Download Boyle MP 2014 - Adler Graduate School

Running head: PREVENTING ANTISOCIAL PERSONALITY DISORDER
Preventing Antisocial Personality Disorder through Clinical Therapy During the
Formative Years of the Limbic System: A Review of Current Literature
A Paper
Presented to
The Faculty of the Adler Graduate School
________________________
In Partial Fulfillment of the Requirements for
The degree of Master of Arts in
Adlerian Counseling and Psychotherapy
________________________
By:
Erin L. Boyle
October, 2014
1
PREVENTING ANTISOCIAL PERSONALITY DISORDER
2
Abstract
As is the case with other severe and persistent mental illnesses, Antisocial Personality
Disorder, or ASPD, is caused by a complicated combination of genetic, biological, and
environmental causes (Benning, Hicks, Blonigen, & Krueger, 2003; Black, 2013). The
following sections of this paper will explore these contributing factors. This paper will
also aim to answer the question of what can be done during the formative years of the
limbic system to potentially offset the symptoms of Antisocial Personality Disorder and
foster pro-social behaviors and attitudes; allowing at risk individuals to live fully
functioning lives in which they feel a sense of belonging, significance, and security. The
targeted population in this paper is American males between the ages of 18 and 25 years
old. The goal of this research will be to answer the question of whether or not therapy is
an effective form of treatment and what makes that therapy more or less successful in
comparison to other forms of treatment.
PREVENTING ANTISOCIAL PERSONALITY DISORDER
3
Table of Contents
I. Introduction …………………………………………………………….………. 4
a. Statement of the Problem ………………………………………………... 5
b. Significance and Purpose of the Study ………………………………….. 6
c. Definition of Terms ……………………………………………………… 7
i. Clinical definition of antisocial personality disorder ……………. 7
ii. Goals of clinical therapy ………………………………………… 8
iii. The limbic system ………………………………………….……. 9
II. Literature Review …………………………………………………………..… 10
a. Developmental Trajectories …………………………………...……….. 10
b. Biological and Neuropsychological Contributing Factors of ASPD ...… 11
i. Genetics ………………………………………….……….…….. 11
ii. Hormones ……………………………………….……………… 12
iii. Neuropsychological dysfunctions ……………….…………..…. 14
c. Environmental Contributing Factor of ASPD ………………………….. 15
i. Trauma, abuse, and neglect ………………………………..…… 15
ii. Secure attachment …………………………………………..….. 16
iii. Evocative interactions and parental relationships …………...…. 17
iv. Paternal antisocial behavior, family dysfunction, and parental
inconsistency ……………………………………………..…….. 18
v. ADHD and peer rejection …………………………………..….. 19
d. The Formative Years as a Window of Opportunity for Change ……..… 20
e. Goals and Objectives for Treatment Planning …………………………. 23
i. Identifying and addressing defense mechanisms ………...…….. 24
ii. Ability to fulfil social roles …………………………………….. 26
iii. Emotion regulation and emotional intelligence …………...…… 27
f. Clinically Effective Treatment Models ……………………………….... 29
i. Family therapy …………………………………………...…….. 30
ii. Long-term integrative psychotherapy ………………………….. 33
iii. Modified therapeutic community treatment …………………..... 34
iv. Multisystem therapy ……………………………………………. 35
v. Pharmacological intervention ……………………………..…… 37
III. Summary, Conclusions, and Recommendations ……………………...…….. 39
a. Restatement of the Problem ……………………………………………. 39
b. Explanation of the Literature ………………………….……………….. 40
c. Recommendations for Future Research Directions and Therapeutic
Implications ……………………………………………………..……… 41
d. Further Questions ……………………………………………….……… 44
e. Conclusion ………………………………………………………...…… 44
IV. References ………………………………………………………………….….. 46
PREVENTING ANTISOCIAL PERSONALITY DISORDER
4
Preventing Antisocial Personality Disorder through Clinical Therapy during the
Formative Years of the Limbic System: A Review of Current Literature
Antisocial personality disorder is a diagnosis that carries more biases and negative
connotations than any other in the Diagnostic Statistical Manual of Mental Illness. Even
the most educated and knowledgeable professionals often associate the term with
violence, danger, and resistance to treatment. While this population rightfully warrants
feelings of apprehension amongst clinicians, it is vitally important to study. Antisocial
personality disorder, or ASPD, is as common as obsessive-compulsive disorder, panic
disorder, and attention deficit hyperactivity disorder (American Psychiatric Association,
2000). Unlike those frequently diagnosed with these common disorders, individuals with
ASPD burden society economically, socially, and emotionally (Cooke, Forth, & Hare,
1998; Harris, Rice, & Cormier, 1991; Black, 2013). Dr. Black, a professor of psychiatry
at the University of Iowa, says that “just about any bad thing in our society from
domestic violence to murder” can be traced back to ASPD. The cost of prosecuting and
incarcerating psychopaths amounts to a staggering $250 billion to $400 billion each year
in the United States (Caldwell, Vitacco, & Van Rybroek, 2006). The clinical diagnostic
criteria for Antisocial Personality Disorder include: pervasive and recurrent behaviors
that violate social norms in all areas of life and continue throughout adulthood.
The most problematic symptoms of ASPD begin to strike individuals during late
adolescence and early adulthood. Unfortunately, choices and behaviors made during this
stage of life have lifelong consequences (Caspi, Elder, & Bem, 1987; Farrington & West,
PREVENTING ANTISOCIAL PERSONALITY DISORDER
5
1990; Baird, Bennett, & Craig, 2006; Black, 2013). Individuals with ASPD frequently
fall behind and are never able to catch up to their peers as they struggle to complete their
education, begin careers, and establish relationships that will help them fulfil social roles
in a positive manner. Early identification and intervention during early adulthood may be
able to help individuals stay on task and out of the criminal justice system later in life.
Furthermore, treatment during this time may help to reduce the emotional and economic
toll ASPD takes on society by minimizing the incidences of victimization caused by the
behaviors these individuals direct against society.
Statement of the Problem
In the United States, adulthood officially begins at age 18. However, the human
brain continues to grow, change, and mature significantly after age 18. The period of
human development between adolescence and adulthood is very important. Trauma and
change during this time can have lifelong implications to the Prefrontal Cortices;
impacting the ability of the individual to modulate emotions. Research has recently
focused on the relationship between what is happening in the lives of the average 18 year
old and the changes occurring in the emerging adult brain (Baird & Bennett, 2006).
According to Abigail Baird (2006), Assistant Professor of Psychological and Brain
Sciences at Dartmouth University, young people rapidly begin to experience many new
things during adolescence, a time that Western society has named the beginning of
adulthood. This time of new experiences brings cognitive, social, and emotional
challenges. The new challenges and experiences create significant changes in the regions
of the brain known to integrate emotion and cognition in individuals ages 18 to 25 (Baird
& Bennett, 2006).
PREVENTING ANTISOCIAL PERSONALITY DISORDER
6
Trauma and stress to the brain during this time can have lifelong implications
(Jacobus, Thayer, Trim, Bava, Frank, & Tapert, 2013). The issue of how to nurture,
protect, and encourage individuals during this critical stage of development is important
to consider. This stage of rapid neurological change, accompanied by the new
independence of legal adulthood could potentially be a critical time to offset the
formation of severe and persistent mental illness, specifically illnesses that offset the
direction of young people’s lives in catastrophic ways.
Significance and Purpose of the Study
The symptoms of personality disorders begin to present themselves long before
age 25, age 18, and even before adolescence (Moffitt & Silva, 1988; Sampson Laub,
1990; Moffitt, 1990; Scott, Briskman, & O’Connor, 2014). Hard wired, genetically
prescribed, character traits often mimic the behaviors that raise red flags to mental health
professionals. These traits have usually been present throughout the duration of their
lives. Negative patterns of thinking, feeling, and behaving seem natural to these
individuals. Individuals who meet the clinical criteria for a personality disorder seldom
recognize that there may be anything wrong with their mental health. Understandably,
they usually blame extrinsic variables or other people for challenges they may encounter
in life. Issues arise when the said challenges begin to out number those that mentally
healthy people encounter on a general basis. Personality disorders cause people to
struggle when trying to relate to situations and to other people. The degree of suffering
correlates directly to the amount of impairment the symptoms have caused in
relationships, social roles, work, school, and other life tasks (Sampson & Laub, 1990;
Riser & Kosson, 2013).
PREVENTING ANTISOCIAL PERSONALITY DISORDER
7
Definition of Terms
Clinical definition of antisocial personality disorder. As is the case with all
personality disorders, people with Antisocial Personality Disorder often have a rigid and
unhealthy pattern of thinking and behaving. Their core character traits lie outside of what
is considered normal for the majority of the population. These character traits fall into
one of three sub groups: affective features, interpersonal features, and behavior patterns.
The affective features present in those with Antisocial Personality Disorder (ASPD) refer
to the absence of guilt and empathy (Black, 2013). The interpersonal features are
narcissism and superficial charm. Typical behaviors of someone with ASPD include
dishonesty, manipulativeness, and reckless risk-taking (Hare, 1993). Western culture has
used the word “Psychopath” to refer to what the Diagnostic Statistical Manual of Mental
Disorders calls Antisocial Personality Disorder. Psychopaths are characterized by an
absence of empathy and poor impulse control; with a total lack of conscience (Hare,
1993). About 1% of the total population can be defined as psychopathic, according to a
detailed psychological profile checklist (Cooke, 1998).
Although the DSM-V (American Psychiatric Association, 2013) states that ASPD
is “also known as psychopathy” (p. 645), ASPD diagnostic criteria focus primarily on
behavioral deviance, whereas psychopathy encompasses a wide range of affective,
interpersonal, and behavioral disturbances. The ASPD criteria do not include many of
these interpersonal and affective features. Nevertheless, it is very difficult to find a true
distinction between ASPD and psychopathy without getting frustrated with the blurred
lines. Many professionals use the two terms interchangeably (Lewis, 1991; Kirkman,
2008; Gurley, 2009). Chronic antisocial behavior is referred to as psychopathy in the
PREVENTING ANTISOCIAL PERSONALITY DISORDER
8
psychological literature and as antisocial personality in the psychiatric literature
(American Psychiatric Association, 2013). Psychopathy and ASPD are highly comorbid
within criminal populations (Coid, 2002; Hare, 2003). Furthermore, both are associated
with substance abuse, (Messina, Wish, Hoffman, & Nemes, 2001; Smith & Newman,
1990) predict treatment failure, (Bucholz, Hesselbrock, Health, Kramer, & Schuckit,
2000; Cunningham & Reidy, 1998; Hare, Clark, Grann, & Thornton, 2000) and
recidivism (Harris, Rice, & Cormier, 1991; Serin & Amos, 1995). These important
similarities suggest that the pathophysiology of the underlying disorders may be the same
(Riser & Kosson, 2013). For the purpose of this paper, the terms ASPD, sociopath, and
psychopathy will be used interchangeably to describe the same set of behaviors and
symptoms.
Goals of clinical therapy. Like other disorders, ASPD lies on a continuum of
severity (Black, 2013; Riser & Kosson, 2013). Serial killers lie at one end while mildly
affected individuals who commit bad acts from time to time lie at the other end. The
targeted population this literature review aims to research lie in the middle of the
spectrum; the symptoms of the disorder affect their lives enough to impact their
functioning in at least one of the five life tasks. While many with ASPD do not report
psychological suffering the same way others would, the suffering that can be prevented
by treating ASPD is that of the victims. Furthermore, many argue that if individuals are
able to remain law abiding, they will be happier in their lives (Krampen & von Eye,
2006; diZerega & Verdone, 2011; Datchi & Thomas, 2013). This assumption would
support the idea that treatment can, in fact, improve the lives of individuals by helping
PREVENTING ANTISOCIAL PERSONALITY DISORDER
9
them to remain law abiding and hence decreasing the degree to which they suffer from
symptoms of the disorder.
Limbic system. The complex of the brain primarily responsible for the emotional
lives of humans is called the limbic system. There are three areas of the limbic system
that function abnormally in the brain of a sociopath: the orbital cortex, the amygdala, and
the narrow strip of limbic cortices that connect the orbital cortex with the amygdala
(Fowles & Dindo, 2006). The orbital cortex is the area of the brain just about the eyes. It
is responsible for the coding of ethics, conscience, and impulse control. The amygdala is
located in the anterior part of the temporal cortex (Gregg & Siegel, 2001). It is one of the
most primitive parts of the human brain, responsible for processing emotion. Lastly, the
limbic cortices that connect the orbital cortex with the amygdala include: a) the cingulate
cortex, which codes for social cues, b) the hippocampal area, which codes for emotional
memories, and c) the insula, which processes empathy and intuition (Harris, Rice, &
Cormier, 1991; Mawson, 1999; Gregg & Siegel, 2001; Fowles & Dindo, 2006). When
the areas of the limbic system are underactive or inactive, a person will feel driven to
compensate for the dulled emotional reactivity by repeatedly pursuing extreme activities
simply to feel satisfied (Mawson, 1999; Baird, Bennett, & Craig, 2006).
Literature Review
Developmental Trajectories
There are three developmental trajectories of ASPD (Loeber & StouthamerLoeber, 1998; Schaeffer, Petras, Ialongo, Poduska, & Kellam, 2003). They each lead to a
different level of criminal involvement and delinquency, or severity of the disorder. The
three pathways are: 1) overt, or life-course persistent (i.e., high levels of aggression in
PREVENTING ANTISOCIAL PERSONALITY DISORDER
10
childhood and violence in adolescence and adulthood). 2) Covert, or limited-duration
(i.e., antisocial acts in childhood and nonviolent crimes later in development), and 3)
authority conflict, or late-onset offenders (i.e., a progression from stubborn behavior,
deviance, and authority avoidance to later status offending).
