Page 53 - Volume 12, Issue 2 - Spring 2012

change the perception of this tone from barely audible to very loud. On the other hand, perceivable changes in loudness level at 1 kHz would require larger changes in SPL. The com- bination of SPL threshold increase and range compression results in poor intensity discrimination at low-frequencies in most people.
However, this audio frequency range is misleading and variable, as inter-individual differences in hearing sensitivity allow some people to detect the “inaudible.” Human hearing thresholds have been reported for frequencies from slightly below 20 Hz to as low as 2 Hz in some cases.6,7 Furthermore, humans encounter and detect many high level infrasound sources on a regular basis, despite their high thresholds.5 Auditory cortical responses and cochlear modulations to infrasound exposure have also been observed, despite the subjects’ lack of tonal perception.8,9 These studies provide strong evidence for infrasound impact on human peripheral and central auditory responses.
Infrasound impact on inner ear responses
While normal sound perception depends on inner hair cell (IHC) function, human sensitivity to infrasound and low frequencies is thought to rely heavily on outer hair cells (OHCs).10 Such differential sensitivity between inner and outer hair cells stems from their distinct relationship to the surrounding inner ear structures. Although IHCs and OHCs both sit atop the basilar membrane, the hair (stereovillar) bundles of the OHCs are embedded in the overlying tectori- al membrane, unlike those of the IHCs. Instead, IHC hair bundles are bathed in endolymphatic fluid within the sub- tectorial space and depend on this fluid movement (“squeez- ing waves”) for their stimulation.11 Mechanical energy must be transferred from the basilar and tectorial membranes to the endolymph to displace the IHC hair bundles. Basilar membrane velocity, however, decreases with decreasing stim- ulus frequency.12 At infrasonic frequencies, the low fluid velocity may effectively eliminate IHC hair bundle displace- ment by fluid motion, rendering IHCs insensitive to infra- sound.
In contrast, OHC stereovilli are stimulated directly by the motion of the basilar membrane relative to the tectorial membrane, as they are embedded in the overlying tectorial membrane. The vibrational amplitude of the basilar mem- brane is proportional to sound pressure level and inversely proportional to frequency.11–13 OHCs’ direct coupling to tec- torial membrane movements results in its maintained sensi- tivity to low-frequency sounds; whereas IHCs’ indirect cou- pling to velocity through fluid movements results in lowered sensitivity. As low-frequency sounds generate significant basilar membrane displacements but low basilar membrane velocities, OHCs are selectively stimulated over IHCs. Furthermore, low-frequency sounds generate minimal endolymphatic viscous forces, allowing maximal stretching of stereovillar tip links for OHC depolarization.14 It is impor- tant, therefore, to keep in mind that high-level, low-frequen- cy stimuli can result in large shearing forces on the OHC stereovilli, but minimal fluid-coupled displacements of IHC stereovilli.
Low-frequency induced OHC intracellular depolariza- tion can be measured as an extracellular voltage change, namely the cochlear microphonic (CM). At 10 Hz (90 dB SPL), CM amplitudes exceed that of the IHC intracellular
10,15
While type I afferent activation by infrasound has not yet been exten- sively studied, these data suggest that infrasound has the potential to induce suprathreshold depolarization in IHCs and type I afferent fibers, through large CMs. Subsequent transmission and interpretation of type I afferent signals in
the brain would be especially interesting to examine.
In addition to CMs, distortion product otoacoustic emis-
sions (DPOAEs) have also demonstrated human inner ear
sensitivity to infrasound. DPOAE recordings allow non-inva-
sive, indirect evaluations of cochlear amplifier characteris-
tics. To elicit DPOAEs, two different pure tones (primaries),
f1 and f2, are introduced into the ear by placing into the ear
canal a sound probe containing two miniature speakers. As
the primaries-generated traveling waves propagate along the
basilar membrane, they interact and produce additional trav-
17
eling waves. These waves propagate out of the inner ear,
52 Acoustics Today, April 2012
potentials as a result of basilar membrane displacement. CM generation in response to this 10 Hz tone provides con- crete evidence for OHC sensitivity to infrasound in the guinea pig. Meanwhile, large CMs generated by OHCs at 40 Hz (112 dB SPL) can electrically stimulate the IHCs to acti-
15,16
vate type I afferent fibers in the spiral ganglion.
generating DPOAEs that are recorded by a microphone in the sound probe. The most prominent and easily measurable DPOAE in humans and other animals is the cubic difference distortion product, 2f1-f2, typically produced by primary tone ratios (f /f ) between 1.2 to 1.3.18
21
Hensel et al. (2007) used primaries of f1=1.6 and f2=2.0
kHz (f2/f1=1.25) at L1=51 and L2=30 dB SPL for their 8
DPOAEs recordings. With the primaries within the normal human audio frequency range, the returning DPOAE repre- sents a typical operating point of the cochlear amplifier. Infrasonic biasing tones (fb) of 6 Hz, 130 dB SPL and 12 Hz, 115 dB SPL were then introduced and resulting DPOAEs were recorded. When compared to the primaries-only-gener- ated DPOAE pattern, fb-generated DPOAEs showed signifi- cant changes in amplitude and phase due to the shifting of the cochlear amplifier operating point. Since the fb-generated DPOAE pattern changed relative to the pattern evoked by the primaries-only-generated DPOAES, it may be then conclud- ed that the infrasonic biasing tones had an observable impact on inner ear function.
High level biasing tones provide large vibrational ampli- tudes that can alter the movement of the cochlear partition, or net pressure across it. The induced pressure gradient in turn shifts the mean position (a DC shift) of the basilar mem- brane. Such a phenomenon parallels the slow motility mech- anism of OHCs. Just as OHC soma contractions alter the dimensions of the subtectorial space to enhance or reduce hearing sensitivity, the shift in basilar membrane position also changes subtectorial volume and adjusts hearing sensi- tivity. In another words, the gain of the cochlear system can be affected by high level infrasound. Moreover, the modula- tions seen in fb-generated DPOAEs reflect differential travel-