It is impossible to make a one-to-one correlation between violence and specific forms of neurological dysfunction or the brain regions involved. There is no “violence center” in the brain, that, when stimulated or destroyed, always produces violent behavior, though occasional case reports of such a sequence exist (Mark and Ervin, 1970; Ashford et al., 1980; St Hilaire 1980). There is no region of the brain identified on positron emission tomography (PET) or other imaging techniques whose abnormal activity allows doctors to predict that the individual whose brain is abnormal will be violent. If one believes, however, that all thought and behavior derive from the brain, including morality ethics (Greene et al., 2001), then the brain would be a reasonable starting point for studies of the origins violence. As we will see below, the neurological status of most violent prisoners is abnormal (Blake et al., 1995); yet the relationship between neurological dysfunction of the brain and the propensity to violence is complex.
Brain Damage
To demonstrate brain damage in violent criminals requires a variety of testing procedures. No single test infallibly provides a touchstone to determine the presence
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or absence of brain damage dysfunction. The history (e.g., learning disorder, epilepsy, brain injury), the physical, neurological examination, neuropsychological tests, the electroencephalogram, and various imaging tests individually may reveal brain dysfunction. (Tranel, 1994; Van Elst et al., 2000). Usually, all these tests are not concordant. Each may fail to identify brain dysfunction, that manifests on another test. In this situation, the abnormal test is definitive. A normal result on one test cannot invalidate or neutralize the diagnostic significance of another abnormal test.
In general, magnetic resonance imaging (MRI) is a very reliable indicator of gross structural disturbances of the brain (tumors, strokes, multiple sclerosis) but seldom provides useful information with regard to primary generalized epilepsy, retardation, dementia, intoxication, learning disorders, clumsiness, and movement disorders. The electroencephalogram (EEG) is better for diagnosing epilepsy than the MRI is. Psychological tests are best for retardation, dementia, and learning disorders. The physical neurological examination is best for clumsiness and movement disorders. A battery of neurological signs provides evidence of diffuse cortical, mainly frontal, dysfunction (Jenkyn et al., 1977, 1985) and the Categories test from Halstead-Reitan battery, Wisconsin Card Sorting Test, Trailmaking A and B, and tests of continuous motor performance engage those portions of the brain that subserve executive functions. Each test of brain function can appear normal in patients with moderate to severe brain disorders that have been revealed in another or other tests. In combination, these tests have virtually always revealed evidence of brain dysfunction in violent individuals (Blake et al., 1995; Wong 1997).
Newer imaging techniques that reflect brain metabolism rather than structure such as PET scans, single photon emission computed tomography (SPECT) scans, and functional magnetic resonance imaging, (fMR) are only beginning to be used evaluate cognition in subjects who have been violent (Soderstrom et al., 2000). Position emission tomography scans, performed during frontal lobe activation and compared to controls, have identified dysfunctional regions of the brain in violent individuals (Raine et al., 1994, 1997). Functional MR has revealed abnormalities in the brains of dyslexic children when they were attempting to carry out reading-related tasks (Shaywitz et al., 1998). Though as many half of prison inmates are dyslexic (Moody et al., 2000), fMR has not yet been applied to violent delinquents.
Many violent individuals have histories of traumatic brain injuries (TBI), and this may be a common source of neurological deficits among them. Repeated mild brain injuries occurring over months or years can result in cumulative neurological and cognitive defects. Mild concussions can have a cumulative effect. In a study of high school football players who were tested before playing and then after apparent recovery from a brain injury sustained in the game, mild concussions caused clinically detectable deficits (McCrea et al., 1997). Athletes
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who have suffered concussions and who recovered are more at risk to be detectably and permanently brain damaged by subsequent head injuries than those who have never had a concussion. This is now called the Second Impact Syndrome (MMWR, 1997). This finding has provided the basis for a position statement of the American Academy Neurology on the management closed-head injuries among athletes, limiting their return to the sport following concussion to prevent serious brain damage (Kelly and Rosenberg, 1998). Cognitive dysfunction is not only a short-term consequence of concussion but also a predisposing risk factor for brain damage from future concussion (Teasdale and Engberg, 1997). Despite general agreement about the hazards of repeated, mild traumatic brain injuries, it is not possible to determine the exact site of injury in every case nor to define the exact role of each episode damaging the brain (Kelly and Rosenberg, 1998).
Brain injury, especially the trauma of child abuse, can have devastating effects on children, as the inflicted injuries are usually recurrent.Ewing-Cobbs et al. (1998) reported that single episodes of inflicted TBI, though comparable in severity to noninflicted TBI, were significantly more likely impair the cognitive function of the victim, even when the TBI did not cause prolonged impairment of consciousness. Mental deficiency was present in 45 percent of the inflicted and 5 percent of the noninflicted TBI groups.
There is no doubt that damage to certain parts of the brain confers a special vulnerability to later violence. Frontal lobe injuries are especially likely facilitate violent behavior. In a study of Vietnam veterans who sustained penetrating brain injuries, those with frontal lobe damage were significantly more likely to be violent in the succeeding years than the veterans who sustained penetrating injuries elsewhere in the brain. Sustaining frontal lobe injury does not guarantee violence; the majority of the frontally injured veterans had not acted violently at follow-up (Grafman et al., 1996). Reduction of frontal neocortical grey matter may underlie the pathophysiology even of the aggression in some patients with epilepsy of temporal lobe origin (Woermann et al., 2000). The temporal and frontal poles, especially the undersurfaces, are the most likely sites of contusion following traumatic brain injury. Repeated concussions, defined as brain injuries that cause temporary cognitive changes, can cause permanent effects even when each is not severe enough to cause bleeding that detectable on computed tomography (CT) scans. Presumably this is the result of the shearing effect of injuries upon axonal nerve processes (Pearl, 1998).
Shaking babies and other abusive acts can produce widespread axonal damage. Beta-amyloid precursor protein has been described by immunohistochemistry in the brain tissue of fatally abused children obtained at autopsy (Shannon et al., 1998). The physical abuse of infants is not rare. In Scotland, for example, the risk of a child suffering nonaccidental head injury by his or her first birthday is 1 in 4065 (Barlow and Minns, 2000). The extent of the changes induced by
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trauma is comparable to the changes induced by severe hypoxia (Gleckman, 1999).
Brain injuries, including those from conditions that generate epilepsy and mental retardation, can impair executive functioning and lead to the disinhibition of impulses, irritability, and poor judgment. Individuals with violent impulses may express them only when disinhibited.
The temporary encephalopathy of intoxication also provides a neurologic basis for disinhibition. More than half of all homicides are committed by intoxicated individuals (Yarvis, 1994). The extent of encephalopathy caused by intoxicants like alcohol can be assessed with clinical testing and with blood urine levels at the time of intoxication. All tests brain structure and function of body fluids are likely to be normal after the intoxicant has been metabolized. Cocaine and amphetamines are especially likely to result in violence as these drugs induce a sense of invulnerability akin to mania (Post, 1975; McIntyre, 1979). This powerful disinhibiting effect is especially sought out by depressed individuals who are treating themselves with street drugs such as PCP, methamphetamine, and cocaine (Cohen, 1984). Prolonged use of these stimulants induces paranoid delusions and a mental state that is difficult to distinguish from paranoid schizophrenia, except that it ultimately clears after the drug has been fully metabolized (Rosse et al., 1994). Stimulants thus induce a form of neurologically based behavioral disinhibition and paranoia, which we regard as two of the three main vulnerabilites to violence (see below). The prevalence of the use of cocaine correlates with and may predict the rise fall of violent crime in U.S. cities (Golub and Johnson, 1994; Blumstein et al., 2000)
Despite the association of violence with brain damage and intoxication, it is very clear that most individuals who are damaged, intoxicated, or both are not violent. It is likely that other factors that interact with neurologic brain dysfunction such as mental illness and the experience of abuse in childhood interact with brain damage/intoxication to produce a vulnerability violent behavior (Loberg, 1983).
