Axial and Radial Diffusivity in Preterm Infants Who Have Diffuse White Matter Changes on Magnetic Resonance Imaging at Term-Equivalent Age

Counsell, Serena J.; Shen, Yuji; Boardman, James P.; Larkman, David J.; Kapellou, Olga; Ward, Philip; Allsop, Joanna; Cowan, Frances; Hajnal, Joseph V.; Edwards, A. David; Rutherford, Mary A.

doi:10.1542/peds.2005-0820

Cited by 221 publications

(197 citation statements)

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“…However, the model described herein employed hypoxia alone. Recent studies have shown similar increases in ADC in premature infants at term with extensive WM signal abnormalities (21,22). In this study, increased ADC likely represents a loss of cellular elements.…”

Section: Discussionsupporting

confidence: 70%

Histopathologic correlation with diffusion tensor imaging after chronic hypoxia in the immature ferret

et al. 2011

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Articles Translational Investigation nature publishing group INTRODUCTION: chronic hypoxia in rodents induces white matter (WM) injury similar to that in human preterm infants. We used diffusion tensor imaging (DTI) and immunohistochemistry to study the impact of hypoxia in the immature ferret at two developmental time points relevant to the preterm and term brain. RESULTS: On ex vivo imaging, the apparent diffusion coefficient (aDc) was decreased throughout the WM after 10 days of hypoxia (hypoxia from postnatal day 10 (P10) to P20 and killed at P20 (early hypoxia P20)), corresponding to increased astrocytosis and decreased myelination. Diffusion values normalized after 10 days of normoxia (hypoxia from P10 to P20 and killed at P30 (early hypoxia P30)), but immunohistochemistry revealed significant astrocytosis and hypomyelination. In contrast, aDc and anisotropy were increased after 10 days of hypoxia at a later developmental time point (hypoxia from P20 to P30 and killed at P30 (late hypoxia P30)), with less astrocytosis and more prominent myelination. DISCUSSION: The patterns of alteration in imaging and histology varied in relation to the developmental time at which hypoxia occurred. Normalization of diffusion measures did not correspond to the normalization of underlying histopathology. METHODS: Ferrets were subjected to 10% hypoxia and divided into three groups: early hypoxia P20, early hypoxia P30, and late hypoxia P30.

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Section: Discussionsupporting

confidence: 70%

Histopathologic correlation with diffusion tensor imaging after chronic hypoxia in the immature ferret

et al. 2011

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“…It is important to stress that the diffusion data were acquired on ex vivo fixed brains, and as such the diffusivity values are lower than those observed in vivo, whereas FA values remain unchanged (31). The reductions in FA observed following LPS were largely due to an increase of D^ (i.e., increased water mobility perpendicular to the mean direction of diffusion) similar to in vivo data after LPS exposure in rat pups (18) and MR studies in preterm infants with WM injury (17,32,33). Increased D^ was attributed to a loss of myelin in adult animal models (34).…”

Section: Discussionmentioning

confidence: 76%

High-field diffusion tensor imaging characterization of cerebral white matter injury in lipopolysaccharide-exposed fetal sheep

et al. 2012

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Background:In gyrencephalic species such as sheep, precise anatomical and microstructural characterization of the consequences of fetal inflammation remains scarce. The goal of this study was to characterize changes in white matter (WM) structure using advanced magnetic resonance imaging (MRI) following lipopolysaccharide (LPS) exposure in the pretermequivalent fetal sheep. Methods: Preterm (0.7 gestation) fetal sheep received vehicle (Sham group) or LPS (LPS group), and fetal brains were collected 10 d later for subsequent ex vivo MRI. T 1 -weighted (T 1 W), T 2 -weighted (T 2 W), and diffusion tensor imaging (DTI) data were collected. results: Fetuses exposed to LPS exhibited reductions in WM volume and corpus callosum thickness at 10 d recovery. characteristic patterns of diffuse and focal WM lesions (necrosis or cysts) could be identified by various T 1 , T 2 , and DTI signal changes. conclusion: Fetal LPS exposure induces a pattern of injury characterized by diffuse and focal WM injury that closely reproduces that observed clinically in preterm infants. This work provides anatomical and microstructural MRI assessment, as well as histopathological correlates, of the consequences of LPS exposure in an animal model with a WM structure similar to that of the human brain. This work will help to further our understanding of MRI changes in preterm infants.

