13 research outputs found
Therapeutic Hypothermia for Neonatal Encephalopathy Results in Improved Microstructure and Metabolism in the Deep Gray Nuclei
BACKGROUND AND PURPOSE: Therapeutic hypothermia has reduced morbidity and mortality and is associated with a lower burden of lesions on conventional imaging in NE. However, its effects on brain microstructure and metabolism have not been fully characterized. We hypothesized that therapeutic hypothermia improves measures of brain microstructure and metabolism. MATERIALS AND METHODS: Forty-one neonates with moderate/severe NE (29 treated with hypothermia, 12 nontreated) and 12 healthy neonates underwent MR imaging, DTI, and (1)H-MR spectroscopy. MR imaging scans were scored by the predominant pattern of brain injury: normal, watershed, and BG/thalamus. ADC, FA, Lac:NAA, and NAA:Cho values from bilateral BG and thalamus ROIs were averaged. T test and linear regression analysis were used to determine the association between hypothermia and MR imaging quantitative measures. RESULTS: Conventional MR imaging findings were normal in 41% of treated neonates; all nontreated neonates had brain injury. Values of MR imaging metrics were closer to normal in treated neonates compared with nontreated neonates: ADC was 63% higher in the BG and 116% higher in the thalamus (both P < .05), and Lac:NAA was 76% lower (P = .04) in the BG. Treated neonates with normal MR imaging findings had normal (1)H-MR spectroscopy metabolites, and ADC was higher by 35% in the thalamus (P = .03) compared with healthy neonates. CONCLUSIONS: Therapeutic hypothermia may reduce disturbances of brain metabolism and preserve its microstructure in the setting of NE, possibly by minimizing cytotoxic edema and cell death. Long-term follow-up studies are required to determine whether early post-treatment DTI and (1)H-MR spectroscopy will be useful biomarkers of treatment response
Cerebellar abnormalities following hypoxia alone compared to hypoxic-ischemic forebrain injury in the developing rat brain
Two-day-old (P2) rat pups were subjected to either a global hypoxia or to electrocoagulation of the right carotid artery followed by 2.5. h hypoxia. Cellular and regional injury in the cerebellum (CB) was studied at 1, 2 and 19. days using immunohistology. Following hypoxia and hypoxia-ischemia, all neuronal populations of the CB were damaged in a subset of Purkinje cells. The decrease in the number of interneurons, as well as the thickness of molecular and granular layers was significant following hypoxia. Diffuse white matter damage, with loss of preoligodendrocytes was more severe following hypoxia than hypoxia-ischemia. Global hypoxia in the rat at P2 produces extensive damage to many cell types in different areas of the CB. The addition of unilateral forebrain ischemia does not increase the severity of these changes. Our data provide insight into the mechanisms of the changes observed in the CB of premature newborns. © 2010 Elsevier Inc
Video-EEG monitoring in newborns with hypoxic-ischemic encephalopathy treated with hypothermia
Quantitative Fiber Tracking Analysis of the Optic Radiation Correlated with Visual Performance in Premature Newborns
Supplementary Material for: Proteomic Analysis of Mouse Cortex Postsynaptic Density following Neonatal Brain Hypoxia-Ischemia
<p>Proteomics of the synapses and postsynaptic densities (PSDs) have
provided a deep understanding of protein composition and signal networks
in the adult brain, which underlie neuronal plasticity and
neurodegenerative or psychiatric disorders. However, there is a paucity
of knowledge about the architecture and organization of PSDs in the
immature brain, and how it is modified by brain injury in an early
developing stage. Mass spectrometry (MS)-based proteomic analysis was
performed on PSDs prepared from cortices of postnatal day 9 naïve mice
or pups which had suffered hypoxic-ischemic (HI) brain injury. 512
proteins of different functional groups were identified from PSDs
collected 1 h after HI injury, among which 60 have not been reported
previously. Seven newly identified proteins involved in neural
development were highlighted. HI injury increased the yield of PSDs at
early time points upon reperfusion, and multiple proteins were recruited
into PSDs following the insult. Quantitative analysis was performed
using spectral counting, and proteins whose relative expression was more
than 50% up- or downregulated compared to the sham animals 1 h after HI
insult were reported. Validation with Western blotting demonstrated
changes in expression and phosphorylation of the N-methyl-D-aspartate
receptor, activation of a series of postsynaptic protein kinases and
dysregulation of scaffold and adaptor proteins in response to neonatal
HI insult. This work, along with other recent studies of synaptic
protein profiling in the immature brain, builds a foundation for future
investigation on the molecular mechanisms underlying developing
plasticity. Furthermore, it provides insights into the biochemical
changes of PSDs following early brain hypoxia-ischemia, which is helpful
for understanding not only the injury mechanisms, but also the process
of repair or replenishment of neuronal circuits during recovery from
brain damage.</p