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Aggression in adolescents
JOURNAL OF ADOLESCENT HEALTH CARE 1:236-243, 1981
REVIEW ARTICLE
Aggression in Adolescents Aspects of Pathogenesis B A R B A R A GELLER, M.D. A N D D O N A L D E. G R E Y D A N U S , M.D.
The violent adolescent presents considerable difficulty to society and to health care professionals. ~ Thus, this discussion overviews some theories of pathogenesis regarding aggression in adolescence. There is special emPhasis on related concepts of neuroanatomy and neurobiochemistry, as well as hormonal influences and the associated psychosocial environment. Literature about the importance of drug abuse and the media is also reviewed. In addition, studies relating aggression to epilepsy and electroencephalographic changes are considered. It is hoped that this paper will aid th e interested clinician discern the vast and multidisciplinary literature describing aggression in adolescence. Future investigative endeavors will provide, it is hoped, more definitive biologic and social measurements to enable specific prevention and intervention strategies. KEY WORDS:
Adolescence Aggression Antisocial behavior Juvenile delinquency Violence
Neuroanatomic Concepts
Aggression in adolescence is often a serious and complex phenomenon. As a symptom per se it has rarely been the target of clinical study (1), but it is not uncommonly investigated as a manifestation of an unsocialized aggressive conduct disorder in children and adolescents or as a manifestation of the
From the Division of Child and Adolescent Psychiatry and the Adolescent Medicine Clinic, University of Rochester Medical Center, Rochester, New York. Direct reprint requests to: Barbara Geller, M.D., R-Wing, Strong Memorial Hospital, 300 Crittenden Boulevard, Rochester, NY 14642. Manuscript accepted December 4, 1980. 236 ISSN 0197-0070/81/010236-08/$02.25
adult equivalent, the antisocial personality. An understanding of the pathogenesis and management of aggressive behavior is particularly important to professionals called upon to evaluate the teenager, because the leading causes of death in this age group are violence related (homicide, accidents, and suicide) (2), and the incidence of violent crime begins to peak in late adolescence (3). Because the literature on aggression (1) includes a voluminous number of contributions by diverse disciplines, we believe a review of biological and psychosocial aspects of aggression in adolescents would be useful. Clinically, physicians are called upon to manage violent adolescents In this manuscript aggression is defined as statements or actions that threaten or produce damage to person or property (4); it does not include adaptive, assertive behavior.
Early investigation into the neuroanatomic basis of aggression began in the 1890s (5), when it was noticed that decorticate animals exhibited angry behaviors (e.g., growling, snarling) similar to those of intact animals who became angered by provocative stimuli in their natural environments. In the 1920s, Cannon coined the term "sham rage" for these phenomena (5). Papez (6), in 1937, made the important observation that actions accompanying emotions (such as the snarling of sham rage) originate in the limbic lobe, whereas the subjective feelings of being angry are based in the cerebral cortex. Papez (6) described the functions of the "limbic lobe", a conceptual rather than an anatomic structure. The limbic lobe comprises the areas of the brain involved with emotional expression and appetitive behavior
© Society for Adolescent Medicine, 1981 Published by Elsevier North Holland, Inc., 52 Vanderbilt Ave., New York, NY 10017
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(behaviors that follow a need-satiation-need pattern such as eating, sleeping, and coital activity) (7). Kluver and Bucy (8), in the late 1930's, resected the amygdala and hippocampal area (parts of the limbic lobe) of monkeys. These animals became hyperphagic and hypersexual. More importantly, they had no fear or anger, because of visual agnosia (inability to distinguish between the dangerous and nondangerous objects in the environment). This report was the first time the amygdala had been associated with aggressive action. This later became the basis for amygdalotomy, a neurosurgical procedure used by several investigators in human populations in an attempt to interrupt violent behavior without producing the appetite and sexual disturbance of the Kluver-Bucy syndrome (9-12). The work of Papez is useful here because the amygdalotomy should work best in patients who are violent in response to subcortical stimuli (limbic) rather than to conscious feelings secondary to environmental stimulation. Current literature indicates that amygdalotomy is a procedure to consider in severely braindamaged, retarded adolescents who are not responsive to pharmacologic intervention (9-12). Indeed, a patient who continually bangs his or her head on the wall over a period of years may be producing more actual brain damage than a precisely performed amygdalotomy.
Hormonal Influences in the Assessment of Aggressive Actions The investigation of hormonal influences during adolescence has been approached from several vantage points. The first question that arose was to what extent the expression of aggression is biologically as opposed to environmentally determined. Evidence for the role of biology is available from animal experiments (13), naturally occurring human experiments (14-18), and cross-cultural investigations (19). Regarding animal experimentation, Harlow's male monkeys who were raised with wire surrogate mothers engage in the same amount of rough and tumble play as male monkeys raised with biologic mothers. Thus, this type of play could not be learned behavior, because wire monkeys could not teach it (13). In cross-cultural studies, rough and tumble play is significantly increased in males compared with females, regardless of rearing methods (19). Thus, these two avenues point to the predominance of biologic factor s , as do the natural human experiments which include girls with congenital adrenal hyperplasia and girls whose mothers received pro-
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gesterone during pregnancy (14,15). Both of these groups as adolescents display increased tomboyishness and decreased feminine interest compared with normal controls. Similarly, boys whose mothers received estrogen during gestation have significantly fewer masculine interests during adolescence when compared with boys whose mothers have not (16). What are the specific biologic factors that have a role in the increased aggression in males? The answer to this question has focused on the role of androgens. Androgens increase three to five times in an 18-24 month span during adolescence (20), and the peak time of violent crimes (e.g., rape or homicide) occurs in late adolescence and young adulthood (from age 15 to 24 years) (21). There is, however, no clear-cut relationship between serum testosterone levels and the expression of violence, which may in part be due to the methodologic difficulties in studying testosterone levels and in studymg violence (22). There are no widely used assessment scales to measure violent actions; therefore, most investigators have develoPed scales to measure the number of assaults (physical and verbal) over a given time. A widely used attitudinal scale devised in 1953 (the Buss-Durkee Hostility Inventory, BDHI) measures attitudes and traits (i.e., not actions) (23). Studies differ as to whether the BDHI correlates with testosterone levels (24,25). In the past decade, a number of studies measured testosterone levels in prisoners (26,27), rapists (28), juvenile delinquents (29), and hockey players (30). In all these studies, there were rio abnormal testosterone elevations; however, there were significant differences between mean testosterone levels in the more Violent subjects when compared with less violent controls. For example, in One study convicts who were more violent and socially dominant in the prison inmate environment also had significantly higher mean testosterone levels compared with the less aggressive and less dominant inmates (27). In this regard, higher levels were also found in rhesus monkeys w h o were in the dominant social position (31). In another study no difference was found between the more aggressive and the less aggressive inmates, but there were significantly higher testosterone levels in young adult convicts who had been arrested for violent crimes when they were 11-16 years of age (26). In a study comparing violent rapists with less violent rapists and normal controls (28), the highest testosterone level was measured in a subject who had murdered his rape victim. As a group, the violent rapists had a significantly higher mean testosterone level than the less violent rapists
