Martens AntisocialandPsychopathicPD Review

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Antisocial and Psychopathic Personality Disorders: Causes, Course, and

Remission—A Review Article
Article in International Journal of Offender Therapy and Comparative Criminology · August 2000

DOI: 10.1177/0306624X00444002
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International Journal of Offender Therapy and
Comparative Criminology
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Antisocial and Psychopathic Personality Disorders: Causes, Course, and Remission—A Review Article
Willem H. J. Martens
Int J Offender Ther Comp Criminol 2000; 44; 406
DOI: 10.1177/0306624X00444002
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International Journal of Offender Therapy and Comparative Criminology
Antisocial and Psychopathic Personality Disorders
Antisocial and Psychopathic Personality

Disorders: Causes, Course, and
Remission—A Review Article
Willem H. J. Martens
Abstract: Antisocial and psychopathic personality disorders can be linked to a number of bio-
chemical abnormalities (e.g., serotonin, monoamine oxidase, and hormone dysfunctions),
genetic and environmental influences, and psychological and social manifestations. Children
with conduct disorders, with or without attention deficit hyperactivity disorder, have an ele-
vated risk for antisocial or psychopathic personality disorders in adolescence and adulthood.
The presence of comorbid disorders such as substance abuse and schizophrenia have a strong
negative predictive value with respect to the course, the prognosis, and the outcome of antiso-
cial and psychopathic disorders. Furthermore, there are substantial gender differences. The
rates for spontaneous remission and improvement of antisocial and psychopathic personality
disorders are possibly relatively high. In fact, these rates are higher for women than for men.
In the fourth decade of life, most of the antisocial and psychopathic personalities are in
remission.
DIAGNOSTIC CRITERIA
There are various diagnostic systems that reflect the different concepts of psy-
chopathy. Although the definitions of psychopathic, antisocial, and dyssocial per-
sonality disorders are related to each other to a high degree, there is no complete
overlap. Despite the same basic set of characteristics—such as irresponsibility,
egocentricity, lack of conscience, social maladjustment, poor development of
relationships, and impulsive/aggressive behavior—there is no agreement on the
precise nature or the right definition of the core disorder.
Today, the official term is antisocial personality disorder as it is defined in the
Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) (American
Psychiatric Association [APA], 1994). The members of the Axis-II study group of
the DSM-IV, Hare, Hart, and Harpur (1991), as well as Kernberg (1992) criticized
the DSM-IV criteria for antisocial personality disorder (ASPD). They pointed out
that these criteria are directed too much at specific behavior and criminality in-
stead of at personality traits and the psychopathological aspects. Hare (1983) pointed
out, in psychometric studies of forensic populations, that there are two separate
factors within the overall construct of ASPD. One reflects consistent criminality,
International Journal of Offender Therapy and Comparative Criminology, 44(4), 2000 406-430
 2000 Sage Publications, Inc.
406

Antisocial and Psychopathic Personality Disorders 407
and the second reflects manipulativeness and a lack of empathy. L. N. Robins and
Regier (1991) found in their large epidemiologic study that only a minority of the
individuals with ASPD have difficulties with the law; Hare (1983) found that only
about half of all prison residents meet the criteria of this disorder. L. N. Robins and
Regier (1991) and Hare (1983) made clear that the relationship between ASPD
and criminality is not as strong and specific as is suggested in the DSM-IV criteria.
Indeed, the relationship between criminality and ASPD is rather complicated.
Hart and Hare (1989) and Stålenheim and von Knorring (1996) studied foren-
sic psychiatric populations and showed that significantly fewer patients suffered
from psychopathic personality disorder (PPD) than from ASPD. They demon-
strated that ASPD and PPD are not identical.
The definitions of PPD of Cleckley (1955/1976) and Hare, Harpur, et al.
(1990) are focused on personality traits. Hare operationalized the concept of
Cleckley when the Psychopathy Checklist (PCL) was developed. The PCL mea-
sures two correlated factors. Factor 1 describes a cluster of affective-interpersonal
traits central to psychopathy. Factor 2 describes traits associated with an unstable
unsocialized lifestyle, or social deviance. Today, only psychopathy as defined by
means of the Psychopathy Checklist by Hare is regarded by some people as a
somehow reliable and valid concept. The DSM-IV field trial of Widiger et al.
(1996) provided mixed support for the proposal to include more traditional traits
of psychopathy such as a glib and superficial charm, lack of remorse, deceitful/
manipulative behavior, lack of empathy, and arrogant self-appraisal.
In the criteria for dyssocial personality disorder of the International Classifica-
tion of Mental and Behavioral Disorders (ICD-10) (World Health Organization,
1992), the criminal aspects were left out of consideration. There is no strong, and a
rather indirect, relationship between criminality and PPD; many psychopaths are
noncriminal (Martens, 1997). Only in the definitions of Cleckley and Hare, the
criteria mendacity, insincerity, and unreliableness were explicitly included. The
concept of PPD is not contained in the DSM-IV or in the ICD-10.
COMORBIDITY
Personality disorders were relegated to Axis II in DSM-III (APA, 1980) to

encourage multiple diagnosis (L. N. Robins & Regier, 1991). ASPD and PPD are
rarely pure disorders and are frequently accompanied and coloured by other men-
tal disorders. Dahl (1998) found that individuals with PPD or ASPD carry a high
risk of comorbid mental disorders. He reported that the presence of comorbid dis-
orders influences PPD and ASPD as to prognosis, treatment response, and the risk
for suicide and violence.

