An Overview of Biological Influences on Violent Behavior

Klaus A. Miczek, Allan F. Mirsky, Gregory Carey, Joseph DeBold, and Adrian Raine

Even the most complex social environmental influences on an individual's propensity to engage in violent behavior may eventually be traced to their biologic bases. In order to sketch such an interactive model, it is useful to begin with a consideration of the genetic influences on violent behavior as studied in animals as well as humans. Steroid and peptide hormones as well as peptides and biogenic amines are critically important in the neural and physiologic mechanisms initiating, executing, and coping with violent behavior. It is here that important endocrine and pharmacologic interventions are targeted. These neurochemical systems mediating violent behavior are specific to discrete neuroanatomic networks. Indirect measures of neural mechanisms of violent behavior may be obtained via neuroimaging and functional neuropsychologic assessments.

GENETIC MECHANISMS

Behavioral genetic research has shown that genes influence individual differences in a wide range of human behaviors—cognition,

Klaus Miczek is at the Department of Psychology. Tufts University; Allan Mirsky is at the National Institutes of Health; Gregory Carey is at the Institute of Behavior Genetics, University of Colorado; Joseph DeBold is at the Department of Psychology, Tufts University; and Adrian Raine is at the University of Southern California.



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Understanding and Preventing Violence: Volume 2, Biobehavioral Influences An Overview of Biological Influences on Violent Behavior Klaus A. Miczek, Allan F. Mirsky, Gregory Carey, Joseph DeBold, and Adrian Raine Even the most complex social environmental influences on an individual's propensity to engage in violent behavior may eventually be traced to their biologic bases. In order to sketch such an interactive model, it is useful to begin with a consideration of the genetic influences on violent behavior as studied in animals as well as humans. Steroid and peptide hormones as well as peptides and biogenic amines are critically important in the neural and physiologic mechanisms initiating, executing, and coping with violent behavior. It is here that important endocrine and pharmacologic interventions are targeted. These neurochemical systems mediating violent behavior are specific to discrete neuroanatomic networks. Indirect measures of neural mechanisms of violent behavior may be obtained via neuroimaging and functional neuropsychologic assessments. GENETIC MECHANISMS Behavioral genetic research has shown that genes influence individual differences in a wide range of human behaviors—cognition, Klaus Miczek is at the Department of Psychology. Tufts University; Allan Mirsky is at the National Institutes of Health; Gregory Carey is at the Institute of Behavior Genetics, University of Colorado; Joseph DeBold is at the Department of Psychology, Tufts University; and Adrian Raine is at the University of Southern California.

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Understanding and Preventing Violence: Volume 2, Biobehavioral Influences academic achievement, personality and temperament (including such traits as aggression and hostility), psychopathology, and even vocational interests and social attitudes (Plomin et al., 1989). Hence, a research finding that criminal or violent behavior had some heritable component would come as no surprise—especially since violent and criminal behaviors are themselves correlated with some of the other behaviors for which genetic relationships have been established. Beyond confirming the existence of heritability in violent behavior, the more interesting intellectual challenges are isolating the precise nature of the mechanisms through which an individual's propensity to engage in or refrain from violent behavior may be inherited; using quantitative methodology to control for heritable influences so that conclusions about environmental influences on violent behavior can be clarified; and quantifying the genetic effect in terms of its importance or triviality in explaining human behavior and the magnitude of its correlation with risk factors for violence. On the first challenge, quantitative genetic studies have not isolated any simple genetic syndrome, either Mendelian or chromosomal, that is invariably associated with violence or, more broadly, with antisocial behavior. Like inherited propensities for other behaviors, a genetic liability toward violence is likely to involve many genes and substantial environmental variation. The existence of such mechanisms may well be confirmed by future quantitative genetic research, but knowledge of their precise nature must await progress in detecting genes—and markers linked to them—that account for small variations in behavior, a problem in molecular biology that lies beyond the scope of this paper. The second challenge suggests a more promising line of research than the reiteration of long-standing, sterile ''nature versus nurture" debates—that genetic research designs may clarify environmental effects. This can best be illustrated by a hypothetical example. Suppose that a propensity toward violent behavior is transmitted from parent to offspring by two mechanisms: one operating through the genes and the other through social learning. How can these two mechanisms be detected and quantified in a study of intact nuclear families? If the parent-offspring correlation is interpreted solely in terms of social learning, then the environmental transmission will be overestimated. On the other hand, if the correlation is interpreted solely in terms of genetic transmission, then the social learning of aggression will be over-looked.

