Antisocial personality disorder

ASPD is extremely difficult to treat, and at present, the prognosis for antisocial individuals typically is considered poor. The empirical treatment literature bearing on ASPD is in its infancy, with few controlled studies having been conducted. In addition, research in this area tends to examine the outcomes of interventions for behaviors associated with ASPD, such as substance abuse and violence, rather than treatments aimed at altering the underlying personality features of the disorder. In addition, relatively little research has examined intervention outcomes with women— and when women are included in samples, results typically are not disaggregated by gender. Nevertheless, the body of literature on this topic has grown over the past decade, and some broad trends are apparent. Several studies have investigated the outcomes of substance abuse treatment among individuals with ASPD. Most results indicate that persons with co-occurring substance abuse problems and ASPD make treatment gains on par with those of individuals in substance abuse treatment without ASPD. However, other studies on this topic suggest less improvement in individuals with ASPD than in others. Furthermore, research suggests that broad classifications such as “substance abuser” may be too generic and that differences based on an individual’s drug of choice and the severity of the impact on daily functioning may be important to treatment outcome. Given the nature of the diagnosis, it is not surprising that most treatment outcome studies on ASPD have been conducted with offender samples. Although at this time, research data do not endorse a specific type of treatment for ASPD, there is strong empirical support for the effectiveness of certain guiding principles. The principles of risk, need, and responsivity indicate that treatment outcome will be maximized as a function of a treatment program’s match with an individual’s level of risk, criminogenic needs (changeable risk factors), and learning style. Meta-analytic reviews indicate that the strongest predictor of success across different correctional programs and offender groups—including both men and women—is treatment that adheres to these three principles. Another aspect of treatment with empirical support is the multimodal hypothesis, which suggests that correctional treatment is most effective when multiple need areas of an offender are targeted. Research demonstrates that multimodal programs that incorporate cognitive-behavioral and social learning strategies are associated with substantially larger treatment gains than are nonbehavioral interventions. In addition, there is a positive association between the number of criminogenic needs targeted for intervention and subsequent reductions in recidivism. In contrast, approaches that are contraindicated for treating ASPD because they are viewed as unresponsive to offenders’ criminogenic needs and/or learning style include traditional “talk” psychotherapy of the psychodynamic, client-centered, and insight-oriented ilk. Programs that include a relapse prevention element are associated with enhanced reductions in recidivism. Relapse prevention is a cognitive-behavioral approach to self-management that entails teaching individuals alternate (more effective) responses to high-risk situations. Components of relapse prevention that seem to be especially effective in reducing recidivism include identifying one’s offense-chain and high-risk situations and, subsequently, role-playing alternate (more effective) ways of handling such situations. Antisocial Personality Disorder Etiology Specifying etiological mechanisms for ASPD is difficult because of the nonspecificity of the disorder. That is, there are innumerable symptom combinations that can give rise to a diagnosis. Furthermore, a diagnosis can arise almost solely from a person having engaged in chronic criminal and violent behavior. That is, there are no pathognomonic, necessary, or sufficient signs of ASPD. Therefore, almost anything that predicts chronic crime and violence ostensibly could be considered a candidate etiological factor for ASPD. Nevertheless, there is evidence for certain genetic, biological, and environmental etiological mechanisms in ASPD. Large-scale twin and adoption research shows a high degree of heritability for PDs generally, as well as for ASPD specifically. An interesting line of research by Robert Krueger and colleagues has shown that ASPD might be construed as part of a heritable externalizing spectrum of psychopathology that includes antisocial personality features and behavior, substance use problems, conduct problems, sensation seeking, and low constraint. Potential biological mechanisms include neurochemical imbalances, such as low serotonin levels, that are related to impulsive and aggressive behavior. Some biological etiological mechanisms have been advanced more specifically for psychopathy, which includes additional interpersonal and emotional deficits. For instance, some experts propose that psychopathy, and as such some cases of ASPD, is associated with functional brain deficits, such as a diminished ability to process emotion or impaired information processing. Other mechanisms could include temperamental deficiencies, such as decreased startle potentiation. Structural, as opposed to functional, neuroanatomic models have been proposed as well, including deficits in prefrontal and temporal lobe gray matter. It is important to note that all such research on the biological mechanisms