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A Sound Therapy-Based Intervention toExpand the Auditory Dynamic Range forLoudness among Persons with SensorineuralHearing Losses: A Randomized Placebo-Controlled Clinical Trial

Craig Formby, Ph.D.,1 Monica L. Hawley, Ph.D.,2

LaGuinn P. Sherlock, Au.D.,3 Susan Gold, M.A.,4 JoAnne Payne, M.S.,1

Rebecca Brooks, M.A.,1 Jason M. Parton, Ph.D.,1

Roger Juneau, B.S.M.E.,5 Edward J. Desporte, M.S.,5 andGregory R. Siegle5

ABSTRACT

The primary aim of this research was to evaluate the validity,efficacy, and generalization of principles underlying a sound therapy–based treatment for promoting expansion of the auditory dynamic range(DR) for loudness. The basic sound therapy principles, originallydevised for treatment of hyperacusis among patients with tinnitus,were evaluated in this study in a target sample of unsuccessfully fit and/or problematic prospective hearing aid users with diminished DRs(owing to their elevated audiometric thresholds and reduced soundtolerance). Secondary aims included: (1) delineation of the treatmentcontributions from the counseling and sound therapy components to thefull-treatment protocol and, in turn, the isolated treatment effects fromeach of these individual components to intervention success; and (2)characterization of the respective dynamics for full, partial, and controltreatments. Thirty-six participants with bilateral sensorineural hearinglosses and reduced DRs, which affected their actual or perceived abilityto use hearing aids, were enrolled in and completed a placebo-controlled(for sound therapy) randomized clinical trial. The 2 � 2 factorial trialdesign was implemented with or without various assignments ofcounseling and sound therapy. Specifically, participants were assigned

1Department of Communicative Disorders, University ofAlabama, Tuscaloosa, Alabama; 2Department of Otolaryn-gology, University of Iowa, Iowa City, Iowa; 3Walter ReedNational Military Medical Center, Bethesda, Maryland;4Retired; previously affiliated with University of MarylandTinnitus & Hyperacusis Center, Baltimore, Maryland;5General Hearing Instruments, Harahan, Louisiana.

Address for correspondence: Craig Formby, Ph.D.,Department of Communicative Disorders, University of

Alabama, 700 University Blvd. E, Room 145, Tuscaloosa,AL 35487 (e-mail: [email protected]).

Sound Therapy-Based Treatment to Expand the Audi-tory Dynamic Range; Guest Editor, Craig Formby, Ph.D.

Semin Hear 2015;36:77–110. Copyright # 2015 byThieme Medical Publishers, Inc., 333 Seventh Avenue,New York, NY 10001, USA. Tel: +1(212) 584-4662.DOI: http://dx.doi.org/10.1055/s-0035-1546958.ISSN 0734-0451.

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mailto:

http://dx.doi.org/10.1055/s-0035-1546958

randomly to one of four treatment groups (nine participants per group),including: (1) group 1—full treatment achieved with scripted counsel-ing plus sound therapy implemented with binaural sound generators;(2) group 2—partial treatment achieved with counseling and placebosound generators (PSGs); (3) group 3—partial treatment achieved withbinaural sound generators alone; and (4) group 4—a neutral controltreatment implemented with the PSGs alone. Repeated measurementsof categorical loudness judgments served as the primary outcomemeasure. The full-treatment categorical-loudness judgments forgroup 1, measured at treatment termination, were significantly greaterthan the corresponding pretreatment judgments measured at baseline at500, 2,000, and 4,000 Hz. Moreover, increases in their “uncomfortablyloud” judgments (�12 dB over the range from 500 to 4,000 Hz) weresuperior to those measured for either of the partial-treatment groups2 and 3 or for control group 4. Efficacy, assessed by treatment-relatedcriterion increases � 10 dB for judgments of uncomfortable loudness,was superior for full treatment (82% efficacy) compared with that foreither of the partial treatments (25% and 40% for counseling combinedwith the placebo sound therapy and sound therapy alone, respectively) orfor the control treatment (50%). Themajority of the group 1 participantsachieved their criterion improvements within 3 months of beginningtreatment. The treatment effect from sound therapy was much greaterthan that for counseling, whichwas statistically indistinguishable inmostof our analyses from the control treatment. The basic principlesunderlying the full-treatment protocol are valid and have generalapplicability for expanding theDR among individuals with sensorineuralhearing losses, who may often report aided loudness problems. Thepositive full-treatment effects were superior to those achieved for eithercounseling or sound therapy in virtual or actual isolation, respectively;however, the delivery of both components in the full-treatment approachwas essential for an optimum treatment outcome.

KEYWORDS: Sound tolerance, loudness discomfort level,

hyperacusis, sound therapy

Learning Outcomes: As a result of this activity, the participant will be able to (1) describe a method for

creating a placebo sound therapy condition and (2) describe the efficacy of sound therapy and counseling as

compared to sound therapy alone, counseling alone, or no treatment.

We report here the findings from a small-scale, randomized, placebo-controlled trial toassess the validity, efficacy, and generality ofprinciples underlying intervention to expandthe auditory dynamic range (DR) for loudnessamong persons with sensorineural hearinglosses. The basic treatment principles, describedoriginally by Hazell and Sheldrake in 1992,1

were designed for treatment of debilitatingtinnitus and associated hyperacusis. Their treat-

ment protocol, which combined low-levelsound therapy with counseling (that encour-aged healthy environmental sound exposure),was later incorporated together with Jastreboff’sneurophysiological model of tinnitus.2,3 Theresulting treatment model and protocol is pop-ularly known today as “tinnitus retraining ther-apy” (TRT).4 TRT has been used withconsiderable success globally to treat tinnitusfor the past two decades. Over this period, the

78 SEMINARS IN HEARING/VOLUME 36, NUMBER 2 2015

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TRT protocol has been modified to categorizeand manage patients with tinnitus differentiallybased upon the individual patient’s hearingstatus, tinnitus, and sound tolerance com-plaints.4 Consequently, protocols now existwithin TRT for managing sound tolerancecomplaints, including hyperacusis, misophonia,and phonophobia, usually in association withtinnitus.4–6

In this project, the basic principles of thesound therapy intervention, described byHazell and Sheldrake, 1 were evaluated in atarget group of hearing-impaired persons, whowere not primarily bothered by tinnitus butwere restricted in the use of amplified soundfrom hearing aids because of their reducedDRs for loudness. Their reducedDRs reflectedtheir elevated audiometric thresholds and, onaverage, lower-than-normal loudness discom-fort levels (LDLs). Our target study group wasmostly individuals who would not routinely beseen in a specialty tinnitus and hyperacusisclinic for their sound tolerance conditions.However, their conditions adversely affectedtheir perceived or expected benefit for aidedsound. Consequently, they often reported hav-ing tried but rejected hearing aid use; assumedthey could not tolerate amplified sound and,therefore, never tried hearing aids; or at-tempted to use amplification, but describedusing it ineffectually. For these individuals tohave been fitted successfully with hearing aids,they typically would have required largeramounts of compression, inordinate decreasesin maximum output level, or diminished pre-scriptive target gains to manage their soundintolerance for amplified sound. The resultingadverse effects of these remedies would vari-ously have manifested as reduced and subopti-mal DRs, diminished hearing aid saturationlevels (which together with compression ef-fects would give rise to enhanced signal dis-tortion), and inadequate amplification levelsset to avoid overstimulation.7 Overamplifica-tion, as perceived by the individual with soundtolerance problems, to achieve aided prescrip-tive target gain levels also may have contribut-ed to hearing aid rejection. Each of theseproblems alone, or in combination, wouldconfound an otherwise successful hearing aidfitting strategy.

Preliminary to describing our study of thistarget group, we consider the historical back-ground for conducting this investigation, be-ginning with early efforts to improve soundtolerance and promote DR expansion amongpersons with hearing loss by presenting repeat-ed exposures to brief high-intensity sounds.8,9

We then consider Hazell and Sheldrake’s low-level sound therapy approach and its evolutionas a primary treatment for hyperacusis anddecreased sound tolerance.1,4 This backgroundsets the stage for the motivation, purpose, andaims of our research.

BACKGROUND

Sound Tolerance Training

The idea of modifying sound tolerance amonghearing-impaired persons to expand their DRsand, concomitantly, to enhance hearing aid useand benefit is a long-standing challenge inaudiology.10 Despite research on this vexingclinical problem formore than half a century, notreatment has proven to be consistently success-ful for modifying sound tolerance.11–13 Theprimary treatment approach heretofore for ex-panding the auditory DR comes out of militaryresearch and related efforts during World WarII. Silverman’s early studies of sound tolerancetraining at the Central Institute for the Deaf arethe most extensive and relevant, and the re-search includes results for normal and hearing-impaired listeners for a range of pure tone andspeech stimuli.9 The approach was based on theidea that a listener’s tolerance to high-levelsounds might be enhanced by brief tougheningtraining exposures to intense sound presentedjust below the hearing-impaired listener’s LDL.Silverman reported �10-dB increases in LDLsfor both normal and hearing-impaired listenersfollowing brief (several minutes) weekly expo-sures to high-level pure tones and speech over a6-week training period.9Most of the incremen-tal LDL shifts reported by Silverman wereachieved between the first and second or thirdtraining sessions. Although there was earlyenthusiasm for Silverman’s sound tolerancetraining strategy,8 the general consensus todayis that this approach is not beneficial.11–13 Itremains unclear whether the resulting

SOUND THERAPY-BASED INTERVENTION/FORMBY ET AL 79

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incremental LDL shifts from sound tolerancetraining are real or simply a practice effect.12

Notwithstanding clarification of this issue,sound tolerance training with high-level soundsmay be an uncomfortable, if not a painful,protocol that is not practiced clinically today.

Hazell and Sheldrake’s Sound Therapy

Treatment

In marked contrast to the brief high-level soundexposures used by Silverman for sound tolerancetraining in normal-hearing and hearing-impaired adults,9 Hazell and Sheldrake’s inno-vative sound therapy strategy evolved fromefforts to manage hyperacusis among theirpatients with tinnitus.1 For the sake of economy,and in the absence of a consensus definition, wewill define hyperacusis as a general intolerance tothe loudness of sounds that would not typicallybe bothersome for most individuals.14 Audio-logically, hyperacusis manifests as an abnormalreduction in the LDLs, usually below �90-dBhearing level (HL) binaurally, across frequen-cies. Hyperacusis may occur with or withouthearing loss or associated tinnitus but is rou-tinely accompanied by subjective reports ofsound intolerance. Pain and/or distress may ormay not accompany these subjective complaintsof reduced sound tolerance.15,16

Hazell and Sheldrake’s novel sound thera-py protocol for treating patients with tinnitusand primary hyperacusis was implemented withcontinuous 6-hour exposures, daily, to low-level, high-frequency emphasis broadbandnoise.1 The noise was produced by behind-the-ear noise maskers fitted with open-canalearmolds. Their sound therapy protocol calledfor the initial presentation of the noise to be“just audible above the threshold.” Subsequent-ly, their patients were instructed to increasegradually, day by day, the volume settings untila point was reached at which the majority oftroubling environmental sounds was toleratedwithout difficulty. The counseling componentof their protocol encouraged their patients “tostop the avoidance of sound in their environ-ment, except when this presented an ordinaryrisk of damage to the ear.” They also advisedtheir patients not to use sound-attenuatinghearing protection during normal daily activi-

ties; Hazell and Sheldrake noted that because ofthe debilitating hyperacusis conditions, hearingprotection was in use by 23 of their 30 patientsprior to the start of treatment. Hazell andSheldrake presented only a limited descriptionof counseling in their brief conference proceed-ings report.1 Sheldrake (personal communica-tion, 2013) indicates counseling was, in fact, animportant component of their protocol acrossthree in-clinic treatment sessions. These ses-sions covered guidance in the theory and appli-cation of the desensitizing sound therapy fortreatment of hyperacusis, and instruction in theuse of the low-level noise maskers for thispurpose. Their hyperacusis counseling strategyeffectively mirrored that outlined by Sheldrakeand colleagues for tinnitus management.17

Hazell and Sheldrake described a remark-able treatment outcome for their hyperacusisgroup, namely, sizable and statistically signifi-cant improvements in LDL judgments acrossaudiometric frequency (excluding 8,000 Hz).1

These positive treatment effects typically re-flected expanded DRs, on the order of 8 to10 dB, which often corresponded to symptom-atic improvements in their patients’ hyperacusisconditions. Hazell and Sheldrake describedgood results as being achieved by 10% of thehyperacusis group within 1 month, 53% within2 months, and 73% within 6 months of begin-ning treatment. Their other patients eitherrequired longer than 6 months for benefit or,in the case of 10% of the group, were not helpedby the intervention. Hazell and Sheldrake notedthat those patients who benefited from treat-ment typically sustained their benefits withoutfurther use of the noise maskers posttreatment.

