The human brain is a complex system composed by several large scale intrinsic networks with distinct functions. The low frequency oscillation (LFO) signal of blood oxygen level dependent (BOLD), measured through resting-state fMRI, reflects the spontaneous neural activity of these networks. We propose to characterize these networks by applying the multiple frequency bands analysis (MFBA) to the LFO time courses (TCs) resulted from the group independent component analysis (ICA). Specifically, seven networks, including the default model network (DMN), dorsal attention network (DAN), control executive network (CEN), salience network, sensorimotor network, visual network and limbic network, are identified. After the power spectral density (PSD) analysis, the amplitude of low frequency fluctuation (ALFF) and the fractional amplitude of low frequency fluctuation (fALFF) is determined in three bands: <0.1 Hz; slow-5; and slow-4. Moreover, the MFBA method is applied to reveal the frequency-dependent alternations of fALFF for seven networks in schizotypal personality disorder (SPD). It is found that seven networks can be divided into three categories: the advanced cognitive networks, primary sensorimotor networks and limbic networks, and their fALFF successively decreases in both slow-4 and slow-5 bands. Comparing to normal control group, the fALFF of DMN, DAN and CEN in SPD tends to be higher in slow-5 band, but lower in slow-4. Higher fALFF of sensorimotor and visual networks in slow-5, higher fALFF of limbic network in both bands have been observed for SPD group. The results of ALFF are consistent with those of fALFF. The proposed MFBA method may help distinguish networks or oscillators in the human brain, reveal subtle alternations of networks through locating their dominant frequency band, and present potential to interpret the neuropathology disruptions.

This study evaluated how change in posttraumatic stress disorder (PTSD) symptoms was associated with residualized change in comorbid personality disorder (PD) features and vice versa over the course of 5-10 years. The sample was comprised of 79 female rape survivors who met criteria for PTSD and who were a part of a larger study examining the effects of trauma-focused therapy. PTSD was assessed with the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) version of the Clinician-Administered PTSD Scale [CAPS-IV (1)] and PD features were assessed with the DSM-IV dimensional PD scales on the Schedule for Non-adaptive and Adaptive Personality [SNAP (2)]. PTSD symptom severity and PD features were assessed at baseline and between 5 and 10 years after completing treatment. Multiple regression analyses revealed that PTSD symptom change was related to residualized change in PD severity for paranoid, schizotypal, antisocial, borderline, avoidant, and dependent PD (βs ranged from -0.23 to -0.33; all ps < 0.05). In addition, for borderline and antisocial PDs, longitudinal stability of the PD was attenuated among those with greater PTSD symptom improvement (i.e., the relationship between these PDs over time was altered as a function of PTSD symptom change; βs ranged from -0.27 to -0.29; all ps < 0.05). Similarly, change in severity of paranoid, schizotypal, antisocial, avoidant, and obsessive-compulsive (OC) PD was associated with residualized change in PTSD symptoms (βs ranged from -0.32 to -0.41; all ps < 0.05), and the longitudinal stability of PTSD was attenuated as a product of change in OC PD (β = -0.27; p < 0.02). These findings suggest that these two sets of disorders may impact one another substantially, altering the course of even chronic, characterological conditions. This carries important clinical implications for the treatment of both PTSD and PDs.

We examined whether personality disorders (PDs) (any, cluster A/B/C) were associated with bone mineral density (BMD) in a population-based sample of Australian women (n = 696). Personality and mood disorders were assessed using semi-structured diagnostic interviews. BMD was measured at the spine, hip, and total body using dual-energy x-ray absorptiometry (GE-Lunar Prodigy). Anthropometrics, medication use, physical conditions, and lifestyle factors were documented. The association between PDs (any, cluster A/B/C) and BMD (spine/hip/total body) was examined with multiple linear regression models. The best models were identified by backward elimination including age, weight, physical activity, smoking status, alcohol consumption, dietary calcium intake, mood disorders, physical multimorbidity, socioeconomic status, and medications affecting bone. The variables were retained in the model if p < 0.05. All potential interactions in final models were tested. Those with cluster A PD, compared to those without, had 6.7% lower hip BMD [age, weight adjusted mean 0.853 (95% CI 0.803-0.903) vs. 0.910 (95% CI 0.901-0.919) g/cm2, p = 0.027] and 3.4% lower total body BMD [age, weight, smoking, alcohol, calcium adjusted mean 1.102 (95% CI 1.064-1.140) vs. 1.139 (95% CI 1.128-1.150) g/cm2, p = 0.056]. No associations were observed between cluster B/C PDs and hip/total body BMD or between any of the PD clusters and spine BMD. To our knowledge, this study is the first to investigate the bone health of women with PD in a population-based sample. Given the paucity of literature, replication and longitudinal research including the examination of underlying mechanisms and sex differences are warranted.