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and normal controls. Hockey players (30) who respond to threats most aggressively have significantly higher mean testosterone levels than their team* mates. Mattson et al. found no difference in mean testosterone levels between Tanner stage 5 juvenile delinquents and normal controls, but did find a sig n nificant difference between these two groups at Tanner stages 3 and 4 (29). The treatment implication must await further delineation of the cause and effect relationship in a homogeneously defined group of subjects. There may be patients whose testosterone levels will be elevated in response to a nonhormonal mechan i s m - e l e v a t e d testosterone levels as an effect of aggression. Another group of patients may have the primary disturbance in an exaggerated androgen production; in this group, the hormonal influence could be the causative factor. A specific treatment implication has been in use during the past decade, which involves treating sex offenders with antiandrogens (20,32,33) such as medroxyprogesterone and cyproterone. This treatment is effective in decreasing the number of sexual offenses, thus allowing the subject to remain in society and not in jail. Definitive studies have not yet been done to determine whether these antiandrogen agents have a general calming effect and are therefore of use in patients committing violent crimes of a nonsexual nature. In one uncontrolled, nonblind study, aggressive temporal lobe epileptics showed a decrease in violent behavior with medroxyprogesterone (34). Finally, XYY males do not have increased testosterone levels (35), although they may have an increased incidence of sexual offenses (36). When the methodologic differences are considered, XYY males do not appear to have an increased incidence of criminal behavior (36,37). In terms of the female aggression, there is evidence that increased aggressivity in females is related to a change in hormonal levels. Dalton (38) showed in 1961 an increase in truancy among adolescents and an increase in number of arrests among older subjects during the premenstrual part of the cycle, when estrogen and progesterone levels are falling, as compared with the incidence of truancy and arrests during the remainder of the menstrual cycle.
Drug Abuse Factors to be considered in the relationship between drugs and violent actions include: the social environment in which the drug was taken; acute vs.
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chronic usage; dose; individual metabolic variations such as differences in enzyme induction; and the psychologic reasons for the choice of a particular drug. Alcohol appears to be the most important substance abused in this regard. Five to ten percent of the general population are alcoholics; 17-48% of convicted felons are alcoholics (28). Also, 20-80% of homicides are committed while the perpetrator is under the influence of alcohol (39). The mechanisms by which alcohol is involved in the process of violent behavior are not understood. Androgen levels usually decrease in the cirrhotic alcoholic; therefore, in this group, this hormonal influence is not likely to be involved (40). Marijuana has been studied in human and laboratory subjects. Its effect on increased or decreased aggressive behavior varies with multiple factors. For example, in Eastern countries, marijuana use has been reported to cause an increase in aggressive behavior (41). However, the Eastern preparation is stronger; is used in higher doses; is used chronically; and the subjects are often underfed, sometimes to the point of starvation at the time of use (41). In the Western world, marijuana has been associated with placidity (42). In the 1960s, in a study of incarcerated adolescents, those convicted of less assaultive crimes said they preferred tetrahydrocannabinol because it lessened their hostility (43). In the same study, adolescent sex offenders preferred L-lysergic acid to lessen hostility. Marijuana has also been reported to transiently decrease serum testosterone levels in direct proportion to the dose (44). Both amphetamine (45) and phencyclidine (46) ("angel dust") have been associated with violent behavior. Amphetamine violence has been reported with chronic abuse, usually 100-500 rag/day, in subjects who, in addition to chronic use, have been exposed to an acute circumstance that might precipitate violent action (45). A recent report indicates that later in life, amphetamine abusers may develop paranoid psychoses (47). Acute paranoid delusions in the chronic abuser are often involved in the violent action. The high dosage used by the chronic amphetamine abuser is far greater than the mean daily dose (10-30 mg) given to children with the syndrome of attention deficit disorder and hyperactivity (48). Violent actions with phencyclidine are related to a toxic psychosis with paranoid ideation (46). The management implication of drug abuse has to do with appropriate psychologic intervention aimed at the addiction problem. In addition, recent
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work with endogenous opiate receptors suggests that there may be important biologic variations (49). This work may pave the way for more specific pharmacologic intervention in the future.
Electroencephalogram and Epilepsy Questions that have been evaluated in regard to the electroencephalogram (EEG) include: (1) whether or not specific EEG abnormalities are seen in violent individuals and (2) how the presence of a seizure disorder affects the expression of violent behavior. It has been known since the 1940s that criminals and juvenile delinquents have slowing and decreased voltage on the EEG (50). This nonspecific finding and more recent evidence from evoked cortical potential studies are interpreted as showing decreased central nervous system arousal and thus a need to seek stimulation to maintain a higher arousal state (51). This is based on the homeostatic theory in which individuals seek to maintain a "normal level of arousal" (51). Evoked potential studies of "actingout adolescents" also shows that these individuals may have lower central nervous system inhibition (52), consistent with their observed impulsivity. More prison inmates have abnormal EEGs than controls, and even more so if one considers prisoners who have committed violent crimes (53). Specific EEG patterns that might be a marker for violent individuals have been sought. With juvenile delinquency it had been postulated that a 14 and 6 spike per second wave pattern is seen more often in association with violent behavior and thus may be a marker for the violent aggressive delinquent (54). Other studies, however, show that this pattern is present in 15-58% of normal child and adolescent subjects (55), which is not more frequent than in juvenile delinquents (56). Furthermore, it is seen more commonly with drowsiness (57). Because criminals have decreased anxiety during the EEG, they show more drowsiness, which may explain why they have more 14 and 6 spike per second patterns (57). Rodin (58) and others (59) have reported that temporal lobe epilepsy is not associated with increased violence during the ictal episode. Several investigations have demonstrated that interictally, epileptics have more behavioral difficulty (60-63). Ounsted (60), in a study of 100 children and adolescents with temporal lobe epilepsy, found that 36% had rages interictally and that for most, the rage episodes began during the early school years. Rutter
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et al. (61) in the pediatric age group, Plutchik et al. (62) in adults, and Shukla et al. (63) in adults and children have demonstrated that interictally epileptics have more psychiatric difficulties and problems in adapting to daily living. Thus, aggression and other behavioral deviations are more prevalent in interictal epileptics. Lewis has described a triad in juvenile delinquents consisting of a history of early head trauma, paranoid ideation, and temporal lobe EEG spikes (64). Consequently, young epileptics merit evaluation for their potential aggressive and behavioral deviations as well as control of their seizures.