Evolution of Hazell and Sheldrake’s

Sound Therapy Principles for

Treatment of Hyperacusis and

Diminished Sound Tolerance

Subsequent to Hazell and Sheldrake’s obscurebut seminal proceedings report,1 Jastreboff andHazell incorporated sound therapy within atreatment protocol for tinnitus, which in duecourse was to become known popularly asTRT.2,4 Their TRT protocol has evolved overtime to include sound therapy and an expandedcounseling protocol in a separate and distinct


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treatment approach for hyperacusis (i.e.,TRT-H). Today, one can find several TRToutcome studies (mostly published in tinnitusconferences proceedings18–20) that supportHazell and Sheldrake’s early use of low-levelsound therapy as a treatment for hyperacusis. Asummary of these treatment effects (i.e., treat-ment-induced incremental LDL shifts) inthe TRT literature reveals appreciably larger(�20-dB) treatment-related LDL shifts formore severely impaired hyperacusis patientscompared to the smaller treatment effects re-ported by Hazell and Sheldrake.1,21 Moreover,sizable but less pronounced secondary treat-ment effects (i.e., secondary to the primarytreatment effects on tinnitus) have been re-ported for patients with tinnitus treated byTRT.22 These positive secondary treatmenteffects appear to be largely independent ofhearing loss for patients with tinnitus whowere able to use noise (or sound) generatorsfor their sound therapy (as long as the audio-metric ceiling was not a confounding factor inthemeasurement range of the LDL values).Wealso now know that the use of sound generatorslike the kind worn for TRT sound therapy canaffect the elevation of LDLs in normal listenersafter 2 to 4 weeks of chronic use without anyassociated counseling.22,23 The resulting treat-ment effects reflect average increases in the DRby 6 to 8 dB, which is slightly smaller than thatreported by Hazell and Sheldrake in theirtreatment of hyperacusis with counseling anddaily low-level noise exposure.1

Purpose and Aims of This Study

A growing body of evidence suggests thatapplications of Hazell and Sheldrake’s soundtherapy and counseling principles may benefit abroad group of hearing-impaired individuals,not just those with debilitating tinnitus and/orprimary hyperacusis.1 Of particular interest inthis study is the application of those principlesto unsuccessful hearing aid users, who weredifficult to fit because of their reduced DRs(resulting from some combination of lower-than-normal LDLs and elevated audiometricthresholds). To the extent that Hazell andSheldrake’s counseling and sound therapy prin-ciples may be applicable and beneficial for a

relatively typical and generic hearing-impairedpatient group with mild sound tolerance prob-lems, and there is no reason a priori to believeotherwise, we would predict successful expan-sion of their DRs, improved sound toleranceand comfort for amplified sounds, and, ulti-mately, enhanced hearing aid benefit and satis-faction following completion of a successfultreatment. That is, the successful treatmentwould achieve the overarching objectives thatDavis et al, early on, had hoped to achieve withhigh-level sound tolerance training.8 Accord-ingly, the primary purpose of this study was toevaluate the validity and efficacy of Hazell andSheldrake’s intervention principles and theirgeneralized applicability (i.e., generality) to arelatively traditional sample of individuals withsensorineural hearing impairments whose hear-ing aid benefit or perceived potential to usehearing aids was limited by their reduced DRsand tolerance for amplified sound.

Of secondary interest in this study was thedelineation of the treatment contributions fromthe counseling and sound therapy componentsin the full-intervention protocol and the respec-tive treatment dynamics. Counseling representsa significant treatment component in the currentTRT-H protocol.4 Refinements in the counsel-ing protocol, with the inclusion of Jastreboff’sneurophysiological model, may explain the cor-respondingly larger incremental LDL shiftsobtained by TRT clinicians in relation to thosereported by Hazell and Sheldrake.1,22,24 If so,then the counseling principles incorporated inthe TRT-H protocol afford a value-added orsynergistic contribution when combined withsound therapy and, together, these combinedeffects are predicted to be greater than thosefrom either sound therapy or counseling alone.Thus, we devised a factorial trial design tocontrol for the treatment effects from counselingseparately from those achieved with soundtherapy, while also allowing for a comparisonof each of these partial treatments with referenceto the full-treatment protocol implementedwith counseling and sound therapy together.These comparisons were achieved with the useof a double-blind placebo control for the soundtherapy component and a no-counseling con-trol, which in combination, also offered a neu-tral (control) treatment condition for this study.


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To summarize, the comprehensive trialdesign allowed us to address the followingaims in a randomized controlled investigationalstudy:

1. To evaluate the validity, efficacy, and gener-ality of the counseling and sound therapyprinciples proposed by Hazell and Sheldrakein a targeted sample of hearing-impairedpersons, who were not troubled by tinnitusnor debilitating hyperacusis but were affect-ed by diminished DRs that impacted theirtolerance for moderately loud and/or ampli-fied sounds.1 Their restricted DRs deterredthem from considering amplification or fromusing hearing aids optimally and/or success-fully prior to treatment.

2. To delineate the contributions of thecounseling and the sound therapy compo-nents in the treatment protocol by comparingthe treatment effects achieved with partialtreatment protocols (i.e., counseling com-bined with placebo sound therapy or soundtherapy without counseling) relative to cor-responding effects from the full-treatmentprotocol (i.e., counseling combined withsound therapy) or the control protocol (i.e.,placebo sound therapy without counseling).

3. To characterize the temporal courses and dy-namics of the resulting treatment effects for thefull, partial, and control treatment protocols.

METHODS

Subjects

Ten adults with normal hearing sensitivityprovided normative results over a period ofalmost 1 year to assess learning effects associat-ed with repeated collection of the primary andsecondary outcome measures. The normal-hearing volunteers included 8 females (ages 39to 73 years, with a mean age of 56 years) and2males (ages 54 and 60 years, with amean age of57 years). These volunteers were recruited lo-cally at the University of Maryland, Baltimore(UMB) under a protocol approved by the insti-tutional Investigational Review Board (IRB).All volunteers provided informed consent.

A total of 32 hearing-impaired adults fromthe UMB and 4 adults from the University of

Alabama (UA) consented, enrolled and, ulti-mately, completed their assigned treatments inthe randomized control trial. The trial protocoland informed consent materials were reviewedand approved by IRBs at UMB and UA. Theage range for the 32 participants who completedthe trial at UMB was 37 to 84 years, with amean age of 67.8 years. The participants in-cluded 12 women and 20 men in the UMBsample. Four female participants, whose agesranged from 58 to 79 years, completed the trialat UA. Their mean age was 70.5 years. Mostparticipants, when questioned, were unable toascribe an onset to their perceived problem oreven verbalize the nature of their conditionother than to state that they had an ill-definedsound tolerance problem that either confound-ed or might confound the benefit of hearing aiduse.

Recruitment and Eligibility Criteria of

Hearing-Impaired Participants for the

Trial

Adults with bilateral hearing loss and com-plaints of reduced sound tolerance, unrelated toprimary misophonia (i.e., dislike of or annoy-ance to specific sounds) or phonophobia (i.e.,fear of exposure to specific sounds),4,15 wererecruited for this study at UMB from a clinicaldatabase and via newspaper advertisements.Recruitment at UA was by known clinicalhistory and direct participant contact. Candi-date participants at UMB were initiallyscreened for eligibility by telephone. Prospec-tive candidates who reported unilateral hearingloss only, current use of hearing aids, or ahistory of otologic surgery were ineligible forthe study. Furthermore, anyone who reportedtinnitus as his or her primary problem wasexcluded.

Prospective candidates who confirmedhearing loss in both ears, noted some degreeof problem in tolerating moderately loudsounds, and denied current hearing aid usewere invited to schedule an eligibility appoint-ment. During the eligibility appointment, ear-specific audiometric thresholds (250, 500,1,000, 2,000, 3,000, 4,000, 6,000, and 8,000Hz) and LDL judgments for pure tones (500,1,000, 2,000, and 4,000 Hz) were measured


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under earphones (ER-3A) (Etymotic Research,Inc., Elk Grove Village, IL). The pure tonestimuli were produced by a clinical audiometer(Grason-Stadler, model GSI-10) (Grason-Stadler, Eden Prairie, MN), calibrated quarter-ly according to standard procedures (AmericanNational Standards Institute 83.6–1996), andpresented to the study candidates via insertearphones (ER-3A). Tympanometry also wasconducted with conventional clinical tympan-ometers (Grason-Stadler, model Tympstar ormodel 33) to verify normal middle ear functionand to rule out confounding middle earpathology.

The audiometric results for each prospec-tive participant were then evaluated to deter-mine whether he or she met the followinginclusion criteria: (1) slight tomoderately severebilateral sensorineural hearing loss of at least20-dB HL for three frequencies and of at least30-dB HL for at least one or more frequenciesin the range of 500 to 4,000 Hz and (2) LDLs� 90-dB HL in the frequency range 500 to4,000 Hz for at least two frequencies or aDR � 60 dB for at least two frequencies orsound tolerance complaints for aided or unaidedlistening for candidates with LDLs below 105-dB HL.

Additional exclusion criteria also wereconsidered in assessing eligibility. Prospectiveparticipants were excluded if any of the follow-ing criteria were violated. (1) Hearing sensitivi-ty for pure tones was within normal audiometriclimits for more than two frequencies in therange 500 to 4,000 Hz. (2) LDLs were � 100-dB HL at more than two frequencies between500 and 4,000 Hz. This latter exclusion criteri-on was necessary because one of the indicatorsof treatment-related change was a measurableincrease in the LDL. Accordingly, if baselineLDL values were 100-dBHL or greater, then asignificant treatment-related incremental shiftin the LDL would have been ceiling limited byaudiometer output constraints. (3) The partic-

ipant’s tympanometric test results were clinical-ly abnormal. (4) The candidate could notconform to the test schedule (e.g., anticipationof multiple scheduling conflicts). (5) The par-ticipant was incapable of completing the func-tional outcome measures (e.g., inconsistentresponses during preliminary LDL measure-ments). (6) The participant exhibited or de-scribed primary complaints consistent withmisophonia or phonophobia. (7) Study person-nel determined that the candidate was unlikelyto be compliant with the study protocol. Eligi-ble and willing candidates who met the inclu-sion criteria and who were not disqualified bythe exclusion criteria voluntarily consented toenroll in the trial by participating in an in-formed consent process. This process culminat-ed with each eligible and willing candidatesigning an IRB-approved informed consentstatement.

Random Treatment Assignments

After providing informed consent, eligible par-ticipants were assigned randomly to one of thefour experimental treatment groups shown inthe 2 � 2 trial design in Table 1. Participants ingroup 1 were assigned to a treatment groundedin the basic principles described by Hazell andSheldrake for treatment of hyperacusis.1 Thisfull-treatment protocol was implemented withcounseling and conventional sound generators(CSGs). Participants in group 2 were assignedto PSGs and counseling. Participants in group 3were assigned to CSGs, and those in group 4were assigned to PSGs, with neither of thelatter two treatment groups receiving thecounseling component.

Nine participants were assigned randomlyto each group at the start of treatment; however,at the end of their treatments three participantswere reclassified to account for PSG failures,which rendered their placebo devices conven-tional in operation as determined by General

Table 1 Study Trial Design and Treatment Groups

Sound Generators Placebo Sound Generators

Counseling Group 1 (n ¼ 11) Group 2 (n ¼ 9)

No Counseling Group 3 (n ¼ 10) Group 4 (n ¼ 6)


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Hearing Instruments (GHI; Harahan, LA)quality control engineers at posttreatment eval-uations. These PSG failures are explained in theappendix (pgs. 106-107). Specifically, one par-ticipant was reclassified from PSG group 2 toCSG group 1, and two participants were re-classified from PSG group 4 to CSG group 3.Additionally, two participants, who were ran-domized to noncounseling treatment, mistak-enly received counseling at their initial fitting.One of these participants was moved fromgroup 3 to group 1 and the other participantwas moved from group 4 to group 2. Accord-ingly, after reclassifying for the PSG failuresand inadvertent counseling errors, the numberof participants evaluated as treated in groups 1,2, 3, and 4 were 11, 9, 10, and 6, respectively.The presentation of the study findings bytreatment group follows from this as-treatedreclassification, which we believe is the mostsensible presentation of the results based on ourknowledge of actual treatments received at the

end of the study. This analysis decision does notchange the overall pattern of the results, whichwe will showwere virtually identical to those forthe as-treated and as-assigned groups afterremoving the PSG failure participants fromthe group analyses.

