we need to treat borderline personality disorder for what it really is – a response to trauma
Introduction
Borderline personality disorder (BPD) is a severe and heterogeneous disorder characterized by chronic instability, with episodes of severe affective and impulsive dyscontrol, interpersonal and identity disturbances (1). Patients with BPD bear witness a marked emotional sensitivity with the incapacity to modulate intense emotional responses and inadequate return to emotional baseline (two).
The prodromal signs and symptoms that prelude to subsequently personality pathology are already nowadays in very young age, in item in boyhood (3), meaning that BPD does non abruptly emerge during adulthood.
Prevalence rate of BPD in non-psychiatric population is ranged between 0.vii and over 5% (4, 5) while in clinical settings reaches 10% of all psychiatric outpatients and 15–xx% of inpatients (vi). BPD is characterized by severe functional impairment, intense use of wellness services, medications, and a suicide rate of 10–50 times higher than the rate in the general population (7).
Psychodynamic theories suggested that BPD arises from precocious distortions in object relations (viii) and characteristic patterns of attachment (9), inducing an intolerance of aloneness, hypersensitivity to environmental stimuli, expectation of detached and hostility from other, and loss of positive memories of dyadic relationship (10).
From early zipper experiences, subjects gain important information about their identity and abilities to regulate inner experiences and behavioral strategies for maintaining proximity to others. Assailment or fail from caregivers may exist experiences contributing to compromise a realistic and balanced view of self and others (10). And so, an insecure model of zipper with caregivers is internalized and could be at the origin of the expectancies for futurity relationships characterized by abuse or rejection (xi). BPD occurs in a precocious context of intolerance toward the manifestations of individual emotions during childhood (12). So, children exposed to these unfavorable conditions are unable to recognize, regulate, and tolerate emotional responses and they fluctuate betwixt extreme emotional lability and emotional inhibition. In 30% up to 90% of cases BPD is associated with abuse and neglect in childhood and these percentages are significantly higher than those registered in other personality disorders (13–15). Some authors proposed affect regulation difficulties as primal mediator in the relationship betwixt babyhood trauma and BPD (16). Interpersonal dysfunctions are a result of early on scarcity of emotional closeness or responsibility from caregivers in early on childhood (17).
Similarly to other psychiatric disorders, the most acknowledged etiopathogenetic theory of BPD suggested that this disturbance was produced by the interaction of biological and psychosocial factors (17–nineteen), in particular biologically based vulnerabilities (temperamental features, genetic polymorphisms) and adverse environment (traumas) during childhood or adolescence. These traumatic experiences could be also associated to neuromorphological abnormalities and to neuroendocrine changes (i.e. hypothalamic-pituitary axis (HPA) activation) that are observed in patients with early BPD and abuse/fail history (20).
The aim of this review is to provide an updated overview on dissimilar types of traumatic events (sexual and physical abuse, neglect, and bullying) that combined with temperamental, genetic, and neurobiological factors may contribute to early manifestations of BPD.
Nosotros searched in Pubmed database studies focused on borderline symptoms and disorder in adolescents up to xx years onetime, published between 2000 and 2021 and using the following terms: (deadline personality disorder) AND (kid OR boyish OR teen OR young) AND (trauma OR abuse OR maltreatment OR neglect OR bullying) AND (temperament) AND (environment) AND (epigenetic factors OR neuroimaging OR neurobiology) AND (suicide OR cocky-injury) AND (cPTSD). Eligibility status for articles was divers by the initial screening of trials on the footing of title and abstract. Papers that passed the initial screening were further selected on the basis of a careful examination of the full manuscript content. The review considered simply articles written in English. We included the post-obit blazon and number of studies: thirty longitudinal, 12 retrospective, nine cross-exclusive, 1 randomized controlled trials. Cess instruments more usually used in the trials were: the Borderline Personality Features Scale for Children (BPFS-C) and a recently developed parent report version of the same measure (BPFS-P); the Revised Diagnostic Interview for Borderlines (DIB-R); the Child Interview for DSM-Iv Deadline Personality Disorder (CI- BPD); the Child Interview for DSM-4 Borderline Personality Disorder. Number of studies participants ranged between 12 and seven,771. Age of patients ranged betwixt ix and 21 years. V studies included only females. Participants were mainly Caucasian.
