Cortico-cortical evoked potentials in response to varying stimulation intensity improves seizure localization

Hays, Mark; Smith, Robert F.; Wang, Yujing; Coogan, Christopher; Sarma, Sridevi V.; Crone, Nathan E.; Kang, Joon Y.

doi:10.1016/j.clinph.2022.08.024

Cited by 11 publications

(11 citation statements)

References 51 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Stimulation artifact limited our ability to assess early responses (<15 ms post-stimulation) in the CCEP waveform. We also exclusively used 3 mA stimulation in order to minimize tissue damage; however, prior studies 13,19,20,39 have found that differences between SOZ and non-SOZ CCEPs begin at 3 mA and are maximal at 6-8 mA. In addition, amplifier saturation near the stimulating electrodes prevented us from quantifying low-frequency oscillations at the stimulation electrode.…”

Section: Methodological Limitationsmentioning

confidence: 99%

Quantifying trial‐by‐trial variability during cortico‐cortical evoked potential mapping of epileptogenic tissue

et al. 2023

View full text Add to dashboard Cite

Objective Measuring cortico‐cortical evoked potentials (CCEPs) is a promising tool for mapping epileptic networks, but it is not known how variability in brain state and stimulation technique might impact the use of CCEPs for epilepsy localization. We test the hypotheses that (1) CCEPs demonstrate systematic variability across trials and (2) CCEP amplitudes depend on the timing of stimulation with respect to endogenous, low‐frequency oscillations. Methods We studied 11 patients who underwent CCEP mapping after stereo‐electroencephalography electrode implantation for surgical evaluation of drug‐resistant epilepsy. Evoked potentials were measured from all electrodes after each pulse of a 30 s, 1 Hz bipolar stimulation train. We quantified monotonic trends, phase dependence, and standard deviation (SD) of N1 (15–50 ms post‐stimulation) and N2 (50–300 ms post‐stimulation) amplitudes across the 30 stimulation trials for each patient. We used linear regression to quantify the relationship between measures of CCEP variability and the clinical seizure‐onset zone (SOZ) or interictal spike rates. Results We found that N1 and N2 waveforms exhibited both positive and negative monotonic trends in amplitude across trials. SOZ electrodes and electrodes with high interictal spike rates had lower N1 and N2 amplitudes with higher SD across trials. Monotonic trends of N1 and N2 amplitude were more positive when stimulating from an area with higher interictal spike rate. We also found intermittent synchronization of trial‐level N1 amplitude with low‐frequency phase in the hippocampus, which did not localize the SOZ. Significance These findings suggest that standard approaches for CCEP mapping, which involve computing a trial‐averaged response over a .2–1 Hz stimulation train, may be masking inter‐trial variability that localizes to epileptogenic tissue. We also found that CCEP N1 amplitudes synchronize with ongoing low‐frequency oscillations in the hippocampus. Further targeted experiments are needed to determine whether phase‐locked stimulation could have a role in localizing epileptogenic tissue.

show abstract

Section: Methodological Limitationsmentioning

confidence: 99%

Quantifying trial‐by‐trial variability during cortico‐cortical evoked potential mapping of epileptogenic tissue

et al. 2023

View full text Add to dashboard Cite

show abstract

“…In complementary paradigms, a site's excitability can be explored by the morphology of the evoked activity in response to stimulation elsewhere or by the morphology and distribution of the responses elicited by stimulation to the single site. For example, the N1 amplitude is generally larger, [7][8][9] with accompanying stronger high-frequency activity [10][11][12] in response sites associated with epileptogenicity, suggesting a greater sensitivity to input stimuli in pathological brain areas (Figure 1A-C). Furthermore, SPES can implicate response regions as pathological through the presence of evoked waveforms such as delayed responses, which resemble interictal epileptiform discharges that occur 100 ms to 1 s after the stimulus.…”

