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Adverse Childhood Experiences and Neurocognition in Borderline Personality Disorder: A Call-to-Action Perspective Review

Estric, Clémentine MD, MSc; Calati, Raffaella PsyD, PhD; Lopez-Castroman, Jorge MD, PhD

Author Information
Harvard Review of Psychiatry: 7/8 2022 - Volume 30 - Issue 4 - p 248-260
doi: 10.1097/HRP.0000000000000344



Borderline personality disorder (BPD) is a chronic and complex mental disorder characterized by emotional dysregulation, impulsivity, and instability of interpersonal relationships as its core features.1 BPD represents a public health issue with prevalences ranging between 0.5% and 5.9% in the general population.2,3 The prevalence is about 6% in primary care settings, 10% of all psychiatric outpatients, and 20% of psychiatric inpatients.4,5 Eighty-five percent of patients with BPD will make multiple suicide attempts, and 10% will die by suicide—50 times more than in the general population.6–8 BPD causes severe functional impairment to individuals, families, and society.9 It is associated with increased health care and treatment utilization,10,11 as well as high societal costs,12,13 explaining the strong current interest in BPD research. Early identification of BPD traits has important clinical implications. Early intervention programs guarantee appropriate treatments and prevent long-term deficits in functioning.14

At present, we have an incomplete understanding of the physio-pathological mechanisms leading to the development of BPD.9,15 A high percentage of patients with BPD suffer adverse childhood experiences (ACEs). For instance, childhood sexual abuse is reported by 16.1%–85.7% of patients with BPD,16 and as many as 71% of patients with BPD report a history of severe maltreatment in childhood.17 The World Health Organization definition of ACEs encompasses all forms of abuse and neglect (sexual, physical, and emotional) against anyone under the age of 18, resulting in actual or potential harm to the child’s health, survival, development, or dignity.18 A review of nationally representative survey data on the prevalence of violence against children in 96 countries estimates that one billion children experienced ACEs in 2014, more than half of all children between the ages of 2 and 17.19 ACEs are strongly associated with emotional problems20 and diverse psychiatric symptoms or diagnoses in childhood, adolescence, and adulthood.21 Indeed, early adversity is a common nonspecific risk factor for the development of most psychiatric disorders, including BPD.

Several findings support the implication of ACEs in the neurocognitive impairments of BPD: (1) ACEs induce changes both in neurocognition and emotional regulation via neurobiological modulations;22 (2) neurocognitive impairments reported in BPD are similar to those reported in adults who experienced ACEs;23,24 (3) several risk factors are commonly associated with both ACEs and BPD;25 and (4) the severity of ACEs is correlated with both the severity of neurocognitive impairments and the severity of BPD.23

Neurocognition comprises many higher mental faculties: attention, memory (episodic or autobiographical), and executive functioning (including 18 subcomponents such as planning, working memory, fluency, inhibition, cognitive flexibility or problem solving, decision making, and impulsivity).26 They correspond to the brain’s ability to select, process, store, produce, and use information to solve problems, reason, adapt to the environment, and respond to needs and desires. Many, if not all, of these faculties can be altered by early trauma.27 For instance, exposure to ACEs induces the stress response system to become hyperreactive and persistently activated. A chronic stress response, reflected by the hyperactivation of the hypothalamic-pituitary-adrenal axis,28 hinders the healthy development of brain structures, neural circuits, and neurotransmitter mechanisms involved in emotional regulation.29 Indeed, many studies have demonstrated the impact of chronic stress on brain structures, such as the hippocampus, the amygdala, and regions of the prefrontal cortex. These regions are directly involved in cognitive functions, such as memory or emotion regulation, and their alteration might lead to the dysfunctional personality traits found in BPD.30

This article aims to provide an overview of the scientific literature on the potential contributory role of neurocognition in the association between ACEs and BPD. Since we did not expect to find many studies specifically examining this triple linkage due to the broad nature of the topic, we conducted a perspective review. The pairwise associations between ACEs and neurocognition, ACEs and BPD, and neurocognition and BPD were also considered. If neurocognition is identified as a robust link between ACEs and BPD, then neuropsychological assessments could offer insight about the severity of early adversity and also facilitate more appropriate treatments for BPD based on therapies for traumatic experiences.


