ライフサイエンスコーパス: TMS

1 TMS at 5 Hz was delivered, in up to 40 daily sessions, t

2 TMS combined with electroencephalography (TMS-EEG) affor

3 TMS delivered at a particular phase of the beta oscillat

4 TMS entrained oscillations, i.e., increased high-beta po

5 TMS inputs arriving at the excitable phase of beta oscil

6 TMS is a method that can be used to assess cortical moto

7 TMS is a noninvasive procedure that reliably and selecti

8 TMS over both SI and V5/hMT+, but not the PPC site, sign

9 TMS over EVC and LOC allowed determining whether these t

10 TMS over the cerebellum produced maximal CBI of PA-evoke

11 TMS parameters were similar to those used in rat infrali

12 TMS studies have provided important pathophysiological i

13 TMS was applied to one of two targets in the left fronta

14 TMS was delivered 10 ms before the end of TUS to the lef

15 TMS was delivered to the motor cortex of healthy human s

16 TMS was either provided after each trial of the ramp pha

17 TMS was given on each trial before stimulus onset either

18 TMS was used to induce controlled perturbations to indiv

19 TMS-EEG waveforms were analyzed through global mean fiel

20 TMS-evoked responses related to phosphene perception wer

21 otation), [Fe(NO)((TMS)PS2)((TMS)PS2H)] (1, (TMS)PS2H(2) = 2,2'-dimercapto-3,3'-bis(trimethylsilyl)di

22 cyclic chlorosilylene nickel(0) complex 1, [(TMS)L(Cl)Si -> Ni(NHC)(2); NHC = :C[( (i)Pr)NC(Me)](2)).

23 tron [bis(NHC)](silylene)Ni(0) complex 1, [((TMS) L)ClSi:-->Ni(NHC)2 ], bearing the acyclic amido-chl

24 ence of 12-crown-4, the reaction with LiCH(2)TMS yields [Ru(PPh(3))(C(6)H(4)PPh(2))(2)H][Li(12-crown-

25 Reaction of [Ru(PPh(3))(3)HCl] with LiCH(2)TMS, MgMe(2), and ZnMe(2) proceeds with chloride abstrac

26 During extinction learning (day 2), TMS was paired with one of the conditioned cues but not

27 Si=E Ni complexes (nickelacycles), [eta(2)-{(TMS)L(H)Si=E(H)}Ni(NHC)(2)] (E = P, 6; E = As, 9).

28 )H(4), 2-CNC(6)H(4), 2-(CO(2)Me)C(6)H(4), 2-(TMS-C=C)C(6)H(4)) present on anilines can be appended to

29 ms after cue onset, total of four trains (28 TMS pulses).

30 ctron-rich bicyclo[1.1.0]butanes by the CF(3)TMS/NaI system.

31 logation of alkenylboronic acids using CF(3)/TMS-diazomethanes in the presence of BINOL catalyst and

32 non-motor regions where less is known about TMS physiology.

33 After TMS, symptom reduction was associated with reduced conne

34 cally relevant changes in connectivity after TMS, followed by leave-one-out cross-validation.

35 lation and memory tasks also increased after TMS to the left angular gyrus relative to the vertex.

36 TMS-evoked neuronal activity 0.8-1 ms after TMS onset.

37 Although TMS treatment produced a clinically meaningful change in

38 silylene and its heavy P- and As-analogues ((TMS)LSi-EH(2); E = N, P, As; (TMS)L = N(SiMe(3))(2,6- (i

39 ood hexamethyldisilazane (HMDS) additive and TMS(2)S by the conjugate base, lithium bis(trimethylsily

40 (CRF) for all combinations of attention and TMS conditions.

41 outcome, while both global connectivity and TMS/EEG changes tracked clinical outcome.

42 ty and causal excitability, resting fMRI and TMS/EEG were performed before and after the treatment.

43 n at individualized intensity for 20 min and TMS was performed at rest (before, during, and after tAC

44 pable of optimizing the stimulation site and TMS coil orientation.