408 International Journal of Offender Therapy and Comparative Criminology
SUBSTANCE ABUSE
Especially in recent years, the relationship between ASPD and PPD on one
hand and substance abuse on the other has been a topic of interest. Nedopil,
Hollweg, Hartmann, and Jaser (1995) and Knop, Jensen, and Mortensen (1998)
found that drug and alcohol use was significantly correlated with the behavioral
characteristics of psychopathy. Whereas a relationship between ASPD and PPD
on one hand and substance use disorder on the other has been frequently observed
(Dinwiddie, 1997; Hesselbrock, Meyer, & Kenner, 1985; Jordan, Schlenger,
Fairbank, & Caddell, 1996; Kessler et al., 1997; E. Robins, Gentry, Munroz, &
Marte, 1977; L. N. Robins & Regier, 1991; Weiss, Martinez, & Hufford, 1996),
the causes of the comorbidity remain unclear (Van den Bree, Svikis, & Pickens,
1998). Men and women with ASPD have much higher rates of lifetime alcohol
(Kessler et al., 1997) and drug disorder (Mulder, Wells, Joyce, & Bushnell, 1994)
in comparison with the general population. Prevalence rates in DSM-III-R (APA,
1987) for substance abuse disorder were 39.3% in persons with ASPD (Kessler
et al., 1997).
The odds for ASPD disorder for drug-dependent men are twice that of women
(Flynn, Craddock, Luckey, Hubbard, & Dunteman, 1996). Men with active ASPD
are 3 times as likely to abuse alcohol and 5 times as likely to abuse drugs as those
without antisocial personality. These rates are even higher for women, 10 times
(Mulder et al., 1994) or 13 times (L. N. Robins & Regier, 1991) for alcohol abuse
and 12 times for drug abuse (L. N. Robins & Regier, 1991). But, not all studies
observed a relationship between alcohol abuse and ASPD. Fils-Aime et al. (1996)
demonstrated that none of 131 investigated alcoholics fulfilled the criteria for
ASPD.
Ross, Glaser, and Germanson (1988) found ASPD and PPD to occur before sub-
stance abuse disorder. Martens (1997) observed that in some cases, depending on
the circumstances, substance abusers have an increased risk for the development
of ASPD or PPD or vice versa. Furthermore, a common biological basis (Deckel,
Hesselbrock, & Bauer, 1996) and a common genetic and environmental founda-
tion (Van den Bree et al., 1998) for ASPD and substance abuse are conjectured.
ANXIETY, DEPRESSION, AND SCHIZOPHRENIA

In the traditional view, the psychopathic personalities lack normal levels of
fear and anxiety and show an absence of neurosis (Cleckley, 1955/1976; Lykken,
1995), delusions, and/or psychosis (Cleckley, 1955/1976, 1955/1988). Eysenck
(1977), however, described psychopaths as people located within a specific space
within a multidimensional model of personality defined by high extraversion,
high neuroticism, and high psychoticism (as core characteristics and not as
comorbidity). But after analyzing relevant studies, Doren (1996) concluded that
the contradictions and omissions make Eysenck’s theory quite questionable.

Some studies found a broad assortment of nonpsychopathic and nonantisocial

symptoms accompanying PPD and ASPD (Dahl, 1998; L. N. Robins & Regier,
1991).
Women with ASPD had high rates of comorbid psychiatric disorders—not
only substance dependence but also depression, anxiety (Jordan et al., 1996;
Kessler et al., 1997; Mulder et al., 1994), and suicidal behavior (Mulder et al.,
1994), whereas men with ASPD did not (Mulder et al., 1994). But according to
L. N. Robins and Regier (1991), although women have higher rates than men,
the comorbidity rates in men are still significantly higher than in the general
population.
Powerful associations between ASPD or PPD on one hand and mania and
schizophrenia on the other were also found (L. N. Robins & Regier, 1991). Ras-
mussen and Levander (1995, 1996) showed that the most frequent comorbidity
was noted between schizophrenia and ASPD. Nedopil et al. (1995), however,
found that there is only a low cooccurrence of psychopathy with schizophrenia.
SUICIDE AS A RESULT OF COMORBIDITY

Antisocial and psychopathic personalities are not generally associated with
suicide and suicide-related factors such as depression and anxiety. Maddocks
(1970) observed, however, 5% suicide in a 3-year follow-up of 59 untreated psy-
chopaths. Patients who made contingent suicide threats were likely to be sub-
stance dependent, antisocial, homeless, unmarried, and in legal difficulty. Data
suggest that there is a significant cooccurrence of psychopathy and other person-
ality disorders (Nedopil et al., 1995) that can be related with suicide ideation.
Axis II comorbidity was observed also in patients with ASPD who committed sui-
cide in Sweden and the United States (Rich & Runeson, 1992).
Two thirds of the women with ASPD reported significant suicidal ideation in
the past, and more than one third had made suicide attempts. Men with ASPD are
12 times more likely to attempt suicide than those without ASPD (Mulder et al.,
1994). Because so few individuals have pure ASPD, the suicidal ideation and
behavior may be largely the result of their comorbid symptoms. Moreover, a
strong relationship was observed between suicide on one hand and substance
abuse, depressive disorders, anxiety disorders, and personality disorders on the
other (Suominen, Isometsä, Henriksson, Ostamo, & Lönnqvist, 1999).
It is possible that male suicidal ideation and behavior might reflect impulsivity
and anger rather than low mood (Mulder et al., 1994). In my opinion, suicide
ideation in women with ASPD is also likely associated with comorbid borderline
personality disorders, anxiety disorder, major depression, schizophrenia, multi-
ple personality disorder, or manic depression. Women showed an evidently differ-
ent spectrum of comorbidity than men did. The consequences of comorbidity for
the prognosis of persons with ASPD will be discussed later in this article.

BIOLOGICAL, PSYCHOLOGICAL,
AND SOCIAL DETERMINANTS
BRAIN INJURIES AND DYSFUNCTIONS

An increasing number of investigations demonstrate the neurobiological
underpinning of PPD and ASPD. Some brain injuries and cerebrovascular disor-
ders can cause antisocial and psychopathic personality changes (Benson &
Blumer, 1975; Robinson & Starkstein, 1997; Silver, Hales, & Yudofsky, 1997).
Individuals with PPD and ASPD have at times a history of frontal lobe lesions
(Deckel et al., 1996; Luria, 1980; Miller, 1987; Silver et al., 1997; Stein et al.,
1993). Disturbances in prefrontal functioning may be a common biological
ground that links ASPD, substance abuse, and biological mechanisms of rein-
forcement (Deckel et al., 1996). Some brain lesions, such as frontal lobe lesions,
are mainly related to specific core features of ASPD and PPDs such as impulsivity
and disinhibition.
Psychopaths were viewed by Hare (1970) as suffering from dysfunctions in the
limbic system of the brain that affects the psychopaths’ ability to inhibit or disrupt
ongoing behavior. One consequence of this dysfunction is that it makes it difficult
for psychopaths to learn to inhibit an action that is known to lead to punishment.
This inhibitory deficiency was presumed by Hare (1970) to cause the preservation
of the most dominant response in any given situation; specifically, psychopaths
will continually act with their most preferred responses regardless of the conse-
quences. Hare employed this theory to explain why psychopaths seem unable to
learn from punishment and appear controlled by their immediate needs with no
thought for the future (Doren, 1996). The preservation theory of psychopathy was
found to be well supported by research if one accepted that psychopaths typically
have cerebral lesions. However, no strong conclusions could be drawn concerning
that issue. Only one type of relevant empirical finding emerged that did not seem
to be in agreement with Hare’s formulations—that of the duration of a psycho-
path’s preservative deficit. Similar to other theories reviewed, this response pres-
ervation theory was seen to be lacking comprehensiveness in explaining psychop-
athy in its entirety (Doren, 1996).
MAO, CSF 5-HIAA, 5-HT, AND HORMONE DYSFUNCTIONS