Neurotransmitters The role of the endogenous compounds involved in impulse transmission between nerve cells (neurotransmitters) has been studied in an effort to elucidate the biochemical processes involved in violent behavior, thus paving the way for specific pharmacologic interventions. Earlier animal investigations sought biochemical correlates of the rage phenomena in decorticate animals, the so-called sham rage, and of the violent phenomena exhibited by animals looking for food, the so-called predatory rage (65). Results showed an increase in circulating norepinephrine in animals with sham rage (66) and when acetylcholine analogs were injected into the cerebral ventricles, the predatory phenomena could be reproduced (67). Serotonin inhibited both rage reactions (68). Another study, however, shows that norepinephrine injected directly into animal brains does not replicate sham rage (69). Work in h u m a n subjects also suggests that noradrenergic mechanisms are involved. Aggressive prisoners have significantly higher serum and urinary levels of norepinephrine than their less violent inmates (70), and aggressive juvenile delinquents excrete significantly more norepinephrine than methylnorepinephrine in the urine (71). In addition, aggressive inmates have significantly more 3-methoxy-4-hydroxyphenylglycol, a product of norepinephrine metabolism, and less 5-hydroxyindolacetic acid, a serotonin metabolite, in their cerebrospinal fluid (72). Recently a peptide has been isolated from the urine of patients with generalized congenital lypodystrophy (73). This peptide produces aggression in laboratory animals, even though the patients are not clinically excessively aggressive. The nature of this peptide has yet to be elucidated. Phenylethylacetic acid, which is a metabolite of phenylethyl-
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amine, an endogenous amine similar to dextroamphetamine, has recently been shown to be increased in the blood of aggressive inmates (74). Neurotransmitter interactions are complex. The data suggest that a balance of compounds in interplay with other physiologic factors, e.g., hormones, individual metabolic variation, are involved in aggressive behavior (69). It is hoped that future investigation will result in more clinical application, specifically in regard to pharmacologic intervention.
Psychosocial Environment Children seem to do best in the context of a consistent, warm, caring relationship which begins early in life with one or a small number of caretakers (75). Deficits in the capacity to experience age-appropriate guilt have been described in deprived youngsters (76). One investigation demonstrated a progression from overly clinging dependent behavior in deprived 7-year-olds to antisocial activities by preadolescence (77). In the well-known West and Farrington studies of English delinquents (78), the most aggressive subjects had parents who were significantly more harsh and cold. The important role of parental modeling is best seen in abused children of parents who frequently have been abused themselves (79,80). In the Gluecks' studies of delinquency (81), inconsistent parenting was a feature of delinquent families. Inconsistent discipline is related to the phenomenon of extinction aggression (82), that is, aggression occurring in a situation where an expected reward does not occur (e.g., kicking the coffee machine after one puts in a quarter and nothing happens). The child who is reprimanded by a parent in a bad mood, when he expects to be rewarded, is in a similar situation. Treatment solutions have been geared to attempts toward producing outpatient counseling and inpatient residential and institutional environments that could prevent or undo deprivational damage. The outpatient counseling by Healy and Bonner (83) in the early part of this century in the juvenile court system attempted to elucidate the background, family history, and character structure of the youngsters. It was hoped that this knowledge would shed light on possible prevention strategies. Unfortunately, this was not the result. In 1939, the well-known Cambridge-Somerville study was begun (84). This project included 325 subjects and 325 controls. All subjects were males between 5 and 13 years of age who lived in a defined area. Subjects attended lay counseling sessions in
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the hope that this would prevent undersocialized behavior. On follow-up there were no differences in conviction rates between the subjects and controls. However, on breakdown of the various factors involved, it was found that there were significantly fewer convictions if counseling had begun early, especially between ages 5 and 8 years and if the children saw their counselor at least once weekly. These two findings are important in that they support the theory that early, intense, consistent, oneto-one interactions with an important adult may make a difference. An additional finding was that adolescents between the ages of 11 and 13 years who had a female counselor also had significantly fewer convictions. This is potentially important in that it is commonly believed that adolescents should be counseled by someone of their own sex. In subsequent years, few studies of the effectiveness of treatment of juvenile delinquent adolescents were done. One example of the type of study done in this area is that performed by the California Youth Authority (85). Juvenile delinquents were randomly divided into institutions that were structured as a prison, reformatory, or work camp. No significant differences in reconviction rates were found on follow-up of youngsters from the three different programs. The problem of violence and delinquent youth is sufficiently widespread to require a public health approach. As an analogy, individual outbreaks of cholera can be medically treated, but a clean water supply or a vaccine has more far-reaching effects. A behavior equivalent to a clean water supply would be a "clean" school system--one that could make a significant difference in the number of delinquent graduates. Such an effort is described in Fifteen Thousand Hours by Rutter et al. (86). This is a landmark study of high school students in England, who as children had been randomly assigned to schools to eliminate any potential of a preselection bias. They found that some schools produced fewer delinquents, fewer dropouts, and more students who passed exams. When they analyzed the factors involved, they found that setting firm limits; expecting the children to be on time, to do homework and to behave; setting difficult, but not too difficult, expectations; giving regular homework assignments; having principals who were interested in the students and could carry the program through with their staffs; and having some students who were high achievers in each class were important factors in producing the best results. They also found that the global ambiance in a particular school was more
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important than the sum of the individual factors. The practical implications of such an approach are enormous. For example, it would not be more of an economic burden to competently staff schools than to hire trained personnel for the special institutions needed when the regular schools fail. Finally, in England, hostels run as six- to eightperson group homes with live-in "parents" worked best when the husband and wife agreed on the approach, set firm limits, and had reasonable (not lax) expectations (87). Here, similar factors to those found in Fifteen Thousand Hours seem also to be operative.
