Jannica Dale and Dr. Wendy Hanks, Audiology
Under the supervision of two of my professors and a graduate student, I participated in research investigating whether or not contralateral suppression affects the hearing system and what any effects may be. We focused on two specific aspects of the hearing system, the acoustic reflex and otoacoustic emissions. Unfortunately, our research could not be completed within the semester time frame and my participation ended just before our first formal 10 subject pilot. We ran into several difficulties with our equipment and our initial procedure, but our failures have prepared the way for a more accurate and valid study. We used the Virtual 310 instrument for the acoustic reflex portion and the ILO88 system for the otoacoustic emissions.
The acoustic reflex is a bilateral mechanism of the ear. When a sound intensity reaches an individual’s acoustic reflex threshold or above (ranging anywhere from 60 to 100 dB HL), the tympanic membrane (the eardrum) and the ossicles (the tiny bones of the middle ear) stiffen, which dampens the sound’s intensity as it enters the inner ear, more specifically the cochlea. We wanted to try to contralaterally suppress this mechanism using whitenoise 5 dB and 30 dB above threshold. For each subject, we established the acoustic reflex at 500 Hz and 2000 Hz, and the whitenoise threshold. A probe inserted in the test ear was responsible for the acoustic reflex and a headphone on the non-test ear introduced the whitenoise. Using the threshold information, we used the following pattern for each trial (total time of 20 seconds): 2 seconds of quiet, at 2 seconds introduce acoustic reflex threshold + 5 dB lasting for 8 seconds, at 10 seconds introduce whitenoise with maintained acoustic reflex + 5 lasting for 6 seconds, at 16 seconds eliminate whitenoise but continue acoustic reflex + 5 dB lasting 4 seconds, at 20 seconds eliminate acoustic reflex + 5 dB and end trial. The pattern was repeated on each ear interchanging the acoustic reflex aspect at 500 Hz and 2000 Hz, and suppression element at 5 dB or 30 dB above whitenoise threshold. This made four trials for each ear for a total of 8 trials.
Otoacoustic emissions (OAEs) are low-level sounds or bursts of energy that are generated in the cochlea, specifically by the outer hair cells, but can be recorded in the external ear canal. Our research called for two types of OAEs, transient otoacoustic emissions (TEOAEs) and distortion product otoacoustic emissions (DPOAEs). For this portion, we continued using whitenoise contralateral suppression at 5 dB and 30 dB above whitenoise threshold at 500 Hz and 2000 Hz. We also ran trials without suppression at 500 Hz and 2000 Hz to compare with the suppression trials. Again, a probe inserted in the test ear introduced the TEOAEs (a series of clicks) or the DPOAEs (a series of tones), and the headphone on the non-test ear introduced the whitenoise with the trials requiring suppression. As a further check, we ran each trial twice, making 12 trials for each ear and a total of 24 trials for this part of our research.
Since the research is incomplete, it is difficult to discuss any clear results or conclusions. We saw some instances of definite acoustic reflex suppression in our group of about 8 subjects, but also saw cases of little to no suppression. In general, the acoustic reflex rarely returned to the original level 69 before the introduced suppression. We also witnessed a great deal of decay at the 2000 Hz level. Naturally, there was usually more obvious suppression using whitenoise thresholds + 30 dB than with an added 5 dB. There are several possibilities for all of these results. The group of 8 subjects we tested was no formal pilot. We screened each subject based on the predetermined criteria, but tested each one regardless of pass or fail in order to practice and evaluate our testing procedure and equipment. This is why I have not bothered to mention our screening criteria. We occasionally had trouble pinpointing a subject’s true acoustic reflex threshold because of our equipment. The trial pattern was not one hundred percent precise for each trial due to human errors since we initialized the acoustic reflex and suppression intervals manually based on time markers. Any of these could have affected our data.
An explanation for the OAE testing is even more vague at this point. The results for the suppression trial versus the non-suppression trials did not appear to be significantly different. Again, it is important to mention not all of the subjects passed the screening criteria because we were more concerned with establishing our procedure at that point of the research. The equipment used for testing OAE is also much more sensitive than that used with the acoustic reflex. This is one of the main reasons that we were unable to get as far with the OAE testing as we were with the acoustic reflex testing.
We did make some changes in our procedure in preparation for a formal pilot of 10 subjects. We altered the trial pattern to the following (total time of 20 seconds): 2 seconds of quiet, at 2 seconds introduce acoustic reflex threshold + 5 dB lasting for 6 seconds, at 8 seconds introduce whitenoise with maintained acoustic reflex + 5 lasting for 6 seconds, at 14 seconds eliminate whitenoise but continue acoustic reflex + 5 dB lasting 4 seconds, at 18 seconds eliminate acoustic reflex + 5 dB, at 20 seconds end trial. This change was to see if the response would be the same in the last 2 seconds as in the initial 2 seconds of quiet, as well as to generally better analyze the suppression data. We also randomized each group of trials for each subject. The minor inconsistencies with manually initiating the acoustic reflex trials and the occasional true acoustic reflex threshold debate have not yet been dealt with. We speculated on eliminating the 2000 Hz acoustic reflex level because there was so much decay, but it is still included.
Based on my participation, I expect there will be consistent acoustic reflex suppression as the research continues. Other research has shown OAE suppression and I think it will be seen here as well. The degree of suppression and the surrounding circumstances will help determine which pathways are involved, but this research has not progressed enough to speculate further at this time.
References
- Martin, Frederick N. and John Greer Clark. 1996. pp. 140. In: Hearing Care for Children Allyn and Bacon, Needham Heights, MA.
- A special thanks to Dr. Hanks, as well as Dr. McPherson and Chris Sanford.