6-3 Final Project Milestone Four: Rough Draft Submit your rough draft. Submit your assignment here. Make sure you’ve included all the required elements by reviewing the guidelines and rubric. The top
Age-Appropriate Milestones and Anomalies
Katherine Alexandre
Southern New Hampshire University
March 24, 2024
Age-Appropriate Milestones and Anomalies
Fairchild, G., Passamonti, L., Hurford, G., Hagan, C. C., von dem Hagen, E. A., van Goozen, S. H., ... & Calder, A. J. (2011). Brain structure abnormalities in early-onset and adolescent-onset conduct disorder. American Journal of Psychiatry, 168(6), 624-633.
Annotation
Fairchild et al. investigate CD neural networks in relation to the age a child onsets CD. The researchers used voxel-based morphometry to evaluate gray matter volumes in several brain regions related to socioemotional processing and found that there were differences between adolescents with early-onset (EO-CD) or adolescent-onset (AO-CD) CD and healthy controls. As a result, the studies demonstrate a loss of volume in the gray matter of the amygdala and insula, essential for emotional processing, in the united group of CD subjects. Even more interestingly, however, both types of CD group presented with decreased amygdala volume, with a specific reduction in the right insula volume only for AO-CD group. Within CD subjects, regression analyses of CD symptoms and right insula volume presented a negative linear relationship. This states that structural brain abnormalities are connected with incidence of CD irrespective of age of onset, with a revision of developmental taxonomic theory of CD etiology. What Fairchild et al. (2011) does is examining brain structural anomalies in conduct disorder (CD) as a function of age onset, helping to clarify answers to neurodevelopmental age-relevant milestones and disturbances. Like Passamonti et al. (2010), this study focuses on neural correlates of CD; however, in terms of methodology, these studies are different but converge in their affixing an important role of neurobiological factors in the development of CD. Both research projects provide insightful views on CD's neurobiological foundations, supplementing each other in their attempt to decode the complex issue.
Abstract from Author
Abstract
Objective:
The developmental taxonomic theory proposes that neurodevelopmental factors play a critical role in the etiology of early-onset conduct disorder, whereas adolescent-onset conduct disorder arises as a result of social mimicry of deviant peers. Recent studies have challenged this theory by demonstrating that adolescents with both early- and adolescent-onset forms of conduct disorder show impaired emotional learning and abnormal neural activation during facial expression processing. The present study extends this work by investigating brain structure in both subtypes of conduct disorder.
Method:
Voxel-based morphometry was used to compare gray matter volumes in four regions of interest (amygdala, insula, anterior cingulate, and orbitofrontal cortex) in male adolescents with early-onset (N=36) or adolescent-onset (N=27) conduct disorder and in healthy comparison subjects (N=27). Whole-brain structural analyses were also performed.
Results:
The combined conduct disorder group displayed gray matter volume reductions in the bilateral amygdala, extending into the insula, relative to healthy comparison subjects. Separate comparisons between healthy subjects and each conduct disorder subgroup revealed lower amygdala volume in both subgroups and reduced right insula volume in the adolescent-onset subgroup. Regression analyses within the conduct disorder subjects alone demonstrated a negative correlation between conduct disorder symptoms and right insula volume.
Conclusions:
The results demonstrate that gray matter volume reductions in brain regions involved in processing socioemotional stimuli are associated with conduct disorder, regardless of age of onset. Brain structural abnormalities may contribute to the emergence of adolescent-onset as well as early-onset conduct disorder.
Passamonti, L., Fairchild, G., Goodyer, I. M., Hurford, G., Hagan, C. C., Rowe, J. B., & Calder, A. J. (2010). Neural abnormalities in early-onset and adolescence-onset conduct disorder. Archives of general psychiatry, 67(7), 729-738.
Annotation
The authors of the study by Passamonti et al. examine the responses of people with early-onset (EO-CD) and adolescent-onset (AO-CD) conduct disorder to emotional stimuli and compare them with a control group consisting of healthy individuals. By using fMRI-based approach, they examine which areas of the brain associated with antisocial behaviors are activated. This research has revealed diminished emotional processing in both CD subtypes compared to controls, contradicting the developmental taxonic theory. In addition, the abnormal amygdala responses to neutral faces and sadness have been observed in both CD subtypes as they manifested more pronounced amygdala hypoactivation compared to the control group. These results imply that neurophysiological defects are responsible for both the subtypes of CD which somewhat goes against the notion that EO-CD is merely neurodevelopmental and AO-CD is only due to social mimicry. The study of Passamonti, et al., (2010) focuses on the neurophysiological responses to emotional stimuli in CD, providing evidence of age-suitable brain functioning. This research is like Fairchild et al, (2011) because both focus on different neural problems in CD, but still concur on the significance of neurobiological factors in experiencing disease symptoms. Two studies describe the neural substrates of CD at different age onsets and together they offer a synergic insight into the disorder, giving a comprehensive idea about the illness.
Abstract from Author
Abstract
Context
Conduct disorder (CD) is characterized by severe antisocial behavior that emerges in childhood (early-onset CD [EO-CD]) or adolescence (adolescence-onset CD [AO-CD]). Early-onset CD is proposed to have a neurodevelopmental basis, whereas AO-CD is thought to emerge owing to social mimicry of deviant peers. However, this developmental taxonomic theory is debated after reports of neuropsychological impairments in both CD subtypes. A critical, although unaddressed, issue is whether these subtypes present similar or distinct neurophysiological profiles. Hence, we investigated neurophysiological responses to emotional and neutral faces in regions associated with antisocial behavior (ie, the amygdala, ventromedial prefrontal cortex, insula, and orbitofrontal cortex) in individuals with EO-CD and AO-CD and in healthy control subjects.
Objective
To investigate whether EO-CD and AO-CD subjects show neurophysiological abnormalities.
Design
Case-control study.
Setting
Government research institute, university department.
Participants
Seventy-five male adolescents and young adults aged 16 to 21 years, including 27 with EO-CD, 25 with AO-CD, and 23 healthy controls.
Main Outcome Measure
Neural activations measured by functional magnetic resonance imaging while participants viewed angry, sad, and neutral faces.
Results
Comparing angry vs neutral faces, participants with both CD subtypes displayed reduced responses in regions associated with antisocial behavior compared with controls; differences between the CD subtypes were not significant. Comparing each expression with fixation baseline revealed an abnormal (increased) amygdala response to neutral but not angry faces in both groups of CD relative to controls. For sad vs neutral faces, reduced amygdala activation was observed in EO-CD relative to AO-CD and control participants. Comparing each expression with fixation revealed hypoactive amygdala responses to sadness in individuals with EO-CD relative to AO-CD participants and controls. These findings were not accounted for by attention-deficit/hyperactivity disorder symptoms.
Conclusions
Neurophysiological abnormalities are observed in both CD subtypes, contrary to the developmental taxonomic theory of CD. Additional amygdala hypofunction in relation to sad expressions might indicate why EO-CD is more severe and persistent than AO-CD.
