Running head: CAUSES AND TREATMENT OF ASPD IN JUVENILES 1

The Causes and Treatment of Antisocial Personality Disorder in Juvenile Offenders

Hannah King

Wofford College

A critical literature review submitted in partial completion of PSY 451 Senior Research

Thesis.

CAUSES AND TREATMENT OF APSD IN JUVENILES 2

The DSM-5 defines individuals with antisocial personality disorder as, those who

engage in repetitive irresponsible, delinquent and criminal behavior. It is a highly

controversial diagnosis. Clinicians and researchers argue that it is too heterogeneous,

over inclusive and demonstrates a considerable overlap with other disorders. Of the

general population, two – three percent have the antisocial personality disorder diagnosis,

with three percent of them being men and one percent being female. However, this

diagnosis is much higher in those who are incarcerated. Of those who are incarcerated,

47% of men and 21% of females are diagnosed with antisocial personality disorder.

Repeated behaviors include, performing acts that are grounds for arrest, lying, fighting or

assaulting, disregard for safety of oneself and others, failure to sustain consistent work

behavior and the mistreatment of other individuals. There are genetic and environmental

components to antisocial personality disorder, which will be discussed later. Genetics

contribute to half of the variance to antisocial behavior, while the environment also plays

a big role. Abnormalities in the brain of patients with antisocial personality disorder have

also been examined with damage in the amygdala and prefrontal cortex playing a role in

the development of antisocial personality disorder (Glenn, Johnson & Raine, 2013).

Deformities in the amygdala may be responsible for antisocial personality

disorder. Lesions and inactivation studies have established that the amygdala is essential

for the perception of fear. It is also essential for the expression of fearful behavior and

acquisitions of fear in response to stimuli that had been paired with aversive outcomes

(Morrison & Salzman, 2010). Although it is generally understood that the amygdala is

associated with fear and negative emotions, new research shows that the amygdala is

CAUSES AND TREATMENT OF APSD IN JUVENILES 3 associated with the processing of positive emotions and stimulus reward learning (Baxter

& Murray, 2002).

The prefrontal cortex is also associated with antisocial personality disorder. When

developed, the prefrontal cortex receives information from all other cortical regions and

functions in order to plan and direct motor, cognitive, affective and social behavior across

time. The prefrontal cortex develops longer than other sections of the brain. Development

might differ when a person is exposed to different environmental stimuli (stress, drugs,

hormones, social situations) (Kolb, Mychasiuk, Muhammad, Li, Frost & Gibb, 2012).

This literature review will examine the causes and treatments of antisocial

personality disorder in juvenile delinquents. The first section will discuss the

psychosocial and behavioral causes of antisocial personality disorder. The second section

will examine how the amygdala and its subregional networks and subneuclei as well as

the presence of gray matter are associated with antisocial behavior in juvenile delinquents

and will examine the structures in the prefrontal cortex and how they differ in juvenile

offenders from non-offenders, the presence of gray matter in the prefrontal cortex. The

last section will examine the use of medication and behavioral rehabilitation to treat

children with antisocial personality disorder.

Psychosocial, Behavioral and Environmental Contributions

Antisocial personality disorder has many possible causes. In this section two types

of causes will be discussed; the psychosocial/behavioral causes and the environmental

causes. Psychosocial and behavioral causes of antisocial personality disorder include the

correlation of serotonergic functioning and attention-deficit hyperactivity disorder

(ADHD), as well as interpersonal callousness. The causes that have been examined the

CAUSES AND TREATMENT OF APSD IN JUVENILES 4 most are the environmental causes of antisocial personality disorder. Environmental

causes of antisocial personality disorder include, abuse and neglect in childhood, parental

history of alcoholism, mental illness and delinquent behavior.

This section will examine the psychosocial and behavioral causes of antisocial

personality disorder in regards to how serotonergic levels are correlated with ADHD

which leads to antisocial personality disorder and how interpersonal callousness can lead

to chronic conduct problems, including antisocial personality disorder. The first

psychosocial/behavioral cause is how ADHD can lead to antisocial personality disorder.

