Ischemic brain metabolism in patients with chronic cerebrovascular disease: Increased oxygen extraction fraction and cerebrospinal fluid lactate

The aim of the present study is to elucidate the existence of chronically ischemic metabolism concomitant with misery perfusion of the brain in patients with chronic cerebrovascular disease. For this purpose, we measured cerebral blood flow (CBF) and oxygen metabolism by positron emission tomography (PET) and also determined cerebrospinal fluid (CSF) lactate as an indicator of the ischemic brain metabolism. Twenty-eight patients with chronic ischemic stroke and transient ischemic attack (TIA), who had angiographically occlusive (n = 11), stenotic (n = 10), and nonstenotic changes (n = 7) of the carotid artery and/or the intracranial major artery, were selected for this study. CBF, oxygen extraction fraction (OEF), cerebral metabolic rate for oxygen (CMRO2), and cerebral blood volume (CBV) were determined by PET, and CSF lactate and pyruvate were determined by enzymatic method in the patients with various grades of stenotic changes of the carotid artery. There were no significant differences in PET parameters and CSF variables among the groups of the occlusive, stenotic, and nonstenotic carotid artery. However, CSF lactate was correlated negatively with mean bilateral hemispheric (m)CBF (R(2) = 0.229, P<.01), positively with mOEF (R(2) = 0.278, P<.005) and more highly with mCMRO2/CBF (absolute extraction of oxygen content to the brain) (R(2) = 0.473, P<.0001) in all patients. There was no correlation between CSF lactate and mCMRO2 or mCBV. None of the cases in the nonstenotic group showed mOEF greater than 0.45, or mCMRO2/CBF greater than 7.9 vol%, while 80% of the cases in the stenotic group and 82% of the cases in the occlusive group showed mOEF and mCMRO2/CBF exceeding the above-mentioned values, respectively. The present findings, that increased mOEF and mCMRO2/CBF were significantly correlated with increased CSF lactate, indicate the brain to be in a metabolically ischemic state or increased anaerobic glycolysis with oxygen metabolism maintained in patients with chronic ischemic stroke.