Studies demonstrated a marked negative relationship between monoamine
oxidase (MAO) activity on one hand and sensation seeking and impulsivity on the
other, both features of psychopathy. For example, an association between low
serotonin (5-hydroxytryptamine, 5-HT) function and aggressive behavior was
found (Dolan, 1994). Various studies uncovered an inverse relationship between
5-hydroxy indoleacetic (CSF 5-HIAA) on one hand and impulsivity, irritability,
hostility, and aggression on the other (Linnoila et al., 1994; Virkkunen, Kallio,
et al., 1994; Virkkunen, Rawlings, et al., 1994).

In a forensic psychiatric population (n = 61 males), elevated triiodothyroine

(T3) levels (Stålenheim, Eriksson, von Knorring, & Wide, 1998) and high con-
centrations of total testosterone (TT) and sex hormone-binding globulin
(Stålenheim, von Knorring, & Wide, 1998) were related to alcoholism and psy-
chopathy as measured by the Psychopathy Checklist-Revised (PCL-R) and a
diagnosis of a DSM-IV (APA, 1994) antisocial disorder. Levels of T3 and
free-thyroxine (T4) were also associated with criminality and an ICD-10
dyssocial disorder (World Health Organization, 1992). Serum levels of T4 were
negatively related to the same disorders and personality traits. Study results indi-
cate an intimate relationship between T3 and T4 and alcohol abuse and antisocial
behavior (Stålenheim, Eriksson, et al., 1998). In the author’s opinion, there is a
possibility that T3 and T4 constitute the same neurobiological basis for alcohol-
ism and ASPD/PPD. Alm, af-Klinteberg, Humble, Leppert, Sorensen, Tegelman,
et al. (1996), however, showed that increased T3 activity was correlated exclu-
sively with more persistent criminality (but not with psychopathic traits) when
compared to that in former delinquents who demonstrated lower T3 values.
In boys, a relationship was observed between low cortisol and aggressive
behavior but not covert antisocial behavior (McBurnett, Pfiffner, Capasso, Lahey, &
Loeber, 1997). When there are low cortisol findings in conduct disorder
(McBurnett et al., 1997; Susman & Ponirakis, 1997; Van Goozen et al., 1998;
Zuckerman, 1994), there should also be low findings in ASPD (Virkkunen, 1985)
as well as low CSF adrenocorticotropic hormone (Virkkunen, Rawlings, et al.,
1994). Susman and Ponirakis (1997) presented findings linking hormones of the
hypothalamic-pituitary-adrenal and hypothalamic-pituitary-gonadal axes to anti-
social behavior in youth. The results of a study of Van Goozen et al. (1998) also
supported an important role for hypothalamic-pituitary-adrenal axis sympathetic
autonomic functioning in persistent antisocial behavior in young boys.
Zuckerman (1994) found that sensation seeking, one of the psychopathic traits,
was related to low levels of MAO and cortisol and high concentrations of gonadal
hormones.
ELECTROENCEPHALOGRAM (EEG) ABNORMALITIES

AND LOW AUTONOMIC ACTIVITY-REACTIVITY
A number of investigations reported an association between PPD and ASPD

on one hand and EEG abnormalities on the other (Hare, 1970; Hare & Cox, 1978;
Howard, 1984; Scarpa & Raine, 1997). Hare (1970) and Hare and Cox (1978)
analyzed the data of 21 relevant studies in reaching this conclusion.
Quay (1965) described the psychopathic disorder as an extreme of stimulation-
seeking behavior, a consequence of pathological underarousal. There were two
facets to Quay’s theory: (a) Psychopaths are characterized by a primary abnor-
mality in their physiological reactions to sensory input that causes a high degree
of optimal stimulation, and (b) psychopaths’ assumed higher optimal levels of

stimulation leads to an extremely high degree of motivation to increase sensory

stimulation so as to compensate for underarousal due to their physiological abnor-
mality. This theory was well supported by investigations of psychopaths’ overt
psychometric and experimentally bound behaviors. Research studying hypothe-
sized physiological substrata of pathological stimulation seeking was not as
impressive in their outcomes (Doren, 1996; Zuckerman, 1994). Nevertheless, a
number of studies indicated that many psychopaths suffer durably from a reduced
cortical arousal (Costin & Draguns, 1989; Raine, 1996; Raine, Venables, &
Mednick, 1997; Raine, Venables, & Williams, 1996).
The neurophysiological reactions of antisocial personalities as a result of prov-
ocation or frustration have been investigated in diverse laboratory settings. Mag-
nusson (1996) presented results indicating that low autonomic activity-reactivity
(i.e., low adrenaline excretion) is strongly associated with persistent antisocial
behavior but not with adolescence-restricted antisocial behavior. Findings of
studies on resting skin conductance and heart rate indicate that antisocial individ-
uals are characterized by a low autonomic activity-reactivity or underarousal
(Raine et al., 1997). Evidence was found for specificity of low heart rate to aggres-
sive forms of antisocial behavior. It was concluded that a low resting heart rate, a
partly heritable trait, and low resting skin conductance, reflecting fearlessness
and stimulation seeking and sensation seeking, are important, diagnostically spe-
cific, well-replicated, and early biological markers for later aggressive behavior
and/or ASPD (Raine et al., 1997). Antisocial behavior was found to be unexpect-
edly related to disruption of vagally mediated, phasic respiratory effects on heart
rate (Mezzacappa et al., 1997).
Zuckerman (1994) found, however, that tonic levels of skin conductance, heart
rate, and blood pressure were lower in high sensation seekers in only a few studies
and that the finding is often limited to one gender (generally women) or is only
found under special conditions. According to Zuckerman, there is no consistent
evidence that sensation seekers are underaroused and seek novel stimulation to in-
crease arousal to optimal levels. The difference between high- and low-sensation
seekers is not based on tonic levels of cortical arousal but on arousability in
response to certain types of stimuli. In this, Zuckerman disagreed with Quay
(1965) and Raine et al. (1997). From the author’s point of view, the states of
underarousal and arousability are two aspects of the same condition, and a split-
ting between them is artificial.
Lykken (1995) found that psychopaths who met Cleckley’s (1955/1976) crite-
ria showed low fearfulness, poor fear conditioning, and poor avoidance learning.
These primary psychopaths demonstrated fewer physiological disturbances, as
was demonstrated from electrical conductance of the skin, in anticipating the
imminent painful electric shock than the nonpsychopaths and the so-called sec-
ondary psychopaths (with neurotic traits). They were also less concerned about
the shock (punishment). Lykken concluded that these primary psychopaths suf-
fered from an innate defect of the central nervous system. As the result of a biolog-
ically changed anxiety level, these individuals are not able to learn from experi-