Serotonergic function disturbances are usually associated with impulsive, aggressive

behavior in adults. However, disturbances in serotonergic function in children produce

different behaviors. Research shows that there is a relationship between childhood

disturbance in serotonergic function and the development of antisocial personality

disorder. Results showed that children who developed ADHD had a lower serotonergic

responsivity that predicts the development of antisocial personality disorder (Flory,

Newcorn, Miller, Harry & Halperin, 2007). The other psychosocial/behavioral cause of

antisocial personality disorder is interpersonal callousness (IP). Interpersonal callousness

includes, being deceitful, manipulative, grandiose, superficially charming, lacking

empathy and guilt, and not accepting responsibility for transgression (Pardini & Loeber,

2008). A longitudinal study showed the association between interpersonal callousness

and the development of chronic conduct problems (CP), such as antisocial personality

disorder. Boys who had high initial levels of IP and CP were at a high risk for developing

antisocial personality disorder (Hawes, Byrd, Waller, Lynam & Pardini, 2016). In

CAUSES AND TREATMENT OF APSD IN JUVENILES 5 conclusion, children who have lower serotonergic responsivity and ADHD or

interpersonal callousness are at a high risk of developing antisocial personality disorder.

Environmental causes of antisocial personality disorder have shown that twins

who have shared environmental factors or influences are at a higher risk of both

developing antisocial personality disorder (Lyons, True, Eisen, Goldberg, Meyer,

Faraone, Eaves, Lindon & Tsuang, 1995). In this section four different environmental

causes of antisocial personality disorder will be examined. These causes are childhood

abuse and neglect, parental alcoholism, parental mental health and parental delinquency.

Childhood abuse and neglect are common environmental causes of disorders like

antisocial personality disorder (Bierer, Yehuda, Schmeidler & Mitropoulou, 2003).

Childhood abuse and neglect greatly increase a person’s risk for being diagnosed with

antisocial personality disorder (Luntz & Widom, 1994). Researchers have looked at the

correlation of childhood abuse and neglect and the later development of personality

disorders. antisocial personality disorder has shown significant associations with sexual

and physical abuse in childhood (Bierer, Yehuda, Schmeidler, Mitropoulou, 2003). There

is also a familial component to the development of antisocial personality disorder; this

component involves the family environment (Carey, 1996). Family environments include,

parental alcoholism, mental health and delinquency. Parental alcoholism studies looked at

the way parents who have alcoholism and antisocial personality disorder contributes to

the risk of their child developing a psychiatric diagnosis, such as antisocial personality

disorder. The children of parents who have only alcoholism, are at a higher risk of

developing ADHD, conduct disorder, antisocial personality disorder and overanxious

disorder. However, children whose parents have both alcoholism and antisocial

CAUSES AND TREATMENT OF APSD IN JUVENILES 6 personality disorder are more likely to develop Oppositional Defiant Disorder (ODD). A

dysfunctional parenting style was associated with the child development of antisocial

personality disorder (Kuperman, Schlosser & Lidral, 1999). Parental mental illness is

also an environmental cause of antisocial personality disorder. Parents who had a history

of mental illness and/or suicide attempts had children who were at a greater risk of being

violent offenders, an act usually associated with antisocial personality disorder (Mok,

Pedersen, Springate, Astrup, Kapur, Antonsen, Morsm & Webb, 2016). The last

environmental cause is parental, especially the mothers’, delinquency. A study that

examined those with antisocial personality disorder and who were aggressive, looked at

the subjects’ mothers and their juvenile behavior. Results showed that those who had

mothers who were juvenile offenders were more likely to develop social adversity, such

as antisocial personality disorder. They were also more likely to use substances during

pregnancy and to offend in adulthood. The early onset of aggression was also associated

with subjects who had mothers that were juvenile offenders (Tzoumakis, Lussier &

Corrado, 2012). A child’s environment plays an important role in determining their fate.

Research shows that the environment of a child can lead to disorders, such as antisocial

personality disorder.

