From Abuse to Violence: Psychophysiological Consequences of Maltreatment

SPECIAL ARTICLE From Abuse to Violence: Psychophysiological Consequences of Maltreatment DOROTHY OTN OW LEWIS, M.D.

Abstract. This paper re views the psychoph ysiolo gical literature related to violent behaviors. It explore s the interacti on s of en viron mental influe nces, pain, stressors, hormones, and neurotransmitters . It presents ways in which malt reatment in the form of ab use or neg lect exace rbates preexisting psychobi ological vulnerabilities. It proposes that whate ver forces increase impu lsivity and irritability, enge nder hypervigile nce and paranoia, diminish judgment and verbal co mpetence, and curtai l the recognition of pain in the self and others, will enhanc e violence, and presents evidence that maltreatment has all of these effects. J. Am. Acad. Child Adolesc. Psychiatry, 1992, 31, 3:38 3- 39 1. Key Words: abuse, violence, psychophysiology. Unlike other species such as rodent s, strains of whic h have bee n bred for aggressive ness (Ebert, 1973 ; Lagerspetz and Lagerspet z, 1971), no parti cul ar ethnic, racial, or religious gro up has shown itself to be innately or enduringly more agg ress ive than any other (although from time to time throughou t history, the peopl e of one co untry or another have attempted to so distinguish them selve s). Th e social and biologic al sciences have come to recognize that probably the most important influences on the development of violent beh avior are environment al or expe riential. Alth ough violen ce does not invariably beget violence (W idom , 1989), there is abundant evi de nce that a history of maltreatm ent is ofte n assoc iated with aggressive behaviors. From co nception onwards, the way s in which living crea tures are treated affec t the ways in which they treat others of their species . Ju st how abusive treatment enge nde rs aggression is not yet entirely und erstood . Th e purp ose of this paper is to ex plore so me of the most import ant psych obiological co nsequences of maltreatment in animals and hum ans and how they may contribute to aggre ssion. Aggression in anima ls and humans is not ident ical. Animal behavio r tend s to fall into two ca tego ries: affec tive and preda tory (F lynn et al., 1970). Predatory aggression is acco mplished with little autonomic activation; it invo lves carefully stalking and qu ickl y subduing the prey in the interest of providin g fast food. Affec tive agg ress ion, on the other hand , ca lls forth inte nse autonom ic activa tion and incl udes among other beh aviors intrama le, fear- induced, and irr itable aggression. Th e nature of hum an aggression is not easil y class ified. The beh aviors of Jack the Ripp er and John D. Rock efeller have both been con sidered aggressive. For purp oses of this discussion, hum an agg ression or violence will be used sirn-

Accepted June 27, 1991. Dr. Lewis is Prof essor of Psychiatry, New York University School of Medicine, Nell' York City. Reprint requests to Dr. Lewis, N YU Medical Center. School of Medicine, New Bellevue, 21525, 550 First Avenue, New York. N Y 10016. 0890-8567/ 92/3 103-0383$03 .00/0© 1992 by the American Aca dem y of Child and Adolesce nt Psychi atry. J. Am .Acad. Child Ad oiese. Psychiatry, 31:3, May 1992

ply to denote recurrent behaviors intended to ca use pain , da mage, or destru cti on to another person. It will not be used as a synonym for ambitiousnes s or asse rtive ness.

Environmental Influences on Aggression Intrauterine Environment The very position in utero of animals with in a litter ha s been found to influence behavior. Female mic e that develop in utero between two males are more aggressive after birth than those positioned bet ween other femal es (vo m Sa al, 1984). Thu s, animals from the same litter who have shared the same uteru s at the same tim e have not had ide ntica l pren atal en vironm ents . Mat ern al stress during pregn anc y has also been show n to affect the beh avior of offs pring (vom Saa l, 1984) long after deli very. In humans, the re is strong evi de nce that di fferent kind s of noxiou s pren atal influences ranging from minor viral infect ions to maternal anxiety and psychological stress have been associated with childhood maladaptation (Pasamanick, 1956, 1961; Rutt er, 1970; Stott , 1973; Stott and Latchford, 1976). The ad verse effec ts of matern al alcoholi sm and other substances on fetal deve lopme nt and on subsequent postnatal social and intellectu al fun ctioning are we ll documented. The exposure of the fetu s to abnormal levels of cert ain gonada l hormones has also been assoc iated wit h behav iora l sequelae (Ehrhardt and Money, 1967 ; Ehrhardt et al., 1968).

Stressful Living Conditions. Isolation. and Neglect Overheating, cro wding, and uncomfortable living conditions have been demonstrated to promote aggression in animals (Griffitt, 1970; Hutchinson , 1972). In hum ans, noxious odors (Jo nes and Bogat, 1978; Rattan et aI., 197 8), high temp eratures, and increase d popul ation density (Griffitt and Veitch , 1971) also have been shown to provoke hostility and agg ression in experimen tal situations . Th ese kinds of stress ors are of special interest because of their possible imp lications for under standing some of the factors that co ntribute to aggression in impoveri shed, cro wded urban en viron me nts. Isol ation of otherwise ge ntle ani m als du rin g critical phases of dev elop ment, an experience analogou s in some

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ways to the neglect of human infants, is an especia lly powerful influence on the ge nesis of aggressi ve behaviors (Brain and Nowell, 1971; Goldsmith et al., 1976; Luciano and Lore, 1976). The work of Spitz (1946), Bowlby (1969, 1975), and Provence and Lipton (1962) illustrates the devastating developmental consequences of isolation for hum an infants. Wherea s almost total stimulus deprivation of infants can lead to extreme developme ntal delays , depression, and even death , lesser degrees of neglect have been associated with extreme ly poor peer relationships and with the development of aggre ssive behaviors (Cicchetti, 1989; Mueller and Silverma n, 1989). In fact , as Widom ( 1989) has noted, there is a need to study neglect separately from abu se because of the ev idence from certain studi es that neglected children may be even more dysfunctional and aggressive than children who are physically abused. Nox ious stimuli may actually be less detr imental to developm ent than no stimulation at all.

Exposure to Aggressive Adults The quality of early parenting also affec ts aggressiveness. Animals bred to have an especia lly gentle nature, if crossfostered by adult females of a violent strain, will become mor e agg ress ive tha n is their usu al nature (Southwi ck, 1968). There is evidence that mice reared in the co mpany of their fathers as well as their mothers grow up to be more aggressive than those raised only by mothers (Mugford and Nowell , 1972). On the other hand , the results of cross fostering aggressive strains of infant rodents with less aggres sive adult animals are more variab le. Cert ain strains of aggre ssive mi ce retai n th ei r aggressi ve ness ev e n whe n reared by less aggressive adults (Southwick, 1968), whereas o ther strains do re spond by beco ming less aggressive (McCarty and So uthwick, 1979; Smith and Si mmel, 1977) when cross -fostered by less aggressive parent surrogates. Thu s, in certain rodents, expo sure to aggressive adults has a more powerful or predictable influence on subsequent adaptive styles than doe s exposure to more docile parent surroga tes. What are the psychological and behavioral co nseque nces of aggressive parenting? We know that aggre ssion can be learned . The re is sound expe rimental evidence that modeling plays an important role in the development of aggressive behaviors both in animals (Hamburg, 1971) and in humans (Bandura, 1973). We also know that aggressi ve behav iors (like more adaptive behaviors) can be acquired through reinforceme nt. Patterson (1977) observed that when children' s aggressive behavi ors were puni shed severely by parents, they tended to con tinue. On the other hand , when positive behaviors were reinforced by praise and aggressive behav iors give n less attention. agg ressive behaviors diminished (Patte rson, 1979). Farrington ( 1978) also found severe physical punishment to be an antecede nt of aggressive delinquency. The author's own studies compar ing extreme ly aggres sive delinqu ent s to their less aggressive delinquent peers indicated that the exposure to ex treme violence within the househol d , particul arl y be t we e n care take rs , was s tro ng ly associated with children's violent behaviors (Lew is et aI., 384

1979). When , however, in a follow-u p study of these delin quents (Lewis et al., 1989), an attempt was made to distin guish between those children raise d in violent households and those who themse lves were physically abused, it was found that th e mo re informa tion th at was obtai ne d, th e clea rer it became that abuse and exposure to other fam ily violence tended to go hand in hand, making it difficult to assess the relative importance of eac h.