ence and cannot avoid negative life events. Lykken did not clarify why these
primary psychopaths suffered from a central nervous system defect because
abnormal electrodermal responses are seen as expressions of arousal and auto-
nomic nervous system dysfunctions. According to Hare (1970), limbic lesions are
the cause of the inability to learn from punishment; there are obviously multiple
neurological causes for this inability.
The control theory of psychopathy states that two major components are nec-
essary for the development of the disorder: cortical underarousal and partial help-
lessness conditioning. Although not fully independent, there is no direct link
between these two. Once both of these conditions exist, a series of learning experi-
ences combine to produce poorly socialized persons who persist in viewing peo-
ple as challenges to be overcome to attain the psychopath’s own immediate
rewards (Doren, 1996). Most of the research supports this conceptualization of
the syndrome. Many of the theoretical relationships, however, have not yet been
empirically investigated in sufficient detail to allow for conclusions or support to
be drawn (Doren, 1996).
GENETIC AND ENVIRONMENTAL INFLUENCES

Recent research data provide increasing evidence that genetic and environ-
mental influences are involved in the development of personality and behavior.
The genetic research of Livesley, Jang, Jackson, and Vernon (1993) and Plomin
(1994) indicated that personality disorders are highly genetically determined. It
was found that psychopath’s children have high rates of conduct problems and
that an antisocial father does not have to live in the home to increase his child’s
risk for PPD and ASPD (L. N. Robins, 1996) because genetic influences play a
major role in these disorders. Ge, Conger, Cadoret, and Neiderhiser (1997) found
that psychiatric disorders of biological parents were also significantly related to
children’s antisocial and hostile behaviors.
Rutter and Rutter (1993); Biederman, Milberger, et al. (1995); and Rutter
(1997) demonstrated the importance of adverse family-environment variables
(severe marital discord, low social class, large family size, paternal criminality,
maternal mental disorder, and foster care placement) as risk factors for children
with attention deficit hyperactivity disorder (ADHD) for adolescent and adult
ASPD. There is an emphasis on the interaction of biological and aversive environ-
mental factors that produce normative and maladaptive patterns of development
and ASPD (Zahn & McBride, 1998). Nevertheless, Faraone, Biederman, Jetton,
and Tsuang (1997) found that ADHD, conduct disorders, and ASPD are substan-
tially genetically determined. A gene-environment interaction also plays an
important role in the development of these disorders.
Poor parent-child relations were associated with aggressive and covert conduct
disorders, and socioeconomic status was associated exclusively with aggressive
conduct disorders in one study (McBurnett et al., 1997). Environmental effects
(Cadoret, Yates, Troughton, Woodworth, & Stewart, 1995) and a gene-environ-

ment interaction (Cadoret et al., 1995; Ge et al., 1997; Lyons et al., 1995) were
found to account for significant variability in adoptee aggressivity, conduct disor-
der, and adolescent and adult antisocial behavior. But, according to Lyons et al.
(1995), who studied 3,226 pairs of male twins, these environmental influences of
the shared or family environment promote antisocial behavior during adulthood
to a much lesser extent than in childhood and early adolescence. Genetic causal
factors were found to be much more prominent for adult than for juvenile antiso-
cial traits (Lyons et al., 1995). In the author’s opinion, Lyons’s research demon-
strated that genetic influences on personality and behavior are more long lasting
than environmental effects.
GENETIC ASPECTS OF COMORBIDITY

Substance abuse in association with ASPD can be (partly) the result of envi-
ronmental influences and a gene-environment interaction (Cadoret et al., 1995).
Results of a study of Cadoret, Yates, Troughton, Woodworth, and Stewart (1996)
indicated that drug abuse and dependency has a genetic etiology that starts with a
biologic parent with antisocial personality whose offspring may manifest conduct
disorder, which leads to aggressivity, drug dependency, or abuse.
Adoption and twin studies have found evidence of both genetic and environ-
mental influences in ASPD and substance use disorders. Therefore, comorbidity
between ASPD and substance abuse may be the result of shared genetic influ-
ences, shared environmental influences, or a combination of the two. However,
only a limited number of adoption and twin studies have addressed this issue, and
the results have not been conclusive (Van den Bree et al., 1998).
BIOSOCIAL, BIOPSYCHOSOCIAL,
AND PSYCHOSOCIAL THEORIES
Only the interaction between biological and psychological risk factors can
induce personality disorders. But social factors such as a chaotic family life,
parental divorce, poor supervision and guidance, criminality, and quarrelsome
and antisocial behavior in the family are also involved in this interaction. Espe-
cially when a child experiences insecurity, a lack of attention, and warmth, there is
a great risk for the development of antisocial personality disorder (Ge et al.,
1997). Also, from a biosocial standpoint, Raine (1996) hypothesized that early
environmental stress and adverse home backgrounds with a lack of psychosocial
motivation may underlie autonomic underarousal and hyporeactivity in antisocial
individuals. The author believes that such negative influences and a lack of
positive stimulation can cause neurophysiological insensitiveness and mental
indifference as an expression of self-protection. McBurnett suggested that low
biological arousal and deviant or rejecting parental behavior represent distinct
mechanisms having differential effects on persistent episodic aggression on inad-

equate internalization of social constraint (McBurnett et al., 1997). Some of the