Knowing the causes of disorders, such as antisocial personality disorder, is

important for reducing the risk of a child developing the disorder. Many of the causes

presented above are causes that are preventable. antisocial personality disorder puts

children at a risk of becoming juvenile offenders. By identifying the causes or risk factors

of antisocial personality disorder, one can help reduce the risk of developing the disorder

and the risk of a child becoming a juvenile offender (Holmes, Slaughter & Kashani,

CAUSES AND TREATMENT OF APSD IN JUVENILES 7 2001). The psychosocial, behavioral and environmental factors of a child are all factors

that can cause the development of antisocial personality disorder.

Brain Structure Association

Much research has been done regarding the associations between antisocial

personality disorder in juvenile delinquents and their brain development. Two major

areas of the brain have been associated with antisocial personality disorder. Those two

areas are the prefrontal cortex and the amygdala. This section will examine the structures

in the prefrontal cortex and how they differ in juvenile offenders from non-offenders, the

presence of gray matter in the prefrontal cortex. It will also examine how the amygdala

and its subregional networks and subneuclei as well as the presence of gray matter are

associated with antisocial behavior in juvenile delinquents.

Psychopathy combines callous-unemotional traits with behavior that is antisocial

and inflexible (Contreras-Rodrigues, Pujol, Batalla, Harrison, Soriano-Mas, Deus, López-

Solá, Maciá, Hernández-Ribas, Pifarré, Menchón & Cardoner, 2014). The brains of

juvenile offenders, who show antisocial behavior, as well as psychopathy, have been

studied and compared to the brains of those who do not commit crimes and show no

antisocial behavior. A normal prefrontal cortex is an important area for reducing the risk

of antisocial behavior and juvenile delinquency. This section will examine the differences

in prefrontal cortexes, damage to the prefrontal cortex and the presence of gray matter in

the prefrontal cortex. Studies examining the prefrontal development in juvenile offenders

as compared to non-juvenile offenders has shown that even though there is no difference

between intelligence in the two groups, incarcerated delinquents are more impulsive,

have lower conceptual levels and flexibility and poorer critical thinking. It is believed

CAUSES AND TREATMENT OF APSD IN JUVENILES 8 that the prefrontal cortices and their limbic inputs are responsible for antisocial behavior

and antisocial personality disorder (Chretien & Persinger, 2000). Previous research done

with patients who have damage to the ventromedial prefrontal cortex show that they have

abnormal judgment responses to a moral dilemma. Researchers took those results and

decided to test if patients who have ventromedial prefrontal cortex damage would have

abnormal judgments of harmful intentions. Their results showed that those with

ventromedial prefrontal cortex damage judged actions that attempted harm, such as

murder, are permissible (Young, Bechara, Tranel, Damasio, Hauser & Damasio, 2010).

These abnormal judgments can also be associated with antisocial personality disorder.

The amount of gray matter volume also plays a role in the presentation of psychopathy in

criminals. Criminals showed less gray matter volume in the prefrontal cortex. An increase

in gray matter volume in the basal ganglia and supplementary motor area was correlated

with antisocial behavior. Higher amounts of gray mater volume in the limbic areas were

also correlated with antisocial behavior as well as a risk of violent recidivism (Leutgeb,

Leitner Wabnegger, Klug, Scharmüller, Zussner & Schienle, 2015). Reductions in

functional connectivity as well as gray matter in the prefrontal cortex are both

contributors to antisocial behavior (Contreras-Rodrigues et al., 2014).

Psychopathy is a psychiatric phenomenon that is characterized by a pathological

constellation of affective (callous, unemotional), interpersonal (manipulative, egocentric),

and behavioral (impulsive, irresponsible) personality traits (Aghajani, Colins, Klapwijk,

Veer, Andershed, Popma, van der Wee & Vereiren, 2016). Those with psychopathy show

antisocial behaviors. The area of the brain that is most frequently associated with

psychopathy and antisocial behaviors is the amygdala. This section will examine the

CAUSES AND TREATMENT OF APSD IN JUVENILES 9 amygdala as a whole, the subregional networks, subnuclei and gray matter volume in the

amygdala and how they are correlated to antisocial behavior in juvenile offenders.