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“…There were three studies that contained both coordinates and fractional anisotropies of the corpus callosum, and therefore a total of 13 studies were included. 20,[29][30][31][32][33][34][35][36][37][38][39][40] The included studies involved a total of 513 children, adolescents or young adults who were born prematurely and were matched with 309 healthy comparison participants. The process of study selection is shown in Figure 1.…”

Section: Resultsmentioning

confidence: 99%

Fractional anisotropy alterations in individuals born preterm: a diffusion tensor imaging meta‐analysis

Sun

Han

et al. 2014

Develop Med Child Neuro

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ALEActivation likelihood estimate DTI Diffusion tensor imaging SMD Standardized mean difference AIM This meta-analysis explored cerebral microstructural changes in individuals born preterm using fractional anisotropy from diffusion tensor imaging.METHOD We used the activation likelihood estimate (ALE) method for the meta-analysis to locate anatomical regions with white matter abnormalities in a group of individuals born preterm and in term-born comparison participants. A statistical analysis of fractional anisotropy was conducted to quantitatively explore the extent of fractional anisotropy changes in the three subregions of the corpus callosum in the preterm group.RESULTS ALE analysis identified 11 regions of decreased fractional anisotropy and four regions of increased fractional anisotropy. Analysis of the corpus callosum revealed the largest decrease in fractional anisotropy in the splenium (standardized mean difference [SMD]=À0.75, 95% confidence interval [CI] À0.93 to À0.57), followed by the body (SMD=À0.73, 95% CI À1.13 to À0.32) and the genu (SMD=À0.65, 95% CI À0.97 to À0.33). INTERPRETATION Significant changes in fractional anisotropy in individuals born pretermreflect white matter abnormalities from childhood to young adulthood, and the mechanism of fractional anisotropy alterations in preterm infants may vary during different stages of white matter development. Furthermore, the variability of fractional anisotropy between studies can primarily be attributed to the age of the individuals at scanning and to the field strength of magnetic resonance scanners.Preterm birth is frequently accompanied by a variety of disabilities, such as cerebral palsy, intellectual disability, deafness, or blindness. The incidence of preterm birth has increased significantly in the past decades, but is associated with higher survival rates 1 and a lower incidence of major disabilities than in the past.2 However, there is strong evidence that preterm survivors without brain malformations, congenital infection, or metabolic disease and with normal outcomes or mild abnormalities on structural brain magnetic resonance imaging (MRI) may experience more problems of motor, cognitive, language, and behavioural functioning throughout childhood and young adulthood. [3][4][5][6] These sequelae have been attributed to perinatal brain injuries, 7,8 which frequently involve white matter, 9 during normal brain maturation. 10 Nevertheless, the location, severity, and mechanism of white matter injuries on neurodevelopment and their impact on future function have not been conclusively determined.11 Additional neuroimaging evidence is necessary to explain the mechanism of white matter injuries and to predict the future influence of these impairments in individuals who are born preterm.Diffusion tensor imaging (DTI), a novel MRI technique, can quantify the fibre orientation and integrity of white matter pathways within neural networks. This technique is superior to conventional MRI methods for the detection of white matter abnormalities becaus...

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Axial and Radial Diffusivity in Preterm Infants Who Have Diffuse White Matter Changes on Magnetic Resonance Imaging at Term-Equivalent Age

Abstract: These findings suggest that DEHSI represents an oligodendrocyte and/or axonal abnormality that is widespread throughout the cerebral WM.

Cited by 221 publications

References 53 publications

Histopathologic correlation with diffusion tensor imaging after chronic hypoxia in the immature ferret

Histopathologic correlation with diffusion tensor imaging after chronic hypoxia in the immature ferret

High-field diffusion tensor imaging characterization of cerebral white matter injury in lipopolysaccharide-exposed fetal sheep

Fractional anisotropy alterations in individuals born preterm: a diffusion tensor imaging meta‐analysis

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