67 resultados para Childhood neurological disorders, Executive function, Preterm, Extremely low birth weight


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Objective: Cortical gray matter thinning takes place during childhood due to pruning of inefficient synaptic connections and an increase in myelination. Alterations in brain structure occur in very preterm born children with prolonged maturation of the frontal lobes and smaller cortical and white matter volume. These findings give rise to the question if age affects cortical thinning differently in very preterm born children compared to controls. The aim of the present study was to investigate the relationship between age and cortical thickness in very preterm born children when compared to controls. Participants and Methods: Forty-one very preterm born children (<32 weeks gestational age and/or < 1500 gram birth weight) and 30term born controls were included in the study (7-12 years). The automated surface reconstruction software FreeSurfer was applied to obtain measurements of cortical thickness based on T1-weighted MRI images. Results: Cortical thickness was lower in bilateral frontal and left parietal regions and higher in left temporal gyri in very preterm born children compared to controls. However, these differences depended on age. In very preterm born children, age correlated negatively with cortical thickness in right frontal, parietal and inferior temporal regions. Accordingly, cortical thickness was higher in young compared to old very preterm born children in bilateral frontal, parietal and temporal regions. In controls, age was not associated with cortical thickness. Conclusions: In very preterm born children, cortical thinning still occurs between the age of 7 and 12 years, mainly in frontal and parietal areas. In controls, however, a substantial part of cortical thinning appears to be completed in these regions before they reach the age of 7 years. These data indicate a delay in cortical thinning in very preterm born children.

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Background: Cortical gray matter thinning occurs during childhood due to pruning of inefficient synaptic connections and an increase in myelination. Preterms show alterations in brain structure, with prolonged maturation of the frontal lobes, smaller cortical volumes and reduced white matter volume. These findings give rise to the question if there is a differential influence of age on cortical thinning in preterms compared to controls. Aims: To investigate the relationship between age and cortical thickness in preterms when compared to controls. Study design and outcome measures: The automated surface reconstruction software FreeSurfer was applied to obtain measurements of cortical thickness based on T1-weighted MRI images. Subjects: Forty-one preterms (< 32 weeks gestational age and/or < 1500 gram birth weight) and 30 controls were included in the study (7-12 years). Results: Cortical thickness was lower in bilateral frontal and left parietal regions and higher in left temporal gyri in preterms compared to controls. However, these differences depended on age. In preterms, age correlated negatively with cortical thickness in right frontal, parietal and inferior temporal regions. Accordingly, cortical thickness was higher in young compared to old preterms in bilateral frontal, parietal and temporal regions. In controls, age was not associated with cortical thickness. Conclusion: In preterms, cortical thinning still seems to occur between the age of 7 and 12 years, mainly in frontal and parietal areas whereas in controls, a substantial part of cortical thinning appears to be completed before they reach the age of 7 years. These data indicate slower cortical thinning in preterms than in controls.

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We investigated whether amygdala activation, autonomic responses, respiratory responses, and facial muscle activity (measured over the brow and cheek [fear grin] regions) are all sensitive to phobic versus nonphobic fear and, more importantly, whether effects in these variables vary as a function of both phobic and nonphobic fear intensity. Spider-phobic and comparably low spider-fearful control participants imagined encountering different animals and rated their subjective fear while their central and peripheral nervous system activity was measured. All measures included in our study were sensitive to variations in subjective fear, but were related to different ranges and positions on the subjective fear level continuum. Left amygdala activation, heart rate, and facial muscle activity over the cheek region captured fear intensity variations even within narrowly described regions on the fear level continuum (here within extremely low levels of fear and within considerable phobic fear). Skin conductance and facial muscle activity over the brow region did not capture fear intensity variations within low levels of fear: skin conductance mirrored only extreme levels of fear, and activity over the brow region distinguished phobic from nonphobic fear but also low-to-moderate and high phobic fear. Finally, respiratory measures distinguished phobic from nonphobic fear with no further differentiation within phobic and nonphobic fear. We conclude that a careful consideration of the measures to be used in an investigation and the population to be examined can be critical in order to obtain significant results.

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Traditionally, researchers have discussed executive function and metacognition independently. However, more recently, theoretical frameworks linking these two groups of higher order cognitive processes have been advanced. In this article, we explore the relationship between executive function and procedural metacognition, and summarize theoretical similarities. From a developmental perspective, the assumed theoretical resemblances seem to be supported, considering development trajectories and their substantial impact on areas that include learning and memory. Moreover, empirical evidence suggests direct relationships on the task level, on the level of latent variables, and in terms of involved brain regions. However, research linking the two concepts directly remains rare. We discuss evidence and developmental mechanisms, and propose ways researchers can investigate links between executive function and procedural metacognition.

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OBJECTIVE To assess whether exposure to high altitude induces cognitive dysfunction in young healthy European children and adolescents during acute, short-term exposure to an altitude of 3450 m and in an age-matched European population permanently living at this altitude. STUDY DESIGN We tested executive function (inhibition, shifting, and working memory), memory (verbal, short-term visuospatial, and verbal episodic memory), and speed processing ability in: (1) 48 healthy nonacclimatized European children and adolescents, 24 hours after arrival at high altitude and 3 months after return to low altitude; (2) 21 matched European subjects permanently living at high altitude; and (3) a matched control group tested twice at low altitude. RESULTS Short-term hypoxia significantly impaired all but 2 (visuospatial memory and processing speed) of the neuropsychological abilities that were tested. These impairments were even more severe in the children permanently living at high altitude. Three months after return to low altitude, the neuropsychological performances significantly improved and were comparable with those observed in the control group tested only at low altitude. CONCLUSIONS Acute short-term exposure to an altitude at which major tourist destinations are located induces marked executive and memory deficits in healthy children. These deficits are equally marked or more severe in children permanently living at high altitude and are expected to impair their learning abilities.

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Little is known about the aetiology of childhood brain tumours. We investigated anthropometric factors (birth weight, length, maternal age), birth characteristics (e.g. vacuum extraction, preterm delivery, birth order) and exposures during pregnancy (e.g. maternal: smoking, working, dietary supplement intake) in relation to risk of brain tumour diagnosis among 7-19 year olds. The multinational case-control study in Denmark, Sweden, Norway and Switzerland (CEFALO) included interviews with 352 (participation rate=83.2%) eligible cases and 646 (71.1%) population-based controls. Interview data were complemented with data from birth registries and validated by assessing agreement (Cohen's Kappa). We used conditional logistic regression models matched on age, sex and geographical region (adjusted for maternal age and parental education) to explore associations between birth factors and childhood brain tumour risk. Agreement between interview and birth registry data ranged from moderate (Kappa=0.54; worked during pregnancy) to almost perfect (Kappa=0.98; birth weight). Neither anthropogenic factors nor birth characteristics were associated with childhood brain tumour risk. Maternal vitamin intake during pregnancy was indicative of a protective effect (OR 0.75, 95%-CI: 0.56-1.01). No association was seen for maternal smoking during pregnancy or working during pregnancy. We found little evidence that the considered birth factors were related to brain tumour risk among children and adolescents.