45 As-analogues ((TMS)LSi-EH(2); E = N, P, As; (TMS)L = N(SiMe(3))(2,6- (i)Pr(2)C(6)H(3))) in the coordi

46 t the sulfur-rich core of the trimeric BACE1 TMS is accessible to metal ions, but copper ions did not

47 Baseline TMS responses were recorded from two intrinsic hand musc

48 We hypothesized that fragments of both TMS(2)S and HMDS had carried out the roles that Bronsted

49 We applied theta-burst TMS to LOC (and a control site) to interfere with an ext

50 e could assess the earliest volley evoked by TMS, and the part 0.6 ms later.

51 gical evaluation of cortical excitability by TMS.

52 (chloro)(silyl)nickel(II) complex 3, {[cat((TMS) L)Si](Cl)Ni<--:BH(NHC)2 }, via the cleavage of two

53 , bearing the acyclic amido-chlorosilylene ((TMS) L)ClSi: ((TMS) L=N(SiMe3 )Dipp; Dipp=2,6-Pr(i)2 C6

54 Clinical TMS for psychiatric applications is advancing rapidly, w

55 alysis of stimulation sites from 14 clinical TMS trials.

56 cyclic amido-chlorosilylene ((TMS) L)ClSi: ((TMS) L=N(SiMe3 )Dipp; Dipp=2,6-Pr(i)2 C6 H4 ) and two NH

57 This combined TMS-fMRI approach provides an opportunity for causal man

58 is not always straightforward as the complex TMS-EEG induced response profile is multi-dimensional.

59 to the acyclic bis(amido)silylene complex [(TMS)L(H(2)N)Si -> Ni(NHC)(2)] 5, which does not undergo

60 controls were also evaluated with concurrent TMS/fMRI.

61 By contrast, TMS measures of cortical excitability and physiological

62 In the control TMS condition, we replicated prior reports of post-encod

63 ther react with [Mn(III)((TMS)PS3)(DABCO)] ((TMS)PS3H(3) = (2,2'2''-trimercapto-3,3',3''-tris(trimeth

64 We conclude that delivering TMS during MI is capable of inducing plastic changes in

65 atible with the idea that applying different TMS currents to the cerebral cortex may reveal cerebella

66 ssive symptoms responded better to different TMS targets across independent retrospective data sets.

67 Overall, we show that directional TMS can probe two distinct cerebellar-cerebral pathways

68 In neurodegenerative disease, TMS has provided novel insights into the function of cor

69 We found a double dissociation: TMS to EBA during the cue period removed validity effect

70 Regulating the evolution of distinctive TMSs is highly desirable but remains challenging to date

71 of anion-regulated evolution of distinctive TMSs, providing a new pathway for enhancing performances

72 wrist flexion or extension movements during TMS delivery (n = 90 trials).

73 Early TMS trials lacked a focal target and thus positioned the

74 t recent studies showing that more effective TMS targets in the frontal cortex are functionally conne

75 etic stimulation and electroencephalography (TMS/EEG) to study cortical reactivity in a cohort of 30

76 TMS combined with electroencephalography (TMS-EEG) affords a window to directly measure evoked act

77 lation combined with electroencephalography (TMS-EEG), breaks down during the loss of consciousness.

78 Behaviorally, post-encoding TMS to LOC selectively impaired associative memory reten

79 This is the first study to evaluate TMS-associated changes in connectivity in patients with

80 Our study examined TMS-EEG responses from the DLPFC in persons with MDD com

81 Specifically, we examined TMS-EEG markers linked to inhibitory and excitatory neur

82 to yield a mononuclear Fe(III) complex, [Fe((TMS)PS2)((TMS)PS2CH(3))] (3).

83 s to the Fe center for the formation of [Fe((TMS)PS2)(2)] (4).

84 framework for the development of RSFC-guided TMS interventions in depression.