Antisocial Personality and the Frontal Lobe
There is a tendency to categorize repeatedly violent behavior as manifestation of antisocial personality disorder (ASPD). Though there is no doubt that murderers have acted antisocially, this diagnosis does not provide an understanding of their antisocial behavior. It is more a moral label than medical diagnosis. The list of symptoms that describes ASPD in DSM-IV is very similar to that which might describe patients with frontal lobe damage (e.g., failure to conform to social norms, impulsivity, irritability, recklessness, irresponsibility, lack of
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remorse, indifference). Thus, ASPD may reflect frontal disease (Damasio et al., 1994).
Quantitative analysis of MRI scans has shown deficient volume the frontal lobes in people with ASPD as compared with normal controls and drug abusers who did not have antisocial personality disorder (Raine et al., 2000). Raine and colleagues (1994, 1997) have compared PET scans of 41 murderers who pleaded “not guilty by reason of insanity” (NGRI) with 41 controls during a continuous performance test. This visual test activates the frontal region of the brain, as it requires focused attention and mental vigilance for a prolonged period. The premotor frontal cortex in the murderers failed to activate. No deficit was found in the temporal or occipital cortex. Murderers tended to show less activation in the left subcortical regions (amygdala, hippocampus, and thalamus) but higher activation than controls in the homologous regions of right hemisphere (Raine et al., 1994, 1997). The frontal lobes project to the corpus striatum, the pallidum, the dorsomedial nucleus of the thalamus, hippocampus, and else-where (Chow and Cummings, 1999). Dysfunction in these regions can give rise to disinhibited “frontal” type behavior, even though they are subcortical or not located in the frontal lobes (Mesulum, 2000).
Neurotransmitters and Hormones
To explain violence, it is not necessary and probably incorrect to reach out to certain commonly invoked factors whose role is uncertain like elevated testosterone levels, low serotonin levels, or genetic influences. Testosterone is not always elevated in violent individuals. It can be nonviolent individuals and lowering the testosterone levels of violent men does not prevent them from committing future violent crimes (Heim and Hursch, 1979; Raboch et al., 1987; Richer and Crismon, 1993; Hall, 1995; Stalenheim et al., 1998).
For approximately 25 years, biologists have reported a correlation between low cerebrospinal fluid concentration of serotonin and various behavioral abnormalities, including violent and criminal behavior. The more than 100 studies published so far are not in accord. At first, the behavior that was reported to be associated with low serotonin was depression, later associations were with aggression, then with impulsive, aggression and still later with alcoholism. Not every individual with low serotonin is depressed, aggressive, impulsive or alcoholic nor does every individual with any or all of these behaviors have low serotonin levels. Alper (1995) reviewed this subject and concluded that the relationship of low levels brain serotonin to behavior was uncertain.
Because discrete behaviors have been associated with specific genetic and chromosomal disorders e.g., OCD (Tourettes), self-destruction (Lesch-Nyhan),
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and insatiable appetite (Prader-Willi) (Nyhan, 1976; Laurance et al., 1981; Pauls et al., 1986), it might be reasonable to postulate that a genetic propensity to violence may exist. This possibility has been eliminated by extensive studies in Scandanavia by Mednick and his colleagues (1984) who compared the rates of violent crime among the biologic parents and adoptive parents of adopted children. These reports have convincingly shown that violent crime is simply not a genetically transmitted characteristic.
Mental Illness
There is strong evidence to support a causal connection between paranoid delusions and violence (Taylor Gunn, 1984; Taylor, 1985;Soderstrom et al., 2000). The degree of schizophrenic symptoms is a predictor of dangerousness in hospitalized schizophrenics (Yesavage, 1984). Among men convicted of homicide and arson, a high proportion were considered definitely to have been driven by psychotic symptoms to commit offenses (Taylor, 1985). Variability over the course of time in the intensity of paranoia is quite characteristic depression, mania, schizophrenia, and drug intoxication may determine the timing of acts of violence. Of 500 British murderers whose psychiatric reports were reviewed, 44 percent had a lifetime history of mental illness, and 14 had mental symptoms at the time of the homicide (Shaw et al., 1999). In Sweden, 63 percent of murderers had had prior psychiatric care, 16 committed suicide, and 70 percent were intoxicated at the time of homicide (Lindquist, 1986). Major mental disorder is thus an important factor in violence, especially when comorbid with the encephalopathy of substance abuse (Rasanen et al., 1998; Steadman et al., 1998; Wallace 1998).
There is also a strong link between mood disorder and violent crime. Homicide and depression are closely connected, along with the experience of child abuse (Rosenbaum and Bennett, 1986). Unipolar depression causes irritability and anger (Fava, 1998) and bipolar affective disorder can also cause anger and aggression (Oquendo et al., 2000). Male and female adolescents adults are more likely to be aggressive when they are clinically depressed (Knox et al., 2000). Intrafamilial violence directed at spouses or children also has been linked to depression (Bourget et al., 2000) and to excessive suspiciousness i.e., paranoia (Rosenbaum and Bennett., 1986). It is not easy to differentiate repetitive nonrepetitive, paranoid and premeditated violence as opposed to unplanned, impulsive violence. Both share similar underlying vulnerabilities (Wong et al., 1997). Intermittent explosive disorders as defined in DSM-IV probably represent bipolar affective disorder and disinhibition, mainly caused by intoxication (McElroy, 1999).
Paranoia is seen not only in patients with disorders that fall within the scope
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of psychiatric practice. It exists on a spectrum ranging from mild excessive suspiciousness to delusions of persecution. All degrees paranoia, even delusions, are nonspecific symptoms. The diseases that can give rise to paranoia vary considerably and include schizophrenia, mania, depression. Neurological conditions can also cause paranoia. Among these conditions is drug intoxication. In fact, any condition of the brain that can cause cognitive impairment: encephalitis, stroke, epilepsy, thyroid disease, vitamin deficiency, Alzheimer's disease, etc. can lead to paranoid thinking.
Despite a strong correlation of paranoid thinking and depression with violence, how can we explain the fact that most paranoid, depressed, manic, psychotic individuals and most mentally ill individuals are not violent? This question is quite similar to the one that could be asked about neurological damage and the answer is the same. Violent individuals may bring other vulnerabilities to their mental symptoms and neurological damage that, under stress, lead to violence. The most important of these is the experience child abuse.
Abuse
The behavioral effects of abuse are noticeable and obvious in primary school years (Feldman et al., 1995). A study of 665 children 9–17 years old revealed a history of abuse in 172. The authors compared the abused with nonabused children. Associated with the experience of physical abuse were global social impairment, poor social competence, major depression, agoraphobia, generalized anxiety as well conduct disorder and oppositional defiant disorder (Flisher et al., 1997; Levitan et al., 1998; Ford 1999).
Child abuse can have devastating consequences for children and for the adults they later become. Abuse early in life correlates with depression (DeBellis et al., 1999; Kauffman et al., 2000), aggression, anxiety, suicide (Fergusson 1996), impulsivity, antisocial personality disorder (Luntz and Widom, 1994), borderline personality disorder (Paris et al., 1996a, b; Gudzer 1999), PTSD (Famularo et al., 1996), and conversion disorders (Wyllie 1999).
