O13 Exploring the modulators of cortical excitability

O13 Exploring the modulators of cortical excitability

e184 Abstracts / Clinical Neurophysiology 128 (2017) e178–e303 O13 Exploring the modulators of cortical excitability—Annika De Goede 1, Michel Van P...

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e184

Abstracts / Clinical Neurophysiology 128 (2017) e178–e303

O13 Exploring the modulators of cortical excitability—Annika De Goede 1, Michel Van Putten 2 (1 University of Twente, Clinical Neurophysiology, Enschede, The Netherlands, 2 University of Twente and Medisch Spectrum Twente, Department of Clinical Neurophysiology and Neurology, Enschede, The Netherlands) Objectives: Fluctuations in cortical excitability is a candidate mechanism involved in the trial-to-trial variation of motor evoked potentials (MEPs) to transcranial magnetic stimulation. We explore if oscillations in the infraslow (0.01–0.1 Hz), delta, theta, alpha and beta frequency bands are possible modulators of cortical excitability. Methods: In ten healthy subjects 200 single pulses were given at the resting motor threshold. Induced motor responses were either regarded as present (MEP amplitude > 50 lV) or absent. Temporal clustering of MEP presence/absence was tested (a = 0.05) using 1 random generated surrogates with a similar presence/absence distribution. Secondly, the phases at stimulation were extracted for each frequency band using the Hilbert transform and divided into 18 equal bins between – p and p. For each phase bin, we determined the absolute value of the difference in percentage MEP presence and MEP absence. We compared the sum over all bins to the sums obtained in surrogates. If the sum was larger than the 75th percentile in surrogates, moderate coupling between phase and MEP presence/absence was assumed. For a sum larger than the 95th percentile, coupling was assumed to be strong. Results: In all ten subjects we found significant temporal clustering of MEP presence/absence. In 30% of the subjects we found moderate, and in 10% strong, coupling between the phase of the infraslow frequency and MEP presence/absence. For the delta/theta/alpha/beta frequency bands coupling was moderate in 40%/20%/20%/30% of the subjects and strong in 20%/50%/30%/10% of the subjects, respectively. Discussion: Temporal clustering of MEP presence/absence suggests oscillatory modulation of cortical excitability instead of randomly generated fluctuations. Our results do not provide strong evidence for one specific oscillatory frequency. Conclusions: Oscillations in the infraslow, delta, theta, alpha and beta frequency band are all possible modulators of cortical excitability. Significance: Gaining insight into the oscillations modulating cortical excitability might provide possibilities to reduce the large trialto-trial variation, as stimulation can be targeted at a specific oscillatory phase. Keywords: Cortical excitability, Transcranial magnetic stimulation, TMS, Phase-amplitude coupling, Trial-to-trial variability doi:10.1016/j.clinph.2017.07.024

O14 Altered recovery from inhibitory repetitive transcranial magnetic stimulation (RTMS) in subjects with photosensitive epilepsy—Tommaso Bocci 1, Matteo Caleo 2, Laura Restani 2, Davide Barloscio 1, Laura Parenti 1, Simone Rossi 3, Ferdinando Sartucci 1 (1 University of Pisa, Department of Clinical and Experimental Medicine, Pisa, Italy, 2 University of Pisa, National Research Council, Pisa, Italy, 3 University of Siena, Department of Neurological and Neurosensorial Sciences, Siena, Italy) Objective: To investigate functional changes underlying photosensitivity, we studied the response of the visual cortex to lowfrequency, inhibitory repetitive transcranial magnetic stimulation (rTMS) in patients with photosensitive seizures and healthy volunteers.

Methods: Visual evoked potentials (VEPs) triggered by grating stimuli of different contrasts were recorded in both hemispheres before and after inactivation of the occipital cortex of one side via low-frequency rTMS (0.5 Hz, 120 % RMT, 200 ). VEPs were recorded before (T0), immediately after (T1) and 450 following rTMS (T2). The display was either centered on the vertical meridian (central stimulation) or positioned in the right hemifield (with its inner edge at a distance of 1 degree from the fixation point). Results: Baseline amplitudes of the VEP components (N1 and P1) were enhanced in photosensitive patients. At T1, rTMS produced an inhibitory effect on VEPs amplitudes at all contrasts in the targeted side and a concurrent facilitation of responses in the contralateral hemisphere. Compared with PSE subjects, VEP amplitudes remained persistently dampened in the stimulated hemisphere of controls (Holm-Sidak post hoc method, p < 0.05). In the contralateral hemisphere, we found a clear enhancement of VEP amplitude in photosensitive subjects but not controls at T2 (Holm-Sidak test, p < 0.001). Conclusions: The rapid recovery of excitability and the persistent transcallosal disinhibition following perturbation of cortical activity may play a role in the pathophysiology of photosensitive epilepsy. Significance: beyond the stereotyped dichotomy between generalized and focal epilepsies, both sets of data seem to indicate PSE as a ‘‘system disease”. Keywords: Photosensitive epilepsy, Corpus callosum, Generalized epilepsies, Transcranial magnetic stimulation, Visual system doi:10.1016/j.clinph.2017.07.025

O15 Long term follow-up study with non-invasive brain stimulation (NBS) (rTMS and TDCS) in parkinson’s disease. strong age dependency in the effect of NBS—Judit Málly 1, Noémi Geisz 1, Elek Dinya 2 (1 Institute of Neurorehabilitation, Sopron, Hungary, 2 Digital Health Department of Semmelweis University, Budapest, Hungary) Parkinson’s disease (PD) produces progressive declines throughout the patient’s life. Its development is not linear and can not be effectively influenced by drugs. Repetitive transcranial magnetic stimulation (rTMS) may slower the progression of the disease compared with dopa substitution (Málly, 2004). The long term mind modification effect of regularly repeated rTMS and tDCS is not known. The predictors for the treatment with non-invasive brain stimulation are not known. In our study we followed 30 patients with PD for 3.5 years. Patients were stimulated with rTMS (1 Hz, low intensity for 7 days), which was repeated every half year for one and half year. After stimulation with 1 Hz the transcranial direct current stimulation (tDCS) over both sides of cerebellum was introduced for the next 2 years as add on therapy to rTMS. Motor disability was assessed by UPDRS and the executive function was measured by Trail Making Test and dual tests. There was a highly significant difference in the deterioration of patients in motor disability 665 yrs and >65 yrs (p < 0.001). Motor disability 665 yrs assessed by UPDRS (onset of the treatment: 19.2 ± 12.4, the end of rTMS: 17.0 ± 7.3, the end of tDCS for 2 years: 17.3 ± 8.8) progression rate 0.13421. The progression above 65 yrs onset of treatment (18.2 ± 7.3, the end of rTMS: 23.2 ± 12.3, the end of tDCS for 2 years: 27.7 ± 13.0, progression rate: 0.23217). The Trail Making test B-A was significantly worse in PD over 65 yrs compared to age match controls and patients with PD under 65 yrs (PD 665 yrs: 30.3 ± 8.3 s, PD > 65 yrs: 62.2 ± 8.1 p < 0.0001).