPD” (p. 172). They believe that the BPD’s hypersensitivity to the social environment, “involves constant vigilance to anticipated rejection and difficulties in regulating emotion, due to low thresholds for stress-related activation of the attachment system and deactivation of controlled mentalization” (p. 188). And they are convinced that these highly sensitive and accurate inferences may exacerbate BPD symptoms, by enhancing emotional dysregulation and dysfunctional interactions.
Ripoll, Snyder, Steele, & Siever (2013) agrees that the empathic dysfunction in the borderline, contributes to interpersonal difficulties. They explain that in early childhood, empathy involves viceral recognition of mental states, by relying on neuronal representation of other peoples feelings, as they are experienced in them self; both experiencing and observing others experiencing mental states. A process that involves shared representations of mental states. Ripoll et al. (2013) proposes that the empathic symptoms in BPD may result from a neurobiological predisposition to persistent, excessively shared representation based attunement, with impairment in mental state attribution. Their tests showed that when someone with BPD evaluates interpersonal stimuli, they show amygdala hyper-reactivity, as well as a lack of habituation. They go on to “hypothesize that dynamic dysregulation of these networks, experienced as ongoing intrapsychic pain, may be mediated by aberrant neuropeptide signaling” (p. 7).
It is believed that with this genetic predisposition, attachment stressors may contribute to shared representation hyper-reactivity and mental state attribution impairment, neuropeptide dysregulation, painful attachment insecurity, and refractory symptoms” (p. 2). This interpersonal hypersensitivity may also affect perceptions of social threat, resulting in attunement and contagion without perspective. And unfortunately, “attachment insecurity, intrapsychic pain, and empathic dysfunction in BPD cause significant distress and disability, despite advances in evidence-based psychotherapy and psychopharmacology” (p. 8).
Daniel Goleman author of Emotional Intellegence sums it up so accurately when saying, “While emotional neglect seems to dull empathy, there is a paradoxical result from intense, sustained emotional abuse, including cruel, sadistic threats, humiliations, and plain meanness. Children who endure such abuse can become hyper alert to the emotions of those around them, in what amounts to a post-traumatic vigilance to cues that have signalled threat. Such an obsessive preoccupation with the feelings of others is typical of psychologically abused children who in adulthood suffer the mercurial, intense emotional ups and downs that are sometimes diagnosed as “borderline personality disorder” (p. 102).

Fonagy and Luyten (2009) highlight, many patients with BPD can only feel that they are loved, if someone is also physically touching them.
When reviewing multiple literature concerning BPD and sexual behaviour, Sansone and Sansone (2011) discovered other authors emphasizing a phenomenon connected to BPD called “pansexuality”, which is an all embracing sexuality, that encompasses promiscuity, “polymorphous perverse sexual practices” and heterosexual/homosexual vacillation (p. 15). Additionally, they found that more than 25% of borderline outpatients exhibit some sort of promiscuity, with many experiencing date rape and younger sexual experiences. They were also more likely to engage in high risk sexual practices, such as not using condoms. Sansone and Sansone (2011) viewed these reactions in BPD sufferers as another result of impulsivity when they wrote, “generally, impulsivity appears to be represented by greater sexual preoccupation, earlier sexual relationships, a greater number of different sexual partners, promiscuity, and homosexual experiences, whereas victimization appears to be represented by a greater number of high-risk sexual behaviours; a greater likelihood of being coerced to have sex, date rape, and/or rape by a stranger; and a high number of sexually transmitted disease” (p. 16).

Treatment for borderline personality disorder includes a mixture of individual sessions, group therapy, family therapy, and psychopharmacology.

Dialectical Behaviour Therapy (DBT)
DBT is an adaptation of cognitive behavioural therapy, designed to target mood instability and impulsive behaviours, while emphasizing empathic responses to distress, and providing validation for the patient’s inner experience (Paris, 2005). Choudhary and Thapa (2013) explains that DBT therapy gives the borderline patient self confidence and coping tools for life outside of treatment. Giving the patient skills such as social skills training, mood awareness and meditative exercises, while providing education on the BPD anomaly, itself.
Gratz et al. (2007) insists that BPD patients with anxiety sensitivity, benefit from “mindful-based interventions that teach them to observe and describe their emotions and thoughts, noticing each internal experience as it occurs in the moment (without trying to push it away or get rid of it) and labelling their emotions and thoughts objectively (i.e., describing an emotion as just an emotion and a thought as just a thought). Teaching BPD patients both to allow thoughts to enter and then leave their mind (without attaching to, reacting to, or acting on these thoughts), and to label thoughts as just thoughts may help reduce the tendency to “buy into” catastrophic thoughts as literally true” (p. 436).

