title: Brain function after resuscitation from cardiac arrest.
abstract: OBJECTIVE
  In industrial countries the incidence of cardiac arrest is still increasing. Almost 80% of cardiac arrest survivors remains in coma for varying lengths of time and full cerebral recovery is still a rare event. After successful cardiopulmonary resuscitation, cerebral recirculation disturbances and complex metabolic postreflow derangements lead to death of vulnerable neurons with further deterioration of cerebral outcome. This article discusses recent research efforts on the pathophysiology of brain injury caused by cardiac arrest and reviews the beneficial effect of therapeutic hypothermia on neurologic outcome along with the recent approach to prognosticate long-term outcome by electrophysiologic techniques and molecular markers of brain injury.
  
  
  RESULTS
  Recent experimental studies have brought new insights to the pathophysiology of secondary postischemic anoxic encephalopathy demonstrating a time-dependent cerebral oxidative injury, increased neuronal expression, and activation of apoptosis-inducing death receptors and altered gene expression with long-term changes in the molecular phenotype of neurons. Recently, nuclear MR imaging and MR spectroscopic studies assessing cerebral circulatory recovery demonstrated the precise time course of cerebral reperfusion after cardiac arrest. Therapeutic hypothermia has been shown to improve brain function after resuscitation from cardiac arrest and has been introduced recently as beneficial therapy in ventricular fibrillation cardiac arrest.
  
  
  CONCLUSIONS
  Electrophysiologic techniques and molecular markers of brain injury allow the accurate assessment and prognostication of long-term outcome in cardiac arrest survivors. In particular, somatosensory evoked potentials have been identified as the method with the highest prognostic reliability. A recent systematic review of 18 studies analyzed the predictive ability of somatosensory evoked potentials performed early after onset of coma and found that absence of cortical somatosensory evoked potentials identify patients not returning from anoxic coma with a specificity of 100%.
authors.affiliation: Department of Medicine IV, Intensive Care Unit, University Hospital of Vienna, Austria. christian.madl@meduniwien.ac.at
authors.forename: Christian
authors.initials: C
authors.lastname: Madl
authors.forename: Michael
authors.initials: M
authors.lastname: Holzer
mesh_terms: D001930:Brain Injuries / Q000209:etiology / Q000503:physiopathology*; D016887:Cardiopulmonary Resuscitation; D003422:Critical Care; D005071:Evoked Potentials; D006323:Heart Arrest / Q000150:complications* / Q000628:therapy; D006801:Humans; D007036:Hypothermia, Induced; D015427:Reperfusion Injury / Q000209:etiology / Q000503:physiopathology