research reviewed supported the neurophysiological component of these
biosocial theories of Raine and McBurnett, while other studies seemed to contra-
dict. The data of the few studies that have reported biosocial interactions suggest,
however, that biological variables can protect against antisocial behavior in
socially vulnerable individuals and that social variables can protect against anti-
social behavior in biologically vulnerable individuals.
Patterson’s (1996) psychosocial theory of the development of antisocial
behavior suggests that chronic antisocial behavior in children is the direct out-
come of a breakdown in parental family management. Patterson constructed a
model of the dual variables that sketches the process that leads to the development
of antisocial children. The parents of antisocial children often come from disad-
vantaged families characterized by increased mobility, financial difficulties, neg-
ative changes in social attitudes, divorce, sexual abuse, and working women.
These children are mostly raised by antisocial and/or single parents, frequently
divorced women or those in transition, or unmarried adolescents. These parents
are frequently unskilled and live isolated in a disorganized neighbourhood. As a
result of an interaction between these factors and other variables (i.e., lack of
parental care, poor diet, and parental substance abuse), their infants and toddlers
become difficult to handle and at an older age show antisocial behavior. This
model of Patterson is well supported by research.
Paris (1996b) investigated a large number of empiric and epidemiologic stud-
ies of ASPD and found cultural differences in the prevalence of this disorder.
Social factors also seem to play a major role in the etiology of ASPD, and Paris
(1993, 1996a) concluded that only a biopsychosocial model can explain this dis-
order. The recent research data indicate consistently the correctness and appropri-
ateness of the biopsychosocial model (Paris, 1993, 1996a, 1996b). The model of
Paris derives from the biopsychosocial model of Siever and Davis (1991), which
conceptualized personality disorders as pathologic manifestations of individual
differences in personality traits. According to Siever and Davis (1991), a number
of specific personality characteristics can constitute a predisposition for personal-
ity disorders. They argued that antisocial behavior is caused by a combination of
neurobiologic-determined impulsivity (low serotonin activity) and an increased
behavior activation that is modulated by high concentrations monoamines.
The investigations of Paris (1993, 1996a, 1996b) demonstrated that psycho-
social factors are crucial in the progression from specific personality traits into
personality disorders. The biopsychosocial model of Paris (1998) hypothesized
that psychopathy will only develop in those individuals who are already vulnera-
ble by virtue of their personality traits, specifically, high impulsivity and high
behavioral activation. If such individuals are also exposed to antisocial parents
and/or to chaotic family environments, the risk of psychopathy is further
increased. However, it is argued that a diagnosable disorder should only appear
when the social environment is sufficiently pathological that it fails to provide
protection against these biological and psychological risks. This model, too, is

well supported by research. Indeed, with the help of the biopsychosocial model,
ASPD and PPD can be explained most completely.
CONDUCT DISORDERS AND ADHD AS PRECURSORS

AND PREDICTORS OF PSYCHOPATHIC AND ASPDS
Many adults with ASPD and PPD have histories of childhood problem behav-
ior such as ADHD and childhood conduct disorders. Although there are predic-
tors of adult conduct disorders, no single individual childhood behavior problem
is a particularly good predictor of antisocial behavior. L. N. Robins and Regier
(1991), who studied a total sample of 516 men and 111 women, concluded that the
best single childhood predictors were running away from home before age 15
(29%), delinquency (25%), and vandalism (21%). Other authors also found that
childhood conduct problems predicted serious antisocial behavior and criminality
in adolescence and adulthood (Biederman, Milberger, et al., 1995; Maddocks,
1970; M. G. Myers, Stewart, & Brown, 1998; L. N. Robins & Regier, 1991;
Satterfield & Schell, 1997). Lynam (1997) concluded that most of the psycho-
pathic boys he investigated at age 12 (n = 430) showed serious, stable, antisocial
behavior in adolescence and early adulthood.
Conduct disorders appeared to be an almost necessary condition for multiple
social disability in adults in one study (Zoccolillo, Pickles, Quinton, & Rutter,
1992), and the childhood-onset type had a generally poor prognosis (Werry,
1997). But L. N. Robins (1996) found in a sample of 536 youngsters that antiso-
cial behavior in childhood is necessary, indeed, but not sufficient to explain adult
antisocial behavior.
Werry (1997) concluded that the comorbidity of conduct problems with other
disorders is common. Children with conduct disorders demonstrate an increased
risk for substance abuse and ASPD in later life (Kazdin, 1991, 1992; L. N.
Robins & Price, 1991; L. N. Robins & Regier, 1991). Comorbid ADHD may be
associated with greater aggression and a poorer prognosis, and comorbid aca-
demic underachievement may be associated with a negative course. Of the
comorbid disorders, ADHD is the most virulent and repeatedly has an overlap
with conduct disorders (Steiner & Dunne, 1997). Findings of the investigation of
Satterfield and Schell (1997) suggest—contrary to the results of the studies of
Biederman, Faraone, Milberger, and Guite (1996) and Mannuzza, Klein, Bessler,
Malloy, and LaPadula (1998)—that only ADHD children with conduct disorders
are at risk for both juvenile and adult criminality. Hyperactive children who do not
have conduct problems are not at increased risk for later criminality. Furthermore,
comorbid anxiety disorder may also be associated with a level of aggression, but
the direction of the correlation appears to differ at different ages, according to
Hinshaw, Lahey, and Hart (1993). The precise nature of the relationship between
anxiety and aggression, however, was not clarified by Hinshaw.

Follow-up studies found that by midadolescence, individuals with ADHD

were at high risk of a wide range of adverse outcomes (Biederman, Faraone, et al.,
1996). The studies of Biederman, Faraone, et al. (1996) and Mannuzza et al.
(1998) strongly suggest that children with ADHD, compared with control per-
sons, are at significantly higher risk for a specific negative course marked by anti-
social and substance-related disorders. Gender differences in ADHD were not
investigated.
There are only a few studies of gender differences with respect to conduct dis-
orders. A large epidemiologic study of 15-year-olds (n = 1,000) reported that
7.5% to 9.5% of the girls met the DSM-III-R (APA, 1987) criteria for conduct dis-
orders, compared to 8.6% to 12.2% of the boys (Fergusson, Horwood, & Lynskey,
1993). The outcome is reported to be better for boys than for girls with conduct
problems (Lipman, Bennett, Racine, Mazumdar, & Offord, 1998). After review-
ing the data of a large epidemiologic study, L. N. Robins (1996) determined the
following gender distinctions: (a) Boys were younger than girls at first conduct
symptoms predictive of adult antisocial behavior, (b) early sexual activity was
more predictive of psychopathy for girls than boys, and (c) psychopathy and
ASPD in women required a more pathological family background. For women,
problems in paternal relationships predicted higher levels of antisocial behavior
(Neighbors, Forehand, & Bau, 1997). These results suggest, in the author’s opin-
ion, that women react in a more destructive way than do men to negative environ-
mental factors and paternal criticism and to immature sexual experiences. Adults
can also develop ASPD. Barrett et al. (1996) investigated the relationship between
combat exposure and adult antisocial behavior in a sample of 2,490 male Army
veterans of the Vietnam War. The results indicated that exposure to traumatic
events can play a major role in the etiology of antisocial personality.
COURSE AND PROGNOSIS
ANTISOCIAL PERSONALITY DISORDER

