At the same time, it should be clarified that while brain death is an operational state that allows transplantation to proceed or typically mandates withdrawal of ventilation and blood pressure support, patients with overwhelming brain injuries need not fulfill these absolute criteria in order for medical support to be withdrawn. If the case for recovery is futile and the family and physician agree, of if the patient’s wishes are unequivocally known from preceding documents or discussions, support can be withdrawn in most jurisdictions and the obligate quest for brain death becomes a trap.
A task force for the determination of brain death in children (updated by Nakagawa et al) has recommended the adoption of essentially the same criteria as for adults. However, the difficulty in evaluating the status of nervous function in relation to perinatal insults, has led this group to suggest that the determination not be made before the seventh postnatal day and that the period of observation should be extended to 48 h. As with adults, the possibility of reversible brain dysfunction from toxins, drugs, hypothermia, and hypotension must always be considered.
The EEG provides one of the most delicate confirmations of the fact that states of impaired consciousness are expressions of neurophysiologic changes in the cerebrum. Some form of alteration of brain electrical activity occurs in almost all disturbances of consciousness except for milder degrees of confusion, delirium tremens, and in catatonia, where the preservation of normal background EEG activity can aid in diagnosis. These alterations usually consist of disorganization of the EEG background pattern, including disappearance of the normal alpha rhythm and replacement by random slow waves of low to moderate voltage in the initial stages of confusion and drowsiness; a more regular pattern of slow, 2to 3-per-second waves of high voltage in stupor; slow low-voltage waves or intermittent suppression of organized electrical activity in deep coma of cerebral hypoxia and ischemia; and, ultimately, complete absence of electrical activity in brain death.
The EEG broadly reflects the depth of certain metabolic comas, particularly those caused by hepatic or renal failure. In these conditions, the slow waves become higher in amplitude as coma deepens, ultimately assuming a high-voltage rhythmic delta pattern and a triphasic configuration. Not all cerebral disorders that cause confusion, stupor, and coma have the same effects on the EEG. In cases of intoxication with sedatives, exemplified by barbiturates and diazepines, fast (beta) activity initially replaces normal rhythms. Coma in which myoclonus or twitching is a major clinical feature may show frequent sharp waves or a sharpness of the background slowing of the EEG. A relatively normal EEG is characteristic of delirium tremens as already commented. The differences in EEG changes among metabolic derangements probably represent biologic distinctions at the neuronal level that have not yet been elucidated (see also Chap. 2).
In some deeply comatose patients, the EEG may transiently show diffuse and variable alpha frequency (8to 12-Hz) activity, which may be mistaken for the normal physiologic alpha rhythm. In addition to these aberrant features, the activity displays no reactivity to sensory stimuli. Alpha coma is associated with pontine or diffuse cortical lesions and has a poor prognosis (see Iragui and McCutchen). An even less common EEG abnormality is “spindle coma,” in which sleep spindles dominate the record (see “Disorders of Sleep Related to Neurologic Disease” in Chap. 18). The EEG may also demonstrate continuous seizure activity (non-convulsive status), making it valuable in the diagnosis of unresponsive states of obscure cause.