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Psychophysiology of Aggression, Psychopathy, and Conduct Problems:
A Meta-Analysis
Michael F. Lorber
State University of New York at Stony Brook
A meta-analysis of 95 studies was conducted to investigate the relations of heart rate (HR) and
electrodermal activity (EDA) with aggression, psychopathy, and conduct problems. Analyses revealed a
complex constellation of interactive effects, with a failure in some cases of autonomic patterns to
generalize across antisocial spectrum behavior constructs. Low resting EDA and low task EDA were
associated with psychopathy/sociopathy and conduct problems. However, EDA reactivity was positively
associated with aggression and negatively associated with psychopathy/sociopathy. Low resting HR and
high HR reactivity were associated with aggression and conduct problems. Physiology–behavior rela-
tions varied with age and stimulus valence in several cases. Empirical and clinical implications are
discussed.
The physiological correlates of antisocial spectrum behavior—
including aggression, psychopathy, conduct problems, and antisocial
personality characteristics—have been the subject of a good deal of
theoretical and empirical attention over the past 45 years (see Scarpa
& Raine, 1997). Understanding possible links between autonomic
physiology and antisocial spectrum behavior may hold special prom-
ise for advancing our understanding of these highly costly behavior
patterns. Autonomic measures move beyond self-reports of psycho-
logical functioning and may be less prone to bias and measure-related
error. They may also be more sensitive indexes of the brain processes
that are ultimately thought to be responsible for the behavior (e.g.,
Fowles, 1980, 1988). Convincingly demonstrating links between an-
tisocial spectrum behavior and autonomic physiology might elucidate
relevant mechanisms and individual differences and potentially lead
to treatment innovations. This is especially important with regard to
antisocial spectrum behavior, because of its enormous cost to society
(e.g., Moffitt, Caspi, Harrington, & Milne, 2002) and its relative
resistance to treatment in many of its forms (e.g., Offord & Bennet,
1994; Richards, Casey, & Lucente, 2003), with the possible exception
of conduct problems in young children (e.g., Brestan & Eyberg,
1998).
Many different theories of antisocial spectrum behavior that in-
volve autonomic psychophysiology have been proposed (Berkowitz,
1994; Eysenck & Gudjonsson, 1989; Fowles, 1980, 1988; Gray,
1987; Hare, 1978a; Quay, 1965; Raine, 1993, 1997; Zillmann, 1994;
Zuckerman & Como, 1983), some with conflicting predictions (e.g.,
Quay, 1965, and Zillmann, 1994). Furthermore, a wide range of
experimental methods and populations have been employed and stud-
ied, respectively. Clear interpretation of the literature has proved
elusive in the face of a mixed pattern of results. In an attempt to clarify
these issues, the present meta-analytic review was designed to quan-
tify the aggregate associations of heart rate (HR) and electrodermal
activity (EDA) with aggression, psychopathy, conduct problems, and
antisocial personality characteristics and to investigate factors that
moderate these relations.
HR and EDA are variables of central interest in many theories
of physiology and antisocial spectrum behavior and have histori-
cally been the most popular measures of psychophysiological
response. Thus, the present analysis was limited to these two
measures. The heart is subject to influence from the sympathetic
(SNS) and parasympathetic (PNS) branches of the autonomic
nervous system, and it is subject to neuroendocrine influences as
well. Chronotropic (i.e., rate-related) cardiac effects are controlled
primarily by the PNS, whereas inotropic effects such as contractile
force and stroke volume are controlled primarily by the SNS. In
contrast, EDA is under exclusive control of the SNS (Blascovich
& Kelsey, 1990; Fowles, 1986). From a perspective dating back to
the seminal work of James and Cannon, HR and EDA are thought
to be tied to emotional responses, with increases reflecting general
emotional arousal, specific emotions, or both (reviewed in Lang,
1994). HR and EDA may also reflect the influence of motivational
systems that control behavior in response to internal and external
cues (e.g., Fowles, 1988; Gray, 1987).
The present meta-analysis focused on three classes of HR and
EDA measures: resting, task, and reactivity. Resting measures
reflect the assessment of autonomic activity in the absence of any
obvious external stimuli. HR and EDA in response to experimental
stimuli are frequently measured in raw form during such presen-
tations (task physiology) or expressed as a change from resting,
baseline, or prestimulus levels (physiological reactivity).
Problems With Interpretation of the Literature
Because of frequent nonreplications and theories that make
competing predictions, the literature on the psychophysiology of
antisocial spectrum behavior is often confusing and seemingly
contradictory. The major thesis of this meta-analytic review is that
these ambiguities are caused in part by two sources: heterogeneity
I would like to thank Theodore Beauchaine, K. Daniel O’Leary, Susan
G. O’Leary, Amy Smith Slep, and Paul Wortman for their helpful com-
ments on earlier versions of this article and Tamara Del Vecchio for her
coding assistance.
Correspondence concerning this article should be addressed to Michael
F. Lorber, Department of Psychology, State University of New York,
Stony Brook, NY 11794-2500. E-mail: michael.lorber@stonybrook.edu
Psychological Bulletin Copyright 2004 by the American Psychological Association
2004, Vol. 130, No. 4, 531–552 0033-2909/04/$12.00 DOI: 10.1037/0033-2909.130.4.531
531
in the behavior construct and heterogeneity in experimental meth-
ods. Furthermore, many of the models of the relation between
physiology and antisocial spectrum behavior have been applied to
adults, adolescents, and children. The generalization of psycho-
physiological models across different age groups is in need of
empirical evaluation given that no study of which I am aware has
examined the association between antisocial spectrum behavior
and physiology in both adults and children.
Heterogeneity in Behavior Construct
Just what form of antisocial spectrum behavior ought to relate to
what specific pattern of physiological response is unclear at
present. Often, multiple behavior patterns are discussed together.
For example, Scarpa and Raine’s (1997) review mixed aggression,
crime, psychopathy, antisocial behavior, and conduct disorder.
Although there is some degree of overlap among these constructs,
there is also some distinctiveness. For example, as Lynam (1996)
pointed out, psychopathy and antisocial personality disorder
(APD) refer to different constellations of behavioral characteris-
tics. Following Cleckly’s (1976) conceptualization, psychopathy
refers to impulsiveness, lack of empathy and guilt, and narcissism,
often accompanied by severe violence. As indicated in the Diag-
nostic and Statistical Manual of Mental Disorders (4th ed.; Amer-
ican Psychiatric Association, 1994), APD is characterized by a
pervasive pattern of disregard for social norms and violation of the
rights of others. In fact, whereas nearly all psychopathic offenders
meet APD diagnostic criteria, only approximately 25% of APD-
diagnosed men meet the criteria for psychopathy (Hare, 1985), as
assessed by Hare’s (1991) Psychopathy Checklist.
Further confusion results from the overuse of the term antiso-
cial. Not all antisocial behavior is equivalent, and not all antisocial
behavior is aggressive. For example, although an individual diag-
nosed with APD and a one-time bar brawler may both exhibit
antisocial behavior (i.e., violation of personal rights, laws, and
social norms), placing them into a single category ignores the
heterogeneity between these individuals. For instance, many indi-
viduals with APD are aggressive, but not all aggressors meet
diagnostic criteria for APD. The non-APD aggressor may not share
the callousness and pervasive violation of the rights of others
exhibited by the APD-diagnosed individual.
Perhaps more important, although psychopathy and APD are as-
sociated with aggression, aggression is not the singular defining
characteristic of these syndromes. It is unclear whether the psycho-
physiological response profiles of psychopathic and antisocial indi-
viduals are specifically related to aggression, to other characteristics,
or to both. For example, aggression is frequently confounded with the
personality characteristics of individuals with psychopathy. Indeed,
Kelsey, Ornduff, McCann, and Reiff (2001) found that the psycho-
physiological responses of individuals high in narcissism—which
plays a prominent part in the personality profiles of psychopaths
(Kernberg, 1989, cited in Kelsey et al., 2001)—in many ways mirror
those of psychopaths. Thus, narcissism may be at the root of the
physiological response patterns of psychopaths.
It is perhaps not surprising, then, that findings differ between
samples of psychopaths and those who exhibit other forms of
antisocial or aggressive behavior, with an important caveat that
psychopathic or antisocial personality characteristics are usually
not assessed in studies of aggressive behavior. For example, the
man who pushes his wife twice per year is probably from a
different population than the felon with multiple convictions for
aggravated assault who exhibits psychopathic tendencies across
contexts. It follows that the psychophysiological profiles of non-
psychopathic and nonantisocial aggressors may also be different
from those of their more pathological counterparts. In the present
article, the term antisocial spectrum behavior is used as shorthand
and may be thought of as a superordinate category that captures the
violation of rules and the rights of others common to aggression,
psychopathy, antisocial personality, and conduct problems.
Heterogeneity in Experimental Stimuli
Even an incomplete list of the experimental stimuli used by
researchers to study the psychophysiology of antisocial spectrum
behavior would reveal substantial variability. Different pockets of
research tend to use characteristic stimuli, reflecting different
theoretical propositions of the circumstances under which physi-
ological changes are associated with antisocial spectrum behavior.
For example, Hinton, O’Neill, Hamilton, and Burke (1980) ex-
posed participants to neutral orienting tones, whereas Milner
(1976) used electric shocks in studying the autonomic responses of
psychopaths. In family aggression research, Frodi and Lamb
(1980) exposed mothers to infant cries and smiles; in studies of
marital aggression (e.g., Jacobson et al., 1994), couples typically
engage in conflict. These differences may be related to apparent
inconsistencies in the literature.
One dimension that may hold promise for disentangling these
inconsistencies is the valence of experimental stimuli. Valence is
defined herein as the hedonic value of a stimulus. Valence cuts
across the stimuli used in the literatures under consideration, thus
allowing for parallel consideration of its impact across these dis-
parate literatures. Furthermore, many of the theoretical perspec-
tives on the psychophysiology of antisocial spectrum behavior
make predictions specific to a negatively valenced antecedent. For
example, Zillmann (1994) posited that physiological reactivity is
elicited by frustrating events, triggering an aggressive response.
Learning theories (e.g., Fowles, 1988) are concerned with an
individual’s ability to inhibit an aggressive/impulsive response
given impending deleterious consequences. Thus, it was hypoth-
esized that studies involving negatively valenced stimuli would be
associated with stronger effects than would studies involving non-
negative stimuli.
Heterogeneity in Age
It is unclear whether autonomic patterns associated with aggres-
sion and antisocial spectrum behaviors generalize across different
age groups. On one hand, there is substantial continuity in antiso-
cial behavior. For example, the previous presence of conduct
disorder in childhood or adolescence is a diagnostic criterion for
APD (American Psychiatric Association, 1994). Childhood con-
duct problems appear to be associated not only with later APD but
with other forms of aggressive and criminal behavior as well. For
example, Huesmann, Eron, Lefkowitz, and Walder (1984) found
that boys identified as aggressive were more likely to abuse their
spouses as adults, as well as to commit serious crimes and drive
while intoxicated. Similarly, Magdol, Moffitt, Caspi, and Silva
(1998) found that children with early problem behaviors were
532
LORBER
more likely to exhibit partner aggression as adults. Thus, it may be
the case that models developed to explain antisocial spectrum
behavior in adulthood apply to children and adolescents as well.
For instance, Lynam (1997) found evidence that children with
early-onset conduct disorder also exhibit personality characteris-
tics that resemble those of adult psychopaths.