There is a growing perception that prolonged child abuse can permanently change the structure and function of the brain (Newport Nemeroff, 2002). Child abuse has thus moved from the purely sociologic and psychological realm of interest into the neurological sphere as well. Abuse can damage brain by direct trauma. More insidiously and pervasively, it can alter the basic developmental anatomy, physiology, and functioning of the brain.
Though the physical and sexual abuse of infants children goes beyond emotional neglect in destructive potential, the effects of neglect were described decades ago and confirmed more recently (Spitz and Cobliner, 1966; Provence, 1967; McClellan et al., 1995; Rutter, 1998). The emotional neglect of institutionalized
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infants in the first years of life can cause long-lasting behavioral-cognitive changes. The early isolation of immature monkeys also induces long-lasting behavioral changes (Harlow et al., 1971). These responses of the immature mammalian brain may be analogous to the imprinting experience of newly hatched goslings (Lorenz, 1970).
What the developing brain registers through its sensory systems about surrounding environment is increasingly recognized as a critical factor that permanently changes the brain by altering its connections. There is an exuberant development of synaptic connections between nerve cells in the first months and years of life and this connectivity is both pared down developed by experience. The changes in synaptic function that occur as an individual matures have been correlated with PET measures of cerebral glucose utilization (Chugani, 1998).
Connections that are not used at critical times lost forever (Huttenlocher and Dabholkar, 1997). The synaptic connections that form in infancy may represent the anatomical substrate for neural plasticity and for early learning as well as the superior capacity of the immature brain to reorganize after injury (Cao et al., 1994). The lack of development synaptic connections may be the substrate for mental retardation and learning disorders (Huttenlocher, 1991).
Experience is critical for the functional and structural maturation of connections in the mammalian cortex. Through experience, immature circuits are “sculpted.” Experience-dependent neural activity endows the brain with an ongoing ability to accommodate changing inputs during development and throughout life (Katz and Shatz, 1996). Deprived of early experience or presented with an abnormal experience during its early development, the functioning of the cortex is disrupted.
The visual system provides a model of the early sensitivity to environment shown by the connections of nerve cells in the brain. If an infant is born with a cataract, the cataract must be removed early because if it is not, vision will never develop in the formerly visually deprived eye. This is not true of adults. If dense cataracts are removed from the sightless eye of an adult, blind for years, vision can be restored. Amblyopia ex-anopsia is permanent blindness that develops in a child with strabismus. This form of blindness occurs only childhood. The development of amblyopia in humans (Grigg et al., 1996; Sengpiel and Blakemore, 1996) illustrates the obliteration of a genetic endowment, present at birth, by abnormal sensory stimulation. Similar permanent changes in the cerebral cortex can occur in other sensory and motor systems when these are manipulated early in life (Singer, 1995). Hearing, somatosensory systems, and motor development all can be permanently affected by early experience (Huntley, 1997), including emotional experience (Joseph, 1998, 1999). Physical abuse can alter the quantitative EEG (Teicher et al., 1997; Ito et al., 1998), MRI (Bremner and Narayan, 1999), behavior (George, 1979).
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Unbearable early stress from severe physical and sexual abuse might cause neurological changes in a number of different ways. A state chronic hyperarousal may lead to neurochemical changes in abused children (Kendall-Tackett, 2000). Stress can alter the development of the hypothalamic-pituitary-adrenal axis. In preclinical studies, levels of corticotropin releasing factor (CRF) correlate with brain changes. Corticotropin releasing factor hypersecretion throughout life may result from severe abuse in childhood and this could underlie the psychopathology that follows abuse (Heim et al., 2000). High concentrations of excitatory amino acids have been found in the ventricular cerebrospinal fluid of badly abused children and this could be a source of excitotoxic damage (Ruppel et al., 2001). Nuclear magnetic resonance studies have directly linked abuse, PTSD, and neuronal loss. A low ratio of N-acetylaspartate to creatine, implying a loss of neural integrity, was reported in the anterior cingulate 11 young victims of abuse who had PTSD, compared with age and sex matched controls (De Bellis et al., 2000).
The memory loss of dissociative amnesia in PTSD may result from the toxic action of high, prolonged levels glucorticosteroids on the hippocampus, which is involved in the storage and retrieval of memories (Joseph, 1999). Quantitative MRI studies of the brain in abused populations reveal decreased brain volumes (Bremner, 1997; Driessen et al., 2000). Positron emission tomography studies of sexually abused women with and without PTSD correlated with dysfunction of the medial premotor cortex, hippocampus, and visual association cortex (Bremner et al., 1999; Shin et al., 1999). The changes seen clinically and on imaging tests may be the result of developmental and neurochemical factors as indicated above or simple physical injury to the brain.
Violence as a Complex Psycho-Social-Biologic Interaction
Raine and his colleagues (1997) classified 4269 male children born living in Denmark according to two variables. The first was whether there were complications at birth (which loosely correlates with neurological impairment). The second was whether the child had been rejected by the mother (whether child was unplanned, unwanted, etc.). This correlates, loosely, with neglect. Looking back 18 years later, the authors found that children who were not rejected and who had no birth complications had roughly the same risk of becoming criminally violent by age 18 years as those with only one of the risk factors, approximately 3 percent. For the children with birth complications who had also been rejected, however, the risk of violence tripled. In fact, children with both problems accounted for 18 percent of all the violent crimes committed by the 4269 children, even though they made up only 4.5 percent of the group.
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It is thus very likely that several factors combine to produce a vulnerability violent behavior (Cadoret et al., 1995).
A considerable body of data adumbrates a plausible environmental, psychological and neurological interaction that leads to violence. Violent behavior is actually a rare event committed by only small number of individuals each whom is not violent all the time. Less than 6 percent of some populations commit up to 70 percent of the violent crimes (Wolfgang, 1975). Considering its rarity, violent crime is abnormal by definition. Certainly one is justified in asking the question, “What is wrong with this (violent) person? Could there be something wrong with his/her brain?” One of us (JHP) has had the opportunity of examining a significant number of murderers and less violent adults delinquents. This experience has led to a hypothesis of the potential causes violent behavior (Pincus, 2001). Findings from studies of seriously violent offenders indicate that three factors often crucially influence the likelihood of violence:
All three factors have been found in about two-thirds of violent juveniles (Lewis et al., 1979) and in murderers (Feldman 1986; Lewis et al., 1986; Blake and Pincus, 1995). No violent individual examined by JHP has been free of all three of these factors.
We think it likely that these correlates of violence play an important role in the causation of violence even though most people with only a one of these factors—abuse, brain damage, or paranoid thinking—are not violent. It is also likely that many individuals who have all three factors are not violent or at least not violent all the time. According to our theory, precipitating factors (such as anger or jealousy) that would ordinarily not produce a violent reaction are sufficient only in individuals who carry these vulnerabilities.
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The concordance of damage, abuse and paranoid thinking was particularly striking in a group of 14 young men who were awaiting execution for crimes committed before they were 18 years old. The 14 men comprised the entire population of juvenile murderers in four states and represented 38 percent the entire population of condemned juvenile murderers in the U.S. at that time. All but one had been physically or sexually abused both. Sixty-four percent had major neurological impairments and only two had full-scale IQ scores over 90. Ten were paranoid, and the rest displayed mood disorders bizarre behavior. Half had actually been psychotic with psychiatric hospitalizations before committing the capital crime (Lewis et al., 1988).
