Dr. Gloss, Director of Epilepsy of the Geisinger Health System, has no relevant financial relationships to disclose.)
In this article, the author discusses the EEG findings in encephalopathic states, both acute and chronic. Encephalopathy is characterized clinically by a generalized alteration of attention, consciousness, or cognition. Acute encephalopathies range from delirium to coma. In the chronic, static, or slowly progressive encephalopathies there may be maintenance of attention initially, but there is loss of cognitive functions as seen in dementia. Electroencephalography (EEG) plays a significant role in the evaluation of patients with acute encephalopathy. Most importantly, EEG can differentiate between a true acute encephalopathy and epileptic states or psychiatric conditions. Although EEG is very sensitive in detecting an acute encephalopathy, it is not usually etiologically specific. The usefulness of EEG in chronic encephalopathy is less clear. Studies are beginning to appear about inter-rater reliability in the EEG literature, and have bearing on 1 of the patterns often seen in encephalopathic states.
• The EEG hallmark of most acute encephalopathies is background slowing.
• The severity of slowing typically corresponds to the degree of impairment.
• EEG findings of encephalopathies are typically of nonspecific etiology.
Historical note and terminology
Electroencephalography (EEG) has been used to assess cerebral dysfunction for more than 70 years. The EEG is very sensitive to changes in the function of the cerebral cortex. Encephalopathy refers to global cerebral dysfunction, which manifests itself as slowing of activity in the cortex. This slowing may be due to dysfunction of the cortical neurons themselves or a reflection of abnormalities in the subcortical gray matter or white matter. EEG has long been used as an objective means of assessing the degree of cerebral dysfunction. In general, it does not help to reveal the etiology of the encephalopathy.
The first reference to the diffuse slowing seen in encephalopathic states appears to have been in a paper by Gibbs and colleagues published in 1935 (Gibbs 1935). In 1936, an article by Davis was published and included mention of this issue (Davis 1936). An article was published in 1937 that looked at encephalopathy caused by medication (Gibbs 1937). Hoagland published another article on this topic in 1937 (Hoagland 1937). Over the years since then, numerous articles have been published looking at EEG changes in a variety of encephalopathies of different etiologies.
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