Neuroplasticity can be defined as the ability of the nervous system to respond to intrinsic or extrinsic stimuli by reorganizing its structure, function and connections. Major advances in the understanding of neuroplasticity have to date yielded few established interventions. To advance the translation of neuroplasticity research towards clinical applications, the National Institutes of Health Blueprint for Neuroscience Research sponsored a workshop in 2009. Basic and clinical researchers in disciplines from central nervous system injury/stroke, mental/addictive disorders, paediatric/developmental disorders and neurodegeneration/ageing identified cardinal examples of neuroplasticity, underlying mechanisms, therapeutic implications and common denominators. Promising therapies that may enhance training-induced cognitive and motor learning, such as brain stimulation and neuropharmacological interventions, were identified, along with questions of how best to use this body of information to reduce human disability. Improved understanding of adaptive mechanisms at every level, from molecules to synapses, to networks, to behaviour, can be gained from iterative collaborations between basic and clinical researchers. Lessons can be gleaned from studying fields related to plasticity, such as development, critical periods, learning and response to disease. Improved means of assessing neuroplasticity in humans, including biomarkers for predicting and monitoring treatment response, are needed. Neuroplasticity occurs with many variations, in many forms, and in many contexts. However, common themes in plasticity that emerge across diverse central nervous system conditions include experience dependence, time sensitivity and the importance of motivation and attention. Integration of information across disciplines should enhance opportunities for the translation of neuroplasticity and circuit retraining research into effective clinical therapies.

Our data suggest that in the absence of normal stimulation there is a sensitive period of about 3.5 yr during which the human central auditory system remains maximally plastic. Plasticity remains in some, but not all children until approximately age 7. After age 7, plasticity is greatly reduced. These data may be relevant to the issue of when best to place a cochlear implant in a congenitally deaf child.

Cortical development is dependent on stimulus-driven learning. The absence of sensory input from birth, as occurs in congenital deafness, affects normal growth and connectivity needed to form a functional sensory system—resulting in deficits in oral language learning. Cochlear implants bypass cochlear damage by directly stimulating the auditory nerve and brain, making it possible to avoid many of the deleterious effects of sensory deprivation. Congenitally deaf animals and children who receive implants provide a platform to examine the characteristics of cortical plasticity in the auditory system. In this review, we discuss the existence of, time limits for, and mechanistic constraints on sensitive periods for cochlear implantation and describe the effects of multimodal and cognitive re-organization that results from long-term auditory deprivation.

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The aim of our research was to estimate the time course of development and plasticity of the human central auditory pathways following cochlear implantation. We recorded cortical auditory-evoked potentials in 3-year-old congenitally deaf children after they were fitted with cochlear implants. Immediately after implantation cortical response latencies resembled those of normal-hearing newborns. Over the next few months, the cortical evoked responses showed rapid changes in morphology and latency that resulted in age-appropriate latencies by 8 months after implantation. Overall, the development of cortical response latencies for the implanted children was more rapid than for their normal-hearing age-matched peers. Our results demonstrate a high degree of central auditory system plasticity during early human development.

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A basic tenet of developmental neurobiology is that certain areas of the cortex will reorganize, if appropriate stimulation is withheld for long periods. Stimulation must be delivered to a sensory system within a narrow window of time (a sensitive period) if that system is to develop normally. In this article, we will describe age cut-offs for a sensitive period for central auditory development in children who receive cochlear implants. We will review de-coupling and reorganization of cortical areas, which are presumed to underlie the end of the sensitive period in congenitally deaf humans and cats. Finally, we present two clinical cases which demonstrate the use of the P1 cortical auditory evoked potential as a biomarker for central auditory system development and re-organization in congenitally deaf children fitted with cochlear implants.Learning outcomes-Readers of this article should be able to (i) describe the importance of the sensitive period as it relates to development of central auditory pathways in children with cochlear implants, (ii) discuss the hypothesis of decoupling of primary from higher order auditory cortex as it relates to the end of the sensitive period, (iii) discuss cross-modal reorganization which may occur after long periods of auditory deprivation, and (iv) understand the use of the P1 response as a biomarker for development of central auditory pathways.