Influence of anisotropic conductivity on EEG source reconstruction: investigations in a rabbit model.

The aim of our work was to quantify the influence of white matter anisotropic conductivity information on electroencephalography (EEG) source reconstruction. We performed this quantification in a rabbit head using both simulations and source localization based on invasive measurements. In vivo anisotropic (tensorial) conductivity information was obtained from magnetic resonance diffusion tensor imaging and included into a high-resolution finite-element model. When neglecting anisotropy in the simulations, we found a shift in source location of up to 1.3 mm with a mean value of 0.3 mm. The averaged orientational deviation was 10 degree and the mean magnitude error of the dipole was 29%. Source localization of the first cortical components after median and tibial nerve stimulation resulted in anatomically verified dipole positions with no significant anisotropy effect. Our results indicate that the expected average source localization error due to anisotropic white matter conductivity is within the principal accuracy limits of current inverse procedures. However, larger localization errors might occur in certain cases. In contrast, dipole orientation and dipole strength are influenced significantly by the anisotropy. We conclude that the inclusion of tissue anisotropy information improves source estimation procedures.

Inhomogeneous propagation of cortical spreading depression-detection by electro- and magnetoencephalography in rats.

Spreading depression (SD) propagates in cortical regions that are different in their morphological and functional characteristics. We tested whether the propagation pattern of spreading depression was different between parts of the cortex. In six adult rats, we recorded the ECoG by a 4 x 4 electrode array that covered parts of the frontal, parietal cortex and the cingulate cortex. Simultaneously a 16-channel magnetoencephalogram was recorded to characterize the development and direction of intracortical ion movements accompanying this phenomenon. Spreading depression was initiated by occipital application of 0.3 molar KCl solution. Depolarization was observed, at first, at lateral cortical regions and then at medial cortical regions. Thereafter, the propagation velocity increased in medial cortical regions and was faster than in lateral regions. Negative potential shifts were detected by all electrodes, but the depolarization reached a maximum over lateral and caudal cortical regions. The recorded magnetic fields indicated the same orientation of currents underlying these fields, which was perpendicular to the wave front and points away from the depolarization region. Overall, the data indicated that propagation patterns of spreading depression differed between parts of the cortex and, thus, propagation was inhomogeneous. This propagation was accompanied by strong currents parallel to the cortical surface.

Effects of discotheque music on audiometric results and central acoustic evoked neuromagnetic responses.

Audiograms and auditory evoked magnetic fields (AEFs) were observed in young male and female adults at different ages before and after being exposed to discotheque music for 4 hours. Sound pressure levels (SPLs) ranged from 95 dB (SPL) up to 130 dB (SPL). After exposure, subjects had temporary threshold shifts up to 20-25 dB, which almost disappeared after 2 hours. The majority of the subjects suffered from tinnitus that lasted approximately as long as the temporary threshold shift. Correspondingly, a transient delay and prolongation of the main component of the acoustically evoked magnetic field (AEF) negative wave, occurring 100 msec after stimulus (N100 m), was seen after this exposure; other components of the AEF (positive wave, occurring 50, 160, and 200 msec after stimulus [P50 m, P160 m, and P200 m, respectively]) occurred less often as compared to nonexposed controls. Because effects of vigilance on the AEF could be excluded, these changes can be related to the loud music, indicating an influence of noise on central auditory processing. The transient tinnitus could be caused by acoustic microinjuries (hidden acoustic predamage) of outer hair cells, leading to the persistent hearing threshold shifts from which many young adults aged 20-24 years are suffering. Occurrence of tinnitus closely coincides with the changes in hearing threshold and AEF, thus, a limitation of loudness in discotheques is needed to prevent this kind of hearing hazard.