Natural history of global and critical brain ischaemia. Part III: cerebral prognostic signs after cardiopulmonary resuscitation. Cerebral recovery course and rate during the first year after global and critical ischaemia monitored and predicted by EEG and neurological signs.

The monitoring and predictive value of the electroencephalography (EEG) and neurological signs was evaluated in 125 patients who had sustained critical brain ischaemia during circulatory arrest of primary cardiovascular aetiology. Cranial nerve areflexia with mydriasis or extension of the upper limb in response to cutaneous stimulation reliably indicated brain death and appearance of the flexion reflex or of intermittent spikes and sharp waves in the EEG predicted an unfavourable outcome; but other EEG configurations and nuerological signs per se were inaccurate variables to assess the outcome. By contrast, the recovery course and rate were accurately assessed by the time for appearance of cerebral functions; the caloric vestibular reflex, decorticate posturing, stereotypic reactivity, intermittent and continuous electrocortical activity were regained within ultimate time limits of 900, 540, 455, 450, and 1020 min, respectively, corresponding to the longest delay compatible with recovery of function at all, and within critical time limits of 165, 180, 180, 200, and 630 min, respectively, corresponding to the longest delay compatible with recovery of consciousness. Moreover, intermittent electrocortical activity, consciousness, speech and ability to cope with personal necessities were regained within supercritical time limits of 3, 47, 156, and 336 h, respectively, corresponding to the longest delay compatible with complete restoration of post-awakening faculties within 1 year of resuscitation. Prognosis was currently ascertained during the period of unconsciousness as cephalic reactivities, and electrocortical activities were regained in an exponential relationship to time. Bradycardia or asystole prior to resuscitation and metabolic acidosis, hypotensive heart failure, recurrent circulatory arrest and pneumonia thereafter influenced the cerebral recovery adversely.