Kelly impulsiveness and feelings of hope, elation, and

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          Kelly GregusED PSYCH 844ODD Research PaperDue 12/15/2017                 Oppositional Defiant Disorder (ODD)Introduction            TheDSM-V defines Oppositional Defiant Disorder (ODD) as a pattern ofangry/irritable mood, argumentative/defiant behavior, or vindictiveness lastingat least six months with an individual who is not a sibling (AmericanPsychological Association, 2013).  Theliterature on ODD prevalence varies, but a meta review by Lahey et al. (1999) found a median prevalencerate of 3.2%.

  It is not unusual forindividuals with ODD to show the behavioral features of the disorder without symptomsnegative mood. However, individuals with the disorder who show theangry/irritable mood symptoms typically show the behavioral features as well(American Psychological Association, 2013).Manifestations ofthe disorder across development appear consistent. Children and adolescents withoppositional defiant disorder are at increased risk for a number of problems inadjustment as adults, including antisocial behavior, impulse-control problems,substance abuse, anxiety, and depression (Kim-Cohen et al. 2003; Nock et al.2007; Rowe et al.

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2010).The purpose of this analysis of ODD is to critique thefindings regarding the etiology of ODD and the issues of gender diversitysurrounding ODD diagnosis and symptomology. The paper will discuss: developmental considerations for ODD in children;the etiology of the disorder, including temperament, neurobiological, geneticfactors; genetic x environment factors; environment factors, genderdifferences; treatment suggestions; and suggestions for future studies.  Developmental Course and ComorbiditySymptoms of ODDusually start during the preschool years rarely later than early adolescence (Roweet al.

2010). ODD is often followed by a diagnosis of conduct disorder,especially for individuals with the childhood onset conduct disorder (Burke etal. 2010). However, many children and adolescents with ODD do not go on to be diagnosedwith conduct disorder. ODD also conveys risk for anxiety disorders and majordepressive disorder, even without conduct disorder. The defiant, argumentative,and vindictive symptoms carry most of the risk for conduct disorder, whereasthe angry-irritable mood symptoms carry most of the risk for emotionaldisorders (Stringaris and Goodman 2009).EtiologyTemperament            Temperamentrefers to enduring patterns of behavior innate to every child that are modifiedwith age.  Early studies of theneurobiology temperament described two systems of temperament that drovebehavior, the Behavioral Inhibition System (BIS) and a Behavioral ActivationSystem (BAS, Pickering & Gray,1999).

  The BIS has beenassociated with anxiety, frustration and sadness, and it is activated by novelstimuli and conditioned by negative stimuli. Some neuroanatomical regions associated with the BIS are the amygdala,right PFC, and hippocampus (Carver & White, 1994; Gray 1978). The BAS has been associated with impulsiveness and feelings ofhope, elation, and happiness, and it is activated by conditioned stimuli thatsignal reward or relief from punishment (Pickering & Gray, 1999; Gray 1978).  Someneuroanatomical regions associated with the BAS are the nucleus acumbens andleft PFC (Barros-Loscertales et al. 2006).   In the AvonLongitudinal Study of Parents and Children (ALSPAC), temperament was assessedat three-years-old using the Emotionality, Activity, and Sociability (EAS)questionnaire, and the same children were tested at seven to eight-years-oldfor psychiatric disorders (Stringaris etal. 2010).  High emotionality andhigh activity were most commonly associated with an ODD diagnosis.

  However, the high activity was only associatedwith ODD when there was a comorbid diagnosis of Attention Deficit HyperactivityDisorder (ADHD), combined type. Additionally, in the Dunedin longitudinal study, researchers studiedcontrol (emotional lability, restlessness, short attention span, and negativity)at ages 3 and 5 years-old.  Later, at 9and 11 years-old, they found that lack of control was associated withantisocial behavior and with conduct disorder at ages 13 and 15 years old.