Of 15 other death row inmates, evaluated only because of the proximity their execution dates, not because of supposed brain damage, 13 had suffered severe physical abuse, sexual abuse, or both by parents (Feldman et al., 1986). Twelve had neurological deficits and had sustained concussions or worse. Six were chronically psychotic, three had been episodically psychotic; two had bipolar mood disorder. Nine of the 15 subjects suffered psychiatric symptoms during childhood severe enough for consultation. Four had attempted suicide in childhood. Eight expressed paranoid ideas at the time of examination (Lewis et al., 1986).
How do neurological deficits, paranoia, and the experience of abuse relate to the etiology of violence? A follow-up study 95 delinquent 15-year-old boys 7 years after initial evaluation suggested that paranoid thinking, neurological dysfunction, and abuse were not merely additive, but that these vulnerabilities interacted to increase the risk and severity of adult violent criminality. The absence of these variables among incarcerated juvenile delinquents at age 15 predicted future nonviolent behavior over the following 7 years 85 percent of the time (Lewis et al., 1989).
Estimates of the prevalence previous physical and sexual abuse among incarcerated violent juvenile delinquents have reached up to 80 percent (Lewis et al., 1979). In prisoners held on death row who have been convicted of homicide, both juveniles (Lewis, 1988) and adults (Feldman, 1986; Blake and Pincus, 1995) have prevalence rates of prior sexual and/or physical abuse in their childhoods that has approached 100 percent. Among nondelinquents matched with delinquents for sex, age, race, and socioeconomic level, the prevalence rate of abuse is much lower (13%) (Lewis et al., 1987). The amount of has never been quantified. It seems reasonable to postulate that severity, frequency, duration of episodes, and years exposure could vary that the worst abuse would be the most harmful.
Despite the high prevalence of severe abuse among violent criminals, causal role of abuse in violent behavior must be complex since only a minority of abused children become violent criminals. Follow-up studies of children who have been subjected to abuse have described increased levels of aggressive behavior
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when compared with controls, but most previously abused children appear to be neither disturbed nor aggressive. In only a minority of families in which abuse was severe enough to lead outside intervention is there child abuse in the next generation (Widom, 1989). Even if under-reporting of abuse seriously reduced the apparent rate of intergenerational abuse, it is very clear that abuse does not always generate abuse, let alone other violent crimes. Abuse alone is not enough to produce a violent criminal under most circumstances. The capacity of many abused people to lead relatively normal lives is a testament the resilience of the human spirit (the plasticity brain), yet some formerly abused people do become violent and dangerous to society, there is a statistical link between the experience of abuse and later violence (Widom, 1989).
Sociological Aspects of Violence
The prevalence of violence varies among different groups and it may be worthwhile to utilize the theory of interacting variables explain this variation. For example, violent crime is much more common among African-Americans. The homicide death rate among all American men aged 15 to 24 rose from 22 per 100,000 in 1987 to 37 per 100,000 1994. The homicide death rate for young African-American males in 1993 was 167 per 100,000 (Bureau of Justice Statistics, 1996). This high homicide rate among African-Americans is not likely to be the result of a genetic vulnerability. The theory that an abnormal gene causes human violent criminal behavior has been definitively contradicted by clinical adoption studies (Mednick et al., 1984; Brennan et al., 1996). There however, solid evidence that the three factors we believe to underlie violence are disproportionately prevalent in the African-American population.
In 1996 the number of cases reported child abuse among African-American children was twice their proportion in the general population (Child Maltreatment 1996; Report from the States to the National Child Abuse and Neglect Data System—U.S. Department of Health and Human Services). Conditions that harm the brain besides physical abuse are also more prevalent in the African-American community. These include lead poisoning (Sargent et al., 1995), traumatic brain injuries (Jager et al., 2000), and drug abuse during pregnancy (Wieman et al., 1994). Schizophrenia may also be more prevalent (Strakowski 1996). If the interplay of abuse, neurologic damage, and mental illness causes violent crime, their overrepresentation in the African-American community may explain the demographic facts.
Socioeconomic level is an important factor in violent crimes. Is this a matter of income and housing or rather the unequal prevalence of abuse, brain damage, and mental illness that varies according to socioeconomic level? According to
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the National Incidence Study (Sedlak and Broadhurst, 1996), the poorest children with family incomes of less than $15,000 per year experienced more than twice the rate of physical abuse as children with annual family incomes $15,000 to $30,000, and 12 times the rate of those children in families with income of over $30,000. The reason that lower income is associated with increased abuse may reflect a greater tendency among the lowest socioeconomic groups to use illicit drugs (Sedlak and Broadhurst, 1996). Serious mental illness, like schizophrenia, is more common in the lower social classes. Child abuse may generate brain damage. Thus, varying rates of neurological damage, abuse, and mental illness depending on socioeconomic group may explain many of the puzzling demographic features of violent crime.
The thesis that the vulnerability to commit violent crimes is the result of interaction of severe abuse in childhood (physical and/or sexual) with neurologic disturbances and mental illness can be utilized to explain the gender difference. Although it would be an overstatement to say that women are not violent, is also true that men commit violent crimes such as homicide more frequently than women by margins of approximately 9 to 1. Men commit 93 to 98 percent gang-related, drug-related, sex-related, and felony murder. The nearly exclusive focus of whatever violence is commited by women lies within the family relationship. Women commit 37 percent of all homicides intimates and 39 of infanticides. Women, mothers, and stepmothers are responsible primarily for 61 percent of the cases physical abuse children (Bureau Justice Statistics 1976-99; Child Maltreatment, 1996). If the theory about the interaction of three factors that produces a vulnerability to violence is correct, we must look at the distribution of these factors in groups that are more likely to be violent, in this case males.
Boys and girls are near parity with regard to the prevalence of abuse mental illness, but neurologic damage is much more common in males. Both the behavioral vulnerability to the effects of abuse and the severity are worse in males.
In this country, 48 percent of physical abuse victims are girls as are 77 of reported sexual abuse victims (Child Maltreatment, 1996). A report from Sweden (Edgardh and Ormstad, 2000) of the prevalence a history sexual abuse in a representative sample of almost 2000 teenagers attending secondary school indicated that 2.3 percent of boys and 7.1 percent girls had been sexually abused. The mean age at the time of first abuse was 9 years for both sexes. 1.2 percent of boys and 3.1 girls reported penetration orally, vaginally, or anally. Suicide attempts other acts of self-harm were reported by 33 percent of the abused boys (and 5% of the nonabused boys) and by 30 percent of the abused girls (and 9% of the nonabused girls). The sexual penetration of children is always likely to be painful and tissue-destructive, especially given the fact that almost two-thirds of the child victims in U.S. are prepubertal
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(less than 11 years old) and 39 percent are less than 7 old (Child Maltreatment, 1996).
Sexual abuse is more damaging to the psyches of boys than girls. Garnefski and Diekstra (1997) compared 745 high school students (151 boys and 594 girls) who reported a history of sexual abuse with a matched group students without such a history. A larger proportion of the sexually abused students reported emotional problems, aggressive and criminal behaviors, addiction-risk behaviors and suicidality. Sexually abused boys had considerably more problems in each of these areas than sexually abused girls did. The differences could not be attributed to the finding that the sexually abused boys were also more likely have been physically abused than were the sexually abused girls. This study indicated that the aftermath of sexual abuse for boys is even worse than it is for girls.
Boys are also more likely to be seriously physically injured by physical abuse (nonsexual) as evidenced by the fact that 56 percent of the children killed abuse are boys (Child Maltreatment, 1996; Mahoney et al., 2000). This is a meaningful gender difference but cannot explain the order of magnitude difference between the sexes in the numbers of homicides committed by men and the almost exclusive focus of serious violence by women within a family relationship.
