Effects of Anti-seizure Medications on Cortico-cortical Evoked Potentials
Serdar Akkol1, Helen Brinyark2, Aparna Vaddiparti1, Rachel Smith2, Benjamin Cox1
1Department of Neurology, 2School of Engineering, University of Alabama at Birmingham
Objective:

To examine the effects of anti-seizure medications (ASM) on cortico-cortical evoked potentials (CCEP).

Background:

ASMs control seizures through distinct neuronal mechanisms leading to multiple cognitive and behavioral side effects thought to be via modulation of brain connectivity. CCEPs helps us measuring the effective connectivity allowing high temporal and spatial resolution in investigating the interactions between brain regions. CCEPs are often performed while the patient is on ASMs, however, the effect of ASMs on CCEPs is largely unknown. We hypothesized that ASMs decrease the amplitude and prolong the latency of the evoked potentials.

Design/Methods:

A 37-year-old female underwent epilepsy monitoring with stereo-EEG electrodes. Due to lack of typical clinical seizures off ASMs, an initial CCEP session was performed as part of clinical care (ASM-OFF). A second CCEP stimulation was later performed once ASMs were resumed as part of research (ASM-ON). We stimulated 3 irritative zone (IZ) and 1 early propagation zone (EPZ) pairs during both sessions. We recorded a total of 156 bipolar channels and stimulated 3 IZ and 1 EPZ pairs with 5mA, 150µsec, 1Hz square wave pulses. EPZ and IZ channels were identified by clinical team based on recorded seizures. We averaged responses for each CCEP pulse at the recorded pairs and measured the delay and voltage of N1, P1 and N2 peaks.

Results:

We found that in response to EPZ channel stimulation, all peaks were 3-5ms earlier and 3-15µV lower in amplitude during ASM-ON compared to ASM-OFF. Similarly, in response to IZ stimulation, peaks were recorded 2-4ms earlier.

Conclusions:

We found that CCEPs were recorded sooner with lower amplitude during patient was on ASMs compared to off ASMs. The shortened CCEP latency on ASMs might be the result of activation of fewer white matter pathways leading to recording of limited number of strong connections, not suppressed by the ASM.

10.1212/WNL.0000000000204612