Swanson, Bland, and Newman (1994) studied 3,258 randomly selected per-
sons and showed that the first signs of antisocial behavior appeared in boys at age
7.6 and in girls at age 9.2. L. N. Robins and Regier (1991) found that antisocial
personality for boys as well as girls typically begins at about age 8 with a variety of
behavior problems at home and in school and is fully expressed by the late 20s or
early 30s.
There are two peaks of antisocial behavior: the highest percentage, between
ages 25 and 34 (Swanson et al., 1994) or between ages 25 and 44 (Karno, 1987;
Swanson et al., 1994), and the lowest percentage, between ages 18 and 24 (Karno,
1987; J. K. Myers et al., 1984; L. N. Robins et al., 1984; Swanson et al., 1994). But
Black, Baumgard, and Bell (1995) observed a peak between ages 24 and 44 and a

diminishing severity of symptoms between ages 45 and 64. The overall rate of
ASPD was 3.1% for life prevalence (Oakley-Browne, Joyce, Wells, Bushuell, &
Hornblow, 1989). The prevalence of ASPD and, to a lesser extent, psychopathy
also declined with age (APA, 1994; Bland, Newman, & Orn, 1997; Harpur &
Hare, 1994). DSM-III (APA, 1980) placed ASPD on Axis II, with the implication
that it is a lifelong disorder; in fact, the remission rate is high and goes up rapidly
with age (Mulder et al., 1994; L. N. Robins & Regier, 1991). Very few elderly per-
sons have recent symptoms of the disorder (L. N. Robins & Regier, 1991). Mulder
et al. (1994) even observed that no one age 45 and older met criteria for ASPD.
Most frequently, an improvement or remission in antisocial personalities happens
in the fourth decade (Adams, Victor, & Ropper, 1997; APA, 1994; Farrington,
1995; Lish, Kavoussi, & Coccaro, 1996; Martin, Cloninger, & Guze, 1982). There
is also a high rate of spontaneous recovery from the conduct problems that are the
childhood version of the disorder, and there is a high rate of remission, as a second
wave, in the third and fourth decades of life (L. N. Robins & Regier, 1991). Rutter
and Rutter (1993) found, nevertheless, that numerous studies have shown that
antisocial behavior shows an unusually strong degree of persistence over time.
Pajer (1998) critically reviewed the data of 20 studies on the adult outcomes of
adolescent girls with antisocial behavior. As adults, antisocial girls manifested
increased mortality rates, a significant increase in the rate of criminality, substan-
tial rates of psychiatric morbidity, and dysfunctional and often violent relation-
ships. Most of the deaths (all natural) in the follow-up of these women occurred in
early adulthood. Seven percent of all girls with conduct disorders died during the
follow-up. Nearly half of these girls developed substance abuse problems as
women, and one third of the girls met as women the criteria for ASPD. Compara-
tive research data of boys are not available.
PSYCHOPATHIC PERSONALITY DISORDER
Age and gender differences in the prevalence and stability of psychopathic

behavior are striking. Most people show temporary or situational psychopathic
behavior, and only a minority continue to manifest this disorder over a long period
of time (Loeber, Stouthamer-Loeber, Van Kammen, & Farrington, 1989).
According to Loeber et al. (1989), an increase of psychopathic behavior
between the ages 7 and 17 is related to a reduction of symptoms between the ages
17 and 30. Psychopathic behavior at age 4 is often permanent, whereas occurrence
at age 7 or older is temporary (Loeber et al., 1989; Martens, 1997; Moffitt,
1993). The prevalence of psychopathic symptoms diminishes with age. After age
21, 2% of all psychopaths are remitting each year (Goldman, 1992). The course of
psychopathy in adulthood is variable, and improvement and remission can occur
at any age (L. H. Robins, 1966; L. N. Robins & Regier, 1991). Most frequently, an
improvement or remission of PPD and ASPD takes place in the fourth decade of

life (Martens, 1997; L. H. Robins, 1966). Obviously, only a minority of the psy-
chopaths suffers from this disorder after age 40.
Hare, McPherson, and Forth (1988) showed that the criminal activity in one
group of nonpsychopaths (n = 317) remained relatively stable in time, whereas
delinquency of psychopaths in another (n = 284) was serious until about age 40
but declined strongly thereafter. Nevertheless, nearly half of the psychopaths
remain involved in criminal activities. But Moffitt (1993) found that only 5% of
the criminal psychopaths age 45 and older render themselves guilty of delinquent
activities. The origins of the difference between the findings of Hare, McPherson,
et al. and Moffitt are unclear.
Some psychopaths, as they age, achieve a certain degree of socially acceptable
behavior, but they seldom lose their egocentric attitude (Hare & Schalling, 1978;
Harpur & Hare, 1994) and manipulative and callous traits (Harpur & Hare, 1994).
Impulsivity decreases, and adaptability increases in most older psychopaths
(Harpur & Hare, 1994).
Black, Baumgard, Bell, and Kao (1996) examined the death rates of 71 male
psychopaths during a four-decade follow-up. Seventeen men died during the follow-
up. Antisocial men younger than 40 years were at excessive risk for premature
death; men between the ages of 40 and 60 years also appeared to be at risk for pre-
mature death, although the increased risk was not statistically significant. The
causes for death were accidents, suicide (1 case), cancer, and diabetes mellitus.
PROGNOSIS AND GENDER
Men are twice as likely as females to be diagnosed with ASPD (Flynn et al.,
1996), but the likelihood of having an ASPD diagnosis decreases with age for
both genders (Bland et al., 1997; Flynn et al., 1996). Mulder et al. (1994) found
that male rates for lifetime prevalence were higher than female rates, although this
was not statistically significant (men = 4.2%, women = 1.9%). They suggested
that the prognosis for men is similar to those of women. L. N. Robins and Regier
(1991), Swanson et al. (1994), and Steels et al. (1998) demonstrated, however,
that women generally have a more satisfactory long-term outcome than men
(Steels et al., 1998). Martin et al. (1982) and Lish et al. (1996) observed that
merely 18% of the female felons with ASPD were still engaged in criminal behav-
ior in the fourth decade of life. L. N. Robins and Regier (1991) reported that 10%
of the women and 27% of the men younger than 30 and only 5% of the females and
20% of the men between the ages 30 and 44 met the criteria of ASPD. And
Swanson et al. (1994) even concluded that none of the women of his research pop-
ulation (n = 3,258) older than 35 suffered from ASPD.
There is some evidence that women are beginning to catch up with men in
meeting these childhood criteria. The disorder is predominantly male, but the
male difference in number between men and women seems to have been reduced

