Adrian Raine

Biosocial Studies of Antisocial and Violent Behavior in Children and Adults: A Review

Despite increasing knowledge of social and biological risk factors for antisocial and violent behavior, we know surprisingly little about how these two sets of risk factors interact. This paper documents 39 empirical examples of biosocial interaction effects for antisocial behavior from the areas of genetics, psychophysiology, obstetrics, brain imaging, neuropsychology, neurology, hormones, neurotransmitters, and environmental toxins. Two main themes emerge. First, when biological and social factors are grouping variables and when antisocial behavior is the outcome, then the presence of both risk factors exponentially increases the rates of antisocial and violent behavior. Second, when social and antisocial variables are grouping variables and biological functioning is the outcome, then the social variable invariably moderates the antisocial–biology relationship such that these relationships are strongest in those from benign home backgrounds. It is argued that further biosocial research is critical for establishing a new generation of more successful intervention and prevention research.

Reduced Prefrontal and Increased Subcortical Brain Functioning Assessed Using Positron Emission Tomography in Predatory and Affective Murderers

There appear to be no brain imaging studies investigating which brain mechanisms subserve affective, impulsive violence versus planned, predatory violence. It was hypothesized that affectively violent offenders would have lower prefrontal activity, higher subcortical activity, and reduced prefrontal/subcortical ratios relative to controls, while predatory violent offenders would show relatively normal brain functioning. Glucose metabolism was assessed using positron emission tomography in 41 comparisons, 15 predatory murderers, and nine affective murderers in left and right hemisphere prefrontal (medial and lateral) and subcortical (amygdala, midbrain, hippocampus, and thalamus) regions. Affective murderers relative to comparisons had lower left and right prefrontal functioning, higher right hemisphere subcortical functioning, and lower right hemisphere prefrontal/subcortical ratios. In contrast, predatory murderers had prefrontal functioning that was more equivalent to comparisons, while also having excessively high right subcortical activity. Results support the hypothesis that emotional, unplanned impulsive murderers are less able to regulate and control aggressive impulses generated from subcortical structures due to deficient prefrontal regulation. It is hypothesized that excessive subcortical activity predisposes to aggressive behaviour, but that while predatory murderers have sufficiently good prefrontal functioning to regulate these aggressive impulses, the affective murderers lack such prefrontal control over emotion regulation.

Prefrontal Structural and Functional Brain Imaging findings in Antisocial, Violent, and Psychopathic Individuals: A Meta-Analysis

Brain-imaging studies suggest that antisocial and violent behavior is associated with structural and functional deficits in the prefrontal cortex, but there is heterogeneity in findings and it is unclear whether findings apply to psychopaths, non-violent offenders, community-based samples, and studies employing psychiatric controls. A meta-analysis was conducted on 43 structural and functional imaging studies, and the results show significantly reduced prefrontal structure and function in antisocial individuals. Effect sizes were significant for both structural and functional studies. With minor exceptions, no statistically significant moderating effects of sample characteristics and methodological variables were observed. Findings were localized to the right orbitofrontal cortex, right anterior cingulate cortex, and left dorsolateral prefrontal cortex. Findings confirm the replicability of prefrontal structural and functional impairments in antisocial populations and highlight the involvement of orbitofrontal, dorsolateral frontal, and anterior cingulate cortex in antisocial behavior.

Annotation: The role of prefrontal deficits, low autonomic arousal, and early health factors in the development of antisocial and aggressive behavior in children

BACKGROUND This article selectively reviews the biological bases of antisocial and aggressive behavior in children with a focus on low autonomic functioning, prefrontal deficits, and early health factors. RESULTS Low resting heart rate is thought to be the best-replicated biological correlate of antisocial and aggressive behavior in child and adolescent populations and may reflect reduced noradrenergic functioning and a fearless, stimulation-seeking temperament. Evidence from neuropsychological, neurological, and brain imaging studies converges on the conclusion that prefrontal structural and functional deficits are related to antisocial, aggressive behavior throughout the lifespan. A prefrontal dysfunction theory of antisocial behavior is advanced. This argues that social and executive function demands of late adolescence overload the late developing prefrontal cortex, giving rise to prefrontal dysfunction and a lack of inhibitory control over antisocial, violent behavior that peaks at this age. Birth complications and minor physical anomalies are selectively associated with later violent behavior, especially when combined with adverse psychosocial risk factors for violence. Cigarette smoking during pregnancy may increase the risk for antisocial and violent behavior in later life by disrupting noradrenergic functioning and enhancement of cholinergic receptors that inhibit cardiac functioning. Malnutrition during pregnancy is associated with later antisocial behavior and may be mediated by protein deficiency. CONCLUSIONS It is argued that early health intervention and prevention studies may provide the most effective way of reversing biological deficits that predispose to antisocial and aggressive behavior in children and adults.

