ПРЛ - Причины
As is the case with other mental disorders, the causes of BPD are complex and not fully agreed upon. Evidence suggests that BPD and post-traumatic stress disorder (PTSD) may be related in some way. Most researchers agree that a history of childhood trauma can be a contributing factor, but less attention has historically been paid to investigating the causal roles played by congenital brain abnormalities, genetics, neurobiological factors, and environmental factors other than trauma. Social factors include how people interact in their early development with their family, friends, and other children. Psychological factors include the individual's personality and temperament, shaped by his or her environment and learned coping skills that deal with stress. These different factors together suggest that there are multiple factors that may contribute to the disorder.
The heritability of BPD is estimated to be 65%. That is, 65 percent of the variability in liability underlying BPD in the population can be explained by genetic differences. (Note that this is different from saying that 65 percent of BPD is "caused" by genes.) Twin studies may overestimate the effect of genes on variability in personality disorders due to the complicating factor of a shared family environment.
Families with twins in the Netherlands were participants of an ongoing study by Trull and colleagues, in which 711 pairs of siblings and 561 parents were examined to identify the location of genetic traits that influenced the development of BPD. Research collaborators found that genetic material on chromosome nine was linked to BPD features. Studies conclude that 42 percent of variation in BPD features was attributable to genetic influences and 58 percent was attributable to environmental influences.
Genes currently under investigation include the 7-repeat polymorphism of the dopamine D4 receptor (DRD4), which has been linked to disorganized attachment, whilst the combined effect of the 7-repeat polymorphism and the 10/10 dopamine transporter (DAT) genotype has been linked to abnormalities in inhibitory control, both noted features of BPD.
A number of neuroimaging studies in BPD have reported findings of reductions in regions of the brain involved in the regulation of stress responses and emotion, affecting the hippocampus, the orbitofrontal cortex, and the amygdala, amongst other areas. A smaller number of studies have used magnetic resonance spectroscopy to explore changes in the concentrations of neurometabolites in certain brain regions of BPD patients, looking specifically at neurometabolites such as N-acetylaspartate, creatine, glutamate-related compounds, and choline-containing compounds.
The amygdalas are smaller and more active in people with BPD. Decreased amygdala volume has also been found in people with obsessive-compulsive disorder. One study has found unusually strong activity in the left amygdalas of people with BPD when they experience and view displays of negative emotions.Since the amygdalas generate all emotions (including "negative" ones), this unusually strong activity may explain the unusual strength and longevity of fear, sadness, anger, and shame experienced by people with BPD, as well as their heightened sensitivity to displays of these emotions in others.
The prefrontal cortex tends to be less active in people with BPD, especially when recalling memories of abandonment. This relative inactivity occurs in the rightanterior cingulate (areas 24 and 32). Given its role in regulating emotional arousal, the relative inactivity of the prefrontal cortex might explain the difficulties people with BPD experience in regulating their emotions and responses to stress.
The hypothalamic-pituitary-adrenal axis (HPA axis) regulates cortisol production, which is released in response to stress. Cortisol production tends to be elevated in people with BPD, indicating a hyperactive HPA axis in these individuals. This causes them to experience a greater biological stress response, which might explain their greater vulnerability to irritability. Since traumatic events can increase cortisol production and HPA axis activity, one possibility is that the prevalence of higher than average activity in the HPA axis of people with BPD may simply be a reflection of the higher than average prevalence of traumatic childhood and maturational events among people with BPD. Another possibility is that, by heightening their sensitivity to stressful events, increased cortisol production may predispose those with BPD to experience stressful childhood and maturational events as traumatic.
Increased cortisol production is also associated with an increased risk of suicidal behavior.
Individual differences in women's estrogen cycles may be related to the expression of BPD symptoms in female patients. A 2003 study found that women's BPD symptoms were predicted by changes in estrogen levels throughout their menstrual cycles, an effect that remained significant when the results were controlled for a general increase in negative affect.
Symptoms experienced due to disturbed levels of estrogen are often misdiagnosed as BPD, like extreme mood swings and depression. As endometriosis is an estrogen responsive disease, severe PMS and PMDD symptoms are observed, that are both physical and psychological in nature. Hormone-responsive mood disorders also known as reproductive depression are seen to cease only after menopause or hysterectomy. Psychotic episodes treated with estrogen in women with BPD show considerable improvement but must not be prescribed to those with endometriosis as it worsens their endocrine condition. Mood-stabilizing drugs used for bipolar disorder do not help patients with disturbed estrogen levels. A correct diagnosis between an endocrine disorder and a psychiatric disorder must be made.
