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      Single ventricle anatomy predicts delayed microstructural brain development

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          Abstract

          Background

          Term newborns with congenital heart disease (CHD) show delayed brain development as early as the third trimester, especially in single ventricle physiology (SVP). Mechanisms causing delayed brain development in CHD are uncertain, but may include impaired fetal brain blood flow. Our objective was to determine if cardiac anatomy associated with obstruction to antegrade flow in the ascending aorta is predictive of delayed brain development measured by diffusion tensor imaging (DTI) and magnetic resonance spectroscopic imaging (MRSI).

          Methods

          Echocardiograms (ECHO) from 36 term newborns with SVP were reviewed for presence of aortic atresia and the diameter of the ascending aorta. Quantitative MR imaging parameters measuring brain microstructural (fractional anisotropy (FA), average diffusivity (Dav)) or metabolic development (N-acetylaspartate (NAA), Lactate/choline (Lac/cho)) were recorded.

          Results

          Increasing NAA/cho and white matter FA, and decreasing Dav and lactate/cho characterize normal brain development. Consistent with the hypothesis that delayed brain development is related to impaired brain perfusion, smaller ascending aortic diameter and aortic atresia were associated with higher Dav and lower white matter FA. ECHO variables were not associated with brain metabolic measures.

          Conclusions

          These observations support the hypothesis that obstruction to fetal cerebral blood flow impairs brain microstructural development.

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          Abnormal brain development in newborns with congenital heart disease.

          Natalie Charlton, Michael Glidden, Duan Xu … (2007)
          Congenital heart disease in newborns is associated with global impairment in development. We characterized brain metabolism and microstructure, as measures of brain maturation, in newborns with congenital heart disease before they underwent heart surgery. We studied 41 term newborns with congenital heart disease--29 who had transposition of the great arteries and 12 who had single-ventricle physiology--with the use of magnetic resonance imaging (MRI), magnetic resonance spectroscopy (MRS), and diffusion tensor imaging (DTI) before cardiac surgery. We calculated the ratio of N-acetylaspartate to choline (which increases with brain maturation), the ratio of lactate to choline (which decreases with maturation), average diffusivity (which decreases with maturation), and fractional anisotropy of white-matter tracts (which increases with maturation). We compared these findings with those in 16 control newborns of a similar gestational age. As compared with control newborns, those with congenital heart disease had a decrease of 10% in the ratio of N-acetylaspartate to choline (P=0.003), an increase of 28% in the ratio of lactate to choline (P=0.08), an increase of 4% in average diffusivity (P<0.001), and a decrease of 12% in white-matter fractional anisotropy (P<0.001). Preoperative brain injury, as seen on MRI, was not significantly associated with findings on MRS or DTI. White-matter injury was observed in 13 newborns with congenital heart disease (32%) and in no control newborns. Term newborns with congenital heart disease have widespread brain abnormalities before they undergo cardiac surgery. The imaging findings in such newborns are similar to those in premature newborns and may reflect abnormal brain development in utero. Copyright 2007 Massachusetts Medical Society.
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            Diffusion tensor imaging of brain development.

            Petra Hüppi, Jessica Dubois (2006)
            Understanding early human brain development is of great clinical importance, as many neurological and neurobehavioral disorders have their origin in early structural and functional cerebral organization and maturation. Diffusion tensor imaging (DTI), a recent magnetic resonance (MR) modality which assesses water diffusion in biological tissues at a microstructural level, has revealed a powerful technique to explore the structural basis of normal brain development. In fact, the tissue organization can be probed non-invasively, and the age-related changes of diffusion parameters (mean diffusivity, anisotropy) reveal crucial maturational processes, such as white matter myelination. Nevertheless, the developing human brain presents several challenges for DTI applications compared with the adult brain. DTI may further be used to detect brain injury well before conventional MRI, as water diffusion changes are an early indicator of cellular injury. This is particularly critical in infants in the context of administration of neuroprotective therapies. Changes in diffusion characteristics further provide early evidence of both focal and diffuse white matter injury in association with periventricular leukomalacia in the preterm infant. Finally, with the development of 3D fiber tractography, the maturation of white matter connectivity can be followed throughout infant development into adulthood with the potential to study correlations between abnormalities on DTI and ultimate neurologic/cognitive outcome.
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              Arrested oligodendrocyte lineage maturation in chronic perinatal white matter injury.

