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Delirium: Phenomenology and Diagnosis—A Neurobiologic View

Published online by Cambridge University Press:  07 January 2005

John P. Blass
Affiliation:
Altschul Laboratory for Dementia Research, Cornell University Medical College at Burke Rehabilitation Center, White Plains, New York, U.S.A.
Karen A. Nolan
Affiliation:
Altschul Laboratory for Dementia Research, Cornell University Medical College at Burke Rehabilitation Center, White Plains, New York, U.S.A.
Ronald S. Black
Affiliation:
Altschul Laboratory for Dementia Research, Cornell University Medical College at Burke Rehabilitation Center, White Plains, New York, U.S.A.
Akira Kurita
Affiliation:
Altschul Laboratory for Dementia Research, Cornell University Medical College at Burke Rehabilitation Center, White Plains, New York, U.S.A.

Abstract

“Delirium” is a reversible confusional state. It results from widespread but reversible interference with the function of cortical neurons, as documented by diffuse slowing on EEG and decreases in cerebral metabolic rate. Delirium can be due to impairments in neuronal metabolism, in neurotransmission (notably cholinergic), or in input from subcortical structures. Engel and Romano (1959) formulated delirium and dementia as the two poles of a spectrum of “cerebral insufficiency,” with delirium resulting from reversible functional impairment and dementia from irreversible anatomic damage. So many disorders can precipitate delirium that the differential diagnosis tests every facet of one's knowledge of medicine. With aging, both normative changes in the brain and the increasing incidence of brain diseases predispose to the development of delirium. The brain damage responsible for a dementia can sensitize to the development of a superimposed delirium.

Type
Description of the Disorder: History, Phenomenology, Nomenclature
Copyright
© 1991 Springer Publishing Company

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