The relationship between anxious/depressed traits and neuromaturation remains largely unstudied. Characterizing this relationship during healthy neurodevelopment is critical to understanding processes associated with the emergence of child/adolescent onset mood/anxiety disorders. In this study, mixed-effects models were used to determine longitudinal cortical thickness correlates of Child Behavior Checklist (CBCL) and Young Adult Self Report Anxious/Depressed scores in healthy children. Analyses included 341 subjects from 4.9 to 22.3 year-old with repeated MRI at up to 3 time points, at 2-year intervals (586 MRI scans). There was a significant "CBCL Anxious/Depressed by Age" interaction on cortical thickness in the right ventromedial prefrontal cortex (vmPFC), including the medial orbito-frontal, gyrus rectus, and subgenual anterior cingulate areas. Anxious/Depressed scores were negatively associated with thickness at younger ages (<9 years), but positively associated with thickness at older ages (15-22 years), with the shift in polarity occurring around age 12. This was secondary to a slower rate of vmPFC cortical thinning in subjects with higher scores. In young adults (18-22 years), Anxious/Depressed scores were also positively associated with precuneus/posterior cingulate cortical thickness. Potential neurobiological mechanisms underlying this maturation pattern are proposed. These results demonstrate the dynamic impact of age on relations between vmPFC and negative affect in the developing brain.
Using a population-based sampling strategy, the National Institutes of Health (NIH) Magnetic Resonance Imaging Study of Normal Brain Development compiled a longitudinal normative reference database of neuroimaging and correlated clinical/behavioral data from a demographically representative sample of healthy children and adolescents aged newborn through early adulthood. The present paper reports brain volume data for 325 children, ages 4.5-18 years, from the first cross-sectional time point. Measures included volumes of whole-brain gray matter (GM) and white matter (WM), left and right lateral ventricles, frontal, temporal, parietal and occipital lobe GM and WM, subcortical GM (thalamus, caudate, putamen, and globus pallidus), cerebellum, and brainstem. Associations with cross-sectional age, sex, family income, parental education, and body mass index (BMI) were evaluated. Key observations are: 1) age-related decreases in lobar GM most prominent in parietal and occipital cortex; 2) age-related increases in lobar WM, greatest in occipital, followed by the temporal lobe; 3) age-related trajectories predominantly curvilinear in females, but linear in males; and 4) small systematic associations of brain tissue volumes with BMI but not with IQ, family income, or parental education. These findings constitute a normative reference on regional brain volumes in children and adolescents.
Background: Understanding the maturation and organization of cognitive function in the brain is a
The neonatal brain possesses higher water content, lower macromolecular concentration, and reduced synaptic density than is found in the brain of a 1-year-old child. Changes in MRI characteristics of brain such as relaxation times accompany rapid changes in brain during early postnatal development. It was hypothesized that T* 2 values found in newborns would be significantly higher than those found in 9-month-old children and adults as measured at 1.5 T. Spoiled gradient echo measurements of T* 2 within the brains of newborns, 9-month-olds, and adults confirmed this hypothesis. The results have implications with regard to functional MRI studies in newborns since, in general, BOLD signal optimization is achieved when echo times TE are set equal to the T* 2 values of the tissue of interest. Since significantly longer T* 2 values are found in newborns, it is suggested that the TE values employed for fMRI studies of newborns should be increased to maximize BOLD signal intensity changes and improve the overall reliability of fMRI results in newborns.
Background and Purpose Arteriopathy is the leading cause of childhood arterial ischemic stroke (AIS). Mechanisms are poorly understood but may include inherent abnormalities of arterial structure. Extracranial dissection is associated with connective tissue disorders in adult stroke. Focal cerebral arteriopathy (FCA) is a common syndrome where pathophysiology is unknown but may include intracranial dissection or transient cerebral arteriopathy (TCA). We aimed to quantify cerebral arterial tortuosity in childhood AIS, hypothesizing increased tortuosity in dissection. Methods Children (1month-18 years) with AIS were recruited within the Vascular Effects of Infection in Pediatric Stroke (VIPS) study with controls from the Calgary Pediatric Stroke Program. Objective, multi-investigator review defined diagnostic categories. A validated imaging software method calculated mean arterial tortuosity of the major cerebral arteries using 3D time-of-flight MR angiography source images. Tortuosity of unaffected vessels was compared between children with dissection, TCA, meningitis, moyamoya, cardioembolic strokes and controls (ANOVA, post-hoc Tukey). Trauma-related versus spontaneous dissection was compared (Student's t-test). Results One hundred fifteen children were studied (median 6.8 years, 43% female). Age and sex were similar across groups. Tortuosity means and variances were consistent with validation studies. Tortuosity in controls (1.346±0.074,n=15) was comparable to moyamoya (1.324±0.038, n=15, p=0.998), meningitis (1.348±0.052, n=11, p=0.989) and cardioembolic (1.379±0.056, n=27, p=0.190) cases. Tortuosity was higher in both extracranial dissection (1.404±0.084, n=22, p=0.021) and TCA (1.390±0.040, n=27, p=0.001) children. Tortuosity was not different between traumatic versus spontaneous dissection (p=0.70). Conclusion In children with dissection and TCA cerebral arteries demonstrate increased tortuosity. Quantified arterial tortuosity may represent a clinically relevant imaging biomarker of vascular biology in pediatric stroke.
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