- May 27, 2020
- 556
- Tinnitus Since
- 2007
- Cause of Tinnitus
- Loud music/headphones/concerts - Hyperacusis from motorbike
I had initially drafted this as a reply to another post, but in the end felt it deserved its own exclusive thread, as I feel this is something that has come up many times in our conversations as hyperacusis sufferers but has not been fully dissected as a point of interest. I would therefore like to make a start on this discussion.
This post was also prompted after reading again that not all hyperacusis sufferers experience relief from Gabapentin and other anticonvulsants, and has therefore made me think a little bit more about the type II afferent fibre theory, which I still believe to be the strongest out there. So let's begin.
The distortion and high frequency issue is something that I haven't been able to get my head around for a while. Why is it that many of us suffer disproportionately with distorted sounds and high frequencies compared to undistorted sounds and lower frequencies, regardless of volume? I have some audio engineering knowledge and what I do know is that, all other things being equal, smaller sound sources tend to produce a frequency spectrum that is more biased towards the high end, but why is this important?
A quick look at the cochlea diagram above shows that the stapes, which "push" into the cochlea after receiving a sound, are closest to the the cochlea base and furthest away from the cochlea apex. We know that the cochlea apex is responsible for low frequencies and the cochlea base is responsible for high frequencies. Now, let's look at the following diagram:
This diagram shows that, on a mechanical level, there is a membrane that displaces the stereocilia to the hair cells. This is the first time I have come across this mechanism. With this mechanism in mind, would it be reasonable to ask: given the distribution of frequency "responsibility" across the cochlea, does the apex of the cochlea, which is closest to the stapes, undergo a disproportionate amount of membrane displacement compared to the base of the cochlea? And I wonder: could this in any way give us some insight into the pathology of hyperacusis? Are the stereocilia of the high frequency OHCs overworked and overinflamed because they undergo excessive displacement compared to their low frequency OHC counterparts? Are they releasing a disproportionate amount of neurotransmitters, which may also play a role in how our brain perceives things? If so, one would imagine that this is also the case in people without hyperacusis, so why are we different? And while I remember, I also remember reading that higher frequencies carry more energy, and I wonder how that fits into the ATP leak theory, where ATP, of course, is the energy source of cells. I include another diagram below for reference with regards to what happens after the membrane displacement.
Moving on from the above, what I also know from my studio production days is that a distorted sound wave looks very different to a normal sound wave. A normal sound wave is usually a sine wave, but distorted waves have more 'square' edges. See diagram below:
A quick google search doesn't get many hits for 'sine waves' in relation to any kind of ear pathologies, but I would be interested to know how such information is processed in the auditory system. Intuitively, I don't see how stereocilia or OHCs could discriminate between a square wave or a sine wave, given that both waves induce a membrane displacement that releases neurotransmitters - a mechanical process, as far as I understand it. Indeed, my intuition would tell me that this distinction in quality of sound is made somewhere further along the auditory path - perhaps in the cochlea nucleus (brainstem) or the auditory cortex. I also know that there are efferent fibres carrying signals from the brain to the ear and am in the dark as to how these could fit into any kind of potential pathology model. I also know that hyperacusis is sometimes seen in children, some of whom grow out of it but others don't, and I wonder what role the brain plays here too. I wonder if in some of us hyperacusis sufferers, the brain or brainstem, for whatever reason I still haven't been able to establish (perhaps neuroinflammation, which has been shown to occur after noise exposure in this study) loses its capacity to process distorted or 'complicated' sounds (I know we also struggle with things like crunching plastic water bottles or scrap paper) and it sends some kind of faulty signal through the efferent fibres which then causes some kind of negative feedback loop where the afferent nerve fibres then come into play. At this point, I'm kind of thinking out loud, but I would very much welcome an open discussion on this @serendipity1996, @100Hz and others.
This post was also prompted after reading again that not all hyperacusis sufferers experience relief from Gabapentin and other anticonvulsants, and has therefore made me think a little bit more about the type II afferent fibre theory, which I still believe to be the strongest out there. So let's begin.
The distortion and high frequency issue is something that I haven't been able to get my head around for a while. Why is it that many of us suffer disproportionately with distorted sounds and high frequencies compared to undistorted sounds and lower frequencies, regardless of volume? I have some audio engineering knowledge and what I do know is that, all other things being equal, smaller sound sources tend to produce a frequency spectrum that is more biased towards the high end, but why is this important?
A quick look at the cochlea diagram above shows that the stapes, which "push" into the cochlea after receiving a sound, are closest to the the cochlea base and furthest away from the cochlea apex. We know that the cochlea apex is responsible for low frequencies and the cochlea base is responsible for high frequencies. Now, let's look at the following diagram:
This diagram shows that, on a mechanical level, there is a membrane that displaces the stereocilia to the hair cells. This is the first time I have come across this mechanism. With this mechanism in mind, would it be reasonable to ask: given the distribution of frequency "responsibility" across the cochlea, does the apex of the cochlea, which is closest to the stapes, undergo a disproportionate amount of membrane displacement compared to the base of the cochlea? And I wonder: could this in any way give us some insight into the pathology of hyperacusis? Are the stereocilia of the high frequency OHCs overworked and overinflamed because they undergo excessive displacement compared to their low frequency OHC counterparts? Are they releasing a disproportionate amount of neurotransmitters, which may also play a role in how our brain perceives things? If so, one would imagine that this is also the case in people without hyperacusis, so why are we different? And while I remember, I also remember reading that higher frequencies carry more energy, and I wonder how that fits into the ATP leak theory, where ATP, of course, is the energy source of cells. I include another diagram below for reference with regards to what happens after the membrane displacement.
Moving on from the above, what I also know from my studio production days is that a distorted sound wave looks very different to a normal sound wave. A normal sound wave is usually a sine wave, but distorted waves have more 'square' edges. See diagram below:
A quick google search doesn't get many hits for 'sine waves' in relation to any kind of ear pathologies, but I would be interested to know how such information is processed in the auditory system. Intuitively, I don't see how stereocilia or OHCs could discriminate between a square wave or a sine wave, given that both waves induce a membrane displacement that releases neurotransmitters - a mechanical process, as far as I understand it. Indeed, my intuition would tell me that this distinction in quality of sound is made somewhere further along the auditory path - perhaps in the cochlea nucleus (brainstem) or the auditory cortex. I also know that there are efferent fibres carrying signals from the brain to the ear and am in the dark as to how these could fit into any kind of potential pathology model. I also know that hyperacusis is sometimes seen in children, some of whom grow out of it but others don't, and I wonder what role the brain plays here too. I wonder if in some of us hyperacusis sufferers, the brain or brainstem, for whatever reason I still haven't been able to establish (perhaps neuroinflammation, which has been shown to occur after noise exposure in this study) loses its capacity to process distorted or 'complicated' sounds (I know we also struggle with things like crunching plastic water bottles or scrap paper) and it sends some kind of faulty signal through the efferent fibres which then causes some kind of negative feedback loop where the afferent nerve fibres then come into play. At this point, I'm kind of thinking out loud, but I would very much welcome an open discussion on this @serendipity1996, @100Hz and others.