Laterobasal amygdalar enlargement in 6- to 7-year-old children with autism spectrum disorder.
ABSTRACT There is substantial imaging evidence for volumetric abnormalities of the amygdala in younger children with autism spectrum disorder (ASD). The amygdala can be divided into functionally distinct laterobasal, superficial, and centromedial subregions. To date, we are not aware of any in vivo reports specifically assessing subregional amygdalar abnormalities in individuals with ASD.
To evaluate alterations in subregional amygdalar morphology in children with ASD compared with typically developing (TD) children and to examine the relationships with ASD symptom severity.
A cross-sectional study encompassing a narrow age range of children with ASD and age-matched TD children that evaluated magnetic resonance imaging-defined subregional morphology of the amygdala using a novel subregional analytic method.
Participants were recruited and clinically evaluated through the University of Washington Autism Center and imaged at the Diagnostic Imaging Sciences Center at the University of Washington. Imaging data were analyzed through the Brain Imaging Laboratory at the Seoul National University.
Fifty-one children 6 to 7 years of age (ASD, n = 31 and TD, n = 20) were assessed using magnetic resonance imaging and behavioral measures.
Volume and subregional measures of the amygdala and measures of social and communication functioning.
The ASD group exhibited larger right and left amygdalae, by 12.7% and 11.0%, respectively, relative to the TD group. Subregional analysis revealed that the ASD group had enlarged laterobasal amygdalar subregions, relative to the TD group, after adjusting for age, sex, and hemispheric cerebral volume (P < .05, false discovery rate corrected and with clustered surface points >15). Exploratory analyses revealed that there were linear trends comparing a strictly defined subgroup of children with autistic disorder, who exhibited the greatest extent of laterobasal enlargement, followed by a subgroup of children with pervasive developmental disorder not otherwise specified and then the group of TD children (P for linear trend <.001). There were linear trends between enlargement of laterobasal subregions and lower levels of social and communication functioning (P < .001, P < .001, and P = .001 for 3 areas in the right laterobasal subregion; P < .001 for 1 area in the left laterobasal subregion).
The current study demonstrates bilateral enlargement of laterobasal subregions of the amygdala in 6- to 7-year-old children with ASD and that subregional alterations are associated with deficits in social and communicative behavior.
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ABSTRACT: Advances in brain imaging research in autism spectrum disorders (ASD) are rapidly occurring, and the amount of neuroimaging research has dramatically increased over the past 5 years. In this review, advances during the past 12 months and longitudinal studies are highlighted. Cross-sectional neuroimaging research provides evidence that the neural underpinnings of the behavioral signs of ASD involve not only dysfunctional integration of information across distributed brain networks but also basic dysfunction in primary cortices.Longitudinal studies of ASD show abnormally enlarged brain volumes and increased rates of brain growth during early childhood in only a small minority of ASD children. There is evidence of disordered development of white matter microstructure and amygdala growth, and at 2 years of age, network inefficiencies in posterior cerebral regions.From older childhood into adulthood, atypical age-variant and age-invariant changes in the trajectories of total and regional brain volumes and cortical thickness are apparent at the group level. There is evidence of abnormalities in posterior lobes and posterior brain networks during the first 2 years of life in ASD and, even in older children and adults, dysfunction in primary cortical areas.
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ABSTRACT: There is now a strong if not urgent call in both the attachment and autism literatures for updated, research informed, clinically relevant interventions that can more effectively assess the mother infant dyad during early periods of brain plasticity. In this contribution I describe my work in regulation theory, an overarching interpersonal neurobiological model of the development, psychopathogenesis, and treatment of the early forming subjective self system. The theory models the psychoneurobiological mechanisms by which early rapid, spontaneous and thereby implicit emotionally laden attachment communications indelibly impact the experience-dependent maturation of the right brain, the "emotional brain." Reciprocal right-lateralized visual-facial, auditory-prosodic, and tactile-gestural non-verbal communications lie at the psychobiological core of the emotional attachment bond between the infant and primary caregiver. These affective communications can in turn be interactively regulated by the primary caregiver, thereby expanding the infant's developing right brain regulatory systems. Regulated and dysregulated bodily based communications can be assessed in order to determine the ongoing status of both the infant's emotional and social development as well as the quality and efficiency of the infant-mother attachment relationship. I then apply the model to the assessment of early stages of autism. Developmental neurobiological research documents significant alterations of the early developing right brain in autistic infants and toddlers, as well profound attachment failures and intersubjective deficits in autistic infant-mother dyads. Throughout I offer implications of the theory for clinical assessment models. This work suggests that recent knowledge of the social and emotional functions of the early developing right brain may not only bridge the attachment and autism worlds, but facilitate more effective attachment and autism models of early intervention.Frontiers in Psychology 09/2014; 5:1049. DOI:10.3389/fpsyg.2014.01049 · 2.80 Impact Factor
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ABSTRACT: Impairments in emotional processing in Autism Spectrum Disorders (ASDs) can be characterised by failure to generate and recognize self-reflective, cognitive-based emotions, such as pride, embarrassment and shame. Among this type of emotions, regret and disappointment, as well as their positive counterparts, result from a counterfactual comparison, that is the comparison between an actual value (“what is”) and a fictive value (“what might have been”). However, while disappointment is experienced when the obtained outcome is worse than the expected outcome that might have occurred from the same choice, regret occurs when one experiences an outcome that is worse than the outcome of foregone choices. By manipulating a simple gambling task, we examined subjective reports on the intensity of negative and positive emotions in a group of adults with High Functioning Autism or Asperger syndrome (HFA/AS), and a control group matched for age, gender and educational level. Participants were asked to choose between two lotteries with different levels of risk under two conditions of outcome feedback: (i) Partial, in which only the outcome of the chosen lottery was visible, (ii) Complete, in which the outcomes of the two lotteries were simultaneously visible. By comparing partial and complete conditions, we aimed to investigate the differential effect between disappointment and regret, as well as between their positive counterparts. Relative to the control participants, the group with HFA/AS reported reduced regret and no difference between regret and disappointment, along with a preserved ability to use counterfactual thinking and similar choice behavior. Difficulties to distinguish the feeling of regret in participants with HFA/AS can be explained by diminished emotional awareness, likely associated with an abnormal fronto-limbic connectivity.Cortex 09/2014; 58. DOI:10.1016/j.cortex.2014.05.008 · 6.04 Impact Factor