The average audiometric thresholds andLDLs for each as-treated group at baseline areshown in Fig. 1. In general, these baselineresults are well matched across groups, reflect-ing mild-to-moderately severe sloping sensori-neural hearing losses and LDLs just below andaround 90-dB HL across frequency. The au-diometric thresholds were unchanged frombaseline to end of treatment.

Measurement Protocol

The participants were scheduled for a practiceappointment subsequent to completing theinformed consent process. This appointmentserved two primary purposes: (1) to verify that

Figure 1 Baseline pure tone air-conduction thresholds and loudness discomfort levels (�1 standard error) forthe left and right ears as a function of frequency for each as-treated group identified in the designated panels.Abbreviation: HL, hearing level.


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the participants continued to meet eligibilitycriteria and (2) to familiarize the participantswith the study measurement protocol. Subse-quently, this same measurement protocol wasadministered at baseline and at all follow-upmeasurement visits to assess treatment efficacy.The protocol included measures of audiometricthresholds; LDLs for pure tone, speech, andwhite-noise stimuli; categorical loudness judg-ments for warbled tones and speech stimuli;evaluation of word-recognition ability at twopresentation levels corresponding to categoricalloudness judgments of Comfortable and Loud,but OK for the individual; and tympanometry.The sequence of the test procedures was ran-domized at each test session. The study meas-urements were performed in a sound-attenuating test suite (IAC, series 1400 ATT)(IAC - Acoustics, Bronx, New York) with theaudiometric equipment previously described.

Ear-specific audiometric thresholds weremeasured for 250, 500, 1,000, 2,000, 3,000,4,000, 6,000, and 8,000 Hz, using the modifiedHughson-Westlake procedure under earphones(ER-3A).25 Ear-specific LDL values, which rep-resent absolute judgments of loudness discomfort,were measured under earphones (ER-3A) forpure tones presented at 1,000 and 8,000 Hz,for spondee words, and for white noise. Stimulusduration for the tones and noise stimuli was�1,000 milliseconds, with an interstimulus inter-val of�400 to 500milliseconds. Participantswereinstructed to press the handheld response buttonwhen the signal level became uncomfortable. Thefollowing instructions were given to each partici-pant: “I am going to present different sounds thatget louder and louder in volume. I want you todecide when the sound is at a level that you thinkis too loud, uncomfortably loud, or annoyinglyloud. By ‘too loud,’ I mean when the sound isabove the level to which you would choose tolisten for any period of time. Push the buttonwhen the sound is at a loudness to which youwould not listen.” Three LDL estimates wereobtained for each stimulus. If there was anintertest difference exceeding 10 dB for a givenstimulus, then a fourth estimate was obtained andthe outlier was discarded.

Categorical loudness judgments were mea-sured for 500-, 2,000-, and 4,000-Hz pulsedwarbled tones (frequency modulation � 5% of

center frequency) per the protocol described byCox and colleagues for the Contour Test ofLoudness.26 Test stimuli were presented inascending level, with the initial starting levelpresented one step above the audiometricthreshold for that frequency; step sizewas 5 dB when audiometric threshold was< 50-dB HL and was 2.5 dB when the thresh-old was � 50-dB HL. Four 200-millisecondspulses of each warbled tone were presented ateach stimulus level. The interstimulus intervalwas typically 1,000 milliseconds, but variedsomewhat based upon the participant responsetime. Participants responded to the perceivedloudness of the signal, after presentation of theseries of tones at a given level, by stating thenumber corresponding to the perceived loud-ness category (e.g., 1 ¼ Very Soft, 2 ¼ Soft,3 ¼ Comfortable but Slightly Soft, 4 ¼ Com-fortable, 5 ¼ Comfortable but Slightly Loud,6 ¼ Loud, but OK, 7 ¼ UncomfortablyLoud). The initial presentation level generallyyielded a response of Very Soft (category 1).Occasionally, the starting level resulted in a ratingof Soft (category 2). When this latter responseoccurred, the starting level was decreased toaudibility threshold. Stimulus intensity subse-quently was increased, and a categorical judgmentof loudness was obtained for each presentationlevel until the participant reported a response ofUncomfortably Loud (category 7), which termi-nated the trial sequence. Three ascending trialsequences were presented at each frequency, withthe test frequency selected in random order. Themedian value for each loudness category wasdetermined from the three trial sequences.

Ear-specific categorical loudness judgmentsalso were obtained under earphones (ER-3A) forrecorded spondaic words (Central Institute forthe Deaf (CID), W-2 Word Lists). The initialstarting level was presented one step above thelowest (best) pure tone threshold across theaudiometric frequency range 250 to 8,000 Hz.A 5-dB step size was used for these measure-ments regardless of the pure tone threshold.Categorical loudness judgments from three as-cending trials were measured for each ear; theorder of presentation was randomized betweenthe ears. Subsequent to completing the categori-cal loudness judgments for the recorded spondeespeech stimuli, word-recognition ability was


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measured using recorded Northwestern Audi-toryTestNo. 6 (NU-6)word lists (50-word lists)at presentation levels corresponding to loudnessjudgments of Comfortable (category 4) andLoud, but OK (category 6).

Some of the study participants at UMBcompleted a pretreatment sound tolerance ques-tionnaire (personal communication with La-Guinn Sherlock and Sue Erdman) and theRevised NEO Personality Inventory (NEOPI-R, Par Inc., Lutz, FL) during the appoint-ment for the practice session.27 The formerinstrument was in development at the start ofthe study and the content is not validated.Therefore, it was not used as a formal baselinenor an outcomemeasure. The latter psychomet-ric tool was administered to assess personalitycharacteristics that might ultimately be predic-tive of treatment success or failure. These latterresults have not been analyzed formally to date.

Bilateral ear canal impressions, for orderingand fabricating the cases of the custom in-the-ear sound therapy devices, were usually madefor the participants at the time of the random-ized treatment assignment. This activity wassometimes postponed and performed at a sub-sequently scheduled practice visit if schedulingor time constraints precluded this step. Thesound therapy device order form was completedby a neutral third party (the division adminis-trator), who determined the sound therapydevice type (i.e., CSG or PSG) that eachparticipant was assigned to receive based upona predetermined randomization schedule. Thestudy audiologists were blinded to the devicetype, as was each study participant.

Participants were scheduled to return fortheir baseline and treatment visit when theirsound therapy devices were ready to be dispensed,typically about 4 weeks after the practice session,but in some cases longer (see the appendix,pg. 107). The baseline test session establishedLDL values, categorical loudness judgments, andword-recognition performance prior to initiatingthe assigned treatment protocol for each partici-pant. In addition, baseline auditory brainstem andmiddle latency response measurements were per-formed for those participants enrolled in the studyat UMB. These results, also measured at follow-up visits throughout the period of treatment, willbe described in a separate report.

Counseling Treatment Protocol

Participants assigned to one of the counselinggroups (groups 1 and 2) received counseling in asingle session. This counseling session followedafter the baseline test measurements and pre-ceded the fitting of their CSGs/PSGs. Thecounseling was performed routinely at UMBand at UA by a single TRT-experienced clini-cian. The audiologist collecting the study datawas not blinded to whether (or not) the partici-pant received counseling as part of his or hertreatment.

Counseling followed a structured protocol,which was administered by the counselingaudiologist in a checklist format. The contentof the counseling protocol was divided into fourbasic components, which typically required atotal time of 1.0 to 1.5 hours to complete. Thefour components of counseling included: (1) anoverview of the counseling protocol and theparticipant’s audiometric results; (2) an over-view of relevant auditory anatomy and neuro-physiology; (3) an overview of central auditorygain control processes in the context of theparticipant’s sound tolerance problem and his orher limited DR; and (4) an introduction to theimportance of sound therapy in treatment of theproblem. The counseling was performed witheach participant’s audiometric and LDL resultsand with visual aids, using flip charts to displayanatomical illustrations and photographs.Additionally, a diagram of Jastreboff’s neuro-physiological model was presented to helpexplain the problem of hyperacusis.24 Themodel was helpful in clarifying hyperacusisand in distinguishing this problem from miso-phonia/phonophobia; again, our sample did notdescribe symptoms consistent with either ofthese latter issues as significant concerns. Thecounseling content also was void of basic infor-mation about tinnitus, which if reported by aparticipant was an unremarkable secondaryissue. Instead, the counseling content was re-fined and restricted to issues relevant to supra-threshold sound-sensitivity problems, soundintolerance, and associated complaints, includ-ing those related to a reduced DR for loudnessas a consequence of sensorineural hearingloss.14 These issues, individually and together,were related to adverse effects on the partic-ipant’s comfortable use of amplification. The


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objectives of the counseling were explained interms of isolating and addressing each partic-ipant’s primary problems, thereby enabling bet-ter management to expand his or her reducedDR for loudness. The counseling also clarifiedthe purpose and goals of the study whileaddressing any study-related questions andconcerns expressed by the study participants.

Sound Therapy Devices

All participants were assigned to a sound ther-apy treatment. The sound therapy treatmentswere implemented with either CSG or PSGdevices via nonoccluding, custom, in-the-earsound generators (GHI Tranquil model). TheCSGs were modified, as described in the ap-pendix, to achieve the desired placebo effect inthe PSGs. Two versions of the PSGs wereimplemented in this study (see the appendix,pgs. 106-108). The typical real-ear frequencyresponses for both CSGs and PSGs werecharacterized by a high-frequency emphasis inthe range of the ear canal resonance frequencies.Perceptually, the sound output was perceived asa soft seashell-like noise. The CSGs producedthe soft noise output continuously at a constantlevel. In contrast, the PSG devices produced ashort-duration dose of the same noise, which isdescribed below.

The novel PSG treatment was crucial tothe success of this project in as much as itenabled us to implement the double-blindsound therapy treatment for the trial. ThePSG strategy took advantage of normalshort-term adaptation processes that may giverise to partial (if not complete) perceptual sounddecay for weak sounds. Additionally, otherperceptual processes ostensibly contributed toauditory gain recalibration effects, followingrepeated exposures to the soft sound therapynoise over extended time of use. Specifically, theplacebo effect was made plausible because weknew clinically that patients with tinnitus andhyperacusis may experience perceptual attenu-ation or decay to the noise during sound therapywith CSGs. Consequently, they often reportbecoming unaware of the low-level sound ther-apy noise from their CSGs over the course ofdaily usage. Also, pilot listening to the CSGdevices by the investigators, even in quiet con-

ditions corresponding to the Comfortable butSoft presentation levels that were used in thisstudy, revealed normal perceptual attenuationof the noise. Accordingly, the PSGs weredesigned to decay to silence after �60 to 70minutes of use. The output of the placebodevices was constant in level during the initial30 to 40 minutes of use and, thereafter, theoutput was systemically attenuated to silence ata rate of�1 dB per minute (see Fig. A3A). Theexpectation of routine sound decay, consistentwith the attenuating PSG function, was rein-forced by clinician instruction. Indeed, all par-ticipants regardless of device assignment wereinformed that they may not hear the noise fromtheir devices because of the adaptation effects,especially in noisy sound environments.

An innovative and critical feature of thefunction of the PSG required the output to resetto the initial, steady-state, unattenuated levelsoon after the device was removed from the ear.This feature was added as a safeguard againstuntoward revelation of the placebo effect,which might otherwise be revealed to theparticipant or to the study audiologist duringan out-of-the-ear listening check of the PSGoutput. This novel resetting feature, whichoperated with a brief resetting time constantof �2 to 3 seconds, was critical for doubleblinding of both the participant and the studyaudiologist to the conventional or placebodevice type. To discourage inadvertent resettingof the PSG output, participants were instructedto insert and position their sound generators(both conventional and placebo) at the startof the day and then to forget about thedevices until removed at the end of daily usage(encouraged for at least 8 hours each day).

Sound Therapy Fitting Protocol

RATIONALE

The essential requirements for sound therapy inthis study were to provide the participants aconsistent and gentle noise source, consistentwith Comfortable but Slightly Soft level (cate-gory 3), to facilitate the intended treatmenteffects from the CSGs, while also minimizinguntoward adverse masking effects while in use.An additional requirement for participant use


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of both the CSG and PSG instruments was tominimize undesirable sound-attenuating occlu-sion effects while wearing the devices. Thelatter occlusion effects might otherwise coun-teract the desired sound-enriching effects of thenoise treatment, as well as restrict daily com-munication while the devices were worn.Specifically, external sound attenuation fromwear of a fully occluding device has been shownto induce counterproductive increases in centralauditory gain, which enhance loudness andthereby reduce sound tolerance and theDR.22,23,28 To minimize untoward occlusioneffects in this study, the CSG and PSG deviceswere encased in open-canal fitted shells, whichallowed speech and environmental sounds topass virtually unattenuated. Accordingly, a suc-cessful CSG sound therapy treatment with anopen-canal fit was expected to reduce (central)auditory gain for the participants,1 fosteringenhanced sound tolerance and expansion of theauditory DR for loudness.

