Cerebral Oxygen Metabolism after Aneurysmal Subarachnoid Hemorrhage

Abstract

Previous studies of cerebral oxygen metabolism and extraction in patients with subarachnoid hemorrhage (SAH) have yielded conflicting results. We used positron emission tomography (PET) to measure the regional cerebral metabolic rate for oxygen (rCMRO2), oxygen extraction fraction (rOEF), and cerebral blood flow (rCBF) 16 times in 11 patients with aneurysmal SAH. All studies were performed preoperatively; no patient had hydrocephalus or intracerebral hematoma on brain CT. Eight patients with no arteriographic vasospasm who were studied on days 1-4 post-SAH had a significant 25% reduction in global CMRO2 compared to age-matched controls, and no significant change in global OEF, suggesting a primary reduction in CMRO2 caused by SAH. Four patients studied seven times during arteriographic vasospasm had significantly increased rOEF with unchanged CMRO2 in arterial territories affected by arteriographic vasospasm compared to territories without vasospasm, indicative of cerebral ischemia without infarction. No brain regions studied with PET were infarcted on follow-up CT. We conclude that the initial aneurysm rupture produces a primary reduction in CMRO2, and that subsequent vasospasm causes ischemia.

Time-Course of Cerebral Perfusion and Tissue Oxygenation in the First 6 h after Experimental Subarachnoid Hemorrhage in Rats

“…This finding supports the hypothesis of a metabolic depression and an uncoupling of CBF and oxidative metabolism and is in accordance with data about cerebral perfusion and metabolism gathered previously by patient studies (Carpenter et al, 1991;Martin et al, 1984;Jakobsen et al, 1990;Voldby et al, 1985). Carpenter et al performed early positron emission tomography studies in SAH patients before aneurysm surgery and observed a significant 25% decrease of CMRO 2 even if patients had no signs of vasospasm in angiograms, suggesting a primary metabolic alteration and uncoupling of CBF and metabolism after SAH (Carpenter et al, 1991). However, in these studies, patients were not examined in the first hours after SAH.…”

“…Voldby et al found a concomitant decrease of CMRO 2 with arterial caliber, indicating secondary metabolic impairment due to cerebral vasospasm (Voldby et al, 1985). Other authors did not observe an additional depression of CMRO 2 with the appearance of delayed vasospasm and advocated a primary reduction of metabolism by SAH (Grubb et al, 1977;Carpenter et al, 1991;Frykholm et al, 2004). All of these studies, however, measured CBF and metabolic parameters in patients at various times after SAH and after hospital admission.…”

“…Although the extent of this phenomenon positively correlated with the patients' clinical state and the amount of subarachnoid blood, it has been observed in patients of all clinical grades and with more or less subarachnoid blood (Jakobsen et al, 1991;Carpenter et al, 1991). Whether there is a relationship between cerebral vasospasm and the depression of oxygen metabolism is discussed with controversy.…”

Quantitative BOLD: The effect of diffusion

“…To analyze the fitted parameters we compare them to gold standard readings from PET studies. OEF is known to be approximately constant across the healthy brain, with quoted average values typically in the range 35%-43% (26,27). This is borne out by the results in Fig.…”

“…There is, however, no established average of vCBV with which we may compare our results. CBV values from PET studies of the healthy brain are typically in the range 3%-4.5% (26,27). Deoxygenated blood is thought to account for the majority of this, but the exact percentage is unknown.…”