224. Phase-Resetting within the Default Mode Network Facilitates Mental Flexibility and is Impaired by Epileptic Dynamics

Authors: Nebras M. Warsi, MD, CM; Simeon Wong; George Ibrahim, MD (Toronto, Canada)

Introduction:

The ability to modulate default mode network (DMN) activity in response to a stimulus facilitates variety of neurocognitive abilities. The phase of oscillatory brain activity encodes a neural syntax that modulates the activity of neural networks. Using stereoelectroencephalographic recordings from children implanted with electrodes within the posterior cingulate cortex (PCC), a hub of the DMN, we tested the hypothesis that visual stimuli induce phase shifts within the DMN that facilitate mental flexibility and are impaired by epileptic dynamics.

Methods:

Four patients with intractable epilepsy underwent stereotactic intracranial depth electrode placement directly into the PCC. All participants performed a set-shifting task during intracranial recordings. Set-shifting is a measure of cognitive flexibility and engages several brain regions including the PCC.  Phase-resetting in PCC was recorded using the Rayleigh Z as a measure of phase consistency.  The effects of concurrent high frequency oscillations (HFOs) on PCC phase were quantified.

Results:

Stimulus presentation induced phase resetting within the PCC in both theta and alpha frequencies.  The physiological process of phase resetting within the PCC was associated with improved mental flexibility, as indexed by task reaction time.  During trials coincident with the expression of epileptic HFOs, phase resetting was impaired and reaction times were prolonged. 

Conclusion:

Here we find that stimulus-induced phase shifts within the DMN are critical for cognitive functions, such as mental flexibility.  Epileptic dynamics disrupt the phase-based neural syntax leading to impairments in behaviors.  The current work provides a critical link between neurophysiological processes, behavior, and neurocognitive deficits in children with epilepsy.  These findings may inform future targeted therapies to address the comorbidities of childhood epilepsy.