Transcranial magnetic stimulation as a biomarker for epilepsy

Bauer, Prisca R.; Goede, Annika A. de; Braack, Esther Maria Spanjer-ter; Putten, Michel J.A.M. van; Gill, Richard D.; Sander, Josemir W.

doi:10.1093/brain/aww345

Cited by 15 publications

(8 citation statements)

References 9 publications

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“…Our retrospective study design did not allow us to go into such detail, limiting the comparison with these studies. It should be noted that the participant cohorts reported in previous studies appear to overlap, potentially leading to multiple publication bias and overestimation of the consistency of these findings (Brigo et al, 2012;Badawy et al, 2017;Bauer et al, 2017).…”

Section: Discussionmentioning

confidence: 97%

Long-interval intracortical inhibition as biomarker for epilepsy: a transcranial magnetic stimulation study

Bauer

Goede

Stern

et al. 2018

Brain

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Cortical excitability, as measured by transcranial magnetic stimulation combined with electromyography, is a potential biomarker for the diagnosis and follow-up of epilepsy. We report on long-interval intracortical inhibition data measured in four different centres in healthy controls (n = 95), subjects with refractory genetic generalized epilepsy (n = 40) and with refractory focal epilepsy (n = 69). Long-interval intracortical inhibition was measured by applying two supra-threshold stimuli with an interstimulus interval of 50, 100, 150, 200 and 250 ms and calculating the ratio between the response to the second (test stimulus) and to the first (conditioning stimulus). In all subjects, the median response ratio showed inhibition at all interstimulus intervals. Using a mixed linear-effects model, we compared the long-interval intracortical inhibition response ratios between the different subject types. We conducted two analyses; one including data from the four centres and one excluding data from Centre 2, as the methods in this centre differed from the others. In the first analysis, we found no differences in long-interval intracortical inhibition between the different subject types. In all subjects, the response ratios at interstimulus intervals 100 and 150 ms showed significantly more inhibition than the response ratios at 50, 200 and 250 ms. Our second analysis showed a significant interaction between interstimulus interval and subject type (P = 0.0003). Post hoc testing showed significant differences between controls and refractory focal epilepsy at interstimulus intervals of 100 ms (P = 0.02) and 200 ms (P = 0.04). There were no significant differences between controls and refractory generalized epilepsy groups or between the refractory generalized and focal epilepsy groups. Our results do not support the body of previous work that suggests that long-interval intracortical inhibition is significantly reduced in refractory focal and genetic generalized epilepsy. Results from the second analysis are even in sharper contrast with previous work, showing inhibition in refractory focal epilepsy at 200 ms instead of facilitation previously reported. Methodological differences, especially shorter intervals between the pulse pairs, may have contributed to our inability to reproduce previous findings. Based on our results, we suggest that long-interval intracortical inhibition as measured by transcranial magnetic stimulation and electromyography is unlikely to have clinical use as a biomarker of epilepsy.

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Section: Discussionmentioning

confidence: 97%

Long-interval intracortical inhibition as biomarker for epilepsy: a transcranial magnetic stimulation study

Bauer

Goede

Stern

et al. 2018

Brain

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“…TMS studies on motor cortex excitability, using muscle responses as indirect readout, noted decreased (134,135), increased (102,136) as well as unaltered (137,138) motor thresholds, thus yielding inconclusive evidence for hyper- or hypo-excitability in this region (89). Combining TMS with EEG (139) could provide direct and objective markers of cortical responsivity including changes in network excitation or inhibition as shown for studies in epilepsy (140,141) but not yet applied in migraine.…”

Section: Clinical Neurophysiology Studies On Cortical Function In Migmentioning

confidence: 99%

Current understanding of cortical structure and function in migraine

2019

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ObjectiveTo review and discuss the literature on the role of cortical structure and function in migraine.DiscussionStructural and functional findings suggest that changes in cortical morphology and function contribute to migraine susceptibility by modulating dynamic interactions across cortical and subcortical networks. The involvement of the cortex in migraine is well established for the aura phase with the underlying phenomenon of cortical spreading depolarization, while increasing evidence suggests an important role for the cortex in perception of head pain and associated sensations. As part of trigeminovascular pain and sensory processing networks, cortical dysfunction is likely to also affect initiation of attacks.ConclusionMorphological and functional changes identified across cortical regions are likely to contribute to initiation, cyclic recurrence and chronification of migraine. Future studies are needed to address underlying mechanisms, including interactions between cortical and subcortical regions and effects of internal (e.g. genetics, gender) and external (e.g. sensory inputs, stress) modifying factors, as well as possible clinical and therapeutic implications.

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“…The GABAergic system is complex and remains a focus of research; used optimally, TMS could contribute to elucidating GABAergic changes in disease. Overall, with expanding use of these measures, and previously voiced concerns, 97 it would be prudent to establish community standards for protocols and quality control.…”

Section: Discussionmentioning

confidence: 99%