Media There has been much concern with whether or not mass media (e.g., television, movies) are responsible for some of the violent aggressive behavior of some children and youth. Here again, there is a concern about what factors in the natural environment are significant in the production of violent individuals. In many studies it can be shown that for a brief period of time, after exposure to a violent television or movie episode, children and adolescents are significantly more aggressive than a control group who have not had a similar exposure (88). By "brief" is meant an hour or two of observation in a laboratory or natural setting. Long-term studies are difficult to design but are needed (89). In an attempt to do this, Berkowitz et al. (90) chose as their subjects adolescents in residential treatment programs in three different countries. In each setting, one cottage of adolescents was shown a violent aggressive movie and another was shown a nonaggressive movie. For the following week they were observed in their natural setting. Those adolescents who had seen the more aggressive movie displayed more verbal and physical aggression afterward. This investigation also included laboratory observations of the "stooge" protocol; in which the subject is told that his behavior influences whether or not another person will receive an electric shock or some other adverse stimulus. The protocol is referred to as "stooge" because, in fact, the person does not receive the shock. They found that those subjects who had been shown the aggressive movie were significantly more hostile in the laboratory setting. Some of the results do not distinguish between adaptive, assertive aggression and violent, antisocial aggression. For example, it was said that the aggressive youngster more often played the parts seen in the violent movie. Perhaps it is adaptive for ad-
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olescents to imitate and play the violent character. This could be preventive for further violence in real life. Here again, more well-controlled studies are needed to assess the impact of the media on behavior. We have reviewed the literature of several aspects of aggression in adolescence. It is hoped that future investigations will provide better understanding of the pathogenesis and delineate more specific treatments and preventive strategies.
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42. Abel EL: Changes in personality response ratings induced by smoking marihuana. Bri J Addict 67:221-223, 1972 43. Tinklenberg JR, Woodrow KM: Drug use among youthful assaultive and sexual offenders, in Aggression. Res Publ Assoc Res Nerv Ment Dis, Vol. 52. Baltimore Williams & Wilkins, 1974 44. Kolodny RC, Masters WH, Kolodny RM, et al: Depression of plasma testosterone levels after chronic intensive marihuana use. N Engl J Med 290:872-874, 1974 45. Ellinwood EH: Assault and homicide associated with amphetamine abuse. Am J Psychiatry 127:1170-1175, 1971 46. Fauman MA, Fauman BJ: Violence associated with phencylidine abuse. Am J Psychiatry 136:1584-1585, 1979 47. McLellan AT, Woody GE, O'Brien CP: Development of psychiatric illness in drug abusers: Possible role of drug preference. N Engl J Med 301:1310-1314, 1979 48. Cantwell DP, Carlson GA: Stimulants, in Werry JS (ed): Pediatric Psychopharmacology. New York, Bruner Mazel, 1978 49. Goldstein A: Opiate receptors and opioid peptides: A tenyear overview, in Lipton MA, DiMascio A, Killam KF (eds): Psychopharmacology: A Generation of Progress. New York, Raven Press, 1978 50. Hill D: Cerebral dysrhythmia, its significance in aggressive behavior. Proc R Soc Med 37:327-390, 1944 51. Zuckerman M: Sensation seeking and psychopathy. In: Hare RD, Schalling D, eds. Psycopathic Behavior: Approaches to Research. New York, John Wiley & Sons, 1978 52. Buchsbaum M: Average evoked response augmenting reducing in schizophrenia and affective disorders, in Freedman DX (ed): Res Publ Assoc Res Nerv Ment Dis, Vol. 54. New York, Raven Press, 1975 53. Pincus JH, Tucker GJ: Behavioral Neurology. 2nd Edition. New York, Oxford University Press, 1978 54. Gibbs EL, Gibbs FA: Electroencephalographic evidence of thalamic and hypothalamic epilepsy. Neurology 1:136-145, 1951 55. Harris R: Relationship between EEG abnormality and aggressive and anti-social behavior--a critical appraisal, in Hersov LA, Berger M, Shaffer D (eds): Aggression and Antisocial Behavior in Childhood and Adolescence. New York, Pergamon Press, 1978 56. Kohen-Raz R, Assael M: EEG and Rorschach findings in a group of juvenile delinquents suspect of organic brain disorder. Acta Paedopsychiatr 33:251-258, 1966 57. Mawson AR, Mawson CD: Psychopathy and arousal: A new interpretation of the psychophysiological literature. Biol Psychiatry 12:49-74, 1977 58. Rodin EA: Psychomotor epilepsy and aggressive behavior. Arch Gen Psychiatry 28:210-213, 1973 59. Gunn J, Fenton G: Epilepsy, automatism and crime. Lancet 1:1173-1176, 1971 60. Ounsted C: Aggression and epilepsy: Rage in children with temporal lobe epilepsy. J Psychosom Res 13:237-242, 1969 61. Rutter M, Tizard J, Yule W, et al: Isle of Wight studies, 1964-1974. Psychol Med 6:313-332, 1976 62. Plutchik R, Climent C, Ervin F: Research strategies for the study of human violence, in Smith WL, Kling A (eds): Issues in Brain/Behavior Control. New York, Spectrum Books, 1976 63. Shukla GD, Srivastava ON, Katiyar BD, et al: Psychiatric manifestations in temporal lobe epilepsy: A controlled study. Br J Psychiatry 135:411-417, 1979 64. Lewis DO: Delinquency, psychomotor epileptic symptomatology and paranoid symptomatology. Am J Psychiatry 133:1395-1398, 1976
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65. Reis DJ: Central neurotransmitters in aggression, in AggresSion. Res Publ Assoc Res Nerv Ment Dis, Vol. 52. Baltimore, Williams & Wilkins, 1974 66. Reis DJ, Gunne LM: Sham rage produced by amygdaloid stimulation led to decrease of brain noradrenaline and adrenal gland adrenaline and noradrenaline. Science 149:450-451, 1965 67. Beleslin BD, Samardzic R: Comparative study of aggressive behavior after injection of cholinomimetics, anticholinesterases, nicotinic and muscarinic ganglionic stimulants into the cerebral ventricles of conscious cats: Failure of nicotinic drugs to evoke aggression. Psychopharmacology 60:147-153, 1979 68. Mandel P, Mack G, Kempf E: Molecular basis of some models of aggressive behaVior, in Sandler M (ed): Psychopharmacology of Aggression. New York, Raven Press, 1979 69. Thiessen DD: Pharmacological and Biochemical Correlates of Aggression. Springfield, Illinois; Charles C. Thomas, 1976 70. Woodman DD, Hinton JW, O'Neil MT: Plasma catecholamines, stress and aggression in maximum security patients. Biol Psychology 6:147-154, 1978 71. Ekkers CL: Catecholamine excretion, conscience function and aggressive behavior. Biol Psychology 3:15-30, 1975 72. Brown GL, Balianger JC, Minichiello MD, et al: Human aggression and its relationship to cerebrospinal fluid 5-hydroxyindoleacetic acid, 3-methoxy4-hydroxyphenylglycol, and homovanillic acid, in Sandler M (ed): Psychopharmacology of Aggression. New York, Raven Press, 1979 73. Reichelt KL, Trygstad OE, Foss I, et al: Purification and characterization of an aggression-inducing peptide from patients with congenital generalized Iipodystrophy, in Sandler M (ed): Psychopharmacology of Aggression. New York, Raven Press, 1979 74. Sandier M, Ruthven CRJ, Goodwin BL, et ah Phenylethylamine in human aggressive behavior, in Sandler M (ed): Psychopharmacology of Aggression. New York, Raven Press, 1979 75. Ainsworth MD: The effects of maternal deprivation: A review of findings and controversy in the context of research strategy, in Deprivation of Maternal Care: A Reassessment of Its Effects. Geneva, World Health Organization, 1962 76. Goldfarb W: Emotional and intellectual consequences of psychological deprivation in infancy, in Hoch PH, Zubin J (eds): Psychopathology of Childhood. New York, Grune & Stratton, 1955
