Notes on Yost Chapter 16: The abnormal auditory system. 253-267.
21 April 2004
Hearing loss can be caused by a variety of agents – excessive noise exposure (perhaps a lifetime accumulation of any noise exposure?); ototoxic drugs; infections and disease; accidents; and aging and heredity. Yost begins with the discussion of “noise-induced hearing loss” (NIHL), because this is very common, and most is known about it. Noise here is not limited to its technical definition (an acoustic waveform with random changes in frequency and amplitude) but in a more social-psychological definition as unwanted or annoying sounds: NIHL can be caused by tones as well as noise, if they are sufficiently intense. It is interesting that perhaps for the first time Yost begins a chapter with a serious concern for physiology, stating that a noise that has caused hearing loss has caused some damage to the inner ear, probably accompanied by changes in the central auditory structures as well.
The effects on the inner ear involve the hair cells, and depending on the degree of severity of the exposure type of noise, other cochlear structures as well. For example, Figure 16.1 shows a cochlea exposed to a very high noise level that pushed the membrane beyond its flexible limits, and thus torn out a section of it. In Figure 16.2 a less intense noise attacked only the stereocilia. In mammals many instances of noise induced hearing loss are permanent, though some low levels of exposure can lead to a temporary form of hearing loss, that might result from metabolic changes or recoverable damage to stereocilia. The first series of figures in the chapter show these various forms of damage in photomicrographs.
Of the several forms of hearing loss that can potentially be caused by noise exposure, the one studied the most is the threshold shift (noise-induced threshold shift, NITS). If it does recover to normal values it is noise-induced temporary threshold shift (NITTS), or if it does not recover it is noise-induced permanent threshold shift (NIPTS): or TTS and PTS. Often noise exposure (in the laboratory with animals, in humans only from real life situations) noise exposure has two effects, in both PTS and TTS, or a “compound threshold shift (CTS). For some exposures TTS reaches a limit at some duration of exposure, and then does not get any worse. This is called the asymptotic threshold shift, ATS.
In the laboratory with human subjects, mild levels of exposure are used and thresholds are determined before and after the exposure, usually 2 or 4 minutes after, these called TTS2 or TTS4. Figure 16.3 shows that the TTS from noise exposure at 2 minutes after noise offset as a function of the duration and level of exposure, and clearly level and duration have independent effects of the TTS. The severity of hearing loss is also affected by the spectral content of the exposure and its temporal pattern (sudden impacts vs. long duration stimuli for example). In addition there seem to be very large individual differences in susceptibility to noise exposure (remember the work by Maison and Liberman in 2000 on the strength of the OCB reflex and hearing loss in chinchillas). For moderate levels of noise (above 70 dB, but less that about 80 to 90 dB) TTS grows more or less linearly with exposure time up to about 8 hours, and there will be no permanent damage for most people. With longer duration and higher exposures then PTS will occur and will accumulate over years of exposure. This often happens in occupational settings, or in people who enjoy noisy recreational activities (shooting, snowmobiles for example). At very high levels (130 dB) hearing loss can be extreme, have a sudden onset, and be permanent, though Yost remarks that its effect will be erratic across individuals, some being more susceptible than others. At 80 to perhaps 105 dB TTS grows logarithmically with exposure time up to 8 to 12 hours. Some investigations indicate that any doubling of exposure time increases the TTS by 5 dB at the 2 minute test time, though others suggest that TTS is related to the energy in the signal and thus goes up by 3 dB whenever the duration (and thus energy in the noise) is doubled.
The amounts of TTS and PTS also depend on the frequency spectrum of the noise and the test stimulus. For short exposures and weak stimuli, Yost writes, maximum TTS occurs at the exposure frequency, which seems highly reasonable – except that for higher exposure levels TTS occurs at frequencies higher that the exposure frequency. So, for wide band noise the maximum effect is between 3 and 6 kHz (see Figure 16.4). How can this be explained? Perhaps in part it is because the resonance of the ear amplifies the higher frequencies; perhaps in part it is because higher level sound elicits the intra-tympanic reflex, which protects against the low frequencies. But also, if a pure tone is used as the “noise” then the amount of TTS depends on the frequency of the noise (perhaps because of resonance and because of the intratympanic reflex). A curious effect is that the frequency of the maximum TTS is progressively higher than the exposure frequency, and is on the order of one octave to one-half octave above the exposure frequency. It seems unlikely that this is because the immediate effect of the exposure tone was greatest at this point, but, instead, it suggests that high frequency hearing is more sensitive to insult than is low frequency hearing. It is possible that high frequency hearing is more sensitive to noise exposure is because all of the frequencies in the noise activate the base of the cochlea, but only the high frequencies activate the apex of the cochlea (think of the asymmetric shape of the traveling wave along the basilar membrane). But this cannot be the whole story because ototoxic drugs have the same effect, of injuring high frequency more than low frequency hair cells. For some reason the high frequency hair cells are more sensitive to insult: it has been suggested that the high frequency cells generate more reactive oxygen species (ROS: highly charged ions that attach themselves to cell membranes and destroy them) or have fewer scavenger molecules that can soak up the ROS before they do their damage.