Pain and Physical Abuse Probably the most powerful generator of aggression in animals and possibly in man is the repeated infliction of pain (Berkowitz, 1984). So strong is this response in animal s that a conventional experimental method for inducing murderous behaviors in mice and rats involves administering painful shocks to their feet (an ethically que stionable prac tice). Physical torment also is an effec tive means of engendering viciousness in fightin g dogs (e.g., pit bulls). The conseq uences of maltreatment in animals include the developme nt of hypervigilance. Defeat in animals tends to engender defensiveness (Flannelly et al., 1984) which in turn is ge nera li ze d to ot her s it ua tions a nd o t her o pp o ne n ts (Leschner, 1981; Seward, 1946). Like animals, children who have been physically abused tend to behav e in more aggre ssive ways than their nonabused peers (Cicchetti, 1989; Widom, 1989). Thes e abused children have been noted to develop a hypervi gilance, to misin terpret their surrou ndings, and, most importa ntly, to lash out when they percei ve ambiguous stimuli as threatening (Dodge et al., 1984; Rieder and Cicc hetti, in press) . The author' s studies of older children and adolesc ents revea led that the symptoms most charac teristic of very violent youngsters were paranoid idea tion and misperceptions, both of which are analogo us to the hypervigilance of abused childre n and animals (Lewis et aI., 1979, 1986). The finding of an association between paran oia and violen ce in delinquents was also consi stent with the findings of Yesavage (1983a, b) who reported that the most important symp tom disti nguishing aggressi ve from nonaggressive psychiatric patients was paranoia. Abusive treatment has been observed to have other de leterious effec ts that are peculi ar to humans and that further contri bute to aggress ion. Maltreatment affect s expressive skills. Abused children have great difficult y putting their feelings into words (Cicchetti and Beeg hly, 1987). Lacking the ability to convey emo tions verba lly, they tend, rather, to demo nstrate their ange r and misery through actions. Ironi cally, abused toddlers speak less about their negative feelings than do children from normal backgr ound s. Cicchetti has hypothesize d that such children develop overcontrolled styles of coping. However, there may be an alternative explanatio n for the clin ical observations in this study sugges t an alternative explana tion. Severely abused children repress and totally deny abusive experiences. The most grotesquely and recurrently maltreated children dissociate themselves from the abusive experiences and often do not eve n recall the abuse . The abuse d child' s inabilit y to identify, much less verbalize, his own distress probably acco unts for his observed difficult y in appr eciating the distress of others J. Am . Acad. Child Ado/esc. Psychiatry. 31:3. May 1992

FROM ABUSE TO VIOLENCE

(Main and Geor ge, 1985). Thi s lack of emp athy noted in abused toddlers is most likely a reflect ion of their conditioned ability to insulate them selves from any stimuli that might reevoke their own painful experiences. In summary, studies of human beings indica te that the same kinds of enviro nmental stresso rs that increase violence in animals (i.e. , intrauteri ne stressors, isolation or neglect, expos ure to violent adults, and the infliction of pain) contribute to aggressive behavi ors in humans. The question remains how such seemingly different kinds of experiences result in similar kinds of aggress ive behavioral changes. So me possible psychophysiological mechani sms by which these kinds of experiences may engender aggression will be explored .

Ph ysiological and Behavioral Consequences of Experiential Stressors The fact that environmental or experiential influences affect the developm ent of aggress ion does not mean that these effects are exclu sively or even primarily psych odynamic or socia l. Children probabl y do not become recurrentl y violent simply as a result of modeling or reinforcem ent, although imitation and conditioned responses are contributory . Studies of animals and humans sugges t that the envi ronmental conditions and stressors that engender aggression are mediated at least in part physiologi cally .

Hormonal Responses to Stressors Environmental stressors affect hormone prod uction. Levels of go nada l hormones are espec ially critical during fetal and neon atal growth (Goy and McEwen , 1980), influencing the devel opment of sexually dimorphi c areas of the brain (Hines, 1982). The presence of androgens prenatally has been show n to be crucial to the normal developm ent of aggressive behaviors in such diverse species as fish, lizards, birds, and chimpanzees (Floody and Pfaff, 1972). Andro gens, which contribute to hypervigilance, are thought to sensitize the parts of the fetal brain that mediate aggressio n. Sens itized animals subsequently are able to respond rapidly and aggressively to stimuli that elicit surges of testosterone (Kamel et aI., 1975). Stud ies have shown that when pregnant female rats are stressed by abnormal periodi c exposure to br ight lights, their serum testo sterone le vels as well as the testosterone levels of their male fetuses rise (vo m Saal, 1984). Of note, episodic eleva tions of testo sterone, especia lly if they occ ur at critical development al stages for the fetus, have been associated with increased postnatal aggres si ve ness . Thus , an en vironme nt al st ressor af fectin g the mother has physiological conseq uences for the fetus and even tual behav ioral co nsequences postnatally. Some effec ts of prenatal expos ure of hum ans to abnormally high levels of androge ns have been observed in girls with congenital adrenal hyperpl asia and in girls exposed in utero to ex oge no us masculini zing pr ogestin s. Thei r increas ed energy and athleticism, and their relative lack of interest in the more tradi tionall y feminine co nce rn s are thought to reflect an early in utero sensitization or masculin ization of the brai n (Ehrhardt et aI., 1968; Ehrha rdt and Money, 1967). l .Am.Acad. Child Ado/esc. Psychiatry, 3 /:3. May 1992