Factors Associated to Early Onset of BPD: Temperamental Traits and Environmental Context
Temperamental Factors
Intrapsychic factors, including temperamental characteristics and personality traits in babyhood and adolescence, must be investigated to recognize predictors of BPD at an early on phase (3). There is a full general consensus that temperamental vulnerabilities combined with childhood adversities play a role in the development of BPD traits (12, 21, 22). Researchers identified several temperamental traits in children or adolescents, including affective instability, negative affectivity, negative emotionality, inappropriate anger, poor emotional control, impulsivity, and aggression, that could predispose to borderline personality disorder (3, 23, 24). Model proposed past Cloninger for personality pathology underlines the role of temperamental characteristics in BPD development (25). Some authors found that loftier harm abstention and novelty seeking (in combination with childhood traumatic experiences and adolescent psychopathology) tin can be considered predictive of early on onset BPD (26). In a randomized controlled written report that compared 33 BPD adolescents with 35 clinical controls and 31 healthy subjects, information technology was observed that loftier damage abstention and novelty seeking, together with depression reward dependence represented a vulnerability for BPD onset (27).
In item, novelty seeking is the temperament dimension that was specifically linked with BPD and differentiated BPD patients from non-clinical patients, patients without personality disorders (PDs), and patients with other PDs (including diagnoses of cluster B disorders) (28).
Amid other temperamental traits, assailment at a very juvenile historic period was associated with precocious onset of BPD (24, 29, 30). Vaillancourt et al. institute in a prospective study performed in 484 children and adolescents that aggression was a predictor for the early on diagnosis of BPD (at 14 years) with some gender differences. In particular, relational aggression was the main predictor in boys, while physical aggression was the strongest predictor in girls. The same authors suggested that negative emotionality, in terms of negative affectivity and poor emotional control, was another temperamental trait oft associated to early BPD (31). Several studies designed to evaluate how negative emotionality and other traits, such as affiliation, constraint, and agency, might impact onset of BPD showed that negative emotionality and low constraint predicted onset of BPD at younger historic period (32, 33), as well as the association of negative affectivity with impulsivity and lower sociability in childhood (34, 35).
Two different longitudinal studies past Gratz and Tragesser identified that three tightly continued traits—depression cocky-control, impulsivity, and melancholia instability—tin can exist considered predictors of early onset BPD (34, 36). One study investigated the impact of the temperamental trait of acrimony on precocious BPD (37). Crawford and colleagues showed a significant clan betwixt acrimony trait and early BPD symptoms in a large sample of 766 children who were followed for 20 years (38).
Bachelor data sustained the hypothesis that temperamental factors may increase vulnerability for the development of BPD, simply they are not sufficient to predict this disorder and demand to interact with ecology negative factors to induce it. Several investigations indicated that the interaction of temperamental vulnerabilities with ecology experiences [i.e., distressing childhood experiences within the context of the family unit (12, 22)] is a pregnant risk gene for the development of BPD in early on age (21, 37).
Environmental Factors
Environmental factors that take been identified equally predisposing conditions for early BPD cover familial maltreatments (abuse and neglect), psychopathology of family members, and parent-child conflicting relationship. It has been supposed that the evolution of knowledge and affectivity, the integration of thinking and emotions, and the ability to discern emotional states are disturbed by early trauma with consequent postal service-traumatic reactions, dissociation, and alexithymia (39).
Children who suffer maltreatments may infer negative characteristics of themselves and others and deduce that they are intrinsically unacceptable and deserve maltreatment. This supposition may pb to see themselves as "helpless, unlovable, or weak and to view other people as dangerous, rejecting, or unavailable". Then, abused children may internalize negative perception about themselves, others, and about relationships with other people (40).
Childhood familial maltreatments may foster BPD through insecure attachment. Driveling children tend to "blame themselves for their maltreatment when the perpetrator is an zipper figure" (41). In item, more severe and chronic experiences of maltreatment may produce a negative image of oneself with consequent expectation to be abandoned (i.e., zipper anxiety) and a simultaneous negative perception of others as unworthy of beingness trusted (i.e., attachment avoidance) (40). Some studies showed that primarily attachment feet, rather than avoidance (more related to father's maltreatment), plays a role in the relation between kid maltreatment and the development of precocious BPD symptoms.
