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.

Objective The aim of the present experiment was to assess the consequences of cochlear implantation at different ages on the development of the human central auditory system. Design Our measure of the maturity of central auditory pathways was the latency of the P1 cortical auditory evoked potential. Because P1 latencies vary as a function of chronological age, they can be used to infer the maturational status of auditory pathways in congenitally deafened children who regain hearing after being fit with a cochlear implant. We examined the development of P1 response latencies in 104 congenitally deaf children who had been fit with cochlear implants at ages ranging from 1.3 yr to 17.5 yr and three congenitally deaf adults. The independent variable was the duration of deafness before cochlear implantation. The dependent variable was the latency of the P1 cortical auditory evoked potential. Results A comparison of P1 latencies in implanted children with those of age-matched normal-hearing peers revealed that implanted children with the longest period of auditory deprivation before implantation—7 or more yr—had abnormal cortical response latencies to speech. Implanted children with the shortest period of auditory deprivation—approximately 3.5 yr or less—evidenced age-appropriate latency responses within 6 mo after the onset of electrical stimulation. Conclusions 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.