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EEG Patterns and Imaging Correlations in Encephalopathy: Encephalopathy Part II

Kaplan, Peter W.*; Rossetti, Andrea O.

Journal of Clinical Neurophysiology: June 2011 - Volume 28 - Issue 3 - p 233–251
doi: 10.1097/WNP.0b013e31821c33a0
Invited Review
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Summary: The EEG patterns seen with encephalopathies can be correlated to cerebral imaging findings including head computerized tomography and MRI. Background slowing without slow-wave intrusion is seen with acute and chronic cortical impairments that spare subcortical white matter. Subcortical/white matter structural abnormalities or hydrocephalus may produce projected slow-wave activity, while clinical entities involving both cortical and subcortical regions (diffuse cerebral abnormalities) engender both background slowing and slow-wave activity. Triphasic waves are seen with hepatic and renal insufficiency or medication toxicities (e.g., lithium, baclofen) in the absence of a significant cerebral imaging abnormality, Conversely, subcortical/white matter abnormalities may facilitate the appearance of triphasic waves without significant hepatic, renal, or toxic comorbidities. More specific syndromes, such as Jakob–Creutzfeldt disease, autoimmune limbic encephalitis, autoimmune corticosteroid-responsive encephalopathy with thyroid autoimmunity, sepsis-associated encephalopathy, and acute disseminated encephalomyelitis, have imaging/EEG changes that are variable but which may include slowing and epileptiform activity. This overview highlighting EEGimaging correlations may help the treating physician in the diagnosis, and hence the appropriate treatment, of patients with encephalopathy.

*Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA

Service de Neurologie, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland.

Address correspondence and reprint requests to Peter W. Kaplan, MBFRCP, B123 Johns Hopkins Bayview Medical Center, 4940 Eastern Avenue, Baltimore, MD 21224, U.S.A.; e-mail: pkaplan@jhmi.edu.

Copyright © 2011 American Clinical Neurophysiology Society