Parallels have been found in psychophysiological research as
well. Low EDA has been found in studies of youth (see Quay,
1993) and adults (see Scarpa & Raine, 1997) who exhibit antiso-
cial spectrum behaviors. Thus, the psychophysiological profiles of
children and adolescents with conduct problems, if sufficiently
stable, may also be predictive of other forms of aggressive or
antisocial behavior in adulthood. On the other hand, although the
retrospective relation of childhood conduct problems to adult
pathology is strong, prospective prediction is far weaker, with a
high false-positive rate. For example, only a minority of children
diagnosed with conduct disorder go on to become diagnosed with
APD as adults (Hinshaw & Anderson, 1996). As illustrated in the
work of Moffitt (1993), as well as Loeber and Stouthamer-Loeber
(1998), this false-positive rate may be attributable to multiple
developmental pathways of antisocial behavior. The majority of
youth with conduct problems exhibit time-limited antisocial be-
havior that appears to peak in adolescence in most individuals and
in the preschool–elementary school age period in others (Loeber &
Stouthamer-Loeber, 1998; Moffitt, 1993). A much smaller group,
which Moffitt labeled life-course-persistent antisocial individuals,
exhibit a relatively continuous course of antisocial behavior be-
ginning in childhood and enduring into adulthood. Thus, psycho-
physiological models developed in research on psychopathic or
antisocial adults may apply to only a subset of children with
conduct problems (i.e., life-course-persistent antisocial children).
Goals of the Present Meta-Analysis
As a means of addressing the problems just outlined, the central
aim of the present meta-analysis was to evaluate the extent to
which the relations of antisocial spectrum behavior with HR and
EDA depend on type of behavior in question, valence of experi-
mental stimuli, and age. Furthermore, the meta-analysis provided
an opportunity to document the aggregate association of each form
of antisocial spectrum behavior with HR and EDA. These issues
were addressed in analyses of resting, task, and reactivity measures
of autonomic physiology. By quantifying these associations and
elucidating potential interactions, it was hoped that some of the
ambiguities that exist in the literature might be resolved.
Method
Literature Searches
Four methods were used to locate studies for the meta-analysis. First,
PsycINFO (1887–2002), MEDLINE (1966–2002), and Dissertation Ab-
stracts International (1861–2002) were searched through January of 2002
through the use of the key words interbeat, heart rate, cardiac, electro-
dermal, skin conductance, skin potential, galvanic, physiology, and psy-
chophysiology, cross referenced with aggression, violence, psychopathy,
conduct disorder, conduct problems, antisocial, oppositional, child abuse,
and spouse abuse. Second, the reference lists of retrieved articles, as well
as several review articles on the relation of psychophysiology with aggres-
sion and antisocial behavior (Fowles, 1980, 1988; Hare, 1978a; Kilzieh &
Cloninger, 1993; Quay, 1993; Scarpa & Raine, 1997), were scanned. Third,
several investigators were contacted in an attempt to locate unpublished
dissertations and articles in press (A. Raine, L. Berkowitz, D. Zillmann, E.
Mezzacappa, T. Zahn, R. Hare, and J. Knutson). Fourth, queries were
posted via relevant Internet sites (e.g., Society for Psychophysiological
Research) and electronic mail discussion groups (e.g., Society for Scien-
tific Clinical Psychology).
Inclusion and Exclusion Criteria
One hundred studies satisfied the inclusion criteria. Publication years of
the retained studies ranged from 1957 to 2001. Inclusion criteria were
liberal by design, in that a substantial goal of the meta-analysis was to test
interactions of effect sizes with study features rather than holding these
features constant. Studies had to include HR, EDA, or both, measured
either during a baseline period or in an experimental task, and an assess-
ment of aggression, antisocial personality characteristics, conduct prob-
lems, or psychopathy/sociopathy. EDA measures had to be either skin
conductance level, amplitude, or frequency. Studies could either compare
the physiology of an antisocial group against a control group or use
correlational methods. Control groups could include less aggressive, psy-
chopathic/sociopathic, antisocial, conduct-disordered, or normal partici-
pants. Furthermore, the studies had to include sufficient data to allow
calculation of effect sizes (pairwise comparisons or correlations, sample
size, and a test statistic or p value for each test of interest). Longitudinal
studies without relevant concurrent tests, studies of animals, articles writ-
ten in languages other than English, and studies of individuals with
developmental disabilities (e.g., autism) were excluded. Studies in which
antisocial spectrum behavior or physiology were manipulated experimen-
tally were also excluded, reflecting my concern with individual differences.
Finally, only journal articles that were either published, in press, or in
advanced stages of review (i.e., “revise and resubmit” status) and disser-
tations were included so as to restrict the sample to work that had under-
gone scientific review. When a study was available both as a dissertation
and as a published article, the published article was selected.
Coding of Moderators
Age. Age groups were coded as follows: child (1–11 years old),
adolescent (12–17 years old), or adult (18 years old or older). Several
studies spanned two age groups. In these cases, age category was deter-
mined by the mean age of the sample. Furthermore, age was not reported
in several studies of incarcerated individuals. In these cases, a code of adult
was assigned.
Behavior type. Behavior type was coded as one of four categories:
psychopathy/sociopathy, aggression, antisocial personality characteristics,
or conduct problems. The psychopathy/sociopathy code was assigned if the
author(s) used (a) a measurement device purporting to measure psychop-
athy or sociopathy, (b) research or clinical interview data, or (c) a combi-
nation thereof to establish group membership or dimensional level of
psychopathy/sociopathy. The aggression code was assigned for studies of
physical behavior intended to harm or injure another person, including
studies of fighting with peers, shocking laboratory confederates, and phys-
ical aggression in families. The antisocial personality characteristics code
1
was assigned for studies of antisocial personality characteristics common
to APD (e.g., failure to conform to social norms, deceitfulness, manipula-
tiveness, and lack of remorse) or diagnosed APD itself. The conduct
problems code was applied for studies of diagnosed conduct disorder,
1
I would have liked to distinguish between antisocial personality charac
-
teristics and formally diagnosed APD. However, there were not enough studies
to include APD as a separate behavior category. Thus, it was included in the
antisocial personality characteristics category.
533
PSYCHOPHYSIOLOGY OF AGGRESSION
delinquency, oppositionality, and other child and adolescent externalizing
behavior problems. Studies of problems involving attention or hyperactiv-
ity (e.g., attention-deficit/hyperactivity disorder; American Psychiatric As-
sociation, 1994), however, were excluded from this category because other
biological contributions to attention-deficit/hyperactivity disorder may
confound the relation between physiology and conduct problems.
Type of physiological measure. Type of HR measure was coded as
resting, task, or reactivity. The resting code was assigned if HR was
measured in the absence of stimuli. In the case of multiple rest periods, the
effect size associated with the first was selected. The task code was
assigned if HR was measured (for any duration of time) while the partic-
ipant performed a task, such as listening to tones or performing mental
arithmetic. The reactivity code was assigned if HR was expressed as
change from a baseline or prestimulus measurement to a task measurement
or if baseline HR was statistically controlled. Coding of EDA followed the
same procedure as HR.
Stimulus valence. Stimuli were coded as either negative or nonnega-
tive. A code of negative was assigned if the stimuli used were designed to
be anger provoking, very loud (e.g., tones ⱖ 90 db), painful (e.g., electric
shock), or otherwise aversive (e.g., pictures of mutilated body parts). A
code of nonnegative was assigned for all other stimuli (e.g., orienting tones
or slides of affectively neutral images).
Reliability. Coding was performed by the author, with 24 articles
coded in parallel by an independent coder unaware of the hypotheses.
Cohen kappa values for age and behavior type were 1.00, with kappas of
.80 and .70 for stimulus valence and type of physiological measure,
respectively.
Computation of Effect Sizes
Cohen’s d. As recommended by Hedges and Olkin (1985), Cohen’s
corrected d statistic was chosen as the measure of effect size; d represents
the difference between treatment and control group means divided by the
pooled standard deviation. The corrected d adjusts for bias resulting from
small sample sizes. Cohen’s d can be calculated from a variety of descrip-
tive and inferential statistics, including means and standard deviations, test
statistics, and p values. Positive effect sizes in the present meta-analysis
represented positive associations between physiology and antisocial spec-
trum behavior. Effect sizes were calculated with Johnson’s (1995) DSTAT
program. Following Cohen’s (1988) recommendations, small, medium,
and large effect sizes were defined by d values of 0.20, 0.50, and 0.80,
respectively.
Multiple effect sizes. It was common for studies to report enough data
to compute multiple effect sizes. The assumption of independence would
be violated by including more than one effect size per study in a given
analysis. Many included baseline and task or reactivity measures of both
HR and EDA. In such cases, no threat to the independence assumption was
present, because analyses of HR and EDA and analyses of baseline and
task-reactivity measures were conducted separately. However, it was com-
mon for studies to include multiple assessments within a given measure
(e.g., EDA in two different tasks).
In addition, there were sometimes multiple types of EDA measurement
(skin conductance level, amplitude, and frequency) and multiple measures
of aggression or antisocial behavior. In these cases, one effect size was
randomly selected for analysis. One exception to random selection was the
case of Babcock, Yerington, Green, and Webb’s (2004) study, which
included analyses of psychopathy, antisocial behavior, and multiple mea-
sures of domestic violence. Because of the low number of studies of family
aggression, one of the analyses pertaining to spousal aggression was
randomly selected. Multiple effect sizes also occurred in studies in which
other (unanalyzed) independent variables were either manipulated or se-
lected. For example, psychopathic individuals and controls might be split
into subgroups high and low in anxiety. In such cases, effects were
averaged across conditions. Also, when studies reported on multiple dis-
tinguishable samples (e.g., men and women, different age cohorts, or
multiple experiments), these samples were treated as independent. Finally,
there were multiple experimental groups in several studies. For example,
psychopathic individuals were often subclassified as exhibiting primary or
secondary psychopathy (e.g., Blackburn, 1979). In the Babcock et al.
(2004) study, abusive husbands were broken into high-level and low-level
groups. In instances in which enough information was provided to do so,
data were averaged to form pairwise comparisons (e.g., individuals with
primary/secondary psychopathy vs. controls or high-level/low-level part-
ner aggressors vs. controls). In other cases, one comparison was randomly
selected for analysis.
Nonsignificant effects. Nonsignificant effects with inadequate infor-
mation to calculate effect sizes (i.e., no test statistic or p value) were
assigned a d value of zero, provided that the comparison was pairwise or
a correlation and the corresponding sample size was reported. This is a
conservative approach that often results in effect size estimates that are too
small. However, excluding such studies leads to inflated effect sizes and
artificially small p values (Rosenthal, 1995). As a result of the desire to
maximize the number of studies and minimize Type I error, the former
approach was adopted.
Data Analysis
In the first step of the data analysis, effect sizes were calculated sepa-
rately for relations of aggression, psychopathy/sociopathy, conduct prob-
lems, and antisocial personality characteristics with resting, task, and
reactivity measures of HR and EDA across age and stimulus categories. As
a means of assessing the impact of age, categorical analyses were per-
formed within behavior types (for effect sizes wherein age could be
determined). Categorical moderation analyses were also performed within
each age group, to assess the generalization of physiology–behavior rela-
tions across behavior patterns,
2
and within behavior categories, to assess
moderation by stimulus valence (for effect sizes wherein valence could be
determined). To be included in moderation analyses, each moderator
category had to comprise three or more studies. Although I would have
liked to use a more conservative criterion, I used this more liberal criterion
so that I could report as much detail as possible. Thus, many of the analyses
should be regarded as preliminary.
The model for categorical moderation analyses roughly follows the logic
of the F ratio. Variability in effect sizes is computed between and within
groups defined by the categories of the moderator variable. A well-
specified model results in maximized between-categories variability in
effect sizes and minimized within-group variability. Between-categories
homogeneity is assessed by the value Q
B
, which is interpreted relative to
a chi-square distribution (df ⫽ number of categories minus 1). Within-
category homogeneity is indexed by Q
W
, also interpreted relative to a
chi-square distribution (df ⫽ number of effect sizes in each category minus
1). Significance tests are computed separately for Q
B
and Q
W
.