In planning the use and fitting of the CSGsfor this trial, we made the decision to maintain aconsistent steady-state volume setting through-out the entire treatment period for each partici-pant. Our treatment protocol therefore differedin an important way from the desensitizingsound therapy protocol originally described byHazell and Sheldrake and currently recom-mended in the TRT-H sound therapy protocolfor treatment of hyperacusis.1,4 Specifically, thedesensitizing sound therapy approach calls forsystematic increases in the sound generatorvolume output over the course of the hyperacusistreatment. Our decision to fix the CSG volumeoutput throughout the period of treatment was,in part, a strategy to offer a known and controlledsound therapy stimulus, which simplified theeventual interpretation of the treatment out-comes. This strategy also was essential for mini-mizing and controlling the low-level maskingproduced by the CSGs. Indeed, minimization oflow-level masking effects was crucial during theprolonged treatment period for our unaided,audibility-challenged, hearing-impaired partici-pants. Otherwise, their everyday communicationand listening abilities, in the absence of useableamplification, would be further compromised bythe low-level masking noise from their CSGs.Thus, to the extent that systematic increases in

the CSG outputs would necessarily have givenrise to incremental low-level masking, eachparticipant’s auditory DR would, in turn, havebeen diminished systematically while the CSGswere in use during the treatment period.Accordingly, we adopted a fixed low-level noisestimulus throughout the period of treatment forgroups 1 and 3. Groups 2 and 4 were similarlymanaged, albeit the outputs of their PSGs werepurposely attenuated to silence after �60 to70 minutes of use.

FITTING PROCEDURE

The participants were instructed in the use,fitting, and care of their open-canal soundgenerators per the treatment protocol describedherein. This instruction always followed afterthe baseline test measures were completed andafter a counseling assignment. Initially, thesound generator instruments were positionedwithin the ear by the study audiologist. Com-fortable physical fits were then verified for eachparticipant, and the noise output was adjustedto a volume corresponding to a loudness ratingof Comfortable but Slightly Soft. The devicevolume was set independently for each ear, anda second loudness rating was then obtained withthe bilateral devices operational. If the bilateralloudness rating changed, then the volume ofeach device was adjusted until the participant’srating of the bilateral noise output level wasagain judged to be Comfortable but SlightlySoft. Next, measurements were performed us-ing a real-ear system (AudioScan, modelRM5000) (AudioScan, Dorchester, Ontario,Canada) to document the device output withineach ear. The probe tube was placed within theear canal to a standardized insertion depth of�28 mm. Measurements were performed withthe devices in the ear, first turned off and thenturned on. The AudioScan output was turnedoff so that the resulting difference between theinstrument settings in the on and off conditionsyielded a measure of the device output withinthe ear canal. Average real-ear responses for thesound generators used in this study are shownseparately for the left and right ears for eachtreatment group in Fig. 2. These responsesreveal the expected high-frequency emphasis,with peak output at 2,000 Hz reflecting thecharacteristic ear canal resonance.


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Behavioral (audiometric) threshold shiftsalso were measured with the bilateral CSGs/PSGs situated within the ears and turned on perthe treatment protocol. The device-inducedmasked (audibility) threshold shifts werechecked at baseline and at each follow-upappointment to verify expected device outputwithin the ear. (Measurements were madewhile the PSG outputs were in the steady state,prior to initiation of the decay phase.) Audibil-ity thresholds were measured between 500 and6,000 Hz using the headphones (Telephonics,model TDH-50) (Telephonics, Farmingdale,NY) encased in supra-aural cushions. Thethreshold measurements were performed,with and without the treatment devices inuse, with the resulting difference in the twosets of thresholds representing the maskedthreshold shifts. Average masked thresholdshifts measured for the sound generators inoperation are shown separately for the leftand right ears for each treatment groupin Fig. 3. Note that the masked threshold shiftsmirror the real-ear response patterns shown

in Fig. 2. The largest masked threshold shifts,typically between 10 and 15 dB, were producedat 3,000 Hz for each group. Otherwise, themasked threshold shifts were not much morethan 5 dB at most frequencies and were notusually reported to be a confounding factor indaily communication for our participants.

CSG/PSG output also was verified electro-acoustically during each test session with theAudioScan real-ear system. The CSG or PSGwas coupled to an HA-1 coupler and its steady-state output was measured at the participant’suse setting. Sound generator outputs were com-pared at each follow-up sessionwith the baselinemeasurements at treatment onset to ensureconsistent outputs. If a follow-up sound gener-ator-output response varied appreciably from itsbaseline value, then the CSG/PSG volumesetting (set manually by potentiometer adjust-ment) was verified. If the volume setting wasconsistent with the baseline value and the outputwas weak, then a visual inspection of the devicewas conducted to rule out a cerumen-occludedreceiver. Subsequent to these efforts, the

Figure 2 Average real-ear frequency responses (�1 standard error) for the conventional sound generators(CSGs) and placebo sound generators (PSGs) measured for the left and right ears for groups 1 and 3 and forgroups 2 and 4, respectively, at Comfortable but Slightly Soft use settings. Abbreviation: SPL, sound pressurelevel.


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treatment device was returned to the manufac-turer for repair or replacement if the outputresponse did not closely match the baselineoutput value.

Participants received written and verbalinstruction in the care and use of their CSGs/PSGs. Again, participants were advised toanticipate naturally occurring perceptual atten-uation of the low-level noise from their soundgenerators. Accordingly, they were forewarnedand were aware that they might not alwaysdetect the outputs from their sound generators.This key information, namely, that perceptualadaptation to the sound generator noise outputwas normal and should be expected, was em-phasized and reinforced at treatment onset andat all follow-up visits for each participant. Thisknowledge was integral to the successful use ofthe PSGs, as well as that of the CSG devices.The instruction to the participants, to inserttheir sound therapy devices within the ears andthen to forget them, also was emphasized. Theparticipants practiced correct placement of theirCSG/PSG devices in the ears, and properplacement was confirmed by the research audi-

ologist or a graduate assistant at each clinic visit.Participants were provided with a supply ofbatteries at each test session and instructed toreplace the batteries weekly, or as needed, tosustain normal function. Last, participants wereinstructed to record their CSG/PSG use timeeach day on a device-use log and to share theirlogs at each follow-up session for clinicianreview. The clinician reviewed the daily-useentries to ensure protocol compliance and, ifnecessary, to counsel the participant if he or shewere noncompliant with prescribed use of thedevice for at least 8 hours daily.

We implemented two follow-up schedulesduring this study to monitor treatment progress.The two schedules were implemented because thedynamics for the full- and partial-treatment ef-fects were uncertain at the start of this study.Hazell and Sheldrake’s early report of theirtreatment dynamics guided our design of theinitial follow-up schedule,1 which coincidedwith the evaluation of the first-generationCSGs/PSGs (see the appendix, pg. 106). Theinitial follow-up schedule encompassed a treat-ment period of about 1 year, which Hazell and

Figure 3 Average masked threshold shifts (�1 standard error) as a function of frequency for groups 1 and 3and for groups 2 and 4, respectively, when using the conventional sound generators (CSGs) and placebosound generators (PSGs) at their Comfortable but Slightly Soft use settings.


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Sheldrake reported to have been sufficient toreveal treatment effects for the majority of theirpatients.1 This early follow-up schedule called forless time between follow-up sessions at the start oftreatment, with increasingly longer intervals be-tween follow-up appointments over the course ofthe assigned treatment protocol. This initialstrategy was necessary to monitor and capturerapid treatment effects (i.e., incremental changesin the categorical loudness judgments) that mightoccur early in the repeated measurements andotherwise be missed. These scheduled follow-upappointments were set at 0.5, 1, 2, 3, 4, 6, 8, 10,and 12months after the baseline/initial treatmentsession. Fourteen participants completed the ini-tial follow-up schedule.

After reviewing the treatment dynamics forthose participants who benefitted from theirinterventions during the initial follow-upschedule, we determined that: (1) primarytreatment-related changes had generally oc-curred during the first 6 months of follow-up,which was consistent with Hazell and Shel-drake’s findings that 73% of their patients withhyperacusis were treated successfully within6 months of beginning treatment,1 and (2)these changes would typically have been cap-tured by monthly visits. We therefore modifiedthe follow-up protocol schedule to reduce theburden on the study participants and to allowthem to be fitted with hearing aids sooner thanwas permitted by the original protocol, whichcalled for an additional 6 months of treatmentwith no further expected improvement fromtheir treatment. The revised follow-up schedulecalled for monthly follow-up appointments for6 months after the baseline/initial treatmentsession. Moreover, the decision was made thatthe treatment and follow-up protocol could beterminated earlier than 6 months if criterionLDL and/or categorical loudness judgments forUncomfortably Loud consistently shifted by10 dB or more for a given measure of uncom-fortable loudness at two consecutive follow-upvisits. This early termination criterion wasdeveloped to allow our participants, who wereall hearing aid candidates, the opportunity to befitted with hearing aids once they had a clini-cally meaningful change in their sound toler-ance. Twenty-two participants completed therevised follow-up schedule.

Participants were interviewed at each fol-low-up test session to determine whether therewere any unexpected changes in their audio-metric or sound tolerance conditions, to ascer-tain any concerns about the fit or function oftheir CSGs/PSGs, and to evaluate self-re-ported use time for their sound therapy devices.Compliance with the upcoming schedule andcontinued interest in study participation alsowere confirmed, and informed consent wasreaffirmed with each participant.

At the termination of their assigned treat-ments, 10 participants who had not received thefull treatment, including counseling and con-ventional sound therapy, were crossed over tothe full-treatment protocol for 6 months. Inaddition, several of the participants in group 1who graduated successfully from the full treat-ment and some participants in other treatmentgroups who benefited from their treatmentselected to try the use of hearing aids at thecompletion of their successful interventions.Unfortunately, during the funding period forthis study, we were only able to follow a few ofthese individuals in their crossover treatmentand/or their postfitting experiences with hear-ing aids. Case examples of posttreatment func-tional benefit will be considered for selectedparticipants in a companion report that willaddress the clinical relevance of the studyoutcomes.

Statistical Analyses

Along with simple descriptive statistics (i.e.,means and standard deviations), the primarystatistical analysis applied in this study focusedon longitudinal change in the categorical loud-ness judgments to reveal treatment-relatedgroup differences. We performed the primaryanalysis of longitudinal change using the Proc-Mixed protocol in SAS software (version 9.3,Cary, NC). Longitudinal change in the loud-ness measures were evaluated and compared,over the course of each treatment, using linearmixed models to evaluate slope inequalities bytreatment group assignment. The analyses werestratified by stimulus-frequency condition, 500,2,000, and 4,000 Hz, for each of the sevenContour loudness categories. Because the studyfollow-up visits were not equally spaced in time


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across the participants, the mixed-model designenabled us to explore various covariance matri-ces to maximize model fit. Additionally, forpurposes of post hoc evaluations, the Bonfer-roni method for correction was used to adjustconfidence limits to maintain a consistent alevel for all paired comparisons.29 As previouslydiscussed, two different follow-up scheduleswere evaluated in this study with differingpoints of treatment termination based on crite-rion changes in the longitudinal loudness meas-ures. This temporal measurement variationinvalidated the standard repeated-measures de-sign, which assumes either that within-partici-pant errors were uncorrelated or that thecorrelation between observations on the sameparticipants was constant regardless of the timelapse between observations. Accordingly, themixed-model approach for this longitudinalstudy incorporated a time-series covariancestructure (i.e., spatial power law) to managethe unequally spaced time points in the analysisthat otherwise would have been susceptible tounderestimates of standard errors and over-estimates of time and time-by-treatment effectsin a standard repeated-measures analysis.

Both linear and nonlinear (quadratic) func-tions were evaluated for best fits to the longitu-dinal data, with minimal difference observedbetween the two fitting functions. Consequent-ly, for economy of description and interpreta-tion, in the absence of compelling evidence tofavor the more complex nonlinear fitting strat-egy, we adopted the linear-fitting strategy forour primary analyses and for reporting of thestudy outcomes.