Literature Search

We searched MEDLINE for articles published up to 1 September 2021 in peer-reviewed journals documenting an association between ACEs, neurocognitive domains, and BPD. The following Medical Subject Headings (MeSH) and search terms were used: (I) [adverse childhood experiences OR childhood abuse OR childhood neglect OR childhood trauma OR early trauma OR early life stress], AND (II) [neuropsycho* OR cognit* OR attention deficit OR memory OR executive function OR decision-making OR impulsivity], AND (III) [borderline personality disorder]. We also conducted a pairwise category search. Titles and abstracts of the screened studies were evaluated by one author (CE). The complete article was thoroughly read by two authors (CE, JLC) if an association between at least two of the three search categories was present in the title/abstract. In case of disagreement on eligibility, consensus was reached through discussion with the third author. Some other studies not found in the database search were selected from the reference lists of the selected articles or added by expert opinion (JLC).

Inclusion/Exclusion Criteria

Inclusion criteria for the studies were the following: (1) peer-reviewed articles published in English, French, Italian, or Spanish with an available abstract, (2) the identification of BPD symptomatology (either as a formal diagnosis or as personality traits), and (3) a study of ACEs or (4) an assessment of neurocognitive functioning using standardized neuropsychological tests. Exclusion criteria were the presence of any neurological disease (e.g., stroke, neurodegenerative disease, or traumatic brain injury resulting from maltreatment or another cause) or any associated psychiatric disorder that could affect cognitive processes, other than BPD or stress-related trauma. There were no restrictions regarding study design, and reviews and meta-analyses were permitted.


The main outcomes were symptom severity scores in BPD and the measures of cognitive and behavioral performance on any specific test. When available, the performance of healthy comparison groups on the same measures was used as a comparator. Any neuroimaging findings reported alongside behavioral data will be mentioned in the qualitative synthesis.

Data Synthesis

The included studies are summarized in the Results section. The highest relevance was attributed to the articles that provided information about the mechanisms connecting ACEs, neurocognition, and BPD (triple linkage). Then, we considered pairwise associations. The relevance of the articles was determined according to their accuracy or novelty in studying the strength of the associations or the mechanisms between ACEs, neurocognition, and BPD. Because of the limited literature on the triple linkage, along with the heterogeneity among the articles, we conducted a perspective review rather than a systematic review. See flowchart in Supplemental Figure 1, Thus, we provide a review of the existing literature and a clinical perspective.

The results will be presented in four sections according to the information they provide on the following: (1) the triple linkage among ACEs, neurocognition, and BPD; (2) the neurocognitive impairments associated with ACEs; (3) the role of ACEs in emerging BPD; and (4) the neurocognitive impairments linked with BPD. Results are ordered starting with systematic reviews and meta-analyses when present, and moving from the earliest age of childhood or adolescence to adulthood.


Using the MeSH terms and search criteria described above, we found the following: 92 studies using (I), (II), and (III); 1834 studies using categories (I) and (II); 1827 studies using (II) and (III); and 320 studies using (I) and (III). After removing duplicates, all abstracts were reviewed. In total, 125 articles meeting the inclusion criteria were fully read and used in this review. Of these, only 2 studies addressed all three areas of interest.

Studies Examining the Triple Linkage

Only one clinical trial in the literature studied alterations in neurocognitive functions induced by exposure to early adversity, in 45 patients with BPD versus 53 non-psychiatric controls.23 BPD diagnoses were established with the Structured Clinical Interview for DSM-IV. Early adversity was examined retrospectively with the Childhood Trauma Questionnaire (CTQ). The study investigators used a comprehensive battery of tests to explore seven neurocognitive functions. Patients with BPD performed more poorly than controls in the areas of verbal comprehension, visuospatial and verbal working memory, sustained attention, and processing speed, but these impairments were not associated with the severity of personality dimensions or the type of ACEs according to the CTQ.