Two strategies were adopted to address bias in effect sizes due to the
tendency of authors to fail to report nonsignificant findings and editors’
tendencies to reject papers with many nonsignificant findings (i.e., the “file
drawer” problem; Begg, 1994). First, an attempt was made to locate as
many unpublished studies as possible. Second, fail-safe N analyses were
calculated for each statistically significant relation reported. The fail-safe N
(N
fs
) indicates the number of studies yielding null findings that would be
necessary to reduce the mean effect to a negligible level. N
fs
was calculated
via the following equation (Hedges & Olkin, 1985):
N
fs
⫽
k共d
⫺ d
c
兲
d
c
,
2
Behavior type moderation was performed within age groups to avoid
confounding age and behavior. For example, studies of psychopathy almost
exclusively involved adult samples; conduct problems refer specifically to
child behavior.
534
LORBER
where k is the number of studies in the analysis, d
is the mean weighted
effect size, and d
c
is a critical d small enough to be negligible. A d
c
of 0.10
(or ⫺0.10 in the case of negative associations) was adopted in the present
meta-analysis. According to Rosenthal’s (1979) conservative guidelines,
N
fs
should exceed 5k ⫹ 10 to effectively overcome the file drawer problem.
However, the file drawer problem may be somewhat less of an issue in the
present meta-analysis, in that multiple analyses were very common and a
large number of nonsignificant findings were reported. Furthermore, sev-
eral of the studies analyzed were unpublished and contained nonsignificant
findings.
Final Sample
The five available studies of antisocial personality characteristics (Brag-
gio, Pishkin, Parsons, Fishkin, & Tassey, 1992; Dinn & Harris, 2000;
Levander, Schalling, Lidberg, & Lidberg, 1979; Mallory, 1983; Raine,
Lencz, Bihrle, LaCasse, & Colletti, 2000) were not sufficient in number to
contribute meaningfully to the meta-analysis. Therefore, these studies were
excluded, and the remaining 95 studies were analyzed.
Results
Resting HR
Study identifying information, coded qualities, and effect sizes
are reported in Tables A1–A6 of the Appendix.
Aggression. Results of analyses involving resting HR are pre-
sented in Table 1. The mean aggregate effect size of the associa-
tion between resting HR and aggression across 16 studies was
⫺0.38, with a 95% confidence interval that excluded zero (⫺0.50,
⫺0.26). Thus, lower resting HR was associated with higher levels
of aggression (N
fs
⫽ 45). According to Cohen’s (1988) standards,
this is a small effect. There was substantial heterogeneity in effect
sizes (p ⬍ .01), with effect sizes ranging from ⫺1.20 to 0.27.
There were enough studies to examine age as a moderator of the
resting HR–aggression relation; studies in all age groups were
compared. The omnibus test was marginally significant, Q
B
(2) ⫽
5.63, p ⬍ .10, and none of the pairwise post hoc tests reached
significance. However, whereas aggression was reliably associated
with low resting HR in children (M ⫽⫺0.51; N
fs
⫽ 25) and adults
(M ⫽⫺0.30; N
fs
⫽ 12), the 95% confidence interval for adoles
-
cents included zero (⫺0.42, 0.12; M ⫽⫺0.15). The significant
negative association for studies of children met Cohen’s criterion
for a medium-sized effect (0.51). Effect sizes were heterogeneous
only in studies of children, with effect sizes ranging from ⫺1.20 to
0.01 (p ⬍ .01).
Psychopathy/sociopathy. The mean effect size of the associa-
tion between resting HR and psychopathy/sociopathy (among
adults only) across 17 studies was 0.06, with a 95% confidence
interval that included zero (⫺0.08, 0.21). Thus, there was no
evidence of an association between HR and psychopathy/sociop-
athy in adults. Statistically significant heterogeneity in effect sizes
was not obtained. With a weighted effect size of 1.06, the Taub
(1972) study was an outlier (the next closest effect size was 0.33).
However, its removal had no impact on the findings, and it was
therefore retained.
Conduct problems. The mean aggregate effect size of the
association between resting HR and conduct problems across 13
studies was ⫺0.33, with a 95% confidence interval that excluded
zero (⫺0.43, ⫺0.23). Thus, lower resting HR was associated with
conduct problems (N
fs
⫽ 30), but the effect was small. Effect sizes
were not significantly heterogeneous. Age could not be determined
in one study of conduct problems (Garralda, Connell, & Taylor,
1991).
There were enough studies to examine age as a moderator of the
resting HR–conduct problems relationship; studies of children and
adolescents were compared. The mean effect size was nearly
identical in child and adolescent studies, Q
B
(1) ⫽ 0.00, ns, with
confidence intervals that excluded zero and no significant hetero-
geneity within either age category.
Behavior type moderation within age groups. Categorical
moderator analyses were performed to examine the association of
effect size with behavior pattern in each age group (where possi-
ble). Mean effect sizes were compared in studies of child aggres-
sion and conduct problems. Although behavior type was not a
significant moderator of effect size, Q
B
(1) ⫽ 2.53, ns, the mean
effect for conduct problems was small (⫺0.34; N
fs
⫽ 17), and the
mean effect for aggression (⫺0.51; N
fs
⫽ 25) met Cohen’s crite
-
rion for a medium effect. Confidence intervals excluded zero in
both cases. There was heterogeneity among effect sizes in studies
of child aggression (p ⬍ .01) but not in studies of child conduct
problems.
Mean effect sizes were also compared in studies of adolescent
aggression and conduct problems. No significant difference was
obtained, Q
B
(1) ⫽ 1.47, ns, despite the fact that resting HR was
significantly associated only with conduct problems. Tests for
heterogeneity were nonsignificant for each behavior construct.
In the case of adults, the mean effects of aggression (⫺0.30) and
psychopathy/sociopathy (0.06) differed significantly, Q
B
(1) ⫽
6.92, p ⬍ .01, indicating that resting HR was more strongly
associated with aggression. There was no significant heterogeneity
in either category.
Task HR
Aggression. Results of analyses involving task HR are pre-
sented in Table 2. The mean aggregate effect size of the associa-
tion between task HR and aggression across 14 studies was ⫺0.02,
Table 1
Categorical Analysis of Resting Heart Rate
Variable k
Mean
d
⫹
95% CI for d
⫹
Q
W
Q
B
Aggression 16 ⫺0.38 ⫺0.50, ⫺0.26 37.27**
Age 5.63†
Child 6 ⫺0.51 ⫺0.68, ⫺0.34 23.32**
Adolescent 4 ⫺0.15 ⫺0.42, 0.12 4.78
Adult 6 ⫺0.30
a
⫺0.53, ⫺0.07 3.54
Psychopathy/sociopathy 17 0.06
a
⫺0.08, 0.21 12.17
Conduct problems 13 ⫺0.33 ⫺0.43, ⫺0.23 17.32
Age 0.00
Child 7 ⫺0.34 ⫺0.47, ⫺0.22 10.21
Adolescent 5 ⫺0.35 ⫺0.52, ⫺0.17 5.72
Note. d
⫹
denotes effect sizes weighted by the reciprocal of their vari
-
ances. Q
W
tests within-category homogeneity of effect size; Q
B
tests
between-categories homogeneity. Significant effect sizes signify rejection
of the null hypothesis of homogeneous effect sizes. Mean effect sizes with
matching subscripts are different from one another at p ⬍ .01. k ⫽ number
of data sets; CI ⫽ confidence interval.
† p ⬍ .10. ** p ⬍ .01.
535
PSYCHOPHYSIOLOGY OF AGGRESSION
with a 95% confidence interval that included zero (⫺0.15, 0.11).
Thus, HR during task responding was not associated with aggres-
sion. There was substantial heterogeneity in effect sizes (p ⬍ .01),
which ranged from ⫺1.14 to 0.69. One study (Thomas, 1982) was
an outlier (the effect size weighted by the reciprocal of its variance
[d
⫹
] was –1.14; the next nearest effect was ⫺0.53). However, its
removal did not affect the results, and it was therefore retained.
Mean effect sizes for task HR and aggression could be com-
pared in the case of children and adults; no significant between-
groups heterogeneity in effect sizes was evident, Q
B
(2) ⫽ 0.05, ns.
Statistically significant heterogeneity was found in child (d
⫹
range: ⫺0.53 to 0.69, p ⬍ .01) and adult (d
⫹
range: ⫺1.14 to 0.60,
p ⬍ .05) studies.
Psychopathy/sociopathy. The mean effect size of the associa-
tion between task HR and psychopathy/sociopathy (among adults
only) across seven studies was ⫺0.16, with a 95% confidence
interval that included zero (⫺0.41, 0.09). Thus, there was no
evidence of an association between task HR and psychopathy/
sociopathy in adults. Statistically significant heterogeneity in ef-
fect sizes was not obtained.
Conduct problems. The mean aggregate effect size of the
association between task HR and conduct problems across eight
studies of children and adolescents was ⫺0.04, with a 95% con-
fidence interval that included zero (⫺0.21, 0.14). Thus, there was
no association between task HR and conduct problems. There was
substantial heterogeneity in effect sizes (p ⬍ .01), with effect sizes
ranging from ⫺1.67 to 0.44.
The difference in effects associated with conduct disorder in
children and adolescents did not differ from chance, Q
B
(1) ⫽ 1.58,
ns, and both confidence intervals included zero. Effect sizes were
heterogeneous only in studies of adolescent conduct problems (d
⫹
range: –1.67 to 0.40, p ⬍ .01), and these studies represented the
entire effect size range for conduct problems.
Behavior type moderation within age groups. The comparison
of child aggression and conduct problems failed to produce a
significant result, Q
B
(1) ⫽ 0.02, ns. Both confidence intervals
included zero, indicating the lack of association in either case.
Significant heterogeneity in effect sizes was observed for studies
of aggression (d
⫹
range: ⫺0.53 to 0.69, p ⬍ .01) but not for
studies of conduct problems.
In the case of adults, the mean effects of aggression and psy-
chopathy/sociopathy did not differ, Q
B
(1) ⫽ 0.53, ns. There was
no significant heterogeneity in effect sizes for studies of psychop-
athy/sociopathy. However, there was significant within-category
heterogeneity of effect sizes in studies of aggression (d
⫹
range:
⫺0.81 to 0.09, p ⬍ .05).
Moderation by stimulus valence. The dependence of effect
size on stimulus valence was examined in studies of aggression
and conduct problems. Valence was a significant moderator in
studies of aggression, Q
B
(1) ⫽ 13.95, p ⬍ .01. The mean effect for
negative stimuli was negative (M ⫽⫺0.23; N
fs
⫽ 9), whereas the
mean effect for nonnegative stimuli was positive (M ⫽ 0.28; N
fs
⫽
11). Both confidence intervals excluded zero. Thus, the direction
of the association depended on stimulus valence. Significant het-
erogeneity was found only in studies of aggression that employed
nonnegative stimuli (p ⬍ .01), with effects ranging from ⫺1.14 to
0.69 (i.e., the highest and lowest effect sizes for task HR and
aggression were found in this category).
Stimulus valence did not moderate the association between task
HR and conduct problems, Q
B
(1) ⫽ 2.66, ns, and could not be
examined with regard to psychopathy/sociopathy (only k ⫽ 2
studies with nonnegative stimuli). Valence could not be deter-
mined in two studies of psychopathy/sociopathy (Pham, Philippot,
& Rime, 2000; Tharp, Maltzman, Syndulko, & Ziskind, 1980) and
in one study of aggression (Chiang, Schuetz, & Soyka, 2001).
HR Reactivity
Aggression. Results of analyses involving HR reactivity are
presented in Table 3. The mean aggregate effect size of the
association between HR reactivity and aggression across 14 stud-
ies was 0.10, with a 95% confidence interval that included zero
(⫺0.03, 0.22). Thus, HR reactivity was not significantly associated
with aggression. There was substantial heterogeneity in effect sizes
(p ⬍ .01), with effect sizes ranging from ⫺0.91 to 1.40.
Mean effect sizes for HR reactivity and aggression were com-
pared among adolescents and adults; no significant between-
groups heterogeneity in effect sizes was evident, Q
B
(1) ⫽ 0.81, ns.
Yet, HR reactivity was related significantly to aggression in stud-
ies of adults (M ⫽ 0.27; N
fs
⫽ 14), and the effect was small.
