CHAPTER 5

The term coma describes a pathologic state of unresponsiveness to arousal. An individual's responsiveness depends on the integrity of anatomical, metabolic, and communicative function of ascending reticular activating system (ARAS)-thalamo-cortical pathway in the brain. Disruption in the function of this pathway could result in a comatose state. The various conditions causing coma are discussed in this chapter. Structural causes include intracranial space-occupying lesions, resulting in brain tissue distortion, shifts, and herniation, whereas metabolic/toxic causes alter the physiology of the ARAS without structural disruptions. In general, the latter results in reversible comatose states, and the former may have permanent sequelae unless reversed in a timely manner. Traumatic brain injury (TBI), vascular lesions, and hypoxia/anoxia are the three major causes of coma. This chapter discusses the various clinical parameters, neurological examination, biochemical markers, neuroimaging, and electrophysiological studies that are carried out for the prognostic evaluation of brain function in comatose patients. The monitoring of comatose patients involves the examination of intracranial pressure, jugular bulb oximetry, brain tissue oxygen tension, microdialysis, and electroencephalography. Coma is not a disease, but a symptomatic presentation of many diseases. The pathophysiology of coma lies in dysfunction of the ARAS and/or its connections, and the clinical examination is aimed at identifying the insult and its location. Neuromonitoring techniques are being refined, with an ultimate goal of identifying "at risk" brain in a timely manner so that appropriate therapy can be instituted and our means to predict outcome, specifically recovery, can be improved.