The distribution of mental illness does not explain the greater male propensity to violence. Males do not have higher rates of mental illness. The prevalence of serious mental illnesses that can cause paranoid delusions, like schizophrenia and bipolar affective disorder, is about equal by gender (Bijl et al., 1998). Schizophrenia starts a bit earlier in men and is generally somewhat more severe, probably because of a preexistent neurologic vulnerability (Leung and Chue, 2000). Males with schizophrenia consistently show poorer cognitive functioning than women before becoming schizophrenic. Males also demonstrate more “negative” symptoms such as withdrawal, apathy, and inability to relate others. These negative symptoms do not respond well to antipsychotic drug treatment. Male schizophrenics have more cognitive deficits, structural brain abnormalities, and neurophysiologic abnormalities. These findings suggest that there is more neurologic disablity among male schizophrenics (Hendrick et al., 2000).
Mania has about the same prevalence in both sexes (Hendrick et al., 2000). Unipolar depression is actually 1.5 to 3 times more prevalent among women (Ustun, 2000), but the overall morbidity of mental illness is approximately the same for both genders in large-population studies (Bijl et al., 1998).
On the other hand, neurological dysfunction is much more common among boys. Attention-deficit hyperactivity disorder (Arnold, 1996), childhood autism (Smalley et al., 1988), pervasive developmental disorders (Volkman et al., 1993), dyslexia (Flannery et al., 2000), developmental dysphasia (Rapin and Allen, 1998), and certain forms of mental retardation are more prevalent among males
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by margins of up to 4 or 5 to 1. These abnormalities may be inherited as X-linked traits, like the Fragile X syndrome, a chromosomal abnormality that causes more cases of mental retardation than Trisomy 21 (mongolism) and affects only males (Boue et al., 1997). Even normal boys demonstrate patterns of behavior that seem to reflect delayed brain development much more frequently than girls do. The behavior of little girls in primary school is, in general, better modulated and mature.
“Immaturity” and “as yet undeveloped” are related concepts given that immaturity has a physiologic and anatomic basis. There is some preliminary evidence that the development of the circuitry brain is slower in males than in females (Benes et al., 1994; Overman 1996; De Bellis 2001). This supports the old hypothesis that testosterone, male hormone, impedes aspects of brain development and makes the male brain more vulnerable to a variety of learning and behavioral disorders (Rapin Allen, 1988) to the kinds of unmodulated, careless motor activity that can result in traumatic brain injury, which is also much more common in boys (Consensus Conference, 1999; Jager et al., 2000).
The unequal distribution of neurologic dysfunction between the sexes may account for much of the greater vulnerability males to violence. The abnormal behavioral patterns imposed by neurologic deficits and delayed development can elicit severe parental responses, especially in abusive homes. In this way neurologic deficits can contribute to abuse and to the alienation of victims who, as a result of abuse, may tend to mistrust others (paranoia).
Supporting the link between abuse and neurologic damage is the fact that in developmentally disabled children, reported abuse is more common than in nondisabled children. In a population-based epidemiologic study (Sullivan and Knutson, 2000), a link between neurologic, educationally relevant disablility and abuse was discovered. Fully 31 percent of disabled children were abused, a rate 3.4 times greater than their nondisabled peers.
Not only are males more likely to be neurologically disabled, and not does disability impose a greater risk of abuse, but males with disability are more likely than females with disability to be abused. In a study of 1834 abused children, disabled boys represented a significantly larger proportion of physically abused, sexually abused, and neglected children than would be expected from the respective proportion of abused and neglected children without disabilities; though half of abused children without disabilities were boys, 65 percent abused children with disabilities were boys (Sobsey et al., 1997).
The combination of neurologic defects with abuse and mental illness is severalfold more common in boys because neurologic defects are severalfold more common in boys, The abuse of damaged boys is more common than that damaged girls and is more harmful to the boys. These links between neurologic deficit and abuse adequately explain the increased prevalence of violence among
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males and these considerations also support the theory of the origins violence that we have presented.
Abuse is humiliating, degrading, and is likely to impose a sense of worth-lessness, helplessness, anxiety, hopelessness, social incompetence, and guilt on children from which they can escape temporarily by exerting the greatest effort to control themselves throughout the remainder of their lives or by employing force in order to victimize others. It takes a good brain keep violent urges check. Damaged by neurological illness or mental illness, the brain may not provide effective social inhibitions to control violence.
To deal with the horrid feelings that abuse imposes, abused women more often than men have a tendency to become sexually active at an early age (Edgardh and Ormstad, 2000), to become promiscuous and/or prostitutes (Widom and Kuhns, 1996), to bear children at an early age (Dietz et al., 1999), and to abuse their children. None of these behaviors is obligatory for abused women, but there is evidence that such behavior more likely in abused females.
It seems probable that mothers would have greater access than fathers to the children with respect to the opportunity abuse them (Rudin et al., 1995), hence the violence of women is focused in the home. The options available to women for temporarily lifting their morale (attracting the opposite sex repeatedly in a short time, becoming pregnant, and abusing their children) are not as available to men. Consequently, for men, the use of their physical size in conflicts with outsiders is a more likely outcome of the same destructive combination factors that is the root of violence for both men and women: the interaction abuse, mental illness, and neurological damage.
Conclusion
Neurologic damage, mental illness, and the experience of unremitting physical and/or sexual abuse in childhood interact to create a vulnerability violent behavior. To explain variations in the rate of violence different social groups one must start with the estimation of the prevalence these three factors in groups being studied. Variations in the distributions and prevalence of three factors by gender, race, and socioeconomic level explain variations in the prevalance of violence in different groups. Violence any group can probably be understood by focusing on these factors.
References
Alper, J. S. Biological influences on criminal behavior: how good is the evidence? BMJ 310: 272, 1995.
P.77
Arnold, L. E. Sex differences in ADHD: conference summary. J Abnorm Child Psychol 24:555, 1996.
Ashford, J. W., S. C. Schultz, F. O. Walsh. Violent automatism in a partial complex seizure. Arch Neurol 37:120, 1980.
Barlow, K. M. R. A. Minns. Annual incidence of shaken impact syndrome in young children. Lancet 356:1571-1572, 2000.
Benes F. M., M. Turtle, Y. Khan, et al. Myelination of a key relay zone in the hippocampal formation occurs in the human brain during childhood, adolescence, and adult-hood. Arch Gen Psychiatry 51:477, 1994.
Bijl R. V, A. Ravelli, G. van Zessen. Prevalence of psychiatric disorder in the general population: results of The Netherlands Mental Health Survey and Incidence Study (NEMESIS). Soc Psychiatry Psychiatr Epidemiol 33:587, 1998.
Blake P. Y., J. H. Pincus, G. Buckner. Neurologic abnormalities in murderers. Neurology 45: 1641, 1995.
Blumstein A., F. P. Rivera, R. Rosenfeld the rise and decline of homicide why. Ann Rev Public Health 21:505, 2000.
Boue J., B. Simon-Bouy. Genetics of fragile X syndrome and its prevention. / Gynecol Obstet Biol Reprod (Paris) 26:273, 1997.
Bourget D., P., Gagne J. Moami. Spousal homicide and suicide in Quebec. J Am Acad Law 28:179, 2000.
Bremner, J. D., M. Narayan L. H. Staib, et al. Neural correlates of memories childhood sexual abuse in women with and without posttraumatic stress disorder. Am J Psychiatry 156:1787, 1999.
Bremner, J. D., P. Randall, E. Vermetten, et al. Magnetic resonance imaging-based measurement of hippocampal volume in post-traumatic stress disorder related to childhood physical and sexual abuse. Biol Psychiatry 41:23, 1997.