The age of onset of aggressive behaviors with comorbid ADHD is believed to
significantly impact the degree and severity of ASPD (Schaeffer, Petras, Ialongo,
Poduska, & Kellam, 2003). Early and persistent aggression (during preschool) is likely
to be related to a biological or genetic vulnerability that is exacerbated by poor parenting
and early school failure (Patterson et al, 1989; Moffitt, 1993; Loeber & StouthamerLoeber, 1998; Schaeffer, Petras, Ialongo, Poduska, & Kellam, 2003). Children with a
middle-childhood onset of aggression without ADHD have been found to respond more
positively to treatment than those with an early onset of aggression and with ADHD
(Tinsley & Parke, 1983; Loeber & Stouthamer-Loeber, 1998; Schaeffer, Petras, Ialongo,
Poduska, & Kellam, 2003; Scott, Briskman, & O’Connor, 2014).
Biological and Neuropsychological Contributing Factors of Antisocial Personality
Disorder
Genetics. Psychological traits and characteristics are affected by genes. At least
a dozen specific genes have been identified as high-risk, violence-related genes
(Mednick, Gabrielli, & Hutchings, 1984; Fallon, 2006; McDermott et al., 2009).
Individuals with the so-called “warrior gene” display higher levels of aggression in
response to provocation compared to individuals without the warrior gene (McDermott et
al., 2009). Monoamine oxidase A (MAOA) is an enzyme that breaks down important
neurotransmitters in the brain, including dopamine, norepinephrine, and serotonin.
PREVENTING ANTISOCIAL PERSONALITY DISORDER
11
MAOA influences aggressive behavior with potentially important implications for
interpersonal aggression, violence, political decision-making, and crime (McDermott et
al., 2009). MAOA earned the nickname “warrior gene” after researchers theorized that
the original purpose of this inherited gene once served the purpose of allowing early
humans to defend themselves against aggressive attackers. Darwinism would suggest
that only the most aggressive humans survived in times of conflict and war. Today,
humans have various forms of the gene, resulting in different levels of enzymatic activity.
People with the low-activity form (MAOA-L) produce less of the enzyme, while the
high-activity form (MAOA-H) produces more of the enzyme (McDermott et al., 2009).
Only about a third of people in Western populations have the low-activity form of
MAOA. Ironically, low-activity MAOA is much more common in some populations that
have a history of warfare. MAOA is less associated with aggression when the degree of
provocation is low in comparison to high-provocation situations where MAOA
significantly predicted aggression (McDermott et al., 2009).
The effects of the MAOA gene express themselves differently in men and
women. Because the gene is found on the X chromosome, females receive either two
normally functioning forms of the gene, or at least one normally functional MAOA
variant that offsets the potentially dangerous implication of the “warrior” form of the
gene. Males, however, only receive one X chromosome. If that one chromosome
contains the “warrior” version of the MAOA gene, there will be no other forms to even
out its effects. This helps to explain why boys and men are much more likely to be very
aggressive or possess more psychopathic traits (Fallon, 2006).
PREVENTING ANTISOCIAL PERSONALITY DISORDER
12
Hormones. Hormones and neurotransmitters also play a vital role in supporting
the biological connection with ASPD. Those with symptoms of impulsivity and
aggression have naturally lower levels of adrenaline in their blood at baseline, and also
when they are excited, irritated, or angry (Hostinar & Gunnar, 2013). The lack of
stimulation resulting from an insufficient amount of adrenaline might cause those with
ASPD to become easily bored. In order to obtain arousal and excitement, these
individuals are more likely to attempt to seek thrills by more dangerous and extreme
measures. A lower concentration of adrenaline also supports the idea that someone with
ASPD is prone to exhibit dangerous behaviors unlike someone who normally experiences
fear and anxiety during dangerous situations. Individuals with ASPD feel less aversion to
initiating and participating in dangerous situation partially because their brains do not
release an adequate amount of adrenaline (Hostinar & Gunnar, 2013).
Neurotransmitters such as serotonin have been targeted in connection with ASPD
(Virkkunen, Goldman, Nielsen, & Linnoila, 1995). Newborns with a family history of
antisocial personality disorder have lower levels of serotonin in the brain at birth than
infants without a family history of the disorder (Constantino, Morris, & Murphy, 1997).
The reduced empathy seen in psychopathy may be associated with the influence
of low acting genes related to the hormones oxytocin and vasopressin (Fallon, 2006).
Oxytocin is a neuropeptide that affects our everyday social interactions and our ability to
behave altruistically and cooperatively; or in opposite ways of which a psychopath
behaves. Oxytocin is also responsible for a variety of virtuous behaviors in humans such
as empathy, generosity and trust (Zak, Kurzban, & Matzner, 2004). The neurotransmitter,
vasopressin, also plays a role in human aggression. Several animal studies have linked
PREVENTING ANTISOCIAL PERSONALITY DISORDER
13
high vasopressin levels to increases in aggressive behavior (Coccaro, Kavoussi, Hauger,
Cooper, & Ferris, 1998).
About five percent of the population does not release oxytocin in the same way as
their peers. The background (character traits, previous behaviors, history of violence) for
individuals who do not release Oxytocin is similar to the population diagnosed with
ASPD (Fallon, 2006). The rest of the population is biologically wired to cooperate and
trust one another. Without oxytocin, there would be no intrinsic intuition telling us
whom we can and cannot trust (Zak, 2005; Beitchman, Zai, Muir, Berall, Nowrouzi,
Choi, & Kennedy, 2012). One of the most dangerous traits of sociopaths is that they lack
empathy. Empathy allows us to understand another’s state of mind. It motivates others
to help those who are in need. Empathy is the basis of morality and social interest. In
one recent study (Barraza & Zak, 2009) participants who showed more empathic concern
(sympathy and compassion) after watching an emotional video had higher levels of
oxytocin than their counterparts. Because oxytocin is related to the pillars of social
interest: generosity, trust, and empathy, it could potentially play a critical role in the
future treatment of ASPD (Beitchman, et al., 2012).
Neuropsychological dysfunctions. Two sorts of neuropsychological deficits are
empirically associated with antisocial behavior: verbal and executive functions. Children
who have verbal neuropsychological deficits exhibit difficulty with listening, reading,
problem solving, expressive speech, writing, and memory (Mednick, Gabrielli, &
Hutchings, 1984; Moffitt & Silva, 1988b; Fallon, 2006; McDermott et al.,, 2009). These
difficulties are pervasive. When coupled with the executive neuropsychological deficits,
which symptoms include inattention and impulsivity, a compartmental learning disability
PREVENTING ANTISOCIAL PERSONALITY DISORDER
14
is produced (Price, Daffner, Stowe, & Mesulam, 1990). Boys with learning disabilities
who score low on tests of language and self-control are more likely than their peers to
exhibit aggressive antisocial behavior (Moffitt, 1990; Moffitt & Henry, 1989; Moffitt &
Silva, 1988).
When a child with neuropsychological deficits feels that he or she does not
belong, or as though he or she is inferior to his or her peers, the child will misbehave as a
way to gain social status. When gaining attention does not work, the child will move to
the next goal: to gain power and control. When the child’s efforts to feel better about
him or herself by gaining power over others are not successful, the child will retaliate out
of anger; hence resorting to what Dreikurs (1964) called the third goal of revenge.
Finally, when all else has failed and the child is left feeling insignificant, insecure,
and as though he or she does not belong in his or her community (family, school,
neighborhood, etc.), the child feels defeated. This is when antisocial behaviors become
persistent enough to define the child. The antisocial behaviors are intertwined with the
child’s sense of self and the child is propelled into a life of persistently antisocial
behavior (Dreikurs, 1964; Moffitt, 1990b; Moffitt & Henry, 1991).
What causes these neuropsychological deficits warrants discussion and
investigation, as they have serious implications for future behavior and may also render
young people more vulnerable to criminogenic environments (Moffitt, 1990b; Lynam,
Moffitt, & Stouthamer-Loeber,1993).
Environmental Contributing Factors of Antisocial Personality Disorder
While there are clear patterns in both the brains and genetics of psychopaths,
these biological markers alone are not enough to create a psychopath or warrant a
PREVENTING ANTISOCIAL PERSONALITY DISORDER
15
diagnosis of Antisocial Personality Disorder. There is a third ingredient involved in the
activation of these abnormalities, or the hindrance of growth in the neurological
development during the formative years in young adulthood. The environment
determines whether or not violence-related genes and certain brain processes are
triggered towards psychopathic behavior (Fallon, 2006; Craig, Catani, Deeley, Latham,
Daly, Kanaan, Picchioni, McGuire, Fahy, & Murphy, 2009).
Trauma, abuse, and neglect. Trauma affects adjustment and may result in
serious personality psychopathology (Tarter, Hegedus, Winsten, & Alterman, 1984;
Milner & McCanne, 1991; Bleiberg, 2002). Trauma is clinically defined as an
experience in the life of an individual that is characterized by its intensity, the incapacity
of that person to react to or cope with it adequately, and the confusion, shock, and longlasting pathogenetic influence on the psychic organization (Laplanche & Pontalis, 1992).
Severe abuse (sexual, physical, or emotional) during early childhood is
instrumental in the stunting of healthy neurological development. The timing of when
various factors come into play is critically important in determining what type of
psychopathological behavior is exhibited (Tarter, Hegedus, Winsten, & Alterman, 1984;
Fallon, 2006; Milner & McCanne, 1991).
Secure attachment. When children are deprived of support at home, antisocial
behavior will subsequently develop (Winnicott, 1953). The optimal relationship between
and infant and caregiver involves a protective and secure environment as well as titration
of gratification and frustration. Right away, an infant should receive undue attention from
his or her caregivers, so that every need is adequately met. The attention and adaptation
of the care giver to the child’s needs provides the child with a sense of control,
PREVENTING ANTISOCIAL PERSONALITY DISORDER
16
omnipotence, and the comfort of being connected with the caregiver, thus establishing a
safe environment and a secure attachment. As the child grows, the caregivers should
gradually adapt less and less, according to the infant’s ability to tolerate frustration and
“inconvenience.” When a parent or caregiver does not adapt to every need of the child,
this helps him or her to adapt to external realities appropriately, as his or her awareness of
personal needs grows concurrently (Winnicott, 1953).
However, if the primary caregiver becomes too distant or too unresponsive, the
child will suffer from early emotional deprivation; a problem that lies at the root of many
psychological issues, including antisocial behavior (Winnicott, 1953; Bandura, 1977;
Dogan, Conger, Kim, & Masyn, 2007). When children experience separations from
parents, and when parents threaten abandonment, children feel intense anger (Bowlby,
1973). When prolonged separations are paired with frightening threats, children are
likely to feel a dysfunctional level of anger toward the parents that often involves intense
hate (Dozier, Stovall, & Albus, 1999). The anger is often repressed and directed toward
others because directing anger toward a parent with antisocial traits and behaviors is too
threatening to the relationship between the child and his or her parent (Bowlby, 1973).
Almost 90% of adults with ASPD have experienced prolonged separations from a
caregiver at some point during their childhood (Zaraini, Gunderson, Marino, Schwartz, &
Frankenberg, 1989). The prolonged separations said to be most indicative of future
maladaptive behavior are from divorce or incarceration of a parent, but not as a result of
death. Parental neglect, lack of warmth, and the deterioration of attachment are most
likely to predicted criminal behavior in studies of secure attachment (Dozier, Stovall, &
Albus, 1999).
PREVENTING ANTISOCIAL PERSONALITY DISORDER
17
Evocative interactions and parental relationships. During infancy, neural
development is obstructed by poor nutrition, a lack of stimulation, and a lack of affection
(Cravioto & Arrieta, 1983; Meany, Aitken, van Berkel, Bhatnagar, & Sapolsky, 1988).
Children with neuropsychological problems evoke a challenge to even the most
resourceful, loving, and patient caregivers. One example of this is seen in studies of lowbirth-weight, premature infants. The complications that accompany premature infants
negatively influence the behavior of their caretakers; they arrive before parents are
prepared, their crying patterns are rated as more disturbing and irritating, and parents
report that they are less satisfying to feed, less pleasant to hold, and more demanding to
care for than healthy babies. Even these early negative experiences contribute to later
dysfunctional parent–child relationships, as the challenge of coping with difficult
behaviors evokes a chain of failed parent-child encounters (Sameroff & Chandler, 1975;
Tinsley & Parke, 1983, Lee & Bates, 1985). Over time, caregivers become discouraged
and subsequently reduce their efforts to actively parent their children and direct their
behavior. They become increasingly less involved in the teaching and parenting process.
(Maccoby & Jacklin, 1983; Lee & Bates, 1985; Anderson, Lytton, & Romney, 1986;
Caspi, Elder, & Bem, 1987).
Evocative interaction occurs when a child's behavior evokes distinctive responses
from others (Maccoby, & Jacklin, 1983; Caspi et al., 1987). Evocative interaction plays
an important role both in promoting antisocial behaviors when the evoked responses from
the interpersonal social environment exacerbate the child’s tendencies (Goldsmith,
Bradshaw, & Rieser-Danner, 1986; Lytton, 1990). This pattern is often maintained
throughout the life of someone who exhibits antisocial behaviors in early childhood
PREVENTING ANTISOCIAL PERSONALITY DISORDER
18
(Caspi, Elder, & Bem, 1987; Moffitt, 1993). In other words, when children “step off on
the wrong foot,” the path remains treacherous at home, as they enter school, and then as
they enter into adulthood. Quay (1987) summarized this pattern by stating: “this youth is
likely to be at odds with everyone in the environment, and most particularly with those
who must interact with him on a daily basis to raise, educate, or otherwise control him….
This pattern is the most troublesome to society, seems least amenable to change, and has
the most pessimistic prognosis for adult adjustment” (p. 121).
Paternal antisocial behavior, family dysfunction, and parental inconsistency.
The behaviors associated with ASPD are socially maladaptive and harmful. Parents with
an antisocial personality structure pose an especially injurious threat to their children.