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Understanding and Preventing Violence: Volume 2, Biobehavioral Influences Twin studies, studies of adoptive parent-offspring pairs, and studies of the biologic parents of adoptees are required to untangle the joint effects of genetic and family environmental transmission. Although such designs are becoming routine in the study of cognitive development, they are rare in the study of violent behavior. The third challenge aims at determining whether a genetic propensity to violence is substantial or trivial and the extent to which it is correlated with other behaviors. Does the genetic influence on intelligence and on alcohol abuse explain genetic liability toward aggression? STUDIES OF HUMANS Studies of the inheritance of violent behavior in humans rely on adoption or twin designs to tease apart the effects of shared family environment from those of shared genes. The adoption design capitalizes on the fact that an adoptee does not receive environmental transmission from a biological parent or genetic transmission from an adoptive parent. Similarly, adoptive siblings share environments but not genes, whereas biological siblings raised apart share genes but not environments. Twin studies rely on the fact that identical twins have all genes in common, whereas fraternal pairs share on average only half their genes (plus a small effect from assortative mating). In both kinds of studies, heritability coefficients—the proportion of observed variation due to genetic variation—may be calculated. As with all human behaviors, the interpretation of these coefficients may be confounded by several factors—selective placement in adoptions, and imitation and co-offending in twins. In addition, the study of violence presents problems of its own. Not only is the base rate for violence low, but it is also more poorly measured than most behaviors studies by behavior geneticists. Despite methodologic weaknesses in the early twin studies, later twin and adoption research suggests important heritability for adult antisocial behavior with perhaps a smaller genetic influence on juvenile criminality (Bohman et al., 1982; Christiansen, 1977; Cloninger and Gottesman, 1987; Mednick et al., 1984). Heritability estimates range from a low of about .20 to a high of almost .70 in Danish samples. Needless to say, such estimates cannot be easily extrapolated to other cultures. In contrast to these data, the evidence for a genetic basis to violent offending is much weaker. Only three samples permit one

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Understanding and Preventing Violence: Volume 2, Biobehavioral Influences to assess the role of genetics in violent offending, and two of the three produced nonsignificant results. These findings suggest at most a weak role for heredity in violent behavior. But studies that use samples at high risk for violent behavior or that measure violent behavior through self-reports rather than arrest records may yet discover genetic relationships that have so far remained hidden—or underestimated—because arrests for violent offenses are rare in samples of the general population. One positive lead is the correlation between violence in biological parents and alcohol abuse in adopted-away sons. This suggests a genetic relationship between the two, an important link given the well-established correlation between alcohol and violent behavior as discussed below (see Miczek et al., Volume 3). Because many violent offenders also commit nonviolent offenses, heritability for criminality per se provides another possible link between genes and violence. Finally and perhaps most importantly, the gene-environment interaction reported for antisocial behavior (Cloninger et al., 1982; Cadoret et al., 1983) may also extend to violence. The principles of quantitative genetics raise strong cautions about the extrapolation of empirical research findings on violence. First, evidence for the heritability of individual differences within a population cannot be used to explain average differences between populations or even within the same population over time. It is unlikely that genetic differences could account for anything but a small fraction of the change in violence over the twentieth century, differences in violent crimes among nations, or variance in rates among certain subgroups within a nation. Second, heritability cannot predict or explain an individual's culpability in a particular violent event. Third, many estimates of heritability are based on data from the Scandinavian countries, where the necessary data are routinely collected in national registries. Because the environmental variance relevant to violence may not be the same in the Scandinavian countries and in the United States, for example, the heritability estimates cannot be readily extrapolated. STUDIES OF ANIMALS A large number of strain comparisons and the successful establishment of selected lines demonstrate significant heritability for rodent aggression (Ebert and Sawyer, 1980; Lagerspetz and Lagerspetz, 1975; Scott, 1942, 1966; van Oortmerssen and Bakker,

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Understanding and Preventing Violence: Volume 2, Biobehavioral Influences 1981). Although there is controversy over the extent to which the genetic mechanisms are the same for male and female aggression in Mus, the testing situation can change the rank order of selected lines (Hood and Cairns, 1988)—females from high-aggression lines exhibit their agonistic behavior mostly in sex-appropriate settings (e.g., postpartum tests). Similarly, studies of selected lines show that aggression may be modified by experience. Thus, although agonistic behavior shows some developmental continuity and cross-situational generality in inbred or selected strains, it is clearly not a single genetic phenomenon that can be studied in isolation from specific contextual cues, social environment, and development (e.g., Cairns et al., 1990; Jones and Brain, 1987). The recent trend in behavior genetic research is less toward demonstrating the fact of the heritability of aggression and more on elucidating its genetic correlates and identifying genetic loci that underlie agonistic behavior. Here, the Y chromosome may contribute to individual differences in male aggression in the mouse, at least in some strains (Carlier et al., 1990; Maxson et al., 1989; Selmanoff et al., 1975). There also appears to be genetic sensitivity to the effects of early neonatal androgens on aggression in mice (e.g., Vale et al., 1972; Michard-Vanhee, 1988). NEUROCHEMICAL MECHANISMS ENDOCRINE MECHANISMS AND VIOLENT BEHAVIOR Steroids Research suggests that testosterone and its androgenic and estrogenic metabolites influence the probability of aggressive responding to environmental events and stimuli through organizational as well as activational mechanisms. Organizational effects are traditionally those exerted, generally permanently, by a hormone during some sensitive period of development. This type of mechanism appears to explain sex differences in anatomy and some aspects of sex differences in behavior. For example, testosterone present during a particular period of fetal development in mammals induces the development of the male reproductive tract and genitalia. If androgen levels are low, as is normally the case in females, this development does not occur and female genitalia develop instead. A similar control for male aggression has been demonstrated in a number of laboratory animal species. For example, female mice given a single injection of testosterone at