The power analysis for the study also wasperformed using a mixed-model design forwhich we modeled between-subjects effectswith the four levels (one level for each treatmentgroup) and a within-subjects effect with sevenlevels (average of time measurements). Bothfactors were designated as having a linear-upeffect pattern, with a conservative detectablemean difference of 1 unit above and below thecomparison mean. For example, a 1-unit de-tectable difference for a reference of a mean of 5would represent the minimal detectable differ-ence in the range of 4.5 to 5.5 for the compari-son mean. Results from this mixed-modelpower calculation consistently resulted in

>80% power for this effect size across samplesranging from 6 to 12 observations (i.e., studyparticipants) per group, which was consistentwith various analyses performed on our unbal-anced group sizes. This study design therefore isunbalanced in its treatment allocations for thedifferent groups. There is a power decline as theallocation ratio deviates from 1.00; however,this effect is not very prominent and moderateimbalances in group sizes, as occurred in ourstudy, can be utilized without great concernabout loss of power or the need to increase totalsample size.30

RESULTS

Overview

The results discussed here address the primaryand secondary aims listed in the introduction.These findings provide the critical tests of thevalidity, efficacy, and generality of the interven-tion principles for treating reduced sound tol-erance and related DR problems among oursample of people with hearing loss.1 The resultsfor the ear-specific LDLs and Contour testingare presented as averages across ears and acrosssubjects in each group.

Control Repeated Measures

Consider first the repeatedmeasurements of thecategorical loudness judgments measured atmonthly intervals over a period of about1 year from the 10 normal-hearing volunteers.There was no consistent trend of improvementover time for any of our repeated measures forindividual participants. The standard deviationsacross sessions for the categorical loudnessjudgments, averaged across participants, were5.4, 4.5, and 10.4 dB at 500, 2,000, and4,000 Hz, respectively.

Changes in Loudness Discomfort with

Treatment

The focus of the treatment effects in this studywas on the change in the categorical loudnessjudgments from baseline to end of treatment.These treatment effects were the primary out-come measure of interest. The LDL judgments


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were used as a secondary outcome measure tosupplement the categorical loudness data forpurposes of establishing treatment termination.Incremental changes from baseline of 10 dB ormore at two consecutive follow-up visits foreither (or both) the 1,000-Hz LDL judgmentsor the Uncomfortably Loud categorical judg-ments, averaged for the 500- and 2,000-Hzmeasurement conditions, qualified a participantto terminate and graduate successfully from theassigned treatment. Based on these criteria fortreatment termination, 82% of the individualsreceiving full treatment in group 1, 25 and 40%of the participants in partial-treatment groups 2and 3, respectively, and 50% of the controlparticipants in group 4 were treated successfullyat the conclusion of their as-treated groupassignments. The latter result for group 4should be interpreted cautiously because onlysix participants contributed to this result.

The magnitudes of the treatment-relatedchanges (in decibels) are shown for each group

in Fig. 4 for the Uncomfortably Loud categoricaljudgments, averaged for the 500-, 2,000- and4,000-Hz frequency conditions. Also shown forcomparison are the corresponding mean changesin the LDL judgments for 1,000 Hz for eachgroup. These data were analyzed in three ways toenable comparison of the results by the: (1) as-assigned (at treatment onset); (2) as-treated (asdetermined at treatment end); and (3) droppedparticipant group designations. The latter desig-nation reflects the deletion of the three partic-ipants with PSG failures from the analysis. Thetrends are similar for all three analyses. The meanchanges for group 1 for both the UncomfortablyLoud and LDL judgments in Fig. 4 were consis-tently greater than those measured for the othergroups. Indeed, the group 1 changes in judgmentsof Uncomfortably Loud posttreatment averaged�15 and 10 dB, respectively, whereas the corre-sponding changes for the other groups typicallyaveraged � 5 dB or less. Similarly, the efficacyrates for the as assigned and dropped participant

Figure 4 Treatment change by group for LDL (1,000 Hz) and Uncomfortably Loud categorical judgments(averaged for 500, 2,000, and 4,000 Hz) between baseline and end of treatment. Shown are the averagechange values (�1 standard error) for the participants in the as assigned, as treated, and dropped fromanalysis treatment groups. Abbreviations: CSG, conventional sound generator; LDL, loudness discomfort level;PSG, placebo sound generator.


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Figure 5 Mean baseline and end-of-treatment loudness-growth functions (�1 standard error), measured for apulsed-warbled tone are presented by group in separate panels for 500, 2,000, and 4,000 Hz. The end-of-treatment functions were constructed by averaging the resulting judgment levels for each loudness categoryacross the last two study visits for each participant. Abbreviation: HL, hearing level.


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analyses were virtually unchanged for group 1 (78and 80%, respectively) from their as-treated effi-cacy rate (82%). These treatment-related changesfor the Uncomfortably Loud judgments are clini-cally significant, reflecting incremental shifts inloudness discomfort in excess of a full category forfull-treatment group 1.

Changes in Loudness Growth with

Treatment

The average loudness-growth functions mea-sured at baseline and at the end of treatment forgroup 1 are consistent with the positive treat-ment effects described above. These results andthose of the other treatment groups are shownin Fig. 5 for the as-treated categorical-loudnessjudgments at 500, 2,000, and 4,000 Hz. Theend-of-treatment function for each group re-flects average results measured over the last pairof treatment visits (for which consistent perfor-mance was required to terminate treatment).Again, the largest treatment effects are apparentfor group 1, for whom the divergence of thebaseline and end-of-treatment functions wasgreatest. For 500 Hz, this divergence beginswith the judgments of Comfortable but SlightlySoft and increases systemically with increasingloudness category; whereas for 2,000 and4,000 Hz, the separation of the baseline andend-of-treatment functions is evident across allcategories from Very Soft to UncomfortablyLoud, and systematically diverges to a greaterextent with increasing loudness category. Con-sequently, the end-of-treatment loudness-growth function for group 1 is extended tohigher levels and, therefore, spans a larger rangeof levels than does the steeper pretreatmentbaseline function. Accordingly, the shallowerend-of-treatment function for group 1 repre-sents an enhanced DR for loudness relative tothe steeper baseline function. A similar but lessprominent effect of treatment is observed in thecorresponding loudness-growth functions forgroup 3, which was treated with CSGs alone.The treatment effects for group 2 were relative-ly smaller than those for group 3, and those forgroup 4 were negligible. Again, group 2 par-ticipants were assigned counseling and PSGs,whereas participants in control group 4 wereassigned no counseling and PSGs. The trends

for the baseline and end-of-treatment loud-ness-growth functions for the respective groupswere largely invariant of the measurementfrequency condition, reflecting the generalityof the treatment effects across frequency.

A two-way analysis of variance comparingthe baseline versus end-of-treatment judgmentsacross Contour loudness category (1 to 7) for eachfrequency condition confirmed the observabletrends in the loudness-growth functions shownin Fig. 5. Specifically, the baseline versus end-of-treatment loudness-growth functions for group 1were significantly different (p < 0.001) for eachfrequency condition. Likewise, the baseline andend-of-treatment loudness-growth functionswere significantly different for group 3 for500 Hz (p ¼ 0.013) and for 4,000 Hz(p ¼ 0.008). In contrast, loudness growth wasnot significantly different between baseline andend-of-treatment for any frequency condition forgroups 2 and 4. No interactions were obtained forany treatment group, precluding the isolation ofan effect for a specific loudness category. Cate-gorical effects of the treatments, however, aresuggested by the increasing separation of thebaseline and end-of-treatment functions withincreasing loudness category for group 1 and, toa lesser degree, for group 3.

Thus, group 1, which was assigned to fulltreatment, achieved the most prominent inter-vention effects as measured by overall changes inloudness growth between baseline and treatmenttermination. These treatment effects were signif-icant statistically and were consistently measuredacross frequency at 500, 2,000, and 4,000 Hz.Significant but less prominent treatment effectsalso were measured at 500 and 4,000 Hz forgroup 3, which received sound therapy alone viaCSGs. No significant treatment effect was mea-sured for control group 4, which was treated onlywith PSGs, nor for group 2, which was assignedcounseling in combination with PSGs. Accord-ingly, we may surmise from this evidence thatCSGs, whichwere assigned for both groups 1 and3 but not for groups 2 and 4, were integral totreatment success.

The conclusion that CSGs were integral totreatment success is highlighted in Table 2 inwhich mean change values are quantified be-tween the baseline and end-of-treatment loud-ness-growth functions from Fig. 5. For each


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Table 2 Mean Treatment Change between Baseline and End-of-Treatment LoudnessJudgments for Each Group as a Function of Contour Loudness Category for Each MeasurementFrequency

Group 1

Contour Loudness Category Frequency (Hz)�D500 2000 4000

1 �0.06 2.61 3.35 1.97

2 0.06 3.69 3.92 2.56

3 3.01 3.69 4.38 3.69

4 5.57 5.06 5.68 5.44

5 7.84 6.99 7.33 7.39

6 9.60 8.81 8.92 9.11

7 11.65 10.00 9.89 10.51P

D 37.67 40.85 43.47 40.66†

Group 2


1 �0.63 �0.21 0.61 �0.07

2 �2.29 �0.69 0.13 �0.95

3 �2.15 �1.39 0.29 �1.08

4 �1.88 �0.76 0.64 �0.67

5 0.14 0.00 0.42 0.19

6 1.39 0.69 0.99 1.02

7 1.32 0.90 1.75 1.32P

D �4.10 �1.46 4.82 �0.25†

Group 3


1 1.69 1.44 1.25 1.46

2 3.00 1.69 1.67 2.12

3 3.38 2.00 1.88 2.42

4 3.81 3.25 1.88 2.98

5 4.75 3.88 3.89 4.17

6 6.31 3.81 3.89 4.67

7 6.44 4.31 4.65 5.13P

D 29.38 20.38 19.10 22.95†

Group 4


1 1.15 3.65 0.52 1.77

2 �0.52 2.19 1.25 0.97

3 �0.52 1.98 �0.31 0.38

4 0.63 2.40 1.46 1.49

5 0.42 2.81 0.83 1.35

6 1.46 3.33 1.77 2.19

7 0.83 3.75 1.46 2.01P

D 3.44 20.10 6.98 10.17†

Corresponding grand mean change values, averaged across measurement frequency for each loudness category.†The summation of the mean change values across category for each frequency and the overall grand mean changevalue.


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group, the mean change in decibels is presentedfor the end-of-treatment loudness judgmentsrelative to the corresponding baseline judg-ments for each Contour loudness categorystratified by measurement frequency. Alsoshown are the mean change values for eachloudness category, stratified by measurementfrequency, and the corresponding grand meanchange values, averaged across measurementfrequency, for each group; the summation ofthe mean change values by frequency and thetotal of these grand mean values for each groupare shown at the bottom of each column. Thelatter total grand mean value represents acomprehensive index, estimated across categoryand frequency, of the respective overall treat-ment change achieved by each group. Theresulting comprehensive index values of treat-ment change were 40.66, �0.25, 22.95, and10.17 dB for groups 1, 2, 3, and 4, respectively.The large and moderate index values of overalltreatment change for groups 1 and 3, respec-tively (in relation to the negligible and smallindex values for groups 2 and 4), confirm theimportance of sound therapy in the treatmentprotocol.

The comprehensive index values of treat-ment change estimated for each groupin Table 2 represent summary outcome meas-ures of overall treatment-related change in thecategorical loudness judgments. The index val-ue for each group can be applied in a factorialanalysis using the equations shown in Table 3 toevaluate formally the respective treatment ef-fects from counseling and conventional soundtherapy in this study.31 The important outcomefrom this factorial analysis is that the treatmenteffect for sound therapy (53.68 dB) is muchlarger than that for counseling (7.29 dB) in thisstudy. Additionally, it is notable that the full-treatment effect for group 1 (40.66 dB) isfourfold that of the control effect for group 4(10.17 dB). Moreover, a relative estimate of theplacebo contribution in the treatment effectscan be garnered from a comparison of the sumof the comprehensive index values for PSG-assigned groups 2 and 4 (9.92 dB) in compari-son with the corresponding summed values forCSG-assigned groups 1 and 3 (63.61 dB). Thiscomparison reveals a negligible role for theplacebo, which is less than a sixth of the

magnitude achieved with conventional soundtherapy for otherwise similar treatmentassignments.

Treatment Dynamics

We used linear mixed models to evaluate sig-nificant mean differences in treatment change(in decibels) from baseline to end of treatmentfor each group (shown in Fig. 5). The p valuesfor time � group interactions were calculatedfor each of the seven Contour loudness catego-ries, stratified by measurement frequency. Thelongitudinal treatment effects for group 1 werethe only ones yielding statistically significantdifferences from the dynamic treatment effectsof the other groups. The longitudinal treat-ment-related changes in the categorical loud-ness judgments for group 1 provide furthersupport for the validity and efficacy of the fulltreatment. Significant time � group interac-tions were evident early, beginning with theSoft categorical loudness judgments for the2,000- and 4,000-Hz warble-tone frequencyconditions. The time � group interactions forthe 500-Hz warble-tone condition for group 1were significantly different for categories great-er than Comfortable but Slightly Loud com-pared to groups 2 and 3, and were greater thancategory Loud compared to group 4. For the2,000-Hz warble-tone condition, group 1 wassignificantly different from groups 2 and 3 forcategories greater than Soft and was differentfrom group 4 for categories greater than Com-fortable. For the 4,000-Hz warble-tone

Table 3 Factorial Analysis Applied in theEvaluation of the Counseling and SoundTherapy Treatment Effects

Sound Generators

Counseling þ �

þ Group 1 (40.66 dB) Group 2 (�0.25 dB)

� Group 3 (22.95 dB) Group 4 (10.17 dB)

Note: Comprehensive index values of treatment change(from Table 2) are shown by group for treatment assign-ments with or without counseling in combination withconventional sound generators or placebo sound gener-ators. Counseling effect ¼ group 1 index value þ group2 index value � (group 3 index value þ group 4 indexvalue) ¼ 7.29 dB; and sound therapy effect ¼ group 1index value þ group 3 index value � (group 2 indexvalue þ group 4 index value) ¼ 53.68 dB.