              Samuel M. McClure, Xi Gong, Ying Wan … (2008)
              Abnormal myelination is a major pathological sequela of chronic periventricular white matter injury in survivors of premature birth. We tested the hypothesis that myelination failure in chronic hypoxia-ischemia-induced periventricular white matter injury is related to persistent depletion of the oligodendrocyte (OL) precursor pool required to generate mature myelinating OLs. A neonatal rat model of hypoxia-ischemia was used where acute degeneration of late OL progenitors (preOLs) occurs via a mostly caspase-independent mechanism. The fate of OL lineage cells in chronic cerebral lesions was defined with OL lineage-specific markers. Acute caspase-3-independent preOL degeneration from hypoxia-ischemia was significantly augmented by delayed preOL death that was caspase-3-dependent. Degeneration of preOLs was offset by a robust regenerative response that resulted in a several-fold expansion in the pool of surviving preOLs in chronic lesions. However, these preOLs displayed persistent maturation arrest with failure to differentiate and generate myelin. When preOL-rich chronic lesions sustained recurrent hypoxia-ischemia at a time in development when white matter is normally resistant to injury, an approximately 10-fold increase in caspase-dependent preOL degeneration occurred relative to lesions caused by a single episode of hypoxia-ischemia. The mechanism of myelination failure in chronic white matter lesions is related to a combination of delayed preOL degeneration and preOL maturation arrest. The persistence of a susceptible population of preOLs renders chronic white matter lesions markedly more vulnerable to recurrent hypoxia-ischemia. These data suggest that preOL maturation arrest may predispose to more severe white matter injury in preterm survivors that sustain recurrent hypoxia-ischemia.
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                Author and article information

                Journal
                Journal ID (nlm-journal-id): 0100714
                Journal ID (pubmed-jr-id): 6400
                Journal ID (nlm-ta): Pediatr Res
                Journal ID (iso-abbrev): Pediatr. Res.
                Title: Pediatric research
                ISSN (Print): 0031-3998
                ISSN (Electronic): 1530-0447
                Publication date Nihms-submitted: 26 February 2013
                Publication date (Electronic): 13 February 2013
                Publication date (Print): May 2013
                Publication date PMC-release: 01 November 2013
                Volume: 73
                Issue: 5
                Pages: 661-667
                Affiliations
                [1 ]Department of Pediatrics, University of California, San Francisco Benioff Children’s Hospital, San Francisco, CA
                [2 ]Department of Pediatrics, University of British Columbia, British Columbia Children’s Hospital, Vancouver, British Columbia, Canada
                [3 ]Department of Radiology, University of British Columbia, British Columbia Children’s Hospital, Vancouver, British Columbia, Canada
                [4 ]Department of Surgery, University of British Columbia, British Columbia Children’s Hospital, Vancouver, British Columbia, Canada
                [5 ]Departments of Surgery, University of California, San Francisco Benioff Children’s Hospital, San Francisco, CA
                [6 ]Department of Radiology, University of California, San Francisco Benioff Children’s Hospital, San Francisco, CA
                Author notes
                Corresponding author: Patrick S. McQuillen, MD, 513 Parnassus Avenue, HSE 1421, San Francisco, CA 94143, Phone: 415-502-4798, Fax: 415-514-0235, McQuillP@ 123456peds.ucsf.edu
                Article
                Manuscript ID: NIHMS447454
                DOI: 10.1038/pr.2013.29
                PMC ID: 3631295
                PubMed ID: 23407116
                SO-VID: 36214068-9d40-4c4d-8f54-787b9d3d6c73
                License:

                Users may view, print, copy, download and text and data- mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use: http://www.nature.com/authors/editorial_policies/license.html#terms

                History
                Funding
                Funded by: National Institute of Neurological Disorders and Stroke : NINDS
                Award ID: R01 NS063876 || NS
                Categories
                Subject: Article

                ScienceOpen disciplines: Pediatrics
                Data availability:
                ScienceOpen disciplines: Pediatrics

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