The pathology of antisocial behavior implies traits such as deceitfulness, irresponsibility,
unreliability, and an incapability to feel guilt, remorse, or even love. This is damaging to
a child’s emotional, cognitive, and social development (Torry & Billick, 2001).
Children with a genetic predisposition to ASPD who are bring raised with a
parental style that triggers the genetic liability are at a clinically significant greater risk
for developing the disorder themselves (Weisz, Sandler, Durlak, & Anton, 2005). A
parent who is impulsive, irritable, and has little concern for their responsibilities is likely
to discipline erratically, be neglectful, and have little to no desire to seek help to improve
his or her parenting styles (Tarter, Hegedus, Winsten, & Alterman, 1984; Weisz, Sandler,
Durlak, & Anton, 2005; Ronis & Borduin, 2007; Torry & Billick, 2011).
ADHD and peer rejection. Boys with chronic aggression have a higher risk for
concentration problems than nonaggressive boys (Patterson, Reid, & Dishion, 1992;
Crijnen, Feehan, & Kellam, 1998). They are also more likely than their nonaggressive
PREVENTING ANTISOCIAL PERSONALITY DISORDER
19
counterparts to experience peer rejection (Coie, Terry, Lenox, & Lochman, 1995;
Bagwell, Coie, Terry, & Lochman, 2000; Deater-Deckard, 2001). These differences
present themselves as early as the fall semester of first grade. The subsequent patterns of
negative interactions with peers and teachers promote the persistence of aggressive and
disruptive behavior over time and heighten the risk of later antisocial behavior in
adolescence and adulthood (Bagwell, Coie, Terry, & Lochman, 2000). The data from
studies on the connections between early aggression, attention, and peer relationships is
consistent with the idea that the aggression exhibited by boys with a chronic high
trajectory may be linked to neuropsychological deficits that are also associated with
ADHD (Patterson, Reid, & Dishion, 1992; Moffitt, 1993; Coie, Terry, Lenox, &
Lochman, 1995; Jensen et al., 1997). Teacher ratings of youths' concentration problems
at school entry may be an important tool for more precisely identifying which children
would benefit most from preventive interventions (Patterson, Reid, & Dishion, 1992).
The Formative Years as a Window of Opportunity for Change
It is not abnormal for teenagers to misbehave or even exhibit antisocial behaviors.
However it is normal for these behaviors to decline after graduating from high school and
entering into adulthood (Elliott & Voss, 1974; Moffitt, 1993). Life changing milestones
that symbolize a coming of age such as: joining the army (Elder, 1986; Mattick, 1960),
getting married (Sampson & Laub, 1990), going to college, or starting a full-time job, are
thought to all be opportunities for young people to gain a sense of significance and
security in their life tasks (West, 1982; Sampson & Laub, 1990; Moffitt, 1993).
Young adults who are able to decrease and eventually stop antisocial behaviors
have had more opportunities to gain confidence and encouragement in their abilities to
PREVENTING ANTISOCIAL PERSONALITY DISORDER
20
behave in a prosocial manner and succeed academically, in comparison to young adults
who meet the clinical criteria for Antisocial Personality Disorder during young
adulthood. Young adults who are vulnerable to being diagnosed with ASPD lack the
social skills and academic achievements that allow their peers to continue on to
postsecondary education, healthy marriages, and desirable careers. These differences are
highlighted during young adulthood, hence threatening the ego, evoking defensive
behaviors, and allowing more opportunities for disadvantaged young people to feel even
further discouraged and inadequate. They often believe that they have less available
alternatives to crime than their peers (Sampson & Laub, 1990; Baird, Bennett, & Craig,
2006; Scott, Briskman, & O’Connor, 2014).
By the end of early adulthood (age 25), the brain is done growing and behavior
modification becomes increasingly difficult. At this time, the neurological damage that
has occurred in the brain of an individual with Antisocial Personality Disorder is likely to
be permanent for the duration of that individual’s life (Gregg & Siegel, 2001; Baird,
Bennett, & Craig, 2006).
The abnormalities in the brain of an adult with ASPD are all found in the limbic
regions. These abnormalities include: 1) A lack of activity in the orbital cortex: the
circuit coding for ethics, conscience and impulse control. 2) A lack of activity in the
anterior part of the temporal cortex, where the amygdala is located: a structure
responsible for the processing of emotion. 3) Under functioning in the narrow strip of
limbic cortices that connect the orbital cortex with the amygdala, namely: the cingulate
cortex, which codes for social cues; the hippocampal area, which codes for emotional
memories; and the insula, which processes empathy and “gut feelings” (Gregg & Siegel,
PREVENTING ANTISOCIAL PERSONALITY DISORDER
21
2001; Craig, Catani, Deeley, Latham, Daly, Kanaan, Picchioni, McGuire, Fahy, &
Murphy, 2009; Fallon, 2006).
The effects of the underactive limbic regions present themselves during aversive
learning, correlating with insensitivity to negative reinforcement (Craig, et al, 2009). The
two defining characteristics of psychopaths, blunted emotional response to negative
stimuli, coupled with poor impulse control, have been measured in psychological and
neuroimaging experiments (Craig, et al, 2009). Several studies have found decreased
responsiveness of the amygdala to fearful or other negative stimuli in psychopaths
(Patrick, Bradley, & Lang, 1993; Zuckerman, 1994; Baird, Bennett, & Craig, 2006;
Craig, et al, 2009).
The poor impulse control observed in psychopaths is correlated to their inability
to control aggressive behaviors. Aggression is typically divided into two categories:
reactive aggression (reacting to a threat), and instrumental (using aggression for a
personal goal). The areas of the brain involved when reacting to a threat either reactively
or instrumentally include the amygdala, the hypothalamus, and the dorsal half of the
periaqueductal gray (PAG) (Gregg & Siegel, 2001).
When one experiences threatening stimuli, the body begins to prepare to defend
itself. Activity is increased in the hypothalamus after the said stimulus has activated the
sympathetic nervous system - awareness becomes heightened and blood pressure is
raised. According to evolutionary theory, this response patterns helps humans remember
significant events and aids in the process of learning from past experience, a necessary
tool for survival (Craig, et al, 2009). Individuals with ASPD do not react the same way
to threatening stimuli as the rest of the population. Even when their safety is at risk, their
PREVENTING ANTISOCIAL PERSONALITY DISORDER
22
most primal instincts do not kick in and they do not respond to or experience fear in the
same way someone with a functional amygdale would. These changes have been
observed through studies focused on: aversive conditioning (Craig, et al, 2009); passive
avoidance learning (Moll, et al, 2005); augmentation of the startle reflex (Patrick, et al,
1993); and fearful face recognition (Zuckerman, 1994; Blair, 2010).
There is a significant difference in cortical thickness between psychopaths and
nonpsychopaths in the precentral gyrus bilaterally (Ly, Motzkin, Philippi, Kirk, Newman,
Kiehl, & Koenigs, 2012). Although the precentral gyrus is primarily known as an area
for motor planning and execution—and thus is not typically theorized to have any
meaningful role in psychopathy—there is mounting evidence that it may indeed impact
functions relevant to psychopathy. Individuals with psychopathic characteristics, such as
violence, are more likely to have a clinically significant amount of thinning in the
precentral gyrus (Narayan, Narr, Kumari, Woods, Thompson, Toga, & Sharma, 2007;
Yang, Raine, Colletti, Toga, & Narr, 2009).
Recent studies have associated precentral gyrus activity with impulsivity in
juvenile offenders (Shannon, Raichle, Snyder, Fair, Mills, Zhang, Bache, Calhoun, Nigg,
Nagel, Stevens, & Kiehl, 2011), abstract emotional meaning (Moseley, Carota, Hauk,
Mohr, & Pulvermuller, 2012), empathy for pain (Fecteau, Pascual-Leone, & Theoret,
2008), and value signals during decision making (Sul, Jo, Lee, & Jung, 2011).
Growing evidence suggests a role for the inferior frontal gyrus in social cognition
and its potential to serve as a neural substrate underlying empathy (Rizzolatti, Fadiga,
Gallese, & Fogassi, 1996; Iacoboni, 2009). Studies aimed at gaining a better
understanding of Autism (Dapretto, Davies, Pfeifer, Scott, Sigman, Bookheimer, &
PREVENTING ANTISOCIAL PERSONALITY DISORDER
23
Iacoboni, 2006; Hadjikhani, Joseph, Snyder, & Tager-Flusberg, 2006; Yamasaki,
Yamasue, Abe, Suga, Yamada, Inoue, & Kasai, 2010) have shown that a lack of “mirror”
activity and a thinning in the inferior frontal gyrus are strongly connected with deficient
empathy and impoverished interpersonal affection; which are also hallmark traits of
ASPD (Kiehl, Smith, Mendrek, Forster, Hare & Liddle, 2004; Shannon, et al., 2011).
Goals and Objectives for Treatment Planning
Because many people who suffer from this disorder will be mandated to therapy,
sometimes in a forensic or jail setting, a client who seems motivated to participate in
therapy is seldom seen. Therapy should focus on life issues that the client is already
interested in changing, such as goals relating to housing, finances, or employment;
improvement in social or family relationships; learning new coping skills, etc. The
therapist must also be sure to discuss the client’s antisocial behavior and feelings (or lack
thereof). A lack of connections between feelings and behaviors is a common sign of
ASPD. Helping the client draw those lines between the two should be included in almost
all treatment plans for clients with ASPD (Black, 2013).
Rather than rationalizing the purpose of therapy by threatening to report
noncompliance to the court or probation officers, a therapist can motivate clients by
helping them find good reasons that they may want to work on this problem further. For
instance, ensuring that they not come into contact with the court system again, be
incarcerated, have to submit themselves to additional psychological examinations, etc.
The symptoms that warrant attention in a treatment plan for someone with ASPD
include: repeated illegal activity (Aos, Phipps, Barnoski, & Lieb, 2001); lying and
deceitfulness; impulsivity; irritability and aggression; disregard for safety of oneself or
PREVENTING ANTISOCIAL PERSONALITY DISORDER
24
others; irresponsibility regarding work, family, or finances; lack of guilt, remorse, or
empathy for others; lack of concern for consequences of behavior; inability to learn from
experience or change behavior based on past outcomes or predicted future outcomes;
bullying or cruelty to animals and/or other humans; and destruction of property (Benning,
Hicks, Blonigen, & Krueger, 2003; Hare, 2003; Caldwell, Vitacco, & Van Rybroek,
2006; American Psychiatric Association, 2013; Black, 2013).
Identifying defense mechanisms. Many professional theorists and clinicians
argue that all symptoms serve a purpose, and that all behavior is purposeful. The
underlying purpose of almost all maladaptive behavior is to essentially defend the
psyche. Freud would refer to this as the ego, whereas Adler would argue that it is the
need to belong and feel significant and secure that is being defended. Just like everyone
else, even those with Antisocial Personality Disorder need to protect their egos and feel a
sense of belonging, significance, and security. By studying what defense mechanisms
those with ASPD are most likely to use, therapists can gain a more clear understanding of
the motivations behind their clients’ behaviors and thus be better equipped to impact
change.
Omnipotence, denial, devaluation, splitting, dissociation, projection,
rationalization, and projective identification are positively associated with ASPD as the
most common defense mechanisms. Repression is negatively associated with ASPD,
meaning it is seldom seen by treatment providers and assessors (Perry, Presniak, &
Olson, 2013). The defense mechanisms used by individuals with ASPD can be
categorized into two groups: image-distorting defenses (i.e., omnipotence, devaluation,
PREVENTING ANTISOCIAL PERSONALITY DISORDER
25
and idealization) and disavowal defenses (i.e., denial, rationalization, and projection)
(Draughon, 1977).
Concurrent with the clinical criteria required for a diagnosis of ASPD, the
distorted view of themselves and others is maintained by disavowal and image-distortion
directed at anything that threatens their omnipotent self-view (Draughon, 1977; Hare,
2003; Hemphäiä & Hodgins, 2014).
Individuals with ASPD intrinsically deny themselves a negative self-image,
resulting in what is referred to as a split-off self-image (Gacono, Meloy, & Berg, 1992).
To many people, self-worth is contingent upon many external factors – intelligence,
monetary earning potential, physical attractiveness, charitable activity. Individuals with
ASPD have already been receiving numerous messages throughout their lives indicating
that they are not capable of being considered a worthwhile human. By early adulthood,
these individuals have successfully managed to perfect defense mechanisms that will
protect them from truly feelings worthless as a human being. They no longer need to
adequately fulfil all social roles in order to feel valuable and worthwhile. The use of
denial and omnipotence/grandiosity as a barrier between them and self-awareness
excuses them from the pressures others feel from the perception of social inadequacy.
Any negative experience that threatens their ego is disavowed by denying the effects of
their behaviors on others, rationalizing their criminal and/or aggressive actions, and
projecting their negative experiences onto others (Gacono et al., 1992; Presniak et al.
2010).
Ability to fulfil social roles. It is common for young men with sociopathic traits
to depend on relatives for assistance with basic needs such as housing, employment, and
PREVENTING ANTISOCIAL PERSONALITY DISORDER
26
health care (diZerega & Verdone, 2011). Looking beyond the bottom rungs of Maslow’s
hierarchy of needs, close and supportive family relationships are an essential component
to the mental health and rehabilitation of young people predisposed to ASPD.
According to recent research on the role of the family and the treatment of ASPD,
the degree of family involvement was indicative of the recidivism rate of male offenders
released from prison (LaVigne & Visher, 2009). Family involvement, specifically the
amount of time spent involved in the daily activities of children, has been associated with
better treatment outcomes for young male offenders who once presented with ASPD
traits (Finney Hairston, 2002; Naser & Visher, 2006).
If the family is able to offer a context in which someone with ASPD traits has the
opportunity to fulfill social roles, relate to others, and feel a sense of purpose, it will serve
as an entry point for minimizing individual and contextual risk factors.
