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Seeing More Clearly Through the Fog of Encephalopathy

Kaplan, Peter W.*; Sutter, Raoul*,†

Journal of Clinical Neurophysiology: October 2013 - Volume 30 - Issue 5 - p 431–434
doi: 10.1097/WNP.0b013e3182a73dec
Invited Review
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Summary: Patients with acute confusional states (often referred to as encephalopathy or delirium) pose diagnostic and management challenges for treating physicians. Encephalopathy is associated with a high morbidity and mortality rate, and the diagnosis rests on clinical grounds but may also be supported by the finding of electroencephalographic (EEG) evidence for diffuse cerebral dysfunction. The myriad cerebral transmitter and metabolic disruptions are generated by systemic organ system failures, principal among which are those of the liver, kidneys, lungs, heart, and endocrine system, along with the effects of exogenous toxins and medications. In most cases, several of these organ failures together contribute to the confusional state, frequently in the context of a diffuse cerebral atrophy that affects the aging brain. This special issue of the Journal of Clinical Neurophysiology is dedicated to exploring the electrophysiology of these conditions. It reviews the pathophysiology, psychiatric manifestations, clinical and imaging correlations of the many causes and types of encephalopathy. A literature review of the EEG abnormalities in the various types of encephalopathy provides an overview that ranges from paraneoplastic causes, through organ system failures, postcardiorespiratory arrest, to postoperative delirium. The issue is supplemented by tables of relevant clinical correlations, graphs, Venn diagrams, and the use of mathematical modeling used to explain how defects in the neuronal interplay might generate the EEG patterns seen in encephalopathy. We hope that this assembly will act as a springboard for further discussion and investigation into the EEG underpinnings, clinical correlations, diagnosis. and prognostication of these common and morbid disturbances of brain function.

*Department of Neurology and

Division of Neurosciences Critical Care, Department of Anesthesiology and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, U.S.A.

Address correspondence and reprint requests to Peter W. Kaplan, MB, BS, FRCP, Department of Neurology, Johns Hopkins Bayview Medical Center, 301 Building, 4940 Eastern Avenue, Baltimore, MD 21224, U.S.A.; e-mail: pkaplan@jhmi.edu.

© 2013 by the American Clinical Neurophysiology Society