- Published on 14 April 2016
For some time now, it is clear how important the brain is for hearing. The result of research by professor emeritus Jos Eggermont from the Hotchkiss Brain Institute of the University of Calgary, Canada, further underlines this. When test animals are exposed to the same noise at a non-traumatic level for a prolonged period of time, no hearing loss will occur. But in the brain things will have changed. And for humans changes like these as a consequence of similar conditions are likely to cause reduced understanding of speech. Eggermont, specialized in brain plasticity, explained the mechanism behind this during his lecture entitled 'Long term non-traumatic noise exposure: a cause of CAPD?' on Wednesday, April 13, during the Academic Research Conference linked to AudiologyNOW!
When presented with incubator noise, dramatic changes took place in the brains of neonatal rats, resulting in retarded auditory cortical development. This was shown by F. Chang and M. Merzenich in 2003 in Science. Outcomes in neonatals were, however, at the time rated as irrelevant for the adult brain based on suppositions of the adult brain’s plasticity. Eggermont: “Dogmas on brain plasticity in adults are that it takes behaviorally relevant events to invoke changes or, alternatively, that it involves training and learning”, says Eggermont.
He spent the first decade of his research on the young brain before switching to research on the plasticity of the adult brain. “This dogma means, translated to sound experiments with test animals, that it is impossible to induce plasticity in the adult animal brain unless the sound is behaviorally relevant. In other words: experiments should for instance be food or safety related to get a response.”
Eggermont: “This fits to our experiments with adult cats, published in 2006. Exposure to sound in more or less the same spectrum from 4 kHz to 20 kHz for three weeks at 80 dB SPL (comparable to 76 dBA) – in the safe range for hearing loss – causes permanent damage to the peripheral auditory system, which results in the reorganization of the cortical tonotopic map. Later we moved to an even lower sound level of 68-70 dB SPL, a quite normal background level for conversation in a crowded place. The results remained the same: the brain turned down the gain for the frequency range of the persistent sounds that were fed to it, in order to ignore it as much as possible.” (See box below.)
Silence heightens sensitivity
Research from Craig Formby PhD, published in the Journal of the Acoustic Society of America in 2003, showed that students rated sounds significantly louder than before after wearing earplugs for 23 hours a day during two weeks. The other way around, after wearing an iPod (at moderate sound levels, ~60 dB) almost permanently for two weeks, they rated the sounds much softer, with typically a 6 dB difference.
It is interesting to notice what happened at the edges of the sound, says Eggermont: “Loss of lateral inhibition occurred, so the sound at the edge-frequencies was emphasized. This enhances the suppressing effect on the 4 to 20 kHz region even more. Normally, every neuron suppresses its neighbor.
"Hearing loss occurs in the ear, hearing problems are in the brain”
This so-called surround suppression mechanism not only occurs in the auditory system, but also in the visual system. Neurons do not respond as much when the stimulus is intensified. When in the 4 to 20 kHz region this suppression takes place, the neighboring regions get the opportunity to go up. This effect can be induced in only three weeks. But the recovery takes three months at the least. It is not farfetched to suppose that a longer exposure would cause permanent effects. And of course, one might suppose that these animal test outcomes go for animals as well as for humans.”
Results in humans
Although it is of course impossible to perform tests like these with humans, there are indications that results indeed do apply to humans. Eggermont: “A Finnish group reported in 2004 on the effects of factory noise on speech understanding. They compared people from the same age group with office jobs to people working in the factory – the latter having used the required sound barrier. It turned out that in both groups no clinical hearing loss could be established. But consonant-vowel phoneme discrimination (e.g., /ba/ vs. /pa/) was significantly less in the factory workers group. There was no difference in hearing, but in the brain there was a difference in the mismatch negativity. This suggested problems with understanding of speech in the factory workers group, which had been exposed to prolonged non-traumatic noise. That is why I say: hearing loss occurs in the ear, but hearing problems are in the brain.”
