Paroxysmal Slow Waves Mark Ictal Networks
Boyer Ayme, F. J. M.; Imtiaz, H.; Prager, O.; Swissa, E.; Abu Ahmad, A.; Serlin, Y.; Aboghazleh, R.; Goldberg, I.; Ben nun Caller, M.; Tamir, I.; Shor, O.; Whatley, B.; Benninger, F.; Friedman, A.
Show abstract
Epilepsy diagnosis and treatment monitoring are hindered by the episodic, heterogeneous expression of seizures and by normal-appearing scalp EEG in many patients. We previously described paroxysmal slow-wave events (PSWEs)--brief epochs of broadband slowing detectable on EEG. Here, using intracerebral and epidural recordings in a paraoxon rat model of temporal lobe epilepsy, we show that PSWEs arise preferentially in temporo-frontal networks, co-occur with global slowing, and increase during both spontaneous and pharmacologically induced seizures. Epidurally recorded PSWEs were temporally coupled to deep temporal discharges and were bidirectionally modulated by GABAergic agents (increased with pentylenetetrazol and decreased with pentobarbital). In long-term video-EEG monitoring (LTM) patients with temporal lobe epilepsy, simultaneous stereo-EEG and scalp EEG showed that scalp PSWEs mirrored hippocampal spike-and-wave activity and were more often observed in the preictal and ictal periods than during interictal baseline. These data indicate that surface PSWEs can index remote epileptiform activity and support their use as a quantitative, noninvasive biomarker for detecting EEG-silent deep foci and for pharmacodynamic.
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