PMC3951777_01
PMC3951777_02
Voxelwise differences in fractional anisotrophy between TBI patient and control group overlaid on mean FA skeleton (in green in the online version) didn't show any significant differences in TBSS analysis (uncorrected p<0.05). No lesion was observed on T2-weighted MRI (right inferior).
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F1
DTI analysis revealed that changes in fractional anisotropy (FA) in the TBI patient did not differ from the findings in the controls (uncorrected p<0.05) (Fig. 1).
A: Percentage of changes in MEPs amplitude after paired-pulse compared to unconditioned TMS pulse, for the TBI patient at week 2, at week 6 and for the group of control subjects (vertical bars indicate standard errors). Positive values indicate facilitation whereas negative values indicate suppression. SICI: short intracortical inhibition is expected with an inter-stimulus interval (ISI) of 3 ms. ICF: intracortical facilitation is expected with an ISI of 12 ms. LICI: long intracortical inhibition is expected with an ISI of 100 ms. The TBI patient had significantly greater ICF at both time points (p<0.01). LICI was absent in the TBI patient at week 2 (p<0.05), but returned to normal at week 6. Healthy controls showed expected patterns of SICI, ICF and LICI. B: Percentage of changes in MEPs amplitude at 0, 5 and 10 minutes after cTBS compared to pre-cTBS, for the TBI patient at week 2, at week 6 and for the group of control subjects (vertical bars indicate standard errors). Positive values indicate facilitation where as negative values indicate suppression. TBI patient had a significant (p<0.01) motor evoked potential (MEP) facilitation at week 2, but displayed predicted MEP suppression at week 6 (p<0.01). Healthy controls show expected MEP depression after cTBS. C: Example of TMS-evoked potentials at all electrodes in healthy controls. D: Topographical maps 50 ms after the TMS pulses, at baseline and at 0, 5 and 10 minutes after cTBS, for controls, and for TBI patient at week 2 and week 6. E: Changes in correlation between the temporal EEG signal recorded at the two contralateral M1 s (electrodes C3-C4), at the stimulated M1 and the ipsilateral frontal area (C3-F5) and at the stimulated M1 and the ipsilateral parietal (C3-P3), were computed at T5 compared to baseline (pre-cTBS) for the TBI patient at week 2, at week 6 and for the group of control subjects (vertical bars indicate standard errors). F: Illustration of the changes in correlation after cTBS.
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F2
SICI in our patient was not different from the control group, which showed expected patterns of SICI, ICF and LICI (Fig. 2A). Contrary to the findings in controls, our patient had significant MEP facilitation at week 2, at 0, 5, 10 and 20 minutes after cTBS, but displayed normal inhibition of MEPs at week 6 (see Fig. 2B for the values up to 10 minutes after cTBS). At week 6, although the activation remained widespread, there was no more massive increase after cTBS (Fig. 2C). TMS) tended to decrease 5 min after cTBS compared to baseline, whereas correlation between the stimulated M1 and the ipsilateral parietal and frontal areas tended to increase. The TBI patient significantly differed from the control subjects with a cTBS-induced increase of left M1-left parietal correlation at week 2, but not at week 6 (Fig. 2D and E).