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Violence and Touch Deprivation in Adolescents

By: Field, Tiffany | Adolescence, Winter 2002 | Article details

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Violence and Touch Deprivation in Adolescents


Field, Tiffany, Adolescence


VIOLENCE AND TOUCH DEPRIVATION

Incidence of Violence

Approximately one-third to one-half of clinic referrals among children and adolescents are for aggression and conduct disorder problems (Vitiello & Stoff, 1997). The homicide rate for adolescents in the U.S. is the highest of the industrialized nations (roughly 20 times higher), and in many community studies, the rates of adolescent fighting and weapon carrying have increased significantly (Orpinas et al, 1995; Sosin et al., 1995).

Early Neglect and Abuse as a Risk Factor

Research has identified a number of risk factors for violence in youth. One of the most commonly cited risk factors is early neglect and abuse. In many studies, aggression and antisocial behavior problems have been found in neglected or abused children and adolescents. For example, Raine et al. (1994) reported that maternal rejection at age one predicted violent crime at age eighteen. Other researchers reported that physical aggression occurred more often in children who had been physically abused (Scarpa, 1998; Scerbo & Kolko, 1995). In a study by Dodge et al. (1990), harmed or abused children had 23% higher aggression ratings by their teachers, 100% higher ratings by their peers, and 30% higher ratings by observers. Further, Widom (1989) found that adolescents who had been abused or neglected during childhood were 42% more likely to have a criminal record as an adult.

The critical need for physical affection is highlighted by a large study on 49 cultures (Prescott, 1990). In that study, the cultures that exhibited minimal physical affection toward their young children had significantly higher rates of adult violence, and, vice versa, those cultures that showed significant amounts of physical affection toward their young children had virtually no adult violence. Some suggest that the absence of physical affection or the presence of physical abuse affects the child's physiological reactivity either through the emotional trauma or through a more direct insult to the brain, and that this acquired overreactivity mediates later aggressive tendencies (Dodge et al., 1990). Others suggest that the early experience of physical neglect or physical abuse heightens sensory thresholds, such as the pain threshold, leading to underresponsivity to stimulation and hence the need for arousal-seeking behavior (Orbach, 1999).

Negative emotional affect, including depression and anxiety, has also been noted to predispose adolescents to impulsive, antisocial or aggressive behavior via a similar mechanism (Scarpa & Raine, 1997). Anxiety and depression are markedly higher in adolescents with conduct disorder (Kovacs, 1981) and, in a longitudinal study, children with comorbid conduct and anxiety disorder showed significant increases in physical aggression over a 4-year period (Lahey & McBurnett, 1992).

EEG and Neurotransmitter / Neurohormone Profiles

Several studies have revealed electroencephalogram (EEG) abnormalities in violent adolescents (Scarpa & Raine, 1997), which are thought to reflect general underarousal or cortical immaturity. The abnormalities have included right hemisphere dominance and excessively slow frequency EEG theta activity (Raine et al., 1990a). In the Raine et al. (1990b) sample of 15-year-old adolescents, evoked potentials including a greater N1 amplitude and faster P300 latency to a warning signal correctly classified 74% of those adolescents who became criminals at age 24. The authors suggested that individuals with chronically low levels of arousal (possibly caused by excessive filtering of stimuli) would seek out risky situations to enhance their arousal level.

In separate studies, aggressive/violent individuals have been noted to have elevated dopamine, low norepinephrine, and low serotonin levels. Elevated dopamine coupled with low levels of norepinephrine and serotonin is thought to lead to impulsive, aggressive behavior. Most studies have targeted serotonin (5-HIAA) as the primary neurotransmitter imbalance and the relationship between low levels of 5-HIAA and aggression (see Stoff et al., 1997, for a review). Their review includes both positron emission tomography (PET) and magnetic resonance imaging (MRI) studies showing lower reuptake of 5-HIAA in the prefrontal cortex. Several primate studies have also highlighted the serotonin/aggression relationship (Higley et al., 1992; Mehlman et al., 1995; Suomi, 1999). In addition, low levels of 5-HIAA have been correlated with aggression as reported by teachers; low serotonin has also been noted in children who torture animals, and children who are unusually hostile to their mothers (Halperin et al., 1997). Further, i n some studies an interaction has been noted between serotonin and testosterone (Bernhardt et al., 1997). In a review of the literature, Coccaro et al. (1989) proposed that reduced serotonin activity reduced the activity of the neuronal processes that inhibit aggression. They described the resulting state as hyperresponsivity to aversive stimuli. In a rat study examining the combined influences of testosterone and serotonin (Bonsan et al., 1994), a serotonin agonist reversed the influence of increased testosterone.

Data that further support the interaction of serotonin and testosterone with aggression are found in studies in which tryptophan decreased predatory aggression (serotonin being derived from tryptophan). Higher levels of 5-HIAA in the hypothalamus and amygdala were associated with decreased aggression. Testosterone in the amygdala was associated with aggressiveness. Both the hypothalamus and amygdala have many receptor sites for testosterone; for example, implants of testosterone in the hypothalamus have been noted to restore aggressive behavior in castrated rats (Christie & Barfield, 1972).

Testosterone has also been shown to interact with cortisol, albeit not consistently. Henry (1992) found that elevated cortisol was accompanied by lower testosterone. Others have reported no relationship between cortisol and testosterone (Scerbo & Kolko, 1994). Studies on cortisol alone have also been mixed, with some reporting reduced levels in adolescents with conduct problems (Lahey & McBurnett, 1992; Susman et

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