Abstract
Neurocritical care focuses on the critical care management of patients with catastrophic neurologic diseases including vascular and traumatic brain damage. Methods commonly used for monitoring the brain in neurocritical care include computed tomographic (CT) scan and magnetic resonance (MR) imaging. Positron emission tomography (PET) is a powerful, noninvasive tool used to study the biochemistry and physiology of the working brain. Positron emitting isotopes are administered via an inhalational or intravenous route, and for imaging of the brain, oxygen (^<15>O) is employed to measure CBF, CBV CMRO_2 and OEF, while fluorodeoxyglucose (^<18>F-FDG) is used to measure cerebral glucose metabolism. PET has been used to evaluate the stage of hemodynamic deficiency in occlusive cerebrovascular disease and the malignancy of the brain tumors. We used PET aggressively to map the pathophysiology in acute vascular and traumatic brain damage. Important findings from our experiences and previous reports are as follows. (1) Acute ischemic stroke studies have shown that a considerable part of the final infarct has already lost cellular integrity and is not accessible to therapy even in the early phase. However, PET detected viable but hypoperfused tissue that is characterized by an elevated OEF and accessibility to acute therapy. (2) A zone of reversible hypoperfusion has been demonstrated around acute intracerebral hemorrhage (ICH). PET studies have shown that CMRO_2 is reduced to a greater degree than CBF in the periclot region in acute ICH, resulting in reduced OEF. Thus, the hypoperfused area observed around acute ICH is not cerebral ischemia. (3) PET studies have shown that global values of CBF CMRO_2 and CBF/CBV ratio are reduced in acute aneurysmal subarachnoid hemorrhage (SAH). Among patients who developed delayed neurological deficits due to vasospasm after SAH, a wide range of CBF disturbance has been observed. (4) Acute-phase ^<18>F-FDG PET studies have revealed that some areas of the brain show a relative increase in glucose utilization in traumatic brain injury (TBI). In addition to the areas showing increased glucose uptake, the human PET studies have also shown decreased glucose utilization in pericontusional and remote areas. Measurements of CBF and CMRO_2 with PET have demonstrated wide regional variations in CBF with consistent decreased CMRO_2 in early TBI patients. In conclusion, recent developments in PET technology provide the neurointensivist with functional information, at the cellular level, that may help guide management in patients with neurocritical care. To understand the absolute values derived from PET, we must consider the effects of anesthetics on cerebral blood flow and metabolism.