The early behavioral effects of go nadal hormones are not immutable; rather, hormones and their beh avioral co ncomitants respond to the vicissitudes of life. In animal soc ieties, such as monkey colonies , levels of circulating andro gen s respond to experie nces of success or defeat and affect domi nance and submissiveness. For example, when a previously domin ant male is bested by another male, his testosteron e may fall as much as 80% , and his place in the hierarchy of animals plummet (Rose et aI., 1971) . In contrast, successful challengers experien ce elevat ions of testostero ne and may assume more assertive roles in the colony. One cannot simply extrapolate from the effects of go nada l hormones on animals to their effects on man. There is some evidence that experiences of success, as in winning a tenni s match or graduating from medical school, are associated with eleva tion of serum testosterone levels in men (Mazur and Lamb, 1980). However, for the most part, results of studies regard ing the relationship bet ween testosterone levels and aggressio n in hum ans have bee n equi vocal (Ehrenkraz et aI., 1974; Kreuz and Rose, 1972; Meyer-B ahlburg, 1974; Monti et aI., 1977 ; Rada et aI., 1976). The use of anabolic steroids in body builders has been assoc iated with extremes of aggressive behavior (Pope and Katz, 1988) and with the de vel opment of pa ran oid sy mpto ms (Pope and Katz, 1987; Tennant et aI., 1988). Of note, although diminishing levels of circul ating androgens in men by means of chemica l or surgica l cas tration has been found to reduce sex ual aggressio n (i.e., rape) (T upin, 1987), it has not been demonstrated to be an effective biological treatment for the suppressio n of other kinds of nonsexual violent behaviors. Its effectiven ess as a deterrent, no doubt, would be consider able. Gonadal hormones are not the only hormones affec ted by envi ronmental stresso rs. Defe at, which tend s to lower testosteron e levels, causes circ ulating corticostero ids to rise (Christian, 1955, 1959). Wh en an animal has been repeatedly exposed to defeat , even exposu re to a potential aggressor wil l cause a surge of cortic osteroi ds (Bro nso n a nd Elftherio u, 1965a, b). Similarly, the administration of high doses of corticosteroids to a domin ant male will induce submiss ive behavior (Flannelly et aI., 1984). The relationship of endocrine statu s to behavior is complex and far from fully under stood. The effects of androgen s, estroge ns, progestins, and corticosteroids, as well as myriad other hormones, vary tremendously. Th e discussion of testosterone and corticosteroids is but an illustration of some of the ways in which experiences can affec t physiological state, and physiologi cal state, in turn , affect behavior. These interactio ns demonstrate the importan t fact that the biological state of the orga nism, animal or man, is not fixed but is, rather, continually chang ing and respondin g to the environment. Thu s what may appear to be"an inherent aggress ive temp erament can, in fact, be the reflection of a physi ologic al state induced and reinforced by envi ronmental stre ssors.

Neurotransmitter Responses to Stressors Just as envi ronmental stressors affect hormone levels, so there is an ever growi ng literature documenting the effec ts of stress on brain levels of neurotran smitters . What is more ,

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studies of animals and hum ans suggest that certain neurotransmitters such as norepin ephrin e, dopamine, and serotonin play important roles in both the genesis and suppression of agg ressive behaviors. For example , aggress ive behaviors in animals have been induced by admini stering precursors of norepin ephr ine and by admi nistering noradrenergic mimet ic drugs (Lal et aI., 1968, 1970; Rand rup and Munk vad, 1966; Reis, 1972). Although the ways in which norepinephrine enhances agg ression are not known, it is thought that its presence in specific parts of the brain inhibits certain brain stem neurons known to suppress aggre ssio n (Reis, 1972). Thu s, it is thought to inhibit inhibitors. (It is important to recall that there are different kinds of aggression in animals. Norepinephrine has been found to facilit ate affective or intermale aggression while inhibiting the predatory behaviors assoc iate d with foo d acquisitio n. Similarly, substances that increase intermale ag gress ion suppress infa nticida l beh aviors [vom Saal, 1979]. Thu s, when considering behavioral effects on animals of particul ar neurotransmitters, it is essenti al that the type of aggre ssion be spec ified.) Dop amine is also thought to play a role in the affective or interm ale aggression of animals. For example, when mice are given methylparatyrosine, an inhibitor of dopamine synthesis, their aggre ssivene ss diminishes (Lycke et al., 1969). The behavioral effects on hum ans of fluctu ations in norepinephrine and dopam ine are uncerta in. Whereas the calming, focusing effects of stimulant medication sugge st that increases in central nervous system dopamine and norepinephrine dimini sh hyp e racti v it y a n d co nseq ue ntly les sen aggressive beha viors, the tranquil izing effec ts of the antipsychotic medications that block dopamin e recep tors suggest an opposite beh avioral effe ct of dopam ine. In short, at this time, it is impossible to ge nera lize about the role of these kinds of neurotransmitters on human aggress ion. One of the most studied neurotransmitters in terms of its influen ce on aggressive behaviors in animals and man is serotonin. For example, Sahakian (198 1) reported low concentrations of serot onin in the cere brospinal fluid of hyperagg re ss i ve rat s. Ot he rs ha ve de m onst ra ted inc rea sed aggress ion in mice and rats whose brains for one reasons or another have been depleted of serotonin (Alpert et aI., 1981; Lyck e et al., 1969). When mice are isolated at cri tical developmental stages, their conc entration of brain sero tonin dimini sh es , and th ese serot o nin -de p leted mi ce becom e agg ressi ve (Ga ratti ni et aI., 1969 ; Va lze lli , 1974 ). Con versely, substances that potent iate serotonin have been demonstrated to dimin ish aggression (Alpert et aI., 1981). In hum ans there is a growing body of literature suggesting a relat ionship between dim inished levels of brain serotonin and self-injuriou s (Asberg et aI., 1976, 1987) as well as outwardly aggre ssive beha viors (Brown et aI., 1979). Based on studies of violent offenders and impulsive fire setters, Linnoila and colleagues ( 1983) suggested that low cere bral serotonin concentration (as reflected in low CS F-5-HIAA) may be associated with impulsive behaviors in general rather than aggressiveness or violence in particul ar. In a follow-up study of these subjects, Virk kunen and his colleague s ( 1989) reported dimini shed concentrations of both 5-HIAA and

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HVA (metabolites of sero tonin and dopamine) in recidi vists as compared to nonrecid ivists, Recentl y, Coccaro and colleagues ( 1989) demo nstrated diminished prolactin responses to fenfluramine (a serotonin-releasing age nt) in impul siveaggressive patients diagnosed as having personality disorders and in depressed suicid al patient s. Con sistent with these data is the fact that many of the antidepressant medicati ons increase serotonin and relieve agitation and suicidal beh avior. Coccaro and co lleag ues (1989 ) hypothesize the existen ce of a psych obi ological susceptibility to impulsiveaggressive behavior, secondary to insuff icient serotonin in the brai n. Thi s theory, however, does not explain why some indiv iduals with dimini shed amounts of serotonin simply becom e unhapp y and irritable whereas other s become aggressive. What else is necessary to cause a person in a serotonin-depleted, irritab le state to aggress agai nst another person rather than bite his own nails or tear at his own flesh?

Brain Function and the Interactions of Hormones and Neurotransmitters Neuroanatomy, hormones, and neurotransmitters cann ot really be studied separately. A few exa mples of their inter actions are offered: I. In vitro studies of the effects of hormones on the embryo nic rat brain show that both estro gen and progesterone enhance the growth of mesenceph alic dopa mine neurons (Reise rt et al., 1987). Thus, hormone s actually affect brain structure. 2. Studies of rats and hamsters reveal that hormones associate d with aggression, such as estradiol and testosterone , co nce ntr ate in specific limbi c sys te m neu cleii (Floody and Pfaff, 1972). 3. T he introduction of testosterone into particular hypothalamic nuclei of castrated rats causes them to resume those aggressive behaviors that were previously suppressed by castration (Herbe rt, 1989). In this study, testosterone seems to act as a neurotransmitter. 4. In vitro studies of the effect of neurotransmitters on testicular tissue in hamsters reveal the role of catecholamine in the produ ction of testosterone (Mayerhofer et aI., 1989). 5. Sero tonin agonists, releasers, precursors, and uptake inhibitors have been found to elevate corticosterone levels in rats (Fuller, 1981). Clearly the actions of hormones cannot be studied without con sideri ng the ir interac tio ns wi th neurotransmitte rs and vice versa. Where in the brain do the neuroph ysiological interactions related to aggression occur? Cli nical data and data from experimentation with anim als have shown that three areas of the brain are especially important in terms of the modul ation of violent behaviors. MacLean ( 1985) and Weiger and Bear ( 1988) have conceptualized a hierarchy of neur al controls that involves particularly the hypothalamu s, amygdala, and orbital prefrontal cortex. The hypothalamu s, which receives input from osmo and chemorece ptors and from the amygdala, affects endocrine respon ses throu gh its influence on the pituitary. For exam ple, dam age to the anterior hypoJ. Am .Acad. Child Ado/esc. Psychia try, 31:3, May 1992

