Antisocial Personality Disorder

Diagnostic Criteria
Criterion A. There is a pervasive pattern of disregard for and violation of the rights or others occurring since age 15years, as indicated by three (or more) of the following:

(1) failure to conform to social norms with respect to lawful behaviors as indicated by repeatedly performing acts that are grounds for arrest

(2) deceitfulness, as indicated by repeated lying, use of aliases, or conning others for personal pleasure or profit

(3) impulsivity or failure to plan ahead

(4) irritability and aggressiveness, as indicated by repeated physical fights or assaults

(5) reckless disregard for safety of self or others

(6) consistent irresponsibility, as indicated by repeated failure to sustain consistent work behavior or honor financial obligations

(7) lack of remorse, as indicated by being indifferent to or rationalizing having hurt, mistreated, or stolen from another

Criterion B. The individual is at least age 18 years.

Criterion C. There is evidence of Conduct Disorder with onset before age 15 years.

Criterion D. The occurrence of antisocial behavior is not exclusively during the course of Schizophrenia or a Manic episode.

Prevalence
The overall prevalence of Antisocial Personality Disorder in community samples is about 3% in males and about 1% in females. Prevalence estimates within clinical settings have varied from 3% to 30%, depending on the predominant characteristics of the populations being sampled. Even higher prevalence rates are associated with substance abuse treatment settings and prison or forensic settings. .

Course
Antisocial Personality Disorder has a chronic course but may become less evident or remit as the individual grows older, particularly by the fourth decade of life. Although this remission tends to be particularly evident with respect to engaging in criminal behavior, there is likely to be decrease in the full spectrum of antisocial behaviors and substance use.

Etiology
There have been many hypotheses about the etioliogical determinants of APD. Many of these take an early developmental stance citing childhood experiences such as child maltreatment or disruptive behavioral disorders in childhood, while others cite the predominance of biology, and others cite the interactions of childhood experiences and biology to mirror a stress-diathesis model.

An example developmental view of APD states child maltreatment (such as physical abuse or emotional abuse) leads to disruption in neurobiological functioning with regards to affect, behavior, and cognition in children (Wicks-Nelson, 2009) and models aggression as a means of successfully dealing with the external environment (Waschbusch, 2002). Consequently, aggressive-disruptive behavior disorders in childhood as such as conduct disorder (CD)— which has been shown to result from physically/verbally abusive, coercive parenting styles —strains relationships with parents, adults and authority figures, retards pro-social behaviors, and eases social acceptance into deviant peer groups (Snyder, 2002). Support for child maltreatment as a precursor of childhood antisocial behaviors such as CD is seen twin studies showing childhood experience of physical abuse is prospectively linked to children antisocial behavior (Jaffee et al., 2004). Support for CD as precursor of APD comes from longitudinal studies showing CD is a robust predictor of APD (Lahey, 2005) and that the strength of the prediction is often independent of adverse family or social factors (Hill, 2003). Notwithstanding, there are some who have cogently, proposed accounting for psychosocial stressors when presented with individuals identified as a belonging to a traditionally oppressed minority groups (Castillo, 1997). Here, historically, unfairly stigmatized individuals may cognitively appraise their environment as unjust and exploitative, and evolve adaptations of victimizing others before allowing themselves to be further victimized. Such psychological adaptations may be diagnosed as APD while signifying an etiological model differentiating the emergence or identification of APD in individuals due to historical and present day, political and socio-economical discrimination.

An example biological view of APD states that dysfunction in the amygdala and prefrontal lobe— the brain areas that oversee emotion processing and executive function, respectively —leads to ease of impulsive and reckless behaviors due to a decrease in the following areas: experiencing of fear, correct interpretation of affect, and behavioral inhibition (Blair et al., 2002; Morgan & Lilienfield, 2000).

Support for amygdala irregularities in persons with APD come studies showing reduced amygdala volume in persons with APD (Blair et al., 2004), decreased speed at differentially categorizing emotional words from neutral words (Kosson et al., 2006), abnormal physiological reactivity to both positive and negative emotional stimuli in persons with APD (Verona et al, 2004), and decreased anxiety as measured by physiological response to impending presentations of aversive stimuli (Fung et al., 2005). Support for prefrontal dysfunction within persons with APD come from studies showing, compared to controls, reduced perseverance and response inhibition in persons with APD on neuro-psychological testing (Blair et al., 2006), and reduced gray matter in the prefrontal lobes of persons with APD (Raine et al., 2000).