Family therapy for these subjects and those closest to them should aim at
increasing the individuals’ understanding of the family’s experience, resolve conflict in
expectations, and build effective strategies for enhanced family support (Shollenberger,
2009). Addressing problematic family transactions is crucial to strengthening
relationships and increasing the positive influence of family support on young men with
sociopathic traits. This treatment component will help to offset the disorder if utilized
during the formative years of early adulthood (Tarter, Hegedus, Winsten, & Alterman,
1984).
Emotion regulation and emotional intelligence. Emotion regulation is the
manipulation of the presence and/or intensity of the psychological and physical
components of an emotional response. Emotion regulation pertains to both subjective
PREVENTING ANTISOCIAL PERSONALITY DISORDER
27
experience and physiological activity (Gross & Thompson, 2007). The ability to regulate
emotions in response to stimuli is essential in the development and maintenance of
mental health (Frazer, Galinsky, Smokowski, Day, Terzian, Rose, & Guo, 2005; Gross &
Muñoz, 2006). Effective treatment plans of psychopathy should always include the goal
of improving emotion regulation ability.
There are two elements to consider when teaching someone to regulate his or her
emotions. The first component focuses on strategies that occur prior to the emotion
generative response. For example, someone with ASPD might actively avoid talking
with an estranged parent to avoid feeling shame or rejection. The second is responsefocused emotion regulation. These behaviors occur after an emotional activation and
involve direct inflection of one or more of the behavioral, physiological, or subjective
response components. An example of this would be practicing relaxation techniques
while anxious or angry to decrease the intensity of physical sensations accompanied by
the emotion (Gross & Muñoz, 1995; Gross & Levenson, 1997).
At some time before adulthood these individuals learned that their initial
responses to emotion triggering stimuli were ineffective. They learned to suppress their
emotions and rely on rigid strategies. These strategies are often inconsistent with longterm goals. For example, one who is seeking security and belonging through friendship
may reach out to his or her peers by initiating conversation. If for some unforeseen
circumstance his or her attempts are met with hostility, this experience would likely
evoke feelings of rejection, embarrassment, shame, or discouragement. Western culture
often encourages maladaptive behaviors. The pattern of expressing maladaptive emotion
regulating behaviors is rewarded every day when young boys are told to “man up.” The
PREVENTING ANTISOCIAL PERSONALITY DISORDER
28
feedback boys receive when they express sadness, fear, or loss implies that their
emotional regulation skills are inherently not only inadequate, but also offensive to the
male population. Young men in particular are taught to cope with feelings of rejection,
embarrassment, shame, and discouragement by dismissing them all together and
expressing only one secondary emotion that accompanies all others: anger. Young men
are encouraged to express their anger. They are frequently given messages that they are
not only entitled to feel anger, but also entitled to express their anger. “You’re not going
to take that from ‘him’, are you?” Is a rhetorical question associated with a tone
implying that something should be done to teach ‘him’ a lesson (Fraser, et al, 2005;
Werner & Gross, 2010).
Young adults with ASPD traits have emotion regulation skills even more
maladaptive than what is normal for young men in Western culture (Benning et al.,
2003). Emotion regulation deficits are associated with psychopathic personality traits
(Gratz & Roemer, 2004). Someone with ASPD traits would likely exhibit specific
behaviors in response to emotional distress. These behaviors include inability to accept
the initial emotion associated with pain (usually rejection, fear, or shame); problems
inhibiting impulsive, goal-directed behavior; and limited perceived access to emotion
regulation strategies (Benning et al., 2003; Patrick et al., 1993). The dual process model
of psychopathy (Fowles & Dindo, 2006) hypothesizes that there are two separate
etiological processes involved in a learned pattern of emotional and behavioral
dysregulation: low-fear temperament and cognitive processing deficits.
PREVENTING ANTISOCIAL PERSONALITY DISORDER
29
Clinically Effective Treatment Models
The most effective strategy currently available to adequately prevent a diagnosis
of antisocial personality disorder is early intervention and the elimination of childhood
abuse. Underdeveloped regions of the prefrontal areas of the brain are most often the
result of abuse during early childhood, before kindergarten. If a child biologically and
genetically predisposed to ASPD remains in an unhealthy environment throughout
childhood and adolescents, maladaptive behaviors are only exacerbated and reinforced by
the already overwhelmed public school system and juvenile justice system (Zuckerman,
1994; Riser & Kosson, 2013).
By the end of adolescents, around age 25, the brain has stopped developing and
neurological impairments become permanent. The developmental pathways have been
formed and the brain is no longer malleable. All change becomes increasingly difficult
after this window of opportunity has closed (Pemment, 2012).
Due to the lack of empathy exhibited by those diagnosed with ASPD, it can be
argued that they are not feeling as though they are suffering from a mental illness. Thus
they are left with no motivation to take responsibility for their behaviors or insight into a
need to change their behavior. Therefore, no one with ASPD is likely to volunteer or
seek treatment. The only treatment would have to be court ordered (Caldwell, Vitacco, &
Van Rybroek, 2006; Pemment, 2012; Black, 2013).
More than any other group of individuals diagnosed with mental illness, those
with ASPD have contact with multiple agencies such as probation officers, social
workers, therapists, etcetera (Duggan, 2009; Black, 2013). A common entry point to link
PREVENTING ANTISOCIAL PERSONALITY DISORDER
30
all these agencies together is essential to ensure the continuity of care and the
accountability of the client – two critical criteria for the optimization of services.
Family therapy. Children begin to understand the concept of empathy first at
home, by learning to see the world through another person’s perspective. A key part of
the multifactorial process involved in the development of empathy is responsive
parenting and parental modeling of caring and empathetic behavior (Bandura, 1977;
Dogan, Conger, Kim, & Masyn, 2007).
There is significant stability in antisocial behavior across generations. Firstdegree relatives of males with ASPD are five times more likely to have the disorder than
the general population, and first-degree relatives of females are ten times more likely to
have the disorder (Baker, Mack, Moffitt, & Mednick, 1989; Dogan, et al., 2007).
During early interventions aimed to redirect antisocial behavior, therapists can
facilitate change by helping parents and caregivers identify ways they can model caring
and empathetic behavior at home. A second goal of family therapy should be to
introduce or increase positive reinforcement to link misbehavior to appropriate
consequences while simultaneously decreasing yelling, threatening, and punishing.
Consequences resulting from the parent’s anger and frustration such as yelling and
threatening do not teach children self-control (Bandura, 1977).
There are two routes of transmission of antisocial behavior from parents to
adolescents: adolescents’ perceptions of parents’ activities, and inept parenting practices
(Dogan, et al., 2007). Both pose unique challenges that warrant clinical intervention.
Awareness of parental deviance often provides a child with “permission” to engage in
similar behaviors (Melby, Conger, Conger, & Lorenz, 1993; Conger & Rueter, 1996).
PREVENTING ANTISOCIAL PERSONALITY DISORDER
31
Children with sociopathic parents will interpret antisocial behaviors as more acceptable
that children with parents who are not sociopathic because the behaviors of parents’ serve
not only as a model but also a mediator of transmission of behavior (Patterson & Capaldi,
1991; Lipsey & Derzon, 1998). Children’s perceptions and interpretations of parents’
behaviors will introduce a cognitive process that will guide future interactions. The
antisocial behaviors in which parents engage are a crucial risk factor for similar behaviors
in their children (Patterson & Forgatch, 1989; Patterson & Capaldi, 1991; Lipsey &
Derzon, 1998; Dogan, et al., 2007).
Facilitating family therapy with a parent who has ASPD is an especially
challenging task for any therapist. Because antisocial personality traits are pervasive and
biologically transmitted, simply having knowledge of how antisocial behaviors are
learned and transmitted will not necessarily alter the behaviors or attitudes of antisocial
parents. Parents with ASPD are likely to minimize the consequences and evidence of
their antisocial behaviors. A lack of remorse, a disregard for others, and the ability to
accept responsibility are all an inherent hallmarks of their personality makeups and of the
disorder. These traits lessen the chance that a parent will be motivated to modify his or
her behavior. The notion that the child is modeling his or her behavior after him or
herself satisfies the narcissistic nature of a parent with ASPD and fulfills the need of
feeling significant and secure in the life task of being a parent. Unless this need for
significance, security, and belonging is addressed creatively through therapeutic
interventions, the antisocial parent will be left with a sense of pride and revel in the
transmission of these personality traits.
PREVENTING ANTISOCIAL PERSONALITY DISORDER
32
The idea of a less difficult child or fewer calls from teachers or social workers
may be enough to entice a parent with ASPD to participate in family therapy. Even
parents with antisocial traits can be taught how to respond to challenging children in
constructive ways. Behavior management skills such as positive discipline, appropriate
supervision, family problem solving, positive reinforcement, and parental involvement
are all ways to engage parents and modify the coercive behaviors of both parents and
children (Patterson, 1982; Lipsey & Derzon, 1998; Dogan, Conger, Kim, & Masyn,
2007).
Long-term integrative psychotherapy. Long-term integrative psychotherapy
oriented at the general psychological therapeutic approach in males with symptoms of
acting out and violence against others has been shown to yield positive long-term
outcomes (Krampen, 2002; Grawe, 2004). Individuals receiving long-term integrative
psychotherapy showed significant symptom reductions and only a few relapses of violent
behaviors. The majority were able to meet their goals of obtaining and/or maintaining
occupations and feel a sense of fulfillment in their social lives.
The key concepts of integrative psychotherapy include an adaptive, flexible set of
psychotherapeutic methods and techniques designed to meet treatment objectives
(Castonguay, 2000; Krampen, 2009). The keys to success in integrative psychotherapy
are: a) structured, plain, and unambiguous objectives that are realistic and relevant to the
present day, b) high frequency of sessions in the initial and major stage of therapy, c) a
clearly defined therapeutic relationship that includes professional distancing of the
therapist as well as systematic alternations of therapists, and d) the therapeutic
involvement of a peer (Krampen, 2009).
PREVENTING ANTISOCIAL PERSONALITY DISORDER
33
The treatment objectives of Integrative Psychotherapy should be to:
1) Enhance social skills and emotional regulation skills, empathy, and morality by
modeling, operant conditioning techniques, role playing, therapeutic homework, moral
dilemma techniques, mirroring, free association, and guided imagery.
2) To reduce psychophysiological arousal by improving impulse control and mastery
(this can be done by using relaxation therapy, self-control techniques, distraction
techniques, thought stop, and delayed negative feedback techniques) (Krampen & von
Eye, 2006)
3) To develop adaptive self-statements by cognitive restructuring of self-defeating
thought patterns and social-cognitive biases that misinterprets the ambiguous behaviors
of others (Draughon, 1977).
4) To reconstruct and improve attachment abilities, trust, and social relationships by
behavior analyses, biographical analyses, development of life projects (narrative therapy),
role playing, and therapeutic homework.
5) To reduce deviant peer influences and improve nondeviant peer relations including
social support and supervision by peers, therapeutic involvement, and modeling
(Krampen, 2009).
The outcomes of treatment were assessed by post session questionnaires designed
to measure clients’ and therapists’ perceptions of psychotherapeutic processes with
reference to progress, stagnation, and backward steps in resource perspective, problem
solving, consciousness, and insight and future outlook of the patient (Krampen, 2002;
Grawe, 2004)
PREVENTING ANTISOCIAL PERSONALITY DISORDER
34
Modified therapeutic community treatment. Modified Therapeutic
Community (MTC) treatment can be effective for individuals diagnosed with ASPD
(McKendrick, Sullivan, Banks, & Sacks, 2006). Results of a recent study (Sacks &
Stommel, 2003) aimed to compare MTC with other mental health treatment showed
significantly lower re-incarceration rates at one-year follow-up for those who received
MTC treatment. This study was preformed within the walls of a prison, with the MTC
program taking place in a special secluded unit. The MTC program was different than
the standard approach to mental health treatment in that it: a) reduced the intensity of
interpersonal interactions, b) individualized treatment planning, and c) increased the
flexibility of treatment programming by including psycho-education classes, cognitivebehavioral protocols, medication interventions, conflict resolution groups, dual recovery
groups, and a variety of other therapeutic techniques tailored to each individual. The
overall goals of MTC were to change the attitudes, behaviors, and lifestyles in the areas
of mental illness, criminal behavior, and substance abuse. The results of the said study
indicated a positive outcome for those diagnosed with ASPD (Sacks & Stommel, 2003).
Multisystemic therapy. Multisystemic Therapy (MST) can successfully reduce
criminal activity in juvenile offenders at high risk of committing additional serious
crimes (Borduin, Schaeffer, & Heiblum, 2009). Many studies (Aos, Phipps, Barnoski, &
Lieb, 2001; Curtis, Ronan, & Borduin, 2004; Weisz, Sandler, Durlak, & Anton, 2005)
have found that family- and community-based interventions, especially those with an
already established evidence base in treating adolescent antisocial behavior, hold
considerable promise in meeting the clinical needs of even particularly challenging
juvenile sexual and violent offenders.
PREVENTING ANTISOCIAL PERSONALITY DISORDER
35
MST targets and responds with individualized interventions to a comprehensive
set of identified risk factors including: individual, family, peer, school, and neighborhood
domains. Clinical services are most effective when provided in home, school, and/or
neighborhood settings at times that are most convenient to the individual or the family
(Borduin, Letourneau, Henggeler, & Swenson, 2003). MST designs interventions that
integrate empirically based clinical techniques that focus on social ecology and then
eventually into a broad-based ecological framework. Behavioral, cognitive-behavioral,
and structural family therapy currently offer the most empirical evidence to show the
effectiveness of MST (Burns & Hoagwood, 2002; Borduin, Letourneau, Henggeler, &
Swenson, 2003). Multisystem individual interventions are used with the clients and their
closest family members to modify the individual's social perspectives, belief systems,
private logic, and attitudes that contribute to antisocial behaviors (Henggeler & Borduin,
1990; Borduin, Schaeffer, & Heiblum, 2009).