Juvenile psychopathy and antisocial behavior, especially callous-unemotional traits, are

similar to the factors that are associated with adult psychopathy. Children with callous-

unemotional traits show lower levels of prosocial reasoning, lower emotional

responsivity and decreased harm avoidance. Brain imaging suggests that children with

these traits have a reduced response of the amygdala and a weaker functional

connectivity between the amygdala and ventromedial prefrontal cortex (Herpers,

Scheepers, Bons, Buitelaar & Rommelse, 2013). Adolescents who scored low on a

certain youth callous and unemotional trait assessment showed a positive correlation

between right amygdala responses and severity of violation ratings. However, when

children viewed pictures that were unpleasant and without moral transgression, the scores

of a youth psychopathy checklist assessment were negatively correlated with

hemodynamic responses in the left amygdala (Harenski, Haresnki & Kiehl, 2014). Many

studies that associated antisocial behavior and psychopathy with the amygdala are just

looking at the amygdala as a whole. However, there are subregional networks that

contribute differently to psychopathy. A study looked at the connectivity of basolateral

and centromedial amygdala networks in relation to the affective, interpersonal and

behavioral traits of psychopathy in juvenile with a history of serious delinquency. Results

showed that different connections in the amygdala are associated with different

psychopathy traits. For example, interpersonal traits of psychopathy are related to the

increase of connectivity of the basolateral and centromedial amygdala networks.

Whereas, affective psychopathic traits are related to the decrease of centromedial

CAUSES AND TREATMENT OF APSD IN JUVENILES 10 amygdala network connectivity (Aghanjani et al., 2016). Since the amygdala is not a

unitary structure, researchers examined how amygdala subnuclei respond to violence.

Segmentation identified the basolateral complex and the central subnucleus. Both are

used as seeds in a functional connectivity analysis to identify the differences in neuronal

coupling that is specific to observed violence (Yoder, Porges & Decety, 2014). Research

found that the full amygdala showed connectivity to the right middle occipital gyrus only,

however the subnuclei seeds revealed different connectivity patterns. The basolateral

complex showed enhanced connectivity with the anterior cingulate and prefrontal

regions, while the central subnucleus showed increase connectivity with the brainstem

(Yoder, Porges & Decety, 2014). Just like in the prefrontal cortex, gray matter in the

amygdala is associated with two temperament dimensions (fearlessness and

disinhibition), which are both present in juvenile offenders. MRI scans showed that the

greater the fearlessness dimension in a juvenile offender, the less gray matter is present in

their amygdala. This fearlessness temperament, as it is associated with gray matter

volume, shows evidence for the association between antisocial behavior in juvenile

offenders and their amygdala (Walters & Kiehl, 2015). Since atypical amygdala function

and connectivity is associated with psychopathy, it is important to show how it is related

to the antisocial behavior in juvenile offenders (Yoder, Porges & Decety, 2014).

In conclusion, brain development, differences and atypical functioning is

important to study for any disorder. By studying the prefrontal cortex and amygdala in

juvenile offenders with antisocial behavior, we are able to determine where the problems

develop. By understanding the structural abnormalities of the prefrontal cortex and the

CAUSES AND TREATMENT OF APSD IN JUVENILES 11 presence of gray matter in the amygdala in juveniles with antisocial behavior, we are able

to treat the problems.

Treatments

It was generally believed that there was no treatment for antisocial personality

disorder; however there has been a significant shift from the view that antisocial

personality disorder is untreatable (Meloy & Yakely, 2010). antisocial personality

disorder generally dissipates by adulthood (Ahmadi-Kadhani & Hechtman, 2014).

However, when antisocial personality disorder is presented in children, it must be treated

in order to lower the risk of the child becoming a juvenile offender. Treatment for

children with antisocial personality disorder can consist of the administration of

medication as well as a variety of psychosocial interventions which include parent-child

therapy, parent training, positive behavioral support and collaborative problem solving

(Ahmadi-Kadhani & Hechtman, 2014). This section will examine the use of medication

and behavioral rehabilitation to treat children with antisocial personality disorder.

