Observations on comatose survivors of cardiopulmonary resuscitation with generalized myoclonus

BACKGROUND: There is only limited data on improvements of critical medical care is resulting in a better outcome of comatose survivors of cardiopulmonary resuscitation (CPR) with generalized myoclonus. There is also a paucity of data on the temporal dynamics of electroenephalographic (EEG) abnormalities in these patients. METHODS: Serial EEG examinations were done in 50 comatose survivors of CPR with generalized myoclonus seen over an 8 years period. RESULTS: Generalized myoclonus occurred within 24 hours after CPR. It was associated with burst-suppression EEG (n = 42), continuous generalized epileptiform discharges (n = 5), alpha-coma-EEG (n = 52), and low amplitude (10 μV <) recording (n = 1). Except in 3 patients, these EEG-patterns were followed by another of these always nonreactive patterns within one day, mainly alpha-coma-EEG (n = 10) and continuous generalized epileptiform discharges (n = 9). Serial recordings disclosed a variety of EEG-sequences composed of these EEG-patterns, finally leading to isoelectric or flat recordings. Forty-five patients died within 2 weeks, 5 patients survived and remained in a permanent vegetative state. CONCLUSION: Generalized myoclonus in comatose survivors of CPR still implies a poor outcome despite advances in critical care medicine. Anticonvulsive drugs are usually ineffective. All postanoxic EEG-patterns are transient and followed by a variety of EEG sequences composed of different EEG patterns, each of which is recognized as an unfavourable sign. Different EEG-patterns in anoxic encephalopathy may reflect different forms of neocortical dysfunction, which occur at different stages of a dynamic process finally leading to severe neuronal loss

NSE and S100 after hypoxia in the newborn pig

Perinatal asphyxia is an important cause of neonatal morbidity and mortality. There is the potential to halt cerebral damage if neural rescue strategies are applied within a short period of time after an insult. It is therefore important to be able to accurately identify neonates who may benefit from neural rescue therapies. Recent studies in asphyxiated neonates have correlated S100B and NSE with outcome; however, interpretation of these studies were difficult, as the timing of the measurements were not consistent. We measured NSE and S100 in I-d-old piglets after a mild or severe hypoxic insult. Measurements were performed at 6-72 h after the insult and correlated with histologic outcome. There were no differences of the NSE or S100 concentrations between controls and the mild hypoxia group. After 24 h, there was a significant difference of NSE between the control/mild insult group and severe insult group. After 48 h, the S100 concentrations were significantly different between the control/ mild insult group and the severe insult group. Both proteins showed good correlation at these time points with outcome as measured by histology score at 72 h. In conclusion, NSE and S100B measured in the serum of piglets after hypoxia increased significantly and correlated with outcome. This increase occurs too late to be used within the first 24 h but might be helpful for the clinician in determining the timing of an insult