Pharmacological interventions for antisocial personality disorder.
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ABSTRACT:
SUBMITTER: Khalifa NR
PROVIDER: S-EPMC8094881 | biostudies-literature | 2020 Sep
REPOSITORIES: biostudies-literature
Publications
Pharmacological interventions for antisocial personality disorder.
Khalifa Najat R NR Gibbon Simon S Völlm Birgit A BA Cheung Natalie H-Y NH McCarthy Lucy L
The Cochrane database of systematic reviews 20200903
<h4>Background</h4>Antisocial personality disorder (AsPD) is associated with rule-breaking, criminality, substance use, unemployment, relationship difficulties, and premature death. Certain types of medication (drugs) may help people with AsPD. This review updates a previous Cochrane review, published in 2010.<h4>Objectives</h4>To assess the benefits and adverse effects of pharmacological interventions for adults with AsPD.<h4>Search methods</h4>We searched CENTRAL, MEDLINE, Embase, 13 other dat ...[more]
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| S-EPMC8094166 | biostudies-literature
Project description:BackgroundDrugs are widely used in borderline personality disorder (BPD) treatment, chosen because of properties known from other psychiatric disorders ("off-label use"), mostly targeting affective or impulsive symptom clusters.ObjectivesTo assess the effects of drug treatment in BPD patients.Search strategyWe searched bibliographic databases according to the Cochrane Developmental, Psychosocial and Learning Problems Group strategy up to September 2009, reference lists of articles, and contacted researchers in the field.Selection criteriaRandomised studies comparing drug versus placebo, or drug versus drug(s) in BPD patients. Outcomes included total BPD severity, distinct BPD symptom facets according to DSM-IV criteria, associated psychopathology not specific to BPD, attrition and adverse effects.Data collection and analysisTwo authors selected trials, assessed quality and extracted data, independently.Main resultsTwenty-eight trials involving a total of 1742 trial participants were included. First-generation antipsychotics (flupenthixol decanoate, haloperidol, thiothixene); second-generation antipsychotics (aripirazole, olanzapine, ziprasidone), mood stabilisers (carbamazepine, valproate semisodium, lamotrigine, topiramate), antidepressants (amitriptyline, fluoxetine, fluvoxamine, phenelzine sulfate, mianserin), and dietary supplementation (omega-3 fatty acid) were tested. First-generation antipsychotics were subject to older trials, whereas recent studies focussed on second-generation antipsychotics and mood stabilisers. Data were sparse for individual comparisons, indicating marginal effects for first-generation antipsychotics and antidepressants.The findings were suggestive in supporting the use of second-generation antipsychotics, mood stabilisers, and omega-3 fatty acids, but require replication, since most effect estimates were based on single studies. The long-term use of these drugs has not been assessed.Adverse event data were scarce, except for olanzapine. There was a possible increase in self-harming behaviour, significant weight gain, sedation and changes in haemogram parameters with olanzapine. A significant decrease in body weight was observed with topiramate treatment. All drugs were well tolerated in terms of attrition.Direct drug comparisons comprised two first-generation antipsychotics (loxapine versus chlorpromazine), first-generation antipsychotic against antidepressant (haloperidol versus amitriptyline; haloperidol versus phenelzine sulfate), and second-generation antipsychotic against antidepressant (olanzapine versus fluoxetine). Data indicated better outcomes for phenelzine sulfate but no significant differences in the other comparisons, except olanzapine which showed more weight gain and sedation than fluoxetine. The only trial testing single versus combined drug treatment (olanzapine versus olanzapine plus fluoxetine; fluoxetine versus fluoxetine plus olanzapine) yielded no significant differences in outcomes.Authors' conclusionsThe available evidence indicates some beneficial effects with second-generation antipsychotics, mood stabilisers, and dietary supplementation by omega-3 fatty acids. However, these are mostly based on single study effect estimates. Antidepressants are not widely supported for BPD treatment, but may be helpful in the presence of comorbid conditions. Total BPD severity was not significantly influenced by any drug. No promising results are available for the core BPD symptoms of chronic feelings of emptiness, identity disturbance and abandonment. Conclusions have to be drawn carefully in the light of several limitations of the RCT evidence that constrain applicability to everyday clinical settings (among others, patients' characteristics and duration of interventions and observation periods).
| S-EPMC4169794 | biostudies-literature
Project description: Not available
| S-EPMC9662763 | biostudies-literature
Project description:Purpose of reviewVariation in the monoamine oxidase A (MAO-A) gene and MAO-A enzyme levels have been linked to antisocial behavior and aggression in clinical and non-clinical populations. Here, we provide an overview of the genetic, epigenetic, and neuroimaging research that has examined MAO-A structure and function in antisocial personality disorder (ASPD) and borderline personality disorder (BPD).Recent findingsThe low-activity MAO-A variable nucleotide tandem repeat genetic polymorphism has shown a robust association with large samples of violent and seriously violent offenders, many of whom had ASPD. A recent positron emission tomography (PET) study of ASPD similarly revealed low MAO-A density in brain regions thought to contribute to the psychopathology of the condition. By contrast, PET has also demonstrated that brain MAO-A levels are increased in BPD and that they relate to symptoms of low mood and suicidality.SummaryCandidate gene studies have produced the most compelling evidence connecting MAO-A genetic variants to both ASPD and BPD. Still, conflicting results abound in the literature, making it highly unlikely that ASPD or BPD is related to a specific MAO-A genetic variant. Future research should strive to examine how MAO-A genotypes interact with broad-spectrum environmental influences to produce brain endophenotypes that may ultimately become tractable targets for novel treatment strategies.
