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Stupor and coma in adults

Author
G Bryan Young, MD, FRCPC
Section Editors
Michael J Aminoff, MD, DSc
Robert S Hockberger, MD, FACEP
Deputy Editor
Janet L Wilterdink, MD

INTRODUCTION

Stupor and coma are clinical states in which patients have impaired responsiveness (or are unresponsive) to external stimulation and are either difficult to arouse or are unarousable. Coma is defined as "unarousable unresponsiveness" [1]. An alert patient has a normal state of arousal. The terms stupor, lethargy, and obtundation refer to states between alertness and coma. These imprecise descriptors should generally not be used in clinical situations without further qualification.

An alteration in arousal represents an acute, life threatening emergency, requiring prompt intervention for preservation of life and brain function [2,3]. Although discussed separately here, the assessment and management are performed jointly in practice (table 1).

ETIOLOGIES AND PATHOPHYSIOLOGY

The ascending reticular activating system (ARAS) is a network of neurons originating in the tegmentum of the upper pons and midbrain, believed to be integral to inducing and maintaining alertness. These neurons project to structures in the diencephalon, including the thalamus and hypothalamus, and from there to the cerebral cortex. Alterations in alertness can be produced by focal lesions within the upper brainstem by directly damaging the ARAS.

Injury to the cerebral hemispheres can also produce coma, but in this case, the involvement is necessarily bilateral and diffuse, or if unilateral, large enough to exert remote effects on the contralateral hemisphere or brainstem. Magnetic resonance imaging (MRI) studies have indicated that coma in supratentorial mass lesions occurs both with lateral forces on the contralateral hemisphere and with downward, brainstem compression [4,5]. (See 'Coma syndromes' below.)

The mechanism of coma in toxic, metabolic, and infectious etiologies and hypothermia is less well understood and to some extent is cause specific. A simplified explanation is that these conditions impair oxygen or substrate delivery, which in turn alters cerebral metabolism or interferes with neuronal excitability and/or synaptic function.

                             

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Literature review current through: Nov 2016. | This topic last updated: Wed May 27 00:00:00 GMT+00:00 2015.
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