Decruitment and the Growth of Loudness in the Ears of Brain-Damaged Adults (1973): A Historical Article Review from the Archives

A Historical Vignette . . .

Editor’s note: Occasionally Pathways will issue a review and discussion of a historical article that at the time of publication that was innovative and of significant value. The following is such an article – with its value carrying over to the present day. This article was brought to our attention by Jim Jerger and created an interest in a number of our doctoral students (Carrie Clancy, Jillian Bushor, and Maggie Schefer) who pursued learning more about the article and writing this review. We also asked Dr. Jerger to comment on the article and review since he was one of the originators of this research and we are most pleased to publish his insightful comments. -FM

 

Background

The Alternate Binaural Loudness Balancing (ABLB) procedure was initially developed as a measure of recruitment, or abnormally rapid loudness growth, which is often seen in cases of cochlear hearing loss (Fowler, 1928). In patients with asymmetrical sensorineural hearing loss, abnormal loudness growth in the poorer ear is often associated with outer hair cell dysfunction; loudness growth abruptly reaches “normal” levels at high intensities, when the inner hair cells engage. In his 1960 study Observations on Auditory Behavior in Lesions of the Central Auditory Pathways, James F. Jerger assessed three listeners with temporal lobe lesions using the ABLB procedure. On the ABLB, he observed that these patients consistently mismatched a fixed-intensity (reference) tone presented to the ear ipsilateral to the lesion and variable higher-intensity tones presented to the contralateral ear. Hallowell Davis and Allan C. Goodman (1966) later confirmed Jerger’s observations in five of their own patients. They explained the observed phenomenon, which they called “decruitment,” in terms of differential interaural rates of loudness growth, where each intensity increase in the ipsilateral ear was accompanied by a disproportionately small increase in loudness growth in the ear contralateral to the side of brain lesion. See Figure 1 for a comparison of recruitment and decruitment effects on loudness balancing.

The Mencher, Clack, and Rupp study Decruitment and the Growth of Loudness in the Ears of Brain-Damaged Adults (1973) addressed several questions raised by procedural details of the Jerger study and the Davis and Goodman study. First, neither of the first two studies used the contralateral ear as a reference to report the presence or absence of similar mismatches in the opposing condition. The original studies using the ABLB procedure assumed normal loudness growth in one ear (the ear ipsilateral to the lesion), and therefore assumed that comparison of loudness growth rates between the two ears would reveal differences, without discrete measurement of loudness growth in each ear individually. Finally, neither of the original studies used a different measure of loudness matching (i.e., ratio scaling) to confirm reliability.

         

 FIG. 1

 

Materials & Methods (Subjects)

The Mencher et al. study compared ABLB results with monaural Sone scale constructions in three groups of listeners: normal listeners with no history of peripheral hearing loss (Group A), patients with non-temporal lobe brain injuries “which should not have involved the auditory system” (Group B), and patients with left hemisphere temporal lobe damage affecting the auditory system (Group C). The twenty-one subjects were matched for age and sex across each of the three groups. All subjects’ hearing thresholds were tested at 1000 Hz to confirm thresholds of 15 dB HL or lower with differences of 5 dB or less between ears. Subjects’ speech reception thresholds were consistent with their pure tone thresholds. All patients with brain damage (Groups B and C) reported tinnitus and having “quality differences” between ears, and the majority of these patients also displayed aphasia and/or apraxia. Site of lesion in each participant was confirmed by results from a minimum of three of the following seven measures: neurological examination, EEG, carotid arteriogram, pneumoencephalographic x-ray, skull x-ray, brain scan, and/or surgical operation. However, the hemisphere of lesion was not specified in the patients with non-temporal lobe lesions.

Procedures

Mencher et al. assessed the results of the ABLB procedure versus Ratio Scaling of Loudness in normal and temporal lobe damaged patients. To begin the ABLB, they presented listeners with a 1000 Hz reference tone to one ear at one of several predetermined intensities (threshold, 10, 20, 30, 40, 50, or 60 dB SL), which were randomly selected for trials to eliminate order effects. A variable-intensity 1000 Hz signal was presented to the participants’ opposite ear, and they were asked to adjust the loudness of the variable signal until it matched the loudness of the reference tone. To ensure good test-retest reliability, researchers obtained loudness-matched values for each intensity level three times over the course of two sessions. Results for the ABLB were obtained using the difference between reference ear intensity and variable ear intensity. These interaural intensity differences were established for both the left and right ear as the reference ear.

