ENO2 and cardiac arrest: In the last few decades, several clinical and electrophysiological variables have been reported to be strongly associated with a poor outcome in comatose survivors of cardiac arrest; these include absence of pupillary and corneal reflexes, absent motor response to pain [2-5], myoclonus or epilepticus status [6,7], an increase of neuron specific enolase (NSE) in serum [8], and a burst-suppression or isoelectric electro-encephalography (EEG) pattern [7,9,10].