A second study using self-reported data found that emotion-regulation difficulties measured with the Difficulties in Emotion Regulation Scale mediated the effect of ACEs severity (particularly emotional abuse and neglect with the CTQ) on impulsivity in BPD (n = 61).31 This mediation was not found in healthy controls (n = 60) or patients suffering from attention-deficit/hyperactivity disorder or substance use disorder without BPD (n = 57).

Neurocognitive Impairments Associated with ACEs

Impact in childhood

Previous systematic reviews and meta-analyses have considered the association between ACEs and neurocognitive deficits in child or adolescent victims.27,32–34 Severity of ACEs exposure in various development periods is linked to intellectual disabilities, especially lower verbal IQ33 and poorer executive functioning, including working memory.34–37 The impact of ACEs on language development is controversial.38 ACEs have also been linked to changes in social-information processing, with heightened perceptual sensitivity to threat, misclassification of negative and neutral emotions as anger, or attention biases toward threat-related cues.39 Children exposed to ACEs also present changes in their emotion-processing abilities, such as an elevated reactivity to threat, low emotional awareness, and difficulties in emotional learning and emotion regulation.39 However, ACEs do not affect all children in the same way; the evidence indicates individual heterogeneity linked to resilience capacity.40 Indeed, early adversity in unstable or unpredictable environments could improve some executive functions such as adaptability,41 which influences later life.42 ACEs could ultimately act as both a risk and protective factor that modifies neurocognitive and emotional development throughout life.

The negative effects of ACEs on neurocognition vary according to the age of exposure (see Figure 1).

Figure 1:
A theoretical modeling of the negative effects of early-life stress and adverse childhood experiences on neurocognition, according to the age of exposure. This theoretical model illustrates a potential linkage between adverse childhood experiences (ACEs) and neurocognition during childhood and adolescence, even before the emergence of personality traits, according to the existent evidence.21 The negative effects of ACEs on neurocognition seem to vary according to the age of exposure.27 Severe lack of positive relational experiences during the perinatal period (the first two months of life) would be associated with delayed cognitive development and sensory integration, as well as self-regulation alterations, whereas stress in childhood (before age 11) would have a higher impact on cognitive functions, behavioral regulation, and attention. During adolescence (after age 11) cognitive factors such as intelligence or academic performance and relational factors would be more affected.32,33,43,44

Delayed cognitive development has been found after early-life stress occurring from infancy to adolescence, especially after substantiated sexual abuse and neglect.32 Severe lack of positive relational experiences during the perinatal period (the first two months of life) seems to be associated with sensory integration and self-regulation alterations, whereas stress in childhood (before the age of 11) seems to have a greater impact on cognitive functions, behavioral regulation, attention, and relational factors.43,44 Importantly, the age at which the ACEs were experienced or the specific neurocognitive assessment was not always specified in the available studies.

Impact in adulthood

Neurocognitive impairments due to early ACEs can shape the cognitive trajectory of youth and adversely affect their mental health in adulthood.45 Indeed, exposure to ACEs has been associated with neurocognitive changes in processing and psychomotor speed, attention, executive function, memory, and learning, as well as academic achievement, literacy comprehension, intelligence, perceptual reasoning, and nonverbal reasoning.32

Differential effects in adults have been described as a result of different types or gradients of ACEs. For instance, working memory seems to be altered specifically after emotional trauma.34 Sexual abuse has been found to be particularly detrimental to impulsivity control and emotion regulation.46 However, intelligence, visual episodic memory, and visuospatial domains seem relatively unaffected by ACEs.35

Modulator variables and confounders

Several features of ACEs, such as type and duration, exposure to different episodes, perceived stress or traumatic impact, or time passed since the events, modify the impact on neurocognition (see Figure 2).