Findings from studies focused on maternal psychopathology emphasize the importance of because the diagnosis of BPD in female parent equally predictor of BPD onset in adolescence (effectually 15 years of age) (42). Maternal externalizing disorders, characterized by poor impulse-control, rule breaking, aggression, and impulsivity were significantly associated with early BPD in offspring (43). Maternal anxiety and low during pregnancy predict early on BPD in sons or daughters. (44).
Among familial relationships, function confusions and disoriented behaviors in parent-child relationship were institute in patients with early BPD symptoms, in detail self-injuries in adolescence (45). Moreover, dysfunctional familial relationships characterized by induction of guilt, psychological command, and triangulation (children who have a function of mediator in the parental marital conflicts), were observed in big samples of adolescents with astringent behavioral and emotional disorders who had already showed BPD symptoms in childhood (46).
Studies on temperamental and environmental factors associated to early on onset BPD are presented in Table i.
Table one. Studies on temperamental and environmental factors associated to early onset BPD.
Traumatic Experiences and Early Onset of BPD
The hypothesis that early traumatic life experiences foster the development of BPD received increasing scientific validation. In particular, early traumas work as triggers for the development of several BPD characteristics, such equally touch on instability, emotion dysregulation, and self-destructive behaviors (47). Traumatic events play a cardinal role equally they seem to impair the ability of mentalizing or symbolizing emotions (48, 49), especially in early phases of life. A recent written report on this focus (50) suggested that the agin childhood experiences (ACEs) involving emotional and physical trauma, parental mental disease, and exposure to poverty in early stages of life were the strongest predictor of BPD symptoms in 14–19-yr-sometime subjects, even when parental psychopathology and poverty were excluded from the analysis. In particular, this report constitute that ACEs in preschool age were particularly impacting on early development of borderline personality features.
In accordance with diathesis–stress theories of borderline etiology (13), precocious traumatic experiences in terms of abuse and neglect and inherited vulnerability (specific temperamental traits and genetic polymorphisms) play a synergistic role to foster borderline personality features. In this perspective, nosotros cannot consider single predisposing factors to early BPD as point insults that produce the disorder by themselves, but rather equally overlapping factors that added to other environmental or biological conditions contribute to the genesis of the disorder. Moreover, in that location is a cumulative effects of traumatic experiences: children who had experienced more than than one type of corruption and maltreatment perpetrated across developmental periods had significantly higher severity of borderline personality features (24, 51–53).
We will hash out below available evidences on this issue, conceiving trauma in terms of abuse or fail conducts from parents and peers that contributed to early on development of borderline pathology. Verbal, emotional, physical, and sexual abuse, together with emotional and physical neglect, and chronic exposure to peer victimization were identified equally potential factors that increment the risk for early BPD.
Some studies that will be reported in the following paragraphs are the same described in the previous section (temperamental factors and ecology factors) as authors investigated the role and interaction of unlike risk factors in early on BPD onset.
Sexual Corruption
Sexual abuse is defined every bit "any sexual deed to which the victim did not consent, could not consent, or was pressured or manipulated into consenting" (54).
Most of studies showed a meaning association between childhood sexual corruption (CSA) and onset of BPD at very young historic period (33, 50, 55–61). Nevertheless, this evidence was not replicated in all studies. In fact, Hect et al. (24) did not find a relationship between BPD and sexual abuse. This upshot should be interpreted considering the study limitations: a small sample size and the possibility that consequences of sexual corruption may manifest later the eye-childhood period, which was the timespan analyzed in Hect's study. Findings from several investigations suggested that adolescents with BPD take a history of sexual trauma more frequently than both salubrious adolescents (57) and not-BPD psychiatric patients (58).