Brennan, P. A., S. A. Mednick, B. Jacobsen. Assessing the role of genetics in crime using adoption cohorts. Ciba Found Sytnp 194:115, 1996.
Bureau of Justice Statistics Homicide Trends in the United States 1976-1999. Department of Justice.http://www.ojp.usdoj.gov:80/bjs/homicide/gender.htm.
Cadoret, R. J., W. R. Yates, E. Troughton. Genetic-environmental interaction in the genesis of aggressivity and conduct disorders. Arch Gen Psychiatry 52:916, 1995.
Cao, Y, E. M. Vikingstad, P. R. Huttenlocher, et al. Functional magnetic resonance studies of the reorganization of the sensorimotor area after unilateral brain injury in perinatal period. Proc Natl Acad Sci 91:9612, 1994.
Child Maltreatment 1996: Reports from the states to the National Child Abuse and Neglect Data System U.S. Department of Health and Human Services pp. 2-14.
Chow, T. W., J. L. Cummings. Frontal-subcortical circuits. In: The Human Frontal Lobes—Functions and Disorders, B. L. Miller, J. L. Cummings, eds. Guilford Press, New York, 1999, p. 3.
Chugani, H. T. A critical period of brain development: Studies cerebral glucose utilization with PET. Prev Med 27:184, 1998.
Cohen, S. Recent developments in the use of cocaine. Bull Narc 36:3, 1984.
Consensus Conference: Rehabilitation of persons with traumatic brain injury. NIH Consensus development panel on rehabilitation of persons with traumatic brain injury. JAMA 282: 974, 1999.
Damasio, H. T. Grabowski, R. Frank. The return of Phineas Gage: clues about the brain from the skull of a famous patient. Science264:1102, 1994.
P.78
DeBillis, M., M. Keshavan, S. Spencer et al. N-Acetylaspartate concentration in the anterior cingulate of maltreated children and adolescents with PTSD. Amer J Psychiatry 157:1175, 2000.
De Bellis, M. D., M. S. Keshavan, S. R. Beers, J. Hall, K. Frustaci, A. Masalehdan, Noll. Sex differences in brain maturation during childhood and adolescence. Cereb Cortex 11:552-557, 2001.
De Bellis, M. D., M. S. Keshaven, et al. Developmental traumatology. Part II Brain development. Biol Psychiatry 45:1271, 1999.
Dietz, P. M., A. M. Spitz, R. F. Anda, et al. Unintended pregnancy among adult women exposed to abuse or household dysfunction during their childhood. JAMA 282: 1359, 1999.
Driessen, M., J. Herrmann, K. Stahl, et al. Magnetic resonance imaging volumes of the hippocampus and the amygdala in women with borderline personality disorder early traumatization. Arch Gen Psychiatry 57:1115, 2000.
Edgardh, K., K. Ormstad. Prevalence and characteristics of sexual abuse in a national sample of Swedish seventeen-year-old boys and girls. Acta Paediatr 89:310, 2000.
Ewing-Cobbs, L., L. Kramer, M. Prasad, et al. Neuroimaging, physical, and developmental findings after inflicted and non-inflicted traumatic brain injury in young children. Pediatrics 102: 300, 1998.
Famularo, R., T. Fenton, R. Kinscherff, et al. Psychiatric comorbidity in childhood post traumatic stress disorder. Child Abuse Negl20:953, 1996.
Fava, M. Depression with anger attacks. J. Clin. Psychiatry 59 (Suppl 18): 18, 1998.
Feldman M., K. Malhoun, D. O. Lewis. Filicidal abuse in the histories of fifteen condemned murderers. Bull Am Acad Psychiatry Law14:345, 1986.
Feldman, R. S., S. Salzinger, M. Zrosario, et al. Parent, teacher, and peer ratings of physically abused and nonmaltreated children's behavior. J Abnorm Child Psychol 23:317, 1995.
Fergusson, D. M., L. J., Horwood, M. T. Lynskey. Childhood sexual abuse and psychiatric disorder in young adulthood: II. Psychiatric outcomes of childhood sexual abuse. J Am Acad Child Adolesc Psychiatry 35:1365, 1996.
Flannery, K. A., J. Liederman, L. Daly, et al. Male prevalence for reading disability is found in a large sample of black and white children free from ascertainment bias. J Int Neuropsychol Soc 6:433, 2000.
Flisher, A. J., R. A. Kramer, C. W. Hoven, et al. Psychosocial characteristics of physically abused children and adolescents. J Am Acad Child Adolesc Psychiatry 36:123-231, 1997.
Ford, J. D., R. Racusin, W. B. Daviss, et al. Trauma exposure among children with oppositional defiant disorder and attention deficit-hyperactivity disorder. J Consult Clin Psychol 67:786, 1999.
Gamefski, N., R. F. Diekstra. Child sexual abuse and emotional behavioral problems in adolescence: gender differences. J Am Acad Child Adolesc Psychiatry 36:323, 1997.
George, C. Social interactions of young abused children: approach, avoidance, and aggression. Child Dev 50:306, 1979.
Gleckman, A. Diffuse axonal injury in infants with nonaccidental craniocerebral trauma: enhanced detection by beta-amyloid precursor protein immunohistochemical staining. Arch Pathol Lab Med 123:146, 1999.
Golub, A., B. D. Johnson. A recent decline in cocaine use among youthful arrestees Manhattan 1987 through 1993. Am J Public Health84:1250, 1994.
P.79
Grafman, J, et al. Frontal lobe injuries, violence, and aggression: a report of the Vietnam Head Injury Study. Neurology 46:1231, 1996.
Greene, J. D., R. B. Sommerville, L. E. Nystrom, et al. An fMRI investigation of emotional engagement in moral judgment. Science293:2105, 2001.
Grigg, J., R. Thomas, F. Billson. Neuronal basis of amblyopia: a review. Indian J Ophthalmol 44:69, 1996.
Gudzer, J., J. Paris, P. Zelkowitz, et al. Psychological risk factors for borderline pathology in school aged children. J Am Acad Child Adolesc Psychiatry 38:206, 1999.
Hall, G. C. Sexual offender recidivism revisited: a meta analysis of recent treatment studies. Consult Clin Psychology 63:802, 1995.
Harlow, H. F., M. K. Harlow, S. J. Suomi. From thought to therapy: lessons from a primate laboratory. How investigation of the learning capability rhesus monkeys has led to the study of their behavioral abnormalities and rehabilitation Am. Sci 59:538, 1971.
Heim, C., D. J. Newport, S. Heit, et al. Pituitary-adrenal and autonomic responses to stress in women after sexual and physical abuse childhood. JAMA 284:592, 2000.
Heim, N., C. J. Hursch. Castration for sex offenders: treatment or punishment? Review and critique of European literature. Arch Sex Behav 8:281, 1979.
Hendrick, V, L. L. Altshuler, M. J. Gitlin, et al. Gender and bipolar illness. J Clin Psychiatry 61:393, 2000.
Huntley, G. W. Differential effects of abnormal tactile experience on shaping representation patterns in developing and adult motor cortex. J Neurosci 17:9220, 1997.
Huttenlocher, P. R. Dendritic and synaptic pathology in mental retardation. Pediatri Neurol 7:79, 1991.
Huttenlocher, P. R., A. S. Dabholkar. Regional differences in synaptogenesis in human cerebral cortex. J Comp Neurol 387:167, 1997.
Ito, Y., M. H. Teicher, C. A. Glod, et al. Preliminary evidence for aberrant cortical development in abused children: a quantitative EEG study. J Neuropsychiatry 10:298, 1998.