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Understanding and Preventing Violence: Volume 2, Biobehavioral Influences birth become much more sensitive to the aggression-enhancing effects of androgens as adults. Prenatal treatment of female rhesus monkeys with testosterone results in females that are male-like in their higher level of "rough and tumble" play as juveniles and more aggressive as adults. In humans, there is evidence for a similar, but reduced in magnitude, modulation of aggression by androgens. This research uses children that were accidentally exposed to inappropriate steroids during fetal development and assesses their behavior though observations, interviews, and psychologic assessments. In girls prenatally exposed to heightened levels of androgens, there is a trend for increased levels of aggression. In boys exposed to estrogens or antiandrogenic steroids during pregnancy, there is a trend for decreased aggressiveness (see Brain, Table 4 in this volume). However, generally these steroids also have had some effect on genital development and the behavioral differences may be due to altered body image or to the affected children being treated differently by parents or peers. Interestingly, prenatal testosterone also alters the development of parts of the preoptic area of the brain. Preoptic area structure and neurochemistry are sexually dimorphic in animals and in humans, and this brain area is also thought to have a role in aggressive behavior. However, a direct link between the sexual dimorphism of the preoptic area and human violent behavior remains elusive. In animals, testosterone (or its metabolites) has effects on the probability of aggressive response to conspecifics or other environmental events. This is frequently referred to as an activational effect although, mechanistically, androgens are not stimulating aggressive behavior in vacuo; more accurately, they appear to be altering the response to aggression-provoking stimuli. In laboratory animals, particularly rodents, there is research that demonstrates the brain sites involved in this action and the importance of the biochemical mechanisms by which testosterone can alter neural activity. The strength of the modulation that testosterone exerts on aggressive behavior seems to decrease in more complex social animals. In nonhuman primates, the correlation between testosterone and aggressiveness or dominance frequently, but not in all studies, exists, but the activational effect of testosterone is more variable and harder to demonstrate. This trend is perhaps more exaggerated in humans. Positive correlations have been reported between androgen levels and aggressive or violent behavior in adolescent boys and in men, but these correlations are not high, they are sometimes difficult to replicate, and importantly, they do not demonstrate causation. In fact there is better evidence

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Understanding and Preventing Violence: Volume 2, Biobehavioral Influences for the reverse relationship (behavior altering hormonal levels). Stress (e.g., from being subject to aggression or being defeated) decreases androgen levels, and winning—even in innocuous laboratory competitions—can increase testosterone. The results of manipulating androgens with antiandrogen therapy in violent offenders are also mixed and difficult to interpret because of confounding influences on the data collection. Some critical reviews have concluded that antiandrogens show promise as an adjunct therapy for violent sex offenders. These may be relying more on the clearer relationship between testosterone and sexual motivation than between testosterone and violence. Another interesting approach will be to study the effects of anabolic steroids, but these studies have just begun and face very difficult methodologic problems. In general, most investigators conclude that there can be an influence of androgens on violence but that it is only one component accounting for a small amount of the variance. Gonadal steroids have also been postulated to be involved in the increased irritability and hostility seen in some women with premenstrual syndrome (PMS). However, the endocrine evidence in support of this view is weak, and most recent papers find that individual differences in estrogens, progestins, and other hormones across the menstrual cycle do not explain the variability in intensity of PMS symptoms. Adrenal steroids (glucocorticoids, such as cortisol and corticosterone) and the pituitary hormone ACTH (adrenocorticotropic hormone) have also been found to be related to aggressive behavior in animals. However, the strongest relationship is a negative one. Chronically increased levels of corticosteroids decrease aggressiveness, and ACTH increases submissiveness and avoidance of attack. These two effects are difficult to separate endocrinologically, but they appear to be mediated by different mechanisms. Correlations between dominance and corticosteroid levels in primates may more directly reflect variations in the ability to adapt to stress. In summary, there is no simple relationship between steroids and aggression, much less violence. The strongest conclusion is that in humans, androgens can influence and be influenced by aggressive behavior. However, they are only one of many influences and not the determining factor. The opposite relationship (i.e., the environment and behavior influencing hormone secretion) is the stronger of the two linkages.

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Understanding and Preventing Violence: Volume 2, Biobehavioral Influences Other Hormones Steroids are not the only hormones that have been related to aggression and violence, but other hormones appear to have less direct or less specific effects. For example, adrenal norepinephrine secretion has been related to the commission of violent crime, but norepinephrine and epinephrine are released in response to a wide variety of arousing or emotional conditions and are important in coping with stress. Animal and clinical studies have found evidence for a role of central nervous system (CNS) norepinephrine in aggressiveness—but when it acts as a neurotransmitter, not as a hormone. Because hormones can alter many aspects of cellular activity and because aggressive behavior involves so many areas of the brain, the potential for indirect or secondary effects of hormones is high. In summary, there is no simple relationship between hormones and aggression, much less violence. The strongest conclusion is that in humans, steroids can influence and be influenced by aggressive behavior. However, they are only one influence of many and not the determining factor. The opposite relationship (i.e., the environment and behavior influence on hormone secretion) is the stronger of the two linkages. NEUROTRANSMITTERS AND RECEPTORS Dopamine Evidence from animal studies points to large changes in brain dopamine systems during aggressive or defensive behavior. At present, evidence for similarly altered dopamine activity in brain regions of violent humans is not available. It is possible that brain dopamine systems are particularly significant in the rewarding aspects of violent and aggressive behavior. However, at present, a "marker" for some aspect of brain dopamine activity that is selective to a specific kind of aggression or violent behavior has not been identified in any of the accessible bodily fluids or via imaging methods in the brain. The most frequently used treatment of violent outbursts in emergency situations and also in long-term medication of violence-prone individuals employs drugs that act principally at dopamine receptors. Particularly, drugs that antagonize the D2 subtype of dopamine receptors represent widely used antipsychotics with frequent application to violent patients. Evidence from animal and human studies emphasizes the many debilitating side effects of these drugs