Brain abnormalities in murderers indicated by positron emission tomography

Murderers pleading not guilty by reason of insanity (NGRI) are thought to have brain dysfunction, but there have been no previous studies reporting direct measures of both cortical and subcortical brain functioning in this specific group. Positron emission tomography brain imaging using a continuous performance challenge task was conducted on 41 murderers pleading not guilty by reason of insanity and 41 age- and sex-matched controls. Murderers were characterized by reduced glucose metabolism in the prefrontal cortex, superior parietal gyrus, left angular gyrus, and the corpus callosum, while abnormal asymmetries of activity (left hemisphere lower than right) were also found in the amygdala, thalamus, and medial temporal lobe. These preliminary findings provide initial indications of a network of abnormal cortical and subcortical brain processes that may predispose to violence in murderers pleading NGRI.

Selective reductions in prefrontal glucose metabolism in murderers.

This study tests the hypothesis that seriously violent offenders pleading not guilty by reason of insanity or incompetent to stand trial are characterized by prefrontal dysfunction. This hypothesis was tested in a group of 22 subjects accused of murder and 22 age-matched and gender-matched controls by measuring local cerebral uptake of glucose using positron emission tomography during the continuous performance task. Murderers had significantly lower glucose metabolism in both lateral and medial prefrontal cortex relative to controls. No group differences were observed for posterior frontal, temporal, and parietal glucose metabolism, indicating regional specificity for the prefrontal deficit. Group differences were not found to be a function of raised levels of left-handedness, schizophrenia, ethnic minority status, head injury, or motivation deficits in the murder group. These preliminary results suggest that deficits localized to the prefrontal cortex may be related to violence in a selected group of offenders, although further studies are needed to establish the generalizability of these findings to violent offenders in the community.

Heart Rate Level and Antisocial Behavior in Children and Adolescents: A Meta-Analysis

OBJECTIVE To assess whether antisocial children are characterized by low heart rate. METHOD A meta-analysis was conducted on 45 independent effect sizes of the resting heart rate-antisocial behavior relationship obtained from 40 studies meeting inclusion and exclusion criteria. Studies were conducted between 1971 to 2002 using a total of 5,868 children. A secondary meta-analysis was also conducted on heart rate during a stressor. RESULTS Significant overall effect sizes were found for both resting heart rate (d = -0.44, p <.0001) and heart during a stressor (d = -0.76, p <.0001). Gender, age, method of recording, use of psychiatric control group, recruitment source, concurrent versus prospective nature of testing, and source of behavioral rating all failed to moderate this relationship. CONCLUSIONS Low resting heart rate appears to be the best-replicated biological correlate to date of antisocial behavior in children and adolescents. Several theoretical interpretations of this relationship are outlined that should be examined in future studies.

Neurocognitive impairments in boys on the life-course persistent antisocial path.

This study addresses 5 unresolved issues in the neuropsychology of antisocial behavior using a community sample of 325 school boys in whom neurocognitive measures were assessed at age 16-17 years. Antisocial behavior measures collected from age 7-17 years were cluster analyzed and produced 4 groups: control, childhood-limited, adolescent-limited, and life-course persistent. Those on the lifecourse persistent path and also on the childhood-limited path were particularly impaired on spatial and memory functions. Impairments were independent of abuse, psychosocial adversity, head injury, and hyperactivity. Findings provide some support for the life-course persistent versus adolescent-limited theory of antisocial behavior and suggest that (a) neurocognitive impairments are profound and not artifactual and (b) childhood-limited antisocials may not be free of long-lasting functional impairment.

Neural foundations to moral reasoning and antisocial behavior

A common feature of the antisocial, rule-breaking behavior that is central to criminal, violent and psychopathic individuals is the failure to follow moral guidelines. This review summarizes key findings from brain imaging research on both antisocial behavior and moral reasoning, and integrates these findings into a neural moral model of antisocial behavior. Key areas found to be functionally or structurally impaired in antisocial populations include dorsal and ventral regions of the prefrontal cortex (PFC), amygdala, hippocampus, angular gyrus, anterior cingulate and temporal cortex. Regions most commonly activated in moral judgment tasks consist of the polar/medial and ventral PFC, amygdala, angular gyrus and posterior cingulate. It is hypothesized that the rule-breaking behavior common to antisocial, violent and psychopathic individuals is in part due to impairments in some of the structures (dorsal and ventral PFC, amygdala and angular gyrus) subserving moral cognition and emotion. Impairments to the emotional component that comprises the feeling of what is moral is viewed as the primary deficit in antisocials, although some disruption to the cognitive and cognitive-emotional components of morality (particularly self-referential thinking and emotion regulation) cannot be ruled out. While this neurobiological predisposition is likely only one of several biosocial processes involved in the etiology of antisocial behavior, it raises significant moral issues for the legal system and neuroethics.

A scale for the measurement of schizotypy

Abstract This paper reports the development of a short scale for the measurement of two aspects of schizotypy for use in general population studies. It was intended for use particularly in a ‘high-risk’ study in Mauritius but only the development of the scale in Britain is described in this paper. The two aspects measured are those concerned with cognitive/perceptual/attentional function, on the one hand; and social dysfunction and anhedonia, and physical anhedonia on the other. These might be called the ‘positive’ and ‘negative’ aspects of schizotypy, possibly having some parallels to the postive and negative symptoms of schizophrenia. The work described indicates that both aspects can be measured with reliability and with stability of factor structure from study to study. A number of studies are described in which the questionnaire, or earlier versions of it are used. These all indicate that the scales have good construct validity.