Cerebral Blood Flow and Cerebral Metabolic Rate of Oxygen Requirements for Cerebral Function and Viability in Humans

1985 ◽  
Vol 5 (4) ◽  
pp. 600-608 ◽  
Author(s):  
William J. Powers ◽  
Robert L. Grubb ◽  
Danielle Darriet ◽  
Marcus E. Raichle

This study was undertaken to determine the minimum CBF and CMRO2 required by the human brain to maintain normal function and viability for more than a few hours. Positron emission tomography (PET) was used to perform regional measurements in 50 subjects with varying degrees of cerebral ischemia but no evidence of infarction. There were 24 normal subjects, 24 subjects with arteriographic evidence of vascular disease of the carotid system, and two subjects with reversible ischemic neurological deficits due to cerebral vasospasm. Minimum values found in the 48 subjects with normal neurological function were 19 ml/100 g-min for regional cerebral blood flow (rCBF) and 1.3 ml/100 g-min for regional cerebral metabolic rate of oxygen (rCMRO2). Minimum values for all 50 subjects with viable cerebral tissue were 15 ml/100 g-min for rCBF and 1.3 ml/100 g-min for rCMRO2. Comparison of these measurements with values from 20 areas of established cerebral infarction in 10 subjects demonstrated that 80% (16/20) of infarcted regions had rCMRO2 values below the lower normal limit of 1.3 ml/100g-min. Measurements of rCBF, regional cerebral blood volume, and oxygen extraction fraction were less useful for distinguishing viable from infarcted tissue. These data indicate that quantitative regional measurements of rCMRO2 with PET accurately distinguish viable from nonviable cerebral tissue and may be useful in the prospective identification of patients with reversible ischemia.

1977 ◽  
Vol 46 (4) ◽  
pp. 446-453 ◽  
Author(s):  
Robert L. Grubb ◽  
Marcus E. Raichle ◽  
John O. Eichling ◽  
Mokhtar H. Gado

✓ Forty-five studies of regional cerebral blood volume (rCBV), regional cerebral blood flow (rCBF), and regional cerebral oxygen utilization (rCMRO2) were performed in 30 patients undergoing diagnostic cerebral angiography for evaluation of a subarachnoid hemorrhage due to a ruptured intracranial aneurysm. Tracer methods employing radioactive oxygen-15 were used to measure rCBV, rCBF, and rCMRO2. The patient studies were divided into groups based on their neurological status and the presence or absence of cerebral vasospasm. Subarachnoid hemorrhage, with and without vasospasm, produced significant decreases in CBF and CMRO2. In general, patients with more severe neurological deficits, and patients with more severe degrees of vasospasm, had a more marked depression of CBF and CMRO2. The most striking finding was a significant (p < 0.001) increase in CBV (to 58% above normal) in patients with severe neurological deficits associated with severe cerebral vasospasm. This large increase suggests that cerebral vasospasm consists of constriction of the large, radiographically visible extraparenchymal vessels accompanied by a massive dilation of intraparenchymal vessels.


1985 ◽  
Vol 62 (4) ◽  
pp. 539-546 ◽  
Author(s):  
William J. Powers ◽  
Robert L. Grubb ◽  
Roy P. Baker ◽  
Mark A. Mintun ◽  
Marcus E. Raichle

✓ Regional cerebral blood flow (rCBF) and regional cerebral metabolic rate of oxygen (rCMRO2) were measured by positron emission tomography (PET) in four patients with subarachnoid hemorrhage and hemiparesis due to cerebral vasospasm. With resolution of the vasospasm, two patients recovered and two remained hemiparetic. Contralateral to the hemiparesis, rCBF was slightly higher in the two patients who eventually recovered (15.0 and 16.2 ml/100 gm/min) than in the two who remained hemiparetic (12.0 and 11.7 ml/100 gm/min). The rCMRO2 measurements showed similar differences, with values of 1.34 and 2.60 ml/100 gm/min in the patients who recovered, and 0.72 and 1.66 ml/100 gm/min in those who did not. These preliminary findings indicate that with PET studies it may be possible to prospectively differentiate patients with neurological deficits due to reversible ischemia from patients with irreversible infarction.


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