Medication is an effective way to treat many disorders. One study looked at how

the drug clozapine affects children with antisocial personality disorder. Even though

clozapine is usually used to reduce aggression in schizophrenics and those with

borderline personality disorder, nothing had been published with how it affects those with

antisocial personality disorder. Researchers found that antisocial personality disorder

patients who were taking clozapine showed significant signs of improvement. Their

impulsive behavior and anger was more controlled. Violent incidents committed by

subjects were also reduced. There was an overall reduction in the severity of antisocial

personality disorder when subjects were taking clozapine (Brown, Larkin, Sengupta,

CAUSES AND TREATMENT OF APSD IN JUVENILES 12 Romero-Ureclay, Ross, Gupta, Vinestock & Das, 2014). This study is the first to show

the effects of clozapine on patients with antisocial personality disorder. Research like this

leads to new ways to treat those who are diagnosed with antisocial personality disorder.

The appropriate prescription of medication can be beneficial in helping prevent children,

with antisocial personality disorder, from becoming juvenile offenders (Meloy & Yakely,

2010).

Another form of treatment for children with antisocial personality disorder is

behavioral rehabilitation. This does not have to involve the use of medication for

treatment. Treatments that have the strongest empirical support among psychotherapies

include parent management training, problem-solving skills training and multisystematic

therapy (Kazdin, 2000). These treatments have been studied and research shows that they

have many strengths. However, long-term treatment is needed because the characteristics

of antisocial personality disorder (impulsivity, deceitfulness, co-morbidity with substance

use) are stable and often resistant to change (Gudonis & Giancola, 2008). Since substance

abuse is associated with juvenile offenders with antisocial personality disorder, it is

suggested that those individuals receive some form of substance abuse treatment. This

helps reduce the prevalence of antisocial behavior (Hatchett, 2015).

Although there is more research on psychotherapy treatment for juveniles with

antisocial personality disorder, there is also research that suggests certain medications can

help reduce antisocial behaviors. Like other disorders, a combination of psychotherapy

and medication is preferred (Meloy & Yakely, 2010). It is important to treat antisocial

behaviors in children because, although antisocial behaviors often go away with age,

failure to treat antisocial personality disorder can result in individuals who are untreatable

CAUSES AND TREATMENT OF APSD IN JUVENILES 13 (Gudonis & Giancola, 2008). It is also important to treat children with antisocial

personality disorder because it ensures that there will be a less likely chance of that child

becoming a juvenile offender.

Conclusions

This literature review examined the causes and treatments of antisocial

personality disorder in juvenile offenders. The previous sections discussed the

psychosocial, behavioral and environmental causes of antisocial personality disorder, the

prefrontal cortex and the amygdala’s role in antisocial personality disorder and the use of

medication and behavioral rehabilitation to treat juvenile offenders with antisocial

personality disorder. It was shown that serotonergic functioning and ADHD as well as

interpersonal callousness play a role in the psychosocial and behavioral causes of

antisocial personality disorder, while abuse and neglect in childhood, parental history of

alcoholism, mental illness and delinquent behavior are aspects of the environmental

effects. Differences in the prefrontal cortex of juvenile offenders and non-delinquent

juveniles as well as a presence of gray matter in the PFC are two of the brain

abnormalities of juveniles with antisocial personality disorder that were discussed. The

amygdala and its subregional networks and subnuclei as well as the presence of gray

matter are also factors of antisocial personality disorder brain abnormalities. A

combination of specific medications and behavioral rehabilitation prove to be the most

effective in treating juvenile offenders with antisocial personality disorder.

The environment appears to play the largest effect on the development of

antisocial personality disorder in juveniles. It is the development of antisocial personality

disorder that plays a large role in the reason why children commit crimes. Children are

CAUSES AND TREATMENT OF APSD IN JUVENILES 14 very susceptible to things when they are growing up, and if they are raised in an

environment that promotes or doesn’t discipline delinquent behavior, they will think it is

okay to act that way. Setting a positive example for children is the best way to prevent

delinquent behavior and the onset of issues like antisocial personality disorder.