Statistically significant heterogeneity was also found in adult stud-
ies (d
⫹
range: ⫺0.06 to 1.40, p ⬍ .01).
Psychopathy/sociopathy. The mean effect size of the associa-
tion between HR reactivity and psychopathy/sociopathy across 14
studies was 0.06, with a 95% confidence interval that included
zero (⫺0.11, 0.23). Thus, there was no evidence of an association
between HR reactivity and psychopathy/sociopathy. Only margin-
ally significant heterogeneity in effect sizes was found (p ⬍ .10),
with effects ranging from ⫺0.66 to 0.99. The only age category
containing 3 or more studies was adult. The mean effect size of the
association between HR reactivity and psychopathy/sociopathy
across these 13 studies was 0.07, with a 95% confidence interval
Table 2
Categorical Analysis of Task Heart Rate
Variable k
Mean
d
⫹
95% CI for d
⫹
Q
W
Q
B
Aggression 14 ⫺0.02 ⫺0.15, 0.11 47.34**
Age 0.05
Child 5 ⫺0.001 ⫺0.22, 0.22 22.84**
Adult 7 ⫺0.04 ⫺0.24, 0.17 19.37*
Stimulus valence 13.95**
Negative stimuli 7 ⫺0.23 ⫺0.41, ⫺0.05 2.51
Nonnegative stimuli 6 0.28 0.08, 0.48 29.50**
Psychopathy/sociopathy 7 ⫺0.16 ⫺0.41, 0.09 6.60
Conduct problems 8 ⫺0.04 ⫺0.21, 0.14 20.07**
Age 1.58
Child 5 0.02 ⫺0.18, 0.22 0.27
Adolescent 3 ⫺0.25 ⫺0.64, 0.13 18.22**
Stimulus valence 2.66
Negative stimuli 5 0.06 ⫺0.15, 0.27 4.17
Nonnegative stimuli 3 ⫺0.27 ⫺0.60, 0.06 13.25**
Note. d
⫹
denotes effect sizes weighted by the reciprocal of their vari
-
ances. Q
W
tests within-category homogeneity of effect size; Q
B
tests
between-categories homogeneity. Significant effect sizes signify rejection
of the null hypothesis of homogeneous effect sizes. k ⫽ number of data
sets; CI ⫽ confidence interval.
* p ⬍ .05. ** p ⬍ .01.
536
LORBER
that included zero (⫺0.11, 0.25). Thus, there was no evidence of
an association between HR reactivity and psychopathy/sociopathy
in adults. Statistically significant heterogeneity in effect sizes was
found (p ⬍ .05), with effects representing the entire range for
studies of psychopathy/sociopathy. Age could not be determined in
one study of psychopathy/sociopathy (Borkovec, 1970).
Conduct problems. The mean aggregate effect size of the
association between HR reactivity and conduct problems across
seven studies of children and adolescents was 0.20, with a 95%
confidence interval that excluded zero (0.05, 0.36). Thus, greater
HR reactivity was associated with conduct problems (N
fs
⫽ 7).
There was substantial heterogeneity in effect sizes (p ⬍ .01), with
effect sizes ranging from –1.24 to 0.49.
Similar effects were found in studies of child and adolescent
conduct disorder, Q
B
(1) ⫽ 0.05, ns. However, whereas the confi
-
dence interval for adolescent studies included zero, the lower
bound of the confidence interval for child studies hovered just
above zero (0.002), indicating that HR reactivity is positively
associated with conduct problems in children (N
fs
⫽ 3). Significant
effect size heterogeneity was found only in adolescent studies
(p ⬍ .01), with effect sizes in this category comprising the entire
range of studies of conduct problems. Age could not be determined
in one study (Garralda, Connell, & Taylor, 1990).
Behavior type moderation within age groups. In the case of
adolescents, the mean effects for aggression and conduct problems
did not differ significantly, Q
B
(1) ⫽ 0.35, ns. Significant within-
category heterogeneity in effect sizes was found in studies of
conduct problems (p ⬍ .01) but not in studies of aggression.
The difference in mean effects for aggression and psychopathy/
sociopathy in studies of adults did not reach statistical significance,
Q
B
(1) ⫽ 2.55, ns; only aggression was significantly associated
with HR reactivity (95% confidence interval: 0.10, 0.43). Signif-
icant heterogeneity in effect sizes was found in both categories
(ps ⬍ .05 and .01 for psychopathy/sociopathy and aggression,
respectively).
Moderation by stimulus valence. The dependence of effect
size on stimulus valence was examined in studies of aggression,
conduct problems, and psychopathy/sociopathy. Valence was a
significant moderator in studies of aggression, Q
B
(1) ⫽ 18.76, p ⬍
.01. In studies of aggression, positive effect sizes were associated
with negative stimuli (M ⫽ 0.31; N
fs
⫽ 17), whereas negative
effect sizes were associated with nonnegative stimuli (M ⫽⫺0.34;
N
fs
⫽ 12). Significant effect size heterogeneity was evident in both
categories (ps ⬍ .01). Effect sizes ranged from ⫺0.06 to 1.40 for
negative stimuli and from ⫺0.91 to 0.84 for nonnegative stimuli.
A similar sign reversal was obtained in studies of conduct
problems. However, the interaction of valence and HR reactivity in
predicting conduct problems was only marginally significant,
Q
B
(1) ⫽ 3.76, p ⬍ .10. Mean effects were 0.26 (N
fs
⫽ 6) for
negative stimuli and ⫺0.20 for nonnegative stimuli. However, the
confidence interval for studies that employed nonnegative stimuli
included zero. Significant effect size heterogeneity was found only
in studies that employed negative stimuli (p ⬍ .01), with effects
that ranged from ⫺1.24 to 0.49.
Stimulus valence did not moderate the association between HR
reactivity and psychopathy/sociopathy, Q
B
(1) ⫽ 0.03, ns. Stimulus
valence could not be determined in one study of psychopathy/
sociopathy (Schachter & Latane, 1964) and in one study of ag-
gression (Smith & Gallo, 1999).
Resting EDA
Aggression. Results of analyses involving resting EDA are
presented in Table 4. Four studies of aggression met criteria for
analysis. The mean aggregate effect size of the association be-
tween resting EDA and aggression across these studies was 0.10,
with a 95% confidence interval that included zero (⫺0.14, 0.34).
Thus, resting EDA was not significantly associated with aggres-
sion. Effect sizes were homogeneous. The only age category
containing three or more studies was adult. The mean aggregate
Table 4
Categorical Analysis of Resting Electrodermal Activity
Variable k Mean d
⫹
95% CI for d
⫹
Q
W
Q
B
Aggression 4 0.10 ⫺0.14, 0.34 0.08
Adult 3 0.08 ⫺0.27, 0.44 0.07
Psychopathy/sociopathy 18 ⫺0.30 ⫺0.46, ⫺0.15 27.31†
Adult 14 ⫺0.29 ⫺0.46, ⫺0.12 23.10†
Conduct problems 11 ⫺0.15 ⫺0.28, 0.001 23.81**
Age 2.81†
Child 8 ⫺0.30 ⫺0.49, ⫺0.07 16.72*
Adolescent 3 ⫺0.03 ⫺0.23, 0.17 4.28
Note. d
⫹
denotes effect sizes weighted by the reciprocal of their vari
-
ances. Q
W
tests within-category homogeneity of effect size; Q
B
tests
between-categories homogeneity. Significant effect sizes signify rejection
of the null hypothesis of homogeneous effect sizes. k ⫽ number of data
sets; CI ⫽ confidence interval.
† p ⬍ .10. * p ⬍ .05. ** p ⬍ .01.
Table 3
Categorical Analysis of Heart Rate Reactivity
Variable k
Mean
d
⫹
95% CI for d
⫹
Q
W
Q
B
Aggression 14 0.10 ⫺0.03, 0.22 69.20**
Age 0.81
Adolescent 4 0.10 ⫺0.21, 0.42 5.04
Adult 8 0.27 0.10, 0.43 30.16**
Stimulus valence 18.76**
Negative stimuli 8 0.31 0.15, 0.47 26.34**
Nonnegative stimuli 5 ⫺0.34 ⫺0.59, ⫺0.10 23.76**
Psychopathy/sociopathy 14 0.06 ⫺0.11, 0.23 23.19†
Adult 13 0.07 ⫺0.11, 0.25 23.13*
Stimulus valence 0.03
Negative stimuli 8 ⫺0.04 ⫺0.17, 0.26 9.74
Nonnegative stimuli 5 0.01 ⫺0.27, 0.30 9.85†
Conduct problems 7 0.20 0.05, 0.36 19.51**
Age 0.05
Child 3 0.19 0.002, 0.39 5.95
Adolescent 3 0.23 ⫺0.05, 0.51 13.42**
Stimulus valence 3.76†
Negative stimuli 4 0.26 0.10, 0.43 14.32**
Nonnegative stimuli 3 ⫺0.20 ⫺0.63, 0.24 1.43
Note. d
⫹
denotes effect sizes weighted by the reciprocal of their vari
-
ances. Q
W
tests within-category homogeneity of effect size; Q
B
tests
between-categories homogeneity. Significant effect sizes signify rejection
of the null hypothesis of homogeneous effect sizes. k ⫽ number of data
sets; CI ⫽ confidence interval.
† p ⬍ .10. * p ⬍ .05. ** p ⬍ .01.
537
PSYCHOPHYSIOLOGY OF AGGRESSION
effect size of the association between resting EDA and aggression
across these three studies was 0.08, with a 95% confidence interval
that included zero (⫺0.27, 0.44) and no significant variation in
effect sizes, further confirming the lack of a reliable relation
between resting EDA and aggression.
Psychopathy/sociopathy. The mean effect size of the associa-
tion between resting EDA and psychopathy/sociopathy across 18
studies was ⫺0.30 (N
fs
⫽ 36), with a 95% confidence interval that
excluded zero (⫺0.46, ⫺0.15). Thus, lower resting EDA was
significantly associated with psychopathy/sociopathy, but the ef-
fect was small. Marginally significant within-category heteroge-
neity of effect sizes was found (p ⬍ .10), with effects that ranged
from –1.87 to 0.57. The only age category containing 3 or more
studies was adult. The mean effect of the association between
resting EDA and psychopathy/sociopathy in these 14 studies was
⫺0.29 (N
fs
⫽ 27), with a 95% confidence interval that excluded
zero (⫺0.46, ⫺0.12) and marginal within-category heterogeneity
of effect sizes (p ⬍ .10), representing the entire range for studies
of psychopathy/sociopathy. This did not differ from the overall
pattern just reported. Age could not be determined in 2 studies of
psychopathy/sociopathy (Fox & Lippert, 1963; Hare, 1965b). With
an effect size of –1.87, the Hinton et al. (1980) study was a
significant outlier (the nearest effect size was –1.17). However, its
removal did not affect the findings reported here, and it was
therefore retained.
Conduct problems. The mean aggregate effect size of the
association between resting EDA and conduct problems across 11
studies of children and adolescents was ⫺0.15, with a 95% con-
fidence interval that included zero (⫺0.28, 0.001). Thus, there was
no reliable association between resting EDA and conduct prob-
lems. There was substantial heterogeneity in effect sizes (p ⬍ .01),
with effect sizes ranging from ⫺1.02 to 0.89.
There were enough studies to examine age as a moderator of the
resting EDA–conduct problems relationship; studies of children
and adolescents were compared. The mean effect size was lower in
child (M ⫽⫺0.30; N
fs
⫽ 16) than in adolescent (M ⫽⫺0.03)
studies, Q
B
(1) ⫽ 2.81, p ⬍ .10, although this difference only
approached statistical significance. Furthermore, the 95% confi-
dence interval excluded zero (⫺0.49, ⫺0.07) in studies of children
but not adolescents, indicating that low resting EDA is reliably
associated with conduct problems only in the case of children.
Significant effect size heterogeneity was found only in studies of
children (p ⬍ .05), with these effects representing the entire range
for conduct problems.
