Abstract
The EEG of patients in non-convulsive status epilepticus (NCSE) often displays delta oscillations or generalized spike-wave discharges. In some patients, these delta oscillations coexist with intermittent epileptic spikes. In this study we verify the prediction of a computational model of the thalamo-cortical system that these spikes are phase-locked to the delta oscillations. We subsequently describe the physiological mechanism underlying this observation as suggested by the model. It is suggested that the spikes reflect inhibitory stochastic fluctuations in the input to thalamo-cortical relay neurons and phase-locking is a consequence of differential excitability of relay neurons over the delta cycle. Further analysis shows that the observed phase-locking can be regarded as a stochastic precursor of generalized spike-wave discharges. This study thus provides an explanation of intermittent spikes during delta oscillations in NCSE and might be generalized to other encephathologies in which delta activity can be observed.
Highlights
Non-convulsive status epilepticus (NCSE), known as petit mal status, absence status, or ictal confusion, refers to a prolonged state in which the subject’s EEG displays epileptiform activity (Brenner, 2004; Kaplan, 2006)
In this study we have verified the prediction of a computational model of the thalamo-cortical system that the epileptic spikes that can be observed in the EEG of patients during NCSE (Ellis, 1978; Granner, 1994; Uthman and Bearden, 2008) are locked to the phases of the background delta oscillations using EEG data from a single patient
The emergence, morphology, and phase-relationship of the spikes to delta oscillations are shaped by the thalamo-cortical system, it does not generate the spikes intrinsically
Summary
Non-convulsive status epilepticus (NCSE), known as petit mal status, absence status, or ictal confusion, refers to a prolonged state in which the subject’s EEG displays epileptiform activity (Brenner, 2004; Kaplan, 2006). It frequently occurs in elderly patients both with and without a history of epileptic seizures (Ellis, 1978; Lee, 1985; Bauer et al, 2007). Most studies are empirical and not much is known about the underlying mechanisms and the structures involved (Brigo, 2011)
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