Abstract
Rationale: Deep brain stimulation (DBS) of the ANT has recently been established as a therapeutic strategy for medically refractory focal epilepsy. However, the mechanistic underpinnings of this novel treatment option are still not sufficiently understood, partly because under normal clinical conditions the analysis of propagation of epileptic activity is restricted to information derived either from surface or intracranial EEG recordings restricted to the accessible cortical structures.
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