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conditions, group 1 was significantly differentfrom groups 2 and 3 for categories greater thanSoft and was different from group 4 for catego-ries greater than Comfortable but Slightly Soft,with the exception of their Comfortable judg-ments. The larger response variation for group4, which consisted of a smaller number of as-treated participants (n ¼ 6) contributing to theaverage treatment effects, likely accounts for thefewer number of conditions yielding statisticallysignificant differences from group 1. Group 4also exhibited larger DRs and shallower meanloudness-growth functions at baseline thanwere measured for any other group; this char-acteristic feature of their results also may be afactor in their statistics.

The corresponding dynamics that charac-terize these longitudinal treatment effects (i.e.,mean treatment change in decibels from base-line to end of treatment) were described for eachgroup by calculating a slope value. The slopevalues were estimated as a linear change frombaseline (in decibels permonth) over the time oftreatment. Slope values were calculated for eachloudness category independently for 500, 2,000,and 4,000 Hz. The intercept values for corre-sponding combinations of loudness categoryand frequency condition were not significantlydifferent across the four treatment groups atbaseline. Thus, on average, the four treatmentgroups began their judgments of loudness fromsimilar starting points for each pairing of Con-tour loudness category and frequency condition.The slope values for group 1 increased system-atically with increasing loudness category foreach frequency condition, ranging from 0.11 to1.56, 0.33 to 1.61, and 0.62 to 1.61 dB/mo at500, 2,000, and 4,000 Hz, respectively. Theslope values were significantly different from a 0slope for loudness categories greater than Com-fortable at 500 Hz and for all Contour loudnesscategories at both 2,000 and 4,000 Hz. Thus,significant dynamic effects measured for group1 were more prominently revealed at 2,000 and4,000 Hz than at 500 Hz, but the full-treat-ment effects generalized across frequency.

The only significant slope values measuredin this study for any of the other treatmentgroups were those for group 2 for Contourcategories Loud, but OK and UncomfortablyLoud, respectively, at 2,000 and 4,000 Hz;

these slope values were less than one third ofthe magnitude of the corresponding slope val-ues for group 1. The appreciably greater slopevalues and dynamic treatment effects for group1, compared to those measured for the othertreatment groups, are highlighted in Fig. 6.Shown are best-fitting linear functions thatrepresent the average treatment change in theUncomfortably Loud categorical judgmentsacross 7 months of treatment for each groupassignment. This 7-month window capturedprimary treatment changes across participantswith differing treatment periods (5 to 12months) and also corresponded generally toour criterion for treatment termination acrossthe individual participants in group 1. Withineach group, the functions are shown to besimilar for 500, 2,000, and 4,000 Hz. Thefull-treatment dynamics are clearly superior tothe smaller effects obtained for the partial andcontrol treatments. The dynamics for controlgroup 4, which are virtually unchanged over thetreatment period, are noteworthy in as much asthese findings are consistent with the isolatedPSG assignment and, therefore, with the im-plementation of a successful placebo control forthe sound therapy treatment in this study.

The normalized (to baseline) treatmentdynamics for group 1, averaged across 500,2,000, and 4,000 Hz, are shown in Fig. 7 foreach of the seven Contour loudness categories.The dynamic effects are shown again across theinitial 7 months of treatment. The slope valuesincreased systematically from a low value of0.29 dB/mo for the Very Soft categorical judg-ments to a high value of 1.66 dB/mo for theUncomfortably Loud categorical judgments.The slope value for the comfortable judgmentswas 0.70 dB/mo. This range of slope valuesreflects aminimum average treatment change of2.03 dB for the Very Soft categorical judgmentsand a maximum average treatment change of11.62 dB for the Uncomfortably Loud judg-ments over this 7-month treatment window. Bycontrast, the isolated effects of counseling forgroup 2 and of sound therapy for group 3 overthis same treatment period typically averaged�3 dB or less for the Uncomfortably Loudcategorical judgments. Again, these variousanalyses reveal that the treatment dynamicsare much more robust for full-treatment group


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1 than for either of the partial treatment groupsor for the control treatment group.

DISCUSSIONThe primary aim of this study was to assess thevalidity of the basic principles underlying Ha-zell and Sheldrake’s protocol for hyperacusis1;their generality for the treatment of a dimin-ished DR and related primary complaintsamong our sample of hearing-impaired indi-

viduals who, prior to treatment, were unsuc-cessful hearing aid users because of theirassociated sound tolerance problems; and theefficacy of the intervention protocol, incorpo-rating CSGs and counseling specific to a di-minished DR as a consequence of reducedsound tolerance and hearing loss (aim 1). Oursecondary study aims were to delineate thecontributions from the counseling and soundtherapy components to the full-treatment pro-tocol by comparing the treatment effects for

Figure 7 Best-fitting (normalized to baseline) linear-regression functions characterize group 1 full-treatmentdynamics for each of the seven loudness categories. Changes in the loudness judgments are shown for eachcategory from Very Soft to Uncomfortably Loud over time of treatment in months.

Figure 6 Best-fitting linear-regression functions for each group highlight mean treatment dynamics forchanges in Uncomfortably Loud categorical judgments (normalized relative to baseline values measured justprior to treatment onset) over time of treatment shown in months. The parameter in each group panel ismeasurement frequency (500, 2,000, and 4,000 Hz), identified by line type in the inset legend. Abbreviations:CSG, conventional sound generator; PSG; placebo sound generator.


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each of the partial treatments with the effectsobtained for full treatment (aim 2) and tocharacterize the associated treatment dynamicsfor the respective treatment assignments (aim3). For purposes of comparison, we also mea-sured the treatment effect and dynamics for acontrol condition that was void of the counsel-ing component and included a placebo soundtherapy component. The study outcomes areconsidered next in terms of these primary andsecondary aims.

Aims

AIM 1: TREATMENT VALIDITY, EFFICACY, AND

GENERALITY

The positive results for full-treatment group 1support the validity and efficacy of the basicintervention principles for treatment of hyper-acusis and related sound tolerance complaintsassociated with a reduced DR. The treatmenteffects also generalize to our sample of hearing-impaired listeners who, on average, were bor-derline for their hyperacusis condition. Specifi-cally, the analyses presented above consistentlyrevealed the full-treatment protocol to be supe-rior in efficacy to both of the partial treatmentsand to the control treatment. Indeed, thecombination of the as-treated efficacy ratesfor individuals in group 2, who receivedcounseling and used PSGs, and for the individ-uals in group 3, who received no counseling andused CSGs, were 25 and 40%, respectively,whereas the efficacy rate for those in group 1was 82%. The efficacy for control group 4(PSGs without any counseling), albeit 50%,must be viewed cautiously in light of havingonly six contributing participants in the analysisat treatment end. Thus, in comparison with theefficacy rate for full-treatment group 1, theefficacy rates for each of the partial treatmentassignments were diminished by at least 40%.Moreover, almost invariably across the variousconditions evaluated statistically, group 1 aloneshowed positive and highly significant treat-ment change over time for the categoricalloudness judgments, and these positive effectswere typically uniform across frequency. Thus,in terms of aim 1, the categorical loudnessjudgments among the group 1 participants

consistently provided substantive support forthe treatment benefits of the combined counsel-ing and sound therapy principles originallydescribed by Hazell and Sheldrake and subse-quently incorporated into the TRT-H protocolby Jastreboff and Hazell.1,4

AIM 2: CONTRIBUTIONS FROM THE

COUNSELING AND SOUND THERAPY

COMPONENTS

The second aim of this research was to delineatethe relative contributions of the counseling andsound therapy components to the full treat-ment. The treatment-related changes in loud-ness growth for group 3 (revealed in thecomprehensive values of treatment changein Table 2) were the only ones, other thanthose measured for group 1, that were differentamong the four treatment groups in this study.That the conventional sound therapy treatment(with CSGs) in isolation yielded a treatmentbenefit for group 3 is not surprising. We andothers, beginning with Hazell and Sheldrake,1

have documented positive treatment effectsfrom use of low-level sound therapy amongnormal-hearing volunteers22,23 and in variouspatient groups.22,32,33 These positive treat-ment-related changes have been ascribed toeffects on central auditory gain control process-es induced by the low-level noise input. We donot know the specific site(s) nor nature of theneuronal mechanisms that are responsible forthese sound-induced treatment effects, andthese processes continue to be speculative.The treatment effects ascribed to counselingwere, on average, negligible in our analysisbased on the results from group 2, who receivedcounseling in combination with sound therapyfrom PSGs. Similarly, the treatment effects forgroup 4, from the PSGs in isolation, were small.

In the virtual absence of an isolatedcounseling effect, and with only a small tomoderate effect from conventional sound ther-apy alone, one wonders how these componentstogether contributed to the much larger full-treatment effect achieved by group 1. As notedabove, the average treatment efficacy rate fromcounseling, assuming negligible treatment ef-fects from their PSGs for group 2, was 25%,whereas the efficacy rate for group 3, whichreceived sound therapy alone from CSGs, was


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40%. In aggregate, the additive contributionsfrom these partial treatment contributions,when measured in isolation, accounted for anefficacy rate (65%) that was 17% less than whenthese individual components were offered to-gether, simultaneously, in the full-treatmentprotocol for group 1 (82%). However, the17% difference between the additive effects ofthe partial treatments and the efficacy estimatefor full treatment may or may not be sensible.Again, combining the partial-treatment efficacyrates is seemingly problematic when one con-siders that the control efficacy rate for the smallnumber of participants in group 4 (n ¼ 6) was50% for the PSG treatment offered in isolation.Results are needed from larger patient samplesto obtain more precise estimates of efficacy forthe partial treatment groups, which on averagewere smaller than for the PSG treatment effectfor control group 4.

In contrast, evidence of a synergistic, ratherthan additive treatment effect for counselingand sound therapy in the full-treatment proto-col seems more compelling. Consider again thecomprehensive index values of treatmentchange in Table 2 (also shown by groupin Table 3). The additive index values forgroups 2 (�0.25 dB) and 3 (22.95 dB), whichwere assigned counseling plus PSGs and CSGsalone, respectively, summed to 22.70 dB,whereas full-treatment group 1 achieved anindex value of 40.66 dB. Thus, the aggregateeffects of counseling and sound therapy in thefull-treatment protocol were almost twofold theadditive treatment effects of these individualcomponents in isolation. It is remarkable thatthe effects of counseling for group 2, whichwere smaller in magnitude than the effects ofthe placebo control treatment for group 4,somehow served to amplify the effects of soundtherapy by a factor of two when combined in thefull-treatment protocol.

The presumptive mechanisms by which thecounseling and sound therapy components con-tribute to the TRT-H treatment for primaryhyperacusis have been explained by Jastreboffand Hazell in the context of Jastreboff’s neuro-physiological model.4,24 Hyperacusis in its pur-est form is assumed in the model to be ananomalous condition or phenomenon that pri-marily, if not exclusively, affects the auditory

pathways. They assume no involvement of keynonauditory brain structures such as the limbicand autonomic nervous systems, which areconjectured to be activated to varying degreesamong persons who suffer misophonia andphonophobia. To the extent that hyperacusisand the related sound tolerance conditionsamong our participants can be represented inthis study as an isolated problem of the auditorypathways, the full-treatment effects, includingthe effect from counseling, seem surprising. Inthis study, the synergistic counseling effects,when considered within the context of the full-treatment results for group 1, were effectivelyequivalent in magnitude to �6 dB in terms ofthe treatment-related incremental shift in theUncomfortably Loud categorical judgments.This estimate of the phantom counseling effectand its contributions to the full treatment effectis in agreement with at least one estimate of theincremental LDL change from counselingalone after 12 months of TRT.34We can derivethis estimate of the counseling effect in the full-treatment protocol based on a known treatmenteffect of �6 dB for normal-hearing subjects insound therapy-alone studies.22,23 However, themeasurable counseling effect in this study wasvirtually absent in terms of the estimate of thecomprehensive index of treatment change forgroup 2 (see Tables 2 and 3). We suppose thisphantom counseling effect might somehow bemediated outside of the classical auditory path-ways by top-down cognitive processes, ostensi-bly via corticofugal efferent modulation. Thesefeedback efferent processes may be involved infacilitating and augmenting the effects of thesound therapy. We and others have conceivedthe mechanism of sound therapy to operatethrough, or on, an anomalous auditory gaincontrol process, probably mediated within thecentral auditory pathways.10 Theoretically,sound therapy down-regulates the abnormallyelevated central-neuronal activity that gives riseto the reduced sound tolerance condition, andthe counseling somehow augments or reinfor-ces the effects of sound therapy.