| S-EPMC5846806 | biostudies-literature
Project description:The pathophysiology of antisocial personality disorder (ASPD) remains unclear. Although the most consistent biological finding is reduced grey matter volume in the frontal cortex, about 50% of the total liability to developing ASPD has been attributed to genetic factors. The contributing genes remain largely unknown. Therefore, we sought to study the genetic background of ASPD. We conducted a genome-wide association study (GWAS) and a replication analysis of Finnish criminal offenders fulfilling DSM-IV criteria for ASPD (N=370, N=5850 for controls, GWAS; N=173, N=3766 for controls and replication sample). The GWAS resulted in suggestive associations of two clusters of single-nucleotide polymorphisms at 6p21.2 and at 6p21.32 at the human leukocyte antigen (HLA) region. Imputation of HLA alleles revealed an independent association with DRB1*01:01 (odds ratio (OR)=2.19 (1.53-3.14), P=1.9 × 10(-5)). Two polymorphisms at 6p21.2 LINC00951-LRFN2 gene region were replicated in a separate data set, and rs4714329 reached genome-wide significance (OR=1.59 (1.37-1.85), P=1.6 × 10(-9)) in the meta-analysis. The risk allele also associated with antisocial features in the general population conditioned for severe problems in childhood family (β=0.68, P=0.012). Functional analysis in brain tissue in open access GTEx and Braineac databases revealed eQTL associations of rs4714329 with LINC00951 and LRFN2 in cerebellum. In humans, LINC00951 and LRFN2 are both expressed in the brain, especially in the frontal cortex, which is intriguing considering the role of the frontal cortex in behavior and the neuroanatomical findings of reduced gray matter volume in ASPD. To our knowledge, this is the first study showing genome-wide significant and replicable findings on genetic variants associated with any personality disorder.
| S-EPMC5048197 | biostudies-literature
Project description:A paucity of cognitive and affective features of empathy can be correlated with violent behavior. We aimed to identify differences in empathy among four groups in a sample of 100 male participants: (1) 27 violent offenders with schizophrenia, (2) 23 nonviolent patients with schizophrenia, (3) 25 patients with antisocial personality disorder, and (4) 25 subjects from the general population, who formed the control group. Schizophrenia symptoms were quantified with the Positive and Negative Syndrome Scale. Empathy was measured with the empathy quotient. Theory of mind was evaluated using (a) the first-order false-belief task, (b) the hinting task, (c) the faux pas recognition test and (d) the "reading the mind in the eyes" test (revised). Differences noted among the groups were age (controls were younger) and educational status (antisocials were less educated). The empathy quotient scoring (p < 0.001) and theory-of-mind tests (p < 0.001) were distinct between the control group and the three other groups of participants, but not among the three patient groups. Patients with antisocial personality disorder, violent psychotic offenders and psychotic nonviolent patients show no remarkable differences in affective or cognitive empathy tests, but they all present deficits in empathy and theory of mind when compared to controls.
| S-EPMC10779118 | biostudies-literature
Project description:Antisocial personality disorder (ASPD) is characterised by a disregard for social obligations and callous unconcern for the feelings of others. Studies have demonstrated that ASPD is associated with abnormalities in brain regions and aberrant functional connectivity. In this paper, topological organisation was examined in resting-state fMRI data obtained from 32 ASPD patients and 32 non-ASPD controls. The frequency-dependent functional networks were constructed using wavelet-based correlations over 90 brain regions. The topology of the functional networks of ASPD subjects was analysed via graph theoretical analysis. Furthermore, the abnormal functional connectivity was determined with a network-based statistic (NBS) approach. Our results revealed that, compared with the controls, the ASPD patients exhibited altered topological configuration of the functional connectome in the frequency interval of 0.016-0.031 Hz, as indicated by the increased clustering coefficient and decreased betweenness centrality in the medial superior frontal gyrus, precentral gyrus, Rolandic operculum, superior parietal gyrus, angular gyrus, and middle temporal pole. In addition, the ASPD patients showed increased functional connectivity mainly located in the default-mode network. The present study reveals an aberrant topological organisation of the functional brain network in individuals with ASPD. Our findings provide novel insight into the neuropathological mechanisms of ASPD.
