Subjects (table I)

Fourteen subjects (ten females and four males) ranging in age from 16 to 74 years of age participated in the study. They received a HiRes90K® cochlear implant from Advanced Bionics Corporation at the Edouard Herriot University Hospital of Lyon (France). All subjects were implanted by the same surgeon and had a full electrode insertion. The electrode array of the HiRes90K® implant is called the HiFocus1j and was described in a previous study by Guiraud et al. (in press). The electrode array was slightly curved and contacts were oriented toward the modiolus wall. These factors intended to focus stimulation towards the nerve fibers and helped reduce neural spread of excitation around contacts. In an unpublished study we have found that N1 latency may be altered within the first months of implant use. Hence, subjects had at least three months of cochlear implant experience at the time of the study when ELAR measurements were made so that duration of implant use would not be a possible confounding variable. To ensure that the effects of the various parameters (duration of deafness, audiogram, M levels) on ELAR latency would not be biased by the duration of implant use, one-way ANOVA tests were performed. Although the p-value for P2 suggests a trend, the duration of implant use had no significant effect on ELAR latency with p = 0.25 for N1, p = 0.08 for P2, and p = 0.11 for N1-P2 (the normality and equal variance tests were passed with p > 0.01 for each test). The mean duration of cochlear implant use was nine months. Subjects were full-time users of their cochlear implant. The known etiologies of deafness included Usher syndrome (N = 1), Turner syndrome (N = 1), Meniere’s syndrome (N = 1), perinatal asphyxia (N = 1), stroke (N = 2), deep pressure traumatism (N = 1), presbyacousia (N = 1), chronic otitis (N = 1), and hereditary origin (N = 1). The duration of profound bilateral deafness varied from 1 to 20 years. The degree of hearing loss varied as shown by pre-operative audiogram. Subjects 1, 3, 4, 7, 8, 9, and 13 were less profoundly deaf as they had less than 100 dB HL audiometric thresholds for 500, 1000, 2000 and 4000 Hz tones (group A1), while the audiometric thresholds for Subjects 2, 5, 6, 10, 11, 12, and 14 were above 100 dB HL for the same frequencies (group A2). All subjects used the HiRes strategy with variable benefit from their cochlear implant as revealed by phoneme scores for the Lafon test (Lafon, 1964), recorded at the time of ELAR recording. Table I summarises this information for each subject. Subjects were fully informed about the experimental procedures in accordance with the decision of the local ethical committee. All subjects signed a consent form prior to participation.

Table I. Demographic information on subjects: etiology and onset of deafness, age at test, duration of profound bilateral deafness prior to implantation and groups, audiogram average and groups, duration of cochlear implant use, and speech perception scores. Two groups of subjects were defined according to duration of deafness: subjects with less than eight years of deafness are in group D1, while group D2 contained subjects with more than eight years of deafness duration. Audiogram groups were defined according to the degree of hearing loss for 500, 1000, 2000, and 4000 Hz. Audiometric thresholds were below 100 dB HL for subjects in group A1 and above 100 dB HL for subjects in group A2. Speech perception scores (percentage of phonemes correctly perceived) were obtained at the time of the study using Lafon lists (lists of three-phoneme words; Lafon, 1964) presented in an open set format in quiet at 65 dB HL in a sound field.

Note: Two of our subjects S12 (16 years old) and S13 (17 years old), are teenagers. S12 became deaf at 3 and S13 probably became deaf at birth. We know that central auditory pathways of the human brain exhibit progressive anatomical and physiological changes through early adulthood (Kraus et al., 1985; Courchesne, 1990; Huttenlocher, 1979; for a review: Wunderlich et al., 2006). However, we decided to keep S12 and S13 in the subject sample because the literature tends to show that it would not affect the study. It appears indeed that, while little or no age-related change in N1 latency was reported in some studies (Ohlrich et al., 1978; Martin et al., 1988; Ponton et al., 1996), others showed that the latency of N1 decreases as age increases (Shibasaki & Miyazaki, 1992; Kurtzberg et al., 1995; Sharma et al., 1997) but that changes may occur only up to 16 years of age (Tonnquist-Uhlen et al., 1995). For P2, this may not be a problem as it may mature earlier than N1 (Barnet, 1975; Courchesne, 1978; Paetau et al., 1995; Bruneau et al., 1997 ; Ceponiené et al., 1998).