The effect size contributed by the investigation of Garralda,
Connell, and Taylor (1989) to studies of conduct problems in
children was an outlier (d
⫹
⫽ 0.89; the next highest effect size was
0.21). However, this study was retained because it did not sub-
stantially leverage the results.
Behavior type moderation within age groups. Mean effect
sizes were compared in studies of adult psychopathy/sociopathy
and aggression. The difference in mean effects for aggression
(M ⫽ 0.08) and psychopathy/sociopathy (M ⫽⫺0.29) fell just
short of statistical significance, Q
B
(1) ⫽ 3.54, p ⬍ .10; only
psychopathy/sociopathy was associated significantly with resting
EDA (i.e., its confidence interval excluded zero). Marginal within-
category effect size heterogeneity was found in studies of psy-
chopathy/sociopathy (p ⬍ .10) but not in studies of aggression.
Task EDA
Aggression. Results of analyses involving task EDA are pre-
sented in Table 5. The mean aggregate effect size of the associa-
tion between task EDA and aggression across four studies was
0.07, with a 95% confidence interval that included zero (⫺0.18,
0.32). Thus, task EDA was not associated with aggression. Effect
sizes were significantly heterogeneous (d
⫹
range: ⫺0.18 to 1.77,
p ⬍ .05). The only age category containing three or more studies
was adult. The mean aggregate effect size of the association
between task EDA and aggression across these three studies was
0.31, with a 95% confidence interval that included zero (⫺0.04,
0.65). Thus, EDA was not associated with adult aggression. Effect
sizes were homogeneous. One study (Wolfe, Fairbank, Kelly, &
Bradlyn, 1983) produced an outlier (d
⫹
⫽ 1.77; the next nearest
effect size was 0.42). Its removal did not affect the results, and it
was therefore retained.
Psychopathy/sociopathy. The mean effect size of the associa-
tion between task EDA and psychopathy/sociopathy across 28
studies was ⫺0.25, with a 95% confidence interval that excluded
zero (⫺0.34, ⫺0.15). Thus, lower task EDA was associated with
psychopathy/sociopathy, but the effect was small (N
fs
⫽ 42).
Statistically significant heterogeneity in effect sizes was found
(p ⬍ .01) with effects ranging from ⫺1.12 to 0.57.
Age was a significant moderator; studies of adult psychopathy/
sociopathy yielded a significant and larger mean effect (M ⫽
⫺0.43; N
fs
⫽ 69), whereas studies of adolescents yielded a non
-
significant and smaller mean effect (M ⫽⫺0.07), Q
B
(1) ⫽ 12.24,
p ⬍ .01. Effect sizes were marginally heterogeneous only in
adolescents (d
⫹
range: ⫺0.62 to 0.06, p ⬍ .10). Age could not be
determined in two studies of psychopathy/sociopathy (Borkovec,
1970; Hare, 1965b).
Table 5
Categorical Analysis of Task Electrodermal Activity
Variable k
Mean
d
⫹
95% CI for d
⫹
Q
W
Q
B
Aggression 4 0.07 ⫺0.18, 0.32 8.38*
Adult 3 0.31
a
⫺0.04, 0.65 4.62
Psychopathy/sociopathy 28 ⫺0.25 ⫺0.34, ⫺0.15 48.59*
Age 12.24**
Adolescent 4 ⫺0.07 ⫺0.21, 0.06 8.78†
Adult 21 ⫺0.43
a
⫺0.57, ⫺0.28 26.26
Stimulus valence 10.98**
Negative stimuli 13 ⫺0.47 ⫺0.65, ⫺0.29 16.45
Nonnegative stimuli 13 ⫺0.11 ⫺0.23, 0.01 15.89
Conduct problems 14 ⫺0.23 ⫺0.35, ⫺0.10 18.81
Age 6.62*
Child 8 ⫺0.46 ⫺0.67, ⫺0.24 6.03
Adolescent 6 ⫺0.10 ⫺0.26, 0.05 6.16
Stimulus valence 0.18
Negative stimuli 4 ⫺0.07 ⫺0.30, 0.16 6.27
Nonnegative stimuli 9 ⫺0.27 ⫺0.44, ⫺0.12 9.50
Note. d
⫹
denotes effect sizes weighted by the reciprocal of their vari
-
ances. Q
W
tests within-category homogeneity of effect size; Q
B
tests
between-categories homogeneity. Significant effect sizes signify rejection
of the null hypothesis of homogeneous effect sizes. Mean effect sizes with
matching subscripts are different from one another at p ⬍ .01. k ⫽ number
of data sets; CI ⫽ confidence interval.
† p ⬍ .10. * p ⬍ .05. ** p ⬍ .01.
538
LORBER
Conduct problems. The mean aggregate effect size of the
association between task EDA and conduct problems across 14
studies of children and adolescents was ⫺0.23, with a 95% con-
fidence interval that excluded zero (⫺0.35, ⫺0.10). Thus, lower
task EDA was associated with conduct problems (N
fs
⫽ 18). There
was no evidence of heterogeneity in effect sizes after removal of
an extreme outlier (Mangina, Beuzeron-Mangina, & Grizenko,
2000; d
⫹
⫽⫺6.71).
The difference in effects associated with conduct problems in
children (M ⫽⫺0.46; N
fs
⫽ 29) and adolescents (M ⫽⫺0.10)
was statistically significant, Q
B
(1) ⫽ 6.62, p ⬍ .05. The associa
-
tion of conduct problems with low task EDA was reliable only
with respect to children (95% confidence interval: ⫺0.67, ⫺0.24).
There was no evidence of effect size heterogeneity in either age
group.
Behavior type moderation within age groups. In the case of
adolescents, the mean effects for psychopathy/sociopathy and con-
duct problems did not differ significantly, Q
B
(1) ⫽ 0.08, ns.
Marginally significant within-category heterogeneity in effect
sizes was found only in studies of psychopathy/sociopathy (d
⫹
range: ⫺0.62 to 0.06, p ⬍ .10).
Among adults, effect size was moderated by behavior type,
Q
B
(1) ⫽ 15.06, p ⬍ .01. A significant negative relation was found
for the 21 studies of psychopathy/sociopathy (M ⫽⫺0.43; N
fs
⫽
69); this was not the case for aggression, in which a nonsignificant
positive mean effect was obtained (M ⫽ 0.31). There was no
evidence of effect size heterogeneity in either group.
Moderation by stimulus valence. Dependence of effect size on
stimulus valence was examined in studies of psychopathy/sociop-
athy and conduct problems. Valence was a significant moderator
only in studies of psychopathy/sociopathy, Q
B
(1) ⫽ 10.98, p ⬍
.01. The mean effect for negative stimuli (M ⫽⫺0.47; N
fs
⫽ 48)
was stronger than the mean effect for nonnegative stimuli (M ⫽
⫺0.11). Furthermore, the task EDA–psychopathy/sociopathy as-
sociation was reliable only when negative stimuli were employed
(95% confidence interval: ⫺0.65, ⫺0.29). There was no evidence
of effect size heterogeneity for stimuli of either valence category.
Valence was not a significant moderator of effect sizes in
studies of conduct problems, Q
B
(1) ⫽ 0.18, ns; a reliable associ
-
ation was obtained only for studies that employed nonnegative
stimuli (mean d
⫹
⫽⫺0.27; 95% confidence interval: ⫺0.44,
⫺0.12; N
fs
⫽ 15). There was no evidence of effect size heteroge
-
neity for either valence category. Stimulus valence could not be
determined in two studies of psychopathy/sociopathy (Hare,
1978b; Herpertz, Werth, et al., 2001) and in one study of conduct
problems (Harden, Pihl, Vitaro, Gendreau, & Tremblay, 1995).
Electrodermal Reactivity
Aggression. Results of analyses involving EDA reactivity are
presented in Table 6. Comparatively fewer studies (k ⫽ 20) re-
ported EDA reactivity. All but two of these were studies of adults.
The one study of conduct problems was not included in EDA
reactivity analyses. The aggregate association across the five stud-
ies of aggression was small (M ⫽⫺0.07), with a 95% confidence
interval that included zero (⫺0.24, 0.10). Thus, there was no
aggregate association between EDA reactivity and aggression.
Significant effect size heterogeneity was found (d
⫹
range: ⫺0.72
to 0.91, p ⬍ .01). The only age class with 3 or more studies was
adult. The aggregate association across these three studies was
small (M ⫽ 0.34; N
fs
⫽ 7), but its 95% confidence interval
excluded zero (0.10, 0.59). Thus, adult aggression was associated
with greater EDA reactivity, with no significant heterogeneity in
effect sizes.
Psychopathy/sociopathy. Across 14 studies, EDA reactivity
was negatively associated with psychopathy/sociopathy (M ⫽
⫺0.31; N
fs
⫽ 29), with a 95% confidence interval that excluded
zero (⫺0.48, ⫺0.13). Effect sizes varied significantly (p ⬍ .01),
from ⫺1.35 to 0.82. The only age class with 3 or more studies was
adult. Across these 13 studies, EDA reactivity was significantly
negatively associated with psychopathy/sociopathy (M ⫽⫺0.33;
N
fs
⫽ 30), with a 95% confidence interval that excluded zero
(⫺0.52, ⫺0.15). Effect sizes varied significantly (p ⬍ .01), rep-
resenting the entire range for psychopathy/sociopathy.
Behavior type moderation within age groups. Studies of adult
psychopathy/sociopathy and aggression yielded nearly identical
effect sizes with opposite signs (⫺0.33 and 0.34, respectively).
This difference was statistically significant, Q
B
(1) ⫽ 18.95, p ⬍
.01.
Moderation by stimulus valence. Because the sample con-
sisted almost exclusively of effects based on the use of negatively
valenced stimuli, moderation by stimulus valence could not be
evaluated.
Discussion
The present meta-analytic review evaluated the associations of
HR and EDA with aggressive, psychopathic, and conduct-
disordered behavior across 95 studies.
3
Analyses were conducted
to examine moderation of effect size by behavior type and age, as
well as valence of experimental stimuli. Results suggest that ag-
gression, conduct problems, and psychopathy/sociopathy are reli-
ably though modestly associated with HR and EDA in many cases.
However, results were mixed and revealed a complex constellation
of interactive effects. Many of the findings are summarized in
Table 7.
With rare exceptions, the effect sizes corresponding to each of
the significant findings reported herein were small according to
Cohen’s (1988) standards. Furthermore, fail-safe N analyses indi-
3
Unfortunately, there were not enough studies of antisocial personality
characteristics to meaningfully contribute to the meta-analysis.
Table 6
Categorical Analysis of Electrodermal Reactivity
Variable k Mean d
⫹
95% for d
⫹
Q
W
Aggression 5 ⫺0.07 ⫺0.24, 0.10 29.62**
Adult 3 0.34
a
0.10, 0.59 2.89
Psychopathy/sociopathy 14 ⫺0.31 ⫺0.48, ⫺0.13 29.30**
Adult 13 ⫺0.33
a
⫺0.52, ⫺0.15 28.23**
Note. d
⫹
denotes effect sizes weighted by the reciprocal of their vari
-
ances. Q
W
tests within-category homogeneity of effect size. Significant
effect sizes signify rejection of the null hypothesis of homogeneous effect
sizes. Mean effect sizes with matching subscripts are different from one
another at p ⬍ .01. k ⫽ number of data sets; CI ⫽ confidence interval.
** p ⬍ .01.
539
PSYCHOPHYSIOLOGY OF AGGRESSION
cated that there might be a file drawer problem. A relatively small
group of studies with very small or opposite-signed effect sizes
could render many of the aggregate findings nonsignificant. Thus,
due caution should be exercised in interpreting the present results.
There were generally more studies of psychopathy/sociopathy
available for analysis, as compared with studies of aggression and
conduct problems. Therefore, with due acknowledgment of the file
drawer problem, confidence in findings involving psychopathy/
sociopathy is greater.