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thalamus of male rats redu ces sexual and aggressive behaviors (Floody and Pfaff, 1972). In addition, hypothalamic projections to the brain stem control stereotyped behaviors, a phenomenon illustrated by the sham rage of decorticate cats (Bard , 1928). Aggressive behaviors can be elicited or suppressed, depending on which parts of the hypothalamus are stimulated or ablated. Acet ylcholine has been show n to be an important neurotransmitte r in this area of the brain (Bandler, 1970; Bear et aI., 1986; Smith et aI., 1970). In hum ans, lesions in the hypothalamus have been associated with unpl anned animal-like attacking beha viors. In contrast with the hypothalamus, the amygdala receives input from all sensory mod alities. It has proje ctions to the hypothalamus and plays a role in the assoc iation of particul ar sensory stimuli with aggressive responses (Dow ner, 1961; Weiger and Bear, 1988). Lesions in the amygdala have been show n to impair an animal's ability to distinguish between appropria te and inappropriate objects for satisfyi ng hunger and sexual drives (Keating, 197 1; Kluver and Bucy, 1939). Expe riments on animals suggest that stimul ation of the amygdala, located deep with in the temporal lobe, is involved in the kind of aggression that occurs in response to fear (Egger and Flynn, 1963; Siege l and Flynn, 1968). On the other hand, damage to the amygdala has been reported to result in a diminution of aggress ive beh aviors in response to novel stimuli. In hum ans, lesions in the amygdaloid area h ave be en associated with ap athy a nd hyp osexualit y, where as abnormal electrical activity in this area has been associated with aggres sion. Whether or not directed aggression eve r occ urs during an actual seizure origina ting in the amygdala or in other limbi c structures of the brain remains a topic of debate. However, interict ally, many patients with epileptic diso rders experience irritability, intensification of feelings, fearfulness, and outright paranoia (Bear and Fulop, 1987; Lewis, 1976; Lewi s et al., 1982). Thi s finding-that a particul ar part of the brain involved in aggression is espec ially responsive to stimuli that elicit fear-is important because, as previously discussed, paranoid mispercepti ons, i.e., fearfulness, hypervigilance, and an unwarranted sense of threat, play such an impor tant role in the etiology of violent behavior in hum an beings. It is durin g these kinds of em otionally intense interictal periods that planned, purp oseful inte rpersonal violence can occur. It is impo rtant to recognize that intenti onally violent behaviors can and do occ ur as a result of brain dysfunction and that premeditation is not necessarily an indication of sanity. The frontal cortex, that part of the brain so esse ntial for abstract thought, plannin g, and j udgme nt, interac ts with the rest of the neocortex as well as the amyg dala and hypothalamus. Lesions of the front al cortex have been associated with apathy, impul sivity, and irritability, depending on their location . Damage to the dorsolateral co nvexity has been linked with apathetic, irresponsible behaviors, whereas damage to the orbital area is more commo nly linked with impulsive, inapprop riate behaviors (Blumer and Benson, 1975 ; Lur ia, 1980). Alth ough attempt s have been made to expl ain specific kinds of criminally aggre ssive beha viors in terms of the J. Am.Acad. Child Adolesc. Psychiatry, 31:3, May 1992

localization of lesions, as yet there are no hard and fast rules that apply invariably to specific hum an behaviors. Th e above exa mples of brain function and dysfunction are, in fact, gross oversimplifications. No part of the brain works in isolation, and, as noted , the structures invo lved in aggressio n have widespread conn ections to other parts of the brain. The essential princ iple to keep in mind is that in real life the expre ssion of violence is not simply the outcome of localized stimulation. Different parts of the brai n are continuo usly interacting with eac h other, and violent beh aviors reflect the result of the equi librium achieved between the stimulation and suppress ion of particular areas at specific points in time.

Are All People Created Equal in Terms of Aggressive Responses to Maltreatment? Are we all created equal or are some of us innatel y more aggressive than others? Studies of infants indicate that we do not enter the world as temperame ntally identical blank slates. Some infan ts are more tense and irritable than others and are more given to temper tantrums when stressed by the ordin ary vicissitudes oflife (Ches s and Tho mas, 1984). The same squeaky chalk will feel more abrasive to some slates than others . However, early temper tantrums are not predictive of a life of violent crime (Kaga n and Moss, 1962), and, althoug h aggressive beh aviors subsequent to age 3 years are often assoc iated with ongoing interpersonal problem s, the majority of aggress ive young children do not become violent adults. Are there any genetic abnormalities that imp art a specific tendency toward violence? With the exce ption of Lesch Nyhan Syndrome (Palmour, 1983), no genetic abnormality has yet been identified that predisposes an individual spec ifically to violent behavior. The findi ngs reported during the 1960s and 1970s suggesting that certain chromosomal abnormalities (e.g., XYY and XXY anom alies) were associated with a predisposition to violence (Casey et aI., 1966 ; Forssman and Ham bert, 1967; Hook, 1973; Nielson, 1968; Telfer, 1968; Witkin et aI., 1976) have been reevaluated, and their conclusions questioned (Baker et al., 1970; Gerald, 1976; Jacobs et aI., 1971; Schiavi et aI., 1984). Most probably, these abnormal constellations of chromosomes, like other abnorma l conditions, pred ispose an individual to a variety of different kind s of adapt ational problem s which, dependin g on upbringing and stressors, may or may not be manifested by aggress ion. The only chromosomal constellation or syndro me that has repeatedly been demo nstrated to be associated with aggres sive behavior is the " XY Sy ndro me." A major feature of the XY Syndrome is a dimin ished violence threshold, and this characteristic is true of most animals as well as man. Wh at is it about the male condition that creates this tend ency to respond aggressively? Given the fact that this quality of temp erament is not pecul iar to hum ans, but rather is equally characteristic of animals, it makes sense to conclude that physiological rather than simply soc ietal influences are at play. It would see m that boys, with their testosteron e-sensitive masculi nized brain s and their physiologica l capacity to secrete large amounts of androgen in respon se to particul ar 387

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stimuli, are, from the outset, more susceptible than girls to the aggress ion-promoting effects of maltreatment. What other physiological conditions or states lower the threshold for violent responses to stressful stimuli? After all, not all abused children, not even all abused boys, become violent. What makes one boy more susceptible than the next to the "slings and arrows of outrageous fortune"? The author's studies of violent individuals suggest that some children are indeed more susceptible than others to the violence engendering effects of abuse and neglect. For example, the studies found that among abused boys, those with psychiatric, neurological, and cognitive impairments are far more likely to act aggressi vely than those whose central nervous system functions are intact (Lewis et al., 1989). Severely neuropsychiatrically impaired girls, on the other hand, even when abused, are far less violent than boys (Lewis et al., 199 1). It seems reasonable, therefore, to conclude that impai red boys, who for any numbe r of reasons already have neurophysiological vulnerabilities, who either start with abnormal neurotransmitter concentrations or abnormal physiological responses to stress, are more likely than their impaired female counterparts or their more neuropsychiatrically intact male counterparts to be affected adversely by the psychobiological consequences of abuse or neglect. The boy who is already intrinsically vulnerable to paranoid misperceptions by virtue of an inherent neurophysiological predisposition to major psychiatric illness, or the boy who suffers from some sort of central nervous system dysfunction that increases irritability and impulsivity, might be expected to respond especially aggressively to the additional psychological and neurophysiologica l insults imposed by neglectful or abusive treatment. We do know that once a physiological response has been established it is easily reevoked by exposure to similar stimuli. It is, therefore , reasonable to hypothesize that ongoi ng abuse and neglect, especially in early childhood, have conditioning effects, setting up the kinds of neurophysiological circuits and respon ses that contribute to violence. The more vulnerable the child is to begin with, the more likely that maltreatment will set up these kinds of circuits and result in recurrent aggressive behavior. What are the most common characteristics of violent individuals? The literature has tended to focus separately on different concomitants of aggression. Some have concentrated primarily on impulsivity and the biochemical abnormalitie s assoc ia te d wit h it; o thers ha ve stresse d th e importance of paranoia in repeatedly antisocial individuals; still others have focused on cognitive or intellectual deficits. In spite of these findings, it is important to rememb er that most brain-damaged , impulsive children are not violent; most psychotic, paranoid children are not violent; and most cognitively impaired, learning disabled, or retarded children are not violent. These separate vulnerabilities do not, in and of themselves, seem to create violence. Furthermore, most abused children do not turn into violent criminals (Widom, 1989). On the other hand, work by the author over the years has suggested that when neuropsychiatric and cognitiv e deficits exist together, maltre atment is an especially potent precipi-