somewhat in recent years as rates for both genders have increased, and women’s
increase has been somewhat greater (Pajer, 1998; L. N. Robins & Regier, 1991).
PROGNOSIS AND COMORBIDITY
A comorbid substance abuse disorder is a strong negative predictive factor in

antisocial individuals (Flynn et al., 1996; Regier et al., 1990). But it is not clear
what substance abuse actually does predict. In one study, ASPD was linked to a
more severe symptomatology of alcoholism and other clinical problems
(Morgenstern, Langenbucher, Labouvie, & Miller, 1997). Black, Monahan,
Baumgard, and Bell (1997) and Dinwiddie and Daw (1998) revealed that alco-
holic individuals with ASPD and PPD had a worse prognosis than their
nonalcoholic counterparts and that their social functioning was significantly
poorer (Knop et al., 1998). The prognosis for antisocial men consuming more
than the average amount of alcohol was worse than that for antisocial women
(Tomasson & Vaglum, 1996). Repo, Virkkunen, Rawlings, and Linnoila (1997)
showed that among arsonists, lifetime criminal recidivism was primarily associ-
ated with alcohol dependence and ASPD.
Personality disorders, particularly ASPD, were found to be predictive of the
course of schizophrenia (Dingemans, Lenoir, & Linszen, 1998). Patients with
ASPD and comorbid schizophrenia had a worse outcome than individuals with
pure ASPD. Most notably, comorbid ASPD or PPD and schizophrenia were asso-
ciated with higher levels of alcohol consumption, more violence (Rasmussen &
Levander, 1995, 1996), and more severe social consequences (Dahl, 1998) than in
persons with exclusively ASPD, PPD, or alcohol disorder (Shumway & Cuffel,
1996).
Generally, differences between the course and prognosis of ASPD and PPD are
indistinct because there are relevant aspects that were investigated in PPD but not
in ASPD. For example, Harpur and Hare (1994) demonstrated a differentiation in
the disappearance of the various psychopathic personality traits in middle-aged
men with PPD, and Black, Baumgard, Bell, et al. (1996) studied the death rates.
These data were not available for persons with ASPD. On the other hand, more
research of individuals with ASPD, in comparison with studies of persons with
PPD, revealed information concerning specific age-, gender-, and comorbidity-
related patterns.
CAUSES OF SPONTANEOUS REMISSION
PSYCHOSOCIAL DETERMINANTS
In juvenile individuals and young adults, diminishing or disappearing of psy-
chopathic and antisocial behavior often occurs when they leave secondary school

(Elliott & Voss, 1974), join the armed services or afterward (Elder, 1986; Mattick,
1960), get married (Mulder et al., 1994; Sampson & Laub, 1990), achieve aca-
demic success (L. N. Robins & Regier, 1991), move from their old neighbourhood
(West, 1982), get positive group influences (McCord & McCord, 1956), live in a
nonfrustrating indulgent environment (McCord & McCord, 1956), or find stable
employment (Sampson & Laub, 1990). Moffitt (1993) pointed out that these
changes can be caused also by biological factors that are associated with age and
structural improvements at school or in the neighbourhood.
Aspects that are found to be correlated with remission or improvement in adult-
hood are the following: relational variables such as marriage or a long-lasting
relationship (Farrington, 1995; Martens, 1997; Mulder et al., 1994; L. H. Robins,
1966); confrontation with other forensic psychiatric patients (Martens, 1997,
1999); influence of a mentor (Black, Baumgard, & Bell, 1995; Martens, 1997,
1999; McCord & McCord, 1956; Vartiainen, Vuorio, Halonen, & Hakola, 1995);
good social integration (Reiss, Grubin, & Meux, 1996); communication, social sup-
port, and positive attention (Martens, 1997; McCord & McCord, 1956; Vartiainen
et al., 1995); parenthood and increased family responsibility (Adams et al., 1997;
Black, Baumgard, & Bell, 1995; Martens, 1997; L. H. Robins, 1966; L. N. Robins
& Regier, 1991); and growing up or maturation (Black, Baumgard, & Bell, 1995;
Martens, 1997; L. H. Robins, 1966). Other variables are fear of custody (L. H.
Robins, 1966), disease (J. K. Myers et al., 1984; L. H. Robins, 1966), religious
experience (Black, Baumgard, & Bell, 1995; L. H. Robins, 1966), academic suc-
cess (Martens, 1997; L. N. Robins & Regier, 1991), stable employment
(Farrington, 1995; L. H. Robins, 1966), and a vacation, excursion, or trip
(Vartiainen et al., 1995). The remission and maturation process continues in most
cases from 30 to 36 years of age (Martens, 1997).
Most of the earlier mentioned studies were based on interviews of former indi-
viduals with ASPD or PPD and observations of neutral authorities. Black,
Baumgard, and Bell (1995) and Vartiainen et al. (1995), however, made use exclu-
sively of self-reported data of former individuals with ASPD and PPD, and Black,
Baumgard, and Bell (1995) also interviewed some partners and/or family mem-
bers of the patients. This method has, however, an increased risk for gathering
incorrect, selective, and incomplete information.
NEUROLOGICAL AND BIOLOGICAL DETERMINANTS

Virkkunen and colleagues (Virkkunen, Kallio, et al., 1994; Virkkunen,
Rawlings, et al., 1994) found that high CSF 5-HIAA concentrations are related to
good impulse control. The subjects’ age may be a critical variable because most of
the patients who exhibit antisocial behavior are believed to remit or settle down in
their 40s (Linnoila et al., 1994; Virkkunen, de Jong, Bartko, Goodwin, & Lin-
noila, 1989). A relationship between (more) normal CSF 5-HIAA and platelet
monoamine oxidase concentrations was found in individuals who demonstrated
decreased or vanished violent, criminal, antisocial, or psychopathic behavior