Section: Using Stimulation To Probe Excitabilitymentioning

confidence: 99%

“…Typically, 30-50 trials of stimulation pulses are delivered at .5-1 Hz, and stimulation occurs at a large percentage of gray matter electrodes, although white matter stimulation is increasingly common. 8,24 The effect of stimulation current on the CCEP has been most studied; there exists a nonlinear positive relationship between current and the N1 peak amplitude, with an eventual plateau of the CCEP amplitude at high stimulation currents. 19,25 Using a biphasic pulse with .15 ms/phase width, reliable CCEP responses emerge with a stimulation current of 2-3 mA and plateau in response amplitude at 5.5-7 mA.…”

Section: Key Pointsmentioning

confidence: 99%

“…19,25 Using a biphasic pulse with .15 ms/phase width, reliable CCEP responses emerge with a stimulation current of 2-3 mA and plateau in response amplitude at 5.5-7 mA. 8,19,24 Slightly higher stimulation currents (or…”

Section: Key Pointsmentioning

confidence: 99%

“…AUC, area under the curve; N.S., not significant; nSOZ, non-SOZ; Stim, stimulation. Figure adapted from Hays et al 8 and Smith et al 16 voltages) can be used in electrocorticographic electrodes due to the increase in electrode surface area; however, the overall charge density should not exceed approximately 57 μC/cm 2 per phase. 26,27 For example, using stereoelectroencephalographic (SEEG) electrodes with a surface area of approximately .06-.08 cm 219,26 and .15 ms/phase width, a stimulation current up to 10 mA remains at <25 μC/cm 2 /phase.…”

Section: Key Pointsmentioning

confidence: 99%

See 2 more Smart Citations

Stimulation to probe, excite, and inhibit the epileptic brain

et al. 2023

View full text Add to dashboard Cite

Direct cortical stimulation has been applied in epilepsy for nearly a century and has experienced a renaissance, given unprecedented opportunities to probe, excite, and inhibit the human brain. Evidence suggests stimulation can increase diagnostic and therapeutic utility in patients with drug‐resistant epilepsies. However, choosing appropriate stimulation parameters is not a trivial issue, and is further complicated by epilepsy being characterized by complex brain state dynamics. In this article derived from discussions at the ICTALS 2022 Conference (International Conference on Technology and Analysis for Seizures), we succinctly review the literature on cortical stimulation applied acutely and chronically to the epileptic brain for localization, monitoring, and therapeutic purposes. In particular, we discuss how stimulation is used to probe brain excitability, discuss evidence on the usefulness of stimulation to trigger and stop seizures, review therapeutic applications of stimulation, and finally discuss how stimulation parameters are impacted by brain dynamics. Although research has advanced considerably over the past decade, there are still significant hurdles to optimizing use of this technique. For example, it remains unclear to what extent short timescale diagnostic biomarkers can predict long‐term outcomes and to what extent these biomarkers add information to already existing biomarkers from passive electroencephalographic recordings. Further questions include the extent to which closed loop stimulation offers advantages over open loop stimulation, what the optimal closed loop timescales may be, and whether biomarker‐informed stimulation can lead to seizure freedom. The ultimate goal of bioelectronic medicine remains not just to stop seizures but rather to cure epilepsy and its comorbidities.

show abstract

Anti-Hu associated paraneoplastic upper and lower motor neuropathy triggered by atezolizumab

Jovanovski,

Mengert,

Lukacs

et al. 2024

Neurol Sci

View full text Add to dashboard Cite

Cortico-cortical evoked potentials in response to varying stimulation intensity improves seizure localization

Cited by 11 publications

References 51 publications

Quantifying trial‐by‐trial variability during cortico‐cortical evoked potential mapping of epileptogenic tissue

Quantifying trial‐by‐trial variability during cortico‐cortical evoked potential mapping of epileptogenic tissue

Stimulation to probe, excite, and inhibit the epileptic brain

Anti-Hu associated paraneoplastic upper and lower motor neuropathy triggered by atezolizumab

Contact Info

Product

Resources

About