We describe the ictal [(18)F]FDG-PET study of a case of absence status showing bilateral thalamic hypermetabolism and frontal cortex hypometabolism. This is the first ictal assessment of absence status by [(18)F]FDG-PET reporting this particular cortical and subcortical involvement. Our findings support the theory of corticothalamic circuitry involvement in the pathophysiology of absence seizures and stress the similarities of the clinical and metabolic pattern observed during absences with the pattern of task-induced interruption of the default state of brain function.
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