High lactate levels have been reported to be associated with ischemia both in SAH patients and patients with head injury (19, 20). However, high lactate levels may also indicate hyperglycolysis (21, 22), explaining its rather low specificity as a biomarker of ischemia (9). Consequently, additional parameters such as L/P-ratio, pyruvate, and CBF should be evaluated to distinguish between ischemia, hyperglycolysis, and mitochondrial dysfunction (5, 23–25). In the current study, there was a significant negative correlation between CBF and lactate. However, the L/P ratio was not significantly correlated with CBF. We have recently reported on high lactate and low CBF during the acute phase following SAH in patients who later developed DCI (26). Different studies report on different levels of CBF thresholds for ischemia. Previous studies using Xenon-CT have reported on cortical CBF in awake normal subjects to be 52 ± 10 ml/100 g/min (27). In an additional study, comatose patients following head injury were compared to normal subjects and CBF threshold of 55.3 ml/100 g/min was defined as hyperemia (28). Our recent report on patients suffering severe SAH showed that patients who later develop DCI have initial low CBF levels of 23.7 ml/100 g/min compared to 37.5 ml/100 g/min in those who do not develop DCI (26). Current results are in line with previous findings and emphasize the important role of lactate in correlation with CBF in patients suffering SAH.