85 However, TMS-evoked activity of individual neurons has remained l

86 all of which can be linked to various human TMS responses recorded at the level of spinal cord and m

87 ely after stimulus onset, triple-pulse 10 Hz TMS was delivered either to IPS or FEF on either side of

88 nerated HNO can further react with [Mn(III)((TMS)PS3)(DABCO)] ((TMS)PS3H(3) = (2,2'2''-trimercapto-3,

89 electronic configuration, whereas [Mn(III)((TMS)PS3)(DABCO)] reacts with NO gas for the formation of

90 e is achieved by the employment of [Mn(III)((TMS)PS3)(DABCO)].

91 D participants demonstrated abnormalities in TMS-EEG markers in the DLPFC.

92 ty, and (3) local and distributed changes in TMS/EEG potentials.

93 as yet unidentified ascaroside components in TMS-derivatized crude nematode exometabolome extracts.

94 ase, all muscles showed similar increases in TMS responses.

95 olution of this role with the supply of S in TMS(2)S caused the iron sulfide impurities.

96 drug condition, frequency, time and space in TMS-induced oscillations.

97 irmed a previous finding in which individual TMS SI1mV (stimulus intensity for 1 mV MEP amplitude) se

98 l magnetic stimulation (TMS), by interacting TMS with stimulation of the median nerve generating an H

99 Intermittent TMS-theta burst stimulation was used to probe long-term

100 d DCC mRNA expression, increased ipsilateral TMS-induced motor evoked potentials, increased fMRI resp

101 mained largely inaccessible due to the large TMS-induced electromagnetic fields.

102 ected the occurrence of prominent sleep-like TMS-evoked slow waves and off-periods-reflecting transie

103 However, post-encoding LOC TMS reduced these processes, such that post-encoding rea

104 Although many TMS targeting methods that use figure-8 coils exist, man

105 1990s, shortly after the invention of modern TMS in 1985 by Barker.

106 those randomly assigned to active NeuroStar TMS monotherapy (n = 48) or sham TMS (n = 55) for 30 dai

107 le proton) with a pendant thiol and [Fe(NO)((TMS)PS2)((TMS)PS2CH(3))] (2) bearing a pendant thioether

108 xes (the Enemark-Felthan notation), [Fe(NO)((TMS)PS2)((TMS)PS2H)] (1, (TMS)PS2H(2) = 2,2'-dimercapto-

109 e formation of a {MnNO}(5) species, [Mn(NO)((TMS)PS3)] (6).

110 ) in organic media to yield anionic [Mn(NO)((TMS)PS3)](-) (5(-)) with a {MnNO}(6) electronic configur

111 notion was supported by previous noninvasive TMS studies of human motor cortex indicating a reduction

112 he alpha band (8-13 Hz), predicted occipital TMS phosphenes, whereas higher-frequency beta-band (13-2

113 mmarize the different uses and challenges of TMS in mental chronometry, perception, awareness, learni

114 o response and examine the optimal dosing of TMS for adolescents with TRD.

115 For comparison purposes, the effect of TMS over M1 was monitored when subjects tracked an exter

116 However, the strongest effects of TMS applied over EVC occurred later than those of LOC, s

117 flex conditioning and directional effects of TMS), we show that a specific set of excitatory inputs t

118 id not differ statistically as a function of TMS site (i.e., number of free associates produced or di

119 Our findings support the introduction of TMS measures in clinical and research settings to monito

120 te of our understanding of the mechanisms of TMS in the context of designing and interpreting psychol

121 Furthermore, the temporal order of TMS effects allowed inferences on the dynamics of inform

122 e assessed the classification performance of TMS parameters in the differential diagnosis of common n

123 Findings illustrate the potential of TMS-EEG perturbation-based biomarkers to characterize ne

124 twork, and salience network as predictors of TMS response and suggest their involvement in mechanisms

125 accuracy, precision, recall, and F1 score of TMS in differentiating each neurodegenerative disorder.

126 ificantly correlated with the specificity of TMS propagation patterns across DAN and DMN, but not wit

127 istent with previous neuroimaging studies of TMS, default mode network connectivity played an importa

128 ed in a randomized, sham-controlled trial of TMS across 13 sites.