Eggermont explains that it is because of results like these that state of the art audiology is moving away from just the pure tone audiogram to establish hearing problems and to use speech in noise discrimination tests in addition. “But outside this setting, for instance in standard annual hearing testing on the work-floor, the pure tone audiogram still dominates. It could be said that an additional speechin- noise test takes too long, which isn’t very practical. Moreover, it will be impossible anyway to bring down noise levels in factories down to a level that doesn’t affect the brain. It is more practical to think of other solutions, such as shifting tasks periodically to environments with different sound characteristics. It probably also matters what sound experiences there are after work.”
In 2009-2013 Eggermont’s group published follow up papers using even lower prolonged sound levels, this time also in relation to tinnitus, an affliction that presently involves ten to fifteen per cent of the general population. “The potential theoretical connection between prolonged non-traumatic noise and tinnitus is as follows”, Eggermont starts explaining. “Tinnitus is the result of increased spontaneous firing of neurons in the cortex, the brain stem and the mid-brain. This means that when there is no sound there still is spontaneous neuron firing activity in the brain. This spontaneous activity can be induced by lack of regular sound input, which for instance is the case with high frequency hearing loss. When the input is reduced, the brain turns up the gain. You then hear the frequencies you are missing as tinnitus, just like phantom pain.” (Read more on tinnitus and retraining therapy).
Without high frequency hearing loss, there still is a connection between prolonged non-traumatic sound exposure and tinnitus. The result is quite the opposite of the earlier experiments with permanent hearing loss. “The presented sound-evoked activity in auditory cortex is suppressed, and also the spontaneous firing rate goes down. This results from the reduction in gain. This situation is sustained until long (> 3 months) after the experiment is stopped. In the same way, as we have seen, the increased driven and spontaneous firing rate at the edges where the gain was up is also sustained. So at these edges we notice a tinnitus response (increased spontaneous firing rate) coming up as a result of prolonged non-traumatic sound exposure, without hearing loss. If such a situation results in tinnitus in humans remains to be explored.
Better tests are needed
“During the last decade, collaboration between audiologist and neuroscientists has become more intense, for good reasons”, says Eggermont. “It is now widely accepted that the mechanisms presented here are real.” It is quite clear: the former dogma no longer holds. Furthermore, although there is no hearing loss, there may still be a problem with understanding speech-in-noise that can only be attributed to changes in the brain.
According to Eggermont, the most pressing conclusion from these research outcomes is that better tests are needed. “It will prove to be very hard indeed to introduce policy changes. It took twenty years to come to the present legislation regarding safe (based on absence of hearing loss) sound levels at work, which was introduced in the late fifties. Before one can expect policies to change regarding effects on the brain, there has to be an undeniable body of evidence from epidemiology, over several years, in various countries and with different noise settings. And that means that speech-innoise testing has to be added to the pure tone audiogram in annual hearing testing, as the latter is not a good indicator for hearing problems. That is what I plead for.”
Eggermont keeps the implications of the research results on Central Auditory Processing Disorder (CAPD) for his keynote lecture. As an introduction he says: “CAPD in general stands for a normal functioning auditory system in combination with problems to understand speech. Mostly there is no structural purely neurological damage. Is it cognitive or developmental then? The label CAPD depends on the outcome of a battery of tests. There can be an array of causes, but there may be a predominant role for problems with temporal processing.”
Jos Eggermont PhD is Professor Emeritus, University of Calgary, Departments of Physiology and Pharmacology, and Psychology. He got his PhD in Physics at Leiden University in his native country The Netherlands in 1972. He is retired since July first, 2013. His research in Calgary comprised most aspects of audition with an emphasis on the electrophysiology of the auditory system in test animals, and was specifically focused on the role played by neural synchrony in the coding of complex sounds in the auditory cortex. His group developed an animal model of noise-exposure induced tinnitus to further understanding of this disorder and, by comparison with the effects of external sounds of similar nature, to investigate how normal and pathological sound sensations are encoded in the central nervous system and the role of cortical reorganization played herein. Lately he focused on the effects of long-term non-traumatic sound exposure on cortical activity and organization.
- Jos Eggermont, Noise and the brain, Experience dependent developmental and adult plasticity, Elsevier 2013
- Jos Eggermont, Auditory temporal processing and its disorders, Oxford University Press 2015