Figure 2:
Perspective of a potential contributory role of neurocognition in the association between adverse childhood experiences and borderline personality disorder. This theoretical model illustrates the potential triple linkage between adverse childhood experiences (ACEs), neurocognition, and borderline personality disorder (BPD). The evidence suggests that early ACEs have a strong impact on brain development and neurocognitive functions.22 ACEs would also be a predictive factor for BPD.16,17,47 Neurocognitive impairments in adults exposed to ACEs and in patients with BPD would arise from similar brain alterations in the amygdala, hippocampus, and prefrontal cortex.23,24,48 The neurocognitive impairments also seem linked with clinical dimensions of BPD.49

Age of onset of ACEs is therefore a crucial moderator. Since the development of cerebral regions is asynchronous, the moment when the ACEs occur will determine a differential impact between brain regions. For example, memory deficits associated with hippocampal dysfunction are found when ACEs happen during the first four years of life.27 Furthermore, the different areas of the brain affected will lead to different neurocognitive alterations. Executive dysfunctions seem to arise due to developmental alterations in the prefrontal cortex,50 and increased stress responsiveness due to alterations in the amygdala.51

Psychiatric disorders, including affective and emotional disorders, are major confounders when studying neurocognitive functioning.52–55 Many studies have examined neurocognitive functioning after ACEs exposure in clinical cohorts affected by posttraumatic stress disorder (PTSD),56 depression,57,58 bipolar disorder,59–61 suicidal behavior,62 psychotic disorders,63,64 substance use disorders,65 or eating disorders.66 However, at least part of the impact of ACEs on adult cognition seems to be independent of comorbid mental disorders. For example, an association between neglect and lack of social cognition has been found regardless of schizophrenia diagnosis.67 Severely traumatized subjects tend to infer contempt or anger in neutral facial expressions, regardless of comorbid PTSD diagnoses.68 High CTQ scores have been linked to an alteration in the specificity of autobiographical memory, regardless of a depressive episode.69

Role of ACEs in emerging BPD

Although a causal link between ACEs and the emergence of BPD in adulthood has not been identified,70,71 patients with BPD report many ACEs during childhood72 and substantially more than patients with other personality disorders.73,74 The causes of BPD are likely multifactorial, with both genetic and environmental roots.75,76 The results of recent gene × environment studies are consistent with this hypothesis.77,78 The heritability level is estimated to be around 37% to 68%.5,79 An interaction between biological (e.g., temperamental) and psychosocial (e.g., ACEs) factors is the most probable explanation of how the condition develops.80,81 ACEs would induce epigenetic modifications that could, in turn, facilitate the emergence of BPD.40,82 Indeed, the methylation levels of the glucocorticoid receptor NR3C1 promoter gene have been correlated with the severity of ACEs in BPD.83

The first study published on BPD reported early history of trauma in 81% of patients, including 68% experiencing sexual abuse.84 A sample of 358 patients with BPD found a prevalence of 91% of abuse and 92% of neglect under age 18.85 The prevalence of around 70% to 90% of ACEs in BPD remains stable, even in population surveys such as the National Epidemiologic Survey on Alcohol and Related Conditions.86,87 Only one study showed a slightly lower prevalence of ACEs in BPD of around 56%, but this figure is still higher than in other mental disorders such as major depression (40%) and schizophrenia (18%).54 Yet, patients with BPD who do not report ACEs may have experienced other forms of early adversity, including an emotionally invalidating developmental context during childhood.81 A complex interaction between inherited predispositions and early adversity leads to the well-known inability to regulate intense emotional responses and impulsive behaviors in BPD.88,89 Other clinical patterns such as chronic shame, social stress, or an unstable sense of identity are associated with severe functional impairments, extreme behaviors, and high rates of comorbid mental disorders, self-injury, and suicidal behavior.16,90

Some studies have described how the type, age at onset, and severity of ACEs affect the development of BPD. Having suffered an experience of sexual abuse before 12 years of age multiplies the odds of developing BPD by almost 20 compared to unaffected controls (95% CI, 4.49–69.26; p < .0001).16 A link has also been shown with other forms of ACEs: physical abuse,91 emotional abuse,92–97 or emotional neglect.98,99 Some studies have found a combined influence of sexual and emotional abuse and emotional neglect in BPD.100–103 BPD appears to have a more severe clinical presentation in cases of severe, combined, or repeated ACEs.72,73