Psychodynamic Therapies – as reported by Paris (2005)
Mentalization-based therapy, tries to teach BPD patients to mentalize, which means to stand outside of their feelings and accurately observe emotions in themselves and others.
Transference-focused psychotherapy, aims to correct distortions in the patient’s perception of significant others and of the therapist.

PHARMACOTHERAPY IN BPD – as reported by Olabi and Hall (2010)
Selective serotonin reuptake inhibitors (SSRIs) have been widely used in the treatment of BPD. In reality though, the only antidepressant to have a positive effect on the symptoms of BPD, outside of major depressive episodes, is Amitriptyline, a tricyclic antidepressant.

*Mood Stabilizers and Anticonvulsants
Cabamazepine is used to decrease impulsivity.
Lithium, Topiramate, Lamotrigine, and Valproate Semiodium is used for mood improvement.

*Antipsychotic Medications
Olanzapine is used to reduce impulsivity, hostility, affective instability, and psychotic symptoms.
Aripiprazole and Haloperidol are used for symptoms of anger.

*Future Prospectives – as reported by Olabi &Hall (2010)
Since brain opioids play an important role in behaviour, such as isolation and exclusion, the future use of opioid antagonists is under investigation. As is Vasopressin antagonists for the use in depression and aggression.
“Future studies may also consider GABA neurotransmission and its importance in the etiology of BPD. The deficiency of GABA receptors might be associated with the clinical phenomenon of an enlarged intolerance against benzodiazepines in BPD patients” (Barnow et al., 2009, p. 317).
And finally, Fonagy and Luyten (2009) argue that a therapeutic intervention that “focuses on the patient’s capacity to mentalize in the context of attachment relationships, can be helpful in improving both behavioural and affective aspects of the condition” (p. 1358).

Continued diligence to find better treatments for borderline personality disorder is imperative. Not only because it is an all encompassing disorder with devastating implications, such as 69 – 75 % of patients having self-injurious behaviours, but also because borderline personality carries between 3 and 9.5% rate of completed suicides . A rate 400 times greater than the general public (Levy, 2005).
Helgeland and Torgersen (2004) present an interesting observation when they write, “according to Millon (2000), the socioculturally amorphous and chaotic state of modern Western society characterized by increased pace of social changes, technological development, urbanization, mobility, migration, and growing dissolution of the traditional family structure and values, deprives children of the stability of life that is so necessary for acquisition of a consistent pattern of feeling and thinking, and may cause “an increase in intrapsychic diffusion and splintering” which is typical of borderline functioning” (p.142 – 143). This writer agrees, if society continues to undermine the importance of family, we are sure to see a continual increase in the numbers of those exhibiting borderline personality disorder.