The goals of MST when working with the families of an individual are to: (a)
reduce parent and youth denial about the behaviors, offences, and the subsequent
consequences, (b) remove barriers to effective parenting, (c) enhance parenting
knowledge, and (d) promote affection and communication among family members
(Henggeler & Borduin, 1990).
Another goal of MST is to address social skills and problem-solving difficulties in
effort to promote the development of friendships and establish a sense of competency
integrating with peers. Therapists help parents facilitate these interventions which should
consist of active support and encouragement of relationship skills, associations with nonproblem peers, as well as discouragement of associations with deviant peers (Ronis &
PREVENTING ANTISOCIAL PERSONALITY DISORDER
36
Borduin, 2007). MST is unique in the support it provides to caregivers and family
members of individuals. MST clinicians help parents develop strategies to monitor and
promote the youth's school performance; interventions in this domain typically focus on
improving communication between parents and teachers and on restructuring after-school
hours to promote academic efforts (Snell-Johns, Mendez, & Smith, 2004).
MST has been clinically effective in helping individuals meet specific treatment
objectives. These objectives include: a) increased cohesion and adaptability amongst
family relations, b) increased emotional bonding and social maturity with decreased
aggression in effort to strengthen peer relations, and improving academic performance by
raising grades. MST has also resulted in decreased behavior problems and decreased
symptoms of depression (Borduin, Schaeffer, & Heiblum, 2009).
Pharmacological intervention. The complex psychosocial-biological markers of
Antisocial Personality Disorder may be a symptom constellation amenable to medical
intervention and drug treatment (Senninger & Laxenaire, 1995; Dinkelacker, Dietl, &
Widman, 2003; Wick, 2013). While there are not currently any medications designed or
intended to specifically treat ASPD, there are several drugs on the market that have been
shown to reduce aggression and other symptoms of the disorder (Crawford, Kakad,
Rendel, Mansour, Crugel, Liu, & Barnes, 2011).
Medications that have typically been known to cause aggression in the majortiy of
the population can have a paradoxical effect when aiming to target disinhibition and
aggression in young adults with symptoms of ASPD. These medications include
benzodiazepines, some anticonvulsants (Phenytoin, or Dilantin), atypical antipsychotics,
and some antidepressants (Senninger & Laxenaire, 1995; Dinkelacker, Dietl, & Widman,
PREVENTING ANTISOCIAL PERSONALITY DISORDER
37
2003; Black, 2006). Lithium Carbonate is currently the most effective medication for
reducing anger and combativeness. It is commonly used among prisoners in correctional
facilities and also in children who are prone to aggressive outbursts (Khanzode, Saxena,
Kraemer, Chang, & Steiner, 2006). Carbamazepine or valproate, can also help to
stabilize moods and may lessen antisocial behavior as well. While antipsychotics may
reduce aggression, they are more likely than mood stabilizers to have irreversible side
effects (Tyrer & Bateman, 2004; Livesley, 2005; Baker-Glenn, Steels, & Evans, 2010).
Although highly addictive, stimulants such as Adderall and Ritalin are often
prescribed to individuals with ASPD because of the high rate of comorbidity with
attention deficit disorder. While they are effective in treating the aggression and
impulsivity that accompany both ASPD and ADD/ADHD, the level of risk is
astronomically high when prescribing a dangerous and addictive drug to a population
with high rates of illegal behavior (Wilens, Biederman, & Spencer, 1998; Crawford,
Sahib, Bratton, Tyrer, & Davidson, 2009).
Individuals who have a history of dangerous sexual behavior can be treated with
injections of medroxyprogesterone acetate, a synthetic hormone that reduces testosterone
levels. Injectable forms of medications are most useful for individuals under civil
commitments, parole, or probation (Crawford, et al., 2009; Wick, 2013).
An interesting idea for the treatment of ASPD is the concept of a drug aimed to
stop arginine vasopressin (AVP) from binding to neurological receptors. This concept
has been tested in hamsters, with results proving the hypothesis of the researchers
(Curraco, 1998). Injection of the hormone AVP into the hypothalamus increases the
number of biting attacks on intruders. Administration of a drug that stops AVP from
PREVENTING ANTISOCIAL PERSONALITY DISORDER
38
binding to receptors in the brain, conversely, inhibits aggression. The relationship
between aggression and AVP levels was much stronger in males than in females.
Serotonin reuptake inhibitors such as Prozac have anti-aggressive effects. It is speculated
that this is due to serotonin’s effect on central AVP (Curraco, 1998).
While Prozac and other SSRIs may treat aggression in patients with ASPD, the
symptoms of depression are not as easily treated in this population. Mood disorders are
among the most commonly dually-diagnosed disorders in clients with ASPD (Livesley,
2005; Black, 2006; Newton-Howes, Tyrer, & Johnson, 2006). However, while mood
disorders are typically easily treated with medications in the general population without
co-occurring personality disorders, depressed patients with personality disorders tend to
not respond as well to antidepressant medications. The details explaining this
discrepancy remain unknown (Newton-Howes, Tyrer, & Johnson, 2006; Wick, 2013).
An artificial increase in levels of the hormone oxytocin has been shown to
increase trusting behavior in humans (Kosfeld 2005). In comparison with a placebo,
participants in a study designed to measure oxytocin’s effect on an individual’s ability to
trust strangers and act altruistically were better at interpreting subtle social cues and were
able to overcome their avoidance of betrayal and take more social risks. Oxytocin may
be a potential key to treating ASP through neuroleptic medications (Kosfeld, 2005;
Domes, 2007; Beitchman, et al., 2012).
Other drugs such as: carbamazepine, valproate, propranolol, buspirone and
trazodone have been successful when used to treat aggression in brain-injured or
developentally delayed patients (Livesley, 2005; Wick, 2013).
PREVENTING ANTISOCIAL PERSONALITY DISORDER
39
Summary, Conclusions, and Recommendations
Restatement of the Problem
The time between adolescence and adulthood is essentially the last chance to
clinically prevent the diagnosis of antisocial personality disorder from having lifelong
effects on the limbic system of the emerging adult brain. If the ability to integrate
emotion and cognition remains intact before age 25, there is a greater chance that
therapeutic interventions can potentially offset the diagnosis of ASPD.
Explanation of the Literature
There are clear patterns in both the brains and genetics of psychopaths (Fallon,
2006). Psychopaths have a clinically significant loss of function in the orbital cortex,
anterior temporal lobes and the strip of limbic cortices connecting the two. Psychopaths
also have one or more several high-risk, violence-related genes, specifically the MAOA
“Warrior Gene.”
At the crossroads of young adulthood, the discrepancy between adolescents who
meet the criteria for antisocial personality disorder and those who are mentally stable
starts to impact all areas of life and have major consequences for the rest of an
individual’s adult life. The developmental histories and personal traits of adolescence
that are able to abstain from deviant behaviors allow them the option of exploring new
life pathways. The histories and traits of life-course-persistent antisocial adolescents have
foreclosed their options, entrenching them in the antisocial path (Pemment, 2012; Riser &
Kosson, 2013).
The majority of treatment services offered to mentally ill adults meeting the
criteria for a diagnosis of ASPD are related to vocational training, educational services,
PREVENTING ANTISOCIAL PERSONALITY DISORDER
40
substance abuse education, and group-based cognitive–behavioral interventions designed
to change criminal thinking, improve moral reasoning, and develop social and problemsolving skills (Datchi & Thomas, 2013). While cognitive–behavioral programs are
effective and easily executed, they do not directly target the environments in which these
individuals will be expected to obtain their goals. Family relationships constitute a
source of social support and play a critical role in keeping young adults with ASPD traits
out of prison (diZerega & Shapiro, 2007). For this reason, family therapy is a critical key
to offsetting the diagnosis of Antisocial Personality Disorder.
There has not yet been any published evaluation of a family therapy program with
the adult offender population, and little is known about the possible impact of family
therapy on the rehabilitation process and the prevention of adult criminal behaviors.
However, family therapy has long been the treatment of choice for youth violence and
substance abuse (Datchi & Thomas, 2013).
Emotion dysregulation warrants continued inquiry in the context of treatment
targets for psychopathy. The majority of empirical investigations into emotion
dysregulation have been conducted in relation to mood and anxiety disorders. Additional
support for the notion that emotion dysregulation is an essential goal of treatment for
antisocial personality disorder would be clinically beneficial.
Recommendations for Future Research Directions and Therapeutic Implications
As is the case with essentially all treatments of any disorder or illness, early
intervention is always the optimal choice. Brief strategic family therapy, functional
family therapy or multisystemic family therapy have been shown to yield the most
effective and long lasting treatment outcomes for children presenting antisocial behaviors
PREVENTING ANTISOCIAL PERSONALITY DISORDER
41
between the ages of eight and eighteen (Duggan, 2009). Clinical trials designed to
examine the moderating effects of various treatment outcomes are needed to improve
interventions to meet the needs of youth presenting with various forms of antisocial
behaviors. Such studies would be able to help clinicians gain insight into commonly
observed trajectories. For example, boys presenting with aggressive behaviors that
gradually increase over time might benefit from parent training or self-control training
programs, whereas boys with a chronic high aggression pattern might require more
intensive interventions such as multisystemic therapy (Henggeler, Schoenwald, Borduin,
Rowland, & Cunningham, 1998).
The goal of social services, educators, parents, and public policy makers should
be to have the infrastructure and resources available to screen children for a
predisposition to psychopathy at an early age. Interventions should be made available to
those identified as at-risk with the goal of preventing or managing the development of
violent or antisocial behaviors. Although further research is needed to more specifically
identify the types of measures that bring about the healthiest outcomes for such
individuals and their caregivers, the available evidence today supports the idea that young
children need an abundant amount of love, support, care, and encouragement in order to
grow into healthy members of society (Fallon, 2006, Scott & O’Connor, 2014).
Schools are the primary setting in which preventive interventions occur (Jensen,
Martin, & Cantwell, 1997). Exploring risk factors that could be assessed within the
school setting is an essential goal for successful early intervention. Identifying risk
factors before first grade can be a cost-effective and efficient way of proving early
intervention to at risk children and their families. Once identified, youths progressing
PREVENTING ANTISOCIAL PERSONALITY DISORDER
42
along a high-risk trajectory could be targeted to receive the limited prevention resources
available (Attar, Guerra, & Tolan, 1994; Jensen, Martin, & Cantwell, 1997; Haselager,
Van Lieshout, Riksen-Walraven, Cillessen, & Hartup, 2002; Broidy, Nagin, Tremblay,
Bates, Brame, Dodge, 2003).
Having an antisocial parent or parents is one of the strongest predictors of violent
behavior or serious delinquency in adolescence and young adulthood (Lipsey & Derzon,
1998; Eddy & Reid, 2001). Early intervention programs aimed to identify high-risk
children and strengthen connections to the school and improve relationships with teachers
encourage cognitive development and foster the acquisition of social skills (Fraser,
Galinsky, Smokowski, Day, Terzian, Rose, & Guo, 2005; Ronis & Borduin, 2007; Scott,
et al., 2014).
Programs with these goals, such as Interpersonal Cognitive Problem
Solving (ICPS) (1988) and Providing Alternative Thinking Strategies (PATHS) (2002),
improve school achievement by strengthening social reinforcements, and in turn,
improving the self-esteem of the children identified as high-risk (Shure & Spivack, 1988;
Shure, 1999; Gottfredson, Wilson, & Najaka, 2002).
Programs designed to include the family in the treatment plan of the high risk
child, such as the Perry Preschool Program (1993) and the Syracuse Family Development
Research Project (1988), feature in-home services, parent training, child cognitive
development activities, and social support and services (Ronald, Mangione, & Honig,
1988; Schweinhart, Barnes, & Weikart, 1993; Barnett, 1996; Schweinhart, Montie,
Xiang, Barnett, Belfield, & Nores, 2005).
Rather than threaten attachment and risk the issues that accompany the perceived
abandonment of a parent, it is preferable to include parents with ASPD in the
PREVENTING ANTISOCIAL PERSONALITY DISORDER
43
multisystemic treatment plan and supplement the lacking positive role model with a
mentoring program. Programs such as The Big Brothers Big Sisters program aim to
reduce violent behavior among youth, and have demonstrated positive evidence in
support of the idea that children at risk of developing ASPD benefit from have a mentor
(Grossman & Tierney, 1998).
Further Questions
People with antisocial personality disorder tend to gradually improve over time.
A certain percentage of those diagnosed with ASPD as young adults will not meet the
clinical criteria later in life (Black, 2013). It is unknown to professionals why symptoms
seem to improve over time. This is a topic that warrants further research.
Conclusion
The integrative psychotherapeutic approach includes multiple treatment
objectives designed to encourage mastery, resource activation, and consciousnesscreation through therapeutic interventions. It is the most promising form of treatment for
offsetting the full effects of ASPD during the formative years of the limbic system
between ages 18 and 25. Although integrative psychotherapy has been shown to produce
positive outcomes in long-term follow-up studies (Grawe, 2004; Krampen, 2002), it must
be noted that there is no reliable psychometric data on treatment outcomes and the
effectiveness of psychological therapeutic intervention. All data at this time has been
found to have strong response biases in participants, or the results have not been able to
be replicated in controlled studies because of internal validity deficiencies.
Unfortunately, there is not enough evidence at this time to prove with concreate
data that any clinical therapy during the formative years of the limbic system can redirect
PREVENTING ANTISOCIAL PERSONALITY DISORDER
44
the behavior of someone who has been exhibiting the signs and symptoms of antisocial
personality disorder and offset the diagnosis and implications for consequences later on.
