• A Kondo, C Sugiura, Y Fujii, T Inoue, Y Maegaki, and K Ohno.
• Division of Child Neurology, Institute of Neurological Sciences, Faculty of Medicine, Tottori University, Yonago, Japan. holbergs@nifty.com
• Neuropediatrics. 2009 Aug 1; 40 (4): 157-61.

AbstractWe report on two children with sepsis-associated encephalopathy. They presented with fulminant neurological damage on clinical, neuroimaging, and neurophysiological findings. At onset, both went into deep coma after status epilepticus, resulting in near brain death. Both patients showed diffuse brain edema on CT and severe brain dysfunction on electroencephalography within a day of onset. Brain magnetic resonance (MR) imaging of one patient on day 2 showed restricted diffusion in the basal ganglia and the subcortical white matter of the frontal and occipital lobes. Brain edema aggravated and lasted for a few months despite a variety of treatments. MR imaging in the chronic phase revealed cracking lesions extending to the cerebral white matter, the cerebellum, and the brainstem. MR angiography showed diminished intracranial major arteries. These serial neuroradiological findings suggested severe brain damage resulting from fulminant elevation of intracranial pressure, which mimicked "brain death" or "respirator brain".Georg Thieme Verlag KG Stuttgart New York.

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