129 neglected previously in the construction of TMSs.

130 , there are often multiple existing forms of TMSs, which are of different natures and catalytic model

131 y spiking within the first 6 ms depending on TMS-induced current orientation and a multiphasic spike-

132 We validated reliability of PARAFAC on TMS-induced oscillations before extracting the features

133 One TMS experiment, conducted in a relatively small sample (

134 Online TMS over rTPJ also impacted on participants' explicit be

135 ctivity might be used to identify an optimal TMS target for use in all patients and potentially even

136 rotocols tested the impact of imagination or TMS alone.

137 ulation using ulnar nerve stimulation and PA TMS pulses over M1, a protocol used in human studies to

138 n of phosphenes after occipital and parietal TMS.

139 eye movement (NREM) sleep following parietal TMS.

140 Hz) power (but not phase) predicted parietal TMS phosphenes.

141 with a pendant thiol and [Fe(NO)((TMS)PS2)((TMS)PS2CH(3))] (2) bearing a pendant thioether, are spec

142 mononuclear Fe(III) complex, [Fe((TMS)PS2)((TMS)PS2CH(3))] (3).

143 nemark-Felthan notation), [Fe(NO)((TMS)PS2)((TMS)PS2H)] (1, (TMS)PS2H(2) = 2,2'-dimercapto-3,3'-bis(t

144 Single- and double-pulse TMS evaluation included measurement of the input-output

145 Online double-pulse TMS over rTPJ 300 ms (but not 50 ms) after target appear

146 -time EEG-triggered single- and paired-pulse TMS in healthy humans of both sexes to assess corticospi

147 Single pulse TMS was administered over the left motor cortex, using a

148 ency disturbance of grip force, single-pulse TMS should also quickly disrupt ongoing eye motion.

149 We translated human single-pulse TMS to rodents and unveiled time-grained evoked activiti

150 We delivered single-pulse TMS to the motor cortex of healthy human volunteers (10

151 healthy participants underwent single-pulse TMS-EEG to assess inhibition and excitation from DLPFC.

152 For 2a (R = TMS), a 1,3-silyl shift gave an intermediary disilene, w

153 d study, intermittent theta-burst rapid rate TMS was applied instead of PAS.

154 d purely by cortical stimulation (rapid rate TMS).

155 Recent TMS work has also revealed markers of motor inhibition d

156 in anxiety expression using 10 Hz repetitive TMS (rTMS).

157 The effect of rhythmic TMS on WM performance was dependent on whether the TMS f

158 Each patient's TMS site was mapped to underlying brain circuits using f

159 cortex was not different than following sham TMS stimulation.

160 e NeuroStar TMS monotherapy (n = 48) or sham TMS (n = 55) for 30 daily treatments over 6 weeks.

161 arge neutral zwitterionic compounds [(Ge9{Si(TMS)3}2)(t)Bu2P]M(NHC(Dipp)) (M: Cu, Ag, Au) (4-6), in w

162 ction with the bis-silylated cluster [Ge9{Si(TMS)3}2](2)(-) yields the novel cluster compound [Ge9{Si

163 ated clusters [Ge9{Si(TMS)3}3](-) or [Ge9{Si(TMS)3}2](2-) with dialkylhalophosphines R2PCl (Cy, (i)Pr

164 -) yields the novel cluster compound [Ge9{Si(TMS)3}2P(t)Bu2](-) (3).

165 sphine (t)Bu2PCl does not react with [Ge9{Si(TMS)3}3](-) due to steric crowding.

166 Reactions of silylated clusters [Ge9{Si(TMS)3}3](-) or [Ge9{Si(TMS)3}2](2-) with dialkylhalophos

167 roups and the tris-silylated cluster [Ge9{Si(TMS)3}3](-) yield the novel neutral cluster compounds [G

168 the novel neutral cluster compounds [Ge9{Si(TMS)3}3PR2] (R: Cy (1), (i)Pr (2)) with discrete Ge-P ex

169 f M1 using an online MRI-guided simultaneous TMS-tACS approach.