Early neuropsychological deficits that cause negative evocative interactions with
caregivers create a discouraging environment first at home and then in school (Caspi,
Elder, & Bem, 1987; Meany, Aitken, van Berkel, Bhatnagar, & Sapolsky, 1988; Moffitt,
1990). Children genetically predisposed to antisocial personality disorder who have also
suffered neuropsychological damage early in life are especially at odds with their
environments (Tarter, Hegedus, Winsten, & Alterman, 1984; Milner & McCanne, 1991).
The reviewed literature supports the statement that early childhood is the best
time to intervene with the intention of preventing antisocial personality disorder (Moffitt
& Henry, 1991; Scott, Briskman, & O’Connor, 2014). The formative years after
adolescence are only a last chance for skilled therapists to potentially encourage change
before the limbic regions have finished growing.
An encouraging conclusion that can be drawn from the literature is that there is
substantial evidence supporting the idea that therapeutic services can be offered to
parents with ASPD to prevent the next generation from following in similar
developmental trajectories as their parents. Early intervention, social skills training,
cognitive development, family therapy, and mentoring programs encourage social interest
in young people and offset the biological and environmental risk factors of antisocial
personality disorder (Patterson, DeBaryshe, & Ramsey, 1989; Schweinhart, Montie,
Xiang, Barnett, Belfield, & Nores, 2005; Dogan, Conger, Kim, & Masyn, 2007).
PREVENTING ANTISOCIAL PERSONALITY DISORDER
45
References
American Psychiatric Association. (2013). Diagnostic and statistical manual of mental
disorders (5th ed.). Arlington, VA: Author.
Anderson, E. (1990). Streetwise. Chicago, IL: University of Chicago Press.
Anderson, K. E., Lytton, H., & Romney, D. M. (1986). Mothers' interactions with normal
and conduct-disordered boys: Who affects whom? Developmental Psychology,
22, 604– 609.
Aos, S., Phipps, P., Barnoski, R., & Lieb, R. (2001). The comparative costs and benefits
of programs to reduce crime. Olympia, WA: Washington State Institute for Public
Policy.
Attar, B. K., Guerra, N. G., & Tolan, P. H. (1994). Neighborhood disadvantage, stressful
life events, and adjustment in urban elementary-school children. Journal of
Clinical Child Psychology, 23, 391– 400.
Bagwell, C. L., Coie, J. D., Terry, R. A., & Lochman, J. E. (2000). Peer clique
participation and social status in preadolescence. Merrill-Palmer Quarterly,
46, 280– 305.
Baird, Abigail A. & Bennett, Craig, M. (2006). Anatomical changes in the
emerging adult brain: A voxel-based morphometry study. Human Brain
Mapping, 27(9), 766–777.
Baker L. A., Mack W., Moffitt T. E., & Mednick S. (1989) Sex differences in property
crime in a Danish adoption cohort. Behavioral Genetics, 19, 355–370
Baker-Glenn W, Steels M, Evans C. (2010). Use of psychotropic medication among
psychiatric out-patients with personality disorder. The Psychiatrist, 34, 83–86.
PREVENTING ANTISOCIAL PERSONALITY DISORDER
46
Bandura A. (1977). Social learning theory. Englewood Cliffs, NJ, Prentice-Hall
Bandura, A. (1979). The social learning perspective: Mechanisms of aggression. In
H.Toch (Ed.), Psychology of crime and criminal justice (pp. 193– 236). Prospect
Heights, IL: Waveland Press.
Barnett, W. S. (1996). Lives in the balance: Age-27 benefit-cost analysis of the
HighScope Perry Preschool Program (Monographs of the HighScope Educational
Research Foundation, 11). Ypsilanti, MI: HighScope Press.
Bateman, A., & Fonagy, P. (2008). Comorbid antisocial and borderline personality
disorders: Mentalization-based treatment. Journal of Clinical Psychology, 64,
181– 194. doi: 10.1002/jclp.20451
Barraza, J., & Zak, P. (2009). Empathy toward strangers triggers oxytocin release and
subsequent generosity Annals of the New York Academy of Sciences, 1167(1),
182-189 DOI: 10.1111/j.1749-6632.2009.04504.x
Beitchman, J., Zai, C., Muir, K., Berall, L., Nowrouzi, B., Choi, E., & Kennedy, J.
(2012). Childhood aggression, callous-unemotional traits and oxytocin genes.
European Child & Adolescent Psychiatry, 21(3), 125-132. doi:10.1007/s00787012-0240-6
Bell, R. Q., & Chapman, M. (1986). Child effects in studies using experimental or brief
longitudinal approaches to socialization. Developmental Psychology, 22, 595–
603.
Benning, S. D., Hicks, P., Blonigen, D. M., Krueger, R. (2003). Factor structure of the
psychopathic personality inventory: validity and implications for clinical
assessment. Psychological Assessment, 15(3), 340-50.
PREVENTING ANTISOCIAL PERSONALITY DISORDER
47
Black, D. (2013). Bad Boys, Bad Men - Confronting Antisocial Personality Disorder
(Sociopathy) (Revised and Updated). New York, NY: Oxford University Press.
Black, D. (2006). Treatment for antisocial personality disorder.
Retrieved on October 12, 2014, from http://psychcentral.com/lib/treatment-forantisocial-personality-disorder/000656
Borduin, C., Schaeffer, C., & Heiblum, N. (2009). A randomized clinical trial of
multisystemic therapy with juvenile sexual offenders: effects on youth social
ecology and criminal activity. Journal of Consulting and Clinical Psychology,
77(1), 26-37. doi:10.1037/a0013035
Borduin, C. M., Letourneau, E. J., Henggeler, S. W., & Swenson, C. C. (2003).
Treatment manual for multisystemic therapy with juvenile sexual offenders and
their families. Unpublished manuscript, University of Missouri—Columbia.
Bowlby J. (1973). Attachment and Loss, Vol. 2, Separation. New York,NY: Basic Books
Broidy, L. M., Nagin, D. S., Tremblay, R. E., Bates, J. E., Brame, B., Dodge, K. A.,
Fergusson, D., Horwood, J. L., Loeber, R., Laird, R., Lynam, D. R., Moffitt, T.
E., Pettit, G. S., & Vitaro, F. (2003). Developmental trajectories of childhood
disruptive behaviors and adolescent delinquency: A six-site, cross-national study.
Developmental Psychology, 39, 222– 245.
Bucholz, K. K., Hesselbrock, V. M., Health, A. C., Kramer, J. R., & Schuckit, M. A.
(2000). Research report. A latent class analysis of antisocial personality disorder
symptom data from a multi-centre family study of alcoholism. Addiction, 95,
553– 567. doi: 10.1046/j.1360-0443.2000.9545537.x
Burns, B. J., & Hoagwood, K. ( Eds.). (2002). Community treatment for youth:
PREVENTING ANTISOCIAL PERSONALITY DISORDER
48
Evidenced-based interventions for severe emotional and behavioral disorders.
New York, NY: Oxford University Press.
Caldwell, M.F., Vitacco, M., Van Rybroek, G. J. (2006). Are violent delinquents worth
treating? A cost–benefit analysis. Journal of Research in Crime and Delinquency,
43, 148-168.
Castonguay, L. G. (2000). A common factors approach to psychotherapy training.
Journal of Psychotherapy Integration, 10, 263– 282.
Caspi, A., Elder, G. H., & Bem, D. J. (1987). Moving against the world: Life-course
patterns of explosive children. Developmental Psychology, 23, 308– 313.
Coccaro, E. F., Kavoussi, R. J., Hauger, R. L., Cooper, T. B., & Ferris, C. F. (1998).
Cerebrospinal fluid vasopressin levels. Correlates with aggression and serotonin
function in personality-disordered subjects. Archives of General Psychiatry,
55(8), 708-714.
Coid, J. (2002). Personality disorders in prisoners and their motivation for dangerousness
and disruptive behaviour. Criminal Behaviour and Mental Health, 12, 209– 226.
Coie, J., Terry, R., Lenox, K., & Lochman, J. (1995). Childhood peer rejection and
aggression as predictors of stable patterns of adolescent disorder. Development
and Psychopathology, 7, 697– 713.
Conger R. D. & Rueter M. A. (1996). Siblings, parents, and peers: A longitudinal study
of social influences in adolescent risk for alcohol use and abuse. Advances in
Applied Developmental Psychology, 10, 1–30
Constantino, J. N., Morris, J. A., & Murphy, D. L. (1997). CSF 5-HIAA and family
PREVENTING ANTISOCIAL PERSONALITY DISORDER
49
history of antisocial personality disorder in newborns. American Journal of
Psychiatry, 154, 1771-1773.
Cooke, D. J., Forth, A. E., & Hare, R. D. (1998). Psychopathy: Theory, research, and
implications for society. Dordrecht, The Netherlands: Kluwer.
Craig, M., Catani, M., Deeley, Q., Latham, R., Daly, E., Kanaan, R., Picchioni, M.,
McGuire, P., Fahy, T., & Murphy, D. (2009). Altered connections on the road to
psychopathy. Molecular Psychiatry, 14(10), 946-953 DOI: 10.1038/mp.2009.40
Cravioto, J., & Arrieta, R. (1983). Malnutrition in childhood. In M. Rutter (Ed.),
Developmental neuropsychiatry (pp. 32– 51). New York, NY: Guilford Press.
Crawford MJ, Sahib L, Bratton H, Tyrer P, Davidson K. (2009). Service provision for
men with antisocial personality disorder who make contact with mental health
services. Personality and Mental Health. 3,165–171
Crawford, M. J., Kakad, S. S., Rendel, C. C., Mansour, N. A., Crugel, M. M., Liu, K. W.,
& Barnes, T. E. (2011). Medication prescribed to people with personality
disorder: the influence of patient factors and treatment setting. Acta Psychiatrica
Scandinavica, 124(5), 396-402. doi:10.1111/j.1600-0447.2011.01728.x
Crijnen, A. A. M., Feehan, M., & Kellam, S. G. (1998). The course and malleability of
reading achievement in elementary school: The application of growth curve
modeling in the evaluation of a mastery learning intervention. Learning and
Individual Differences, 10, 137– 157.
Curtis, N. M., Ronan, K. R., & Borduin, C. M. ( 2004). Multisystemic treatment: A metaanalysis of outcome studies. Journal of Family Psychology, 18, 411– 419.
Dapretto M., Davies M. S., Pfeifer J. H., Scott A. A., Sigman M., Bookheimer S.
PREVENTING ANTISOCIAL PERSONALITY DISORDER
50
Y., Iacoboni M. (2006). Understanding emotions in others: mirror neuron
dysfunction in children with autism spectrum disorders. Nature Neuroscience. 9,
28–30
Datchi, C. C., & Thomas L. (2013). Can family therapy have an effect on adult criminal
conduct? Initial evaluation of functional family therapy. Couple and Family
Psychology: Research and Practice, 2(4), 278-293. doi: 10.1037/a0034166
Davidson, K. M., Tyrer, P., Tata, P., Cooke, D., Gumley, A., Ford, I., Crawford, M. J.
(2009). Cognitive behaviour therapy for violent men with antisocial personality
disorder in the community: An exploratory randomized controlled trial.
Psychological Medicine, 39, 569– 577. doi: 10.1017/S0033291708004066
Deater-Deckard, K. (2001). Annotation: Recent research examining the role of peer
relationships in the development of psychopathology. Journal of Child
Psychology and Psychiatry and Allied Disciplines, 42, 565– 579.
Dinkelacker, V., Dietl, T., Widman, G. (2003). Aggressive behavior of epilepsy patients
in the course of levetiracetam add-on therapy: report of 33 mild to severe cases.
Epilepsy Behav., 4, 537-547.
diZerega, M., & Verdone, J. (2011). Setting an agenda for family-focused justice
reform. New York, NY: Vera Institute of Justice.
diZerega, M. & Shapiro, C. (2007). Asking about family can enhance reentry.
Corrections Today, 69(6), 58-61.
Dogan S.,J., Conger R. D., Kim K. J., & Masyn K. E. (2007). Cognitive and parenting
pathways in the transmission of antisocial behavior from parents to adolescents.
Child Development, 78(1), 335–349
PREVENTING ANTISOCIAL PERSONALITY DISORDER
51
Domes, G., Heinrichs, M., Michel, A., Berger, C., & Herpertz, S. (2007). Oxytocin
improves “mind-reading” in humans Biological Psychiatry, 61(6), 731-733
DOI:10.1016/j.biopsych.2006.07.015
Dozier M., Stovall K. C., & Albus K. (1999). Attachment and psychopathology in
adulthood. In: J. Cassidy & P. R. Shaver (Eds) Handbook of attachment: Theory,
research, and clinical applications (pp. 497-519). New York, NY: The Guilford
Press.
Draughon, M. (1977). Ego-building: An aspect of the treatment of psychopaths.
Psychological Reports, 40, 615– 626.
Dreikurs, R. (1964). Children: The challenge. New York, NY: Hawthorn Books.
Duggan, C. (2009). A treatment guideline for people with antisocial personality disorder:
Overcoming attitudinal barriers and evidential limitations. Criminal Behaviour &
Mental Health, 19(4), 219-223. doi:10.1002/cbm.726)
Eddy J. M. & Reid J. B. (2001). The antisocial behavior of the adolescent children of
incarcerated parents: A Developmental Perspective. In: U.S. Department of
Health and Human Services, Asst Secretary for Planning and Evaluation,
Substance Abuse and Mental Health Services Administration, (Eds). From prison
to home: The effect of incarceration and reentry on children, families, and
communities. Washington, DC, U.S. Department of Health and Human Services
Elder, G. H., Jr. (1986). Military times and turning points in men's lives. Developmental
Psychology, 22, 233– 245.
Elliott, D. S., & Voss, H. L. (1974). Delinquency and dropout. Lexington, MA: Heath.
