A common finding in developmental neurobiology is that patterned stimulation must be delivered to a sensory system within a narrow window of time (a critical period) during development in order for that sensory system to develop normally. Experiments with congenitally deaf children fit with cochlear implants at different times during childhood have allowed us to establish the existence and time limits of a critical period for the development of central auditory pathways in humans. Using the latency of cortical auditory evoked potentials (CAEPs) as a measure we have found that central auditory pathways are maximally plastic for a period of about 3.5 years. If stimulation is delivered within that period CAEP latencies reach age-normal values within 3- 6 months following the onset of stimulation. However, if stimulation is withheld for more than 7 years, we find that plasticity in central auditory pathways is greatly reduced. In late-implanted children, CAEP latencies decrease significantly over a period of approximately one month following the onset of stimulation then remain constant or change very slowly over months or years.
The loss of central auditory plasticity in congenitally deaf children implanted after age 7 is correlated with relatively poor development of oral speech and language skills. We suppose the link is, in fact, causal. Animal models suggest that primary auditory cortex may be functionally disconnected from higher-order auditory cortex, due to restricted development of inter- and intra-cortical connections, in late-implanted children (Kral et al., in press). This would account for late-implanted children who ëhearí by means of the implant but who experience very slow development of speech and language skills. Another aspect of plasticity that works against late-implanted children is the take over of higher-order auditory cortex by other function, e.g. vision. Lee et al. (2001) have shown via PET scans that after the age of 4-5 higher-order auditory cortex in congenitally deaf children is not ëquietí as would be expected in the absence of auditory stimulation, but rather is active, suggesting take over by other functions. The hypothesis of a decoupling of primary cortex from higher-order auditory and language cortex in children deprived of sound for a long period provides an account for the oral language-learning difficulties of children who receive an implant after the end of the critical period.