In early stages of development, peripheral stimulation helps organize the sensory cortex, a process commonly referred to as neural plasticity. Neural plasticity may be best thought of as continuous reorganization throughout early life in which neural pathways are formed, but abandoned if not frequently used, in favor of other more active pathways.
In the auditory and visual systems, sensory deprivation during CNS development causes deficient organization, or detrimental reorganization of the cortex that may lead to permanent deficits.1 For example, in amblyopia (“lazy eye”), affecting about 2% of children, one eye is less functional than the other. If untreated, the visual cortex will “ignore” the less-coherent signals from the lazy eye and its neural pathways will degenerate, leading to blindness of that eye.
The central auditory system likewise undergoes sensory-deprivation-based detrimental reorganization in the event of peripheral deafness. In the absence of peripheral stimuli, the auditory cortex can be subsumed by the more active processes of the visual system, especially in signers. This cross-modal adaptation has been associated with poor outcomes when cochlear implantation is delayed.2 Although electrical stimulation with cochlear implants can establish central auditory pathways and diminish takeover by the visual system early in development, after 5 years of age, restitution of the auditory cortex may be minimal.3,4
Clinical experience has demonstrated the value of cochlear implantation prior to the age of 18 months and many feel that the ideal age is less than 12 months. Controlled studies confirm the time-sensitive nature of successful implantation. Based on ABR findings, Sharma, Dorman and Spahr demonstrated that progressively worse CI outcomes occur in prelinguistically deaf children who had delayed implantation.
What’s (kind of) New
Normal development of the central auditory system may be thought of in three stages: 1. Establishment of connectivity; 2. Pruning of underused synapses; and 3. Consolidation. During the establishment phase, repeated stimulation of adjacent neurons forms a persistent pathway. First described by Hebb in 19496 (clearly not new), Hebb’s postulate explains that when an axon of one cell stimulates another cell persistently, an efficient pathway is formed. Otherwise stated, cells that fire together, wire together. Of course, other forces are also active in establishment, for example growth of axons from the mid-brain (thalamus) to the primary auditory cortex (A1) is targeted to specific cells of the cortex by chemotrophic guidance (chemical attraction).
Lack of stimulation during sensitive periods can result in “negative plasticity”, a term sometimes used to describe lack of Stage 1. stimulus-driven establishment of connectivity, as occurs in sensory deprivation.
Strides have been made in understanding cellular level mechanisms of neural plasticity, but much remains unclear. Short-term potentiation of auditory (and other) synapses is pre-synaptic and results from repeated-use-based calcium ion accumulation that, on a temporary basis, increases release of neurotransmitter. Long-term hebbian potentiation (LTP) is another story, lasting for weeks to months. It involves the post-synaptic glutamine receptor NMDA. Many other receptors are now being recognized for LTP and its opposite, long-term depression of underused synapses. Consolidation, on the other hand, is influenced by an acetylcholine-based neurotransmitter system.
Establishment stage properties of electrical stimulation (electrical neurotrophism) through a cochlear implant have been demonstrated in development of the brainstem, midbrain and cortex. This is especially significant in the cortex where electrical stimulation promotes normal appearing, layer-specific function of A1 in kittens but not in mature cats. This is consistent with findings of CI electrical neurotrophism in primates dating back to the 1983.7
Neural plasticity is a process of peripheral stimulation that guides structural and functional development, and modification, of the central auditory system. Auditory deprivation during early life results in failure to establish neural pathways that are necessary for cochlear implants to provide excellent outcomes.8 In the absence of early implantation, primary and secondary auditory cortices are “taken over” by the visual system. However, early implantation provides electrical neurotrophism sufficient to establish functional central auditory pathways and preclude cross-modal takeover by elements of the visual cortices.
1. Kaas J., editor. (ed.). (2001). Mutable Brain: Dynamic and Plastic Features of the Developing and Mature Brain. Amsterdam: Harwood Academic Publishers.
2. Sandmann P., Eichele T., … Dillier N., et al. . (2009). Evaluation of evoked potentials to dyadic tones after cochlear implantation. Brain 132, 1967–1979.
3. Kral A., Sharma A. (2012). Developmental neuroplasticity after cochlear implantation. Trends Neurosci. 35, 111–122.
4. Dorman M. F., Sharma A., … Roland P. (2007). Central auditory development: evidence from CAEP measurements in children fit with cochlear implants. J. Commun. Disord. 40, 284–294.
5. Sharma A., Dorman M. F., Spahr A. J. (2002). A sensitive period for the development of the central auditory system in children with cochlear implants: implications for age of implantation. Ear Hear. 23, 532–539.
6. Hebb, D.O. (1949). The Organization of Behavior. New York: Wiley & Sons.
7. Larsen SA, Asher DL, Balkany TJ, Rucker N. Histopathology of the auditory nerve and cochlear nucleus following intracochlear electrical stimulation. Otolaryngol Clin N Am 1983;16:233-248.
8. Gama NM, Lehmann A. Compensatory plasticity: time matters. Front Neurosci 2015, 9:348.