Kelly impulsiveness and feelings of hope, elation, and

 

 

 

 

 

 

 

 

 

 

Kelly Gregus
ED PSYCH 844
ODD Research Paper
Due 12/15/2017

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Oppositional Defiant Disorder (ODD)

Introduction

            The
DSM-V defines Oppositional Defiant Disorder (ODD) as a pattern of
angry/irritable mood, argumentative/defiant behavior, or vindictiveness lasting
at least six months with an individual who is not a sibling (American
Psychological Association, 2013).  The
literature on ODD prevalence varies, but a meta review by Lahey et al. (1999) found a median prevalence
rate of 3.2%.  It is not unusual for
individuals with ODD to show the behavioral features of the disorder without symptoms
negative mood. However, individuals with the disorder who show the
angry/irritable mood symptoms typically show the behavioral features as well
(American Psychological Association, 2013).

Manifestations of
the disorder across development appear consistent. Children and adolescents with
oppositional defiant disorder are at increased risk for a number of problems in
adjustment 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. 2010).The purpose of this analysis of ODD is to critique the
findings regarding the etiology of ODD and the issues of gender diversity
surrounding ODD diagnosis and symptomology. 
The paper will discuss: developmental considerations for ODD in children;
the etiology of the disorder, including temperament, neurobiological, genetic
factors; genetic x environment factors; environment factors, gender
differences; treatment suggestions; and suggestions for future studies. 

Developmental Course and Comorbidity

Symptoms of ODD
usually start during the preschool years rarely later than early adolescence (Rowe
et al. 2010). ODD is often followed by a diagnosis of conduct disorder,
especially for individuals with the childhood onset conduct disorder (Burke et
al. 2010). However, many children and adolescents with ODD do not go on to be diagnosed
with conduct disorder. ODD also conveys risk for anxiety disorders and major
depressive disorder, even without conduct disorder. The defiant, argumentative,
and vindictive symptoms carry most of the risk for conduct disorder, whereas
the angry-irritable mood symptoms carry most of the risk for emotional
disorders (Stringaris and Goodman 2009).

Etiology

Temperament

            Temperament
refers to enduring patterns of behavior innate to every child that are modified
with age.  Early studies of the
neurobiology temperament described two systems of temperament that drove
behavior, the Behavioral Inhibition System (BIS) and a Behavioral Activation
System (BAS, Pickering & Gray,
1999).  The BIS has been
associated with anxiety, frustration and sadness, and it is activated by novel
stimuli 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 of
hope, elation, and happiness, and it is activated by conditioned stimuli that
signal reward or relief from punishment (Pickering & Gray, 1999; Gray 1978).  Some
neuroanatomical regions associated with the BAS are the nucleus acumbens and
left PFC (Barros-Loscertales et al. 2006).   

In the Avon
Longitudinal Study of Parents and Children (ALSPAC), temperament was assessed
at three-years-old using the Emotionality, Activity, and Sociability (EAS)
questionnaire, and the same children were tested at seven to eight-years-old
for psychiatric disorders (Stringaris et
al. 2010).  High emotionality and
high activity were most commonly associated with an ODD diagnosis.  However, the high activity was only associated
with ODD when there was a comorbid diagnosis of Attention Deficit Hyperactivity
Disorder (ADHD), combined type. 
Additionally, in the Dunedin longitudinal study, researchers studied
control (emotional lability, restlessness, short attention span, and negativity)
at ages 3 and 5 years-old.  Later, at 9
and 11 years-old, they found that lack of control was associated with
antisocial behavior and with conduct disorder at ages 13 and 15 years old.  Similarly, the Australian Temperament Project
found that 7-8 year-olds with aggressive behavior and hyperactivity had more
difficult temperaments, as measured at 4-8 months-old. 

Neurobiology

Androgens

Connor (2002),
performed a meta-analysis of aggression studies and found that nine studies
show a positive correlation between aggression/delinquency with higher salivary
testosterone and/or serum testosterone. 
Conversely, four studies did not find this correlation, but these
studies were done in pre-pubescent children. 
Additionally, two studies have found a correlation with a testosterone
precursor, dehydroepiandrosterone, and ODD or CD in children (Van Goozen et al. 1998; Van Goozen et al. 2000b).  Interestingly, some studies suggest that
cortisol can moderate the effect of testosterone.  Pompa and colleagues (2007) found that there
was a significant correlation between testosterone and overt aggression in
individuals with low cortisol levels, but this correlation was lost with
individuals with high cortisol. 

Punishment Sensitivity

Children usually
naturally learn to avoid antisocial behavior by aversive conditioning.  They begin to feel afraid when they
anticipate punishment or the guilt of seeing someone else hurt by your actions
(Kochanska, 1993).  The amygdala, sympathetic
nervous system (SNS), and the hypothalamic-pituitary-adrenal (HPA) axis.  Many fMRI studies have shown abnormal amygdala
functioning in CD.  However, two fMRI studies
have found reduced activation of the amygdala in response to fearful faces in
individuals with ODD (Marsh et al. 2008;
White et al. 2012).  Additionally, negative emotionality has been
associated with the amygdala, and behavioral inhibition has been related to
amygdala projections to the prefrontal cortex (PFC, Kagan, 1988).  Additionally, the amygdala is connected to the
anterior cingulate cortex (ACC).  The ACC
is involved in negative feedback loops to the amygdala (Stefanacci &
Amaral, 2002).  Thus, weaker connections
results in less deactivation of the amygdala and more negative
emotionality. 

