Neural processing of speech in children with sensorineural hearing loss

Although the primary damage associated with sensorineural hearing loss lies in the cochlea,
its consequences extend throughout the entire auditory pathway. Despite having significant
residual hearing, children with mild (21-40 dB HL) to moderate (41-70 dB HL) sensorineural
hearing loss (MMHL) experience deficits with general auditory processing, which puts them at risk
of encountering language difficulties. Here, I will present two studies aimed at better understanding
the neural consequence of partial degradation of the auditory input in children with MMHL. The
first study examines the developmental effects of childhood MMHL on auditory discrimination of
speech, “speech-like” and “nonspeech” stimuli, using the Mismatch Negativity (MMN). We tested
46 children with MMHL and 44 normally-hearing chronological age-matched controls (CA).
Children were divided into two age groups: “younger” (8-11 years) and “older” (12-16 years). Our
main result indicated that, while present in younger children with MMHL, there was no significant
MMN in older MMHL children, whatever the condition. In an attempt to replicate this finding,
fourteen children from the initial younger group participated in a longitudinal follow-up study
again 6 years later (age range: 14-17 years). Although this group had a significant MMN when they
were aged 7-11 years, this was only the case for speech when they reached 14-17 years. Our
findings suggest that even a mild or moderate levels of hearing loss during childhood may entail a
persistent damage of auditory cortical functioning. A second study was conducted to evaluate the
benefit of hearing aid amplification at various levels of the auditory pathway in children with
MMHL. The frequency following response (FFR) was used as an index of speech processing at
the subcortical level. Both the MMN and the intra-class correlation (ICC) coefficients were used
to index processing of sounds at the cortical level. The results suggest that, as a group, children
with MMHL have smaller ICC coefficients than NH controls in both unamplified and amplified
conditions, and do not show an MMN. In contrast, at the subcortical level, they show an FFR that
was smaller than that of NH controls in the unamplified condition only. With simulated
amplification, children with MMHL demonstrate an FFR that was comparable to that observed in
NH controls. Our findings suggest that the neural processing of unamplified speech may be
impaired at both subcortical and cortical levels in children with MMHL. Results will be discussed
with respect to the existing literature on profoundly deaf children with cochlear implant and animal
studies, which highlight long-term consequences of MMHL on the neural processing of sounds.

Acknowledgments
This research was supported by an Economic and Social Research Council (ESRC) First Grants
Award (RES-061-25-0440) to LH and a European Union ITN