Journal
NEUROCRITICAL CARE
Volume 9, Issue 3, Pages 319-325Publisher
HUMANA PRESS INC
DOI: 10.1007/s12028-008-9119-2
Keywords
Head injury; Oxygen metabolism; Glucose metabolism; Ischemia; Positron emission tomography; Traumatic penumbra
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Funding
- MRC [G0600986, G0001237, G9439390] Funding Source: UKRI
- Medical Research Council [G9439390, G0600986, G0001237] Funding Source: researchfish
- Medical Research Council [G0001237, G0600986, G9439390] Funding Source: Medline
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Introduction Conclusive evidence of cerebral ischemia following head injury has been elusive. We aimed to use O-15 and (18)Fluorodeoxyglucose positron emission tomography (PET) to investigate pathophysiological derangements following head injury. Results Eight patients underwent PET within 24 h of injury to map cerebral blood flow (CBF), cerebral oxygen metabolism (CMRO2), oxygen extraction fraction (OEF), and cerebral glucose metabolism (CMRglc). Physiological regions of interest (ROI) were generated for each subject using a range of OEF values from very low (< 10), low (10-30), normal range (30-50), high (50-70), and critically high (70%). We applied these ROIs to each subject to generate data that would examine the balance between blood flow and metabolism across the injured brain independent of structural injury. Discussion Compared to the normal range, brain regions with higher OEF demonstrate a progressive CBF reduction (P < 0.01), CMRO2 increase (P < 0.05), and no change in CMRglc, while regions with lower OEF are associated with reductions in CBF, CMRO2, and CMRglc (P < 0.01). Although all subjects demonstrate a decrease in CBF with increases in OEF > 70%, CMRO2 and CMRglc were generally unchanged. One subject demonstrated a reduction in CBF and small fall in CMRO2 within the high OEF region (> 70%), combined with a progressive increase in CMRglc. Conclusions The low CBF and maintained CMRO2 in the high OEF ROIs is consistent with classical cerebral ischemia and the presence of an 'ischemic penumbra' following early head injury, while the metabolic heterogeneity that we observed suggests significant pathophysiological complexity. Other mechanisms of energy failure are clearly important and further study is required to delineate the processes involved.
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