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tant of aggression. That is, when impulsivity, hypervigilan ce , and cog n it ive ex pressive defi cits coex ist, th e psychophysiological stage is set for violence to occur. What is it about these kinds of vulnerabilities that create a matrix for violence? First, brain dysfunction of almost any kind is often associated with irritability, impatience, and mood labil ity. Second , paranoi d idea tio n and mi spercept ion s, symptoms associated with so many different kinds of psychiatric disorders, increase fearfulness and a tendency to retaliate for both genuine and imagined threats. Finally, cognitive deficits not only impair judgment but also diminish the ability to conceptualize feelings and put them into words rather than actions. How might on e und er st and the ways in which maltreatment in the form of abuse or neglect exacerb ates these vulnerabilities and enco urages violence? Certa inly, maltreatment has psychodynamic consequences, engendering rage and providing a model of violent beha vior. In addition, extrapolating from the researc h on animals, maltreatment modifies the physiology of the organism itself. It is reaso nable to hypothesize that abusive, neglectful treatment diminishes co nce ntra tio ns in the brain of subs tances such as serotonin that ordinarily help to modulate feelings; maltreatment seems to increase the outpouring of substances such as dopamine and testosterone that enhance competitive and retaliatory aggression . These same substances also contribute to hypervigilance, and thus increase the fearfulness and paranoia that give rise to violent acts. There is also another way in which these kinds of physiological reactions to maltreatment may possibly contribute to aggress ion. We know that testosterone and other hormones affect the very structure of the brain. The delayed verbal skills of boys compared to girls is thought to be a reflection in part of the action of testosterone on the developing brain (Hines, 1982). The special difficulties that abused toddlers have expressing feelings in words may not be simply a reflection of psychol ogical intimidation but rather a manifestation of neuroanatomical and neurophysiological changes secondary to abusive or neglectful treatment. Furthermore, the apparent lack of empathy of abused aggressive children noted previously may be a manifestat ion of a centrally mediated expressive deficit coupled with a conditioned imperviousness to certai n painful stimuli and not simply a reflection of nastiness or character pathology. Studies of abused young children indicate that they do not suffer from a lack of moral development. Abused children, as well as normal children, consider it wrong to cause physical harm (Smetana and Kelly, 1989). It would seem, rather, that abused children are unable to act on their intellectual understanding of moral principles when they are stressed. When such traumatized children also happen to be paranoid (which is frequently the case), they tend to adopt defensive, contemptuous attitudes toward the rest of the world, thus seeming to complete the picture of sociopathy. In short, whatever increases impulsivity and irritability, engenders hypervigilance and paranoia, diminishes judgment and verbal competence, and curtails the ability to recognize one's own pain and the pain of others, also enhances the tendency toward violence. Abusive, neglectful caretakI. Am. Acad. Child Adolesc. Psychiatry, 31:3, May / 992

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ing does all of these things. In a resilient child, maltreatment (i.e., abuse or neglect) may not engender aggression. In an already vulnerable child with tendencies toward impul sivity, hypervigil ance, expressive difficulties, and dissoci ati on from painful feeling s, maltreatment is often sufficient to create a very violent individu al. To the extent that testosterone contributes to this constellation of vulnerabilities, persons with the XY Syndrom e are at special risk. What are the implications of the above psychobi ological phenomena for the treatment and prevention of violence ? Clearly, interventions that help control impulsi vity, dimini sh irritability, enhance a child's sense of security, alleviate paranoid feelings, improve cognition and verbal expressiveness, and encourage recogn ition of one ' s own pain and the pain of others, will diminish the likelihood of violence. To date, programs addressing each of these issues individually and specifically do not exist. On the other hand, ironically, our correctional system reproduces all of the ingredients known to promote violence: isolation, discomfort, exposure to other aggressive individuals, insecurity, and lack of intellectual stimulation. If in our prisons we have demonstrated our ability to make a laboratory which predictably produce s and reinforces aggres sive behavior, surely the possibility exists that with a little ingenuity we might, just as reliably, be able to create an environment to produce and encour age the opposite. References Alp ert, J. E., Coh en , D. J., Sha ywitz, B. A. & Picci rillo, M. (198 1), Neurochemica l and beh avioral orga nization: disord ers of attentio n, ac tivity , and aggression. In : Vulnerab ilities to Delinquency, ed . D. O. Lewis. New York: Spectrum, pp. 109-171. Asberg, A ., T raskma n, L. & Th oren, P. (19 76), 5-HIAA in cerebrospinal fluid : a biochemical suicide predi ctor? Arch. Gen. Psychiat ry 33 :1193 - 1196. Asberg, M ., Schalling, D., Traksm an-B end z, L. & Wagner, A . ( 1987) , A psych ob iology of suicide, imp ulsiv ity, and related phen omena. In : Psychopharmacology: Third Generation of Progress, ed. H. Y. Meltzer. New York: Raven Pre ss, pp. 655 - 688. Ba ker , D., Telfer, M. A., Rich ard son , C. E. & Clark, G. R. (1970), Chro moso me errors in men wit h antisoc ial beha vior: co mpariso n of selected men with " Klinefelter's syndrome" and XYY chromosome pattern. JAMA, 2 14:869-878. Bandler, R . J. (1970) , Ch olinergic syna pses in the lateral hypothal amu s fo r the control of predatory aggression in the rat. Brain Res. 20:4 09-424. Bandu ra, A . (197 3), Aggression: A Social Learn ing Analysis. Englewoo d C liffs, NJ : Prentice Hal l. Bard , P. (19 28) , A dien ceph alic mechan ism for the exp ress ion ofrage with spe cial reference to the sympathe tic nervous system. Am. J. Physiol . 84 :490-5 15. Be ar, D. M . & Fulop, M . (19 87 ), Th e ne uro log y of emo tion. In: Behavioral Biology in Medicine, ed . A. Hobson. So uth Norwa lk, CT : Meduration , Inc. - - Ros enbaum , J. F. & Norman, R. (19 86), Aggression in ca t and man precipitated by a ch olin esterase inh ibitor. Psych osomati cs 26 :535-536. Berkowit z, L. (1984) , Ph ysical pain an d the inclination to agg ress ion. In : Biological Perspectives on Aggression, eds . K. J. Flannelly, R. J. Blan ch ard & D. C. Blan chard . New York : Liss, pp. 27-47 . Blu mer, D. & Ben son, D. F. (1975 ), Personality changes with fronta l an d temporal lobe lesion s. In : Psychiatric Aspec ts of Neuro logic Disease, eds. D. F. Benson & D. Blumer. New York: Gru ne and Stra tton, pp. 151-1 70 . Bowlby, J. ( 1969), Attachment and Loss, vol. I. New York: Basic Books.