To examine personality/temperament features and mental health vulnerability in offspring of mothers with bipolar disorders (BD), including dimensions which may impact psychological characteristics or therapeutic measures.

Personality disorder symptomatology (PD-Sx) can result in personal distress and impaired interpersonal functioning, even in the absence of a clinical diagnosis, and is frequently comorbid with psychiatric disorders such as substance use, mood, and anxiety disorders; however, they often remain untreated, and are not taken into account in clinical studies. To investigate brain morphological correlates of PD-Sx, we measured subcortical volume and shape, and cortical thickness/surface area, based on structural magnetic resonance images. We investigated 37 subjects who reported PD-Sx exceeding DSM-IV Axis-II screening thresholds, and 35 age, sex, and smoking status-matched control subjects. Subjects reporting PD-Sx were then grouped into symptom-based clusters: N = 20 into Cluster B (reporting Antisocial, Borderline, Histrionic, or Narcissistic PD-Sx) and N = 28 into Cluster C (reporting Obsessive-Compulsive, Avoidant, or Dependent PD-Sx); N = 11 subjects reported PD-Sx from both clusters, and none reported Cluster A (Paranoid, Schizoid, or Schizotypal) PD-Sx. Compared to control, Cluster C PD-Sx was associated with greater striatal surface area localized to the caudate tail, smaller ventral striatum volumes, and greater cortical thickness in right prefrontal cortex. Both Cluster B and C PD-Sx groups also showed trends toward greater posterior caudate volumes and orbitofrontal surface area anomalies, but these findings did not survive correction for multiple comparisons. The results point to morphological abnormalities that could contribute to Cluster C PD-Sx. In addition, the observations parallel those in substance use disorders, pointing to the importance of considering PD-Sx when interpreting findings in often-comorbid psychiatric disorders.

Borderline personality disorder (BOR) is determined by environmental and genetic factors, and characterized by affective instability and impulsivity, diagnostic symptoms also observed in manic phases of bipolar disorder (BIP). Up to 20% of BIP patients show comorbidity with BOR. This report describes the first case-control genome-wide association study (GWAS) of BOR, performed in one of the largest BOR patient samples worldwide. The focus of our analysis was (i) to detect genes and gene sets involved in BOR and (ii) to investigate the genetic overlap with BIP. As there is considerable genetic overlap between BIP, major depression (MDD) and schizophrenia (SCZ) and a high comorbidity of BOR and MDD, we also analyzed the genetic overlap of BOR with SCZ and MDD. GWAS, gene-based tests and gene-set analyses were performed in 998 BOR patients and 1545 controls. Linkage disequilibrium score regression was used to detect the genetic overlap between BOR and these disorders. Single marker analysis revealed no significant association after correction for multiple testing. Gene-based analysis yielded two significant genes: DPYD (P=4.42 × 10-7) and PKP4 (P=8.67 × 10-7); and gene-set analysis yielded a significant finding for exocytosis (GO:0006887, PFDR=0.019; FDR, false discovery rate). Prior studies have implicated DPYD, PKP4 and exocytosis in BIP and SCZ. The most notable finding of the present study was the genetic overlap of BOR with BIP (rg=0.28 [P=2.99 × 10-3]), SCZ (rg=0.34 [P=4.37 × 10-5]) and MDD (rg=0.57 [P=1.04 × 10-3]). We believe our study is the first to demonstrate that BOR overlaps with BIP, MDD and SCZ on the genetic level. Whether this is confined to transdiagnostic clinical symptoms should be examined in future studies.