In BPD adolescents some authors found a higher rate of sexual corruption-related events, than in depressed and healthy control adolescents (55). In addition, sexual abuse events were significantly associated to suicidal conducts in youths with BPD (62). Psychological brunt of CSA experiences does not subtract with the disclosure. On the contrary, this tin exist a delicate menstruum with increased risk of suicide and development of personality disorders (sixty). In particular, a accomplice study that compared the presence of several psychiatric diagnoses in adolescents who had been victims of CSA, reported that BPD was the only diagnosis non nowadays at all before the disclosure of CSA experience, but it was establish in the showtime year, and its charge per unit drastically increased in the second twelvemonth afterwards the offset registered CSA experience (61). These findings supported the specificity of the relationship between precocious sexual abuse experiences and early on BPD onset.
Sexual corruption was plant the simply 1, among unlike types of abuses (due east.g. fail, physical, and sexual abuse), to reach an independent significant relation with early on BPD development in a written report performed in a sample of adolescent females with BPD, compared with a clinical control group with mixed psychiatric diagnoses (59). Precocious sexual abuse could alter clinical manifestations and worsen the course of BPD. Some authors observed a significant relationship between sexual corruption and psychotic-like experiences in young patients with deadline personality features (63) and a more severe general clinical film in BPD patients with prolonged childhood sexual corruption than subjects who had not experienced these traumas (50, 64). Moreover, adolescent BPD females who did not remit four years after initial presentation of symptoms were significantly more likely to have self-reported babyhood sexual abuse, concomitant depressive symptoms, or substance use disorder (56). On the other mitt, BPD symptoms significantly improved from ages sixteen to 18 amid BPD adolescent girls who did non study experiences of sexual abuses (33).
Physical and Verbal Abuse
Physical abuse consists of "the non-adventitious infliction of physical injury on the other person (due east.g., bruises, welts, burns, choking, and broken bones), while exact abuse involves some sort of verbal interaction that causes a person's emotional harm (e.g. blaming, criticism, judging, and name-calling)" (24). Several studies found a relationship betwixt concrete or verbal abuse and BPD development (23, 24, 37, 59, 65).
Children who were physically maltreated developed more than BPD symptoms at age 12 compared to non-maltreated peers and were especially vulnerable if they had relatives with psychiatric disorders (23). Harsh treatment and inherited vulnerability seem to play a synergistic role to foster borderline personality features. Not only family unit history, but too children temperamental characteristics tin facilitate manifestation of BPD symptoms if concrete corruption is suffered: children with a low level of the temperamental trait of affiliation who were physically abused showed an earlier onset and a higher severity of BPD symptoms (37). The relationship between perpetrated maltreatments and temperament is circuitous and debated: maltreatment could promote the onset of BPD in patients who had a biological vulnerability (specific temperamental traits). Still, it is also possible that precocious and repeated familial maltreatments influence at to the lowest degree some of the temperamental features related to BPD. Timing of measurement of temperamental features constitutes a limitation as it is hard to distinguish temperamental traits in personality of developed patients.
The result of physical trauma affects many domains of personality, such every bit affective dysregulation, identity diffusion, disturbed relationships, and self-harm. Physically abused children presented higher scores on each domain in comparison with a not-maltreated children control grouping. Moreover, they had higher overall deadline trait scores and were more probable to be recognized as individuals at high gamble for BPD (24).
Non all studies are consequent about the specific relationship between physical abuse and early BPD development. Infurna et al. (59) institute a pregnant association betwixt physical abuse from male parent and BPD onset when univariate regression was used, while this association was lost when results were analyzed by means of a multivariate regression model, including other types of abuse experiences. Biskin et al. (56) establish no deviation between BPD and clinical comparing groups on self-reports of physical abuse.
As regards the effects of verbal abuse, data are limited. Some authors suggested that the impact of harsh speech can be traumatic also as physical abuse. Johnson et al. (65) plant that children who experienced exact abuse from mother were more decumbent to borderline, narcissistic, obsessive-compulsive, and paranoid PDs in adolescence or early on machismo compared to subjects who did not experience verbal abuse.
Fail
In the context of caregiving, fail is a kind of abuse characterized by "failure to supervise the child properly, leading to concrete or emotional harm" (65). Neglect concept includes concrete neglect, which is the failure to meet fairly the physical needs of children, and emotional neglect, which is represented by emotional detachment by the caregivers to the requests for attention and care of children (66).