(Alm, Alm, et al., 1994). Another study found a significant negative correlation
between platelet MAO activity and the degree of criminal psychopathy or ASPD
(Alm, af-Klinteberg, Humble, Leppert, Sorensen, Thorell, et al., 1996). A rela-
tionship was observed between low triiodothyronine (T3) activity and less persis-
tent criminalility, but there was no association with psychopathic traits (Alm,
af-Klinteberg, Humble, Leppert, J., Sorensen, Tegelman, et al., 1996). Dolan
(1994) concluded that normalized CSF 5-HIAA and MAO functions, and the
interaction between these factors, are associated with the absence or reduced anti-
social and psychopathic impulsivity. There is thus some evidence that normalized
neurobiological functions correlate with improvement or remission of persons
with ASPD or PPD. Until now, the biochemical functions of remitted psychopaths
were not investigated.
Deckel et al. (1996) found that increased frontal left hemisphere EEG activa-
tion is associated with a decreased likelihood of ASPD diagnosis. A diminishing
of EEG deviations was observed in the older, mostly middle-aged (former) psy-
chopaths and antisocial personalities. In these men, the increased (slow wave)
theta activity disappeared or was reduced (Hill, 1942; Kiloh, McComas, &
Osselton, 1972; Knott & Gottlieb, 1943; Monroe, 1970, 1978; Silverman, 1944;
Williams, 1969). Because most of the middle-aged psychopaths and antisocial
personalities are in remission—only 2% of the women and 10% of the men
between age 45 and 65 meet the criteria for ASPD (L. N. Robins & Regier,
1991)—it is likely that most of these antisocial and psychopathic persons
with normalized EEG patterns have achieved a certain degree of psychological
maturity.
Beneficial effects of traumatic brain injury are rarely described. Labbate, War-
den, and Murray (1997) reported two cases of patients who sustained frontal trau-
matic brain injury and who showed an improvement in impulsive and antisocial
behavior.
CONCLUSIONS
Different diagnostic systems or versions are used in the various studies, and the
results are not always consistent. As a consequence, it is at times difficult to match
and interpret the findings. Moreover, it is very confusing that many authors used
psychopathy as an equivalent of ASPD. There is some evidence that ASPD and
PPD are not identical. Since ASPD was introduced as an official diagnosis and
term, there has been a constantly decreasing amount of research that has been
directed at individuals who really met criteria for psychopathic personalities.
Criminality is frequently associated with PPD and ASPD. But the exact nature
of this relationship is obscure. There are many noncriminal individuals with PPD
and ASPD. Criminality in individuals with PPD—it was noted earlier that crimi-
nality is not a core feature of PPD—can be rather seen as a consequence of the
interaction of other traits such as impulsivity, disinhibition, moral dysfunction, a

lack of empathy, and irresponsibility. Hare (1983) and L. N. Robins and Regier
(1991) found that this trait is present in only some of the persons with ASPD and
that the association between criminality and ASPD is complicated and unclear.
Children with conduct disorders, with or without ADHD, are at high risk for
ASPD/PPD, substance abuse disorder, and criminality. The relationship between
conduct disorders and/or ADHD and ASPD/PPD is quite obscure, and more
research is needed, particularly with respect to other risk factors such as an
absence of stimulation of empathic abilities, positive coping behavior, exposure
to moral instruction, and related neurologic complications.
There are gender differences in the prevalence of antisocial and psychopathic
personality, in risk factors, in the presence of specific comorbid disorders, and in
prognosis and age-related remission rates. As a result, intervention, prevention,
and treatment programs for men and women should be specifically tailored to suit
them.
Men have twice the likelihood as women of having an ASPD diagnosis, but
this prevalence decreases for both sexes with age. The presence of comorbid dis-
orders such as substance abuse and schizophrenia in psychopathic and antisocial
personalities is associated with a poorer outcome when compared to antisocial
individuals without such disorders. There is some evidence that the prognosis of
alcoholic men with ASPD or PPD is poorer than that of alcoholic women with
ASPD or PPD.
As stated earlier, the neurologic and biochemical status of antisocial and psy-
chopathic persons in remission has not been the subject of investigation, although
there has been an increased interest in the psychosocial aspects of remission.
More knowledge concerning the neurologic and biochemical functioning of anti-
social and psychopathic personalities is necessary for the construction of
biopsychosocial-oriented treatment and prevention programs.
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Willem H. J. Martens, M.D., Ph.D.

Chairman and Advisor of the Dutch College of Psychiatric Ethics
Beatrixstraat 62
3921 BR
Elst (Utrecht), the Netherlands
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Antisocial and Psychopathic Personality Disorders: Causes, Course, and

Article in International Journal of Offender Therapy and Comparative Criminology · August 2000

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Antisocial and Psychopathic Personality

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Personality disorders were relegated to Axis II in DSM-III (APA, 1980) to

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ANXIETY, DEPRESSION, AND SCHIZOPHRENIA

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Some studies found a broad assortment of nonpsychopathic and nonantisocial

SUICIDE AS A RESULT OF COMORBIDITY

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BRAIN INJURIES AND DYSFUNCTIONS

MAO, CSF 5-HIAA, 5-HT, AND HORMONE DYSFUNCTIONS

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In a forensic psychiatric population (n = 61 males), elevated triiodothyroine

ELECTROENCEPHALOGRAM (EEG) ABNORMALITIES

A number of investigations reported an association between PPD and ASPD

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stimulation leads to an extremely high degree of motivation to increase sensory

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GENETIC AND ENVIRONMENTAL INFLUENCES

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GENETIC ASPECTS OF COMORBIDITY

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equate internalization of social constraint (McBurnett et al., 1997). Some of the

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CONDUCT DISORDERS AND ADHD AS PRECURSORS

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Follow-up studies found that by midadolescence, individuals with ADHD

COURSE AND PROGNOSIS

ANTISOCIAL PERSONALITY DISORDER

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PSYCHOPATHIC PERSONALITY DISORDER

Age and gender differences in the prevalence and stability of psychopathic

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PROGNOSIS AND GENDER

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PROGNOSIS AND COMORBIDITY

A comorbid substance abuse disorder is a strong negative predictive factor in

CAUSES OF SPONTANEOUS REMISSION

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NEUROLOGICAL AND BIOLOGICAL DETERMINANTS

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Willem H. J. Martens, M.D., Ph.D.

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