Cerebral oxygen metabolism and neuroelectrophysiology in a clinical study of severe brain injury and mild hypothermia

Mild hypothermia has an important role in the treatment of severe brain injury and there are therapeutic windows for this technique for patients with severe brain injury. We used a randomized, controlled, clinical study to investigate indexes of cerebral oxygen metabolism and neuroelectrophysiology to evaluate the efficacy of mild hypothermia treatment in severe brain injury. A total of 148 patients (106 males and 42 females), aged 18 to 64 years with acute severe brain injury were selected from June 1998 to June 2004 from the Department of Neurosurgery at The First Affiliated Hospital of Chongqing Medical University. All patients met the inclusion criteria: admission to hospital within 10 hours of injury; Glasgow Coma Scale (GCS) score ⩽ 8; age < 65 years; no other severe combined visceral injury; and no severe co-morbidities of the heart, lung, liver, kidney, or other visceral organs. Patients were divided into groups according to brain injury severity: GCS scores 7–8, 5–6, and 3–4. Patients in each GCS score group were randomly assigned to two subgroups: hypothermia and normothermia. Brain oxygen metabolism indexes (partial pressure of oxygen in brain tissue [PbrO2] and regional cerebral oxygen saturation [rSaO2]) as well as neuroelectrophysiology indexes (short-latency somatosensory evoked potential [SLSEP] and brain-stem auditory evoked potential [BAEP]) were recorded in the normothermia and hypothermia subgroups (32–34 °C) prior to and after cooling for 5 days. Brain oxygen metabolism indexes (PbrO2 and rSaO2) and neuroelectrophysiology indexes (SLSEP and BAEP) were also compared for patients who underwent mild hypothermia and those who did not. For patients with GCS 7–8, SLSEP, BAEP and rSaO2 following cooling were significantly improved in the hypothermia subgroup and the PbrO2 was less in the hypothermia subgroup. For patients with GCS 5–6, the SLSEP, BAEP and rSaO2 were improved following hypothermia on some days, and the PbrO2 was greater in the hypothermia subgroup on some days. For patients with GCS 3–4, there was no difference between the hypothermia and normothermia subgroups. We conclude that hypothermia had a significant therapeutic effect on severe brain injury of patients with GCS 7–8, had no effect on patients with GCS 3–4, and an uncertain effect on patients with GCS 5–6. The indexes of cerebral oxygen metabolism and neuroelectrophysiology indicated primary and secondary brain injury, respectively, and provided an effective way to evaluate brain injury.