The association between neglect and early BPD development was reported past several studies (24, 37, 57, 59, 67, 68). The most significant findings showed that: adolescents with BPD and concomitant depression had significantly higher rates of neglect than good for you controls (57); physical fail was associated with BPD features onset at an earlier historic period (24); the combination betwixt specific temperamental features and physical/emotional neglect may speed up the onset of BPD and antisocial personality disorder (ASPD) symptoms (37); and neglect from both parental figures was reported more often amongst BPD adolescents in comparison with other clinical populations (59).
The impact of specific kinds of neglect (i.e. childhood supervision neglect and maternal withdrawal) was investigated in two studies (67, 68). Childhood supervision fail, including the failure to set limits, to nourish to misbehavior, to know child's whereabouts and friends, was associated with higher risk for Cluster B personality disorders in adolescence and early on adulthood (67). Maternal withdrawal in infancy, a kind of neglect in which female parent creates physical and verbal distance from her baby, was a robust predictor of both BPD symptoms and cocky-injuries or suicidality in adolescence (68).
Bullying
"Bullying is a systematic abuse of power and is defined as ambitious behavior or intentional impairment doing past peers that is carried out repeatedly and involves an imbalance of ability, either actual or perceived, between the victim and the smashing" (69).
Bullying includes both physical and verbal acts of aggression or indirect cracking victimization denoted by social exclusion (lxx, 71). In a psychological perspective, victimization may affect upon inner working models that pertain the relationships, disturbing the capacity to trust and collaborate with others in a right manner, and leading to unstable relationships, misconstrue perceptions, and emotional dysregulation (72).
Several studies reported that beingness bullied during the menstruum of master schoolhouse is a strong predictor of early on BPD onset (73, 74) approximately upwards to 2–six years later on the bullying conducts (73). Feelings of loneliness, acrimony, and loss of trust that are due to victimization by peers were oft described by victims of bullying who had developed BPD in young age and were observed too during experimental social trust games (75, 76).
Wolke and colleagues (73) conducted one report in guild to explore the clan betwixt peer victimization and BPD symptoms. Authors considered peer victimization during master school as a potential predictor of the disorder'south onset at about 12 years and observed that children who were exposed to chronic bullying (at viii and 10 years) had an augmented risk of BPD symptoms with a dose-response relationship. Children who experienced relational and repeated peer victimization had 7 times increased risk to early on BPD symptoms compared to those that were non bullied. In our previous investigation aimed to identify which factors are independently associated to early onset of BPD, nosotros found that earlier onset of BPD is associated to traumatic experiences, including corruption, fail, and dysfunction in household surroundings. A significant traumatic status that was identified in our analysis of early on BPD gamble factors is bully victimization (74). Studies on precocious traumas (sexual abuse, concrete/exact abuse, neglect, bullying) and early onset BPD are displayed in Tabular array 2.
Table 2. Studies on precocious traumas (sexual corruption, physical/verbal abuse, neglect, and bullying) and early onset BPD.
Neurobiology, Neuro-Morphology and Epigenetic in Early on Trauma and BPD
There is a general consensus in retaining that alterations in several biological systems and brain anatomical features are related to traumas in childhood and to early BPD. Some authors have examined the effect of early stressful events on biological systems in order to place biomarkers that could be involved in BPD vulnerability. These markers might allow an early detection of individuals at high adventure for BPD (2).
Precocious traumatic experiences atomic number 82 to chronic "hyperarousal" of the hypothalamic-pituitary- adrenal axis (HPA), resulting in higher levels of cortisol. Several investigators found an increment of cortisol levels (urinary, salivary, and claret) in patients with BPD, hallmarking HPA activation (78–lxxx). The cortisol hyper-stimulation of the hippocampus can generate a distorted estimation of signals from the environment equally constant menaces, therefore sending this danger signals to amygdala, that modulates fear and aggression (20). Intense emotional responses to small stress with a greater latency for returning to baseline conditions are common in young BPD patients. Moreover, over-operation of the prefrontal cortex generates loss of rationality, reasoning, and decision- making capacity in BPD patients (20, 81).
