Impact of Infant Thoracic Non-cardiac Perioperative Critical Care on Homotopic-Like Corpus Callosum and Forebrain Sub-regional Volumes.

Previously, we reported quantitatively smaller total corpus callosum (CC) and total forebrain size in critically ill term-born and premature patients following complex perioperative critical care for long-gap esophageal atresia (LGEA) that included Foker process repair. We extended our cross-sectional pilot study to determine sub-regional volumes of CC and forebrain using structural brain MRI. Our objective was to evaluate region-specific CC as an marker for decreased myelination and/or cortical neural loss of homotopic-like sub-regions of the forebrain.

Infant study of hemispheric asymmetry after long-gap esophageal atresia repair.

Objectives: Previous studies have demonstrated that infants are typically born with a left-greater-than-right forebrain asymmetry that reverses throughout the first year of life. We hypothesized that critically ill term-born and premature patients following surgical and critical care for long-gap esophageal atresia (LGEA) would exhibit alteration in expected forebrain asymmetry.

Methods: Term-born (n = 13) and premature (n = 13) patients, and term-born controls (n = 23) <1 year corrected age underwent non-sedated research MRI following completion of LGEA treatment via Foker process.

Infant Corpus Callosum Size After Surgery and Critical Care for Long-Gap Esophageal Atresia: Qualitative and Quantitative MRI.

Previous studies in preterm infants report white matter abnormalities of the corpus callosum (CC) as an important predictor of neurodevelopmental outcomes. Our cross-sectional study aimed to describe qualitative and quantitative CC size in critically ill infants following surgical and critical care for long-gap esophageal atresia (LGEA) - in comparison to healthy infants - using MRI. Non-sedated brain MRI was acquired for full-term (n = 13) and premature (n = 13) patients following treatment for LGEA, and controls (n = 20) <1 year corrected age.

Neurologic Injury and Brain Growth in the Setting of Long-Gap Esophageal Atresia Perioperative Critical Care: A Pilot Study.

We previously showed that infants born with long-gap esophageal atresia (LGEA) demonstrate clinically significant brain MRI findings following repair with the Foker process. The current pilot study sought to identify any pre-existing (PRE-Foker process) signs of brain injury and to characterize brain and corpus callosum (CC) growth. Preterm and full-term infants ( = 3/group) underwent non-sedated brain MRI twice: (PRE-Foker scan) and (POST-Foker scan) completion of perioperative care.

Neonatal functional brain maturation in the context of perioperative critical care and pain management: A case report.

Introduction: Remarkable plasticity during the first year of life imparts heighted vulnerability of the developing infant brain. Application of resting-state functional magnetic resonance imaging (rs-fMRI) in infants may contribute to our understanding of neuroplastic changes associated with therapeutic interventions and/or brain insults. In addition to showing clinically relevant incidental brain MRI findings, the objective of our pilot study was to test feasibility of rs-fMRI methods at this early age in the context of pediatric perioperative critical care.

Infant Brain Structural MRI Analysis in the Context of Thoracic Non-cardiac Surgery and Critical Care.

To determine brain magnetic resonance imaging (MRI) measures of cerebrospinal fluid (CSF) and whole brain volume of full-term and premature infants following surgical treatment for thoracic non-cardiac congenital anomalies requiring critical care. Full-term ( = 13) and pre-term ( = 13) patients with long-gap esophageal atresia, and full-term naïve controls ( = 19) < 1 year corrected age, underwent non-sedated brain MRI following completion of thoracic non-cardiac surgery and critical care treatment. Qualitative MRI findings were reviewed and reported by a pediatric neuroradiologist and neurologist.

Identifying Rodent Resting-State Brain Networks with Independent Component Analysis.

Rodent models have opened the door to a better understanding of the neurobiology of brain disorders and increased our ability to evaluate novel treatments. Resting-state functional magnetic resonance imaging (rs-fMRI) allows for exploration of large-scale brain networks with high spatial resolution. Its application in rodents affords researchers a powerful translational tool to directly assess/explore the effects of various pharmacological, lesion, and/or disease states on known neural circuits within highly controlled settings.

Resting-State Functional Connectivity in the Infant Brain: Methods, Pitfalls, and Potentiality.

Early brain development is characterized by rapid growth and perpetual reconfiguration, driven by a dynamic milieu of heterogeneous processes. Postnatal brain plasticity is associated with increased vulnerability to environmental stimuli. However, little is known regarding the ontogeny and temporal manifestations of inter- and intra-regional functional connectivity that comprise functional brain networks.

Bringing CLARITY to gray matter atrophy.

Gray matter atrophy has been shown to be a strong correlate to clinical disability in multiple sclerosis (MS) and its most commonly used animal model, experimental autoimmune encephalomyelitis (EAE). However, the relationship between gray mater atrophy and the spinal cord pathology often observed in EAE has never been established. Here EAE was induced in Thy1.

Estrogen mediates neuroprotection and anti-inflammatory effects during EAE through ERα signaling on astrocytes but not through ERβ signaling on astrocytes or neurons.

Estrogens can signal through either estrogen receptor α (ERα) or β (ERβ) to ameliorate experimental autoimmune encephalomyelitis (EAE), the most widely used mouse model of multiple sclerosis (MS). Cellular targets of estrogen-mediated neuroprotection are still being elucidated. Previously, we demonstrated that ERα on astrocytes, but not neurons, was critical for ERα ligand-mediated neuroprotection in EAE, including decreased T-cell and macrophage inflammation and decreased axonal loss.