Bad Boy. Bad Boy. Is It Conduct Disorder?

Defining the line between normal childhood behavior and more serious problems like conduct disorder (CD) is important.

Conduct disorder is linked to a significant risk for a lifelong problem with aggression. 

Identifying CD early in life provides the hope that early intervention might reduce the later consequences of the disorder.

The American Academy of Child and Adolescent Psychiatry has an excellent online resource center to understand conduct disorder. They note the condition is characterized by four key diagnostic features with onset in childhood:

• Aggression toward people and animals
• Destruction of property
• Frequent lying/theft
• Chronic violation of rules

A recent research study by Benjamin Lahey and Irwin Waldman analyzed the validity of conduct disorder in relationship to the other common childhood forms of psychopathology.

They note a key diagnostic challenge is to differentiate conduct disorder from a similar disorder known as oppositional defiant disorder or ODD. The main conclusions from their literature review included the following:

1. CD appears distinct from ODD in many ways
2. CD more strongly predicts adult antisocial behavior compared to ODD
3. It may be of value to identify the type of aggressive behavior in cases of CD: proactive vs reactive, physical vs non-physical aggression towards other
4. Age of onset of CD may be an important signal. Early age of onset appears to have a worse prognosis
5. CD in the context of a callous, unemotional, without regret may also be an important marker for severity
6. CD is a male predominant disorder and there may be important differences in the manifestation of the disorder between boys and girls
7. Factor analysis finds CD to cluster in a broad group of externalizing disorders that includes ODD, ADHD hyperactivity and impulsivity and inattention
8. This externalizing group of disorders appears distinct from a group of childhood internalizing disorders that includes social anxiety, obsessive compulsive disorder, separation anxiety and phobias including agoraphobia
9. Externalizing disorders appear to share some distinct genetic risk
10. Although genetic factors appear key in CD and other externalizing disorders, environmental factors may interact with genetic risk to effect outcome
11. Future research implications from this review include the methods needed for refining the CD phenotype, molecular genetic studies, nonshared environmental studies and studies of the neurobiology of CD and studies of gender difference
12. It is likely that CD will share "neurobiological mechanisms with other prevalent forms of psychopathology" although is is likely there are mechanisms that will be specific or unique to CD

This review is a good place to start in understanding the phenotype of CD and how it is understood from a current research prospective.

Readers with more interest in this topic can access the free full-text manuscript by clicking on the PMID link in the citation below.

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Lahey BB, & Waldman ID (2012). Annual research review: phenotypic and causal structure of conduct disorder in the broader context of prevalent forms of psychopathology. Journal of child psychology and psychiatry, and allied disciplines, 53 (5), 536-57 PMID: 22211395

The Neurobiology of Anxiety Disorders

A key question in the classification of anxiety disorders is whether the DSM-IV classification system describes distinct useful categories.  There is a great deal of overlap in clinical populations.  You do not find many individual who have one unique disorder.  Typically, someone with say panic disorder is likely to have one or more additional anxiety disorder such as social phobia or PTSD.  A key question is whether there is a broader anxiety disorder phenotype that might include a variety of symptoms found in specific anxiety disorders.

If specific anxiety disorders describe specific phenotypes, there should be evidence from what we know about the neurobiology of these disorders.  A recent comprehensive review of this issue has been published in the 2009 September issue of Psychiatric Clinics of North America and has been republished in Clinical and Laboratory Medicine.  The authors of this review make the argument that “there exist many distinguishing features that support the continued classification of individual anxiety disorders that are distinct from each other and from major depression.”  I will summarize some of their highlights for several of the individual anxiety, disorders.  The authors group their findings into anatomical and functional imaging findings, neuroendocrine and neurotransmitter, and genetic domains.  I will focus on the anatomical and functional imaging domains and refer the reader to the original manuscript for the other domains.

Panic Disorder

• Decreased glucose metabolism in parietal lobe and overall decreased cerebral blood flow
• Elevated glucose metabolism in amygdale, hippocampus, thalamus, midbrain and cerebellum
• Elevations normalize with successful treatment with behavioral or pharmacotherapy
• Panic attacks are linked with hyperactivity burst in right amygdale
• Anxious visual stimuli provoke increased activity in inferior frontal cortex, hippocampus, anterior and posterior cingulated cortex and orbitofrontal cortex

Posttraumatic Stress Disorder

• Severity of PTSD linked to greater activation of amygdale in response to fearful faces
• Ventral activation of anterior cingulate cortex with fearful faces predicts poor response to cognitive behavioral therapy
• PTSD patients activate the executive function network with combat-related images—this network is typically not activated in normals for emotional/affective processing tasks
• PTSD patients anxiety overwhelms brain inhibitory network producing more errors with cognitive tasks

Social Phobia

• Anticipation of public speaking tasks excessively elevates activation of subcortical, limbic and lateral paralimbic regions
• Response to trazodone in social phobia linked to decreased blood flow to ventral and dorsl anterior cingulate cortex and prefrontal cortex and increased cerebral blood flow to middle cingulated cortex, left hippocampus and parahippocampal gyrus
• Misinterpretation of social cues due to dysfunction of the cortico-striato-thalamic network

Generalized Anxiety Disorder

• Pediatric patients with generalized anxiety show enlargement of amygdale
• Elevated prefrontal cortex resting activity felt to be an anxiety compensatory response
• Elevated amygdala and insular cortex activation with angry faces
• Venlafaxine drug response tied to lower pretreatment amygdala activity and higher anterior cingulated activity

One of the methodological problems with imaging, neurotransmitter and genetic studies in anxiety disorders is the issue of identifying individuals with a unique anxiety disorder.  Even this strategy may be problematic.  Studying a young adult patient with a unique panic disorder diagnosis does not account for the possibility of later development another anxiety disorder such as social phobia or PTSD.

Although a great deal of progress has been made in the neurobiology of anxiety disorders, the challenge of understanding the best classification strategies remain.  Clinicians are typically, left with a implementing a trial of a selective serotonin re-uptake inhibitor or cognitive behavior therapy in patients with a single or multiple anxiety disorder diagnoses.  The jury is out whether neurobiology can lead to improved and more specific treatments.  

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Martin EI, Ressler KJ, Binder E, & Nemeroff CB (2009). The neurobiology of anxiety disorders: brain imaging, genetics, and psychoneuroendocrinology. The Psychiatric clinics of North America, 32 (3), 549-75 PMID: 19716990