The most simple and compelling results were obtained with
respect to EDA and psychopathy/sociopathy, studied primarily in
adults. Psychopathy/sociopathy was associated with lower EDA at
rest and during tasks and as a change from baseline. Consistent
with predictions, the negative association between psychopathy/
sociopathy and EDA during tasks was evident only for stimuli of
negative valence; this interaction achieved statistical significance.
A similar pattern was obtained for child conduct problems,
which were associated with attenuated EDA in the absence of
stimulation. As was psychopathy/sociopathy, conduct problems
were associated with low task EDA. However, this was found only
in the case of studies of conduct problems that involved nonnega-
tive stimuli. This finding was the opposite of what was predicted
and was in contrast to the findings for psychopathy/sociopathy.
The attenuated EDA of psychopathic individuals relative to con-
trols was evident only under conditions of exposure to negatively
valenced stimuli. Thus, despite the considerable overlap in these
two constructs and the status of childhood conduct problems as a
risk factor for antisocial adult behavior (Loeber, 1982), the present
meta-analytic results suggest that the nature of underlying psycho-
pathology may differ between children with conduct problems and
adults with psychopathy. The latter are thought to almost invari-
ably exhibit conduct problems as children (Lynam, 1996). How-
ever, the majority of children with conduct problems will not
become psychopathic or even antisocial adults (Robins, 1978);
thus, if a group of “fledgling psychopaths” exists (with autonomic
characteristics of psychopathic adults), their contribution to the
relations between task EDA and conduct problems would be
washed out by the majority.
A very different pattern of results was obtained with respect to
EDA and aggression. Although aggression was not associated with
either resting or task EDA in any age group, adult aggression was
positively associated with EDA reactivity, the opposite of findings
for psychopathy/sociopathy. Considering the EDA findings as a
whole, and in spite of overlaps in the behavior constructs being
studied (e.g., violations of personal rights, laws, and social norms
are common to all of them), a degree of behavioral specificity was
evidenced in this aspect of autonomic functioning.
In contrast to the consistent relation between EDA and psychop-
athy/sociopathy, psychopathy/sociopathy was not associated with
HR in any analysis, irrespective of the valence of experimental
stimuli. On the other hand, HR proved to be a reliable correlate of
conduct problems and aggression. Conduct problems in children
and adolescents were associated with lower resting HR. Conduct
problems were also associated with greater HR reactivity, but only
among children. Because of the small effect size difference be-
tween studies of children and adolescents, however, future meta-
analyses may indeed reveal a positive relation between HR reac-
tivity and conduct problems in adolescents. Consistent with the
valence hypothesis, reliable associations between conduct prob-
lems and HR reactivity were found only for negative stimuli. The
association of conduct problems with HR, combined with a lack of
any HR findings for psychopathy/sociopathy, further highlights the
distinctiveness of the psychopathologies constituting these two
behavior patterns.
As with conduct problems, both child and adult aggression were
associated with low resting HR, but only adult aggression was
marked by greater HR reactivity. Although no aggregate associa-
tion between task HR and aggression was found, negative task
HR–aggression relations emerged for stimuli of negative valence,
whereas positive relations were obtained for nonnegative stimuli.
The opposite pattern was found with respect to HR reactivity.
Clinical Implications
Limitations notwithstanding, the results of this meta-analysis
may have clinical implications. Iacono (1991) pointed out the
value of psychophysiological assessment in assisting with differ-
ential diagnoses and identification of different forms of psycho-
pathology. From this perspective, the autonomic differentiation of
adult aggression and psychopathy/sociopathy provides the clearest
information. Broadly, aggression appears to be more tightly tied to
HR than to EDA, with the converse being true of psychopathy/
sociopathy. Differences between mean effects were significant in
only half of the contrasts reported. However, in no case were
aggression and psychopathy/sociopathy reliably associated with
either EDA or HR in the same direction. This set of findings
further accentuates the distinctiveness of these two constructs.
In contrast to the relative autonomic distinctiveness of aggres-
sion and psychopathy/sociopathy in adults, there was no evidence
of differing physiology–behavior relations between conduct prob-
Table 7
Summary of Main Effects
Category
Resting
HR
Task
HR
HR
reactivity
Resting
EDA
Task
EDA
EDA
reactivity
Aggression 2 —— ———
Child 2 —? ?? ?
Adolescent ? — — ? ? ?
Adult 2 — 1 —— 1
Negative stimuli 21 ??
Nonnegative stimuli 12 ??
Psychopathy/sociopathy — — — 22 2
Child ? ? ? ? ? ?
Adolescent ? ? ? ? — ?
Adult — — — 22 2
Negative stimuli ? — 2 ?
Nonnegative stimuli ? — — ?
Conduct problems 2 — 1 — 2 ?
Child 2 — 122?
Adolescent 2 —— —— ?
Negative stimuli — 1 —?
Nonnegative stimuli — — 2 ?
Note. 1 denotes a significant (i.e., 95% confidence interval excludes
zero) positive main effect; 2 denotes a significant negative main effect.
Dashes denote nonsignificant main effects (i.e., 95% confidence interval
includes zero). Question marks indicate insufficient number of studies for
analysis. HR ⫽ heart rate; EDA ⫽ electrodermal activity.
540
LORBER
lems and aggression in children and adolescents. The strongest
findings concern conduct problems in children. Children with
conduct problems had autonomic patterns in common with adult
aggressors (low resting HR; also found with regard to child ag-
gression) and psychopathic/sociopathic individuals (low resting
EDA). This pattern is consistent with the theoretical and empirical
literature indicating that children with conduct problems are at risk
for both adult aggression and psychopathy/sociopathy (e.g., Ly-
nam, 1996; Moffitt et al., 2002). HR and EDA appear to mark
nonspecific risk, with other factors determining which develop-
mental trajectory children follow.
To the extent that autonomic measures reflect the presence of
specific symptoms or dimensional attributes that underlie a disor-
der (Iacono, 1991), the autonomic variables identified here may
also be useful indices of change. Where psychopathology is con-
cerned, treatment outcome studies most often assess changes in
behavioral indicators only. However, if part of the pathology of
antisocial spectrum behavior is inherently biological—and the
results of the present meta-analysis support this contention—
behavioral indicators cannot capture all of the relevant aspects of
change. Changes in autonomic measures may ultimately prove to
be most feasible with children (e.g., Raine et al., 2001), given their
relative neural plasticity.
Contributors to Variability in Effect Sizes
The present analyses of effect size heterogeneity have several
empirical implications. Researchers of antisocial spectrum behav-
ior may in many cases assume a degree of specificity in
physiology–behavior relations, these being tied to theory. For
example, Lykken (1957) hypothesized that psychopathic individ-
uals have deficient fear conditioning. This was tested by measuring
EDA responses to a conditioned stimulus that had previously been
associated with shocks. In contrast, Hare (1968) hypothesized that
psychopathic individuals are deficient in orienting. This was tested
by measuring EDA in response to novel tones. However, this
degree of specificity may not always exist. Despite the fact that the
antisocial constructs were measured differently, different stimuli
were employed, and different subclasses of physiological measures
were used, effect sizes did not significantly vary in many cases.
Significant heterogeneity was found in 42.86% of the cases in
which it was tested (30.43% for EDA, 51.52% for HR). In the
cases in which significant aggregate effects were accompanied by
nonsignificant heterogeneity in effect sizes, a degree of generality
is suggested. That is, these associations were potentially insensi-
tive to construct measurement, stimuli used, and subtype of phys-
iological measure. Also, in cases in which aggregate effects were
not reliable, with nonsignificant heterogeneity in effect sizes,
methodological differences could not have caused false nonsignif-
icant findings.
Of course, in instances in which heterogeneity was found, it
could have been due to any one of these factors or to other
methodological and substantive differences among studies. The
presence of such interactive effects could not be evaluated here
because of the relatively low number of studies included in each
subanalysis; however, single studies or future quantitative reviews
might address this issue.
One methodological contributor to unexplained variability in
effect sizes may have been construct heterogeneity within coding
definitions. For example, studies by Hare and colleagues, who
used a consistent operationalization of psychopathy over several
studies of psychopathy and EDA reactivity, enjoyed a notably high
replication rate relative to the pool of studies contributed by other
investigators, within which varied psychopathy assessment meth-
ods were used. One of the main themes in this article is that
physiology–behavior relations depend on which behavior con-
struct is being studied. Therefore, heterogeneity in behavior op-
erationalizations seems to be an important candidate as a contrib-
utor to variability in effect sizes. More studies will be required to
make finer distinctions in future quantitative reviews.
Within behavior patterns, the mixed degree of clinical deviation
in participants of the studies included in the present meta-analysis
may also have contributed to effect size heterogeneity.
Physiology–behavior relations may apply only to more “clinical”
groups, such as psychopathic individuals low in anxiety (vs. all
psychopathic individuals) or those in the upper ranges of aggres-
sion (vs. simply higher than average). Single studies and future
meta-analyses could address this concern. For example, Babcock
et al. (2004) found that the relation between HR reactivity and
psychopathy differed among low- and high-level domestically
violent men.
Gender is another potentially important moderator of the rela-
tions investigated herein, and it may have contributed to effect size
heterogeneity. Although the majority of studies included in the
present meta-analysis were conducted exclusively with male par-
ticipants, female participants were included in several of the stud-
ies, probably more so in studies of children and adolescents. Most
of these studies, however, did not report separate findings by
gender. This prevented examination of gender interactive effects.
Such questions are important, and they should be addressed in
future studies and, eventually, meta-analyses.
With some notable exceptions (e.g., Raine, Brennan, Farrington,
& Mednick, 1997; Raine & Venables, 1981), the field has focused
primarily on main effects. Identification of methodologically and
theoretically warranted moderators will continue to advance this
area of inquiry.
Further Implications for Research
Cross-sectional work with multiple age cohorts would also be
helpful to resolve issues pertaining to generalization of findings
across development. Longitudinal studies would help in this regard
as well, with both aggressive/antisocial behavior and autonomic
patterns measured contemporaneously at all time points. Longitu-
dinal studies have begun to yield findings similar to the cross-
sectional ones reported here. For example, Raine and his col-
leagues have found that low resting HR at the age of 3 years
predicts aggression at 11 years (Raine, Venables, & Mednick,
1997). This group has also found evidence that poor conditioning
(judged by electrodermal responses) in adolescence is a risk factor
for adult crime (Raine, Venables, & Williams, 1996). More pro-
spective longitudinal studies will be necessary to address impor-
tant, as-of-yet-unresolved developmental problems, such as iden-
tification of autonomic variables that predict the transition from
childhood conduct problems to adult psychopathy.
541
PSYCHOPHYSIOLOGY OF AGGRESSION
The impact of stimulus valence on physiology–behavior rela-
tions also merits further study. Broad support was not found for the
hypothesis that stimuli of negative valence would produce stronger
physiology–behavior relations. In fact, the only clear support for
the valence hypothesis was found with respect to task EDA and
psychopathy/sociopathy. Significant valence moderation was
found in other cases. However, the results were mixed, with
frequent sign reversals. Although these results did not support a
priori hypotheses in most cases, the impact of stimuli valence is
clearly worthy of attention. To my knowledge, there is no existing
theory that predicts such patterns. Thus, revisions to theory may be
in order. On the other hand, it is possible that valence was con-
founded with design characteristics that were ultimately responsi-
ble for the observed patterns. This possibility could perhaps best be
tested in future studies and should be clarified before theory
modification.
In addition to paying more attention to moderators in future
quantitative reviews, measuring multiple forms of antisocial and
aggressive behavior within studies would allow for comparisons of
autonomic patterns. The Babcock et al. (2004) study is an excellent
example of this approach. The present results suggest that, in many
cases, autonomic patterns differ according to the behavior under
consideration; however, the comorbidity of different forms of
antisocial spectrum behavior decreases clarity of interpretation.
For example, it is impossible to know to what degree aggressive
samples were populated with psychopathic individuals or individ-
uals with multiple antisocial personality characteristics.