Alternatively, as discussed earlier, additiveefficacy rates for counseling and sound therapydo not necessarily rule out two independentadditive processes contributing to the full treat-ment. The counseling contribution to the full


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treatment would presumably be from cognitivesources and the sound therapy contributionwould derive from operations on central audi-tory pathway processes.

Baguley and Andersson have been criticalof the idea that hyperacusis is an isolatedproblem of the auditory pathways.15 They arguethat this notion is too simplistic and thathyperacusis likely involves an associated com-ponent of distress, with contributions fromnonauditory processes, including the limbicand autonomic nervous systems and other brainstructures. If so, then hyperacusis would bebetter represented in the Jastreboff model as acombined condition with misophonia (i.e., anemotional response to sound characterized bydislike or annoyance to specific sounds), whichmay often evolve into an associated conditionwith primary hyperacusis.24,35 Indeed, Hazellet al analyzed 187 consecutive patients with adiagnosis of decreased sound tolerance andconcluded that virtually all of these patientshad some degree of misophonia.36 Consistentwith the complex nature of the hyperacusisproblem is recent evidence from neuroimagingstudies suggesting that mild hyperacusis likelyinvolves neuronal activity in multiple centralnervous system structures within the midbrain,thalamus, and primary auditory cortex.37 Ac-cordingly, the underlying treatment mecha-nisms and the sites on which the counselingand sound therapy components in our full-treatment protocol achieved their effects almostcertainly include actions on structures andprocesses within and external to the classicalauditory pathways. Consequently, we mightreasonably conjecture that the phantomcounseling effect discussed previously may bedue to a counseling-induced reduction in theparticipant’s level of distress or anxiety over thecourse of the full treatment. Unfortunately, wedo not have data to support or refute this idea.However, anecdotally, few if any of our partic-ipants noted sound-related distress or anxiety atbaseline as a major issue.

Notwithstanding the multiple issues thatcloud the understanding of the relative contri-butions of the counseling and sound therapycomponents, it is evident that these two treat-ment components, when offered together, sub-stantially augment full-treatment efficacy.

Simply put, this means that the full-treatmentapproach is better than either of the partialtreatments delivered in isolation. Both treat-ment components are necessary to achieve anoptimum outcome for alleviating mild or sub-clinical conditions of hyperacusis and relatedsound tolerance complaints that restrict the DRfor persons with mild-to-moderately severesensorineural hearing losses.

AIM 3: TREATMENT DYNAMICS

Our third aim was to characterize the dynamicsfor the full treatment, each partial treatment,and the control treatment. Group 1 yieldedsignificantly different longitudinal treatmenteffects relative to the treatment dynamics ofthe other groups; these longitudinal effectsgeneralized across frequency from 500 to4,000 Hz. The associated slope values furtherhighlighted the prominent positive dynamics ofthe treatment effects over time of treatment forgroup 1, which were routinely different from azero slope across all loudness categories for2,000 and 4,000 Hz and across categoriesSoft through Uncomfortably Loud for 500Hz. The slope values for group 2 for categoriesLoud, but OK and Uncomfortably Loud at2,000 and 4,000 Hz were the only valuesamong any of the other treatment groups reach-ing statistical significance. Thus, on average,the full-treatment protocol yielded a superioroutcome when compared to the dynamiceffects for either of the partial treatments orfor the control treatment. Moreover, these full-treatment dynamics and the positive treatmenteffects may have been underestimated in asmuch as our revised follow-up schedule cur-tailed treatment as soon as consistent shifts of�10 dB were measured in the loudnessjudgments.

Finally, we noted in the presentation of theslope values that the dynamic treatment effectsfor counseling in effective isolation (group 2)and for sound therapy (group 3) were small butpositive. When these average partial effectswere summed together for the UncomfortablyLoud categorical judgments, the resulting pro-jection after 7 months of treatment is that thesummed partial effects amount to less than halfof their combined full-treatment effects (i.e.,4.9 dB versus 11.6 dB, respectively). This


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analysis of the treatment dynamics also indi-cates that the combined counseling and soundtherapy contributions in the full treatment arelikely synergistic rather than additive.

SUMMARY AND CONCLUSIONSNotwithstanding the small scale of this ran-domized controlled trial and the uneven groupsizes in our as-treated analyses, the overwhelm-ingly positive full-treatment effects, the subtlebut positive treatment effects achieved for con-ventional sound therapy alone, and the negligi-ble and small effects measured for thecounseling (combined with PSGs) and thecontrol protocols, respectively, are consistentwith the nature and efficacy of each treatmenttype in this study. Accordingly, in aggregate,the study outcome data and our analyses lendsubstantive support for the validity, efficacy,and generality of the full-intervention approachand the underlying treatment principles de-scribed by Hazell and Sheldrake for remediat-ing mild degrees of hyperacusis and expandingthe auditory DR for loudness among the hear-ing-impaired persons sampled in this study.1

Our full-treatment findings for group 1 (1)replicate both the magnitude and dynamics ofthe uncontrolled treatment effects reported byHazell and Sheldrake1 and (2) are in agreementwith a growing literature that reveals variousforms of enriched, wideband sound therapy, incombination with counseling, may significantlyenhance sound tolerance in clinical popula-tions.22 This literature includes the Neuro-monics approach for tinnitus treatment,which Davis and colleagues report yields incre-mental LDL shifts equivalent to those reportedfor patients treated with TRT.38,39

Norena and Chery-Croze described sur-prisingly large and rapid treatment effects for asound therapy-alone protocol among a group ofhearing-impaired subjects with varying degreesof high-frequency deficits and primary hyper-acusis.33 Their sound therapy approach, whichused a weighted, temporally complex, pure tonecomposite stimulus tailored to the frequencies ofthe hearing loss, called for daily exposure underheadphones to the low-level composite stimu-lation for 1 to 3 hours. Most of their treatmenteffects, based on incremental changes in cate-

gorical loudness judgments, were obtainedwithin a couple of weeks of beginning treatmentand were on the order of that measured for ourfull-treatment group 1. These rapid treatmenteffects for sound therapy alone deserve furtherstudy. Indeed, one wonders whether counselingcombined with Norena and Chery-Croze’ssound therapy approach might further enhancetheir treatment benefit. Clearly, counselingcontributed significantly to an optimum full-treatment benefit in the current study—whetherby virtue of participant understanding of theintervention and goals of the treatment, promo-tion of participant treatment compliance, en-couragement of participant motivation, top-down modulation and/or reinforcement of thesound therapy effects, reduction in associateddistress, or some other way.

The findings from our study potentiallyhave broad clinical relevance for managing andtreating sensorineural hearing loss, with impli-cations of the intervention principles extendingbeyond the treatment of hyperacusis and tinni-tus. Consider that our participants, on average,were representative of a subgroup of patientswhom Jastreboff and Jastreboff have distin-guished from individuals suffering primary hy-peracusis.35 They describe this subgroup ashaving decreased sound tolerance/no tinnitus,with average LDLs of � 85-dB HL. Thissubgroup presumably corresponds to hyperacusiscategory 1 on theHyperacusisNetworkWeb site(see http://www.hyperacusis.net/hyperacusis).The main concerns among our study samplewere consistent with their hearing losses andnominal sound intolerance, as revealed by theirborderline-reduced LDLs, which together di-minished their DRs. These problems are consis-tent with those of patients whom one mightroutinely manage in a traditional hearing aid/audiological practice. Indeed, the most promi-nent problems among our sample of participantswere reported when amplification was fittedunsuccessfully or dismissed without trial becauseof perceived or potential sound intolerance. Thefull-treatment protocol as described in this studymay, therefore, offer benefit for widespreadtreatment of diminished DR and sound-intoler-ance conditions across the general hearing-impaired population. This benefit includes thetreatment of persons with classical loudness


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http://www.hyperacusis.net/hyperacusis

recruitment for whom no intervention has pre-viously been available. If so, then we haveachieved with low-level sound therapy thelong-standing, elusive clinical goal and tooloriginally sought by Davis et al and Silverman,who championed the repeated presentation ofbrief high-level sound exposures to expand theauditory DRs of hearing-impaired persons.8,9

Finally, we have focused exclusively ongroup results to address the study aims inthis report. We also acquired unique caseresults that highlight compelling treatmenteffects and benefits for individual participantsover their course of treatment and postinter-vention. This evidence will be considered in aseparate report that provides a deeper discus-sion of the clinical relevance of the full-treat-ment protocol and associated implications ofthe intervention.

ACKNOWLEDGMENTS

This research was supported by a Public HealthService research award (parent grant NIDCDR01DC04678) from the National Institutes ofHealth to Craig Formby and by a pair ofcompanion supplement awards, including ded-icated support for Monica Hawley. Work wasstarted while Craig Formby, Monica Hawley,LaGuinn Sherlock and Susan Gold were at theUniversity of Maryland, Baltimore. We grate-fully acknowledge student assistance in con-ducting this study fromKimberly Block, JustineCannova, Allyson Segar, and Christine Gmit-ter. We also thank Charles Schroder for his aidin randomizing and maintaining documenta-tion of the blinded treatment assignments forour study participants, and Karen Tucker forpreparing multiple drafts of this manuscript.General Hearing Instruments, Inc. and theaffiliated authors’ roles in this project wererestricted to development, production, andquality-assurance testing of the sound generatortreatments; preparation of the information con-tained in the appendix, describing the soundgenerator products; and collaboration withclinical study staff to achieve double blindingof the sound therapy treatment assignments andmaintenance of the associated records andproduct documentation.

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2. Jastreboff PJ, Hazell JWP. A neurophysiologicalapproach to tinnitus: clinical implications. Br JAudiol 1993;27(1):7–17

3. Jastreboff PJ, Gray WC, Gold SL. Neurophysio-logical approach to tinnitus patients. Am J Otol1996;17(2):236–240

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5. Jastreboff PJ, Jastreboff MM. Tinnitus RetrainingTherapy (TRT) as a method for treatment oftinnitus and hyperacusis patients. J Am AcadAudiol 2000;11(3):162–177

6. Jastreboff MM, Jastreboff PJ. Decreased soundtolerance and tinnitus retraining therapy (TRT).Aust N Z Audiol 2002;21:74–81

7. Sammeth CA, Birman M, Hecox KE. Variabilityof most comfortable and uncomfortable loudnesslevels to speech stimuli in the hearing impaired. EarHear 1989;10(2):94–100

8. Davis H, Hudgins CV, Marquis RJ, et al. Theselection of hearing aids. Laryngoscope 1946;56:85–115, 135–163

9. Silverman SR. Tolerance for pure tones and speechin normal and defective hearing. Ann Otol RhinolLaryngol 1947;56(3):658–677

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19. Hazell JWP, ed. Proceedings of the Sixth Interna-tional Tinnitus Seminar. London, UK: The Tinni-tus and Hyperacusis Centre; 1999

20. Patuzzi R, ed. Proceedings of the Seventh Interna-tional Tinnitus Seminar. Perth, Australia: TheUniversity of Western Australia; 2002

21. Formby C, ed. Hyperacusis and Related SoundTolerance Complaints: Differential Diagnosis,Treatment Effects, and Models. Semin Hear2007;28(4):(Monograph)

22. Formby C, Sherlock LP, Gold SL, Hawley ML.Adaptive recalibration of chronic auditory gain.Semin Hear 2007;28(4):295–302

23. Formby C, Sherlock LP, Gold SL. Adaptiveplasticity of loudness induced by chronic attenua-tion and enhancement of the acoustic background. JAcoust Soc Am 2003;114(1):55–58

24. Jastreboff PJ. Clinical implication of the neuro-physiological model of tinnitus. In: Reich GE,Vernon JA, eds. Proceedings of the 5th Interna-tional Tinnitus Seminar. Portland, OR: AmericanTinnitus Association; 1994:500–507

25. Carhart R, Jerger JF. Preferred method for clinicaldetermination of pure-tone thresholds. J SpeechHear Disord 1959;24:330–345

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28. Munro KJ, Blount J. Adaptive plasticity in brain-stem of adult listeners following earplug-induceddeprivation. J Acoust SocAm2009;126(2):568–571