ACEs are also associated with an early onset of BPD,17 especially for sexual abuse in childhood and adolescence.104 Moreover, young age at the first traumatic event is correlated with severity of BPD symptoms73,105—even prenatal events.106

Exposure to certain forms of ACEs leads to the expression of particular clinical dimensions of BPD. Early sexual abuse has been associated with suicidal behaviors72,107,108 and parasuicidal behaviors.16,109,110 The risk of acting out could increase tenfold after early sexual abuse.111,112 Sexual abuse has also been linked to identity disruption or dissociative symptoms110 and social-cognitive disabilities.113 Emotional adversity (with early traumatic memories, emotional amplification, neglect of negative emotions, or parental psychological control) is strongly correlated with emotional dysregulation25,113,114 and rejection sensitivity.115 Early exposure to adversity factors could also be predictive of BPD associated with anxiety disorders,116 addictive comorbidities,117 PTSD,72 or significant psychosocial impact.16

Finally, some BPD features such as emotional dysregulation seem to be associated with revictimization phenomena after exposure to ACEs,118,119 as presented in Figure 2.

Neurocognitive Impairments Linked with BPD

Several meta-analyses and reviews have reported neurocognitive impairments in patients with BPD compared to healthy controls in memory, attention, executive functioning, decision making, visuospatial ability, and verbal intelligence.24,120–124 These impairments are similar to those found in non-BPD people exposed to ACEs. By contrast, no association has been found with global intelligence, nonverbal intelligence, or language skills. Neurocognitive impairments in BPD are linked with education levels and psychiatric comorbidities such as anxiety or depressive disorders or PTSD,23 but not with demographic features such as age, sex, ethnicity, or antidepressant use.24

Neurocognitive impairments could be considered as correlates of the clinical symptoms of BPD. Dysexecutive disorders (orbitofrontal cortex processes) could be linked with increased impulsivity. Impaired emotional recognition, a type of social cognition, could be related to unstable interpersonal relationships. Emotional interferences on the coding and retrieval of autobiographical memories could facilitate dissociative symptoms.15,49 Moreover, the hyperresponsiveness of patients with BPD in interpersonal relationships is correlated with temporal-limbic dysfunction, and relational avoidance may be used to compensate executive dysfunctions.125

A history of ACEs may contribute to specific neurocognitive deficits or to trauma-related disorders such as BPD,125 but according to a meta-analysis, people suffering from psychiatric disorders (BPD: k = 1; MDD: k = 1; and PTSD: k = 10) and maltreatment have worse global cognitive performance than people of similar ages in the general population (moderate effect size, g = −0.59) or with maltreatment alone.21 In BPD and first psychotic episodes, early sexual and physical abuse has been associated with poor facial emotion recognition: neutral or happy faces are often interpreted as angry or scared.126

Finally, neurocognitive impairments have also been considered as risk factors for the development of BPD traits.127,128 In a longitudinal cohort of 1116 pairs of same-sex twins followed from birth to age 12,47 BPD traits measured at age 12 were found to be more frequent in children with poor neurocognitive function, impulsivity, and behavioral or emotional problems, such as depression, anxiety and psychosis, at age 5. In addition, exposure to ACEs before the age of 10 was correlated with BPD traits at the age of 12, particularly when there was a family history of psychiatric problems. This study supports the hypothesis that, after an exposure to early trauma, neurocognitive alterations appear in parallel to BPD traits in children and adolescents. Enhanced social support after early sexual aggression seems to be a good prognostic factor to prevent the appearance of BPD traits.129

Neurobiological Aspects of the Triple Linkage

Structural magnetic resonance imaging (MRI) studies found reduced amygdala volumes in BPD compared to controls,130–132 as well as hippocampal volume reduction in females with BPD and a history of ACEs.74 Morphological changes found in BPD are noticeably similar to those described after ACEs.48 High CTQ scores have been correlated with decreasing volumes of gray matter in the orbitofrontal cortex (OFC), anterior cingulated gyrus (ACG), hippocampus, insula, and caudate nucleus.133 A recent study in a large sample, however, found no association of BPD traits with any structural brain change, despite a robust correlation between behavioral symptoms and ACEs.134

