Proefschrift_vd_Beek

the basal contacts to the modiolus (Figure 2, Table 4), the T-levels increased at the basal end of the cochlea, and an increased electrode-to-modiolar distance was ruled out as the cause of this increase toward the base.

A T-level profile with increased levels toward the basal end (Figure 3) has been frequently reported in the literature [Polak et al., 2005;Botros and Psarros, 2010;Smoorenburg et al., 2002;Lai et al., 2009;Thai- Van et al., 2001;Miller et al., 2008;Baudhuin et al., 2012;D’Elia et al., 2012;Vargas et al., 2012;Cafarelli et al., 2005;van der Beek et al., 2015]. However, there is no clear explanation for this phenomenon. Elucidating the causes of this phenomenon could provide insights for improving fitting and future electrode development. Although a clear increase in the T-levels toward the basal end was observed in various sub- groups (Figure 5A), not all of the subjects showed such an increase. The variation among the subjects could be caused by different factors. However, 20% of the intra-patient variation was related to the basal increase in the T-levels, suggesting that there is a common cause for this occurrence (Figure 3B, quadratic fit, r=0.2). An increased threshold level suggests a suboptimal neural-electrode interface. If the basal increase is caused by central pathways, no possible improvements at this particular site can be expected in the near future; this would also be the case if neural degeneration is the cause of the increase. If other peripheral aspects cause the deterioration of the neural-electrode interface and cause differences along the array, determining their contribution might lead to improvements in future electrode designs. Based mainly on data obtained using experimental animals, Shibata et al. concluded that deafness generally causes neural degeneration that leads to a progressively smaller number of SGCs [Shibata et al., 2011]. However, Rask-Andersen et al. showed that even with degeneration of the organ of Corti, the SGCs were preserved [Rask-Andersen et al., 2010]. In our population, neither a longer duration of deafness nor an increased age at implantation affected the absolute levels or their profile along the array (Figure 7). Because SGCs can survive even after a long duration of deafness [Rask-Andersen et al., 2010] and the duration of deafness had no clear effect on the stimulation levels (Figure 7), the progressive degeneration of the neural elements, starting in those involved with the high frequencies, appears not to be the cause of the wide variation in the levels or the basal increase in the levels. Other factors (e.g., etiology) are likely to affect neural excitability and therefore the stimulation levels. However, although the patients’ T-levels varied greatly, the level profiles did not depend on the T-level (cf. also Van der Beek et al., 2015), and all of the sub-groups consistently showed a basal increase in the T-levels, as Figure 5 shows. The widely varying overall levels are generally thought to be correlated with an etiology-of-deafness-based factor or another patient- specific factor, making it less likely that the consistent, level-independent basal increase is associated with the same factor. In contrast, Propst et al. showed that patients who presumably had experienced neural degeneration that was equally distributed along the cochlea (GJB2 patients) had the same eCAP thresholds along the array, whereas the non-GJB2 patients had different thresholds along the array. Unfortunately, no direct connection between Propst et al.’s data and neural degeneration can be made because they did not conduct histological evaluations [Propst et al., 2006]

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