Edge Frequency Plasticity and the Central Auditory Nervous System

Dr. Frank Musiek
March 10, 2021

Frank Musiek, Ph.D., University of Arizona


Edge frequency plasticity (EFP) of the central auditory nervous system (CANS) is a phrase that reflects some current interest in the research of auditory plasticity. It is also related to cochlear implants – especially for high frequency sensorineural hearing loss (HFSNHL), trans-synaptic degeneration, frequency discrimination, and even the pure tone audiogram. We will touch upon each of these sub topics in this overview.

Perhaps the best place to begin is with the concept of trans-synaptic degeneration research that lies at the underpinnings to our brief commentary on EFP. Though there were other researchers involved in the early studies on trans-synaptic degeneration, Kent Morest, a friend and colleague, was perhaps one of, if not the key figure in this kind of research. In the early 1980s Morest presented a paper at a major symposium on hearing and noise. In this presentation, Morest related his research on how damage to hair cells in the cochlea resulted in compromise of nuclei in the auditory brainstem (Morest and Bohne, 1983). This appeared to be a degenerative situation related to lack of input from the end organ to the CANS. This, from our view, was one the early accounts of trans-synaptic degeneration. Many studies were to follow showing this same pathophysiological action not only affected the brainstem but likely the alteration, in some manner, of the entire auditory pathway due to inappropriate neural input (usually decreased input) to the CANS.

Given the early work on trans-synaptic degeneration as a backdrop let us move ahead to the late 1980s and 1990s. In this time period, some very interesting studies emerged. One of the key studies in this time period was by Robertson and Irvine (1989). They showed in animals with induced HFSNHL that the auditory cortex tonotopically reorganized to keep the cortex physiologically viable despite lack of input. That is, the area of the auditory cortex that was responsible for high frequencies (where hearing loss was present) shifted its frequency to the next lower frequency where the hearing was normal or near normal allowing input to this area of cortex. This in turn created an expanded area of the cortex that was available to what now has been termed the “cut off” frequency (fc) or last frequency of good hearing sensitivity before the occurrence of hearing loss. This tonotopic shift of the auditory cortex away from the frequencies with hearing loss also potentially indicated that the auditory cortex really did not have access to the neural substrate to respond to these frequencies. This study by Robertson and Irvine was followed by other studies supporting their results. This tonotopic shift was evidence of edge frequency plasticity i.e., auditory cortex plasticity – likely to stave off degeneration of cortical tissue from lack of input. In addition, there was considerable speculation surrounding this research with clinical implications. One of these was if there was lack of auditory cortex substrate to support high frequency hearing, what would happen if amplification devices at the hearing loss frequencies were applied?

Given that with HFSNHL there is a tonotopic shift in the auditory cortex, it would be interpreted that now for the fc (cut off frequency) there would be more auditory cortex volume devoted to supporting this frequency area. Another key question now emerges. Because there is more neural substrate would auditory performance at the fc be improved? Actually, von Bekesy (von Bekesy and Wever, 1960) posed a similar question in reference to the somatosensory system many years ago – perhaps this work spawned some theories regarding the auditory system. There has been some evidence that indicated that hearing sensitivity improved at the fc but this data seems a little underwhelming but certainly probable (Thai-Van, 2010). It is important to note however, that there is some substantial data that shows auditory performance other than sensitivity is enhanced at the fc. McDermott and colleagues (1998) conducted a study on frequency discrimination that revealed difference limens (DLs) for the fc were smaller (improved) when compared to other frequencies with normal hearing sensitivity. This was a compelling study and was followed up with research by Thai-Van and colleagues (2002) showing similar findings, and also smaller DLs as a function of the steepness of the hearing loss. It should be mentioned that though these studies are indeed eye opening there needs to be additional research in this regard, not only for frequency discrimination but also for other auditory functions.

If DLs for frequency improve at fc when hearing loss is present, would DLs become worse if hearing was regained at fc — certainly a key question. Despite a fair amount of research into this question there seems to be a paucity publications on this regarding HFSNHL. Interestingly, Thai-Van and associates (2010) conducted a study involving patients with HFSNHL for which DLs for the fc were established. This group was then fit with amplification. Approximately 1 month after wearing hearing aids, DLs for the fc were again determined. The results indicated a trend towards altered DLs consistent with the hypothesis of the researchers. These findings are not with controversy but they were a critical first step towards showing possible reorganization of auditory cortex back to normal tonotopic status. This kind of investigation is sorely needed to determine if rehabilitative approaches with hearing aids and cochlear implants can reverse auditory cortex reorganization related to HFSNHL. It appears that using frequency DLs to monitor these kinds of changes could prove to be of value in monitoring tonotopic changes, but more data is needed.

It is also important to understand that there is a fair amount of data showing cortex reorganization in those with profound hearing loss, as well as those who have been implanted. Plasticity changes in these patients show auditory as well as extra auditory cortical changes. This topic however, is beyond the scope of this commentary but might be discussed in future pathways articles.



  1. McDermott, H. J., M. Lech, M. S. Kornblum, and D. R. F. Irvine. 1998. Loudness perception and frequency discrimination in subjects with steeply sloping hearing loss: possible correlates of neural plasticity. The Journal of the Acoustical Society of America 104, no. 4: 2314-2325
  2. Morest, D. K., and B. A. Bohne. 1983. Noise-induced degeneration in the brain and representation of inner and outer hair cells. Hearing Research 9, no. 2: 145-151.
  3. Robertson, D., and D. R. Irvine. 1989. Plasticity of frequency organization in auditory cortex of guinea pigs with partial unilateral deafness. Journal of Computational Neuroscience, 282,  3: 456-471
  4. Thai-Van, H., Veuillet, E., Norena, A., Guiraud, J., & Collet, L. (2010). Plasticity of tonotopic maps in humans: Influence of hearing loss, hearing aids and cochlear implants. Acta Oto-laryngologica, 130(3), 333–337.
  5. Thai-Van, H., Micheyl, C., Norena, A., & Collet, L. (2002). Local improvement in auditory frequency discrimination is associated with hearing-loss slope in subjects with cochlear damage. Brain: A Journal of Neurology, 125(Pt 3), 524–537.
  6. von Békésy, G., & Wever, E. G. (1960). Experiments in hearing. New York: McGraw-Hill.

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