¹David Geffen School of Medicine at UCLA, UCLA Medical Center, University of California, Los Angeles, California, USA

Correspondence: Dr Paul Vespa, David Geffen School of Medicine at UCLA, CHS 18-218, UCLA Medical Center, University of California, Los Angeles, CA 90095, USA. E-mail: PVespa@mednet.ucla.edu

Received 7 June 2004; Revised 20 September 2004; Accepted 22 November 2004; Published online 16 February 2005.

Abstract

Brain trauma is accompanied by regional alterations of brain metabolism, reduction in metabolic rates and possible energy crisis. We hypothesize that microdialysis markers of energy crisis are present during the critical period of intensive care despite the absence of brain ischemia. In all, 19 brain injury patients (mean GCS 6) underwent combined positron emission tomography (PET) for metabolism of glucose (CMRglu) and oxygen (CMRO₂) and cerebral microdialysis (MD) at a mean time of 36 h after injury. Microdialysis values were compared with the regional mean PET values adjacent to the probe. Longitudinal MD data revealed a 25% incidence rate of metabolic crisis (elevated lactate/pyruvate ratio (LPR)>40) but only a 2.4% incidence rate of ischemia. Positron emission tomography imaging revealed a 1% incidence of ischemia across all voxels as measured by oxygen extraction fraction (OEF) and cerebral venous oxygen content (CvO₂). In the region of the MD probe, PET imaging revealed ischemia in a single patient despite increased LPR in other patients. Lactate/pyruvate ratio correlated negatively with CMRO₂ (P<0.001), but not with OEF or CvO₂. Traumatic brain injury leads to a state of persistent metabolic crisis as reflected by abnormal cerebral microdialysis LPR that is not related to ischemia.