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Understanding and Preventing Violence: Volume 2, Biobehavioral Influences that render them problematic as treatment options, representing little more than a form of "chemical restraint." Antipsychotic drugs that are antagonists at D2 dopamine receptors show a wide range of behavioral activities and, when used chronically, lead to various neurologic problems. Cocaine and amphetamine activate behavior and engender euphoria in all likelihood via action on brain dopamine receptors. The broad spectrum of behavioral and mood-elevating effects of these drugs may also include the aggression-enhancing effects that are seen in animals under certain conditions and that may be relevant to the occasional incidence of human violence after psychomotor stimulants. More important, however, are the psychopathic conditions that precede chronic amphetamine or cocaine use in predicting violent outbursts. Whether the paranoid psychosis due to amphetamine or cocaine use represents the causative condition for occasional violent behavior or the psychopathology preceding drug use is unclear at present. The relatively infrequent occurrences of violent activities in stimulant abusers appear to result from brain dopamine changes that are counteracted by treatment with antipsychotic drugs. Norepinephrine Behavioral events involving intense affect are accompanied by adrenergic activity, in both the peripheral and the central nervous system. For several decades, the adrenergic contribution to the "flight-fight" syndrome in the form of increased sympathetic innervation as well as adrenal output has been well established. More recently, large changes in noradrenergic neurotransmitter activity in limbic, diencephalic, and mesencephalic regions, while preparing for, executing, and recovering from highly arousing activities—among them aggressive and violent behavior—have been documented. So far, in neither animal nor human studies have noradrenergic "markers" emerged that selectively identify the propensity to engage in an aggressive or violent act. Rather, noradrenergic activity, either measured in the form of metabolite levels in a bodily fluid or indirectly assessed in a sympathetically innervated end organ, is correlated with the level of general arousal, degree of behavioral exertion and activation, and either positive or negative affect, but not with a specific behavior or mood change such as a violent act. The most significant development during the past dozen years in applying noradrenergic drugs in the management and treatment of retarded, schizophrenic, or autistic patients with a high rate of

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Understanding and Preventing Violence: Volume 2, Biobehavioral Influences violent behavior is the use of beta-blockers primarily for their effects on the central nervous system rather than for their autonomic effects. Drugs that block adrenergic beta-receptors also act on certain subtypes of serotonin receptors, and their aggression-reducing effects may be derived from their action on these latter sites. Beta-blockers have not been compared in effectiveness and side effects, particularly during long-term treatment, with other therapeutic agents that reduce aggressive and violent activities. Clonidine, an adrenergic drug that targets a specific alpha-receptor subtype, has been used with success in managing withdrawal from alcohol, nicotine, and opiate addiction. Evidence from animal and human studies demonstrates that withdrawal states are often associated with irritability and a higher incidence of aggressive and defensive acts. The application of therapeutic agents with increasing selectivity for adrenergic receptor subtypes to managing and treating patients with violent outbursts represents an important therapeutic alternative to the classic antipsychotics. Serotonin (5-Hydroxytryptamine) For the past 30 years, the most intensively studied amine in violent individuals has been serotonin. Evidence from studies ranging from invertebrates to primates highlights marked changes in aspects of serotonin activity in bodily fluids or neural tissue in individuals that have engaged in violent and aggressive behavior on repeated occasions. There is considerable evolutionary variation in the role of serotonin in mediating aggressive or violent behavior across animal species, functionally divergent roles even being represented at the nonhuman primate level. In psychiatric studies, deficits in serotonin synthesis, release, and metabolism have been explored as potential "markers" for certain types of alcoholic and personality disorders with poor impulse control. It is very difficult to extract, from single measures of whole brain serotonin or blood levels, activity information that is specific to past violent behavior, or represents a risk for future propensity, without also considering seasonal and circadian rhythmicity, level of arousal, nutritional status, or past drug history, particularly alcohol abuse. No single type or class of violent activity has emerged as being specifically linked to a "trait" serotonin metabolite level. However, challenges with pharmacologic probes and physiologic or environmental stresses begin to reveal an important profile of serotonin-mediated response patterns.

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Understanding and Preventing Violence: Volume 2, Biobehavioral Influences During the past decade, remarkable advances in serotonin receptor pharmacology have promised to yield important new therapeutic options. Evidence from animal studies suggest that drugs with specific actions at certain serotonin receptors selectively decrease several types of aggressive behavior. A new class of antianxiety drugs that target certain serotonin receptors is currently finding acceptance in clinical practice. However, specific antiaggressive effects have not been demonstrated for the serotonin anxiolytics. In humans, brain imaging of serotonin receptors begins to point to distinct alterations in serotonin receptor populations in subgroups of affectively disordered patients. These ongoing developments promise to be significant for diagnostic and therapeutic applications to violent individuals. Sensational incidents of violence have been linked to the use of hallucinogens that act at distinct serotonin receptor subtypes. However, little is known as to whether or not the action at serotonin receptors is the actual mechanism by which these substances engender violent outbursts in rare, possibly psychopathic individuals. Gamma-Aminobutyric Acid—Benzodiazepine Receptors Thirty percent of all synapses in the brain use gamma-aminobutyric acid (GABA), and many of the GABA-containing neurons are inhibitory in nature. This cellular inhibitory role has been postulated to apply also to the physiologic and behavioral levels, including aggression. However, the present neurochemical evidence from animal studies finds inhibitory as well as excitatory influences of GABA manipulations on different aggressive patterns in discrete brain regions. Interest in GABA is currently intense because one subtype of GABA receptor (GABA-A) forms a supramolecular complex that also localizes benzodiazepine receptors and that also is the site of action for certain alcohol effects. These receptors are the site of action for the most important antianxiety substances that have also been used for their antiaggressive properties. Evidence from animal and human studies documents the effectiveness of benzodiazepine anxiolytic for their calming and quieting effects. However, under certain pharmacologic and physiologic conditions, at low doses benzodiazepine anxiolytics may increase aggressive behavior in animals and humans, leading sometimes to violent outbursts that are termed "paradoxical rage." The study of the benzodiazepine-GABA-A receptor complex in

