Objective:

To analyze the neurophysiology of generalized tonic-clonic (GTC) seizures using intracranial-EEG and surface-EMG data.

Background:

The precise mechanism of a GTC seizure is not well understood. A polygraphic analysis with intracranial-EEG (iEEG) and surface-EMG (sEMG) offers a unique opportunity to study this mechanism from a neurophysiological standpoint.

Design/Methods:

We studied two patients with refractory focal epilepsy, admitted to the epilepsy-monitoring unit with iEEG and sEMG. Both patients underwent direct electrical cortical stimulation for cortical mapping. iEEG and EMG signals were recorded using Nihon-Kohden’s JE-120 256-channel amplifier with a sampling rate of 2000Hz. A GTC seizure was provoked in both patients during their respective stimulation sessions.

Results:

The tonic phase demonstrated continuous spike activity in iEEG with highest power in 50-100Hz range. The sEMG activity demonstrated an interference pattern in both agonists and antagonists, consistent with a tetanic contraction with a very similar power spectrum as the iEEG.

The clonic phase was characterized by polyspike and slow-wave pattern. The polyspikes and slow-waves were time-locked with synchronized tetanic sEMG bursts and silent-periods in agonists and antagonists, respectively. The polyspikes were superimposed with ~400-600Hz high-frequency oscillations (HFOs). The frequency of the serrations of the motor unit potentials in the sEMG bursts was a subharmonic of the HFOs. The iEEG-sEMG latency was ~17-21ms, consistent with corticospinal conduction. There was a progressive increase of the sEMG burst and silent-period duration during the clonic phase, associated with corresponding increases in the polyspike and slow-wave durations.

Conclusions:

This study shows a very close relationship between iEEG and sEMG activity in a GTC seizure. The very similar power spectra of the iEEG and sEMG activities indicate that a GTC seizure is a direct result of cortical electrical activity varying in a crescendo-decrescendo manner. The transition from tonic to clonic phase is due to the “weakening” of the seizure discharge intensity.