A prominent stress diathesis model concerning development of APD is the MAO (specifically, monoamine oxidase A) theory of APD in which a genetic polymorphism on the gene coding for MAOA, an enzyme that degrades neurotransmitters raised during stress, moderates the development of APD after exposure to child maltreatment (Butcher, 2010). Support for this stress diathesis model comes from studies showing low MAO activity in female victims of childhood sex abuse with APD compared to female victims of childhood sex abuse without APD (Ducci et al., 2008) differences in. Similarly, results of a meta-analysis showed MAO activity was shown male victims of childhood trauma with APD compared to male victims without (Kim-Cohen et al., 2006).

ReferencesReferences

Wicks-Nelson, R., Israel, A. C. (2008). ''Abnormal Child and Adolescent Psychology (7th Ed). Upper Saddle River, NJ: Prentice Hall.''

Waschbusch, D. A.(2002). A meta-analytic examination of comorbid hyperactive-impulsive- attention problems and conduct problems.Psychological Bulletin, 128(1), 118-150

Snyder, J. (2002). Reinforcement and coercion mechanisms in the development of antisocial behavior: peer relationships. In Reid, J.B., and Snyder, J. (Eds.), Antisocial behavior in children and adolescents: A developmental analysis and model for intervention. Washington, DC: American Psychological Association.

Jaffee, S.R., Caspi, A., Moffitt, T. E., Taylor, A. Physical maltreatment victim to antisocial child:Evidence of an environmentally mediated process.(2004). Journalof Abnormal Psychology, 113(1), 44-55

Lahey, B.B., Loeber, R.;Burke, J.D., Applegate, B.(2005).Predicting future antisocial personality disorder in males from a clinical assessment in childhood.Journal of Consulting and Clinical Psychology, 73(3),389-399.

Castillo, R. J. (1997). ''Culture and Mental Illness: A client-centered approach. '' New York: Brooks/Cole.

Hill, J. (2003). Early identification of individuals at risk for antisocial personality disorder. British Journal of Psychiatry, 182(144), 11-14.

Blair, R. James, R.1; Mitchell, D. G., Richell, R.A.,Kelly, S.,Newman, C.,[http://csaweb110v.csa.com/ids70/p_search_form.php?field=au&query=scott+sophie+k&log=literal&SID=ij7do2ikr1qa1rnf73tg6v89k5 Scott, S.K.(2002). ]Turning a deaf ear to fear: Impaired recognition of vocal affect in psychopathic individuals.Journal of Abnormal Psychology, 111(4), 682-686

Morgan, A. B., & Lilienfield, S. O. (2000). A meta-analytic review of the relation between antisocial behavior and neuropsychological measures of executive function. Clinical Psychology Review, 20, 113–136.

Blair, R. J. R., Mitchell, D. G. V., Leonard, A., Budhani, S., Peschardt, K. S., & Newman, C. (2004). Passive avoidance learning in individuals with psychopathy: Modulation by reward but not punishment. Personality and Individual Differences, 37, 1179–1192.

Kosson, D. S., Lorenz, A.R.,Newman, J.P.Effects of comorbid psychopathy on criminal offending and emotion processing in male offenders with antisocial personality disorder. Journal of Abnormal Psychology, 115(4), 798-806

Verona, E., Patrick, C. J.,Curtin, J.J., Bradley, M., Lang, P. J., Psychopathyand Physiological Response to Emotionally Evocative Sounds.Journal of Abnormal Psychology, 113(1), 99-108

Fung, M.T., Raine, A.,Loeber, R.,Lynam, D.R., Steinhauer, S.R., Venables, P. H., Stouthamer-Loeber, M.(2005). Reduced electrodermal activity in psychopathy-prone adolescents.Journal of Abnormal Psychology, 114(2), 187-196

Blair, K. S., Newman, C., Mitchell, D.G.V., Richell, R.A., Leonard, A., Morton, J., Blair, R. J. R.(2006). Differentiating among prefrontal substrates in psychopathy: Neuropsychological test findings.Neuropsychology, 20(2), 153-165

Raine, A., Lencz, T., Bihrle, S., LaCasse, L., & Colletti, P. (2000). Reduced prefrontal gray matter volume and reduced autonomic activity in antisocial personality disorder. Archives of General Psychiatry, 57,119–127.

Butcher, J.N. (2010). ''Abnormal Psychology. ''(14th ed.). Boston, MA: Pearson Education, Inc.

Ducci F., Enoch, M.A., Hodgkinson, C., Xu, K., Catena M., Robin, R.W., Goldman, D. (2008). Interaction between a functional MAOA locus and childhood sexual abuse predicts alcoholism andantisocial personality disorder in adult women. Molecular Psychiatry, 13(3), 334‐347.

Kim‐Cohen, J., Caspi, A., Taylor, A., Williams, B., Newcombe, R., Craig, I.W., Moffitt, T.E. (2006). MAOA, maltreatment, and gene‐environment interaction predicting children's mental health: New evidence and a meta‐analysis.Molecular Psychiatry, 11(10), 903‐913.

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