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Understanding and Preventing Violence: Volume 2, Biobehavioral Influences individuals with a high rate of violent behavior promises to enhance the currently available diagnostic and therapeutic tools for the management of violence. BRAIN MECHANISMS AND VIOLENT BEHAVIOR NEUROANATOMIC APPROACH Physiologic research on aggression in animals has discovered that different neural circuits appear to underlie ''predatory attack" behavior as opposed to "affective defense" in animals (Siegel and Edinger, 1981, 1983; Siegel and Brutus, 1990). Sites in which electrical stimulation elicits predatory attack behavior in the cat include midbrain periaqueductal gray matter, the locus ceruleus, substantia innominata, and central nucleus of the amygdala. Brain sites that mediate affective defense reactions in the cat include the medial hypothalamus and the dorsal aspect of periaqueductal gray matter. In general, limbic structures such as the amygdala, hypothalamus, midbrain periaqueductal gray, and septal area, as well as cortical areas such as the prefrontal cortex and the anterior cingulate gyrus, contain networks of excitatory and inhibitory processes of different kinds of aggressive and defensive behavior. Aggression in animals largely reflects an adaptive response when viewed within an evolutionary framework. Whether or not violent offending in humans constitutes an instrumental act that can be viewed as adaptive is open to question. Nevertheless, the distinction between quiet, predatory, planned attack, on the one hand, and affective, explosive aggression occurring in the context of high autonomic arousal may be of heuristic value for understanding human violence. Possibly, cat (or rat) models could serve as effective screening methods to identify new drugs—some for control of "cold calculated" aggression, others for control of "explosive" aggression. Neuroanatomic and neuropsychologic studies are needed, however, to determine whether disruption of different brain mechanisms is indeed implicated in these two forms of aggression in humans. Data on the neuroanatomy of violence in humans stem largely from clinical studies of the effects of epileptic activity and other forms of brain damage on behavior, as well as from reports of the effects of brain resections on control of violent behavior (i.e., psychosurgery). Psychosurgical studies in Japan, India, and the United States have aimed at destroying portions of the limbic system, especially the amygdala and medial hypothalamus, in cases

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Understanding and Preventing Violence: Volume 2, Biobehavioral Influences of patients with uncontrollable violence. Other symptoms have been targeted for psychosurgical treatment, as well. Favorable outcomes are reported, but clinical improvement has been variable; moreover, the basis for assessing success is controversial (see Mirsky and Siegel, in this volume; O'Callaghan and Carroll, 1987). Several studies suggest a link between violence and temporal lobe epilepsy, although violence occurring during a seizure is extremely rare (Mirsky and Siegel, in this volume). The question remains unanswered as to whether some patients with seizure disorders are more violence prone (because of their putative heightened emotionality) than other persons. Another important question that remains unanswered to date concerns whether these limbic system structures (portions of the temporal lobe, hippocampus, amygdala, hypothalamus) are also implicated in ostensibly "normal" criminally violent offenders who are not preselected under the suspicion of neural abnormalities. Brain imaging techniques constitute one relatively new methodology for addressing such questions. Clinical case studies of patients with damage to the prefrontal lobes provide some support for a link between this area and features of psychopathic behavior; however, the overlap between these two syndromes is only partial. Given the animal data implicating the prefrontal cortex in the inhibition of aggression, together with neuropsychologic data on frontal dysfunction in violence, it would seem important to pursue research linking this brain site with violence. Studies are needed that combine brain imaging and social, cognitive, emotional or affective measures in order to assess both direct and indirect relationships between the prefrontal cortex and violence in humans. NEUROPSYCHOLOGIC APPROACH A large number of studies have found that violent offenders have brain dysfunction as reflected in deficits on neuropsychologic tests (e.g., Bryant et al., 1984; see review in Mirsky and Siegel, in this volume). Although the etiological implications of these deficits are not fully understood, there is converging evidence that cognitive deficits may underlie early school failure, dropouts, alcohol and drug use, and ultimately, encounters with the legal system as violent offenders. An important issue requiring resolution concerns whether neuropsychologic disturbances are a cause or an effect of violence. Left-hemisphere dysfunction that disrupts linguistic processing may be causal with respect to violence in that poorer verbal comprehension