In functional MRI studies (fMRI) of BPD, an overactivation of the amygdala has been reported during the recall of negative life events or when viewing aversive facial expressions.135 A meta-analysis of 19 fMRI studies in BPD found that the left amygdala presented functional hyperactivity but smaller gray matter volume compared to healthy controls.136 Interestingly, the hyperactivity of the amygdala seemed to be moderated by the use of psychotropic medication among patients. Also, high CTQ scores have been correlated with a hyperactivated amygdala response to fear stimuli.137,138

Neural activity seems to mediate the association between ACEs and an increased downstream impulsivity. An fMRI study showed that high scores of ACEs were associated with a lower neural response during the n-back task.139 In the n-back task, commonly used to measure working memory, participants are presented with a sequence of stimuli one-by-one. For each stimulus, participants must decide if the current stimulus is the same as the one presented n trials ago. Similarly, the electroencephalogram trace of patients exposed to ACEs showed a lack of inhibition and frontal lobe dysfunction during the go/no-go task.140 The go/no-go task measures impulsiveness by testing a person’s capacity not to respond, which is a core construct in cognitive control and self-regulation. In fMRI studies, changes in limbic or prefrontal regions of the brain associated with emotional and cognitive control have been reported in BPD compared to controls. This was illustrated by an attenuated activation in anterior cingulate cortex to fear,141 increased blood oxygen level–dependent responses in bilateral OFC facing pictures of solitary and social situations,142 or a stronger activation in dorsolateral prefrontal cortex (DLPFC) when subjected to painful heat stimuli during fMRI.143 Moreover, patients with both BPD and PTSD showed a decreased activation of the amygdala when exposed to thermic pain–induction.135 The authors suggested that differential neural patterns of traumatic memory exist among subgroups of patients with BPD.

Regional brain blood flow can be measured by script-driven imagery of abandonment in BPD versus controls during [15O] H2O PET tracer uptake. Memories of abandonment were associated with underactivity of the OFC, greater increases in blood flow in the DLPFC, and greater decreases in the right ACG in women with BPD compared to controls.144 Autobiographical memories of abuse events in traumatized women without BPD were accompanied in PET by increased blood flow in the prefrontal cortex (right DLPFC, right ACG, and left OFC) but decreased blood flow in left DLPFC, whereas women with child abuse histories and BPD failed to activate these regions.145,146 Thus, patients with BPD do not seem to engage the cognitive-control regions to distance themselves from unpleasant emotions, which may contribute to the affective instability of this disorder. It should be noted, however, that in these studies most BPD subjects were on psychoactive medications, whereas most controls were not.


This perspective overview summarizes the available data regarding the potential contributory role of neurocognition in the association between ACEs and BPD. Three main arguments support this role. First, evidence suggests a strong impact of early ACEs on brain development and neurocognitive functions. Second, maltreated, abused, and emotionally invalidated children are more likely to present emerging borderline personality traits or BPD.17,47 Third, the scientific literature shows that patients without BPD who have suffered ACEs have neurocognitive impairments that are similar to those reported in patients with BPD.23,24 That is, comparable neuroanatomical and neurofunctional changes in the amygdala, hippocampus, and prefrontal cortex are present in patients with BPD and in those exposed to ACEs but without BPD.48 Furthermore, the neurocognitive impairments of ACEs can be roughly linked to the main clinical dimensions of BPD. For instance, increased impulsivity can be linked to altered inhibitory control (belonging to a general lower executive functioning), and dissociative experiences can be linked to unspecific autobiographical memory and emotionally biased facial recognition. Thus, the results of this perspective review suggest that the strong association of ACEs and BPD is founded, at least partly, on neurocognitive changes that act as mediating factors.