170 ition of the left amygdala induced by single TMS pulses to the right dorsolateral prefrontal cortex;

171 troduction of active transition metal sites (TMSs) in carbon enables the synthesis of noble-metal-fre

172 hira reaction utilizing CsF-mediated in situ TMS-alkyne desilylation followed by Sonogashira coupling

173 n a generalized approach to subject-specific TMS targeting that is capable of optimizing the stimulat

174 , side effects were consistent with standard TMS, and blinding was successful.

175 on transcranial magnetic brain stimulation (TMS) in healthy human subjects.

176 ivity via transcranial magnetic stimulation (TMS) abolished the adaptation of M100 attenuation, while

177 combining transcranial magnetic stimulation (TMS) and electroencephalography (EEG), we investigated t

178 combined transcranial magnetic stimulation (TMS) and fMRI to test the role of awake consolidation pr

179 tex using transcranial magnetic stimulation (TMS) and measured the impact of these disruptions on aud

180 RI-guided transcranial magnetic stimulation (TMS) and simultaneous electroencephalography (EEG) to ch

181 Transcranial magnetic stimulation (TMS) at beta frequency has previously been shown to incr

182 pled to a transcranial magnetic stimulation (TMS) coil.

183 gle-pulse transcranial magnetic stimulation (TMS) concurrent with fMRI to examine whether predictive

184 or random transcranial magnetic stimulation (TMS) delivered to the right Frontal Eye Field (FEF) prio

185 preceding transcranial magnetic stimulation (TMS) each significantly predicted motor-evoked potential

186 of 10-Hz transcranial magnetic stimulation (TMS) for adolescents with TRD.

187 refrontal transcranial magnetic stimulation (TMS) for treatment of depression (discovery sample, N=30

188 Transcranial magnetic stimulation (TMS) has been suggested as a reliable, noninvasive, and

189 rhythmic transcranial magnetic stimulation (TMS) in either theta or alpha frequency to prefrontal an

190 he use of transcranial magnetic stimulation (TMS) in the study of psychological functions has entered

191 CM with a transcranial magnetic stimulation (TMS) intervention that transiently perturbed the LPFC.

192 focus of transcranial magnetic stimulation (TMS) investigational studies.

193 Transcranial magnetic stimulation (TMS) is a noninvasive method to stimulate the cerebral c

194 Transcranial magnetic stimulation (TMS) is an accessible, non-invasive technique to study c

195 Transcranial magnetic stimulation (TMS) is an effective treatment for depression but is lim

196 Transcranial magnetic stimulation (TMS) measures of corticospinal excitability, GABA(A) (sh

197 ation and transcranial magnetic stimulation (TMS) of fM1 was 15-30 ms.

198 ften used transcranial magnetic stimulation (TMS) of hand motor cortex (M1) as a model, but in this m

199 Transcranial magnetic stimulation (TMS) of human occipital and posterior parietal cortex ca

200 tained by transcranial magnetic stimulation (TMS) of M1 using an online MRI-guided simultaneous TMS-t

201 oint with transcranial magnetic stimulation (TMS) of the motor cortex generated plastic changes in mo

202 ility via transcranial magnetic stimulation (TMS) of the primary motor cortex and the measurement of

203 rectional transcranial magnetic stimulation (TMS) over M1.

204 means of transcranial magnetic stimulation (TMS) over the hand area of the primary motor cortex (M1)

205 pulses of transcranial magnetic stimulation (TMS) over the primary motor cortex (M1) appear to activa

206 red-pulse transcranial magnetic stimulation (TMS) protocols to evaluate the excitation index, a bioma

207 Transcranial magnetic stimulation (TMS) represents a novel approach to PTSD, and intermitte

208 clinical transcranial magnetic stimulation (TMS) since the mid-1990s, shortly after the invention of

209 epetitive transcranial magnetic stimulation (TMS) therapy can modulate pathological neural network fu

210 RI-guided transcranial magnetic stimulation (TMS) to assess whether temporary disruption of hippocamp

211 RI-guided transcranial magnetic stimulation (TMS) to assess whether temporary disruption of the left

212 by using transcranial magnetic stimulation (TMS) to block consolidation, we report the first direct

213 , we used transcranial magnetic stimulation (TMS) to briefly alter cortical excitability and determin

214 gnals and transcranial magnetic stimulation (TMS) to deliver information noninvasively to the brain.

