The D values primarily reflect overall brain water content. The A sigma values are more sensitive to tissue microstructure (e.g., white matter packing and myelination). The D and A sigma images reveal information and not apparent on T1- and T2-weighted images.

Background and Purpose WM injury is the dominant form of injury in preterm infants. However, other cerebral structures, including deep GM and cerebellum, can also be affected by injury and/or impaired growth. Current MRI injury assessment scales are subjective and challenging to apply. Thus, we developed a new assessment tool and applied it to MRI studies obtained from VPT infants at term-equivalent postmenstrual age to describe the spectrum of brain abnormalities. Methods MRI scans from 97 VPT infants (<30 weeks gestation) and 22 healthy term-born infants were evaluated retrospectively. The severity of brain injury (defined by signal abnormalities) and impaired brain growth (defined with biometrics) was scored in the WM, cortical GM, deep GM and cerebellum. Perinatal variables for clinical risks were collected from medical records. Results Of 97 VPT infants, brain injury was observed in WM (n=23), deep GM (n=5) and cerebellum (n=23). Combining measures of injury and impaired growth showed moderate-severe abnormalities most commonly in WM (n=38) and cerebellum (n=32), but still notable in cortical GM (n=16) and deep GM (n=11). None of 22 term-born infants had moderate-severe abnormalities. Multiple clinical risk factors, including prolonged intubation, prolonged parenteral nutrition, postnatal corticosteroid use and postnatal sepsis, were associated with increased global MRI abnormality. Conclusions VPT infants demonstrate a high prevalence of injury and growth impairment in both WM and GM. This MRI scoring system provides a more comprehensive and objective classification of the nature and extent of abnormalities in VPT infants than existing measures.

Objective To evaluate associations between neonatal intensive care unit (NICU) room type (open ward and private room) and medical outcomes; neurobehavior, electrophysiology and brain structure at hospital discharge; and developmental outcomes at two years of age. Study design In this prospective longitudinal cohort study, we enrolled 136 preterm infants born <30 weeks gestation from an urban, 75-bed level III NICU from 2007-2010. Upon admission, each participant was assigned to a bedspace in an open ward or private room within the same hospital, based on space and staffing availability, where they remained for the duration of hospitalization. The primary outcome was developmental performance at two years of age (n=86 infants returned for testing, which was 83% of survivors) measured using the Bayley Scales of Infant and Toddler Development, 3rd Edition. Secondary outcomes were 1) medical factors throughout the hospitalization, 2) neurobehavior, and 3) cerebral injury and maturation (determined by magnetic resonance imaging and electroencephalography). Results At term equivalent age, infants in private rooms were characterized by a diminution of normal hemispheric asymmetry and a trend toward having lower amplitude integrated electroencephalography cerebral maturation scores [p= 0.02; β=−0.52 (CI −0.95, −0.10)]. At age two years, infants from private rooms had lower language scores [p= 0.006; β=−8.3 (CI −14.2, −2.4)] and a trend toward lower motor scores [p= 0.02; β=−6.3 (CI −11.7, −0.99)], which persisted after adjustment for potential confounders. Conclusion These findings raise concerns that highlight the need for further research into the potential adverse effects of different amounts of sensory exposure in the NICU environment.

TH slows the evolution of diffusion abnormalities on MRI following HIE in term infants.

Pulsed gradient spin echo (PGSE) sequences have been used to measure the signal loss of 19F in perfluorinated hydrocarbon blood substitutes moving within the vasculature of the rat brain in the experimental conditions of the study. The signal loss is not characterized by a single apparent pseudodiffusion coefficient. A simple vascular network model based on self-similarity has been used to calculate the shape of the signal loss. Excellent agreement with the experiment has been obtained showing that the IVIM measurements are sensitive to flow over a wide range of vessel diameters and flow rates. This model of vascular structure may serve well for other MR measurements that are sensitive to perfusion.

Animal models with complex cortical development are useful for improving our understanding of the wide spectrum of neurodevelopmental challenges facing human preterm infants. Magnetic resonance imaging (MRI) techniques can define both cerebral injury and alterations in cerebral development with translation between animal models and the human infant. We hypothesized that the immature ferret would display a similar sequence of brain development (both grey (GM) and white matter (WM)) to that of the preterm human infant. We describe postnatal ferret neurodevelopment with conventional and diffusion MRI. The ferret is born lissencephalic with a thin cortical plate and relatively large ventricles. Cortical folding and WM maturation take place during the first month of life. From the mid-second through the third week of postnatal life, the ferret brain undergoes a similar, though less complex, pattern of maturational changes to those observed in the human brain during the second half of gestation. GM anisotropy decreases rapidly in the first three weeks of life, followed by an upward surge of surface folding and WM anisotropy over the next two weeks.

Cerebral periventricular white matter injury stands as a leading cause of cognitive, behavioral and motor impairment in preterm infants. There is epidemiological and histopathological evidence demonstrating the role of prenatal or neonatal inflammation in brain injury in preterm infants. In order to define the effect of an inflammatory insult in the developing brain on magnetic resonance (MR) imaging, we obtained high resolution conventional and diffusion MR images of the brain of rat pups after an inflammatory injury. Rat pups were subjected on postnatal day 5 (P5) to a stereotaxic injection of lipopolysaccharide in the corpus callosum and then imaged at 11.7 Tesla on days 0, 2 and 4 following the injury. They were subsequently sacrificed for immunohistochemistry. Diffusion tensor imaging (DTI) acquired at high spatial resolution showed an initial reduction of the apparent diffusion coefficient (ADC) in the white matter. This was followed by an increase in ADC value and in T2 relaxation time constant in the white matter, with an associated increase of radial diffusivity of the corpus callosum, and a 10-fold increase in ventricular size. On histology, these MR changes corresponded to widespread astrogliosis, and decreased proportion of the section areas containing cresyl violet positive stain. The increase in radial diffusivity, typically attributed to myelin loss, occurred in this case despite the absence of myelin at this developmental stage.

Sepsis has been reported to cause mitochondrial dysfunction and inhibition of key enzymes that regulate the tricarboxylic acid (TCA) cycle. We investigated the effect of sepsis on high-energy phosphates, glycolytic and TCA cycle intermediates, and specific amino acids that are involved in regulating the size of the TCA cycle pool during changes in metabolic state of the heart. Sepsis was induced in 12 female rats by the cecal ligation and perforation technique under halothane anesthesia; seven control rats underwent cecal manipulation without ligation. At 36-42 h postsurgery, the rats were reanesthetized, the chest was opened, and the hearts were freeze-clamped. Perchloric acid extracts of the hearts were analyzed with fluorometric enzymatic methods and 31P nuclear magnetic resonance spectroscopy. There were no significant differences in the levels of the TCA cycle intermediates or high-energy phosphates between the septic and control rats. The major metabolic changes were the 28% decrease in alanine and the 31% decrease in glutamate in the septic hearts compared with control (P less than 0.05 and P less than 0.005, respectively). Phosphocholine, a component of membrane phospholipids, was increased by 91% in the septic hearts (P less than 0.01). We conclude that sepsis does not impair the TCA cycle or induce significant cellular ischemia in the heart. The increase in phosphocholine may represent significant cellular membrane disruption during sepsis.