  Similarly, the Australian Temperament Projectfound that 7-8 year-olds with aggressive behavior and hyperactivity had moredifficult temperaments, as measured at 4-8 months-old.  NeurobiologyAndrogensConnor (2002),performed a meta-analysis of aggression studies and found that nine studiesshow a positive correlation between aggression/delinquency with higher salivarytestosterone and/or serum testosterone. Conversely, four studies did not find this correlation, but thesestudies were done in pre-pubescent children. Additionally, two studies have found a correlation with a testosteroneprecursor, dehydroepiandrosterone, and ODD or CD in children (Van Goozen et al. 1998; Van Goozen et al.

2000b).  Interestingly, some studies suggest thatcortisol can moderate the effect of testosterone.  Pompa and colleagues (2007) found that therewas a significant correlation between testosterone and overt aggression inindividuals with low cortisol levels, but this correlation was lost withindividuals with high cortisol.  Punishment SensitivityChildren usuallynaturally learn to avoid antisocial behavior by aversive conditioning.  They begin to feel afraid when theyanticipate punishment or the guilt of seeing someone else hurt by your actions(Kochanska, 1993).  The amygdala, sympatheticnervous system (SNS), and the hypothalamic-pituitary-adrenal (HPA) axis.  Many fMRI studies have shown abnormal amygdalafunctioning in CD.  However, two fMRI studieshave found reduced activation of the amygdala in response to fearful faces inindividuals with ODD (Marsh et al.

2008;White et al. 2012).  Additionally, negative emotionality has beenassociated with the amygdala, and behavioral inhibition has been related toamygdala projections to the prefrontal cortex (PFC, Kagan, 1988).  Additionally, the amygdala is connected to theanterior cingulate cortex (ACC).  The ACCis involved in negative feedback loops to the amygdala (Stefanacci &Amaral, 2002).  Thus, weaker connectionsresults in less deactivation of the amygdala and more negativeemotionality.

  The SNS nervous systemis also involved in fear conditioning. Gao and colleaues (2010a) found that poor fear conditioning viaelectrodermal stimulation was correlated with aggression at age eight.  Additionally, Gao and colleagues (2010b)found that poor fear conditioning at age three was correlated with criminalhistory at age 23.

 Skin conductivity isanother measure of punishment sensitivity. Studies have found that children with lower skin conductivity are more likelyto have conduct problems or ODD (Lorber 2004; Van Goozen et al. 2000a).    Additionally, in a follow up study of the childrenwho had ODD, lower basic skin conductance was a predictor of externalizingproblems and maintenance of ODD (Van Bokhoven et al. 2005).  Serotonin has beenimplicated in punishment sensitivity as well. Matthys et al.

(2013) showedthat serotonin was negatively correlated with aggressive behavior in childrenand adolescents with ODD and CD.  However,studies of rhesus monkeys show that the environment can influence serotonin levelsas well (Shannon et al. 2005).  Reward Sensitivity             Theamygdala, orbitofrontal cortex, and striatum are all implicated in the neurobiologyof reward sensitivity.

  Genetic            Eavesand colleagues (2000) found a large genetic correlation in liability forODD.  Rhee and Waldman (2002) conducted ameta-analysis that estimates that antisocial behavior, in general, is 41%heritable.  The same meta-analysis byMoffitt (2005b) estimated the heritability to be 50%.  Environmentalx Genetic It is alsoimportant to note that there are gene x environment interactions as well. Malnutritionat age three has been correlated with more aggressive behavior at age eight,externalizing problems at age 11, and conduct disorder at age 17 (Liu et al. 2004).  Additionally, the link between poor nutritionand behavior problems was mediated by IQ, thus the authors concluded that malnutritionpredisposes children to neurocognitive deficits, which can lead to behavior problems.

  Additionally, mothers who use opiates andcocaine during the fetal development period have been shown to have childrenwith greater behavior problems at age four (Bennet et al. 2002).  Maternalsmoking has also been shown to be a statistically significant predictor ofconduct problems (Brennan et al. 2003)Sometimes anenvironment will affect people differently based upon their genotype.  For example, one MAOA genotype is associatedwith negative emotionality, reward dependence, and antisocial behavior.  Additionally, victims of maltreatment arealso at risk for these same factors. However, if victims of maltreatment do not have this particular allelefor MAOA genotype, their genotype serves as a protective factor (Caspi 2002).