J. Am. Acad. Child Adolesc. Psychiat ry, 31:3, Ma y 1992

- - ( 1975), Attachment and Loss, vol. 2. Harmondsworth: Penguin. Brain , P . F. & Nowell, N. W . (197 1), Isolati on versus grouping effects on adre nal and gonada l fun ct ion in albino mice . I. Th e male. Gen. Compo Endocrinol., 16:149. Bron son , F. H. & Ele ftheriou, B. E. (l 965a) , Adre nal response to figh tin g in mice: sep aration of phy sical and psychological causes. Scien ce 147:627. - - - - ( 1965b) , Relati ve effec ts of fight ing on bo und and unb ound cort ico stero ne . Proc. Soc. Exp. Biol. Med. 118: 146. Brown , G. L., Ballenge r, J. c., Min ichi ell o, M. D. & Good win, F. K. ( 1979), Human aggression and its re lationship to cerebro spinal fluid 5-hydroxy-indoleacetic acid , 3-m ethoxy-4-hydroxy-phenyl-glycol, and homo vanillic acid . In : Psychopharm acology of Aggression, ed . M. Sandl er. New Yor k: Raven Press, pp . 13 1-148. Ca sey, L. 1., Sega ll, D. R. Stre et, K. & Blank, C . E . (1966), Sex chromoso mes abnorma lities in two state hospitals for patient s requiring spe cial security. Nature, 209:64 1- 642. Chess, S. E. & T homas, A. (1984) , Origins and Evolution ofBeha vior Disorders. Ne w York: Brunner and Ma zel. Christian, J. J. (1955 ), Effect of popul ation size on the adre nal glands and reprod uctiv e orga ns of male mice in popul ati on s of fi xed size. J. Physiol . (Lo nd. ) 182:292 . - - (1959), Lack of correlation between adrenal weight and injury from fighting in gro uped male albino mice . Proc. Soc. Exp. Biol. Med. 101:166. C icche tti, D. (19 89), How research on child maltr eatm ent has inform ed the study of child developm ent : per specti ves from develop mental psych opathology . In : Child Maltreatm ent: Theory and Research on the Causes and Consequences of Child Abuse and Neglect, ed s. D. Cic chetti & V. Carl son. Ne w York: Ca mb ridg e University Press, pp. 377-43 1. - - Beegh ly, M. (19 87), Symbo lic developme nt in maltre atment youngsters: an orga niza tional perspective. In: A typical Symbolic Development, eds. D. Cicchetti & M. Be eghly. San Fran cisco: Jos sey -Ba ss. Coccaro, E. F., Sie ver , L. J., Klar, H. M. , Ma urer, G. et al. (1989), Sero tonergic studies in patient s with affec tive and person ality disorde rs. Arch. Gen. Psychiatry, 46:587-598. Dodge, K., Murphy, R. & Buchsbaum, K. C. (19 84), Th e assessment of intention-cue detection skills in children: implication s for de velopme ntal psych opathology. Child Dev. 55 :163- 173. Down er, J. L. (196 1), Change s in visual gnostic func tion s and emo tional beh aviour follow ing unilateral te mpo ral pole dam age in the " split-brain" monk ey. Nature, 191 :50-5 1. Ebert, P. D. (1983) , Selection for aggression in a natural population. In: Aggressive Behavior: Genetic and Neural Approaches, eds . E. C. Himmel, M . E. Hahn & J. K. Walte rs, Hi llsdale , NJ: Laur ence Erl baum, pp . 103-1 27. Egger, M . D. & Flynn , J. P. (19 63) , Effec ts of electr ica l stimulation of the amygda la on hypo thalami cally elic ited attack behavior in cats. J. Neu rophys iol., 26:705-720. Ehrenkranz, J., Bliss, E. & Sheard, M. H. ( 1974), Plasma testoste rone: correl ation w ith aggressive beh avior and soc ial domin an ce in ma n. Psychosom. Med. 36:469-475. Ehrhardt, A. A. & Mon ey, J. ( 1967), Progestin-induced herm aph roditism: lQ and psych osexual identity in a sample of ten girl s. Journal of Sex Research , 3:83-100. - - Ep stein , R. & Mon ey, J. (1968), Fetal androg ens and fem ale gender identity in the early treat ed adre noge nita l syndro me. Johns Hopkins Medical Journal, 122: 160-1 67. Farringt on, D . P. (1 97 8), Th e family bac kgrounds of ag gress ive youths . In: Aggression and Antisocia l Behavio r in Childhood and Ado lescence, eds. L. A. Hersov, M . Ber ger & D. Shaffer. Oxford : Pergamon , pp . 73-93 . Flan nelly , K. J., Flannelly, L. & Blanch ard , R. J. (\984) , Adult experience and the expressio n of ag gres sion: a co mpara tive analysi s. In: Biological Perspec tives on Aggre sssion, eds. K. J. Flannelly, R. J. Blanch ard & D. C. Blanch ard . New York: Liss, pp. 207 -259 . Floody, O. R. & Pfaff, D. W . ( 1972 ), Steroid horm on es and agg res sive beh avior: approach es to the study of horm on e-sensitive bra in mechanis ms fo r beh avior, S. H. Frazi er. Agg ression , 52:149- 184. Flynn, J. P., Vanega s, H., Foote, W . & Edward, S. (19 70 ), Neural