Following the ABLB, participants’ were tasked with constructing a monaural Sone scale using a reference point of 1 Sone, where 1 Sone was considered to be equivalent to a 1000 Hz tone at 40 dB SL for each participant. Participants were alternately presented with this 1 Sone reference and variable-intensity tones, which the participants were instructed to adjust until they sounded “twice as loud” or “half as loud” as the original reference tone. Participants were allowed to refer back to the reference tone at any point in testing to confirm their adjustments. Repeated measures allowed researchers to construct individual Sone scales based on the doubling and halving of intensities each participant demonstrated.

Results

Mencher and his colleagues analyzed the mean level differences in the ABLB results of the three groups, and noticed a few significant trends. For Group A, they noted two visible trends. First, at 30 dB SL and below, there was consistent representation of negative and positive intensity for the right and left ear reference conditions respectively. Second, at 60 dB SL, all but one subject in Group A underestimated the equal intensity level. In Group B, the mean imbalances followed the underestimation trends set by the normals. In addition, five of the seven participants in Group B yielded greater mismatching of loudness levels; these, however, were still within the normal range. The Group C patients displayed interaural level differences no less than twice those of Groups A and B. Group C patients also tended to greatly overestimate loudness with a 40 dB SL reference tone in the left ear condition. Group B patients tended to underestimate equal intensity levels with a 40 dB SL reference tone in the right ear reference condition; conversely, researchers observed the same underestimations in the left ear condition for three members of Group C.

Mencher, Clack, and Rupp concluded that there was no significant variance in loudness balancing between Groups A and B, yet Group C performed significantly differently in regard to both individual variability and mean decibel level difference when balancing loudness to the contralateral ear. They found that in the contralateral reference condition, there was still some variability, but all three groups rated interaural intensity differences much more consistently. Ultimately, variability was greatest in the temporal lobe group, which is indicative of “decruitment” (Davis & Goodman, 1966) occurring for all subjects in Group C. In contrast to the results of the ABLB, when Mencher et al. analyzed the individually constructed Sone scales, they were unable to find any significant differences among the groups.

Comments & Discussion

Though the ABLB was conceived as a measure of recruitment in cochlear hearing loss, the three studies referenced here–Jerger (1960), Davis and Goodman (1966), and Mencher, Clack, and Rupp (1973)–used the ABLB to look at a seemingly opposite phenomenon, namely decruitment, or abnormally slow loudness growth, in cases of known CANS abnormality. Without the benefit of modern equipment or imaging techniques, these researchers combined a classic but underutilized audiologic evaluation technique and a novel research approach to conclude that decruitment in patients with temporal lobe damage is not indicative of abnormal loudness balancing per se, but rather abnormal binaural integration of auditory information in the CANS. Mencher and his colleagues took the further step of comparing these patients’ ABLB results to their monaural Sone scale constructions, and the differences in those results highlight the particular potential for clinical utility of the ABLB in cases of CANS involvement.

Unlike the monaural Sone scaling task, the ABLB measure is easy to administer and can be accomplished on most audiometers equipped with two channels. Unfortunately, the ABLB has been forgotten or underutilized by most audiologists for some time now. Though its primary purpose is measuring recruitment in unilateral or asymmetric hearing loss, it could also be used to determine the amount of gain needed for hearing aids. Additionally, the ABLB can be a very efficient test, when the poorer ear is used as the reference, to assess for the presence of decruitment (Jerger, 1962).

Though recruitment is usually understood as a cochlear phenomenon, more recent thinking points to possible CANS involvement in recruitment as well. For example, if loudness correlates with the number of neurons carrying the auditory signal, and if the number of operational neurons is somehow reduced by an injury or a lesion such as acoustic tumor, it would follow that the representation of loudness in the CANS would also be reduced on the affected side. Recent animal studies, such as Salvi et al. (1996) and Kujawa and Liberman (2009) have demonstrated a reorganization of neural response patterns in the auditory nerve and CANS after cochlear hearing loss. These studies might seem to implicate “brain gain”, or the central nervous system’s ability to compensate for compromised sensory input, as a possible component in abnormal perception of loudness growth (Musiek, 2016). If these effects can be observed on a simple clinical test like the ABLB, then there is justification for adapting and including that test in the auditory assessment battery for cases where auditory nerve or CANS involvement is suspected.

