No abstract

A basic finding in developmental neurophysiology is that some areas of the cortex cortical areas will reorganize following a period of stimulus deprivation. In this review, we discuss mainly electroencephalography (EEG) studies of normal and deprivation-induced abnormal development of the central auditory pathways in children and in animal models. We describe age cut-off for sensitive periods for central auditory development in congenitally deaf children who are fitted with a cochlear implant. We speculate on mechanisms of decoupling and reorganization which may underlie the end of the sensitive period. Finally, we describe new magentoencephalography (MEG) evidence of somatosensory cross-modal plasticity following long-term auditory deprivation.

Congenital deafness leads to atypical organization of the auditory nervous system. However, the extent to which auditory pathways reorganize during deafness is not well understood. We recorded cortical auditory evoked potentials in normal hearing children and in congenitally deaf children fitted with cochlear implants. High-density EEG and source modeling revealed principal activity from auditory cortex in normal hearing and early implanted children. However, children implanted after a critical period of seven years revealed activity from parietotemporal cortex in response to auditory stimulation, demonstrating reorganized cortical pathways. Reorganization of central auditory pathways is limited by the age at which implantation occurs, and may help explain the benefits and limitations of implantation in congenitally deaf children.

We used the latency of the P1 cortical auditory-evoked potential (CAEP) as a biomarker for the development of central auditory pathways in three children who received intervention through hearing aids and/or cochlear implants. Our goal was to examine the clinical feasibility of using the latency of the P1 CAEP as an objective tool to evaluate whether acoustic amplification for hearing-impaired children has provided sufficient stimulation for normal development of central auditory pathways. If clinicians have such a marker, then they can more confidently make a decision about whether to provide a child with a cochlear implant following an appropriate hearing-aid trial. Using the same marker, clinicians will also be able to monitor the maturation of central auditory pathways once electrical stimulation is initiated.

No abstract