Researchers have wondered about the effects of varying the temporal pattern of the noise exposure. Yost suggests that the outcome is too complex to for him to cover. For example, a repetitive noise may allow the auditory system to recover between noise bursts, and thus increase its sensitivity to the insult. Or, it may allow the intratympanic reflex to recover, which would reduce the insult, at least for low frequencies. Or it may be a loud impulse noise, which produces mechanical damage rather than metabolic damage. Thus there seem to be no general principles, though I suspect in general for any noise energy it would be best to spread it out in time, rather that compress it into a very short burst.
The general conclusion about recovery from hearing loss seems to be that recovery from TTS will describe an exponential decay curve, and will be complete with 24 hours, at least when ATS is less than 30 dB. There are a number of studies showing at a gross level that permanent threshold changes are correlated with hair cell damage, most sensitively with stereocilia damage. Experiments on this relationship use trained laboratory animals who are exposed to noise under different conditions, then are killed and the state of the cochlea assessed. Observations of the relationship in humans have been made in patients who have donated their temporal bones (and the remaining hair cells within the temporal bones) to hearing science, and have had their hearing assessed prior to their death, their hair cells counted after their death. Both types of observations show a general relationship, though it is far from perfect. (See Figure 16.6). In part this may result because hair cell loss, which is the basic observation, is only a gross indicator of loss of hair cell function.
The effects of environmental noise include permanent or temporary hearing loss and go beyond these to include interference and distraction at work, speech interference, and loss of sleep and general annoyance. Part of the acoustics profession is concerned with environmental noise, and these people in part act like detectives, sneaking around airports etc. with their noise level meters. For many years it has been recognized that human beings are commonly exposed to noise in two situations. One is factory work, the second is military service. The progression of hearing loss with age shows a steadily increasing loss with many years of exposure, beginning with the high frequencies and then growing increasing severe and proceeding to ever lower frequencies. Nowadays there are OSHA standards for noise limits in the work place that are designed to avoid work related hearing loss, but it is still common to see people working on roads with jack-hammers, and not wearing ear-protectors. Military service provides a constant new source of persons with noise induced hearing loss (as do rock concerts, personal listening devices with ear phone attachments, and shooting expeditions).
Ototoxic drugs which include a number of very useful antibiotics and anti-cancer agents seem to share mechanisms with noise in destroying haircells, including their liberating ROS. Some (aspirin for example in high quantities) can cause tinnitus (“ringing in the ears”) which is another effect of noise exposure, thought to be due to adaptation of inhibitory central processes (GABA) following over stimulation. There are lots of therapies for tinnitus: in fact, that there are so many indicates than none is very effective.
Mammals have been thought not to form new neurons following embryonic development (with some interesting and sometimes controversial exceptions), and when hair cells are severely damaged they die and are not replaced. In other vertebrates neurons do continue to form in adulthood, including hair cells, and the most recent data obtained in birds and in reptiles is that these hair cells are functional. Figure 16.8 shows the bird’s homologue of the basilar membrane after noise exposure, and then (in another bird) this structure 90 days after the noise exposure. Ryals and her coworkers were interested largely in finding out if these effects were characteristic of all groups of birds, and in general the answer was that they were, with differences dues largely to basic differences in the numbers of haircells in the different species: those with more haircells, quail and budgerigars, being more sensitive to noise, and less able to rebuild their hearing, than birds with fewer hair cells, canaries and zebra finches. But all of the birds recovered considerable numbers of hair cells and considerable function.
Although mammalian hair cells do not recover there are certainly changes in the central auditory nervous system that occur as a consequence of hearing loss. (Actually avian hair cells do not recover either, they are replaced by stem cells that differentiate into hair cells. There is presently a lot of interest in getting mammalian stem cells to do similar things in the mammalian nervous system, not so much in hearing that I know about, anyway, but for Alzheimer’s Disease and Parkinson’s.) Willott has found in the aging C67BL mouse with a high frequency hearing loss the formerly high frequency cells become sensitive to low frequencies: whether this is a good thing or not is presently controversial: does it help as compensation? or does it hurt, as distortion, or, perhaps tinnitus? Profoundly deaf individuals respond to other sensory modalities in the auditory cortex, though this changes after cochlear implants. This area of neuroplasticity, and the search for ways to improve and control its limits, is certainly going to be one of the major fields of activity in future years of research.