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This paper means something to me because I was diagnosed with borderline personality disorder about 15 years ago. I endure all of the symptoms that this paper talks about, and more. But fortunately, because I am a fighter like my mother, I fought to find really good cognitive treatments. I was so fortunate to receive the Dialectical behavioural therapy (DBT) when I did, because I was at a beneficial age to want to absorb it.
One aspect about my personality that does not mesh with everything written about borderline though, is that I was born with the gift of dance. I literally danced before I was able to walk. I danced incessantly, and in true borderline fashion, I had no balance and was driven by the dance. I used to tell people I was afraid that my dance was going to kill me like the girl in the movie ‘The Red Shoes’.
The dance gave me an internal escape from my mental anguish, and solace for many years; until there was too much drama, too long for my body to handle, and it started shutting down. For me in particular, the thyroid system was most affected. At least, this is what I thought until writing this paper.
I have refused the normal psychotrophic pills and stuck to natural preventatives. Exercise and diet with vitamins and minerals, plus herbs; concentrating on stress reduction. While I was in Dialectical treatment for the borderline, I was diagnosed with an extreme case of post traumatic stress disorder (PTSD), as a result of having so much trauma throughout my life. To name only a few: I have been molested by my own brother, who committed suicide over it many years later; raped by my first boyfriends father; married and divorced three times; first husband committed suicide from his schizophrenia, kicked out of AA, and pushed away at one time or another, by everyone I know. I now understand why it happened and even why my loved ones felt the way they did, at the time. After all, I was enraged and lashing out so many times in my life. And even though it wasn’t my fault, it wasn’t their fault either. I wouldn’t have wanted to be around my rage, if I was them, either.
But I do wonder how much sooner I could have healed, if I had actually had proper support from others when I was younger; if someone had stuck it out with me. To feel valuable enough for someone to put up with me, and look over my indiscretions.
I now feel I am supported by my family, and fortunately I am blessed with a true friend who has tried to stick by me throughout the years. But I can still feel their own type of PTSD towards me. Waiting and fearful I will go back to destroying myself with drugs and alcohol, or afraid I will start screaming at any minute. Triggering their PTSD symptoms just with my presence, similar to a Pavlov’s response.
I now believe though, that because I know how I am affecting them, I can change the reaction my loved ones give to me. I need to be patient and continue to strive for lasting, self-loving changes. Hopefully then, my loved ones can begin to heal, as I feel I am actively doing.
Neither one of my children have borderline personality disorder, yet they both have similar reactions in times of really bad stress. Thank heavens, they are not wrapped in the blanket of borderline, like I am though. Both have a type of post traumatic stress when they are around me. Like the kind I used to feel around my mother. Even though I never beat on my kids, I did scream excessively, and made so many situations way more stressful than necessary. Nothing was ever good enough. I even belittled and made fun of my children from time to time.
I didn’t find out that I had BPD until both my children were in their late teens. The funny thing is though, I know my children dearly love me. They genuinely respect and honour me, for the changes I have been able to make over the last decade; but it still doesn’t take their PTSD away, when they are around me. I used to believe that they didn’t love me, because they don’t seem to want to spend any time with me, unless necessary. Which they do lovingly and happily, but I can feel their agitation. After writing this paper though, it no longer hurts me. I understand their reaction to me. I know it will change given enough time; enough time with me not stressing them out. I have also figured out why they are not borderline and why it did not get absorbed into them. See, even though I was an angry person sometimes, I was also a very happy person, who loved my kids and cooked and cleaned happily. We danced and sang and laughed. Not all the time, but enough. I didn’t allow addictions around my kids either, until they were much older. But the clincher on why they didn’t become borderline is because when they had their normal crazed period, like every teen goes through, I fought to keep them with me. I fought to not leave each other. With my son, I fought to keep him with me, but it didn’t work and he went anyway. He went to live my mother, which he apologized for, years later. My daughter on the other hand, stayed. We worked it out and didn’t abandon each other. I fought her, my mom, her friends, her boyfriend, the school, the cops, and even child welfare, but I won to keep my daughter with me. I knew if I let her go, she would feel like I do. Abandoned! And then she would lose her ‘self’.
When I was growing up, my mother told me many times, that my father didn’t want me. That he had run around telling everyone that I was not his. And then when it came to my crazy, hormonal, teen time, she pushed me out. She beat me with her fists, and I couldn’t hit her back; she was my mom – you don’t hit your mom. It’s just wrong on so many levels. And in all fairness to her, it was the only beating my mother ever gave me. But I had experienced her wrath many times via my brothers, as I am exceedingly empathic; and she beat them mercilessly. When she was done beating me that day though, she told me to get my stuff ready because I was going somewhere, and she didn’t care where, and then left me there at my aunt’s. She came back the next day and had the money for me to go. I left BC and went back to the States….
My mother was cruel. Even though she didn’t practice voodoo, she once made a voodoo doll for my grand father and told him he would die on a certain day, hoping to give him a heart attack. Mind you, this was the very same man who had raped her in her late teens. I forgive my mother for the things that she was, because she was abandoned by her family; alone, scared, hurt, and enraged. But she was also fun and adventurous, taking us fishing or exploring many weekends. She showed me the true meaning of strength and how not wallow in your own pity. My mom had no one in life. Her mother stayed with the man that had raped her and then threw her out of the house. Mom’s saving grace was an aunt that took her in. The rest of the family tortured her emotionally and ostracized her, and every man treated her as if she was worthless. The reason I admire and love my mom so much though, is that over the years she has made a great effort to change her personality and better herself. Yes my mother still has borderline personality and she still has enduring habits especially towards me, but she has mellowed through age and continues to adjust her personality, the best she can. I am proud of her for over coming so much horror, to turn into such a loving person.
I do still feel abandoned though. I think it is because I don’t have someone to belong to. I am the person who should not be alone, as all the information on BPD says, it is not good for my psyche. Yet I have been alone, except for my heavenly father, for almost 15 years! Yes I have time with friends and family, but very little; I am physically alone most of the time. I have adapted but I am not really ok with it. I won’t be ok until I find a man to belong to. And I have full faith that that will come soon enough. My emotional growth is ready now. I believe I could now be in a relationship and not push them away, or scream constantly. I have learned so much from school about normal growth and development from so many angles, that I have grown leaps and bounds inside. Differently than the rest of the people. I have gained a sense of self, that I didn’t have before. I have become a friend to myself, because there is a self to be a friend to; a person as important as everyone around me. I now have true compassion for myself. I am no longer a bad person in my own mind. I truly feel like a caterpillar morphing into a butterfly. I feel amazing things all around me. The sky is the limit…
Thank you Les for making me write this paper, it truly changed my life. And I think you can see that every time you look into my eyes lately… Thank you with all my heart.

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