Regional Brain Volumes and Their Later Neurodevelopmental Correlates in Term and Preterm Infants

Abstract Context: IGF-I and IGF binding protein-3 (IGFBP-3) are essential for growth and maturation of the developing brain. Objective: The aim of this study was to evaluate the association between postnatal serum concentrations of IGF-I and IGFBP-3 and brain volumes at term in very preterm infants. Design: Fifty-one infants with a mean (sd) gestational age (GA) of 26.4 (1.9) wk and birth weight (BW) of 888 (288) g were studied, with weekly blood sampling of IGF-I and IGFBP-3 from birth until 35 gestational weeks (GW) and daily calculation of protein and caloric intake. Magnetic resonance images obtained at 40 GW were segmented into total brain, cerebellar, cerebrospinal fluid, gray matter, and unmyelinated white matter volumes. Main Outcome Measures: We evaluated brain growth by measuring brain volumes using magnetic resonance imaging. Results: Mean IGF-I concentrations from birth to 35 GW correlated with total brain volume, unmyelinated white matter volume, gray matter volume, and cerebellar volume [r = 0.55 (P < 0.001); r = 0.55 (P < 0.001); r = 0.44 (P = 0.002); and r = 0.58 (P < 0.001), respectively]. Similar correlations were observed for IGFBP-3 concentrations. Correlations remained after adjustment for GA, mean protein and caloric intakes, gender, severe brain damage, and steroid treatment. Protein and caloric intakes were not related to brain volumes. Infants with BW small for GA had lower mean concentrations of IGF-I (P = 0.006) and smaller brain volumes (P = 0.001–0.013) than infants with BW appropriate for GA. Conclusion: Postnatal IGF-I and IGFBP-3 concentrations are positively associated with brain volumes at 40 GW in very preterm infants. Normalization of the IGF-I axis, directly or indirectly, may support normal brain development in very preterm infants.

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Abstract 36: Association of Parental Stroke with Cognitive and Brain MRI Measures in Offspring - The Framingham Heart Study

Stroke ◽

10.1161/str.43.suppl_1.a36 ◽

2012 ◽

Vol 43 (suppl_1) ◽

Author(s):

GALIT WEINSTEIN ◽

Alexa Beiser ◽

Rhoda Au ◽

Charles DeCarli ◽

Philip A Wolf ◽

...

Keyword(s):

Executive Function ◽

Brain Injury ◽

Verbal Learning ◽

Brain Mri ◽

Abstract Reasoning ◽

Parental History ◽

Brain Volumes ◽

Regional Brain ◽

Increased Risk ◽

History Of

Objectives- Parental stroke is related to an increased risk of stroke among the offspring. Vascular related brain changes, however, often occur before clinical stroke and the association of parental history of stroke and structural brain measures and cognition has not been fully explored. We hypothesized that prospectively verified parental stroke will be associated with increased vascular brain injury and poorer cognitive performance. Methods- A total of 1,297 Framingham offspring (mean age: 61 ± 9 years, 54% women) were studied. Of these, 9.9% had prospectively identified stroke in one or both parents before age 65. Volumetric brain MRI measures of total cerebral brain volume (TCBV), regional brain volumes, white matter hyperintensity volume (WMHV), and covert brain infarcts (CBI) and performance on tests of verbal memory, abstract reasoning, verbal learning and visuospatial memory (VRd) were compared for offspring with and without parental history of stroke. All measures were assessed cross-sectionally and longitudinally (mean duration of follow-up was 6.1±1.2 years). We used models adjusted only for age, sex, education and also additionally adjusted for vascular risk factors and for WMHV as an index of subclinical vascular brain injury. GEE models were used to adjust for sibling relationships among offspring. Results- Higher WMHV (β±SE=0.17±0.08;p=0.027) and lower VRd scores (β±SE=-0.80±0.34; p=0.017) at baseline were found in offspring with parental history of stroke. In addition, participants with parental stroke by age 65 years were more likely to be in the highest quintile of increase in WMHV (OR=1.87;p=0.04) as well as worsening executive function (Trails B-A) (OR:1.81;p=0.03). Parental stroke was not associated with total and regional brain volumes or with memory, abstract reasoning and verbal learning. Conclusions- In our community-based sample of middle-aged asymptomatic subjects, the occurrence of parental stroke by age 65 years is associated with higher baseline WMHV and with a more rapid increase in WMHV. Further, parental stroke is also associated with poorer performance on VRd and a decline in executive function. The effects on baseline WMH and VRd were substantial equivalent to 2.8 and 7 years of brain aging, respectively.

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Circulatory insulin-like growth factor-I and brain volumes in relation to neurodevelopmental outcome in very preterm infants

Pediatric Research ◽

10.1038/pr.2013.135 ◽

2013 ◽

Vol 74 (5) ◽

pp. 564-569 ◽

Cited By ~ 36

Author(s):

Ingrid Hansen-Pupp ◽

Holger Hövel ◽

Chatarina Löfqvist ◽

Lena Hellström-Westas ◽

Vineta Fellman ◽

...

