# {#article-title-2} To the Editor: Andrade et al.1 described 3 patients with anti-LGI1 limbic encephalitis and abnormal movements involving different body regions. The authors stated that these paroxysmal attacks are tonic seizures and suggested that may indicate anti-LGI1 encephalitis.1 Features of tonic seizures include the following: sudden-onset tonic extension or flexion of the head, trunk, or extremities; duration of less than 60 seconds; varying degrees of impairment of consciousness; and occurrence either shortly after the person falls asleep or just after awakening.2 In the EEG, the ictal correlate of tonic seizures is an electrodecremental response: a high-frequency discharge in the β frequency with relatively low amplitude. Moreover, EMG activity is dramatically increased in tonic seizures. Unfortunately, no EMG trace was available in the single ictal EEG recording reported by Andrade et al.1 While we agree that the motor movements in their patients were longer than myoclonic seizures, the extrapyramidal nature of these fits cannot be dismissed. The authors' ictal recordings did not identify definite EEG changes and the inconsistent response to different antiepileptic drugs (AEDs) also argues for an alternative, nonepileptic origin. Considering that these neurologic manifestations are not readily evocative of any seizure type currently recognized by the International League Against Epilepsy classification, Irani et al.3 termed them faciobrachial dystonic seizures. Most of their patients' neuroimaging studies showed altered glucose metabolism in different cerebral regions including the basal ganglia. They also acknowledged that “it seems likely that the ictal dystonia in these patients reflects basal ganglia involvement.”3 Neurophysiologic characterization of these attacks by multichannel EEG-EMG recordings and jerk-locked back averaging analysis are needed to clarify the nature of attacks and affected brain areas before definitely considering them “epileptic.” However, the distinctive semiology should prompt testing for VGKC-complex/Lgi1 antibodies and possible immunotherapy.
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Andrade et al. (2011) studied this question.
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