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From the Departments of Pediatrics (Drs. Juhász, Chugani, Muzik, Asano, and Chugani), Neurology (Drs. Shah and Chugani), Radiology (Drs. D.C. Chugani, Muzik, Mangner, Chakraborty, and H.T. Chugani), and Neurosurgery (Dr. Sood), Children’s Hospital of Michigan and Harper University Hospital, Detroit Medical Center, Wayne State University School of Medicine, Detroit, MI.
Address correspondence and reprint requests to Dr. Harry T. Chugani, Pediatric Neurology/PET Center, Children’s Hospital of Michigan, 3901 Beaubien Blvd., Detroit, MI 48201; e-mail: hchugani{at}pet.wayne.edu
Background: In children with tuberous sclerosis, the PET tracer 
[11C]methyl-L-tryptophan (AMT) has been shown to be selectively taken up by epileptogenic tubers, thus allowing differentiation from nonepileptogenic tubers in the interictal state.
Objective: To determine whether cortical areas showing increased AMT uptake in children without tuberous sclerosis complex with intractable neocortical epilepsy indicate the epileptogenic zone, and to assess the relative contributions of AMT and 2-deoxy-2[18F]fluoro-D-glucose (FDG) PET abnormalities to the localization of epileptogenic cortical regions.
Methods: Areas of increased AMT and decreased FDG uptake were marked objectively as regions with abnormal asymmetry using an in-house written software in 27 children who underwent comprehensive evaluation for resective epilepsy surgery. The marked PET abnormalities were compared to the locations of scalp and subdural EEG epileptiform abnormalities, as well as histology and surgical outcome.
Results: Focal cortical increases of AMT uptake were found in 15 patients. The lobar sensitivity (39.0%) of AMT PET for seizure onset was lower, but its specificity (100%) was higher (p < 0.0001) than that of hypometabolism on FDG PET (sensitivity 73.2%, specificity 62.7%). AMT PET abnormalities were smaller than corresponding FDG PET hypometabolic regions (p = 0.002), and increased AMT uptake occurred in two patients with nonlocalizing FDG PET. Histologically verified cortical developmental malformations were associated with increased AMT uptake (p = 0.044). Subdural electrodes adjacent to the area of increased AMT uptake were most often involved in seizure onset.
Conclusions: Focal increase of cortical AMT uptake in children is less sensitive but more specific for the lobe of seizure onset than corresponding FDG PET hypometabolism, and it is often associated with epileptogenic cortical developmental malformations. AMT PET can assist placement of subdural electrodes even when MRI and FDG PET fail to provide adequate localizing information. Cortical areas adjacent to increased AMT uptake should be carefully addressed by intracranial EEG because these regions often show a high degree of epileptogenicity.
This article has been cited by other articles:
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  D. K. Lachhwani, E. Pestana, A. Gupta, P. Kotagal, W. Bingaman, and E. Wyllie Identification of candidates for epilepsy surgery in patients with tuberous sclerosis Neurology, May 10, 2005; 64(9): 1651 - 1654. [Abstract] [Full Text] [PDF]
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 P. Curatolo, R. Bombardieri, M. Verdecchia, and S. Seri Topical Review: Intractable Seizures in Tuberous Sclerosis Complex: From Molecular Pathogenesis to the Rationale for Treatment J Child Neurol, April 1, 2005; 20(4): 318 - 325. [Abstract] [PDF]
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P. Curatolo, R. Bombardieri, M. Verdecchia, and S. Seri Topical Review: Intractable Seizures in Tuberous Sclerosis Complex: From Molecular Pathogenesis to the Rationale for Treatment J Child Neurol, March 1, 2004; 19(3): 318 - 325. [Abstract] [PDF]
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