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77. Fish B, Shapiro T: A typology of children's psychiatric disorders. J Am Acad Child Psychiatry 4:32-52, 1965 78. West DJ, Farrington DP: Who Becomes Delinquent? London, Heineman Educational Books, 1973 79. Spinetta JJ, Rigler D: The child-abusing parent: A psychological review. Psychol Bull 77:296-304, 1972 80. Steele BF, Pollack D: A psychiatric study of parents who abuse children and small infants, in Helfer RE, Kempe CH (eds): The Battered Child. Chicago, University of Chicago Press, 1968 81. Glueck S, Glueck E: Unraveling Juvenile Delinquency. Cambridge, Harvard University Press, 1950 82. Kelly DD: The experimental imperative: Laboratory analysis of aggressive behaviors, in Aggression. Res Publ Assoc Res Nerv Ment Dis, Vol. 52: Baltimore, Williams & Wilkins, 1974 83. Healy W, Bronner AF: New Light on Delinquency and Its Treatment. New Haven, Yale University Press, 1936 84. McCord J, McCord W: A follow-up report on the Cambridge-Somerville Youth Study. Ann Am Acad Pol Soc Sci 322:89-96, 1959 85. Burchard JD, Harig TP: Behavior modification and juvenile delinquency, in Leitenberg H (ed): Handbook of Behavior Modification and Behavior Therapy. Englewood Cliffs; New Jersey, Prentice-Hall, 1976 86. Rutter M, Maughan B, Mortimore P, et ah Fifteen Thousand Hours. Cambridge, Harvard University Press, 1979 87. Clarke RVG, Cornish DB: The effectiveness of residential treatment for delinquents, in Hersov LA, Berger M, Shaffer D (eds): Aggression and Antisocial Behavior in Childhood and Adolescence. New York, Pergamon Press, 1978 88. Stein AH, Friedrich LK: Impact of television on children and youth, in Hetherington EM (ed): Review of Child Development Research, Vol. 5. Chicago, University of Chicago Press, 1975 89. Eron LD, Huesmann LR, Lefkowitz MM, et al: How learning conditions in early childhood--including mass media--relate to aggression in late adolescence. Am J Orthopsychiatry 44:517-531, 1974 90. Berkowitz L, Parke RD, Leyens JP, et al: Experiments on the reactions of juvenile delinquents to filmed violence, in Hersov LA, Berger M, Shaffer D (eds): Aggression and Antisocial Behavior in Childhood and Adolescence. New York, Pergamon Press, 1978
REVIEW ARTICLE
Aggression in Adolescents Aspects of Pathogenesis B A R B A R A GELLER, M.D. A N D D O N A L D E. G R E Y D A N U S , M.D.
The violent adolescent presents considerable difficulty to society and to health care professionals. ~ Thus, this discussion overviews some theories of pathogenesis regarding aggression in adolescence. There is special emPhasis on related concepts of neuroanatomy and neurobiochemistry, as well as hormonal influences and the associated psychosocial environment. Literature about the importance of drug abuse and the media is also reviewed. In addition, studies relating aggression to epilepsy and electroencephalographic changes are considered. It is hoped that this paper will aid th e interested clinician discern the vast and multidisciplinary literature describing aggression in adolescence. Future investigative endeavors will provide, it is hoped, more definitive biologic and social measurements to enable specific prevention and intervention strategies. KEY WORDS:
Adolescence Aggression Antisocial behavior Juvenile delinquency Violence
Neuroanatomic Concepts
Aggression in adolescence is often a serious and complex phenomenon. As a symptom per se it has rarely been the target of clinical study (1), but it is not uncommonly investigated as a manifestation of an unsocialized aggressive conduct disorder in children and adolescents or as a manifestation of the
From the Division of Child and Adolescent Psychiatry and the Adolescent Medicine Clinic, University of Rochester Medical Center, Rochester, New York. Direct reprint requests to: Barbara Geller, M.D., R-Wing, Strong Memorial Hospital, 300 Crittenden Boulevard, Rochester, NY 14642. Manuscript accepted December 4, 1980. 236 ISSN 0197-0070/81/010236-08/$02.25
adult equivalent, the antisocial personality. An understanding of the pathogenesis and management of aggressive behavior is particularly important to professionals called upon to evaluate the teenager, because the leading causes of death in this age group are violence related (homicide, accidents, and suicide) (2), and the incidence of violent crime begins to peak in late adolescence (3). Because the literature on aggression (1) includes a voluminous number of contributions by diverse disciplines, we believe a review of biological and psychosocial aspects of aggression in adolescents would be useful. Clinically, physicians are called upon to manage violent adolescents In this manuscript aggression is defined as statements or actions that threaten or produce damage to person or property (4); it does not include adaptive, assertive behavior.
Early investigation into the neuroanatomic basis of aggression began in the 1890s (5), when it was noticed that decorticate animals exhibited angry behaviors (e.g., growling, snarling) similar to those of intact animals who became angered by provocative stimuli in their natural environments. In the 1920s, Cannon coined the term "sham rage" for these phenomena (5). Papez (6), in 1937, made the important observation that actions accompanying emotions (such as the snarling of sham rage) originate in the limbic lobe, whereas the subjective feelings of being angry are based in the cerebral cortex. Papez (6) described the functions of the "limbic lobe", a conceptual rather than an anatomic structure. The limbic lobe comprises the areas of the brain involved with emotional expression and appetitive behavior
© Society for Adolescent Medicine, 1981 Published by Elsevier North Holland, Inc., 52 Vanderbilt Ave., New York, NY 10017
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(behaviors that follow a need-satiation-need pattern such as eating, sleeping, and coital activity) (7). Kluver and Bucy (8), in the late 1930's, resected the amygdala and hippocampal area (parts of the limbic lobe) of monkeys. These animals became hyperphagic and hypersexual. More importantly, they had no fear or anger, because of visual agnosia (inability to distinguish between the dangerous and nondangerous objects in the environment). This report was the first time the amygdala had been associated with aggressive action. This later became the basis for amygdalotomy, a neurosurgical procedure used by several investigators in human populations in an attempt to interrupt violent behavior without producing the appetite and sexual disturbance of the Kluver-Bucy syndrome (9-12). The work of Papez is useful here because the amygdalotomy should work best in patients who are violent in response to subcortical stimuli (limbic) rather than to conscious feelings secondary to environmental stimulation. Current literature indicates that amygdalotomy is a procedure to consider in severely braindamaged, retarded adolescents who are not responsive to pharmacologic intervention (9-12). Indeed, a patient who continually bangs his or her head on the wall over a period of years may be producing more actual brain damage than a precisely performed amygdalotomy.