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32. Dauman R, Bouscau-Faure F. Assessment andamelioration of hyperacusis in tinnitus patients.Acta Otolaryngol 2005;125(5):503–509

33. Norena AJ, Chery-Croze S. Enriched acousticenvironment rescales auditory sensitivity. Neuro-report 2007;18(12):1251–1255

34. McKinney CJ, Hazell JWP, Graham RL.Changes in loudness discomfort level and sensi-tivity to environmental sound with habituationbased therapy. In: Hazell J, ed. Proceedings ofthe Sixth International Tinnitus Seminar. Lon-don, UK: The Tinnitus and Hyperacusis Centre;1999:499–501

35. Jastreboff PJ, Jastreboff MM. Decreased soundtolerance. In: Snow JB, ed. Tinnitus: Theory andManagement. Hamilton, Ontario, Canada: Deck-er; 2004:8–15

36. Hazell JWP, Sheldrake JB, GrahamRL.Decreasedsound tolerance: predisposing factors, triggers andoutcomes after TRT. In: Patuzzi R, ed. Proceed-ings of the Seventh International Tinnitus Semi-nar. Crawley, Perth, Australia: University ofWestern Australia; 2002:255–261

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APPENDIX: DESIGN/IMPLEMENTATION OF THEPLACEBO SOUND THERAPYTREATMENT

First-Generation Placebo Devices

The implementation of the PSGs by GHI wasintegral to the success of this clinical trial. Theplacebo activation, triggered by in- and out-of-the ear detection circuitry, was achieved withtwo different strategies in this project. Thefirst-generation PSGs were implemented witha gold-plated shell or case. The purpose of thisunique shell design was to optimize the detec-tion and capture of electrical activity emittedfrom the skin of the external ear and ear canal.Specifically, this electrical signal activated andpowered the placebo-detection circuitry bymaximizing electrical conductivity and shell-surface contact with the skin. The resultingvoltage signal from the human body then couldbe optimized for detection of the placebo devicewithin the ear and for activation of the placebocircuitry.

The detection strategy was implementedwith a detector circuit that used an integratedcircuit (IC) timer. A voltage applied to thetimer input produced a pulse at the output ofthe timer. The input signal to the timer was thesmall voltage signal produced from the skin ofthe external ear and ear canal. For this smallelectrical skin signal to be usable for control of

the placebo circuitry, the signal had to bemaximized for detection and transformed to ahigher voltage. Two large conductivity platesserved to maximize the collection of the smallvoltage signal from the skin. The plates wereimplemented on the acrylic shell surface of theplacebo device as pictured in Fig. A1A. Oneplate detected the body voltage and the otherestablished a ground-plane reference to thebody. Gold, because of its excellent propertiesof electrical conductivity, was selected as thematerial for constructing the plates. The appli-cation of the gold to the acrylic shell wasachieved through a mercury-free sputteringprocess. The initial step in the process was tomask the shell surface to outline the two plates;a base metal then was applied to the shell tooptimize the adherence of the gold material;and, finally, the gold was deposited electroni-cally onto the base-metal surface of the shell toachieve the plates. Two 1-mm holes were thendrilled through the gold-plating material toconnect the plates and the internal placebocircuitry via a pair of gold-plated pins.

Despite the elegance of the gold-platingprocess and the placebo design, two primarymodes of device failure were identified over theperiod of use of the first-generation PSGs. Onefailure mode was associated with the wear andloss of the electrically conductive epoxy adhe-sive connections between the gold-surface pinsand plates. This problemwas readily resolved by

Figure A1 Photographs of first-generation sound generators/placebo sound generator shells. (A) Unworndevice prior to participant use. (B) Worn device at end of treatment when placebo device failure wasdetermined by General Hearing Instruments (GHI, Harahan, LA) for the participant assigned to group 2 butmoved to as-treated group 1. Note the significant erosion of the gold plating from the surface of the failedworn device, which precluded normal placebo function.


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cleaning the shell surface and reapplying theconductive epoxy. The second and appreciablymore serious failure mode occurred when thebond between the base metal and the acrylicshell was eroded or disrupted. The causes of thislatter form of device failure were multifacetedand resulted from any one or a combination ofthe following factors, including rough handlingof the device; acids in the cerumen of the earcanal that disrupted the acrylic-base bond;excessive cleaning of the shell and/or applica-tion of abrasive cleaning products; and flawedbonding of the base metal to the acrylic materialof the shell during the sputtering process.

The latter failure mode is obvious whencomparing the pictures of unworn (Fig. A1A)and worn (Fig. A1B) failed first-generationPSGs. Note the significant erosion of thegold plating from the surface of the worn faileddevice in Fig. A1B in relation to the unworndevice shown in Fig. A1A. In the absence of thegold plating, little or no residual contact wasachieved between the connective pins and thebase metal on the surface of the shell. Althoughwe suppose it may have been possible for suchdamaged PSGs to continue to function via pinconductivity alone, this seems highly unlikelygiven the unique placebo design, which re-quired a consistent voltage path of sufficientstrength, maximized by the gold plating, toactivate the placebo circuitry. We know thatsignificant damage or erosion to the gold-platedsurface of failed devices, like that shownin Fig. A1B, consistently rendered the placebofunction inoperable. Consequently, these failedPSGs acted as conventional (nondecaying)sound generators. This conventional operationby the failed placebo units was measured andconfirmed by the manufacturer using standardquality control and failure assessment methodsposttreatment.

Fortunately, only 5 of the 17 participantswho were fitted with first-generation soundtherapy treatments were assigned to PSGs.There was no indication of undue damage orwear to the device cases for two of the fiveparticipants assigned to the placebo devices,and GHI engineers confirmed that the placebooperation remained functional for both of theirPSGs at treatment end.We do not know at whatpoint in treatment the damaged PSGs failed for

the three affected participants; however, thefailures appear to have occurred early in treat-ment because of unexpectedly robust treatmenteffects (of the kind measured for full treatment).

The first-generation devices also wereproblematic economically in that they werecostly to manufacture and required extendedperiods of time to produce. The first-generationgold-plated shells, used for both conventionaland placebo devices, were made in batches of 10or more at an added cost of $50.00 per shell. Abatch of 10 or more shells for a processing runby the outside vendor required an accumulationof at least five study participants and theiracrylic shells prior to placing a batch order forapplication of the gold-plating. Moreover, atleast a month was allotted for the outsidevendor to gold-plate the shells and return theplated shells to GHI, which in turn typicallyrequired an additional 2 weeks to build and shipa pair of devices to the study center to start/restart treatment. Thus, literally months wentby for some participants between the time theywere enrolled in the study and the time at whichthey began treatment with their assigned soundgenerator. This problem was further confound-ed for a period of almost 1 year during which nodevices were built or repaired because of Hur-ricane Katrina damage to the GHImanufactur-ing operation and facilities in New Orleans,Louisiana.

Second-Generation Placebo Devices

In light of the above problems with the first-generation PSGs, GHI re-engineered the pla-cebo instruments. The detector circuitry for thesecond-generation PSGs relied on detection ofskin capacitance rather than skin voltage andwas sensitive to skin proximity and touch.Consequently, dual plating on the device shellwas not required as was the case for the first-generation devices. Instead, a 6-mm-roundcontact pin was mounted into the helix of theshell, which provided sufficient capacitive pick-up and stability within the ear to preventundesirable resetting of the placebo circuitry.This pin-contact configuration, as visualizedfrom the outside of the shell, is shownin Fig. A2. The conducting-pin contact trans-mitted the skin-conductance signal to the


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placebo detector circuitry, which was imple-mented with a charge-transfer q-touch IC(Quantum Research Group, model QT 100)(Atmel, San Jose, CA). Upon insertion of thePSG into the ear, the QT 100 IC self calibratedto obtain threshold and reference capacitancelevels. The output of the QT 100 IC, whichtriggered placebo detection within the ear and,ultimately, activation of the circuitry that con-trolled the sound-decay process, then remainedactive while in the ear until there was a changein capacitance below a prescribed thresholdlevel. The capacitance change was monitoredfor 10 counts (i.e., 70 milliseconds per count orcircuit cycle of the QT 100 IC) to preventerroneous readings of the capacitance change.Upon removal of the PSG from the ear, a largechange (decrease) in the skin-capacitance levelwas detected and the QT 100 IC recalibrated tothe out-of-the ear state. The IC remained idleuntil the PSG was returned to the ear, whichreinitiated detection of another incrementalchange in skin capacitance. This incrementalchange in capacitance reactivated the self-cali-brate in-the-ear state of the PSG circuitry.Thus, if device contact with the skin of theear was lost for a period of time > 700 milli-seconds, then the PSG unit recalibrated.

Operationally, if the PSG was removedfrom the ear for more than �1 second, thenthe placebo-detection circuitry triggered a pro-cess of resetting such that within �3 second ofits removal from the ear the PSG output wasrestored to its original, full-on, steady-statevolume setting. This operational strategy wasintegral to successful double blinding of both theclinician and study participant as to soundtherapy treatment assignment. Specifically, sub-sequent to the clinician performing a listening

check to confirm the out-of-the-ear deviceoutput, reinsertion of the PSG within the earactivated the IC detection circuitry to recalibratefor in-the-ear operation. In turn, this recalibra-tion process retriggered activation of the placebooutput decay process, which was controlled withcircuitry described below. This latter circuitrywas common to both the first- and second-generation placebo devices.

Placebo Device Circuitry

The first- and second-generation detectioncircuits activated the same volume control cir-cuitry for the PSGs. Both detection circuitsgenerated an output voltage, either high or low,to designate whether the placebo devices wereoperating in an in-the-ear or out-of-the-earstatus, respectively. This control-voltage signalwas applied to the gates of a quad MOSFETswitch (Analog Devices, model AD6783) (An-alog Devices, Norwood, MA) to regulate: anelectronic volume control (Sound DesignTechnologies, model lv-560) (Sound DesignTechnologies, Burlington, Ontario, Canada);the up and down electronic volume-controllogic (i.e., for augmentation or attenuation ofthe noise output), and the time constants of theelectronic volume control. The time constantscontrolled the timing of: (1) the rapid restora-tion of the full-on steady-state volume outputafter removal of the PSG from the ear and (2)activation of the sound decay function after 30to 40 minutes of in-the-ear placebo operation.At power on, a high pulse applied to the gate ofthe quad MOSFET switch put the electronicvolume control into the volume up mode with avery fast time constant (i.e., seconds). Thisrapid activation of the volume-up mode setthe noise output to the clinician-set maximumvolume. The circuit remained in this state untilthe PSG was inserted into the ear, at whichtime the quad MOSFET switch activated thevolume-down mode of the electronic volumecontrol with a very long time constant (i.e.,minutes). The output of the PSG remainedconstant for 30 to 40 minutes, subsequent towhich the circuit triggered a decrease in thenoise volume (as the countdown capacitorscharged and discharged between one- andtwo-thirds voltage regulators). This decay

Figure A2 Photograph of second-generation soundgenerator shell.


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process systematically attenuated the noise out-put of the placebo device below the audibilitythreshold of the participant. The duration ofthe sound-decay process, subsequent to itsinitiation, was usually complete within 20 to30 minutes. The duration of the decay ulti-mately was dependent on the magnitude of theparticipant’s dynamic range set by the placebooutput steady-state suprathreshold noise levelsand the threshold-dependent subaudible noiselevels. The PSG remained in the subaudiblesilent state until removed from the ear, which inturn generated a reset pulse to the volumecircuitry to restore maximum noise output.

A transconductance block, housed withinthe electronic volume control circuit, wasused as a feedback resistance to control thegain of a linear-d amplifier (Sound DesignTechnology, model gs-3024). The analogoutput of this amplifier was then routed to

the input of a pulse width modulator(Knowles Electronics, model cd3418)(Knowles Electronics, Itasca, IL), which con-verted the analog signal into an on/off pulsed-duty-cycle signal. This latter signal then wassent through a set-screw volume control,which attenuated the full-on, steady-statemaximum output from the electronic volumecontrol circuit to regulate the amount of noisedelivered to the participant. The same signalwas routed to the receiver for control of theacoustical output of the PSG.

An example of a typical output-decayresponse versus time-after-activation (uppergraph of decay curve) function for the resultinganalog PSG is shown in Fig. A3A. Shownin Figs. A3B and A3C are typical frequencyresponse (lower left graph) and output response(lower right graph displaying dynamic range)curves for this PSG.

Figure A3 Output decay response curve (A), frequency response curves at minimum and maximum outputsettings (B), and dynamic range response (C) of a typical placebo sound generator used in this study.


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a sound therapy-based intervention to expand the auditory … · ed to hearing aid rejection. each...

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