It is important for places like juvenile detention centers, children’s homes and

even schools need to have better treatment plans for children who display delinquent

behavior with antisocial personality disorder as well as other disorders. It might be the

case of some juvenile detention centers that the mental healthcare the juveniles were

receiving is not always effective. It is hard for a couple of therapists to give their full

attention to every single juvenile at the detention center because the number of juveniles

severely outnumbers the amount of therapists available. It might also be the case that

therapists do not always their job at all at a detention center. Therapists will refuse to

meet with any juveniles, and if they did they would not try to do anything about the

juvenile’s behavior issues. Although there are a number of good therapists, there are also

therapists in juvenile detention centers that are not helpful in the rehabilitation of a

juvenile offender’s behavior. The population these therapists are counseling are a difficult

group to counsel because they might not always be willing to change or think that they

can change. This is an issue because, if the juvenile does not receive effective behavioral

rehabilitation, they will revert to their delinquent behavior when they are released back

into society. Medication is also an issue when offenders are not in a detention center. The

juveniles receive medication while they are in a detention center and their behavior is

modified. While they are incarcerated their behavior is regulated because they are able to

receive the proper medication. However, once they are released, they are only given

CAUSES AND TREATMENT OF APSD IN JUVENILES 15 medication for a certain amount of time. Many of the juvenile offenders do not have the

resources to continue to receive medication or behavioral rehabilitation once they are

released from a detention center. Their disorders like, antisocial personality disorder,

cannot be managed and which can result in more delinquent behaviors, since the brain

structures in those with antisocial personality disorder will always be different from those

without the disorder. Antisocial juveniles can take medication and go to therapy to relieve

the symptoms of their disorder, but if they do not continue with their treatment, they will

revert back to previous antisocial behaviors because their brain structures have not

changed.

It is very important for juvenile offenders with antisocial personality disorder to

receive treatment (behavioral and medication) after they are released from a juvenile

detention center. If the proper treatment is not received in the detention center, they will

have a harder time reintegrating back into society. If they do not continue treatment

outside of a detention center, they will be more likely to repeat their delinquent behavior

since their disorder is not under control.

CAUSES AND TREATMENT OF APSD IN JUVENILES 16 References

Aghanjani, M., Colins, O., Klapwijk, E., Veer, I., Andershed, H., Popma, A., van der

Wee, N., Vermeiren, R. (2016). Dissociable relations between amygdala

subregional networks and psychopathy trait dimensions in conduct-disordered

juvenile offenders.

Ahmadi-Kashani, Y., Hechtman, L. (2014). Antisocial behavior in children with ADHD:

clinical presentation, epidemiology, etiology, prognosis and treatment approaches.

Antisocial behavior: Etiology, genetic and environmental influences and clinical

management. 113-132.

Baxter, M., Murray, E. (2002). The amygdala and reward. Nature Reviews Nueroscience.

563.

Bierer, L., Yehuda, R., Schmeidler, J., Mitropoulou, V., New, A., Silverman, J., Siever,

L. (2003). Abuse and neglect in childhood: relationship to personality disorder

diagnoses. CNS Spectr, 8(10). 737-754.

Brown, D., Larkin, F., Sengupta, S., Romero-Ureclay, J., Ross, C., Gupta, N., Vinestock,

M., Das, M. (2014). Clozapine: an effective treatment for seriously violent and

psychopathic men with antisocial personality disorder in a UK high-security

hospital. CNS Spectr, 19(5). 391-402.

Carey, G. (1996). Family and genetic epidemiology of aggressive and antisocial

behavior. Aggression and Violence: Genetic, Neurobiological and Biosocial

Perspectives. 3-21.

Chetein, R., Persinger, M. (2000). “Prefrontal deficits” discriminate young offenders

from age-matched cohorts: juvenile delinquency as an expected feature of the

CAUSES AND TREATMENT OF APSD IN JUVENILES 17

normal distribution of prefrontal cerebral development. Psychol Rep, 87(3). 1196-

1202.

Contreras-Rodríguez, O., Pujol, J., Batalla, I., Harrison, BJ., Soriano-Mas, C., Deus, J.,

López-Solà, M., Macià, D., Pera, V., Hernández-Ribas, R,. Pifarré, J,. Menchón,

JM., Cardoner, N. (2015). Functional connectivity bias in the prefrontal cortex of

psychopaths. Biol Psychiatry, 78(9). 647-655.