Hormonal Influences in the Assessment of Aggressive Actions The investigation of hormonal influences during adolescence has been approached from several vantage points. The first question that arose was to what extent the expression of aggression is biologically as opposed to environmentally determined. Evidence for the role of biology is available from animal experiments (13), naturally occurring human experiments (14-18), and cross-cultural investigations (19). Regarding animal experimentation, Harlow's male monkeys who were raised with wire surrogate mothers engage in the same amount of rough and tumble play as male monkeys raised with biologic mothers. Thus, this type of play could not be learned behavior, because wire monkeys could not teach it (13). In cross-cultural studies, rough and tumble play is significantly increased in males compared with females, regardless of rearing methods (19). Thus, these two avenues point to the predominance of biologic factor s , as do the natural human experiments which include girls with congenital adrenal hyperplasia and girls whose mothers received pro-
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gesterone during pregnancy (14,15). Both of these groups as adolescents display increased tomboyishness and decreased feminine interest compared with normal controls. Similarly, boys whose mothers received estrogen during gestation have significantly fewer masculine interests during adolescence when compared with boys whose mothers have not (16). What are the specific biologic factors that have a role in the increased aggression in males? The answer to this question has focused on the role of androgens. Androgens increase three to five times in an 18-24 month span during adolescence (20), and the peak time of violent crimes (e.g., rape or homicide) occurs in late adolescence and young adulthood (from age 15 to 24 years) (21). There is, however, no clear-cut relationship between serum testosterone levels and the expression of violence, which may in part be due to the methodologic difficulties in studying testosterone levels and in studymg violence (22). There are no widely used assessment scales to measure violent actions; therefore, most investigators have develoPed scales to measure the number of assaults (physical and verbal) over a given time. A widely used attitudinal scale devised in 1953 (the Buss-Durkee Hostility Inventory, BDHI) measures attitudes and traits (i.e., not actions) (23). Studies differ as to whether the BDHI correlates with testosterone levels (24,25). In the past decade, a number of studies measured testosterone levels in prisoners (26,27), rapists (28), juvenile delinquents (29), and hockey players (30). In all these studies, there were rio abnormal testosterone elevations; however, there were significant differences between mean testosterone levels in the more Violent subjects when compared with less violent controls. For example, in One study convicts who were more violent and socially dominant in the prison inmate environment also had significantly higher mean testosterone levels compared with the less aggressive and less dominant inmates (27). In this regard, higher levels were also found in rhesus monkeys w h o were in the dominant social position (31). In another study no difference was found between the more aggressive and the less aggressive inmates, but there were significantly higher testosterone levels in young adult convicts who had been arrested for violent crimes when they were 11-16 years of age (26). In a study comparing violent rapists with less violent rapists and normal controls (28), the highest testosterone level was measured in a subject who had murdered his rape victim. As a group, the violent rapists had a significantly higher mean testosterone level than the less violent rapists
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and normal controls. Hockey players (30) who respond to threats most aggressively have significantly higher mean testosterone levels than their team* mates. Mattson et al. found no difference in mean testosterone levels between Tanner stage 5 juvenile delinquents and normal controls, but did find a sig n nificant difference between these two groups at Tanner stages 3 and 4 (29). The treatment implication must await further delineation of the cause and effect relationship in a homogeneously defined group of subjects. There may be patients whose testosterone levels will be elevated in response to a nonhormonal mechan i s m - e l e v a t e d testosterone levels as an effect of aggression. Another group of patients may have the primary disturbance in an exaggerated androgen production; in this group, the hormonal influence could be the causative factor. A specific treatment implication has been in use during the past decade, which involves treating sex offenders with antiandrogens (20,32,33) such as medroxyprogesterone and cyproterone. This treatment is effective in decreasing the number of sexual offenses, thus allowing the subject to remain in society and not in jail. Definitive studies have not yet been done to determine whether these antiandrogen agents have a general calming effect and are therefore of use in patients committing violent crimes of a nonsexual nature. In one uncontrolled, nonblind study, aggressive temporal lobe epileptics showed a decrease in violent behavior with medroxyprogesterone (34). Finally, XYY males do not have increased testosterone levels (35), although they may have an increased incidence of sexual offenses (36). When the methodologic differences are considered, XYY males do not appear to have an increased incidence of criminal behavior (36,37). In terms of the female aggression, there is evidence that increased aggressivity in females is related to a change in hormonal levels. Dalton (38) showed in 1961 an increase in truancy among adolescents and an increase in number of arrests among older subjects during the premenstrual part of the cycle, when estrogen and progesterone levels are falling, as compared with the incidence of truancy and arrests during the remainder of the menstrual cycle.
Drug Abuse Factors to be considered in the relationship between drugs and violent actions include: the social environment in which the drug was taken; acute vs.
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chronic usage; dose; individual metabolic variations such as differences in enzyme induction; and the psychologic reasons for the choice of a particular drug. Alcohol appears to be the most important substance abused in this regard. Five to ten percent of the general population are alcoholics; 17-48% of convicted felons are alcoholics (28). Also, 20-80% of homicides are committed while the perpetrator is under the influence of alcohol (39). The mechanisms by which alcohol is involved in the process of violent behavior are not understood. Androgen levels usually decrease in the cirrhotic alcoholic; therefore, in this group, this hormonal influence is not likely to be involved (40). Marijuana has been studied in human and laboratory subjects. Its effect on increased or decreased aggressive behavior varies with multiple factors. For example, in Eastern countries, marijuana use has been reported to cause an increase in aggressive behavior (41). However, the Eastern preparation is stronger; is used in higher doses; is used chronically; and the subjects are often underfed, sometimes to the point of starvation at the time of use (41). In the Western world, marijuana has been associated with placidity (42). In the 1960s, in a study of incarcerated adolescents, those convicted of less assaultive crimes said they preferred tetrahydrocannabinol because it lessened their hostility (43). In the same study, adolescent sex offenders preferred L-lysergic acid to lessen hostility. Marijuana has also been reported to transiently decrease serum testosterone levels in direct proportion to the dose (44). Both amphetamine (45) and phencyclidine (46) ("angel dust") have been associated with violent behavior. Amphetamine violence has been reported with chronic abuse, usually 100-500 rag/day, in subjects who, in addition to chronic use, have been exposed to an acute circumstance that might precipitate violent action (45). A recent report indicates that later in life, amphetamine abusers may develop paranoid psychoses (47). Acute paranoid delusions in the chronic abuser are often involved in the violent action. The high dosage used by the chronic amphetamine abuser is far greater than the mean daily dose (10-30 mg) given to children with the syndrome of attention deficit disorder and hyperactivity (48). Violent actions with phencyclidine are related to a toxic psychosis with paranoid ideation (46). The management implication of drug abuse has to do with appropriate psychologic intervention aimed at the addiction problem. In addition, recent
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work with endogenous opiate receptors suggests that there may be important biologic variations (49). This work may pave the way for more specific pharmacologic intervention in the future.