The SNS nervous system
is also involved in fear conditioning. 
Gao and colleaues (2010a) found that poor fear conditioning via
electrodermal stimulation was correlated with aggression at age eight.  Additionally, Gao and colleagues (2010b)
found that poor fear conditioning at age three was correlated with criminal
history at age 23.  Skin conductivity is
another measure of punishment sensitivity. 
Studies have found that children with lower skin conductivity are more likely
to have conduct problems or ODD (Lorber 2004; Van Goozen et al. 2000a).    Additionally, in a follow up study of the children
who had ODD, lower basic skin conductance was a predictor of externalizing
problems and maintenance of ODD (Van Bokhoven et al. 2005). 

Serotonin has been
implicated in punishment sensitivity as well. 
Matthys et al. (2013) showed
that serotonin was negatively correlated with aggressive behavior in children
and adolescents with ODD and CD.  However,
studies of rhesus monkeys show that the environment can influence serotonin levels
as well (Shannon et al. 2005). 

Reward Sensitivity

            The
amygdala, orbitofrontal cortex, and striatum are all implicated in the neurobiology
of reward sensitivity. 

Genetic

            Eaves
and colleagues (2000) found a large genetic correlation in liability for
ODD.  Rhee and Waldman (2002) conducted a
meta-analysis that estimates that antisocial behavior, in general, is 41%
heritable.  The same meta-analysis by
Moffitt (2005b) estimated the heritability to be 50%. 

Environmental
x Genetic

It is also
important to note that there are gene x environment interactions as well. Malnutrition
at 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 nutrition
and behavior problems was mediated by IQ, thus the authors concluded that malnutrition
predisposes children to neurocognitive deficits, which can lead to behavior problems.  Additionally, mothers who use opiates and
cocaine during the fetal development period have been shown to have children
with greater behavior problems at age four (Bennet et al. 2002).  Maternal
smoking has also been shown to be a statistically significant predictor of
conduct problems (Brennan et al. 2003)

Sometimes an
environment will affect people differently based upon their genotype.  For example, one MAOA genotype is associated
with negative emotionality, reward dependence, and antisocial behavior.  Additionally, victims of maltreatment are
also at risk for these same factors. 
However, if victims of maltreatment do not have this particular allele
for MAOA genotype, their genotype serves as a protective factor (Caspi 2002).  Thus, the MAOA genotype moderates the
response to the environment. 

Environment

            Family

            In 2013, a study showed that 18% of
children live in poverty, and 7% live in extreme poverty (Capella et al. 2013).  Lower family economic status has been related
to more involvement in juvenile crime and more instances of disruptive behavior
problems (Sampson and Lamb 1993; Barry et
al. 2005).  Additionally, families in
low SES households generally have higher levels of depression, which also
influences conduct problems (Conger et
al. 1994). 

            Parenting Practices

            Peer Factors

            Community

Gender Differences

            Gender
differences in ODD are inconsistent across studies.  However, most data suggest that ODD is more prevalent
in boys than girls or that there is no difference at all (Loeber et al. 2000). Recent studies show that
ODD is best characterized as two separate disorders, one behavioral and one
affective, 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 the
behavioral and affective dimensions. 

            Peer
rejection: Peer rejection can predict delinquency in boys but not in girls
(Miller 1999). 

Eme (2007) also discusses further potential
leads in this area that warrant investigation; particularly why girls with
congenital adrenal hyperplasia (CAH), a foetal disorder that leads girls to be
exposed to male levels of androgens in utero, tend to have high rates of behavioral
problems.

 

Boys
and girls follow different trajectories in the development of antisocial
behaviors. Boys usually have a child-onset, or an adolescent onset (Crick and
Zahn-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 and
middle childhood. It is suspected that girls might be protected against
child-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 to
understand as it is associated with greater risk of difficulties and serious
psychopathology 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 of
disruptive behavior in child and            adolescent
twins. Behav Genet 30:321–334

Lahey, 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: Model
comparisons, gender and longitudinal     invariance. Journal
of 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 the
past 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 peer
rejection and aggression and adolescent            delinquency
severity and type among African American youth. Journal of Emotional
and      Behavioral Disorders, 7(3),
137-146

White, S. F., Marsh, A. A., Fowler, K. A.,
Schechter, J. C., Adalio, C., Pope, K., … & Blair, R. J.     R. (2012). Reduced amygdala response in
youths with disruptive behavior disorders and            psychopathic
traits: decreased emotional response versus increased top-down attention to            nonemotional features. American
Journal of Psychiatry, 169(7), 750-758.