Nevertheless, the paucity of literature on the triple linkage precludes any strong interpretation of the findings. Only two studies addressed this triple association. These studies were methodologically limited by small sample sizes and cross-sectional designs. The first study did not find an association between neurocognitive impairments and severity of personality traits in ambulatory patients with BPD.23 But since ambulatory patients are clinically stabilized and have relatively less severe symptoms than BPD inpatients, a weaker association could be expected. The second study, based on self-report and retrospective data, suggests that emotional dysregulation plays a mediating role in the association between ACEs and impulsivity.31 Neither of these studies was specifically designed to test the hypothesis that neurocognitive changes mediate the relationship between ACEs and BPD symptoms. Further research is warranted to test this hypothesis by examining if neurocognitive changes precede BPD development and by identifying the potential progression from ACEs to the neurocognitive impairments to BPD.

Several points should be considered in designing such studies: (1) prospective and longitudinal cohort studies starting in childhood or adolescence are required to gain insights into causal relationships; (2) the clinical severity of the target population should be taken into account since it may be related to the neurocognitive changes; and (3) the studies should focus on clinician ratings, experimental tasks, and neurobiological findings, rather than self-report measures, to increase the validity of the results. Indeed, given the different levels of data that would be explored, future studies could be founded on a bottom-up epistemological approach such as the National Institute of Mental Health–supported Research Domain Criteria (RDoC) to enable cross-level analyses.

Various factors complicate the task of investigating the triple linkage between ACEs, neurocognitive changes, and BPD. It is difficult to untangle the role of neurocognitive impairments since they can be an independent variable, a preceding risk factor, or a symptom of the psychopathological development of BPD. Likewise, the importance of their mediating effect on the clinical severity of BPD is still to be determined, but they seem to facilitate the self-maintenance of some clinical symptoms—for instance, when impulsivity traits are sustained by deficient inhibitory executive control.49,125 It would be informative to track patients with BPD over time to trace how the progression of cognitive functioning correlates with BPD symptomatology. Also, neurocognitively impaired patients could constitute a BPD cluster with more severe clinical symptomatology and with increased suicidal and self-harm behaviors. Notably in this context, the literature has identified a cluster of patients, often corresponding to young adults between 16 and 25 years of age,147,148 who are less studied and respond only partially to classical therapy programs.149,150

Neurocognitive functions are usually considered as good predictors of social functioning and recovery after the onset of a mental disorder, and could be the target of early interventions among those who have experienced ACEs. Cognitive remediation therapy, which has been widely validated in schizophrenia and bipolar disorder, has received little attention in BPD;151,152 approaches based on neurocognition could lead to new preventive and therapeutic strategies. Many psychotherapeutic programs are already targeting cognitive abnormalities such as attentional bias, risky decision-making, impulsivity, and problem-solving deficits.151 Such programs often involve cognitive and behavioral techniques, including neurocognitive remediation or problem solving. They could also be considered in combination with what recent guidelines consider the most effective therapies for BPD153—dialectical behavior therapy, mentalization-based therapy, or good psychiatric management for BPD—to help protect or stimulate the cognitive abilities of patients with BPD.154–156 Facial-expression recognition training might be used to counteract negativity bias in individuals who experienced ACEs and suffer from BPD. It would also be interesting to further investigate whether a history of ACEs or neurocognitive impairments influences the developmental trajectory of BPD157 and could be used to predict suicidal behaviors.158,159 Thus, although the neurocognitive approach in BPD has been little studied to date, it offers an innovative perspective to understand the disorder and improve its treatment. A few studies have emphasized the clinical usefulness of adjunctive therapy targeting neurocognitive functions and note the potential value of studying the combined effect of cognitive remediation with other integrative psychotherapeutic models.153,160 Moreover, the results of one study with 70 BPD outpatients suggest that cognitive rehabilitation could be efficacious in improving long-term psychosocial functioning.161

