• Nobuyuki Kawai, Takehiro Nakamura, Takashi Tamiya, and Seigo Nagao.
• Department of Neurological Surgery, Kagawa University School of Medicine, 1750-1 Miki-cho, Kita-gun, Kagawa 761-0793, Japan. nobu@med.kagawa-u.ac.jp
• Acta Neurochir. Suppl. 2008 Jan 1;102:241-5.

BackgroundCerebral ischemia is believed to be an important mechanism of secondary neuronal injury in traumatic brain injury (TBI).MethodsIn this study, we performed 15O2 positron emission tomography (PET) studies to measure the cerebral blood flow (CBF) and oxygen metabolism (CMRO2) in the pericontusional region in a total of 15 patients (11 males, 4 females, aged 15-81 years) who sustained TBI with contusional hematoma. PET studies were performed a mean of 13.5 +/- 9.1 days (range 2-33 days) after TBI occurred.FindingsThe areas of pericontusional tissues located 10 mm away from the cerebral contusion exhibited mildly decreased CBF (89%) and severely suppressed CMRO2 (67%) when comparison was made with the remote cerebral cortex. Severely suppressed oxygen metabolism in the pericontusional tissue was observed not only in the acute stage, but also in the subacute stage after TBI, whereas blood flow was slightly recovered in the subacute stage. We also compared the PET findings obtained in the acute or subacute stage after TBI and structural abnormalities on late-stage MRI in 5 patients. The area of flow defect on the CBF-PET image developed into irreversible tissue damage (necrosis) in the chronic stage. The area of hypoperfusion surrounding the lesion partly resulted in tissue necrosis: however, a large part of the hypoperfused tissue survived in the chronic stage. Again, a significant portion of oxygen hypometabolism surrounding the lesion did not develop into tissue necrosis.ConclusionsWe conclude that impaired cerebral blood flow and metabolism in the pericontusional region is observed even in the subacute stage after TBI and is unlikely to cause severe further neuronal damage.

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