Increasing evidence has documented subtle changes in brain morphology and function in patients with borderline personality disorder (BPD). However, results of magnetic resonance imaging volumetry in patients with BPD are inconsistent. In addition, few researchers using voxel-based morphometry (VBM) have focused on attachment and childhood trauma in BPD. This preliminary study was performed to investigate structural brain changes and their relationships to attachment and childhood trauma in a homogenous sample of young adults with BPD.

Emerging neuroimaging research suggests that antisocial personality disorder (ASPD) may be linked to abnormal brain anatomy, but little is known about possible impairments of white matter microstructure in ASPD, as well as their relationship with impulsivity or risky behaviors. In this study, we systematically investigated white matter abnormalities of ASPD using diffusion tensor imaging (DTI) measures: fractional anisotropy (FA), axial diffusivity (AD), and radial diffusivity (RD). Then, we further investigated their correlations with the scores of impulsivity or risky behaviors. ASPD patients showed decreased FA in multiple major white matter fiber bundles, which connect the fronto-parietal control network and the fronto-temporal network. We also found AD/RD deficits in some additional white matter tracts that were not detected by FA. More interestingly, several regions were found correlated with impulsivity or risky behaviors in AD and RD values, although not in FA values, including the splenium of corpus callosum, left posterior corona radiate/posterior thalamic radiate, right superior longitudinal fasciculus, and left inferior longitudinal fasciculus. These regions can be the potential biomarkers, which would be of great interest in further understanding the pathomechanism of ASPD.

Borderline personality disorder (BPD) is characterized by "stable instability" of emotions and behavior and their regulation. This emotional and behavioral instability corresponds with a neurocognitive triple network model of psychopathology, which suggests that aberrant emotional saliency and cognitive control is associated with aberrant interaction across three intrinsic connectivity networks [i.e., the salience network (SN), default mode network (DMN), and central executive network (CEN)]. The objective of the current study was to investigate whether and how such triple network intrinsic functional connectivity (iFC) is changed in patients with BPD. We acquired resting-state functional magnetic resonance imaging (rs-fMRI) data from 14 patients with BPD and 16 healthy controls. High-model order independent component analysis was used to extract spatiotemporal patterns of ongoing, coherent blood-oxygen-level-dependent signal fluctuations from rs-fMRI data. Main outcome measures were iFC within networks (intra-iFC) and between networks (i.e., network time course correlation inter-iFC). Aberrant intra-iFC was found in patients' DMN, SN, and CEN, consistent with previous findings. While patients' inter-iFC of the CEN was decreased, inter-iFC of the SN was increased. In particular, a balance index reflecting the relationship of CEN- and SN-inter-iFC across networks was strongly shifted from CEN to SN connectivity in patients. Results provide first preliminary evidence for aberrant triple network iFC in BPD. Our data suggest a shift of inter-network iFC from networks involved in cognitive control to those of emotion-related activity in BPD, potentially reflecting the persistent instability of emotion regulation in patients.

Caregivers encounter serious and substantial challenges in managing hypertension in patients with subclinical or clinical borderline personality disorder (BPD). These challenges include therapeutic conflicts resulting from harmful drug-drug, and drug-disease interactions. Current guidelines provide no recommendations for concurrent psychotropic and antihypertensive treatment of hypertensive BPD patients who are at even greater cardiovascular risk.

There is a general agreement that physical pain serves as an alarm signal for the prevention of and reaction to physical harm. It has recently been hypothesized that "social pain," as induced by social rejection or abandonment, may rely on comparable, phylogenetically old brain structures. As plausible as this theory may sound, scientific evidence for this idea is sparse. This study therefore attempts to link both types of pain directly. We studied patients with borderline personality disorder (BPD) because BPD is characterized by opposing alterations in physical and social pain; hyposensitivity to physical pain is associated with hypersensitivity to social pain, as indicated by an enhanced rejection sensitivity.