 

Comment from Jim Jerger

Thanks very much for the review; and my compliments to your three students for a very nice job. Their point about using ABLB as a diagnostic procedure in more central disorders is well taken. Another point illustrated by the sequence of the three articles (Jerger, Davis & Goodman, and Mencher et al.) is that we usually get into trouble when we stray from operational definitions of diagnostic measures into the hazardous practice of naming procedures according to what we think we are measuring. Many years ago, for example I did quite a bit of ABLB testing on patients with Meniere’s Disease. Using a method of adjustment, I would instruct the patient as follows, “You will hear a sound that alternates between ears. Turn this knob until the alternating sound has the same loudness in both ears”. More often than not the patient would reply. “ I cannot do it because the sound in one ear is not the same as the sound in the other ear.” It sounds more like a noise in my bad ear”. I became wary of the procedure after that. I should have stopped using the word loudness right then and there because it clearly was not a “balancing of loudness”. But I persisted for some years. Davis and Goodman introduced the term “decruitment,” and that confounded the problem to a newer level by conflating “loudness “ with “recruitment”, another non-operationally defined term. Mencher et al. proposed to stab at the heart of the problem by having the listeners do halving and doubling operations, but halving and doubling of what? If it doesn’t sound right to begin with, does halving and doubling tell you anything about loudness? 

I think that all three of us used the term loudness too freely. If it doesn’t sound the same in the two ears, then more than ever one should avoid speculating about equivalence of loudness and just stay with the operations leading to the observed curious data.

 

References

  1. Colin, D., Micheyl, C., Girod, A., Truy, E., & Gallego, S. (2016). Binaural diplacusis and its relationship with hearing-threshold asymmetry. PLoS ONE, 11(8).
  2.  Davis, H., & Goodman, A.C. (1966). Subtractive hearing loss, loudness recruitment and decruitment. Annals of Otology, Rhinology & Laryngology, 75(1), 87–94. doi:10.1177/000348946607500106
  3. Fowler, E.P. (1928). Marked deafened areas in normal ears. Archives of Otolarynglogy, 8:151-155.
  4. Fowler, E.P. (1937). Measuring the sensation of loudness: A new approach to the physiology of hearing and the functional and differential diagnostic tests. Archives of Otolaryngology, 26(5):514–521. doi:10.1001/archotol.1937.00650020568002
  5. Hoth, S., & Baljić, I. (2017). Current audiological diagnostics. GMS Current Topics in Otorhinolaryngology, Head and Neck Surgery, 16.
  6. Jerger, J.F. (1960). Observations on auditory behavior in lesions of the central auditory pathways. Archives of Otolaryngology, 71(5):797-806. doi:10.1001/archotol.1960.03770050057009
  7. Jerger, J.F. (1962). Comparative evaluation of some auditory measures. Journal of Speech and Hearing Research, 5(1).
  8. Carver, W.F. (1978). Loudness balance procedures. In J. Katz, Handbook of Clinical Audiology, 2nd ed. (pp. 164-178). Baltimore, MD: Williams & Wilkins, Co.
  9. Kujawa, S.G. & Liberman, M.C. (2009). Adding insult to injury: Cochlear nerve degeneration after “temporary” noise-induced hearing loss. Journal of Neuroscience, 29(45):14077-14085. doi:10.1523/JNEUROSCI.2845-09.2009
  10. Mencher, G.T., Clack, T.D., & Rupp, R.R. (1973). Decruitment and the growth of loudness in the ears of brain-damaged adults. Cortex, 9(4):335-45.
  11. Musiek, F.E., (2016, August 3). Loudness recruitment: a commentary. Retrieved from https://hearinghealthmatters.org/pathways/2016/loudness-recruitment-commentary/
  12. Pastore, R.E., & Flint, J. (2011). Magnitude judgments of loudness change for discrete, dynamic, and hybrid stimuli. Attention, Perception and Psychophysics, 73(3):886-907.
  13. Salvi, R.J., Wang, J., & Powers, N. (1996). Rapid functional reorganization in the inferior colliculus and cochlear nucleus after acute cochlear damage. In: R.J. Salvi, et al. (Eds.), Auditory Plasticity and Regeneration (pp. 275-295) New York: Thieme Medical Publishers.
  14. Teghtsoonian, R., Teghtsoonian, M., & Canévet, G. (2005). Sweep-induced acceleration in loudness change and the “bias for rising intensities”. Perceptual Psychophysics, 67(4):699-712.

 

Carrie Clancy is a first year AuD student at the University of Arizona. She has received Bachelor of Arts degrees in Music and Speech-Language Pathology/Audiology and a Master of Music degree from the University of Nebraska.

Jillian Bushor is a first year AuD student at the University of Arizona. She has received a Bachelor of Science degree in Communication Sciences and Disorders from the University of Vermont.

Maggie Schefer is a first year AuD student at the University of Arizona. She has received Bachelor of Science degree in Communication Sciences and Disorders from the University of Vermont.

About Pathways

Pathways is both a column that covers topics related to CAPD and Neuroaudiology and a society for people interested in central auditory disorders that regularly meets to discuss these issues.

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