Jager, T. E., H. B. Weiss, J. H. Cohen, et al. Traumatic brain injuries evaluated in U.S. emergency departments 1992-1994. Acad Emerg Med 7:134, 2000.
Jenkyn, L. R., D. B. Walsh, C. M. Culver, A. G. Reeves. Clinical signs in diffuse cerebral dysfunction. J Neurol Neurosurg Psychiatry40:956, 1977.
Jenkyn, L. R., A. G. Reeves, T. Warren. Neurologic signs in senescence. Arch Neurol 42:1154, 1985.
Joseph, R. Traumatic amnesia, repression, and hippocampus injury due to emotional stress, corticosteroids, and enkephalins. Child Psychiatry Hum Dev 29:169, 1998.
Joseph, R. The neurology of traumatic “dissociative” amnesia: commentary and literature review. Child Abuse Negl 23:715, 1999.
Katz, L. C., A. Shatz. Synaptic activity and the construction of cortical circuits. Science 4:1133, 1996.
Kaufman, J., P. M. Plotsky, C. B. Nemeroff, et al. Effects of early adverse experiences on brain structure and function. Clinical implications. Biol Psychiatry 48:778, 2000.
Kelly, J. P., J. H. Rosenberg. The development of guidelines for the management of concussion in sports. JH Trauma Rehabil 13:53, 1998.
Kendall-Tacket, K. A. Physiological correlates of childhood abuse: chronic hyperarousal in PTSD, depression, and irritable bowel syndrome. Child Abuse Negl 24:799, 2000.
Knox, M, C. King, G. L. Hanna, et al. Aggressive behavior in clinically depressed adolescents. J Am Acad Child Adolesc Psychiatry 39:611, 2000.
P.80
Laurance, B. M., A. Brito, J. Wilkinson. Prader-Willi syndrome after age 15 years. Arch Dis Child 56:191, 1981.
Leung, A., P. Chue. Sex differences in schizophrenia, a review of the literature. Acta Psychiatr Scand (Suppl) 401:3, 2000.
Levitan, R. D., S. V. Parikh, A. D. Lesage, et al. Major depression in individuals with a history of childhood physical or sexual abuse: relationship to neurovegetative features, mania, and gender. Am J Psychiatry 155:1746, 1998.
Lewis, D., S. Shanock, J. Pincus, et al. Violent juvenile delinquents. J Amer Acad Child Adolesc Psychiat. 18:307, 1979.
Lewis, D. O., J. H. Pincus, B. Bard, et al. Neuro-psychiatric, psychoeducational and family characteristics of fourteen juveniles condemned to death in the United States. Am J Psychiatry 145:584, 1988.
Lewis, D. O., J. H. Pincus, M. Feldman, et al. Psychiatric, neurological, and psychoeducational characteristics of 15 death row inmates in the United States. Am J Psychiatry 143:838, 1986.
Lewis, D., R. Lovely, C. Yeager, et al. Toward a theory of violence. J Amer Acad Child Adolesc Psychiat. 29:150, 1989.
Lewis, D. O., J. H. Pincus, R. Lovely, et al. Biosocial characteristics of matched samples of delinquents and non-delinquents. J Am Acad Child Adolsc Psychiatry 26:744, 1987.
Lindquist, P. Criminal homicide in northern Sweden 1970-1981: alcohol intoxication, alcohol abuse, and mental disease. Int J Psychiatry8:19, 1986.
Loberg, T. Belligerence in alcohol dependence. Scand J Psychol 24:285, 1983.
Lorenz, K. Studies in Animal and Human Behavior, Vol. 1. Translated by Robert Martin Methuen and Co. Ltd., London, 1970.
Luntz, B. K., C. S. Widom. Antisocial personality disorder in abused and neglected children grown up. Am J Psychiatry. 151:670, 1994.
Mahoney, A., W. O. Donnelly, T. Lewis, et al. Mother and father self-reports of corporal punishment and severe physical aggression toward clinic-referred youth. J Clin Child Psychology 29:266, 2000.
Mark, V H., F. Ervin. Violence and the Brain. Harper and Row, New York, 1970.
McClellan, J., J. Adams, D. Douglas, et al. Clinical characteristics related to severity of sexual abuse: a study of seriously mentally ill youth. Child Abuse Negl 10:1245, 1995.
McCrea, M., J. P. Kelly, J. Kluge, et al. Standardized assessment of concussion in football players. Neurology 48:586, 1997.
McElroy, S. Recognition and treatment of DSM IV intermittent explosive disorder. J Clin Psychiatry, 60(Suppl 15): 12, 1999.
Mclntyre, J. S. Mania: the common symptom of several illnesses. Postgrad Med 66:145, 1979.
Mednick, S. A. W. F. Gabrielli, Jr., B. Hutchings. Genetic influences in criminal convictions: Evidence from an adoption cohort. Science224:891, 1984.
Mesulum, M. Principles of Behavioral and Cognitive Neurology, 2nd Ed. Oxford University Press, New York, 2000, p. 55.
MMWR. Sports related recurrent brain injuries—United States, MMWR 46:224,1997.
Moody, K. C., C. E. Holzer 3rd, M. J. Roman, et al. Prevalence of dyslexia among Texas prison inmates. Tex Med 96:69, 2000.
Newport, J., C. Nemeroff. Childhood trauma: psychiatric and neurobiologic consequences, of aggressivity and conduct disorders. Arch Gen Psychiary, 52:916, 1995.
P.81
Newport, J. and Nemeroff, C. Childhood Trauma, Semin Clin Neuropsychiatry (2), 2002.
Nyhan, W. L. Behavior in the Lesch-Nyhan Syndrome. J Autism Child Schizophr 6:235, 1976.
Oquendo, M. A., C. Waternaux, B. Brodsky, et al. Suicidal behavior in bipolar mood disorder: clinical characteristics of attempters and nonattempters. J Affect Disord 59: 107, 2000.
Overman, W. H., J. Bachevalier, E. Schuhmann, et al. Cognitive gender differences in very young children parallel biologically based cognitive gender differences in monkeys. Behav Neurosci 110:673-684, 1996.
Paris, J., H. Zweig-Frank, J. Gudzer. Risk factors for borderline personality in male outpatients. J Nerv Ment Dis 182:375, 1994a.
Paris Psychological risk factors for borderline personality disorder in female patients. Compr Psychiatry 35:301, 1994b.
Pauls, D. L., J. F. Leckman. The inheritance of Gilles de la Tourette syndrome and associated behaviors. Evidence for autosomal dominant transmission. N Engl J Med 315:993, 1986.
Pearl, G. S. Traumatic neuropathology. Clin Lab Med 18:39, 1998.
Pincus, J. H. Base Instincts: What Makes Killers Kill. Norton, New York, 2001.
Post, R. M. Cocaine psychoses: a continuum model. Am J Psychiatry 132:225, 1975.
Provence, S. Infants in Institutions: A Comparison of their Development Through the First Year of Life With Family Reared Children.International Universities Press, New York, 1967.
Raboch, J., H. Cerna, P. Zemek. Sexual aggressivity and androgens. Br J Psychiatry 151:398, 1987.
Raine, A., P. Brennan, S. A. Mednick Interaction between birth complications and early maternal rejection in predisposing individuals to adult violence: specificity serious early-onset violence. Am J Psychiatry 154:1265, 1997.
Raine, A., M. S. Buchsbaum, D. LaCasse. Brain abnormalities in murderers indicated by positron emission tomography. Biol Psychiatry42:495, 1997.