Another implication for future empirical work is tied to ener-
vation of the heart. As reviewed in the introduction, HR is con-
trolled by both the SNS and the PNS. However, the PNS ordinarily
exerts a stronger influence on HR—via the vagus nerve—than the
SNS (Porges, 2001). Because aggression was found to be associ-
ated with HR (low resting HR and high HR reactivity), it follows
that aggression may be tied to vagal functioning, particularly that
which originates in the nucleus ambiguus of the medulla, an area
tied to social affective behavior (Beauchaine, 2001; Porges, 1995,
2001). At present, however, the literature assessing such relations
(e.g., Umhau et al., 2002) is too limited to allow any firm conclu-
sions. Investigations of vagal functioning and antisocial spectrum
behavior may hold a great deal of promise for advancing our
understanding of these forms of psychopathology, particularly
when studied in the context of other aspects of autonomic func-
tioning (see Beauchaine, 2001).
Finally, there is a critical need for studies focusing on psycho-
physiological correlates of antisocial personality characteristics. I
was surprised at the relative lack of such studies, too few to have
made a meaningful contribution to the present meta-analysis. It is
ironic that the most commonly invoked construct in this area of
inquiry—“antisocial”—has apparently been studied the least.
Conclusion
This meta-analysis highlights the significance of autonomic
markers of antisocial spectrum psychopathology. Although aggre-
gate relations were small, HR and EDA measures proved to be
reliable correlates of aggression, psychopathy/sociopathy, and
conduct problems in enough cases to suggest that they be taken
seriously. At the same time, the present meta-analysis underscores
the complexity of research in this area. This too is a useful
contribution inasmuch as it points to several open empirical issues,
the resolution of which will doubtlessly advance our knowledge of
this most socially costly set of behaviors.
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Appendix
Characteristics and Effects Sizes for Studies in the Meta-Analysis
Table A1
Coded Qualities and Weighted Effect Sizes of Studies of Resting Heart Rate
Study Age Behavior pattern N
e
N
c
d
⫹
Arnett et al. (1993) Adult Psychopathy/sociopathy 31 32 0.00
Babcock et al. (2004) Adult Aggression 72 30 ⫺0.32
Blackburn (1979) Adult Psychopathy/sociopathy 18 14 ⫺0.23
Chiang et al. (2001) Adult Aggression 14 16 ⫺0.79
Cohn (1995)
a
Adolescent Aggression 21 21 ⫺0.31
Cohn (1995)
a
Adolescent Aggression 19 19 0.19
Cohn (1995)
a
Adolescent Aggression 21 21 0.27
Davies & Maliphant (1971) Adolescent Conduct problems 14 14 ⫺0.73
Delamater & Lahey (1983) Child Conduct problems 19 17 ⫺0.58
Frodi & Lamb (1980) Adult Aggression 14 14 0.00
Garralda et al. (1989) Child Conduct problems 7 8 ⫺1.02
Garralda et al. (1991) Uncodable Conduct problems 25 25 0.00
Gerra et al. (1997) Adult Aggression 15 15 ⫺0.08
Haldeman (1973) Adult Psychopathy/sociopathy 30 10 0.08
Hare & Craigen (1974) Adult Psychopathy/sociopathy 17 17 0.00
Hare (1968) Adult Psychopathy/sociopathy 39 12 1.00
Hare (1982) Adult Psychopathy/sociopathy 16 15 0.00
Hare et al. (1978) Adult Psychopathy/sociopathy 24 40 0.00
Herpertz, Wenning, et al. (2001) Child Conduct problems 26 21 ⫺0.47
House & Milligan (1976) Adult Psychopathy/sociopathy 32 32 0.00
Ingersoll (1977) Adult Psychopathy/sociopathy 9 11 ⫺0.32
Kindlon et al. (1995)
a
Child Aggression 51 0 ⫺0.52
Kindlon et al. (1995)
a
Adolescent Aggression 44 0 ⫺0.42
Maliphant et al. (1990) Adolescent Conduct problems 12 20 ⫺1.11
Marchel (1993) Adolescent Conduct problems 40 40 ⫺0.16
McBurnett (1989) Child Conduct problems 15 37 ⫺0.18
McLaughlin (1995) Child Aggression 29 0 ⫺0.14
McNamara & Ballard (1999)
a
Adult Psychopathy/sociopathy 49 0 0.02
McNamara & Ballard (1999)
a
Adult Psychopathy/sociopathy 47 0 0.26
Milner (1976) Adult Psychopathy/sociopathy 29 0 0.33
Ogloff & Wong (1990) Adult Psychopathy/sociopathy 16 16 ⫺0.29
Pham et al. (2000) Adult Psychopathy/sociopathy 14 15 ⫺0.32
Pitts (1993) Child Aggression 65 38 ⫺0.75
Raine & Jones (1987) Child Aggression 40 0 ⫺0.64
Raine & Venables (1984a) Adolescent Conduct problems 101 0 ⫺0.28
Rogeness et al. (1990)
a
Child Conduct problems 374 0 ⫺0.39
Rogeness et al. (1990)
a
Adolescent Conduct problems 61 145 ⫺0.34
Scarpa et al. (2000) Adult Aggression 54 0 ⫺0.36
Schachter & Latane (1964)
a
Adult Psychopathy/sociopathy 15 15 0.00
Schachter & Latane (1964)
a
Adult Psychopathy/sociopathy 9 9 0.00
Smithmyer (2001) Child Aggression 67 0 0.01
Taub (1972) Adult Psychopathy/sociopathy 15 15 1.06
Tucker (1991) Child Conduct problems 32 44 ⫺0.25
van Goozen et al. (1998) Child Aggression 52 0 ⫺1.20
Wolfe et al. (1983) Adult Aggression 7 7 0.18
Zahn & Kruesi (1993) Child Conduct problems 27 31 0.37
Note. N for studies that reported correlations or other single-group analyses is reported in the N
e
column. N
e
⫽ number of participants in experimental
(i.e., aggressive, psychopathic/sociopathic, conduct problems) group; N
c
⫽ number of participants in control group; d
⫹
⫽ effect size weighted by reciprocal
of variance.
a
Multiple independent samples from a single study.
(Appendix continues)
547
PSYCHOPHYSIOLOGY OF AGGRESSION
Table A2
Coded Qualities and Weighted Effect Sizes of Studies of Task Heart Rate
Study Age Behavior pattern Stimulus valence N
e
N
c
d
⫹
Babcock et al. (2004) Adult Aggression Negative 72 30 ⫺0.32
Chiang et al. (2001) Adult Aggression Uncodable 14 16 ⫺0.45
Davies & Maliphant (1971) Adolescent Conduct problems Negative 14 14 ⫺0.47
Edguer & Janisse (1994) Adult Aggression Nonnegative 50 0 0.60
Eisenberg et al. (1996) Child Conduct problems Negative 92 0 0.00
Friedrich et al. (1985) Adult Aggression Negative 14 15 0.00
Haldeman (1973) Adult Psychopathy/sociopathy Negative 10 10 ⫺0.06
Harden & Pihl (1995) Adolescent Conduct problems Negative 28 0 0.44
Harden et al. (1995) Child Conduct problems Negative 18 15 0.19
House & Milligan (1973) Adult Psychopathy/sociopathy Nonnegative 32 32 0.00
Ingersoll (1977) Adult Psychopathy/sociopathy Nonnegative 9 11 ⫺0.80
Jacobson et al. (1994) Adult Aggression Negative 60 32 ⫺0.04
Jennings & Matthews (1984) Child Aggression Nonnegative 17 17 ⫺0.53
Maliphant et al. (1990) Adolescent Conduct problems Nonnegative 12 20 ⫺1.67
Marchel (1993) Adolescent Aggression Negative 80 0 ⫺0.20
McBurnett (1989) Child Conduct problems Nonnegative 15 37 0.00
McLaughlin (1995) Child Aggression Nonnegative 29 0 ⫺0.30
Milner (1976) Adult Psychopathy/sociopathy Negative 29 0 0.09
Ogloff & Wong (1990) Adult Psychopathy/sociopathy Negative 16 16 ⫺0.81
Pelham et al. (1991) Child Aggression Negative 10 10 ⫺0.49
Pham et al. (2000) Adult Psychopathy/sociopathy Uncodable 14 15 ⫺0.15
Pitts (1993) Child Aggression Negative 65 38 ⫺0.41
Tharp et al. (1980) Adult Psychopathy/sociopathy Uncodable 15 15 0.00
Thomas (1982) Adult Aggression Nonnegative 13 0 ⫺1.14
Tucker (1991) Child Conduct problems Nonnegative 32 44 0.00
van Goozen et al. (1998) Child Conduct problems Negative 21 31 0.05
Winkel et al. (1987) Adolescent Aggression Nonnegative 28 0 0.51
Wolfe et al. (1983) Adult Aggression Negative 7 7 ⫺0.10
Zahn & Kruesi (1993) Child Aggression Nonnegative 63 0 0.69
Note. N for studies that reported correlations or other single-group analyses is reported in the N
e
column. N
e
⫽ number of participants in experimental
(i.e., aggressive, psychopathic/sociopathic, conduct problems) group; N
c
⫽ number of participants in control group; d
⫹
⫽ effect size weighted by reciprocal
of variance.
548
LORBER
Table A3
Coded Qualities and Weighted Effect Sizes of Studies of Heart Rate Reactivity
Study Age Behavior pattern Stimulus valence N
e
N
c
d
⫹
Arnett et al. (1997) Adult Psychopathy/sociopathy Nonnegative 13 19 0.62
Babcock et al. (2004) Adult Aggression Negative 102 0 ⫺0.06
Borkovec (1970) Uncodable Psychopathy/sociopathy Nonnegative 19 46 0.00
Cohn (1995)
a
Adolescent Aggression Negative 21 21 0.54
Cohn (1995)
a
Adolescent Aggression Nonnegative 21 21 ⫺0.10
Cohn (1995)
a
Adolescent Aggression Nonnegative 19 19 0.32
Davies & Maliphant (1971) Adolescent Conduct problems Negative 7 7 ⫺1.24
Eisenberg et al. (1996) Child Conduct problems Negative 95 0 ⫺0.02
Eisenberg et al. (1996) Child Conduct problems Negative 92 0 0.47
Frodi & Lamb (1980) Adult Aggression Negative 14 14 0.73
Garralda et al. (1990) Uncodable Conduct problems Nonnegative 4 5 0.00
Gerra et al. (1997) Adult Aggression Nonnegative 15 15 0.84
Gerra et al. (2001)
a
Adult Aggression Negative 20 0 1.14
Gerra et al. (2001)
a
Adult Aggression Negative 20 0 1.40
Hare (1968) Adult Psychopathy/sociopathy Nonnegative 21 12 ⫺0.65
Hare (1982) Adult Psychopathy/sociopathy Negative 14 12 ⫺0.66
Hare & Craigen (1974) Adult Psychopathy/sociopathy Negative 17 17 0.00
Hare et al. (1978) Adult Psychopathy/sociopathy Negative 24 40 0.59
House & Milligan (1976) Adult Psychopathy/sociopathy Negative 32 32 0.00
Ishikawa et al. (2001) Adult Psychopathy/sociopathy Negative 13 26 0.35
Johnson & Rule (1986) Adult Aggression Negative 40 0 0.51
Keltikangas-Jarvinen & Keinonen (1988) Adolescent Aggression Nonnegative 19 16 ⫺0.41
Levenston et al. (2000) Adult Psychopathy/sociopathy Nonnegative 17 18 0.56
Maliphant et al. (1990) Adolescent Conduct problems Nonnegative 12 20 ⫺0.55
Marchel (1993) Adolescent Conduct problems Negative 80 0 0.49
McBurnett (1989) Child Conduct problems Nonnegative 15 37 0.00
Meehan et al. (2001) Adult Aggression Negative 19 39 0.00
Milner (1976) Adult Psychopathy/sociopathy Negative 29 0 ⫺0.05
Ogloff & Wong (1990) Adult Psychopathy/sociopathy Negative 16 16 ⫺0.39
Patrick et al. (1994) Adult Psychopathy/sociopathy Nonnegative 35 18 ⫺0.33
Raskin & Hare (1978) Adult Psychopathy/sociopathy Negative 10 7 0.00
Schachter & Latane (1964) Adult Psychopathy/sociopathy Uncodable 9 9 0.99
Smith & Gallo (1999) Adult Aggression Uncodable 60 0 0.00
Smithmyer (2001) Child Aggression Negative 67 0 0.23
Zahn & Kruesi (1993) Child Aggression Nonnegative 63 0 ⫺0.91
Note. N for studies that reported correlations or other single-group analyses is reported in the N
e
column. N
e
⫽ number of participants in experimental
(i.e., aggressive, psychopathic/sociopathic, conduct problems) group; N
c
⫽ number of participants in control group; d
⫹
⫽ effect size weighted by reciprocal
of variance.
a
Multiple independent samples from a single study.
