Consciousness and the Electroencephalogram

Bremer^[22] and Moruzzi and Magoun ^[23] demonstrated the essential role of the brainstem reticular core in activating the cortical EEG (see Chapter 31 ). Segundo and associates^[24] showed that destruction of the brainstem reticular core leads to a loss of consciousness in laboratory animals. These observations gave birth to the concept of the ascending reticular activating system (ARAS). Although the central insight of this concept, that structures in the brainstem regulate the state of consciousness, still holds true, the ARAS is no longer regarded as a monolithic unit, nor is it restricted to the classically defined reticular nuclei of the brainstem. Maintenance of wakefulness or control of the sleep-wake cycle does not depend exclusively and unalterably on any single region of the brain.^[25] In brain death, the patient is believed to have no consciousness, no intellectual activity, and therefore no true humanity. This state is defined as deep coma and is the basis for the concept of brainstem death.

Hockaday and colleagues^[26] and Schwab and coworkers^[27] studied the EEGs of 550 comatose patients, analyzed EEGs for 26 cases of sudden cardiac arrest and 13 cases of respiratory arrest, and classified abnormalities on EEGs into five grades according to final outcome. The prognosis for patients belonging to grade I was favorable. The determination of the prognosis for grade II and III patients required repeated recording of the EEG. When the EEG showed improvement on the day 2 or 3 recording session, the prognosis was favorable. When the EEG tended to deteriorate, the prognosis was poor. In this system, grade Vb represented the EEG for brain death. Significant electroencephalographic changes occur^[28] when blood flow falls below 18 mL/100 g/min, and it becomes isoelectric when blood flow is in the range of 12 to 15 mL/100 g/min.^[29] However, Paolin and associates^[30] reported that 7 of 15 patients with clinical diagnosis of brain death showed persistent electrical activity, although cerebral blood flow measurements with xenon 133 and selective cerebral angiography showed intracranial circulatory arrest.