• Neurocritical care · Oct 2016

    Case Reports

    Neuroglucopenia and Metabolic Distress in Two Patients with Viral Meningoencephalitis: A Microdialysis Study.

    • Mario Kofler, Alois Schiefecker, Ronny Beer, Florian Sohm, Gregor Broessner, Paul Rhomberg, Peter Lackner, Bettina Pfausler, Claudius Thomé, Erich Schmutzhard, and Raimund Helbok.
    • Neurological Intensive Care Unit, Department of Neurology, Medical University of Innsbruck, Anichstrasse 35, 6020, Innsbruck, Austria.
    • Neurocrit Care. 2016 Oct 1; 25 (2): 273-81.

    IntroductionViral encephalitis is an emerging disease requiring intensive care management in severe cases. Underlying pathophysiologic mechanisms are incompletely understood and may be elucidated using invasive multimodal neuromonitoring techniques in humans.MethodsTwo otherwise healthy patients were admitted to our neurological intensive care unit with altered level of consciousness necessitating mechanical ventilation. Brain imaging and laboratory workup suggested viral encephalitis in both patients. Invasive neuromonitoring was initiated when head computed tomography revealed generalized brain edema, including monitoring of intracranial pressure, brain metabolism (cerebral microdialysis; CMD), brain tissue oxygen tension (in one patient), and cerebral blood flow (in one patient).ResultsBrain metabolism revealed episodes of severe neuroglucopenia (brain glucose <0.7 mM/l) in both patients, which were not attributable to decreased cerebral perfusion or hypoglycemia. CMD-glucose levels changed depending on variations in insulin therapy, nutrition, and systemic glucose administration. The metabolic profile, moreover, showed a pattern of non-ischemic metabolic distress suggestive for mitochondrial dysfunction. Both patients had a prolonged but favorable clinical course and improved to a modified Rankin Scale Score of 1 and 0 three months later.ConclusionInvasive multimodal neuromonitoring is feasible in poor-grade patients with viral meningoencephalitis and may help understand pathophysiologic mechanisms associated with secondary brain injury. The detection of neuroglucopenia and mitochondrial dysfunction may serve as treatment targets in the future.

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