(Appendix continues)
549
PSYCHOPHYSIOLOGY OF AGGRESSION
Table A4
Coded Qualities and Weighted Effect Sizes of Studies of Resting Electrodermal Activity
Study Age Behavior pattern N
e
N
c
d
⫹
Arnett et al. (1993) Adult Psychopathy/sociopathy 31 32 ⫺0.30
Babcock et al. (2004) Adult Aggression 72 30 0.11
Beauchaine et al. (2001) Adolescent Conduct problems 20 22 ⫺0.65
Blackburn (1979) Adult Psychopathy/sociopathy 18 14 0.57
Blair (1999) Adolescent Psychopathy/sociopathy 16 15 ⫺0.37
Delamater & Lahey (1983) Child Conduct problems 21 0 ⫺1.02
Fox & Lippert (1963) Uncodable Psychopathy/sociopathy 10 10 ⫺1.17
Frodi & Lamb (1980) Adult Aggression 14 14 0.00
Garralda et al. (1989) Child Conduct problems 7 8 0.89
Haldeman (1973) Adult Psychopathy/sociopathy 30 10 ⫺0.42
Harden et al. (1995) Child Conduct problems 18 15 0.00
Hare (1965b) Uncodable Psychopathy/sociopathy 10 10 ⫺0.28
Hare (1968) Adult Psychopathy/sociopathy 39 12 ⫺0.51
Hare (1982) Adult Psychopathy/sociopathy 16 15 0.00
Hare & Craigen (1974) Adult Psychopathy/sociopathy 17 17 ⫺0.57
Hare et al. (1978) Adult Psychopathy/sociopathy 24 40 0.00
Herpertz, Wenning, et al. (2001) Child Conduct problems 26 21 ⫺0.09
Hinton et al. (1980) Adult Psychopathy/sociopathy 7 7 ⫺1.86
House & Milligan (1976) Adult Psychopathy/sociopathy 32 32 ⫺0.70
Ingersoll (1977) Adult Psychopathy/sociopathy 9 11 ⫺0.34
Ishikawa et al. (2001) Adult Psychopathy/sociopathy 29 26 ⫺0.36
Lippert & Senter (1966) Adolescent Psychopathy/sociopathy 21 21 0.00
Marchel (1993) Adolescent Conduct problems 40 40 0.07
McBurnett et al. (1993) Child Conduct problems 31 26 ⫺0.53
Milner (1976) Adult Psychopathy/sociopathy 30 0 0.11
Ogloff & Wong (1990) Adult Psychopathy/sociopathy 16 16 ⫺0.91
Schmidt et al. (1985) Child Conduct problems 11 11 ⫺0.29
Smithmyer (2001) Child Aggression 69 0 0.11
Steinberg & Schwartz (1976) Adult Psychopathy/sociopathy 10 12 0.00
Tucker (1991) Child Conduct problems 32 44 ⫺0.56
Witkin-Lanoil (1977) Adolescent Conduct problems 128 0 0.04
Wolfe et al. (1983) Adult Aggression 5 5 0.08
Zahn & Kruesi (1993) Child Conduct problems 27 31 0.21
Note. N for studies that reported correlations or other single-group analyses is reported in the N
e
column. N
e
⫽ number of participants in experimental
(i.e., aggressive, psychopathic/sociopathic, conduct problems) group; N
c
⫽ number of participants in control group; d
⫹
⫽ effect size weighted by reciprocal
of variance.
550
LORBER
Table A5
Coded Qualities and Weighted Effect Sizes of Studies of Task Electrodermal Activity
Study Age Behavior pattern Stimulus valence N
e
N
c
d
⫹
Aniskiewicz (1979) Adult Psychopathy/sociopathy Negative 13 13 ⫺0.81
Arnett et al. (1997) Adult Psychopathy/sociopathy Negative 29 29 ⫺0.78
Babcock et al. (2004) Adult Aggression Negative 72 30 0.13
Blackburn (1979) Adult Psychopathy/sociopathy Negative 18 14 0.00
Blair (1999) Child Psychopathy/sociopathy Negative 16 16 ⫺0.12
Blair et al. (1997) Adult Psychopathy/sociopathy Nonnegative 18 18 ⫺0.03
Borkovec (1970) Uncodable Psychopathy/sociopathy Nonnegative 19 46 ⫺0.49
Delamater & Lahey (1983) Child Conduct problems Nonnegative 19 17 ⫺0.63
Garralda et al. (1989) Child Conduct problems Nonnegative 15 7 0.04
Garralda et al. (1991) Child Conduct problems Nonnegative 25 25 ⫺0.52
Haldeman (1973) Adult Psychopathy/sociopathy Negative 30 10 ⫺0.16
Harden & Pihl (1995) Adolescent Conduct problems Negative 28 0 0.00
Harden et al. (1995) Child Conduct problems Uncodable 18 15 ⫺0.56
Hare (1965a) Uncodable Psychopathy/sociopathy Negative 10 10 ⫺0.52
Hare (1965b) Adult Psychopathy/sociopathy Nonnegative 12 12 ⫺0.84
Hare (1972) Adult Psychopathy/sociopathy Nonnegative 16 16 ⫺1.00
Hare (1978b) Adult Psychopathy/sociopathy Uncodable 32 32 ⫺0.66
Herpertz, Wenning, et al. (2001) Adult Psychopathy/sociopathy Uncodable 25 24 ⫺0.69
Herpertz, Werth, et al. (2001) Child Conduct problems Negative 26 21 ⫺0.74
Hinton et al. (1980) Adult Psychopathy/sociopathy Nonnegative 7 7 0.00
Ingersoll (1977) Adult Psychopathy/sociopathy Nonnegative 9 11 ⫺0.28
Ishikawa et al. (2001) Adult Psychopathy/sociopathy Nonnegative 29 26 ⫺0.24
Levenston et al. (2000) Adult Psychopathy/sociopathy Nonnegative 17 16 ⫺0.44
Lippert & Senter (1966) Adolescent Psychopathy/sociopathy Negative 21 21 ⫺0.62
Lykken (1957) Adult Psychopathy/sociopathy Negative 14 11 ⫺0.82
Mangina et al. (2000) Child Conduct problems Nonnegative 10 10 ⫺6.71
Marchel (1993) Adolescent Conduct problems Negative 40 40 ⫺0.05
McBurnett et al. (1993) Child Conduct problems Nonnegative 31 26 ⫺0.74
Milner (1976) Adult Psychopathy/sociopathy Negative 30 0 0.20
Plovnick (1976) Adolescent Psychopathy/sociopathy Nonnegative 311 0 0.00
Raine (1987) Adult Psychopathy/sociopathy Nonnegative 36 0 ⫺1.00
Raine & Venables (1981)
a
Adolescent Psychopathy/sociopathy Negative 41 0 ⫺0.55
Raine & Venables (1981)
a
Adolescent Conduct problems Negative 52 0 0.16
Raine & Venables (1984b)
a
Adolescent Psychopathy/sociopathy Nonnegative 49 0 0.06
Raine & Venables (1984b)
a
Adolescent Conduct problems Nonnegative 44 0 ⫺0.36
Schmidt et al. (1985) Child Conduct problems Nonnegative 11 11 0.00
Siddle et al. (1973) Adolescent Conduct problems Nonnegative 15 20 ⫺0.69
Sutker (1970) Adult Psychopathy/sociopathy Nonnegative 12 12 0.00
Tharp et al. (1980) Adult Psychopathy/sociopathy Negative 15 15 ⫺0.74
Tong (1959) Adult Aggression Nonnegative 19 22 0.42
Tucker (1991) Child Conduct problems Nonnegative 32 44 ⫺0.18
Waid (1975) Adult Psychopathy/sociopathy Nonnegative 10 17 ⫺0.77
Waid & Orne (1982) Adult Psychopathy/sociopathy Nonnegative 9 11 ⫺1.12
Waid et al. (1979) Adult Psychopathy/sociopathy Negative 12 13 ⫺0.82
Witkin-Lanoil (1977) Adolescent Conduct problems Nonnegative 128 0 ⫺0.09
Wolfe et al. (1983) Adult Aggression Negative 5 5 1.76
Zahn & Kruesi (1993) Child Aggression Nonnegative 63 0 ⫺0.18
Note. N for studies that reported correlations or other single-group analyses is reported in the N
e
column. N
e
⫽ number of participants in experimental
(i.e., aggressive, psychopathic/sociopathic, conduct problems) group; N
c
⫽ number of participants in control group; d
⫹
⫽ effect size weighted by reciprocal
of variance.
a
Multiple independent samples from a single study.
(Appendix continues)
551
PSYCHOPHYSIOLOGY OF AGGRESSION
Received March 7, 2002
Revision received October 18, 2003
Accepted October 20, 2003 䡲
Table A6
Coded Qualities and Weighted Effect Sizes of Studies of Electrodermal Reactivity
Study Age Behavior pattern Stimulus valence N
e
N
c
d
⫹
Babcock et al. (2004) Adult Aggression Negative 102 0 0.32
Friedrich et al. (1985) Adult Aggression Negative 14 15 0.00
Frodi & Lamb (1980) Adult Aggression Negative 14 14 0.91
Garralda et al. (1990) Uncodable Conduct problems Nonnegative 4 6 0.00
Hare (1965c) Adult Psychopathy/sociopathy Negative 11 11 ⫺0.88
Hare (1982) Adult Psychopathy/sociopathy Negative 14 12 ⫺0.66
Hare & Craigen (1974) Adult Psychopathy/sociopathy Negative 17 17 ⫺0.71
Hare et al. (1978) Adult Psychopathy/sociopathy Negative 12 52 ⫺0.50
Hare & Quinn (1971) Adult Psychopathy/sociopathy Negative 18 18 ⫺0.67
House & Milligan (1976) Adult Psychopathy/sociopathy Negative 32 32 ⫺0.77
Lippert & Senter (1966) Adolescent Psychopathy/sociopathy Nonnegative 21 21 0.00
Lykken (1957) Adult Psychopathy/sociopathy Negative 18 11 ⫺0.76
Marchel (1993) Adolescent Aggression Negative 80 0 ⫺0.72
Mathis (1970) Adult Psychopathy/sociopathy Uncodable 20 20 0.00
Milner (1976) Adult Psychopathy/sociopathy Negative 29 0 0.21
Patrick et al. (1994) Adult Psychopathy/sociopathy Nonnegative 35 18 0.00
Raskin & Hare (1978) Adult Psychopathy/sociopathy Negative 24 24 0.00
Schmauk (1970) Adult Psychopathy/sociopathy Negative 10 10 ⫺1.35
Smithmyer (2001) Child Aggression Nonnegative 69 0 ⫺0.12
Sutker (1970) Adult Psychopathy/sociopathy Negative 12 12 0.82
Note. N for studies that reported correlations or other single-group analyses is reported in the N
e
column. N
e
⫽ number of participants in experimental
(i.e., aggressive, psychopathic/sociopathic, conduct problems) group; N
c
⫽ number of participants in control group; d
⫹
⫽ effect size weighted by reciprocal
of variance.
552
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