With regards to neuroimaging investigations, several preclinical studies have delineated the effects of early on stressors on specific brain regions. Corpus callosum and other myelinate areas are potentially vulnerable to the affect of early on exposure to higher levels of stress hormones, that suppress glial cell segmentation crucial for myelination (82) and determine a reduced size of the corpus callosum (83, 84). These results were confirmed in clinical investigations. De Bellis and colleagues observed the reduction of volume of corpus callosum size in children with a history of abuse and post-traumatic stress disorder (PTSD) (85). Reduction of the corpus callosum size may lead to a macerated communication between the hemispheres, with an increased hemispheric laterality (82).
The clan between decreased hippocampal volume, early on traumatic events, and development of psychiatric disorders in early phases of life was too investigated (86, 87). In item, an average of 16% reduction in hippocampal volume bilaterally was seen in BPD females with a history of babyhood victimization (88). Some authors observed a directly proportional correlation between the amount of volume reduction in the mentioned areas and severity of trauma exposure in babyhood (89). In addition to the volumetric reduction that was observed in corpus callosum, hippocampus, and prefrontal cortex, some abnormalities in activity were found in amygdala, in particular in BPD females with traumatic experiences in childhood (90).
Despite the detrimental consequences of child maltreatment on developmental processes, some subjects show resilience, with depression level of psychopathology, while others develop astringent disorders. Factor-surroundings interaction model can aid u.s.a. to better understand the function of trauma on genetic predisposition to develop early BPD. An interconnection betwixt genes and environment in relation to beliefs was firstly reported by Caspi et al. (91). In item, authors observed that maltreated children who developed behave disorder and hating personality disorder had a genotype that resulted in low levels of monoamine oxidase A (MAOA) expression (92).
Some studies evaluated how serious life events (SLE) (i.e., physical abuse, rape, and childhood sexual abuse—CSA) collaborate with polymorphisms of genes in producing behavioral patterns characteristic of BPD. In BPD patients trauma was found associated with a decrease or an increase of impulsivity depending on the genotype: lower impulsivity after SLE was associated to SS and SL genotypes and higher impulsivity was associated to LL carriers of the long/short (L/S) polymorphism of the serotonin transporter promoter (five-HTTLPR) (93). Interactions between trauma and the rs4680 COMT polymorphism involved in dopaminergic functioning (COMT Val158Met) was also evaluated. Results reported that the Val/Val genotype (but non the Val/Met and Met/Met genotypes) was associated with lower impulsive assailment in BPD (94).
Martin Blanco and colleagues (95) performed a written report aimed to written report the interaction of HPA genetic polymorphisms and babyhood trauma in BPD. Authors found that two FKBP Prolyl Isomerase 5 (FKBP5) alleles (rs3798347-T and rs10947563-A) were more frequent in BPD subjects who experienced physical abuse and emotional neglect and two Corticotropin-releasing factor receptor 2 (CRHR2) variants (rs4722999-C and rs12701020-C) were more common in BPD subjects sexually and physically abused (95). These findings can suggest that childhood trauma modulates the onset of this disorder (92).
In order to better understand the influence of the surround on gene, some epigenetic studies were performed. Perroud et al. (96) investigated epigenetic changes of serotonin 3A receptor (5-HT3AR) in patients with childhood maltreatment and several psychiatric disorders. They found that epigenetic modification of 5-HT3AR was related to a history of childhood maltreatment and more astringent psychiatric disorders, including BPD, in adulthood (96). Another study showed a higher methylation of glucocorticoid receptor gene NR3C1 in patients with BPD and childhood traumas (97).
Studies on neurobiological, neuro-morphological, and epigenetic factors in early onset BPD are described in Table iii.
Table 3. Studies on neurobiological, neuro-morphological, and epigenetic factors in early on onset BPD.
BPD and Circuitous PTSD: Contempo Traumatic Experiences Could Reactivate Precocious Traumas?
