Magnetic resonance imaging of the brain in a cohort of extremely preterm infants

Maalouf, Elia F.; Duggan, Philip; Rutherford, Mary A.; Counsell, Serena J.; Fletcher, Alison; Battin, Malcolm; Cowan, Frances; Edwards, A. David

doi:10.1016/s0022-3476(99)70133-2

Cited by 302 publications

(236 citation statements)

References 17 publications

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“…These signal changes had microstructural correlates of increased D ⊥ and decreased FA. These lesions show the same properties as the diffuse WM hyperintensity well described in human premature infants (35). Histological correlates showed an alteration of tissue structure as demonstrated by reduced AF/T and neurofilament stain and organization.…”

Section: Diffuse Changessupporting

confidence: 70%

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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Section: Diffuse Changessupporting

confidence: 70%

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

et al. 2012

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“…Both cystic PVL and diffuse white matter disease are characterized by reduced white matter volume, reduced brain growth and features, suggesting abnormal myelination by magnetic resonance imaging. [68][69][70] Up to 25% of patients suffering from PWMI develop cerebral palsy, 71,72 while as many as 50% may display cognitive and learning disabilities by the time they reach school age. 73 Since a prominent feature of white matter injury is a chronic disturbance in myelination, it was hypothesized that OLs are the major target cells in PWMI.…”

Section: Ols and Diseasementioning

confidence: 99%

Maturation-dependent sensitivity of oligodendrocyte lineage cells to apoptosis: implications for normal development and disease

2008

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Apoptosis plays a crucial role in brain development by ensuring that only appropriately growing, migrating, and synapse-forming neurons and their associated glial cells survive. This process involves an intimate relationship between cell-cell interactions and developmental cues and is further impacted by environmental stress during neurogenesis and disease. Oligodendrocytes (OLs), the major myelin-forming cells in the central nervous system, largely form after this wave of neurogenesis but also show a selective vulnerability to cell death stimuli depending on their stage of development. This can affect not only embryonic and early postnatal brain formation but also the response to demyelinating pathologies. In the present review, we discuss the stagespecific sensitivity of OL lineage cells to damage-induced death and how this might impact myelin survival and regeneration during injury or disease. Apoptosis is a major form of programmed cell death required for the normal development of metazoan tissues, including the brain. 1 During embryonic development of the brain, many more cells than ultimately needed are generated and then selection occurs, resulting in the apoptotic depletion of the surplus cells. The importance of the apoptotic pathway in early brain development has been demonstrated by the targeted deletion in mice of the death-specific cysteine proteases caspase-3 or caspase-9, or of the co-activator Apaf-1, all of which cause severe brain overgrowth and perinatal death. 2,3 In the adult brain, 90% of the cells belong to the glial lineage, which includes oligodendrocytes (OLs), astrocytes and microglia. The glia ensures proper development, function and repair of the neuronal network. This is possible through continuous cross-talk between the glia and neurons mediated by neurotransmitters, cytokines, growth and trophic factor secretion and signaling in a reciprocal manner. [4][5][6][7] In the central nervous system (CNS), OLs are responsible for axon myelination, which insulates the electrical signals transmitted between neurons. OL and neuron development is tightly regulated and the myelin sheath is constructed only when OLs reach maturity and neurons have grown appropriately. In response to injury or during the course of neurological diseases, the neuron-glia network can be replenished to some extent but the degree of repair is dependent on the developmental stage of the OL. This complexity is compounded by the differential sensitivity of OL lineage cells to apoptotic stimuli. In the present review, we will first briefly examine the stages of differentiation of OL cells and then discuss several diseases that are impacted by OL apoptosis, noting how the stage of cell differentiation governs the sensitivity to apoptosis. Defined Stages of OL DevelopmentOligodendrocyte development can be divided into four distinct stages according to the temporal expression of cell surface markers and morphology (Table 1). 8 In the first stage, OL progenitor cells (OPCs) originate from the neuroepithelium of the ventricul...

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“…MR studies in recent years have linked premature birth to white matter (WM) abnormalities or myelination delays (Maalouf et al, 1999;Miller et al, 2002;Arzoumanian et al, 2003), and to abnormalities of gray matter development (Inder et al, 2005). These effects have sometimes been observed as early as term-equivalent age.…”

Section: Introductionmentioning

confidence: 99%

Accelerated cerebral white matter development in preterm infants: A voxel-based morphometry study with diffusion tensor MR imaging

et al. 2008

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Twenty-seven preterm infants were compared to 10 full-term infants at term equivalent age using a voxel-based analysis of diffusion tensor imaging of the brain. Preterm infants exhibited higher fractional anisotropy values, which may suggest accelerated maturation, in the location of the sagittal stratum. While some earlier findings in preterm infants have suggested developmental delays, the results of this study are more consistent with accelerated white matter development, possibly as a result of increased sensorimotor stimulation in the extrauterine environment. These results are the first to suggest that the increased intensity of stimulation associated with preterm birth may advance the process of white matter maturation in the human brain. Questions remain about whether these findings reflect acceleration of the process of white matter maturation generally, or localized alterations induced specifically by activity in affected pathways.

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Magnetic resonance imaging of the brain in a cohort of extremely preterm infants

Cited by 302 publications

References 17 publications

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

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

Maturation-dependent sensitivity of oligodendrocyte lineage cells to apoptosis: implications for normal development and disease

Accelerated cerebral white matter development in preterm infants: A voxel-based morphometry study with diffusion tensor MR imaging

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