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Understanding and Preventing Violence: Volume 2, Biobehavioral Influences and communication may contribute to a misinterpretation of events and motives in an interpersonal encounter; this in turn could precipitate a violent encounter. Similarly, poor verbal abilities and communication skills could contribute to peer rejection in childhood, which in combination with other later social and situational factors could predispose to alienation and, ultimately, to violence. Alternatively, left-hemisphere dysfunction could result in verbal deficits that lead to school failure, which in turn could lead to violence. Left-hemisphere dysfunction may, however, be a result (rather than the cause) of violent behavior, since blows to the head and falls may result in concussion and damage to the cortex. Another major source of damage to the brain that may have profound and irreversible consequences for adaptive behavior is in environmental toxins. Maternal use of ethanol (as in beverage alcohol) has effects on the fetus that may persist for many years, and are manifest in poorer attention at ages 4, 7, and older (Streissguth et al., 1984, 1986, 1989). The effects of lead on cognitive and social adaptation have been the focus of investigation by Needleman and collaborators (1990); even relatively "small" elevations of lead in the body are associated with poor attention, academic failure, and other impairment in life success. Maternal use of cocaine, opiates, and tobacco has also been shown to have a deleterious effect on the neurobehavioral capacities of the infant and developing child. These early effects may be associated, as well, with long-term academic and social failures (summarized in Mirsky and Siegel, in this volume). Large-scale epidemiologic and prospective studies are required in order to help elucidate the etiologic significance of neuropsychologic impairment for violence. One limitation of neuropsychologic studies, however, is that they are only indirect measures of brain dysfunction; additional statements regarding brain dysfunction in violence can be made on the basis of future studies that combine neuropsychologic testing with electroencephalogram (EEG) and positron emission tomography (PET) measures of brain activity. PSYCHOPHYSIOLOGIC APPROACH Neurochemical, neuroanatomic, and neurophysiologic research on violent behavior faces formidable difficulties. Measurement of the central neurologic processes is costly, often invasive, and difficult to implement so as to observe the processes during reactions to transitory situations in the social environment. To cope with these difficulties, an alternative approach to the study of

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Understanding and Preventing Violence: Volume 2, Biobehavioral Influences some types of violent offenders has been provided by the measurement of psychophysiologic variables (i.e., assaying autonomic and CNS functions by means of recordings from the periphery of the body). Included among these variables are heart rate and skin conductance (autonomic nervous system variables), as well as EEG and event-related brain potentials (central nervous system variables). Differences among criminals, delinquents and conduct-disordered children on the one hand, and control subjects, on the other, have been shown to exist in resting heart rate (lower in offenders and in persons characterized as fearless) (Raine et al., 1990a; Raine and Jones, 1987; Venables and Raine, 1987; Kagan, 1989). Some offenders have also been shown to have lower skin conductance responses to orienting stimuli than controls, although the reverse may be true for criminal offenders designated as psychopathic (Siddle et al., 1973; Raine et al., 1990b). With respect to EEG studies, many have reported an excess of slow wave activity in the records of incarcerated criminal offenders. It is unclear whether this is best interpreted as the effects of underarousal in the prison setting, developmental anomalies, or the sequela of brain damage (Williams, 1969; Hare, 1980). Event-related brain potentials (ERPs), in particular the P300 component, have been studied in a number of disordered populations. The P300 wave, which is an index of the allocation of attention to a stimulus (Duncan, 1990), is an example of a "cognitive" component of the ERP. These components vary as a function of some information processing requirement or task administered to the subjects. The P300 has been found to be larger in some groups of psychopathic criminals (Raine and Venables, 1988). The interpretation of this finding is unclear, although it suggests that these persons process information differently from normal subjects. NEUROIMAGING APPROACH Perhaps the most recent technical development in research into the antecedents of violence involves the application of new brain imaging techniques. Positron emission tomography and regional cerebral blood flow (RCBF) techniques allow direct and indirect assessments of glucose metabolism (or blood flow in the case of RCBF) throughout the brain either during a resting state or during performance of a certain task. As such, PET and RCBF techniques assess brain function. Conversely, computerized tomography and magnetic resonance imaging (MRI) techniques, while providing detailed images, assess brain structure only.

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Understanding and Preventing Violence: Volume 2, Biobehavioral Influences Although studies suggest differences between violent and nonviolent offenders, sample sizes have been relatively small, and findings should be viewed as preliminary. Nevertheless, brain imaging is clearly a new field that has enormous potential for addressing questions concerning altered brain structure and function in violent offenders. For example, PET studies would be capable of directly assessing differential effects of alcohol administration on brain glucose metabolism in violent and nonviolent offender groups, and could help address the issue of whether some violent offenders constitute a subgroup that is particularly susceptible to the disinhibitory effects of alcohol on specific brain areas. Studies that combine both MRI and PET techniques are clearly desirable in that assessments of both structure and function would allow more complete statements to be made with regard to brain dysfunction in violence. Studies that combine brain imaging assessment with neuropsychologic, cognitive-psychophysiologic, and hormonal assessments in violent and nonviolent subjects would allow us to address the potentially important interactions between different biologic systems in predisposing to violence. HYPOGLYCEMIA, DIET, AND VIOLENT BEHAVIOR Some studies have observed that violent offenders, particularly those with a history of alcohol abuse, are characterized by reactive hypoglycemia (Virkkunen, 1986). Although there have been no demonstrations to date that violent individuals are hypoglycemic at the time of the commission of violence, it is possible that low blood glucose levels (hypoglycemia) could be conducive to aggressive behavior. Increased irritability is one symptom of hypoglycemia (Marks, 1981), and this could be the first step in the development of a full-blown aggressive outburst. Anthropologic studies, studies of aggressive personality in "normal" subjects, and experimental studies in animals all support a link between hypoglycemia and aggression (Venables and Raine, 1987). Acute symptoms of hypoglycemia are reported as maximal at 11.00–11.30 a.m. (Marks, 1981), and this time corresponds to peaks in assaults on both staff and other inmates in prison, both of which reach their maximum at 11.00–11.30 a.m. (Davies, 1982). A number of studies have claimed that dietary changes aimed at reducing sugar consumption reduce institutional antisocial behavior in juvenile offenders, but these studies have methodological weaknesses that preclude drawing any firm conclusions at the present time (see Kanarek, in this volume). There is also some