Raine, A., M. S. Buchsbaum, J. Stanley, et al. Selective reductions in prefrontal glucose metabolism in murderers. Biol Psychiatry, 36:365, 1994.
Raine, A., T. Lencz, S. Bihrle, et al. Reduced frontal prefrontal gray matter volume and reduced automatic activity in antisocial personality disorder Arch Gen Psychiatry 57:119, 2000.
Rapin, I., D. A. Allen Syndromes in developmental dysphasia and adult aphasia. Assoc for Res in Nerv Ment Dis 66:57, 1988.
Rasanen, P., J. Tiihonen, M. Isohanni, et al. Schizophrenia, alcohol abuse, and violent behavior: a 26-year follow-up study of an unselected birth cohort. Schizophr Bull 24:437, 1998.
Richer, M., M. L. Crismon. Pharmacotherapy for sexual offenders. Am J Psychiatry 143:367, 1986.
Rosnebaum, M., B. Bennett. Homicide and depression. Amer J Psychiatry 143:367, 1986.
Rosse, R. B., J. P. Collins, M. Fay-McCarthy, et al. Phenomenologic comparison of the idiopathic psychosis of schizophrenia and drug induced psychoses: a retrospective study. Clin Neuropharmacol 17: 359, 1994.
Rudin, M. M., C. Zalewski, J. Bodmer-Turner. Characteristics of child sexual abuse victims according to perpetrator gender. Child Abuse Negl 19:963, 1995.
P.82
Ruppell, R. A., P. M. Kochanek, P. D. Adelson, et al. Excitatory amino acid concentrations in ventricular cerebrospinal fluid after severe traumatic brain injury infants and children: the role of child abuse J Pediatr 138:18, 2001.
Rutter, M. Developmental catch-up and deficit following adoption after severe global, early privation. English and Romanian Adoptees (ERA) Study Team. J Child Psychol Psychiatry, 39:405, 1998.
Saint-Hilaire, J. M., M. Gilbert, G. Bouner. Aggression as an epileptic manifestation: two cases with depth electrode study. Epilepsia21:184, 1980.
Sargent, J. D., M. J. Brown, L. Freeman, et al. Childhood lead poisoning in Massachusetts communities: its association with socioeconomic and housing characteristics. Am J Public Health 85:528, 1995.
Sedlak, A. J., D. D. Broadhurst. U.S. Department of Health and Human Services, National Incidence Study, September 3, 1996.
Sengpiel, F, C. Blakemore. The neural basis of suppression and amblyopia in strabismus. Eye 10:250, 1996.
Shannon, P., C. R. Smith, J. Deck, et al. Axonal injury and the neuropathology of shaken baby syndrome. Acta Neuropathol 95:625, 1998.
Shaw, J. L., T. Appleby, G. Amos, et al. Mental disorder and clinical care in people convicted of homicide: national clinical survey. BMJ318:1240, 1999.
Shaywitz, S. E., B. A. Shaywitz, K. R. Pugh, et al. Functional disorganization for reading in the brain in dyslexia. Proc Nat Acad Sci USA95:2636, 1998.
Shin, L. M., R. J. McNally, S. M. Kosslyn, et al. Regional cerebral blood flow during script-driven imagery in childhood sexual abuse-related PTSD: a PET investigation. Am J Psychiatry 156:575, 1999.
Singer, W. Development and plasticity of cortical processing architectures. Science 270:758, 1995.
Smalley, S. L., R. F. Asarnow, M. A. Spence. Autism and genetics. Arch Gen Psychiatry 45:953, 1988.
Sobsey, D., W. Randall, R. K. Parilla. Gender differences in abused children with and without disabilities. Child Abuse Negl 21:707, 1997.
Soderstrom, H., M. Tullberg, C. Wikkelso, et al. Reduced regional blood flow in nonpsychotic violent offenders. Psychiatry Res 98:29, 2000.
Spitz, R., G. Cobliner. First Year of Life: A Psychoanalytic Study Normal and Deviant Development of Objective Relations. International Universities Press, Madison, CT, 1966.
Stalenheim, E. G. Testosterone as a biologic marker in psychopaths Psychiatry Res 77:79, 1998.
Steadman, H. J., E. P. Mulvey, J. Monahan, et al. Violence by people discharged from acute psychiatric inpatient facilities and by others in the same neighborhoods. Arch Gen Psychiatry 55:393, 1998.
Strakowski, S. M., M. Flaum, X. Amandor, et al. Racial differences in the diagnosis of psychosis. Schizophr Res 21:117, 1996.
Sullivan, P. M., J. F. Knutson. Maltreatment and disabilities: a population-based epidemiological study. Child Abuse Negl 24:1257, 2000.
Taylor, P. J. Motives for offending among violent psychotic men. Br J Psychiatry 147:491, 1985.
Taylor, P. J., J. Gunn. Violence and psychosis. I. Risk of violence among psychotic men. BMJ 30;288, 1984.
Teasdale, T. W., A. Engberg. Duration of cognitive dysfunction after concussion and cognitive dysfunction as a risk factor: a population study of young men. BMJ 315: 569, 1997.
P.83
Teicher, M. H., et al. Preliminary evidence for abnormal cortical development in physically and sexually abused children using EEG coherence and MRI. Ann NY Acad Sci 821: 160, 1997.
Tranel, D. Acquired sociopathy, the development of sociopathic behavior following focal brain damage. Prog Exp Pers Psychopathol Res17:285, 1994.
Ustun, T. B. Cross-national epidemiology of depression and gender. J Gend Spec Med 3:54, 2000.
Van Elst, L., F. Woerman, L. Lemieux, et al. Affective aggression in patients with temporal lobe epilepsy: a quantitative study of the amygdala. Brain 123:234, 2000.
Volkman, F. R., P. Szatmari, S. S. Sparrow. Sex differences in pervasive developmental disorders J Autism Dev Disord 23: 579, 1993.
Wallace, C, P. Muller, P. Burgess, et al. Serious criminal offending and mental disorder case linkage study. Br J Psychiatry 172:477, 1998.
Widom, C. S. The cycle of violence. Science 244:160,1989.
Widom, C. S., Kuhns, J. B. Childhood victimization and subsequent risk for promiscuity, prostitution, and teenage pregnancy: a prospective study. Am J Public Health 86:1607, 1996.
Wiemann, C. M., A. B. Berenson, V. V. San Miguel. Tobacco, alcohol, and illicit drug use among pregnant women. Age and racial/ethnic differences J Reprod Med 39:769, 1994.
Woermann, F., L. van Elst, M. Koepp, et al. Reduction of frontal neocortical grey matter associated with affective aggression in patients with temporal lobe epilepsy: an objective voxel by voxel analysis of automatically segmented MRI. J Neurol Neurosurg Psychiatry 68:162, 2000.
Wolfgang, M. Delinquency and violence from the viewpoint of criminality. In: Neural Bases of Violence and Aggression, W. S. Fields, H. Sweet, eds. Warren Green, St. Louis, 1975, p. 456.
Wong, M., P. Fenwick, G. Fenton, et al. Repetitive and non-repetitive violent offending behavior in male patients a maximum security mental hospital-clinical and neuroimaging findings. Med Sci Law 37:150, 1997.
Wyllie, E., J. P. Glazer, S. Benbadis, et al. Psychiatric features of children and adolescents with pseudoseizures. Arch Pediatr Adolesc Med153:244, 1999.
Yarvis, R. M., Patterns of substance abuse and intoxication among murderers. Bull Am Acad Psychiatry Law 22:133, 1994.
Yesavage, J. A., Correlates of dangerous behavior by schizophrenics in a hospital. J Psychiatr Res 18:225, 1984.