The broad term, epilepsy surgery, when applied to children refers to either corpus callosotomy, hemispherectomy, or focal corticectomy. This report discusses the role of positron emission tomography (PET) with [18F]deoxyglucose (FDG) for planning surgery in children undergoing either hemispherectomy or focal corticectomy for uncontrolled seizures. Since the pioneer ing work by Goldring [1] and Goldring and Gregorie [2], epilepsy surgery has gained steady acceptance among the Neurology and Pediatric communities as a viable therapeutic modality for medically intractable epilepsy in children. Most centers that perform pediatric epilepsy surgery evaluations in children now agree that candidates for this procedure should be subjected to a rigorous, standardized, presurgical evaluation process to select those who stand the best chance of benefitting from epilepsy surgery and thus reduce the risk of operating unnecessarily. Typically, the evaluation process goes from the least to the most invasive. At our institution, phase one of this process consists of history, physical, antiepileptic drug profile, psychosocial evaluation, neuropsychologic evaluation, speech and hearing, psychiatric evaluation, electroencephalography (EEG) video recording to capture several typical seizures, enhanced and unenhanced computed tomography (CT) and magnetic resonance imaging (MRI), and when possible, FDG-PET. The latter, although helpful, is quite expensive and often not authorized by third-party payors; theretore, it is not always possible to obtain this study. At the end of phase one, the decision is made by the epilepsy surgery team whether enough evidence of potential benefit to the patient exists to proceed. Phase two consists of intracarotid amytal or Wada testing to determine cerebral dominance, neuroophthalmologic evaluation, and somatosensory evoked responses. During phase three, customdesigned subdural electrode grids are placed in order to determine the epileptogenic zone via extraoperative ictal recordings. In addition, eloquent areas of neurologic function are determined by stimulation through the grid. Phase four consists of removal of the grids followed by focal corticectomy or hemispherectomy as indicated by all test results. This process of patient selection, as well as the epilepsy surgery itself, is expensive and labor intensive, but logical and data driven with the ultimate potential to provide dramatic improvement in seizure control in children who are uniformly devastated by epilepsy. The question before us is simple: Can one eliminate the need for ictal recordings from subdural grids (i.e., phase three testing) when one has an area of hypometabolism defined by FDG-PET, the surgical removal of which results in the same or better outcome as if phase three testing had been performed? If the answer to this question were yes, then by definition the epileptogenic zone, that is the area of seizure origin, which we currently define by ictal recordings from subdural grids, must be identical in anatomic boundaries to the area of hypometabolism observed on FDG-PET. If this finding were true then only interictal electrocorticography would need to be performed under anesthesia to localize the epileptogenic zone at the time of focal corticectomy/hemispherectomy. Our answer to this question is no. A yes answer assumes that the neurons in the epileptogenic zone always have the same functional deficit (i.e., decreased glucose utilization); however, no evidence exists to support this premise. Each diagnostic procedure performed during presurgical evaluation is designed to provide data concerning disparate areas of brain function. For example, each neuroimaging method provides different information based on different physical properties of brain tissue. CT measures densities of cerebral tissue by attenuation of an X-ray beam passed through the cranium. Standard MRI is based on the signal intensities given off by resonating water molecules. The signal intensity depends on both the amount of water present and how the water molecules interact with their surrounding environment. FDG-PET is based on cellular uptake and metabolism of glucose. Thus, PET provides a measure of only one aspect of neuronal metabolism which compliments, but does not replace CT and MRI. Similarly, FDG-PET visualizes properties of brain that are different from those elicited during ictal electrocorticography from subdural grids; therefore, it is fallacious to conclude that the area of abnormality of cellular metabolic function, as defined by FDG-PET, al-