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Understanding and Preventing Violence: Volume 2, Biobehavioral Influences limited evidence that food additives may contribute to hyperactivity, although the data on sugar intake and hyperactivity are inconclusive (Kanarek, in this volume). There have been reports however that home environment mediates dietary effects on behavior. Although data are limited at the present time, further double-blind studies into the effects of dietary manipulation on aggression and violence in institutions seem warranted. Furthermore, investigation of the interconnections between hypoglycemia or diet and other factors at both biological and social levels seems warranted. Since alcohol increases the susceptibility to hypoglycemia through its capacity to increase insulin secretion (Marks, 1981), it may well be that predispositions to both hypoglycemia and alcohol abuse would make an individual particularly predisposed to violence. Hypoglycemia has also been theoretically linked to both low heart rate and EEG slowing, factors that have been found to characterize violent offenders (Venables, 1988). The fact that children from a supportive home environment show more dietary improvement than those from an unsupportive home (Rumsey and Rapoport, 1983) also suggests an interaction between diet and family environment in antisocial behavior. Clearly, diet and hypoglycemia should not be studied independently of interactions with factors at other levels. REFERENCES Bohman, M., C.R. Cloninger, S. Sigvardsson, and A.L. von Knorring 1982 Predisposition to petty criminality in Swedish adoptees: I. Genetic and environmental heterogeneity. Archives of General Psychiatry 39:1233–1241. Bryant, E.T., M.L. Scott, C.D. Tori, and C.J. Golden 1984 Neuropsychological deficits, learning disability, and violent behavior. Journal of Consulting and Clinical Psychology 52:323–324. Cadoret, R.J., C. Cain, and R.R. Crowe 1983 Evidence for a gene-environmental interaction in the development of adolescent antisocial behavior. Behavior Genetics 13:301–310. Cairns, R.B., J.-L. Gariepy, and K.E. Hood 1990 Development, microevolution and social behavior. Psychological Review 97:49–65. Carlier, M., P.L. Roubertoux, M.L. Kottler, and H. Degrelle 1990 Y chromosome and aggression in strains of laboratory mice. Behavior Genetics 20:137–156.

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Understanding and Preventing Violence: Volume 2, Biobehavioral Influences Christiansen, K.O. 1977 A review of studies of criminality among twins. In S.A. Mednick and K.O. Christiansen, eds., Biosocial Bases of Criminal Behavior. New York: Gardner. Cloninger, C.R., and I.I. Gottesman 1987 Genetic and environmental factors in antisocial behavioral disorders. Pp. 92–109 in S.A. Mednick, T.E. Moffitt, and S.A. Stack, eds., The Causes of Crime: New Biological Approaches. New York: Cambridge University Press. Cloninger, C.R., S. Sigvardsson, M. Bohman, and A.L. von Knorring 1982 Predisposition to petty criminality in Swedish adoptees: II. Cross-fostering analysis of gene-environmental interaction. Archives of General Psychiatry 39:1242–1247. Davies, W. 1982 Violence in prisons. In P. Feldman, ed., Developments in the Study of Criminal Behavior. Vol. 2: Violence. London: Wiley. Duncan, C.C. 1990 Current issues in the application of P300 to research on schizophrenia. In E.R. Straube and K. Hahlweg, eds. Schizophrenia: Concepts, Vulnerability, and Intervention. New York: Springer-Verlag. Ebert, P.D., and R.G. Sawyer 1980 Selection for agonistic behavior in wild female Mus musculus. Behavior Genetics 10:349–360. Gorenstein, E. 1982 Frontal lobe functions in psychopaths. Journal of Abnormal Psychology 91:368–379. Hare, R.D. 1980 Psychopathy: Theory and Practice. New York: Wiley. Hood, K.E., and R.B. Cairns 1988 A developmental-genetic analysis of aggressive behavior in mice: II. Cross-sex inheritance . Behavior Genetics 18:605–619. Jones, S.E., and P.F. Brain 1987 Performances of inbred and outbed laboratory mice in putative tests of aggression. Behavior Genetics 17:87–96. Kagan, J. 1989 Temperamental contributions to social behavior. American Psychologist 44:668–674. Lagerspetz, K.M.J., and K.Y.H. Lagerspetz 1975 The expression of the genes of aggressiveness in mice: The effect of androgen on aggression and sexual behavior in females. Aggressive Behavior 1:291–296. Marks, V. 1981 The regulation of blood glucose. In V. Marks and F.C. Rose, eds., Hypoglycemia. Oxford: Blackwell. Maxson, S.C., A. Didier-Erickson, and S. Ogawa 1989 The Y chromosome, social signals, and offense in mice. Behavioral and Neural Biology 52:251–259.