Electroencephalogram and Epilepsy Questions that have been evaluated in regard to the electroencephalogram (EEG) include: (1) whether or not specific EEG abnormalities are seen in violent individuals and (2) how the presence of a seizure disorder affects the expression of violent behavior. It has been known since the 1940s that criminals and juvenile delinquents have slowing and decreased voltage on the EEG (50). This nonspecific finding and more recent evidence from evoked cortical potential studies are interpreted as showing decreased central nervous system arousal and thus a need to seek stimulation to maintain a higher arousal state (51). This is based on the homeostatic theory in which individuals seek to maintain a "normal level of arousal" (51). Evoked potential studies of "actingout adolescents" also shows that these individuals may have lower central nervous system inhibition (52), consistent with their observed impulsivity. More prison inmates have abnormal EEGs than controls, and even more so if one considers prisoners who have committed violent crimes (53). Specific EEG patterns that might be a marker for violent individuals have been sought. With juvenile delinquency it had been postulated that a 14 and 6 spike per second wave pattern is seen more often in association with violent behavior and thus may be a marker for the violent aggressive delinquent (54). Other studies, however, show that this pattern is present in 15-58% of normal child and adolescent subjects (55), which is not more frequent than in juvenile delinquents (56). Furthermore, it is seen more commonly with drowsiness (57). Because criminals have decreased anxiety during the EEG, they show more drowsiness, which may explain why they have more 14 and 6 spike per second patterns (57). Rodin (58) and others (59) have reported that temporal lobe epilepsy is not associated with increased violence during the ictal episode. Several investigations have demonstrated that interictally, epileptics have more behavioral difficulty (60-63). Ounsted (60), in a study of 100 children and adolescents with temporal lobe epilepsy, found that 36% had rages interictally and that for most, the rage episodes began during the early school years. Rutter
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et al. (61) in the pediatric age group, Plutchik et al. (62) in adults, and Shukla et al. (63) in adults and children have demonstrated that interictally epileptics have more psychiatric difficulties and problems in adapting to daily living. Thus, aggression and other behavioral deviations are more prevalent in interictal epileptics. Lewis has described a triad in juvenile delinquents consisting of a history of early head trauma, paranoid ideation, and temporal lobe EEG spikes (64). Consequently, young epileptics merit evaluation for their potential aggressive and behavioral deviations as well as control of their seizures.
Neurotransmitters The role of the endogenous compounds involved in impulse transmission between nerve cells (neurotransmitters) has been studied in an effort to elucidate the biochemical processes involved in violent behavior, thus paving the way for specific pharmacologic interventions. Earlier animal investigations sought biochemical correlates of the rage phenomena in decorticate animals, the so-called sham rage, and of the violent phenomena exhibited by animals looking for food, the so-called predatory rage (65). Results showed an increase in circulating norepinephrine in animals with sham rage (66) and when acetylcholine analogs were injected into the cerebral ventricles, the predatory phenomena could be reproduced (67). Serotonin inhibited both rage reactions (68). Another study, however, shows that norepinephrine injected directly into animal brains does not replicate sham rage (69). Work in h u m a n subjects also suggests that noradrenergic mechanisms are involved. Aggressive prisoners have significantly higher serum and urinary levels of norepinephrine than their less violent inmates (70), and aggressive juvenile delinquents excrete significantly more norepinephrine than methylnorepinephrine in the urine (71). In addition, aggressive inmates have significantly more 3-methoxy-4-hydroxyphenylglycol, a product of norepinephrine metabolism, and less 5-hydroxyindolacetic acid, a serotonin metabolite, in their cerebrospinal fluid (72). Recently a peptide has been isolated from the urine of patients with generalized congenital lypodystrophy (73). This peptide produces aggression in laboratory animals, even though the patients are not clinically excessively aggressive. The nature of this peptide has yet to be elucidated. Phenylethylacetic acid, which is a metabolite of phenylethyl-
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amine, an endogenous amine similar to dextroamphetamine, has recently been shown to be increased in the blood of aggressive inmates (74). Neurotransmitter interactions are complex. The data suggest that a balance of compounds in interplay with other physiologic factors, e.g., hormones, individual metabolic variation, are involved in aggressive behavior (69). It is hoped that future investigation will result in more clinical application, specifically in regard to pharmacologic intervention.