Driemeyer, W., Spehr, A., Yoon, D., Richter-Appelt, H., Briken, P.J. (2013). Comparing

sexuality, aggressiveness, and antisocial behavior of alleged juvenile sexual and

violent offenders. Forensic Sci,58(3),711-718.

Emmelkamp, P., Vedel, E. (2010). Psychological treatments for antisocial personality

disorder: Where is the evidence that group treatment and therapeutic community

should be recommended? Personality and Mental Health, 4(1). 30-33.

Flory, J., Newcorn, J., Miller, C., Harty, S., Halperin, J. (2007). Serotonergic function in

children with attention-deficit hyperactivity disorder; relationship to later

antisocial personality disorder. The British Journal of Psychiatry, 190. 410-414.

Glenn, A., Johnson, A., Raine, A. (2013). antisocial personality disorder: A current

review. Psychiatry Rep, 15(427).

Gudonis, L., Giancola, P. (2008). Commentary A: Misunderstandings surrounding the

treatment of juvenile delinquency. Leading-edge Cognitive Disorders Research.

1-4.

Harenski, C., Harenski, K., Kiehl, K. (2014). Neural processing of moral violations

among incarcerated adolescents with psychopathic traits. Dev Cogn Neurosci, 10.

181-189.

CAUSES AND TREATMENT OF APSD IN JUVENILES 18 Hatchett, G. (2015). Treatment guidelines for clients with antisocial personality disorder.

Journal of Mental Health Counseling, 37(1). 15-27.

Hawes, S., Byrd, A., Waller, R., Lynam, D., Pardini, D. (2016). Late childhood

interpersonal callousness and conduct problem trajectories interact to predict adult

psychopathy. Child Psychol Psychiatry.

Herpers, P., Scheepers, F., Bons, D., Buitelaar, J., ROmmelse, N. (2014). The cognitive

and neural correlates of psychopath and especially callous-unemotional traits in

youths:a systematic review of the evidence. Dev Psychopathol, 1.245- 273.

Holmes, S., Slaughter, J., Kashani, J. (2001). Risk factors in childhood that lead to the

development of conduct disorder and antisocial personality disorder. Child

Psychiatry and Human Development, 31(3). 183-193.

Hutton, EL., Woodworth, M. (2014). Violent female youth: an examination of

instrumental violence, psychopathy, and offense characteristics. Behav Sci Law,

32(1). 121-134.

Kazdin, A. (2000). Treatments for aggressive and antisocial children. Child and

Adolescent Psychiatric Clinics of North America, 9(4). 841-858.

Kolb, B., Mychasiuk, R., Muhammad, A., Li, Y., Frost, D., Gibb, R. (2012). Experience

and the developing prefrontal cortex. PNAS, 109(2). 17186-17193.

Kuperman, S., Schlosser, S. Lidral, J. (1999). Relationship of child psychopathology to

parental alcoholism and antisocial personality disorder. Journal of the American

Academy of Child & Adolescent Pschiatry, 38 (6). 686-692.

Lahey, B. (2008). Oppositional defiant disorder, conduct disorder, and juvenile

delinquency. Child and Adolescent Psychopathology, 335-369.

CAUSES AND TREATMENT OF APSD IN JUVENILES 19 Lang, F., Otte, S., Vasic, N., Jäger, M., Dudeck, M. (2015). Impulsivität bei

kurzzeitgefangenen mit einer antisozialen persönlichkeitsstörung. Psychiatrische

Praxis, 42(5). 274-277.

Leutgeb, V., Leitner, M., Wabnegger, A., Klug, D., Scharmüller, W., Zussner, T.,

Schienle, A. (2015). Brain abnormalities in high-risk violent offenders and their

association with psychopathic traits and criminal recidivism. Neuroscience, 308.

194-201.

Levy, T., Orlans, M. (1999). Kids who kill: attachment disorder, antisocial personality

and violence. The Forensic Examiner, 8(3-4). 19-24.

Luntz, B., Widom, C. (1994). antisocial personality disorder in abused and neglected

children grown up. The American Journal of Psychiatry, 151(5). 670-674.

Lyons, M., True, W., Eisen, S., Goldberg, J., Meyer, J., Faraone, S., Eaves, L., Lindon, J.,

Tsuang, M. (1995). Differential heritability of adult and juvenile antisocial traits.