PREVENTING ANTISOCIAL PERSONALITY DISORDER
52
Fallon, J. H. (2006). Neuroanatomical background to understanding the brain of the
young psychopath. Ohio State Journal of Criminal Law, 3, 341-367. Retrieved
from http://moritzlaw.osu.edu/osjcl/Articles/Volume3_2/Symposium/Fallon-PDF03-29-06.pdf
Farrington, D. P., & West, D. J. (1990). The Cambridge study of delinquent
development: A long-term follow-up of 411 London males. In H. J. Kerner &
G.Kaiser ( Eds.), Kriminalitat (pp. 117– 138). New York, NY: Springer-Verlag.
Fecteau S., Pascual-Leone A., Theoret H. (2008). Psychopathy and the mirror neuron
system: preliminary findings from a non-psychiatric sample. Psychiatry Res.,
160, 137–144
Finney Hairston, C. (2002). Prisoners and their families: Parenting issues during
incarceration. Paper presented at From Prison to Home: The Effect of
Incarceration and Reentry on Children, Families and Communities, a conference
hosted by the U.S. Department of Health and Human Services and Urban
Institute, Washington DC.
Fraser, M. W., Galinsky, M. J., Smokowski, P. R., Day, S. H., Terzian, M. A., Rose, R.
A., & Guo, S. (2005). Social information-processing skills training to promote
social competence and prevent aggressive behavior in the third grades. Journal of
Consulting and Clinical Psychology, 73, 1045– 1055.
Fowles, D. C., & Dindo, L. (2006). A dual-deficit model of psychopathy. In C. J. Patrick
(Ed.) Handbook of psychopathy (pp. 14-34). New York, NY: Guilford Press.
Gacono, C. B., Meloy, J. R., & Berg, J. L. (1992). Object relations, defensive operations,
PREVENTING ANTISOCIAL PERSONALITY DISORDER
53
and affective states in narcissistic, borderline, and antisocial personality disorder.
Journal of Personality Assessment, 59, 32-49.
Goleman, D. (2005). Emotional intelligence: Why it can matter more than IQ (10th
Anniversary ed.). New York, NY: Bantam Books.
Goldsmith, H. H., Bradshaw, D. L., & Rieser-Danner, L. A. (1986). Temperament as a
potential developmental influence on attachment. In J. V. Lerner & R. M. Lerner
(Eds.), Temperament and social interaction during infancy and childhood (pp. 5–
34). San Francisco, CA: Jossey-Bass.
Gottfredson, D. C., Wilson, D. B., & Najaka, S. S. (2002). The schools. In J. Petersilia &
J. Q. Wilson (Eds.), Crime: Public policies for crime control (pp. 149-189).
Oakland, CA: Institute for Contemporary Studies Press.
Gratz, K. L., & Roemer, L. (2004). Multidimensional assessment of emotion regulation
and dysregulation: Development, factor structure, and initial validation of the
difficulties in emotion regulation scale. Journal of Psychopathology and
Behavioral Assessment, 26(1), 41-54.
Grawe, K. (2004). Psychological therapy. Cambridge, MA: Hogrefe & Huber.
Gregg, T. R., & Siegel, A. (2001). Brain structures and neurotransmitters regulating
aggression in cats: Implications for human aggression. Progress in NeuroPsychopharmacology & Biological Psychiatry, 25, 91–140.
Gross, J. J., & Thompson, R.A. (2007). Emotion regulation: Conceptual foundations. In J.
J. Gross (Ed.) Handbook of emotion regulation (pp. 3-26). New York, NY:
Guilford Press.
Gross, J. J., & Levenson, R. W. (1997). Hiding feelings: Acute effects of inhibiting
PREVENTING ANTISOCIAL PERSONALITY DISORDER
54
negative and positive emotion. Journal of Abnormal Psychology, 106(1), 95-103
0021-843X/97/.
Grossman, J. B. & Tierney, J. P. (1998). Does mentoring work? An impact study of the
big brothers big sisters program. Evaluation Review, 22(3), 403-426
Gurley, J. R. (2009). A history of changes to the criminal personality in the DSM. History
of Psychology, 12, 285– 304. doi: 10.1037/a0018101
Hadjikhani N., Joseph R. M., Snyder J., Tager-Flusberg H. (2006). Anatomical
differences in the mirror neuron system and social cognition network in autism.
Cereb Cortex, 16, 1276–1282
Haselager, G. J. T., Van Lieshout, C. F. M., Riksen-Walraven, J. M. A., Cillessen, A. H.
N., & Hartup, W. W. (2002). Heterogeneity among peer-rejected boys across
middle childhood: Developmental pathways of social behavior. Developmental
Psychology, 38, 446– 456.
Hare, R. D., Hart, S. D., Forth, A. E., Harpur, T. J., & Williamson, S. E. (1993).
Psychopathic personality characteristics: Development of a criteria set for use in
the DSM-IV antisocial personality disorder field trial. DSM-IV Update, Office of
Research, American Psychological Association, January/February, (pp. 6-7).
Hare, R. D., Clark, D., Grann, M., & Thornton, D. (2000). Psychopathy and the
predictive validity of the PCL-R: An international perspective. Behavioral
Science and the Law, 18, 623– 645. doi: 10.1002/10990798(200010)18:5<623::AID-BSL409>3.0.CO;2-W
Hare, R. D. (2003). The Hare psychopathy checklist—Revised (2nd ed.). Toronto, ON:
Multi-Health Systems.
PREVENTING ANTISOCIAL PERSONALITY DISORDER
55
Harris, G. T., Rice, M. E., & Cormier, C. A. (1991). Psychopathy and violent
recidivism. Law and Human Behavior, 15, 625– 637. doi: 10.1007/BF01065856
Heewon, Yangdong Su, A. (2013). Examination of personal and socio-behavioral
characteristics as predictors of aggressive behavioral tendencies of university
students. College Student Journal, 47(1), 41-52.
Hemphäiä, I., & Hodgins, S. (2014). Do psychopathic traits assessed in mid-adolescence
predict mental health, psychosocial, and antisocial, including criminal outcomes,
over the subsequent 5 years? Canadian Journal of Psychiatry. 59(1), 40-49.
Henggeler, S. W., Schoenwald, S. K., Borduin, C. M., Rowland, M. D., & Cunningham,
P. B. (1998). Multisystemic treatment of antisocial behavior in children and
adolescents. New York, NY: Guilford Press.
Henggeler, S. W., & Borduin, C. M. (1990). Family therapy and beyond: A
multisystemic approach to treating the behavior problems of children and
adolescents. Pacific Grove, CA: Brooks/Cole.
Hostinar, C. E. & Gunnar, M. R. (2013). The developmental psychobiology of stress and
emotion in childhood. In I. B. Weiner, D. K. Freedheim, & R. M. Lerner (Eds.),
Handbook of psychology (2nd ed., pp. 121-141). Hoboken, NJ: Wiley.
Jacobus, J., Thayer, R. E., Trim, R. S., Bava, S., Frank, L., & Tapert, S. (2013). White
matter integrity substance use and risk taking in adolescence. Psychology of
Addictive Behaviors, 27(2), 431-442. doi:10.1037/a0028235.
Iacoboni M. (2009). Imitation, empathy, and mirror neurons. Annual Review of
Psychology, 60, 653–670.
Jensen, P. S., Martin, D., & Cantwell, D. P. (1997). Comorbidity in ADHD: Implications
PREVENTING ANTISOCIAL PERSONALITY DISORDER
56
for research, practice, and DSM-V. Journal of the American Academy of Child
and Adolescent Psychiatry, 36, 1065– 1079.
Khanzode, L. A., Saxena, K., Kraemer, H., Chang, K., & Steiner, H. (2006). Efficacy
profiles of psychopharmacology: Divalproex sodium in conduct disorder. Child
Psychiatry & Human Development, 37(1), 55-64. doi:10.1007/s10578-006-0019-4
Kiehl K. A., Smith A. M., Mendrek A., Forster B. B., Hare R. D., & Liddle P. F.
(2004). Temporal lobe abnormalities in semantic processing by criminal
psychopaths as revealed by functional magnetic resonance imaging. Psychiatry
Res., 130, 27–42
Kilduffa, M. (2014). Strategic use of emotional intelligence in organizational
settings: Exploring the dark side. Research in Organizational Behavior, 30, 129–
152
Kirkman, C. A. (2008). Psychopathy: A confusing clinical construct. Journal of Forensic
Nursing, 4, 29– 39.
Kosfeld, M., Heinrichs, M., Zak, P., Fischbacher, U., & Fehr, E. (2005). Oxytocin
increases trust in humans Nature, 435 (7042), 673-676 DOI: 10.1038/nature03701
Krampen, G. (2002). Stundenbogen für die Allgemeine und Differentielle
Einzelpsychotherapie, STEP [ Postsession questionnaires for patients and
therapists]. Göttingen, Germany: Hogrefe.
Krampen, G. (2009). Psychotherapeutic processes and outcomes in outpatient treatment
of antisocial behavior: An integrative psychotherapy approach. Journal of
Psychotherapy Integration, 19(3), 213-230. doi:10.1037/a0017069
Krampen, G., & von Eye, A. (2006). Treatment motives as predictors of acquisition and
PREVENTING ANTISOCIAL PERSONALITY DISORDER
57
transfer of relaxation methods to everyday life. Journal of Clinical Psychology,
62, 83– 96.
LaVigne, N. J., & Visher, C. (2009). The familial relationships of former prisoners:
Examining the link between residence and informal support mechanisms. Journal
of Contemporary Ethnography, 38(2), 201-224.
Lee, C. L., & Bates, J. E. (1985). Mother-child interaction at age two years and perceived
difficult temperament. Child Development, 56, 1314– 1323.
Lee, J. H. (1999). The treatment of psychopathic and antisocial personality disorders: A
review. Crowthorne, Berks., UK: Clinical Decision Making Support Unit,
Broadmoor Hospital, Berkshire.
Lewis, C. E. (1991). Neurochemical mechanisms of chronic antisocial behavior
(psychopathy). A literature review. Journal of Nervous and Mental Disease, 179,
720– 727. doi: 10.1097/00005053-199112000-00002
Lipsey M. W. & Derzon J. H. (1998). Predictors of violent or serious delinquency in
adolescence and early adulthood: A synthesis of longitudinal research. In R.
Loeber & D. P. Farrington (Eds) Serious & violent juvenile offenders: Risk
factors and successful interventions (pp. 86-105). Thousand Oaks, CA, Sage
Publications, Inc.
Livesley, W. (2005). Principles and strategies for treating personality disorder.
Canadian Journal of Psychiatry, 50(8), 442-450.
Loeber, R., & Stouthamer-Loeber, M. (1998). Development of juvenile aggression and
violence: Some common misconceptions and controversies. American
Psychologist, 53, 242– 259.
PREVENTING ANTISOCIAL PERSONALITY DISORDER
58
Ly, M., Motzkin, J .C., Philippi, C. L., Kirk, G. R., Newman, J. P., Kiehl, K. A., Koenigs,
M. (2012). Cortical thinning in psychopathy. American Journal of Psychiatry.
169, 743-749. doi:10.1176/appi.ajp.2012.11111627
Lynam, D., Moffitt, T., & Stouthamer-Loeber, M. (1993). Explaining the relation
between IQ and delinquency: Class, race, test motivation, school failure, or selfcontrol? Journal of Abnormal Psychology, 102, 187– 196.
Lytton, H. (1990). Child and parent effects in boys' conduct disorder: A
reinterpretation. Developmental Psychology, 26, 683– 697.
Lynam, D., Moffitt, T., & Stouthamer-Loeber, M. (1993). Explaining the relation
between IQ and delinquency: Class, race, test motivation, school failure, or selfcontrol? Journal of Abnormal Psychology, 102, 187– 196.
Maccoby, E. E., & Jacklin, C. N. (1983). The “person” characteristics of children and the
family as environment. In D.Magnusson & V. L.Allen (Eds.), Human
development: An interactional perspective (pp. 75– 92). San Diego, CA:
Academic Press.
Mattick, H. W. (1960). Parolees in the army during World War II. Federal Probation, 24,
49– 55.
Mawson, A. R. (1999). Stimulation-induced behavioral inhibition: A new model for
understanding physical violence. Integrative Physiological & Behavioral Science,
34(3), 177-198.
McDermott, R., Tingley, D., Cowden, J. Frazzetto, G., & Johnson, D. D. P. (2009).
Monoamine oxidase A gene (MAOA) predicts behavioral aggression following
PREVENTING ANTISOCIAL PERSONALITY DISORDER
59
provocation. Proceedings of the National Academy of Sciences, 106(7), 21182123. Retrieved from http://www.pnas.org/content/106/7/2118.full.pdf+html
McKendrick, K., Sullivan, C., Banks, S., & Sacks, S. (2006). Modified therapeutic
community treatment for offenders with MICA disorders: Antisocial personality
disorder and treatment outcomes. Journal of Offender Rehabilitation, 44(2/3),
133-159.
McRae, L. (2013). Rehabilitating antisocial personalities: treatment through selfgovernance strategies. The Journal of Forensic Psychiatry & Psychology, 24(1),
48–70, http://dx.doi.org/10.1080/14789949.2012.752517
Mednick, S. A., Gabrielli, W. F., & Hutchings, B. (1984). Genetic influences in criminal
behavior: Some evidence from an adoption cohort. Science, 224, 891– 893.
Melby J. N., Conger R. D., Conger K. J., & Lorenz F. O. (1993). Effects of parental
behavior on tobacco use by young male adolescents. Journal of Marriage and the
Family, 55, 439–454.
Meany, M. J., Aitken, D. H., van Berkel, C., Bhatnagar, S., & Sapolsky, R. M. (1988).
Effect of neonatal handling on age-related impairments associated with the
hippocampus. Science, 239, 766– 768.
Milner, J. S., & McCanne, T. R. (1991). Neuropsychological correlates of physical child
abuse. In J. S.Milner Ed., Neuropsychology of aggression (pp. 131– 145).