389

LEWIS mechanisms involved in a eat's attack on a rat. In: N eural Control of Beha vior, eds. R. E. Whalen et al., New York: Academic Press, p. 135. Forssman, H. & Hambert, G. (1967), Chromosomes and antisocial behavior. Exerpta Crim ino logica, 7: 113- 117. Fuller, R. W. (198 1), Serotonergic stimulation of pituitary-adrenocortical functions in rats. Neuroendocrino logy, 32:118- 127 . Garatt ini, S ., Gi acolon e , E. & Valz ell i, L. (1969 ), Bi och emi cal changes during isolation- induced aggressiv eness in mice. In: Ag gress ive Behavior, eds. S. Garattini & E. Sigg. New York: Wiley. Ger ald, P. S. (1976), Current concepts in genetics: sex chromoso me disorders. New England Journal of Medicine, 294:706 . Gold smith, J. F., Brain, P. F. & Benton, D. (1976 ), Effects of age at differential housing and the duration of individua l housing/gro uping on intermale fighting behavio r and adrenocortical activity in T. O. strain mice. Ag gressive Behavior, 2:307-323. Goy, R. W. & McEwen, B. S. (1980 ), Sexua l Differentiation of the B rain. Cambridge, MA: MIT Pre ss. Griffitt, W. (1970), Environmental effec ts on interpersonal affective behavior: ambient effe ctive tempera ture and attraction. J. Pers. Soc . Psycho/., 15:240 . - - Veitch, R. (197 1), Hot and crow ded, influence of population de nsity and temperature on interp ersonal affective beha vior: ambient effec tive temperatu re and attraction. J. Pers. Soc. Psych o!. 17:92-98. Hamburg, D. A. (197 1), Psychobi ological studies of aggressive behaviour. Nature. 230:19- 23. Herbert, J. (1989), The physiology of aggressi on. In: A ggression and War : Thei r Biological and Social Bases, eds. J. Groebel & R. A. Hinde. New York : Cambr idge University Press, pp. 58-71. Hines, M. (1982) , Prenatal gonadal hormones and sex differences in hum an behavior. Psychol . Bull. 92(1):56-80. Hook, E. B. (1973 ), Behavioral implications of the human XYY genotype. Science, 179:139- 150. Hutchinson, R. R. (1972), The environmental causes of aggression. In: Neb raska Symposium on Motivation, eds. J. K. Cole & D. D. Jensen. Linco ln: Univerity of Nebr aska Press. Jacobs, P. A., Price, W. H., Richmond, S. & Ratcliff, R. A. W. (197 1), Chromosomes survey s in penal institutions and approve d schools. J. Med. Genet. 8:49 -58 . Jones, J. W. & Bogat, G. A. (197 8), Air pollution and human aggression. Psycho!. Rep. 4 3:721. Kagan, 1. & Mo ss, H. (1962), From Birth to Maturity. New York: John Wiley. Kamel, F., Mock , E. J., Wright, W . W. & Frankel, A. I. (1975), Alteration s of plasma concentrations of testosterone, LH, and prolactin associated with mating in the male rat. Horm. Beha v. 6:277. Keating, E. G. (197 1), Soma tosensory deficit produced by parietotemporal disconnection. An at. Rec. 169:353- 354 . Kluver, H. & Bucy, P. C. (1939), Preliminary analysis of functions of the temporal lobes in monkeys . Archive s of Neurology and Psychiatry 42 :979-1 000 . Kreuz, L. E. & Rose, R. M. ( 1972), Assess ment of aggressive behavior and plasma testosterone in a young criminal pop ulation. Psychosom. Med. 34 :32 1- 332 . Lagerspetz, K. M. 1. & Lagerspetz, K. Y. H. (1971), Changes in the aggress iveness of mice resulting from selective breeding, learning and social isolati on. Scand. J. Psychol. 12:24 1- 248. Lal, H., De Feo , J. J. & Thut, P. (196 8), Effect of amphetamine on pain-induced aggression. Communica tions in Behavioral Biology, 1:333. - - Nesson, B. & Smith, N. (1970), Amphetamine-induced agg ression in mice pretreated with dihydroxyphenylalanine (DOPA) and! or reserpine. Bioi. Psychiatry, 2:299 . Leshner, A. 1. (198 1), The role of hormones in the contro l of submissiveness. In: A Mul tidiscipl inary Approach to Aggressi on Research, eds. P. F. Brain & D. Benton. Amsterda m: ElsevierlNorth Holland Press, pp. 309-322. Lewis, D. O. (1976 ), Delinquency, psycoh motor epileptic symptoms, and paranoid ideation: a triad. Am. J. Psychiatry, 133: 1395-1398. - - Shanok, S., Pincus, J. & Glaser, G. (1979), Violent juvenile

390

delinqu ents: psychiatric, neurological, psycological and abuse factors. J. Am. Acad. Child Adolesc. Psychiatry, 18:307- 3 19. - - Pincus, J., Shanok, S. & Glaser, G. ( 1982), Psychomotor epilepsy and violence in a group of incarcerated adoles cent boys. Am. J. Psychia try, 139:882- 887. - - Lovely, R., Yeager , C. & Della Femi na, D. (1989), To ward a theory of the genesis of violence: a follow-up study of deli nquents. J. Am. Acad. Child Ado lesc . Psychiatry 28:43 1-436. - - Pincus, J. H., Feldman, M., Jackson, L. & Bard, B. (1986), Psychiatric, neurological, and psychoeducational characteristics of 15 death row inmates in the United States. Am. J. Psy chiatry , 143:838- 845. - - Yeager, c., Cob ham- Portorreal, C. S., Klein, N., Showa lter, C. & Anthony, A. ( 1991), A follow-up female delinquents: materna l contributions to the perpetuation of devia nce. J. Am. Acad. Child Ado lesc. Psychiatry , 30: 197-20 1. Linnoila, M., Virkkunen, M., Scheinin, M., Nuutila, A., Rimo n, R. & Goodwin, F. K. (1983), low cerebrospinal fluid 5-hydroxyindoleacetic acid concentration differentiates imp ulsive from nonimpulsive violent behavior. Life Sc i. 33:2609-26 14. Luciano, D. & Lore, R. (1975), Aggression and social experience in do mesticated rats. J. Comp o Physiol. Psychol., 88:9 17. Lur ia, A. R. (1980 ), Higher Cortica l Function s in Man. New York: Basic Books. Lycke, E., Modigh, K. & Roos, B. E. (1969), Aggression in mice associated with changes in the monoami ne-metab olism of the brain . Experientia 25 :95 1-953. Macl.ean, P. (1985), Brain evolution relating to fami ly, play and the separation call. A rch. Gen. Psychiatry, 42:405-41 7 . Main, M. & George, C. (1985), Response of abused and disadvantaged toddlers to distress in agitate s: a study in the day care setting. Developmental Psychology, 21:407-4 12. Mayerhofer, A., Bartke, A. & Steger, R. W. (1989), Catecholamine effec ts on testicular testosterone production in the go nadally active and the gonadally regressed adult golden hamster. Bioi. Reprod. 40:752- 761. Mazur, A. & Lamb, T. A. (1980), Testosterone, status and mood in hum an males. Horm. Behav. 14:236-246. McCarthy, R. & Southwick, C. H. ( 1979), Parental enviro nment: effec ts on survival, growth and aggressiv e behaviors of two roden t species. Del'. Psychobiol. 12:269- 279. Meyer-Bahlburg, H. F. L. (1974 ), Aggression, and androgens and the XYY syndrome . In: Sex Differences in Behavior, eds. R. C. Friedman, R. M. Richart & R. L. Vande Wiele. New York: John Wiley, pp. 433-453. Monti, P. M., Brown, W . A. & Corriveau, M. A. (1977 ), Tes tosterone and components of aggressive and sexual beha vior in man. Am . J. Psychiat ry, 134 :692- 694 . Mueller, E. & Silverm an, N. (1989) , Peer relations in maltreated children. In: Child Maltreatment: Theory and Resea rch on the Causes and Consequence s of Child Ab use and Ne glect, eds. D. Cicc hetti, & V. Carlson. New York: Cambridge University Press, pp. 529-578. Mugford, R. A. & Nowell, N. W. (1972), Patern al stimulation d uring infancy: effe cts upon aggression and open-field performance of mice . Jo urn a l of Co mpa ra tive an d Ph ys io logi ca l Psy chology, 79:30-36. Nielson, 1. (196 8), The XXY synd rome in a ment al hospital. British Journal of Criminology, 8:186- 203. Owen, D. R. (1972), The 47XYY male: a review. PsychoI. Bu ll. 79:209-233. Palmour R. M. (1983), Genetic models for the study of aggressive behavior. Prog, Neuro psychopharmacol. Biol. Psychiatry 7 :5 135 17. Pasamanick, B. (1956 ), Pregnancy experience and the development of behavior disorders in children. Am . J. Psych iat ry 112:613--{)1 7. - - ( 1961), Epidemiological investigations of some prenatal factors in the production of neuropsychiatric disorder. In: Comparative Epidemiology fo r Mental Disorders, eds. P. H. Hoch & J. Zubin . New York: Grune & Stratton , pp. 260-275. Patterson, G. R. (1977 ), Accelerating stimuli for two classes of coercive behaviors. J. Ab norm. Child Psyc hol., 5:335 - 350. J. Am.A cad. Ch ild Adol esc. Psy chia try, 31:3, Ma y 19 92

