Does the region of epileptogenicity influence the pattern of change in cortical excitability?

Badawy, Radwa A.B.; Vogrin, Simon; Lai, Alan; Cook, Mark

doi:10.1016/j.clinph.2014.05.029

Cited by 14 publications

(43 citation statements)

References 54 publications

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“…The re-digitalized curves are shown in Fig. 1A; (ii) The curve of the new-onset temporal lobe epilepsy group, based on six subjects (Badawy et al, 2013a), appears the same as the one from a report based on 10 subjects (Badawy et al, 2015) (Fig. 1B); and (iii) The curve from the group with new onset generalized epilepsy with tonic-clonic seizures only (n = 7) (Badawy et al, 2013a), appears the same as the curve of the same patient group with a different sample size (n = 12) (Badawy et al, 2013b) and as the curve of the new-onset generalized epilepsy group with tonic-clonic, myoclonic and/or absence seizures (n = 20) (Badawy et al, 2014) (Fig.…”

Section: Sirmentioning

confidence: 62%

“…We read with interest the report by Badawy et al (2013a) highlighting changes in cortical excitability in subjects with epilepsy and their siblings. It adds to the body of work of this group consistently showing that cortical excitability, measured by transcranial magnetic stimulation (TMS) may have potential as an epilepsy biomarker (Badawy and Jackson, 2012;Badawy et al, 2013bBadawy et al, , 2014Badawy et al, , 2015. Responses to TMS were shown to have a relatively large interindividual variability (see for example Valls-Solé et al, 1992;Du et al, 2014).…”

Section: Sirmentioning

confidence: 99%

See 1 more Smart Citation

Transcranial magnetic stimulation as a biomarker for epilepsy

Bauer

Goede

Braack

et al. 2017

Brain

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Section: Sirmentioning

confidence: 62%

Section: Sirmentioning

confidence: 99%

Transcranial magnetic stimulation as a biomarker for epilepsy

Bauer

Goede

Braack

et al. 2017

Brain

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“…In epilepsy, LICI was mainly studied by one group of investigators who, in several studies, showed facilitation instead of inhibition at ISIs of 50, 150, 250 and 300 ms in groups of drug-naïve subjects with different types of genetic generalized epilepsy (Brodtmann et al, 1999;Badawy et al, 2007Badawy et al, , 2010bBadawy et al, , 2013Badawy et al, , 2013bBadawy et al, , c, 2014. In drug-naïve focal epilepsy, cortical excitability was consistently increased in the hemisphere ipsilateral to the epileptic focus, but not in the contralateral hemisphere, at ISIs 250 and 300 ms (Badawy et al, 2007(Badawy et al, , 2010b(Badawy et al, , 2013(Badawy et al, , 2013a(Badawy et al, , b, d, 2014(Badawy et al, , 2015. In successfully treated epilepsy, hyperexcitability normalized over time in seizure-free groups, becoming more similar to controls, but it remained increased in refractory groups (Badawy et al, 2010a(Badawy et al, , 2013(Badawy et al, , 2013c.…”

Section: Introductionmentioning

confidence: 99%

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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“…This finding revealed the characteristics of cortical hyperexcitability in different types of patients and indicated that this abnormality was reversible under certain conditions (28). The motor cortical excitability was influenced in varying degrees by most focal epilepsy syndromes, regardless the epileptogenic foci (29,46). Cortical excitability of patients with juvenile myoclonic epilepsy was higher than that of either the juvenile absence epilepsy or generalized epilepsy with tonic-clonic seizures, while all three types of epilepsy caused significant cortical hyperexcitability (30,45).…”

Section: Cortical Excitability Measurementmentioning

confidence: 78%

A facilitation tool: transcranial magnetic stimulation in epilepsy research

Zhou

2016

Eur J Bio Med Res

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Transcranial magnetic stimulation (TMS) is a noninvasive and relatively safe method to modulate the cortical activities and thus becomes popular in clinical research such as epilepsy studies. These studies mainly focus on the use of paired-pulse TMS as biomarkers and the effects of repetitive TMS (rTMS) in epilepsy treatment. Paired-pulse TMS measures the cortical excitability under different pathological circumstances by deriving and analyzing paired-pulse recovery curve, which has been proved reliable and widely used to study the physiological and pharmacological mechanisms in epilepsy. rTMS is able to modulate the brain functions and has been considered as a potential treatment for epilepsy, yet the evidence is insufficient and further exploration is required. This review intends to examine the methodologies and outcomes presented by relevant studies and to discuss the pros and cons of current TMS research. This review gives a brief introduction to background and principle of TMS. It reviews the methods measuring cortical excitability and the key findings in accordance with the mechanisms of epilepsy. It also reviews the existing controlled studies in therapeutic effectiveness of rTMS and analyzes the advantages of different designs and parameter choices.In the end, this review suggests directions for future research.

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Does the region of epileptogenicity influence the pattern of change in cortical excitability?

Cited by 14 publications

References 54 publications

Transcranial magnetic stimulation as a biomarker for epilepsy

Transcranial magnetic stimulation as a biomarker for epilepsy

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

A facilitation tool: transcranial magnetic stimulation in epilepsy research

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