Norwell, MA: Kluwer Academic.
Moffitt, T. E. (1993). Adolescence-limited and life-course-persistent antisocial behavior:
A developmental taxonomy. Psychological Review, 100(4), 674-701.
doi:10.1037/0033-295X.100.4.674
PREVENTING ANTISOCIAL PERSONALITY DISORDER
60
Moffitt, T. E. (1990a). Juvenile delinquency and attention-deficit disorder:
Developmental trajectories from age 3 to 15. Child Development, 61, 893– 910.
Moffitt, T. E. (1990b). The neuropsychology of delinquency: A critical review of theory
and research. In N.Morris & M.Tonry (Eds.), Crime and justice ( Vol. 12, pp. 99–
169). Chicago, IL: University of Chicago Press.
Moffitt, T. E., & Henry, B. (1989). Neuropsychological assessment of executive
functions in self-reported delinquents. Development and Psychopathology, 1,
105– 118.
Moffitt, T. E., & Silva, P. A. (1988). Neuropsychological deficit and self-reported
delinquency in an unselected birth cohort. Journal of the American Academy of
Child and Adolescent Psychiatry, 27, 233– 240.
Moffitt, T. E., & Henry, B. (1991). Neuropsychological studies of juvenile delinquency
and violence: A review. In J. Milner (Ed.), The neuropsychology of aggression
(pp. 67– 91). Norwell, MA: Kluwer Academic.
Moll, J., Zahn, R., de Oliveira-Souza, R., Krueger, F. & Grafman, J. (2005). The neural
basis of human moral cognition. Nature Reviews Neuroscience, 6, 799-809.
Moseley R., Carota F., Hauk O., Mohr B., Pulvermuller F. (2012). A role for the
motor system in binding abstract emotional meaning. Cereb Cortex (Epub ahead
of print, Mar 14, 2012). Retrieved from
http://cercor.oxfordjournals.org/content/early/2011/09/12/cercor.bhr238.full.pdf+
html
Messina, N., Wish, E., Hoffman, J., & Nemes, S. (2001). Diagnosing antisocial
PREVENTING ANTISOCIAL PERSONALITY DISORDER
61
personality disorder among substance abusers: The SCID versus The MCMIII. The American Journal of Drug and Alcohol Abuse, 27, 699– 717. doi:
10.1081/ADA-100107663
Narayan V. M., Narr K. L., Kumari V., Woods R. P., Thompson P. M., Toga A.
W., & Sharma T. (2007). Regional cortical thinning in subjects with violent
antisocial personality disorder or schizophrenia. American Journal of Psychiatry.
164, 1418–1427
Naser, R., & Visher, C. (2006). Family members’ experiences with incarceration and
Reentry. Western Criminology Review, 7(2), 20-31.
Newton-Howes G., Tyrer P., Johnson T. (2006). Personality disorder and the outcome of
depression: meta-analysis of published studies. Br J Psychiatry, 188, 13–20.
Patterson G. (1982). A social learning approach to family intervention III: Coercive
family process. Eugene, OR, Castalia.
Patterson G. & Capaldi D. (1991). Antisocial parents: Unskilled and vulnerable. In:
P. E. Cowan & M. Hetherington (Eds) Family transitions (pp. 195-218).
Hillsdale, NJ: Erlbaum.
Patterson G., DeBaryshe B. D., & Ramsey E. (1989). A developmental perspective on
antisocial behavior. American Psychologist 44, 329–335
Patterson G. & Forgatch M. (1989). Some amplifying mechanisms for pathologic
processes in families. In M. R. Gunnar & E. Thelen (Eds) Systems and
development. Minnesota symposium on child psychology, Vol. 22 (pp. 167-209).
Hillsdale, NJ: Erlbaum.
Patterson, G. R., Reid, J. B., & Dishion, T. J. (1992). A social learning approach. IV:
PREVENTING ANTISOCIAL PERSONALITY DISORDER
62
Antisocial boys. Eugene, OR: Castalia
Patrick C. J., Bradley M. M., Lang P. J. (1993). Emotion in the criminal psychopath:
Startle reflex modulation. Journal of Abnormal Psychology, 102, 82–92.
Pemment, J. (2012). The neurobiology of antisocial personality disorder: The quest for
rehabilitation and treatment. Aggression and Violent Behavior, 18(1), 79-82.
http://dx.doi.org/10.1016/j.avb.2012.10.004
Perry, J., Presniak, M. D., & Olson, T. R. (2013). Defense mechanisms in schizotypal,
borderline, antisocial, and narcissistic personality disorders. Psychiatry:
Interpersonal & Biological Processes, 76(1), 32-52.
doi:10.1521/psyc.2013.76.1.32
Presniak, M. D., Olson, T. R., & MacGregor, M. W. (2010). The role of defense
mechanisms in borderline and antisocial personalities. Journal of Personality
Assessment, 92, 137-145.
Price, B. H., Daffner, K. R., Stowe, R. M., & Mesulam, M. M. (1990). The
comportmental learning disabilities of early frontal lobe damage. Brain, 113,
1383– 1393.
Pruitt D. B. (1998). Your child. New York, NY: American Academy of Child &
Adolescent Psychiatry.
Quay, H. C. (1987). Patterns of delinquent behavior. In H. C.Quay ( Ed.), Handbook of
juvenile delinquency (pp. 118– 138). New York, NY: Wiley.
Riser, R. E., & Kosson, D. S. (2013). Criminal behavior and cognitive processing in male
PREVENTING ANTISOCIAL PERSONALITY DISORDER
63
offenders with antisocial personality disorder with and without comorbid
psychopathy. Personality Disorders: Theory, Research, and Treatment, 4(4), 332340. doi:10.1037/a0033303
Rizzolatti G., Fadiga L., Gallese V., Fogassi L. (1996). Premotor cortex and the
recognition of motor actions. Brain Res Cogn Brain Res. 3, 131–141
Ronald, J. L., Mangione, P. L., & Honig, A. S. (1988). The Syracuse University Family
Development Research Program: Long-range impact on an early intervention with
low-income children and their families. In D. R. Powell and I. E. Sigel (Eds.),
Parent education as early childhood intervention: Emerging direction in theory,
research, and practice. Annual Advances in Applied Developmental Psychology,
Volume 3 (pp. 79-104). Norwood, NJ: Ablex Publishing Corporation.
Ronis, S. T., & Borduin, C. M. ( 2007). Individual, family, peer, and academic
characteristics of male juvenile sexual offenders. Journal of Abnormal Child
Psychology, 35, 153– 163.
Sacks, S., Sacks J.Y. & Stommel, J. (2003). Modified TC for MICA inmates in
correctional settings: A program description. Corrections Today, 90-99.
Sameroff, A., & Chandler, M. (1975). Reproductive risk and the continuum of caretaking
casualty. In F. Horowitz, M. Hetherington, S. Scarr-Salapatek, & G. Siegel
(Eds.), Review of child development research (Vol. 4, pp. 187– 244). Chicago, IL:
University of Chicago Press.
Sampson, R. J., & Laub, J. H. (1990). Crime and deviance over the life course: The
salience of adult social bonds. American Sociological Review, 55, 609– 627.
Schaeffer, C. M., Petras, H., Ialongo, N., Poduska, J., & Kellam, S. (2003). Modeling
PREVENTING ANTISOCIAL PERSONALITY DISORDER
64
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. doi:10.1037/0012-1649.39.6.1020
Schweinhart, L. J., Barnes, H. V., & Weikart, D. P. (1993). Significant benefits: The
HighScope Perry Preschool study through age 27 (Monographs of the HighScope
Educational Research Foundation, 10). Ypsilanti, MI: HighScope Press.
Scott, S., Briskman, J., & O’Connor, T. G. (2014). Early prevention of antisocial
personality: Long-term follow-up of two randomized controlled trials comparing
indicated and selective approaches. American Journal of Psychiatry, 171(6), 649657. doi:10.1176/appi.ajp.2014.13050697
Serin, R. C., & Amos, N. L. (1995). The role of psychopathy in the assessment of
dangerousness. International Journal of Law and Psychiatry, 18, 231– 238. doi:
10.1016/0160-2527(95)00008-6
Senninger, J. L. & Laxenaire, M. (1995). Violent paradoxal reactions secondary to the
use of benzodiazepines. Ann Med Psychol (Paris), 153, 278-281.
Shannon B. J., Raichle M. E., Snyder A. Z., Fair D. A., Mills K. L., Zhang D.,
Bache K., Calhoun V. D., Nigg J. T., Nagel B. J., Stevens A, A., Kiehl K.
A. (2011). Premotor functional connectivity predicts impulsivity in juvenile
offenders. Proc Natl Acad Sci. 108, 11241–11245
Shollenberger, T. L. (2009). When relatives return: Interviews with family members of
returning prisoners in Houston, Texas. Washington, DC: Urban Institute.
://www.urban.org/UploadedPDF/411903_when_relatives_return.pdf.
Shure, M. B. (1999). Preventing violence the problem-solving way. Juvenile Justice
PREVENTING ANTISOCIAL PERSONALITY DISORDER
65
Bulletin. Washington, DC: U.S. Department of Justice, Office of Juvenile Justice
and Delinquency Prevention. NCJ 172847.
Shure, M. B., and Spivack, G. (1988). Interpersonal Cognitive Problem Solving. In R.
H. Price, E. L. Cowen, R. P. Lorion, & J. Ramos-McKay (Eds.), Fourteen Ounces
of Prevention: A Casebook for Practitioners (pp. 69-82). Hawthorne, NY: Aldine.
Smith, S. S., & Newman, J. P. (1990). Alcohol and drug abuse—dependence disorders in
psychopathic and nonpsychopathic criminal offenders. Journal of Abnormal
Psychology, 99, 430– 439. doi: 10.1037/0021-843X.99.4.430
Snell-Johns, J., Mendez, J. L., & Smith, B. H. ( 2004). Evidence-based solutions for
overcoming access barriers, decreasing attrition, and promoting change with
underserved families. Journal of Family Psychology, 18, 19– 35.
Stephenson A. L., Henry C. S., & Robinson L. C. (1996). Family characteristics and
adolescent substance abuse. Adolescence, 31, 59–77.
Sul J. H., Jo S., Lee D., Jung M. W. (2011). Role of rodent secondary motor cortex
in value-based action selection. Nat Neuroscience, 14, 1202–1208.
Tarter, R. E., Hegedus, A. M., Winsten, N. E., & Alterman, A. L. (1984).
Neuropsychological, personality and familial characteristics of physically abused
delinquents.Journal of the American Academy of Child Psychiatry, 23, 668– 674.
Tinsley, B. R., & Parke, R. D. (1983). The person–environment relationship: Lessons
from families with preterm infants. In D.Magnusson & V. L.Allen (Eds.), Human
development: An interactional perspective (pp. 93– 110). San Diego, CA:
Academic Press.
Torry, Z., & Billick, S. (2011). Implications of antisocial parents. Psychiatric Quarterly,
PREVENTING ANTISOCIAL PERSONALITY DISORDER
66
82(4), 275-285. doi:10.1007/s11126-011-9169-z
Tyrer P. & Bateman A. (2004). Drug treatment for personality disorders. Advanced
Psychiatric Treat., 10, 389–398
Virkkunen M, Goldman D, Nielsen DA, & Linnoila M. (1995). Low brain serotonin
turnover rate (low CSF 5-HIAA) and impulsive violence. J Psychiatry Neurosci.
20, 271–275
Weisz, J. R., Sandler, I. N., Durlak, J. A., & Anton, B. S. (2005). Promoting and
protecting youth mental health through evidence-based prevention and treatment.
American Psychologist, 60, 628– 648.
Werner, K., & Gross, J. J. (2010). Emotion regulation and psychopathology: A
conceptual framework. In A. Kring & D. Sloan (Eds.). Emotion regulation and
psychopathology. (pp. 13-37) New York, NY: Guilford Press.
West, D. J. (1982). Delinquency. Cambridge, MA: Harvard University Press.
Wick, J. Y. (2013). Violence & aggression: Nature or nurture—Can meds help?
Retrieved from
http://www.pharmacytimes.com/publications/issue/2013/March2013/Violenceand-Aggression-Nature-or-Nurture-Can-Meds-Help#sthash.lKwfBVnm.dpuf
Wilens, T. E., Biederman, J. J., & Spencer, T. J. (1998). Pharmacotherapy of attention
deficit hyperactivity disorder in adults. CNS Drugs, 9(5), 347-356.
Winnicott D. (1953). Transitional objects and transitional phenomena. International
Journal of Psychoanalysis, 34, 89–97
Yamasaki S., Yamasue H., Abe O., Suga M., Yamada H., Inoue H., Kasai K.
PREVENTING ANTISOCIAL PERSONALITY DISORDER
67
(2010). Reduced gray matter volume of pars opercularis is associated with
impaired social communication in high-functioning autism spectrum disorders.
Biol Psychiatry, 68, 1141–1147
Yang Y., Raine A., Colletti P., Toga A. W., & Narr K. L. (2009). Abnormal
temporal and prefrontal cortical gray matter thinning in psychopaths. Mol
Psychiatry, 14, 561–562
Zak, P., Kurzban, R., & Matzner, W. (2004). The neurobiology of trust. Annals of the
New York Academy of Sciences, 1032(1), 224-227 DOI: 10.1196/annals.1314.025
Zak, P., Kurzban, R., & Matzner, W. (2005). Oxytocin is associated with human
trustworthiness Hormones and Behavior, 48(5), 522-527
DOI:10.1016/j.yhbeh.2005.07.009
Zanarini M. C., Gunderson J. G., Marino M. F., Schwartz E. O., & Frankenberg F. R.
(1989). Childhood experiences of borderline patients. Comprehensive Psychiatry
30, 18–25
Zuckerman, M. (1994). Behavioral expressions and biosocial bases of sensation-seeking.
New York, NY: Cambridge University Press.