To study the pathophysiologic mechanism of astatic seizures in a patient with myoclonic astatic epilepsy of early childhood, ictal magnetoencephalography was recorded and the neuronal pathway involved was analyzed. The patient was a 12-year-old female who developed myoclonic and astatic seizures including nodding and sudden falling at the age of 4. The current source of spikes during nodding attacks was located in the bilateral frontal area with left predominance, possibly in the premotor cortex. Although we could not claim, on the basis of our findings, that myoclonic astatic epilepsy of early childhood is a type of focal epilepsy, it seems likely that the premotor cortex might be more excitable than other areas. Thus we speculate that the functionally altered premotor-reticulospinal tract which normally controls postural adjustment might play an important role in the generation of myoclonic astatic seizures. Furthermore, the underlying mechanism in the brainstem seems to be common, at least in part, for infantile spasms when considering the efficacy of synthetic adrenocorticotropic hormone for nodding seizures.