There is a strong correlation between child abuse, especially child sexual abuse, and development of BPD. Many individuals with BPD report a history of abuse and neglect as young children. Patients with BPD have been found to be significantly more likely to report having been verbally, emotionally, physically, or sexually abused by caregivers of either gender. They also report a high incidence of incest and loss of caregivers in early childhood.
Individuals with BPD were also likely to report having caregivers of all sexes deny the validity of their thoughts and feelings. Caregivers were also reported to have failed to provide needed protection and to have neglected their child's physical care. Parents of all sexes were typically reported to have withdrawn from the child emotionally and to have treated the child inconsistently. Additionally, women with BPD who reported a previous history of neglect by a female caregiver and abuse by a male caregiver were significantly more likely to experience sexual abuse by a non-caregiver.
However, none of these studies provide evidence that childhood trauma necessarily causes or contributes to causing BPD. Rather, both the trauma and the BPD could be caused by a third factor. For example, it could be that many caregivers who tend to expose children to traumatic experiences do so partly because of their own heritable personality disorders, the genetic predisposition for which they may pass on to their children, who develop BPD as a result of that predisposition and other factors, and not as a result of prior mistreatment.
Other developmental factors
The intensity and reactivity of a person's negative affectivity, or tendency to feel negative emotions, predicts BPD symptoms more strongly than does childhood sexual abuse. This finding, differences in brain structure (see Brain abnormalities), and the fact that some patients with BPD do not report a traumatic history,suggest that BPD is distinct from the post-traumatic stress disorder, which frequently accompanies it. Thus, researchers examine developmental causes in addition to childhood trauma.
Newer research published in January 2013 from Dr. Anthony Ruocco at the University of Toronto has highlighted two patterns of brain activity that may underlie the dysregulation of emotion indicated in this disorder: There has been described, increased activity in the brain circuits responsible for the experience of heightened negative emotions, coupled with reduced activation of the brain circuits that normally regulate or suppress these generated negative emotions. These two neural networks are seen to be dysfunctionally operative in the frontolimbic regions, but the specific regions vary widely in individuals, which calls for the analysis of more neuroimaging studies. Also, differing from earlier studies, sufferers of BPD showed less activation in the amygdala in situations of increased negative emotionality than the control group. Dr. John Krystal, Editor of Biological Psychiatry, added that, "This new report adds to the impression that people with borderline personality disorder are 'set-up' by their brains to have stormy emotional lives, although not necessarily unhappy or unproductive lives".
Writing in the psychoanalytic tradition, Otto Kernberg argues that a child's failure to achieve the developmental task of psychic clarification of self and other and failure to overcome splitting might increase the risk of developing a borderline personality.
A child's inability to tolerate delayed gratification at age 4 does not predict later development of BPD.
Mediating and moderating factors
While high rejection sensitivity is associated with stronger symptoms of borderline personality disorder, executive function appears to mediate the relationship between rejection sensitivity and BPD symptoms. That is, a group of cognitive processes that include planning, working memory, attention, and problem-solving might be the mechanism through which rejection sensitivity impacts BPD symptoms. A 2008 study found that the relationship between a person's rejection sensitivity and BPD symptoms was stronger when executive function was lower and that the relationship was weaker when executive function was higher. This suggests that high executive function might help protect people with high rejection sensitivity against symptoms of BPD.
A 2012 study found that problems in working memory might contribute to greater impulsivity in people with BPD.
Family environment mediates the effect of child sexual abuse on the development of BPD. An unstable family environment predicts the development of the disorder, while a stable family environment predicts a lower risk. One possible explanation is that a stable environment buffers against its development.
Self-complexity, or considering one's self to have many different characteristics, appears to moderate the relationship between Actual-Ideal self-discrepancy and the development of BPD symptoms. That is, for individuals who believe that their actual characteristics do not match the characteristics that they hope to acquire, high self-complexity reduces the impact of their conflicted self-image on BPD symptoms. However, self-complexity does not moderate the relationship between Actual-Ought self-discrepancy and the development of BPD symptoms. That is, for individuals who believe that their actual characteristics do not match the characteristics that they should already have, high self-complexity does not reduce the impact of their conflicted self-image on BPD symptoms. The protective role of self-complexity in Actual-Ideal self-discrepancy, but not in Actual-Ought self-discrepancy, suggests that the impact of conflicted or unstable self-image in BPD depends on whether the individual views self in terms of characteristics that they hope to acquire or, in terms of characteristics, that they should already have acquired.
A 2005 study found that thought suppression, or conscious attempts to avoid thinking certain thoughts, mediates the relationship between emotional vulnerability and BPD symptoms. A later study found that the relationship between emotional vulnerability and BPD symptoms is not necessarily mediated by thought suppression. However, this study did find that thought suppression mediates the relationship between an invalidating environment and BPD symptoms.