Keyword(s):

Growth Factor ◽

Preterm Infants ◽

Neurodevelopmental Outcome ◽

Insulin Like Growth Factor ◽

Brain Volumes ◽

Very Preterm Infants ◽

Very Preterm ◽

Factor I ◽

Growth Factor I

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Subclinical Agoraphobia Symptoms and Regional Brain Volumes in Non-clinical Subjects: Between Compensation and Resilience?

Frontiers in Psychiatry ◽

10.3389/fpsyt.2018.00541 ◽

2018 ◽

Vol 9 ◽

Cited By ~ 5

Author(s):

Bianca Besteher ◽

Letizia Squarcina ◽

Robert Spalthoff ◽

Marcella Bellani ◽

Christian Gaser ◽

...

Keyword(s):

Brain Volumes ◽

Regional Brain

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Regional neurodegeneration correlates with sleep–wake dysfunction after stroke

SLEEP ◽

10.1093/sleep/zsaa054 ◽

2020 ◽

Vol 43 (9) ◽

Author(s):

Elie Gottlieb ◽

Natalia Egorova ◽

Mohamed S Khlif ◽

Wasim Khan ◽

Emilio Werden ◽

...

Keyword(s):

White Matter ◽

Sleep Duration ◽

A Priori ◽

Sleep Efficiency ◽

Poor Sleep ◽

Subcortical Structures ◽

Whole Brain ◽

Brain Volumes ◽

Regional Brain ◽

Long Sleep

Abstract Sleep–wake disruption is a key modifiable risk factor and sequela of stroke. The pathogenesis of poststroke sleep dysfunction is unclear. It is not known whether poststroke sleep pathology is due to focal infarction to sleep–wake hubs or to accelerated poststroke neurodegeneration in subcortical structures after stroke. We characterize the first prospective poststroke regional brain volumetric and whole-brain, fiber-specific, white matter markers of objectively measured sleep–wake dysfunction. We hypothesized that excessively long sleep (>8 h) duration and poor sleep efficiency (<80%) measured using the SenseWear Armband 3-months poststroke (n = 112) would be associated with reduced regional brain volumes of a priori-selected sleep–wake regions of interest when compared to healthy controls with optimal sleep characteristics (n = 35). We utilized a novel technique known as a whole-brain fixel-based analysis to investigate the fiber-specific white matter differences in participants with long sleep duration. Stroke participants with long sleep (n = 24) duration exhibited reduced regional volumes of the ipsilesional thalamus and contralesional amygdala when compared with controls. Poor sleep efficiency after stroke (n = 29) was associated with reduced ipsilesional thalamus, contralesional hippocampus, and contralesional amygdala volumes. Whole-brain fixel-based analyses revealed widespread macrostructural degeneration to the corticopontocerebellar tract in stroke participants with long sleep duration, with fiber reductions of up to 40%. Neurodegeneration to subcortical structures, which appear to be vulnerable to accelerated brain volume loss after stroke, may drive sleep–wake deficiencies poststroke, independent of lesion characteristics and confounding comorbidities. We discuss these findings in the context of the clinicopathological implications of sleep-related neurodegeneration and attempt to corroborate previous mechanistic-neuroanatomical findings.

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Regional brain volumes, microstructure and neurodevelopment in moderate–late preterm children

Archives of Disease in Childhood - Fetal and Neonatal Edition ◽

10.1136/archdischild-2019-317941 ◽

2020 ◽

Vol 105 (6) ◽

pp. 593-599 ◽

Cited By ~ 1

Author(s):

Claire E Kelly ◽

Deanne K Thompson ◽

Alicia J Spittle ◽

Jian Chen ◽

Marc L Seal ◽

...

Keyword(s):

White Matter ◽

Grey Matter ◽

Diffusion Tensor ◽

Brain Mri ◽

Developmental Outcomes ◽

Late Preterm ◽

Brain Volumes ◽

Regional Brain ◽

White Matter Microstructure ◽

Cortical Grey Matter

ObjectiveTo explore whether regional brain volume and white matter microstructure at term-equivalent age (TEA) are associated with development at 2 years of age in children born moderate–late preterm (MLPT).Study designA cohort of MLPT infants had brain MRI at approximately TEA (38–44 weeks’ postmenstrual age) and had a developmental assessment (Bayley Scales of Infant and Toddler Development and Infant Toddler Social Emotional Assessment) at 2 years’ corrected age. Relationships between cortical grey matter and white matter volumes and 2-year developmental outcomes were explored using voxel-based morphometry. Relationships between diffusion tensor measures of white matter microstructure (fractional anisotropy (FA) and axial (AD), radial (RD) and mean (MD) diffusivities) and 2-year developmental outcomes were explored using tract-based spatial statistics.Results189 MLPT children had data from at least one MRI modality (volumetric or diffusion) and data for at least one developmental domain. Larger cortical grey and white matter volumes in many brain regions, and higher FA and lower AD, RD and MD in several major white matter regions, were associated with better cognitive and language scores. There was little evidence that cortical grey matter and white matter volumes and white matter microstructure were associated with motor and behavioural outcomes.ConclusionsRegional cortical grey matter and white matter volumes and white matter microstructure are associated with cognitive and language development at 2 years of age in MLPT children. Thus, early alterations to brain volumes and microstructure may contribute to some of the developmental deficits described in MLPT children.

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