Limited evidence exists regarding fitness-to-drive for people with the mental health conditions of schizophrenia, stress/anxiety disorder, depression, personality disorder and obsessive compulsive disorder (herein simply referred to as 'mental health conditions'). The aim of this paper was to systematically search and classify all published studies regarding driving for this population, and then critically appraise papers addressing assessment of fitness-to-drive where the focus was not on the impact of medication on driving.

Personality disorder (PD) is associated with elevated suicide risk, but the level of risk in primary care settings is unknown. We assessed whether PD among primary care patients is linked with a greater elevation in risk as compared with other psychiatric diagnoses, and whether the association is modified by gender, age, type of PD, and comorbid alcohol misuse.

Attention-deficit/hyperactivity disorder (ADHD) is an established risk factor for developing alcohol use disorder (AUD), and AUD-ADHD comorbidity is associated with additional psychiatric diagnoses. Several lines of evidence support the role of impulsivity as a pathway of these relationships; however, impulsivity is not a unitary construct. Thus, we sought to explore whether separate aspects of impulsivity may explain the relationship between ADHD symptoms and psychiatric comorbidity among inpatients (N = 136) with AUD. Methods: We assessed ADHD symptoms (childhood ADHD [Wender Utah Rating Scale], adult ADHD [Adult ADHD self-report scale]), health-related quality of life (HRQL; EQ-5D-5L), psychiatric comorbidity (Mini International Neuropsychiatric Interview), and impulsive personality traits (Urgency, Premeditation, Perseverance, Sensation seeking [UPPS] scale). Results: 19% of patients screened positive in the retrospective assessment of childhood ADHD, and 17% for adult ADHD. Participants reported moderate levels of problem severity in the HRQL dimensions, and 65% had ≥1 current psychiatric disorders other than AUD and ADHD. Multiple mediation indicated that there was a significant direct effect of childhood ADHD symptoms on psychiatric comorbidity (β = 0.224, 95% CI [0.080, 1.114]), and indirect effects of both reacting impetuously when experiencing negative emotions (negative urgency; β = 0.999, 95% CI [0.043, 0.461]) and the tendency to not finish tasks (lack of perseverance; β = 0.075, 95% CI [0.002, 0.297]). Conclusions: The subcomponents of impulsivity to react rashly when experiencing negative emotions and the tendency to not persist in activities seem to contribute to the relationship between ADHD symptoms (particularly those in childhood) and psychiatric comorbidity among patients with severe AUD.

Borderline personality disorder (BPD) and history of prior suicide attempt (SA) have been shown to be high predictors for subsequent suicide. However, no previous study has examined how both factors interact to modify clinical and suicide severity among adolescents.

Background: Comorbid Posttraumatic Stress Disorder (PTSD) increases the already high symptom burden of patients with Borderline Personality Disorder (BPD). As the gold standard for BPD treatment, Dialectical Behavior Therapy (DBT), does not focus on PTSD, other treatment approaches are needed. Narrative Exposure Therapy (NET) was designed to address multiple traumatic events and may be especially useful in this patient group. The aim of the present study was to determine the efficacy of NET compared to DBT based treatment (DBT-bt) in a randomized controlled trial. Methods: Female patients (n = 60) with BPD and comorbid PTSD were randomized to either a 10-week residential NET or DBT-bt. The primary outcome was change in PTSD severity as assessed by the Clinician Administered PTSD Scale (CAPS). Mixed linear models as well as reliable change, remission, and response rates were used to compare improvement across treatment groups. Results: Mixed linear model showed that patients in both treatments improved significantly over time across all outcome measures. This improvement was not more pronounced in NET (no significant time × type of treatment effect). However, NET resulted in a higher remission rate as compared to DBT-bt. PTSD remission was accompanied by BPD remission in all cases. Conclusions: This study shows the value of trauma-focused therapy in patients with BPD and PTSD for recovery in both disorders. To shorten the duration of both illnesses as much as possible, future studies should focus on the factors predicting treatment success and enabling patients to benefit from trauma-focused treatment as soon as possible. Trial registration: ClinicalTrials.gov, identifier: NCT02517723.