| S-EPMC4891727 | biostudies-literature
Project description:There is a high prevalence of antisocial personality disorder (ASPD) in individuals affected by substance use disorders (SUD). However, there is limited information on the specific patterns of association of ASPD with SUD severity and specific SUD diagnostic criteria. We investigated the association of alcohol, cannabis, cocaine, opioid, and tobacco use disorders (AUD, CanUD, CocUD, OUD, and TUD, respectively) in 1660 individuals with ASPD and 6640 controls matched by sex (24% female), age, and racial/ethnic background in a sample ascertained for addiction-related traits. Generalized linear regressions were used to test ASPD with respect to the five DSM-5 SUD diagnoses, their severity (i.e., mild, moderate, severe), and their diagnostic criteria. We found that ASPD is associated with the diagnosis and severity of AUD (Odds Ratio, ORs = 1.89 and 1.25), CanUD (ORs = 2.13 and 1.32), and TUD (ORs = 1.50 and 1.21) (ps < 0.003). Of the specific diagnostic criteria, the "hazardous use" criterion showed the strongest association with ASPD across the five SUDs investigated (from ORTUD = 1.88 to ORCanUD = 1.37). However, when criteria of different SUDs were included in the same model, ASPD was independently associated only with TUD "hazardous use" and CocUD "attempts to quit". Attempting to quit cocaine was inversely related to the presence of ASPD and remained significant (OR = 0.57, 95% confidence interval = 0.36-0.89) after controlling for interactive effects with sex. The current work provides novel insights into ASPD-SUD comorbidity, supporting the existence of different SUD patterns among individuals affected by ASPD.
| S-EPMC11358160 | biostudies-literature
Project description:Antisocial personality disorder (ASPD) is closely connected to criminal behavior. A better understanding of functional connectivity in the brains of ASPD patients will help to explain abnormal behavioral syndromes and to perform objective diagnoses of ASPD. In this study we designed an exploratory data-driven classifier based on machine learning to investigate changes in functional connectivity in the brains of patients with ASPD using resting state functional magnetic resonance imaging (fMRI) data in 32 subjects with ASPD and 35 controls. The results showed that the classifier achieved satisfactory performance (86.57% accuracy, 77.14% sensitivity and 96.88% specificity) and could extract stabile information regarding functional connectivity that could be used to discriminate ASPD individuals from normal controls. More importantly, we found that the greatest change in the ASPD subjects was uncoupling between the default mode network and the attention network. Moreover, the precuneus, superior parietal gyrus and cerebellum exhibited high discriminative power in classification. A voxel-based morphometry analysis was performed and showed that the gray matter volumes in the parietal lobule and white matter volumes in the precuneus were abnormal in ASPD compared to controls. To our knowledge, this study was the first to use resting-state fMRI to identify abnormal functional connectivity in ASPD patients. These results not only demonstrated good performance of the proposed classifier, which can be used to improve the diagnosis of ASPD, but also elucidate the pathological mechanism of ASPD from a resting-state functional integration viewpoint.
| S-EPMC3625191 | biostudies-literature
Project description:INTRODUCTION:Aggression is a clinical symptom of various psychiatric disorders that can be conceptualised as a physical act towards another person with the intent to cause harm. In antisocial personality disorder (ASPD), aggression is a frequent manifestation that differently compromise therapeutic and prognostic goals according to its impulsive or premeditated categorisation. ASPD is characterised by high levels of impulsivity, psychopathic traits, and a high prevalence of co-morbid substance use disorders (SUDs). Aggression in ASPD patients may determine long and recurrent imprisonment thus representing a challenge clinicians and legal experts face. OBJECTIVES:Our aims were to characterise impulsive and premeditated aggression in male ASPD offenders as well as to determine the potential role of SUDs, impulsivity, and psychopathic traits as predictors. MATERIALS AND METHODS:In this cross-sectional study we evaluated a sample of ASPD offenders with a battery of clinical and psychometric, standardised instruments: the Psychopathy Checklist-Revised (PCL-R), the European Version of the Addiction Severity Index (EuropASI), the Barratt Impulsivity Scale Version 11 (BIS-11), and the Impulsive/Premeditated Aggression Scale (IPAS). RESULTS:We used a total sample of 134 offenders, all of whom were male. ASPD patients (n = 96) had a 71.9% prevalence of impulsive aggression and a 28.1% prevalence of premeditated aggression. ASPD patients with impulsive aggression had significantly lower scores of total PCL-R (p<0.01) factor 1 and interpersonal facet 1 (p<0.05), compared with ASPD patients with premeditated aggression. ASPD patients with impulsive aggression and ASPD patients with premeditated aggression had comparable BIS-11 mean scores, and exhibited an equal prevalence of SUDs. The interpersonal facet 1of the PCL-R predicted the aggression type (p<0.05) in ASPD patients, and the exponential beta value for facet 1 was 1.42 (CI = 1.03; 1.95). CONCLUSIONS:The aggression type that is associated with ASPD is mainly impulsive in nature. ASPD patients who have higher scores of psychopathic traits have a lower probability of exhibiting impulsive aggression and a higher probability of exhibiting premeditated aggression. Although ASPD patients have high levels of impulsivity and a high frequency of SUDs, these two variables were not predictors of the aggression type.
| S-EPMC7059920 | biostudies-literature