Repeated traumatic events provoked past caregivers or intimate partners involve the run a risk of developing a constellation of psychiatric symptoms. Complex Post Traumatic Stress Disorder (cPTSD) was originally conceptualized to indicate the reaction to multiple, perpetrated traumatic events with onset in early on life (98). More recently the diagnosis of cPTSD referred to a "clinical syndrome post-obit experiences of interpersonal traumatic victimization and is characterized by difficulties in emotion regulation, interpersonal relationships, and self-concept" (99). So, cPTSD shows some overlapping with BPD, including dissociative symptoms, dysregulation of emotions, self and relational disturbances (100). In fact, chronic precocious traumatic experiences often outcome in more than pervasive disorders than unproblematic PTSD with impairment in attachment style and in the ability to modulate emotions. Trauma tin can produce its effects on behavioral, emotional, physiologic, and neuroanatomical levels. Assaults atomic number 82 to hyperarousal states that tin can interfere with right judgment of the relationships and situations. After stressors tend to exist experienced by victims of trauma as a reactivation of the precocious traumatic experiences (101).
Prolonged and repeated traumas, peculiarly in early life, promote a chronic disability to modulate emotions, that can result in behavioral patterns feature of BPD, such as disturbed relationships, substance abuse, and self-injuries behaviors, in which precocious traumatic events are re-enacted over time (102).
Despite the great interest in this topic, systematic investigations focused on the relationship between precocious traumas, present traumatic experiences, complex post traumatic disorder and BPD psychopathology are still scarce. One of the primary reasons is that complex PTSD has been proposed by several investigators, only has been included as an official diagnosis only very recently in ICD-11. So, only now well-defined diagnostic criteria are bachelor for PTSD and BPD in DSM- 5 and for cPTSD in ICD-xi. A comparison of these criteria in clinical samples volition allow to identify more clearly differences and similarities of these psychopathological constructs.
One written report was performed in club to determine whether patterns of melancholia dysregulation, relational damage, and identity alterations, mediate the relationship between exposure to interpersonal traumatic stressors in childhood and present clinical symptoms in a sample of adults diagnosed with severe cPTSD/BPD. Results of the written report demonstrated that the relationship between childhood exposure to trauma and cPTSD/BPD symptoms in adulthood was mediated by the three factors: relational damage, touch dysregulation, and identity alterations (103). Some authors hypothesized that emotion dysregulation and impulsivity in BPD may increase vulnerability to be re-exposed to traumatic events due to high appraisal of threat, macerated coping resources, increased exposure to risky situations, and intense emotional responding peri-traumatically (104, 105). Exposure to multiple traumatization afflicted the sense of self and emotion regulation strategies (106). These key alterations of personality can evolve into BPD or cPTSD. Emotional dysregulation may also increase the trend to perceive new events every bit threatening and traumatic (107).
Studies on BPD and complex PTSD are presented in Table 4.
Tabular array 4. Studies on BPD and circuitous PTSD.
Conclusions
On the ground of the results discussed in the previous sections, we tin can conclude that the interaction of temperamental, environmental, and genetic factors with early on traumatic experiences can promote onset of BPD in young age. Available data suggested that experiences of corruption, fail, and smashing victimization in childhood, temperamental traits of impulsive aggression and negative affectivity interacting with dysfunctional familial environment, volumetric and functional abnormalities in fronto-limbic areas associated to precocious trauma and specific polymorphisms of genes (MAOA; 5-HTTLPR; FKBP5; CRHR2; 5HTTR; COMT) characterize subjects at loftier risk to develop BPD. In accordance with our preliminary model of risk factors in early BPD (three), the outcome of the interaction of different run a risk factors is more decisive than the separate effects of unmarried factors in early on development of BPD. So, the furnishings of traumatic experiences are enhanced when the dysfunctional familial surroundings that produces traumas interacts with the kid'south innate temperamental traits or specific genetic polymorphisms.
The mechanisms of interaction of dissimilar predisposing factors are only partially known and farther studies are required to sympathise which factors have an independent effect and which produce their action as mediators or modulators.
Author Contributions
All authors provided their contribution to collection and analysis of data and preparation of manuscript.
Conflict of Interest
The authors declare that the inquiry was conducted in the absence of any commercial or financial relationships that could be construed as a potential disharmonize of involvement.
Publisher'south Notation
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