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Objectives: The prospective longitudinal Mannheim Study of Children at Risk followed the development of children from the age of 2 years up to the age of 8 years. Are there differences between the developmental risk load in toddlers (psychopathology, cognition, motor or neurological development. and educational differences) who suffer from a hyperactive disorder at age 8 and that of undisturbed children of the same age? Are there specific harbingers of hyperkinetic disorders for the group concerned? Methods: In terms of their developmental risk load at the age of 2 years, 26 primary school children with hyperkinetic disorders were compared to 241 healthy primary school children, as well as to 25 children of the same age with emotional disturbances and 30 children of the same age with socially disruptive behavior. Results: A significant combination of predictors of later hyperkinetic disorders at primary school age proved to be increased fidgetiness and irritability, as well as a reduced language comprehension, at the age of two. Conclusions: The predictive value of symptoms in early childhood for later hyperkinetic disorder in children of primaryschool age is higher than that of symptoms assessed in infancy, which although expected is without relevant specificity.
Objectives: Are there any differences (organic, psychosocial, psychopathological, cognitive or educational, respectively differences in the motor or neurological development) between infants who later on at the age of 8 years suffer from a hyperactive disorder and those who later on at the same age are undisturbed? Are there specific harbingers for hyperactive disorders in the group concerned? Methods: With regard to their developmental risk load at the age of 3 months, 26 primary school children with hyperactive disorders were compared with 241 healthy children, 25 children with emotional disturbances, and 30 children with socially disruptive behaviour, all of the same age. Results: Identified as the most important predictors for the onset of hyperactive disorders were a reduced birth weight, the mother's origin from a shattered family, early contact impairments on the part of the child, and the mother's neglect of the infant. Conclusions: Altogether, however, the prediction of later hyperactivity in primary school children on the basis of salient features in the infant children remains unsatisfactory and unspecific.
Ventral striatum and amygdala activity as convergence sites for early adversity and conduct disorder
(2017)
Childhood family adversity (CFA) increases the risk for conduct disorder (CD) and has been associated with alterations in regions of affective processing like ventral striatum (VS) and amygdala. However, no study so far has demonstrated neural converging effects of CFA and CD in the same sample. At age 25 years, functional MRI data during two affective tasks, i.e. a reward (N = 171) and a face-matching paradigm (N = 181) and anatomical scans (N = 181) were acquired in right-handed currently healthy participants of an epidemiological study followed since birth. CFA during childhood was determined using a standardized parent interview. Disruptive behaviors and CD diagnoses during childhood and adolescence were obtained by diagnostic interview (2–19 years), temperamental reward dependence was assessed by questionnaire (15 and 19 years).
CFA predicted increased CD and amygdala volume. Both exposure to CFA and CD were associated with a decreased VS response during reward anticipation and blunted amygdala activity during face-matching. CD mediated the effect of CFA on brain activity. Temperamental reward dependence was negatively correlated with CFA and CD and positively with VS activity. These findings underline the detrimental effects of CFA on the offspring's affective processing and support the importance of early postnatal intervention programs aiming to reduce childhood adversity factors.
Converging evidence has highlighted the association between poverty and conduct disorder (CD) without specifying neurobiological pathways. Neuroimaging research has emphasized structural and functional alterations in the orbitofrontal cortex (OFC) as one key mechanism underlying this disorder. The present study aimed to clarify the long-term influence of early poverty on OFC volume and its association with CD symptoms in healthy participants of an epidemiological cohort study followed since birth. At age 25 years, voxel-based morphometry was applied to study brain volume differences. Poverty (0 = non-exposed (N = 134), I = exposed (N = 33)) and smoking during pregnancy were determined using a standardized parent interview, and information on maternal responsiveness was derived from videotaped mother infant interactions at the age of 3 months. CD symptoms were assessed by diagnostic interview from 8 to 19 years of age. Information on life stress was acquired at each assessment and childhood maltreatment was measured using retrospective self-report at the age of 23 years. Analyses were adjusted for sex, parental psychopathology and delinquency, obstetric adversity, parental education, and current poverty. Individuals exposed to early life poverty exhibited a lower OFC volume. Moreover, we replicated previous findings of increased CD symptoms as a consequence of childhood poverty. This effect proved statistically mediated by OFC volume and exposure to life stress and smoking during pregnancy, but not by childhood maltreatment and maternal responsiveness. These findings underline the importance of studying the impact of early life adversity on brain alterations and highlight the need for programs to decrease income-related disparities.