Archives of General Psychology, 52(11). 906-915.

McGruffin, P., Thapar, A. (1998). Genetics and antisocial personality disorder.

Psychopathy: antisocial, criminal, and violent behavior. 215-230.

Meloy, J., Yakeley, J. (2010). Psychodynamic treatment of antisocial personality

disorder. Psychodynamic Psychotherapy for Personality Disorders: A Clinical

Handbook. 311-336.

Mitchell, J. (1992). Linkages among deviance in adolescence, antisocial personality

disorders in adulthood, and work behavior. Economics and Mental Health, 182-

192.

CAUSES AND TREATMENT OF APSD IN JUVENILES 20 Mok, P., Pedersen, C., Springate, D., Astrup, A., Kapur, N., Antonsen, S., Morsm O.,

Webb, R. (2016). Parental psychiatric disease and risk of attempted suicide and

violent criminal offending in offspring: a population-based cohort study. JAMA

Psychiatry.

Monahan, K., Steinberg, L., Cauffman, E., Mulvey, E. (2013). Psychosocial (im)maturity

from adolescence to early adulthood: distinguishing between adolescence-limited

and persisting antisocial behavior. Dev Psychopathol, 25(4). 1093- 1105.

Morrison, S., Salzman, C. (2010). Revaluing the amygdala. Current Opinion in

Neurobiology, 20(2). 221-230.

Otero, M., Carrillo-de-la-Peña, M., Mirón, L. (1994). Dimensions of antisocial behavior

in juvenile delinquency: A study of personality variables. Psychology, Crime &

Law, 1(1), 27-37.

Pardini, D., Loeber, R. (2008). Interpersonal callousness trajectories across adolescne.

Criminal Justice Behavior, 35(2), 173-196.

Pincham, H., Bryce, D., Pasco Fearon, R. (2015). The neural correlates of emotion

processing in juvenile offenders. Dev Sci, 18(6). 994-1005.

Rafferty, F. (1976). Juvenile delinquency and antisocial behavior. Psychiatric Annals,

6(7). 18-26.

Schaeffer, C., Petras, H., Ialongo, N., Poduska, J., Kellam, S. (2003). Modeling growth in

boys’ aggressive behavior across elementary school: links to later criminal

involvement, conduct disorder, and antisocial personality disorder.

Developmental Psychology, 39 (6). 1020-1035.

CAUSES AND TREATMENT OF APSD IN JUVENILES 21 Simon, L. (1998). Does criminal offender treatment work? Applied & Preventive

Psychology, 7(3). 137-159.

Sosyukalo, O., Ermolina, L., Bryun, E., Voloshin, V., Zhurnal Nevvropatologii, P.

(1990). Clinico-epidemiological characterization of deviant behavior in

adolescents. 90(8). 50-52.

Tzoumakis, S., Lussier, P., Corrado, R. (2012). Female juvenile delinquency,

motherhood, and the intergenerational transmission of aggression and antisocial

behavior. Behavioral Sciences & the Law, 30(2). 211-237.

Walters, G., Kiehl, K. 2015. Limbic correlates of fearlessness and disinhibition in

incarcerated youth: exploring the brain-behavior relationship with the Hare

Psychopathy Checklist: Youth Version. Psychiatry Res, 230(2). 205-210.

Wygant, D., Sellbom, M., Sleep, C., Wall, T., Appelgate, K., Krueger, R., Patrick,

C.(2016). Examining the DSM -5 alternative personality disorder model

operationalization of antisocial personality disorder and psychopathy in a male

correctional sample. Personality Disorders: Theory, Research and Treatment,

7(3). 229-239.

Yoder, K., Porges, E., Decety, J. (2015). Amygdala subnuclei connectivity in response to

violence reveals unique influences of individual differences in psychopathic traits

in a nonforensic sample. Hum Brain Mapp, 36 (4). 1417- 1428.

Young, L., Bechara, A., Tranel, D., Damasio, H., Hauser, M., Damasio, A. (201).

Damage to ventromedial prefrontal cortex impairs judgment of harmful intent.

Neuron, 65 (6). 845- 851.