Borderline personality disorder (BPD) is a prevalent, complex, and serious mental disorder involving multiple symptoms and maladaptive behaviour. The underlying psychobiological mechanisms involved are not yet fully understood, but increasing evidence indicates that changes in hypothalamic-pituitary-adrenal stress axis (HPA) activity may contribute to BPD. Whilst various studies have demonstrated elevated levels of cortisol (the end-product of the HPA axis) in BPD sufferers, others have presented opposite findings. Inconsistent findings may be attributable to comorbidities, collection and measurement methods, gender, and sample size. Considering these discrepancies, the aim of this systematic review and meta-analysis was to assess available studies in the scientific literature examining basal/ baseline cortisol levels in patients diagnosed with borderline personality disorder compared to non-psychiatric controls.

Previous research has demonstrated that patients with borderline personality disorder (BPD) are more sensitive to negative emotions and often show poor cognitive empathy, yet preserved or even superior emotional empathy. However, little is known about the neural correlates of empathy. Here, we examined empathy for pain in 20 patients with BPD and 19 healthy controls (HC) in a functional magnetic resonance imaging (fMRI) study, which comprised an empathy for pain paradigm showing facial emotions prior to hands exposed to painful stimuli. We found a selectively enhanced activation of the right supramarginal gyrus for painful hand pictures following painful facial expressions in BPD patients, and lower activation to nonpainful pictures following angry expressions. Patients with BPD showed less activation in the left supramarginal gyrus when viewing angry facial expressions compared to HC, independent of the pain condition. Moreover, we found differential activation of the left anterior insula, depending on the preceding facial expression exclusively in patients. The findings suggest that empathy for pain becomes selectively enhanced, depending on the emotional context information in patients with BPD. Another preliminary finding was an attenuated response to emotions in patients receiving psychotropic medication compared to unmedicated patients. These effects need to be replicated in larger samples. Together, increased activation during the observation of painful facial expressions seems to reflect emotional hypersensitivity in BPD.

Dialectical behaviour therapy (DBT) is noted to be an intervention with a growing body of evidence that demonstrates its efficacy in treating individuals diagnosed with borderline personality disorder (BPD). Evidence for the effectiveness of DBT in publicly funded community mental health settings is lacking however. No study to our knowledge has been published on the effectiveness of a 12 month standard DBT programme without adaptations for individuals with BPD in a publicly funded community mental health setting and no study has included data across multiple time-points. The main objective of the current study was to determine if completion of a 12 month DBT programme is associated with improved outcomes in terms of borderline symptoms, anxiety, hopelessness, suicidal ideation, depression and quality of life. A secondary objective includes assessing client progress across multiple time-points throughout the treatment.

According to the nosological classification, Bipolar Disorder (BD) and Borderline Personality Disorder (BPD) are different syndromes. However, these pathological conditions share a number of affective symptoms that make the diagnosis difficult. Affective symptoms range from abnormal mood swings, characterizing both BD and BPD, to regulation dysfunctions, more specific to BPD. To shed light on the neural bases of these aspects, and to better understand differences and similarities between the two disorders, we analysed for the first time gray and white matter features of both BD and BPD. Structural T1 images from 30 patients with BD, 20 with BPD, and 45 controls were analysed by capitalizing on an innovative whole-brain multivariate method known as Source-based Morphometry. Compared to controls, BD patients showed increased gray matter concentration (p = .003) in a network involving mostly subcortical structures and cerebellar areas, possibly related to abnormal mood experiences. Notably, BPD patients showed milder alterations in the same circuit, standing in the middle of a continuum between BD and controls. In addition to this, we found an altered white matter network specific to BPD (p = .018), including frontal-parietal and temporal regions possibly associated with dysfunctional top-down emotion regulation. These findings may shed light on a better understanding of affective disturbances behind the two disorders, with BD patients more characterized by abnormalities in neural structures involved in mood oscillations, and BPD by deficits in the cognitive regulation of emotions. These results may help developing better treatments tailored to the specific affective disturbances displayed by these patients.