Psychosocial Environment Children seem to do best in the context of a consistent, warm, caring relationship which begins early in life with one or a small number of caretakers (75). Deficits in the capacity to experience age-appropriate guilt have been described in deprived youngsters (76). One investigation demonstrated a progression from overly clinging dependent behavior in deprived 7-year-olds to antisocial activities by preadolescence (77). In the well-known West and Farrington studies of English delinquents (78), the most aggressive subjects had parents who were significantly more harsh and cold. The important role of parental modeling is best seen in abused children of parents who frequently have been abused themselves (79,80). In the Gluecks' studies of delinquency (81), inconsistent parenting was a feature of delinquent families. Inconsistent discipline is related to the phenomenon of extinction aggression (82), that is, aggression occurring in a situation where an expected reward does not occur (e.g., kicking the coffee machine after one puts in a quarter and nothing happens). The child who is reprimanded by a parent in a bad mood, when he expects to be rewarded, is in a similar situation. Treatment solutions have been geared to attempts toward producing outpatient counseling and inpatient residential and institutional environments that could prevent or undo deprivational damage. The outpatient counseling by Healy and Bonner (83) in the early part of this century in the juvenile court system attempted to elucidate the background, family history, and character structure of the youngsters. It was hoped that this knowledge would shed light on possible prevention strategies. Unfortunately, this was not the result. In 1939, the well-known Cambridge-Somerville study was begun (84). This project included 325 subjects and 325 controls. All subjects were males between 5 and 13 years of age who lived in a defined area. Subjects attended lay counseling sessions in
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the hope that this would prevent undersocialized behavior. On follow-up there were no differences in conviction rates between the subjects and controls. However, on breakdown of the various factors involved, it was found that there were significantly fewer convictions if counseling had begun early, especially between ages 5 and 8 years and if the children saw their counselor at least once weekly. These two findings are important in that they support the theory that early, intense, consistent, oneto-one interactions with an important adult may make a difference. An additional finding was that adolescents between the ages of 11 and 13 years who had a female counselor also had significantly fewer convictions. This is potentially important in that it is commonly believed that adolescents should be counseled by someone of their own sex. In subsequent years, few studies of the effectiveness of treatment of juvenile delinquent adolescents were done. One example of the type of study done in this area is that performed by the California Youth Authority (85). Juvenile delinquents were randomly divided into institutions that were structured as a prison, reformatory, or work camp. No significant differences in reconviction rates were found on follow-up of youngsters from the three different programs. The problem of violence and delinquent youth is sufficiently widespread to require a public health approach. As an analogy, individual outbreaks of cholera can be medically treated, but a clean water supply or a vaccine has more far-reaching effects. A behavior equivalent to a clean water supply would be a "clean" school system--one that could make a significant difference in the number of delinquent graduates. Such an effort is described in Fifteen Thousand Hours by Rutter et al. (86). This is a landmark study of high school students in England, who as children had been randomly assigned to schools to eliminate any potential of a preselection bias. They found that some schools produced fewer delinquents, fewer dropouts, and more students who passed exams. When they analyzed the factors involved, they found that setting firm limits; expecting the children to be on time, to do homework and to behave; setting difficult, but not too difficult, expectations; giving regular homework assignments; having principals who were interested in the students and could carry the program through with their staffs; and having some students who were high achievers in each class were important factors in producing the best results. They also found that the global ambiance in a particular school was more
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important than the sum of the individual factors. The practical implications of such an approach are enormous. For example, it would not be more of an economic burden to competently staff schools than to hire trained personnel for the special institutions needed when the regular schools fail. Finally, in England, hostels run as six- to eightperson group homes with live-in "parents" worked best when the husband and wife agreed on the approach, set firm limits, and had reasonable (not lax) expectations (87). Here, similar factors to those found in Fifteen Thousand Hours seem also to be operative.
Media There has been much concern with whether or not mass media (e.g., television, movies) are responsible for some of the violent aggressive behavior of some children and youth. Here again, there is a concern about what factors in the natural environment are significant in the production of violent individuals. In many studies it can be shown that for a brief period of time, after exposure to a violent television or movie episode, children and adolescents are significantly more aggressive than a control group who have not had a similar exposure (88). By "brief" is meant an hour or two of observation in a laboratory or natural setting. Long-term studies are difficult to design but are needed (89). In an attempt to do this, Berkowitz et al. (90) chose as their subjects adolescents in residential treatment programs in three different countries. In each setting, one cottage of adolescents was shown a violent aggressive movie and another was shown a nonaggressive movie. For the following week they were observed in their natural setting. Those adolescents who had seen the more aggressive movie displayed more verbal and physical aggression afterward. This investigation also included laboratory observations of the "stooge" protocol; in which the subject is told that his behavior influences whether or not another person will receive an electric shock or some other adverse stimulus. The protocol is referred to as "stooge" because, in fact, the person does not receive the shock. They found that those subjects who had been shown the aggressive movie were significantly more hostile in the laboratory setting. Some of the results do not distinguish between adaptive, assertive aggression and violent, antisocial aggression. For example, it was said that the aggressive youngster more often played the parts seen in the violent movie. Perhaps it is adaptive for ad-
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olescents to imitate and play the violent character. This could be preventive for further violence in real life. Here again, more well-controlled studies are needed to assess the impact of the media on behavior. We have reviewed the literature of several aspects of aggression in adolescence. It is hoped that future investigations will provide better understanding of the pathogenesis and delineate more specific treatments and preventive strategies.
References 1. Crabtree JM, Moyer KE: Bibliography of Aggressive Behavior: A Reader's Guide to the Research Literature. New York, AR. Liss, 1977 2. Holinger PC: Adolescent suicide: An epidemiological study of recent trends. Am I Psychiatry 135:754-756, 1978 3. Shaffer D: Suicide in childhood and early adolescence. J Child Psychol Psychiatry 15:275-291, 1974 4. Marini JL, Sheard MH: Antiagressive effect of lithium ion in man. Acta Psychiatr Scand 55:269-286, 1977 5. Glusman M: The hypothalamic "savage" syndrome, in Aggression. Res Publ Assoc Nerv Ment Dis. Baltimore, Williams & Wilkins, 1974 6. Papez JW: A proposed mechanism of emotion. Arch Neurol Psychiatry 38:725-743, 1937 7. Rapaport D: On the psychoanalytic theory of motivation. Nebr Symp Motivation 8:173-224, 1960 8. Kluver H, Bucy PC: Preliminary analysis of functions of the temporal lobes in monkeys. Arch Neurol Psychiatry 42:979, 1939 9. Narabayashi H, Nagao T, Saito Y, et al: Stereotaxic amygdalotomy for behavior disorders. Arch Neurol 9:11-26, 1963 10. Gunn J: Evaluation of violence. Proc R Soc Med 66:1133-1135, 1973 11. Hitchcock E: Amygdalotomy for aggression, In Sandler M (ed): Psychopharmacology of Aggression. New York, Raven Press, 1979 12. Small IF, Heimburger RF, Small JG, et al: Follow-up of stereotaxic amygdalotomy for seizure and behavior disorders. Biol Psychiatry 12:401-411, 1977 13. Hutt C: Biological bases of psychological sex differences. Am J Dis Child 132:170-177, 1978 14. Money J, Ehrhardt AA: Man and Woman, Boy and Girl. Baltimore, Johns Hopkins University Press, 1972 15. Reinisch J: Effects of prenatal hormone exposure on physical and psychological development in humans and animals: With a note on the state of the field, in Sachar EJ (ed): Hormones, Behavior and Psychopathology. New York, Raven Press, 1976 16. Yalom ID, Green R, Fish N: Prenatal exposure to female hormones: Effect on psychosexual development in boys. Arch Gen Psychiatry 28:554-561, 1973 17. Rose RM: Neuroendocrine correlates of sexual and aggressive behavior in humans, in Lipton MA, DiMascio A, Killam KF (eds): Psychopharmacology: A Generation of Progress. New York, Raven Press, 1978 18. Imperato-McGinley J, Peterson RE, Gautier T, et al: Androgens and the evolution of male-gender identity among male pseudohermaphrodites with 5 a-reductase deficiency. N Engl J Med 300:1233-1237,1979
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