Congenital heart disease and brain development.
ABSTRACT Brain and heart development occur simultaneously in the human fetus. Given the depth and complexity of these shared morphogenetic programs, it is perhaps not surprising that disruption of organogenesis in one organ will impact the development of the other. Newborns with congenital heart disease show a high frequency of acquired focal brain injury on sensitive magnetic resonance imaging studies in the perioperative period. The surprisingly high incidence of white matter injury in these term newborns suggests a unique vulnerability and may be related to a delay in brain development. These abnormalities in brain development identified with MRI in newborns with congenital heart disease might reflect abnormalities in cerebral blood flow while in utero. A complete understanding of the mechanisms of white matter injury in the term newborn with congenital heart disease will require further investigation of the timing, extent, and causes of delayed fetal brain development in the presence of congenital heart disease.
SourceAvailable from: Johanna Calderon[Show abstract] [Hide abstract]
ABSTRACT: This longitudinal study investigates executive functions (EF) in children with transposition of the great arteries (TGA) compared to typically developing children at a key age period between 5 and 7 years. We explored the presence and evolution of specific impairments on three core EF components (inhibition, working memory, and cognitive flexibility). Ninety children were evaluated for three consecutive years. Results demonstrated significant delays in inhibition and cognitive flexibility despite normal working memory. Impairments did not systematically worsen with age. EF impairments after TGA are dynamic and may affect selective components. Cyanotic congenital heart disease is associated with altered EF development.Developmental Neuropsychology 08/2014; In press. DOI:10.1080/87565641.2014.916709 · 2.67 Impact Factor
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ABSTRACT: Injury to the preterm brain has a particular predilection for cerebral white matter. White matter injury (WMI) is the most common cause of brain injury in preterm infants and a major cause of chronic neurological morbidity including cerebral palsy. Factors that predispose to WMI include cerebral oxygenation disturbances and maternal–fetal infection. During the acute phase of WMI, pronounced oxidative damage occurs that targets late oligodendrocyte progenitors (pre-OLs). The developmental predilection for WMI to occur during prematurity appears to be related to both the timing of appearance and regional distribution of susceptible pre-OLs that are vulnerable to a variety of chemical mediators including reactive oxygen species, glutamate, cytokines, and adenosine. During the chronic phase of WMI, the white matter displays abberant regeneration and repair responses. Early OL progenitors respond to WMI with a rapid robust proliferative response that results in a several fold regeneration of pre-OLs that fail to terminally differentiate along their normal developmental time course. Pre-OL maturation arrest appears to be related in part to inhibitory factors that derive from reactive astrocytes in chronic lesions. Recent high field magnetic resonance imaging (MRI) data support that three distinct forms of chronic WMI exist, each of which displays unique MRI and histopathological features. These findings suggest the possibility that therapies directed at myelin regeneration and repair could be initiated early after WMI and monitored over time. These new mechanisms of acute and chronic WMI provide access to a variety of new strategies to prevent or promote repair of WMI in premature infants. GLIA 2014Glia 11/2014; 62(11). DOI:10.1002/glia.22658 · 5.47 Impact Factor
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ABSTRACT: We studied brain structure abnormalities in adolescents and young adults who had undergone the neonatal arterial switch operation for transposition of the great arteries and related them to the neurologic and psycho-intellectual outcomes.Journal of Thoracic and Cardiovascular Surgery 05/2014; 148(5). DOI:10.1016/j.jtcvs.2013.10.087 · 3.99 Impact Factor