Striatal stimulation causing movements mimicking faciobrachial dystonic seizures

Faciobrachial dystonic seizures (FBDS) are characteristic of anti‐LGI1 encephalitis. The pathophysiological mechanisms underlying FBDS are unknown, with scalp EEG correlates consistent with cortical initiation and basal ganglia hypermetabolism implicating the involvement of subcortical structures. In a patient with non‐encephalitic drug‐resistant temporal lobe epilepsy undergoing brain mapping during a stereotactic‐EEG investigation, we identified neurophysiologic evidence that lateralized movements similar to FBDS can result from direct striatal activation. Stimulation of putaminal depth electrode contacts resulted in brief contralateral dystonic movements resembling the FBDS seen in anti‐LGI1 encephalitis. The evoked movements lagged stimulation initiation and outlasted stimulation, reminiscent of the delay between scalp EEG infraslow activity and FBDS in anti‐LGI1 encephalitis. Unlike FBDS in anti‐LGI1 encephalitis, no scalp EEG change preceded the stimulation‐induced movements. These findings suggest that the putamen may be a part of the symptomatogenic zone for anti‐LGI1 encephalitis‐related FBDS, and that in the encephalitic scenario transient cortical epileptic discharges are ipsilaterally propagated to the striatum to cause FBDS.