FROM ABUSE TO VIOLENCE

- - (1979) , A performance theory for coercive family interaction. In: The Analysis of Social Interactions: Methods. Issues. and Illustratio ns, ed. R. B. Caines. Hillsdale, NJ: Laurence Erlbaum. Pope, H. G. & Katz, D. L. (1987), Bodybuilder' s psychosis. Lancet, 1:863. - - - - (1988), Affective and psychot ic symptoms associated with anabolic steroid use. Am . 1. Psyc hiatry, 145:487-490 . Provence, S. & Lipton, R. (1962), Infants in Insti tutions. New York: Internationa l Universities. Rada, R. T., Laws, D. R, & Kellner, R. (1976), Plasma testosterone levels in the rapist. Psychosom. Med. 38 :257- 268 . Randrup , A. & Munkvad , 1. (1966), DOPA and other naturally occurring substances as causes of stereotype and rage in rats. Acta. Psychiatr. Scand. 42[Suppl. 19]:193. Reis, D. 1. (1972), Central Neurotran smitters in Aggression, S. F. Frazier. Aggression, 52:1 19- 147 . Reisert, I., Han, V., Lieth, E., Toran, A. D., Pilgrim, C. & Lauder, J. (1987), Sex steroids promote neurite growth in mesenceph alic tyrosine hydroxylase immunoreactive neuron in vitro. Internati onal Journal of Developmental Neuroscience , 5:91-98. Rieder, C. & Cicchetti, D. (1989), An organizational perspective on cognitive contro l function ing and cognitive-affecti ve balance in maltreated children. Developm ental Psychology , 25:382- 393. Rose, R., Holaday, J. & Bernstein, 1. (1971), Plasma testosterone, dominance rank and aggressive behaviour in male rhesus monkeys. Nature, 231:366. Rotton, J., Barry, T., Frey, J. & Soler, E. ( 1978), Air pollution and interpersonal attraction. J. Appl. Soc. Psyc hol, 8:57. Rutter, M. (1970), Sex differences in response to family stress. In: The Child and His Fam ily. eds, E. J. Antho ny & C. Kompernik. New York: Wiley. Sahakian, B. J. (1981), The neurochemic al basis of hyperactivity and aggression induced by social deprivation. In: Vulnerabilities to Delinquency, ed. D. O. Lewis. New York: Spectrum, pp. 173- 186. Schiavi, R., Theilgaard, A., Owen, D. et al. (1984), Sex chromosome anom alies, hormones and aggressivity. Arch . Gen . Psy chiatry, 41:93- 99. Seward, J. P. (1946), Aggressive behavior in the rat: IV. Submission determin ed by conditioning, extinction and disuse. J. Compo Psychol., 39:5 1. Siegel, A. & Flynn, J. P. (1968), Differential effects of electrical stimulation and lesions of the hippocampus and adjacent regions upon attack behavior of cats. Bra in Res. 7 :252-267 . Smetana, J. G. & Kelly, M. ( 1989), Social cognition in maltreated children. In: Child Maltreatm ent, eds. D. Cicchetti & V. Carlson. Cambridge: Cambridge U. Press, pp. 620-646.

Smith, D. E., King, M. D. & Hoebel, B. G. (1970 ), Lateral hyppothalamic control of killing: evidence for a cholinoceptive mechanism. Science 167 :900-90 1. Smith, M. L. & Simmel, E. C. ( 1977), Paternal effects on the development of social behavior in Mus Mu sculu s. in: Child Maltreatm ent: Theory and Research on the Causes and Consequen ces of Child Abuse and Neglect, eds. D. Cicchetti & V. Carlson. New York: Cambridge University Press, pp. 620-646. Southwick, C. H. (1968). Effect of maternal environment on aggressive behavior of inbred mice. Communications in Behavioral Biology, 1:129-1 32. Spitz, R. A. (1946), Anaclitic depression. Psychoanal. Study Child, 2:3 13- 342. Stott, D. H. (1973), Follow-up study from birth of the effect s of prenatal stresses. Del'. Med. Child Neural . 15:770- 787. - - Latchford, S. A. (1976), Prenatal antecedents of child health, development and behavior. 1. Am . Acad. Child Adoles c. Psychiatry 15:161- 191. Telfer, M. A. ( 1968), Are some criminals born that way? Think, 34:24-28. Tennant, F., Black, D. L. & Voy, R. O. (1988), Anabolic steroid dependence with opioid-type features. N. Engl. J. Med. 3 19-578. Tup in, J. P. (1987), Psychopharmacology and aggression. In: Clinical Treatm ent of the Violent Person, ed. L. H. Roth. pp. 79-94. Valzelli, L. (1974), 5-Hydroxytryptamine in aggressiveness. In: Advances in Bi ochem ica l Psycop ha rmacology, cd s, E. Costa, G. Gessa & M. Sandler. New York: Raven. Virkkunen , M., DeJong, J., Bartko, J., Goodwin, F. K. & Linnoila , M. (1989), Relationship of psychobiological variables to recidivism in violent offenders and impulsive fire setters. A rch. Gen. Psychiatry 46 :600-603. vom Saal, F. S. (1979), Prenatal exposure to androgen influences morphology and aggressive behavior of male and female mice. Horm. Behav. 12: I. - - (1984), The intrauterine positio n phenomenon: effects on physiology, aggressive behavior and population dynamics in house mice. In: Biological Perspe cti ves on Aggression. eds. K. J. Flannelly, R. J. Blancahard & D. C. Blanchard. New York: Liss. pp. 135- 179. Weiger, W. A. & Bear, D. M. (1988), An approach to the neurology of aggression. J. Psychiat. Res. 22 :85-98. Widom, C. S. (1989), The cycle of violence. Science, 244:160- 166. Witkin, H. A., Mednick, S. A., Schuylsinger, F. et al. ( 1976), Criminality in XYY and XXY men. Scien ce 193:547-555 . Yesavage, J. A. (I 983a), Bipolar illness: correlates of dangerous inpatient behavior. Br. J. Psychiatry 143:554-557 . - - (l983b), Correla tes of dangerou s behavior by schizophrenics in hospital. J. Psychoso m. Res. 18:225-231 .

From Pediatrics

Safety Practices and Living Conditions of Low-Income Urban Families. Lisa J. Santer, M.D., and Carol B. Stocking, Ph.D. Abstract. Inj uries remain the leading cause of mortalit y in children and disproportionately affect poor children. Prior injury prevention efforts have neglected the injury prevention needs of these children. One hundred thirty-three care givers of medically indigent urban children younger than 6 years old were interviewed regarding living conditions, previous injuries, and safety practices and knowledge. Functional smoke detectors and fire extinguishers were present in 75% and 27% of homes, respectively. Few respondents, regardless of previous poisoning experience, were cognizant of ipecac, had it in their homes, or had a good response to possible poisoning. Few homes had locked storage space, and most hazards were stored suboptimally. While the frequency of the use of automobiles was low, rides in a variety of vehicles were common with 63% of children who usually were restrained inadequately. Additionally, 89% of children aged 35 to 59 months and 6% of those younger than 3 years old sometimes bathed without adult supervision. These findings indicate the dramatic need for injury prevention programs focused on low-income urban families. Specific concerns include exposure to fires and burns, falls, hazardous travel conditions, dangerous chemical, choking, and drown ing. Lack of information and isolated care givers may result in poor supervision and response s to injur y of these children. We suggest potential interventions in each area. Pediatrics 199 1;88 :11 12-1118. J. Am. A ca d. Child A do lesc . Psych iat ry, 3 1:3, Ma y 1992

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