  Thus, the MAOA genotype moderates theresponse to the environment.  Environment            Family            In 2013, a study showed that 18% ofchildren live in poverty, and 7% live in extreme poverty (Capella et al. 2013).  Lower family economic status has been relatedto more involvement in juvenile crime and more instances of disruptive behaviorproblems (Sampson and Lamb 1993; Barry etal. 2005).  Additionally, families inlow SES households generally have higher levels of depression, which alsoinfluences conduct problems (Conger etal.

1994).              Parenting Practices            Peer Factors             CommunityGender Differences            Genderdifferences in ODD are inconsistent across studies.  However, most data suggest that ODD is more prevalentin boys than girls or that there is no difference at all (Loeber et al.

2000). Recent studies show thatODD is best characterized as two separate disorders, one behavioral and oneaffective, because these are more comparable for boys and girls (Lavigne et al. 2015).

  Additionally, Herzhoff & Tackett (2016)show evidence of less gender differences when diagnosis is split by thebehavioral and affective dimensions.              Peerrejection: Peer rejection can predict delinquency in boys but not in girls(Miller 1999).  Eme (2007) also discusses further potentialleads in this area that warrant investigation; particularly why girls withcongenital adrenal hyperplasia (CAH), a foetal disorder that leads girls to beexposed to male levels of androgens in utero, tend to have high rates of behavioralproblems.

 Boysand girls follow different trajectories in the development of antisocialbehaviors. Boys usually have a child-onset, or an adolescent onset (Crick andZahn-Waxler 2003). In contrast, the child-onset pathway in girls is rare (10:1 boys:girls;Eme 2007; Moffitt and Caspi 2001),with most girls who develop antisocial behaviors doing so during adolescence(1.5:1 in favour of boys; Moffitt and Caspi 2001).This likely impacts the male:female prevalence ratios of DBDs during early andmiddle childhood. It is suspected that girls might be protected againstchild-onset due to various factors including their earlier physical maturation,and better-developed language, social and emotional skills compared to boys(Crick and Zahn-Waxler 2003; Keenan and Shaw 1997).

For both genders the child-onset pathway is particularly important tounderstand as it is associated with greater risk of difficulties and seriouspsychopathology into adulthood compared to the adolescent-onset pathway(Moffitt and Caspi 2001; Silverthorn and Frick 1999).   Treatment      References: American Psychiatric Association. (2013).

 Diagnostic and statistical manual of mental disorders (5th ed.). Arlington, VA:American Psychiatric Publishing.Eaves L, Rutter M, Silberg JL, Shillady L,Maes H, Pickles A (2000), Genetic and environmental            causes of covariation in interview assessments ofdisruptive behavior in child and            adolescenttwins. Behav Genet 30:321–334Lahey, B. B., Miller, T.

L., Gordon, R.A., & Riley, A. W. (1999). Developmental epidemiology  of the disruptive behavior disorders.

In Handbook of disruptive behavior disorders(pp.  23-48). Springer US.  Lavigne, J.

V., Bryant, F. B., Hopkins,J.

, & Gouze, K. R. (2015). Dimensions of oppositional    defiant disorder in young children: Modelcomparisons, gender and longitudinal     invariance. Journalof Abnormal Child Psychology, 43(3), 423-439.Loeber, R., Burke, J. D.

, Lahey, B. B.,Winters, A., & Zera, M. (2000). Oppositional defiant and            conduct disorder: a review of thepast 10 years, part I. Journal of the American Academy            of Child & Adolescent Psychiatry, 39(12),1468-1484.

Miller-Johnson, S., Coie, J. D.,Maumary-Gremaud, A., Lochman, J.

, & Terry, R. (1999).            Relationship between childhood peerrejection and aggression and adolescent            delinquencyseverity and type among African American youth.

 Journal of Emotionaland      Behavioral Disorders, 7(3),137-146White, S. F., Marsh, A.

A., Fowler, K. A.,Schechter, J. C., Adalio, C.

, Pope, K., … & Blair, R.

J.     R. (2012). Reduced amygdala response inyouths with disruptive behavior disorders and            psychopathictraits: decreased emotional response versus increased top-down attention to            nonemotional features. AmericanJournal of Psychiatry, 169(7), 750-758. 

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