Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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Glaser, N.S. et al.

Glaser, Wootton-Gorges, Marcin, Buonocore, Dicarlo, Neely, Barnes, Bottomly, Kuppermann,

Mechanism of cerebral edema in children with diabetic ketoacidosis.

OBJECTIVES: Cerebral edema during diabetic ketoacidosis (DKA) has been attributed to osmotic cellular swelling during treatment. We evaluated cerebral water distribution and cerebral perfusion during DKA treatment in children. STUDY DESIGN: We imaged 14 children during DKA treatment and after recovery, using both diffusion and perfusion weighted magnetic resonance imaging (MRI). We assessed the apparent diffusion coefficients (ADCs) and measures reflecting cerebral perfusion. RESULTS: The ADC was significantly elevated during DKA treatment (indicating increased water diffusion) in all regions except the occipital gray matter. Mean reductions in the ADC from initial to postrecovery MRI were: basal ganglia 4.7 +/- 2.5 x 10(-5) mm(2)/s (P=.002), thalamus 3.7 +/- 2.8 x 10(-5) mm(2)/s, (P=.002), periaqueductal gray matter 4.3 +/- 5.1 x 10(-5) mm(2)/s (P=.03), and frontal white matter 2.0 +/- 3.1 x 10(-5) mm(2)/s (P=.03). In contrast, the ADC in the occipital gray matter increased significantly from the initial to postrecovery MRI (mean increase 3.9 +/- 3.9 x 10(-5) mm(2)/s, P=.004). Perfusion MRI during DKA treatment revealed significantly shorter mean transit times (MTTs) and higher peak tracer concentrations, possibly indicating increased cerebral blood flow (CBF). CONCLUSIONS: Elevated ADC values during DKA treatment suggests a vasogenic process as the predominant mechanism of edema formation rather than osmotic cellular swelling.[1]

References

Mechanism of cerebral edema in children with diabetic ketoacidosis. Glaser, N.S., Wootton-Gorges, S.L., Marcin, J.P., Buonocore, M.H., Dicarlo, J., Neely, E.K., Barnes, P., Bottomly, J., Kuppermann, N. J. Pediatr. (2004) [Pubmed]

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