of psychopathy and ASPD is in its infancy and cannot yet support definitive statements about clear etiological factors. Environmental factors also may elevate the risk of the development of ASPD. For instance, abusive, inconsistent, or permissive parental disciplinary styles predict delinquency and adult criminality. Similarly, other family-of-origin and formative experiences predict delinquent and criminal behavior, such as parental criminality, violence, and substance use problems. Social learning theory would posit that such parental behaviors model criminal behavior for children, who then learn to use crime and violence in their own lives. Of course, many such parental factors could be acting as mere proxies for genetic etiological mechanisms, and future research will need to disentangle genetic from environmental risk factors. Some interesting emerging research has started to do so. For instance, parental physical maltreatment of children has been found to predict antisocial behavior above and beyond the heritable aspects of parental antisociality. Furthermore, research is starting to address gene-environment interactions vis-a-vis antisocial behavior and personality, which posit that genetic and environmental factors might be multiplicative in their influence on such outcomes rather than merely additive. Antisocial Personality Disorder Controversies The ASPD diagnosis has generated controversy on several fronts. The debate that has received the most commentary pertains to whether the diagnostic criteria should emphasize objective behaviors or personality features. The introduction of ASPD into the DSM was intended to reflect the clinical disorder known as psychopathy, which includes features such as callousness, remorselessness, guiltlessness, superficiality, and shallow affect. The ASPD criteria were written with a behavioral focus in the service of the decreasing subjectivity involved in rating personality features, thereby increasing reliability. In the current diagnostic nomenclature, ASPD is presented as being largely the same as psychopathy—even though many of the descriptors traditionally associated with psychopathy are absent from the diagnostic criteria. That the two disorders are not in fact synonymous is highlighted by the results of contemporary prevalence studies demonstrating that about three quarters of prisoners meet the criteria for ASPD whereas only about one quarter, or less, meets the criteria for psychopathy. Additionally, the criteria have been criticized for lacking specificity; for instance, meeting diagnostic criteria may arise from a boggling number of permutations of the 7 adult disorder and 15 CD symptoms. An important impact of the imprecision with which the outcome of ASPD is delineated is that it renders investigation into the disorder’s causal factors much more challenging, as noted above. Moreover, the validity of ASPD has been challenged in light of the paucity of available longitudinal data. Critics of the ASPD criteria also argue that they are underinclusive (in that individuals will not be identified who have the core antisocial personality features but have not been criminally sanctioned or who demonstrate antisociality during adulthood but for whom there is no evidence of CD). In contrast, others advance concerns that the criteria are overinclusive (in that there likely are several etiological bases for antisociality, only one of which may be psychopathy). As noted earlier, the criteria largely reflect the behavioral difficulties associated with crime and substance use. This is noted to be problematic because behaviors can be influenced by external circumstances, whereas personality traits are viewed as being more reflective of underlying pathology. Another controversy surrounding the diagnostic criteria is the apparent diagnostic biases they invoke. Although the prevalence of ASPD genuinely may be higher among men (estimated at 3% of the population) than among women (estimated at 1%), research has documented elevated rates among men even when men and women do not differ in symptomatology. Some researchers have argued in favor of amending the diagnostic criteria to include behaviors associated specifically with antisociality in women in an effort to make the criteria more gender-neutral. Finally, concerns also have been raised that ASPD may be disproportionately overdiagnosed among prisoners and persons with substance use problems in light of the behavioral focus of the criteria. References:

1. American Psychiatric Association. (2000). Diagnostic and statistical manual of mental disorders (4th ed., text revision). Washington, DC: Author.

2. Fowler, K. A., & Lilienfeld, S. O. (2006). Antisocial personality disorder. In J. E. Fisher & W. T. O’Donohue (Eds.), Practitioner’s guide to evidence-based psychotherapy (pp. 57-67). New York: Springer.

3. Krueger, R. F., Markon, K. E., Patrick, C. J., & Iacono, W. G. (2005). Externalizing psychopathology in adulthood: A dimensional-spectrum conceptualization and its implications for DSM-V. Journal of Abnormal Psychology, 114, 537-550.

4. Moffitt, T. E. (2005). The new look of behavioral genetics in developmental psychopathology: Gene-environment interplay in antisocial behaviors. Psychological Bulletin, 131, 533-554.

5. Patrick, C. J. (2006). Handbook of psychopathy. New York: Guilford.

6. Widiger, T. A., Cadoret, R., Hare, R., Robins, L., Rutherford, M., Zanarini, M., et al. (1996). DSM-IV antisocial personality disorder field trial. Journal of Abnormal Psychology, 105, 3-16.