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Understanding and Preventing Violence: Volume 2, Biobehavioral Influences Mednick, S.A., W.F. Gabrielli, and B. Hutchings 1984 Genetic influences in criminal convictions: Evidence from an adoption cohort. Science 224:891–894. Michard-Vanhee C. 1988 Aggressive behavior induced in female mice by an early single dose of testosteroned is genotype dependent. Behavior Genetics 18:1–12. Needleman, H.L., A. Schnell, D. Bellinger, A. Leviton, and E. Allred 1990 Long term effects of childhood exposure to lead at low dose: An eleven-year follow-up report. New England Journal of Medicine 322:83–88. O'Callaghan, M.A.J., and D. Carroll 1987 The role of psychosurgical studies in the control of antisocial behavior. In S.A. Mednick, T.E. Moffitt, and S.A. Stack, eds., The Causes of Crime: New Biological Approaches. New York: Cambridge University Press. Plomin, R., J.C. DeFries, and G.E. McClearn 1989 Behavior Genetics: A Primer, 2nd ed. San Francisco: W.H. Freeman. Raine, A., and F. Jones 1987 Attention, autonomic arousal, and personality in behaviorally disordered children. Journal of Abnormal Child Psychology 15:583–599. Raine, A., and P.H. Venables 1988 Enhanced P3 evoked potentials and longer P3 recovery times in psychopaths . Psychophysiology 25:30–38. Raine, A., P.H. Venables, and M. Williams 1990a Relationships between central and autonomic measures of arousal at age 15 and criminality at age 24 years. Archives of General Psychiatry 47:1003–1007. 1990b Autonomic orienting responses in 15-year-old male subjects and criminal behavior at age 24. American Journal of Psychiatry 147:933–937. Rumsey, J.M., and J.L. Rapoport 1983 Assessing behavioral and cognitive effects of diet in pediatric populations. Pp. 101–162 in R.J. Wurtman and J.J. Wurtman, eds., Nutrition and The Brain, Vol. 6. New York: Raven Press. Scott, J.P. 1942 Genetic differences in the social behavior of inbred strains of mice. Journal of Heredity 33:11–15. 1966 Agonistic behavior of mice and rats: A review. American Zoologist 6:683–698. Selmanoff, M.K., J.E. Jumonville, S.G. Maxson, and B.E. Ginsburg 1975 Evidence for a Y chromosome contribution to an aggressive phenotype in inbred mice. Nature 253:529–530. Siddle, D.A.T., A.R. Nicol, and R.H. Foggit 1973 Habituation and over-extinction of the GSR component of the orienting response in anti-social adolescents. British Journal of Social and Clinical Psychology 12:303–308.

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Understanding and Preventing Violence: Volume 2, Biobehavioral Influences Siegel, A., and M. Brutus 1990 Neural substrates of aggression and rage in the cat. Pp. 135–233 in A.N. Epstein and A.R. Morrison, eds., Progress in Psychobiology and Physiological Psychology. San Deigo, Calif.: Academic Press. Siegel, A., and H. Edinger 1981 Neural control of aggression and rage. Pp. 203–240 in P. Morgane and J. Panksepp, eds., Handbook of the Hypothalamus. New York: Marcel Dekker. 1983 Role of the limbic system in hypothalmatically elicited attack behavior. Neuroscience and Biobehavioral Reviews 7:395–407. Streissguth, A.P., D.C. Martin. H.M. Barr, B.M. Sandman, G.L. Kirchner, and B.L. Darby 1984 Intrauterine alcohol and nicotine exposure: Attention and reaction time in 4-year-old children. Developmental Psychology 20(4):533–541. Streissguth, A.P., H.M. Barr, P.D. Sampson, J.C. Parrish-Johnson, G.L. Kirchner, and D.C. Martin 1986 Attention, distraction and reaction time at age 7 years and prenatal alcohol exposure. Neurobehavioral Toxicology and Teratology 8:717–725. Streissguth, A.P., P.D. Sampson, and H.M. Barr 1989 Neurobehavioral dose-response effects of prenatal alcohol exposure in humans from infancy to adulthood. Annals of the New York Academy of Sciences 562:145–158. Vale, J.R., D. Ray, and C.A. Value 1972 The interaction of genotype and exogenous neonatal androgen: Agonistic behavior in female mice. Behavioral Biology 7:321–334. van Oortmerssen, G.A., and C.M. Bakker 1981 Artificial selection for short and long attack latencies in wild Mus musculus domesticus. Behavior Genetics 11:115–126. Venables, P.H. 1988 Psychophysiology and crime: Theory and data. In T.E. Moffitt and S.A. Mednick, eds., Biological Contributions to Crime Causation . Dordrecht, Netherlands: Martinus Nijhoff. Venables, P.H., and A. Raine 1987 Biological theory. Pp. 3–28 in B. McGurk, D. Thornton, and M. Williams, eds., Applying Psychology to Imprisonment: Theory and Practice . London: Her Majesty's Stationery Office. Virkkunen, M. 1986 Reactive hypoglycemia tendency among habitually violent offenders. Nutrition Reviews 44:94–103. Williams, D. 1969 Neural factors related to habitual aggression: Consideration of those differences between those habitually aggressive and others who have committed crimes of violence. Brain 92:503–520.