215 , we used transcranial magnetic stimulation (TMS) to evaluate the causal role of two key regions of t

216 ffered by transcranial magnetic stimulation (TMS) to explore the impact of pre-morbid individual diff

217 tion with transcranial magnetic stimulation (TMS) to induce plasticity in the human motor system.

218 gle-pulse transcranial magnetic stimulation (TMS) to interfere with postmovement activity in M1 in tw

219 , we used transcranial magnetic stimulation (TMS) to measure cortical inhibition/excitation (n = 51),

220 , we used transcranial magnetic stimulation (TMS) to probe the excitability of distinct sets of excit

221 ice-daily transcranial magnetic stimulation (TMS) to the cerebellar midline.

222 ble-pulse transcranial magnetic stimulation (TMS) while moving a single tactile point across the fing

223 ng online transcranial magnetic stimulation (TMS) with computational modeling of behavioral responses

224 sponse to transcranial magnetic stimulation (TMS) with electroencephalography (EEG) offers unique ins

225 Using transcranial magnetic stimulation (TMS), 25 motor-evoked potentials (MEPs) were recorded be

226 icited by transcranial magnetic stimulation (TMS), by interacting TMS with stimulation of the median

227 reaction, transcranial magnetic stimulation (TMS), functional magnetic resonance imaging (fMRI) under

228 RMT) with transcranial magnetic stimulation (TMS), is known to be associated with chronic pain condit

229 h ECT and transcranial magnetic stimulation (TMS), offering a new framework for the development of RS

230 probed by transcranial magnetic stimulation (TMS).

231 ons using transcranial magnetic stimulation (TMS).

232 ed online transcranial magnetic stimulation (TMS).

233 ses using transcranial magnetic stimulation (TMS).

234 ing using transcranial magnetic stimulation (TMS).

235 navigated transcranial magnetic stimulation (TMS).

236 SE) using transcranial magnetic stimulation (TMS).

237 s such as transcranial magnetic stimulation (TMS).

238 LOC and OPA: relative to vertex stimulation, TMS over LOC selectively impaired the recognition of obj

239 In stroke, TMS methodology has facilitated the understanding of cor

240 in the targeted regions predicted subsequent TMS effects across subjects supporting a model by which

241 Observers received two successive TMS pulses around their occipital pole while the stimuli

242 TUS safely suppressed TMS-elicited motor cortical activity, with longer sonica

243 Using a combined tACS-TMS approach, we demonstrate that driving gamma frequenc

244 s provide evidence that hippocampal-targeted TMS can specifically modulate episodic simulation and di

245 STATEMENT The present work demonstrates that TMS disruption of M1 activity impairs the consolidation

246 and a preregistered protocol, we found that TMS over object-selective cortex (lateral occipital comp

247 Results indicated that TMS over the right FEF significantly reduced the behavio

248 Results revealed that TMS did not influence adaptation to the new visuomotor r

249 ta from 20 humans (13 females) revealed that TMS over both EVC and LOC impaired illusory size percept

250 tatus, stimulation, and word type, such that TMS increased the disadvantage for spelling-sound atypic

251 As the TMS-EEG waveform and its components index inhibitory and

252 sed as a general method to optimize both the TMS coil site and its orientation.