Various factors also contribute to the heterogeneity and discrepancies between studies in the current literature. First, the heterogeneity of BPD diagnosis itself, with all the potential permutations of diagnostic criteria and symptom dimensionality, is itself a complication. As mentioned above, the triple association might characterize a particular subpopulation of patients with BPD but not others. Likewise, the ontological issue of the diagnostic entity of BPD and its large phenotypic heterogeneity is still actively debated.162 The incorporation of dimensional measures of personality psychopathology—for instance, with the Alternative Model of Personality Disorders measured by the Personality Inventory for DSM-5 (PID-5)163 or with the International Classification of Diseases, 11th revision—may help complete the dimensional/categorical conceptualization of the clinical phenomena. Second, ACEs are a powerful transdiagnostic risk factor associated with elevated risk for multiple forms of psychopathology across development (see Figure 1). Although the differing features of ACEs seem to determine their consequences (see Figure 2), they remain poorly or unevenly studied in the literature. Importantly, the scales for ACEs currently used in clinical studies—such as the CTQ92 or the Childhood Experience of Care and Abuse Questionnaire164—may not be adapted to the personal experience of patients suffering from BPD for two reasons: (1) some experiences that patients consider traumatic may not be sufficiently covered (e.g., emotional non-validation, bullying, or witnessing domestic violence), and (2) reports on early trauma might be biased by later experiences and the psychopathology of BPD itself, such as feelings of shame or the tendency to present an overgeneral autobiographical memory. We should also investigate the intergenerational transmission of violence through heredity or learning during childhood, as well as family profiles (hyper-demanding, overprotective, or insecure), yet to our knowledge, no specific scale has been validated to explore early traumatic experiences in BPD.

Chronic shame felt after a traumatic history is rarely assessed in clinical settings. It has been shown, however, to be a central dimension of BPD.165 A particularly interesting study on patients with BPD showed significantly higher levels (2.6 times) of shame over 16 years of follow-up compared to other Axis II disorders. Severity of childhood sexual abuse and neglect have been associated with persistent feelings of shame.166 Furthermore, chronic shame is a prime influence in suicidal behaviors. Negative perception biases toward signals of social threat or cognitive distortions involving perceived abandonment underlie the relational difficulties linked to a persistent feeling of shame in patients with BPD.167

This review must be considered in light of some limitations. First, only one database was thoroughly searched, given the large number of articles in pairwise searches. Even so, a substantial number of additional sources from reference lists of screened records or expert opinion (n = 63) were added. Second, title and abstract screening was done by only one author. Third, we did not consider positive publication biases, which are likely to exist. Fourth, the heterogeneity of the available studies in terms of populations, methods or design, and limitations of statistical analysis (biased tests, underpowered samples) prevented assessment as a systematic review. For instance, the instruments used for exploring neurocognitive functions or for collecting the history of ACEs differed between studies. Most questionnaires were self-reported and retrospectively completed by adults, suggesting a memory bias. Finally, the included studies were heterogeneous, and many had small sample sizes. Important information about the conditions of study was also frequently omitted—for instance, the age at the moment of exposure to ACEs, the duration and severity of the traumatic events, or the use of psychoactive medications in BPD.

ACEs induce changes in brain structure and function, and these changes are probably related to the emergence of psychiatric disorders, such as BPD, in adulthood. As suggested elsewhere,22 however, ACE-related changes may involve plastic adaptions to a hostile environment and should not necessarily be considered as pathological. That is, the brain structures and connections of people exposed to ACEs may have been modified to react quickly when a fearful stimulus appears or is anticipated.141 If so, the symptoms of BPD could partly result from the need to resettle into a non-hostile environment some years later, once brain development has ended. Neurocognitive changes may thus take the form of dysfunctional personality traits in adulthood. An instrument combining relevant clinical and neuropsychological elements to identify the subjects most at risk of suicide in BPD could be helpful in psychiatric emergency and post-emergency departments. Assessing the emotional and neurocognitive response of patients with BPD exposed to ACEs could lead to new research opportunities and innovative preventive or therapeutic targets.

Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the article.

We thank Sarah Kabani for substantive editing help.


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borderline personality disorder; childhood trauma; early adversity; neurocognitive impairments; neuropsychology

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