253 natomical scans of each subject to guide the TMS coil, starting at 25% of maximum stimulator output (

254 facilitates a new level of insight into the TMS-brain interaction that is vital for developing this

255 methods allow for precise positioning of the TMS coil over a specific brain location, but leveraging

256 elective modulation of the later part of the TMS volley, as expected if this part of the volley is se

257 atographic fingerprint characteristic of the TMS-4,4'-desmetylsterol derivative fraction of several m

258 acked a focal target and thus positioned the TMS coil over the prefrontal cortex using scalp measurem

259 WM performance was dependent on whether the TMS frequency matched or mismatched the expected underly

260 ng altered size representations in EVC, then TMS effects over EVC should be observed simultaneously o

261 Therefore, TMS extinguished the effect of exogenous attention.

262 We used near-threshold TMS with concurrent EEG recordings to measure how oscill

263 tution by cyanide upon treatment with TMSCN (TMS=trimethylsilyl).

264 irect in vivo electrophysiological access to TMS-evoked neuronal activity 0.8-1 ms after TMS onset.

265 There were no overall changes to TMS measured GABAergic inhibition with this low dose of

266 Analyses used a priori seeds relevant to TMS, posttraumatic stress disorder, or MDD (subgenual an

267 The EEG response to TMS stimulation is altered by drugs active in the brain,

268 reliability, inter-individual sensitivity to TMS accounted for a modest percentage of the variance in

269 discusses the application of trimethylsilyl (TMS)-4,4'-desmethylsterols derivatives chromatographic f

270 ) (PEOH), was silylated with trimethylsilyl (TMS) groups followed by cross-linking with a bis-silyl e

271 For each of two TMS sessions, continuous theta-burst stimulation (cTBS)

272 isease Rating Scale total motor score [UHDRS-TMS] >=25 points), and reduced independence (UHDRS indep

273 idine did not significantly change the UHDRS-TMS at 26 weeks compared with placebo at any dose.

274 Pridopidine did not improve the UHDRS-TMS at week 26 compared with placebo and, thus, the resu

275 ry efficacy endpoint was change in the UHDRS-TMS from baseline to 26 weeks, which was assessed in all

276 However, the mechanisms underlying TMS-evoked EEG potentials (TEPs) remain largely unknown.

277 All patients underwent TMS assessment at recruitment (index test), with applica

278 paration, focusing on studies that have used TMS to monitor changes in the excitability of the cortic

279 We used TMS to quantify motor cortical excitability and physiolo

280 of cortical function measures obtained using TMS and how such measures may provide insight into brain

281 ceptual advances in behavioral studies using TMS.

282 her, we built group-level maps that weighted TMS-induced electric fields and diffusion magnetic reson

283 This effect did not take place when TMS was delivered over adjacent dorsal premotor cortex o

284 d Parkinson's disease are key examples where TMS has led to advances in understanding of disease path

285 reduced skin conductance responses, whereas TMS to target 2 had no effect.

286 our understanding of the mechanism by which TMS exerts its antidepressant effect is minimal.

287 y impaired the recognition of objects, while TMS over OPA selectively impaired the recognition of sce

288 lectively impaired object recognition, while TMS over scene-selective cortex (occipital place area) s

289 oms of both disorders can be alleviated with TMS therapy.

290 Restoration of network connectivity with TMS corresponded to amelioration of negative symptoms, s

291 g motor point stimulation of FDS or EDC with TMS.

292 Combined with hydrodechlorination with TMS(3)SiH, direct chlorination provides access to five o

293 Extensor imagination with TMS increased MEPs in extensor muscles only.

294 Flexion imagination with TMS increased MEPs in flexors and an intrinsic hand musc

295 tinction recall (day 3), the cue paired with TMS to target 1 showed significantly reduced skin conduc

296 e then combined the adaptation paradigm with TMS.

297 an be reliably and selectively targeted with TMS, even when defined based on group-average fMRI coord

298 complex LPt(IV)F(2)(Ar)(py) is treated with TMS-X (TMS = trimethylsilyl; X= NMe(2), SPh, OPh, CCPh)

299 s of various targeted reactions related with TMSs.

300 x LPt(IV)F(2)(Ar)(py) is treated with TMS-X (TMS = trimethylsilyl; X= NMe(2), SPh, OPh, CCPh) it also