Evidence-based treatment of paralytic dysphonia: making sense of outcomes and efficacy data

Evidence-based treatment of paralytic dysphonia: making sense of outcomes and efficacy data

Otolaryngol Clin N Am 37 (2004) 75–104 Evidence-based treatment of paralytic dysphonia: making sense of outcomes and efficacy data Alison Behrman, PhD,...

316KB Sizes 0 Downloads 30 Views

Otolaryngol Clin N Am 37 (2004) 75–104

Evidence-based treatment of paralytic dysphonia: making sense of outcomes and efficacy data Alison Behrman, PhD, CCC-SLPa,b,* a

Director of Voice Research, Center for the Voice, The New York Eye and Ear Infirmary, 310 East 14th Street, 6th Floor, New York, NY, USA b Department of Otolaryngology, New York Medical College, Valhalla, NY, USA

The decision for surgical or behavioral intervention for patients with vocal fold paralysis is driven by patient perception of vocal handicap and the expectation on the part of the surgeon, voice therapist, and patient that treatment will address the patient’s primary concerns. Incompetent glottal valving can cause interference with all laryngeal functions: airway protection, perception of ease of breathing, stabilization of the body core during physical activity, and phonation. Dysphonia, however, is generally the primary concern of the patient and the focus of the treatment team. The specific nature of the dysphonia may vary among patients: insufficient loudness, vocal fatigue, globus sensation, nonspecific ‘‘hoarseness,’’ effortful voicing, impaired singing quality (professional or recreational), difficulty in reading children’s stories to grandchildren, sensation of breathlessness on exertion or speaking, and intermittent laryngospasm. Although it is evident that impaired vocal fold adduction underlies these symptoms, significant clinical questions regarding treatment efficacy and outcome remain unanswered. For the patient, unrealistic expectations can lead to unnecessary frustration and complicate the course of treatment. For the voice therapist and surgeon, unmet treatment expectations further obscure the criteria that inform clinical decision making. The unanswered clinical questions regarding diagnosis and treatment outcome result from a dearth of outcomes and efficacy data generated from well-designed clinical research. This is partially a result of the varied symptomatology, which defies easy characterization for the purposes of clinical inquiry. This phenomenon, combined with variability of normative * Correspondence. Department of Otolaryngology, The New York Eye and Ear Infirmary, 310 East 14th Street, 6th Floor, New York, NY 10003, USA. E-mail address: [email protected] 0030-6665/04/$ - see front matter Ó 2004 Elsevier Inc. All rights reserved. doi:10.1016/S0030-6665(03)00169-5

76

A. Behrman / Otolaryngol Clin N Am 37 (2004) 75–104

data, has prevented the establishment of uniform, or even widely agreed on, measures of outcomes and efficacy. The result is an often insurmountable challenge to extract meaning from variable and disparate measures of treatment across different studies. The virtual absence of randomized controlled clinical trials (RCTs) addressing this patient population obliges the surgeon and voice therapist to extrapolate data from cohort and case-control studies that may not provide the best evidence to inform treatment decisions. The purpose of this article is to offer a guide to the critical interpretation of available measures of outcome and efficacy for the problem of dysphonia associated with vocal fold paralysis. Such data form the basis for the practice of evidence-based medicine and voice therapy, essential if the standard of care is to evolve to the benefit of the patient. A better understanding of the potentials and limitations of each measure is important for treatment planning and patient counseling and, ultimately, for the conception of future well-designed clinical research. The complex issues regarding outcomes measurement are addressed here within the context of current treatment literature on vocal fold paralysis. Particular emphasis is placed on realistic data gathering within clinical practice. This article includes a survey of the outcomes and efficacy literature on treatment for vocal fold paralysis (Table 1). Table 1 was obtained by searching Index Medicus using the key words ‘‘vocal fold’’ or ‘‘vocal cord’’ combined with ‘‘paralysis,’’ ‘‘paresis,’’ ‘‘immobility,’’ ‘‘augmentation,’’ ‘‘medialization,’’ or ‘‘reinnervation’’; ‘‘recurrent laryngeal nerve paralysis’’ or ‘‘paresis’’; ‘‘superior laryngeal nerve paralysis’’ or ‘‘paresis’’; ‘‘medialization laryngoplasty’’; ‘‘arytenoid adduction’’; and ‘‘thyroplasty.’’ Articles were limited to those published in English language peer-reviewed journals from 1975 through July, 2003. Articles were included in Table 1 only if they addressed treatment for dysphonia caused by unilateral vocal fold paralysis and included pre- and posttreatment data analysis. Therefore, many excellent research studies are specifically excluded from this listing, including (1) basic science animal studies; (2) human studies of the pathophysiology of untreated vocal fold paralysis; (3) exploration of diagnostic procedures, such as laryngeal electromyography (EMG), CT, or other imaging studies; (4) review articles of surgical procedures; (5) treatment outcome studies that considered only nonvoice factors, such as swallowing or complication rate; (6) case studies or series describing unique etiologies; and (7) the numerous retrospective chart reviews of incidence, prevalence, etiology, and treatment, where treatment outcome was determined only by the final physician note in the clinical record. Also excluded were articles that seemed to be duplicates, published within the same year in two different journals containing a similar author listing and abstract content. Table 1 includes 101 treatment studies, reflecting a substantial body of literature on unilateral vocal fold immobility. Despite the number, however, there remains a lack of data regarding selection of optimal treatment modalities, outcomes of treatment for specific patient groups, and the relative efficacy of treatments.

Table 1 Survey of outcomes and efficacy literature on treatment for vocal fold paralysis Injection augmentation (no group comparison)

Arytenoid adduction (no group comparison)

[73] 28 titanium 2003

[109] 80 autologous fat 2003

[74] 112 Gore-Tex 2003

[110] 7 collagen 2002

[75] 14 Gore-Tex 2003 [77] 70 ML (35 longstanding UVFP, 35 short-term UVFP) 2002 [78] 11 ML, 12 ML + AA (all acute repair) 2002

[111] 8 autologous fat 2002 [56] 12 acellular dermis 2002

[112] 14 minced fascia 2002

Table 1 (continued )

Reinnervation (no group comparison)

Voice therapy (no group comparison)

One treatment group and control normals group only

Two or more treatment groups

[128] 22 AA paramedian approach with strap muscle 2002 [144] 23 AA, 3 AA + ML 2000

[67] 9 using XII as donor 2000

[69] 20 yawnbreathing technique 1991

[55] 13 IA (fat), 8 ML with voice therapy 2000

[141] 8 REINN, 4 ML 2003

[135] 52 all with ML silastic 1997

[72] 12 reinnervation, 12 N 1998

[146] 9 arytenopexy + ML 1998 [147] 11 1994

[136] 8 1996

[27] 5 ML (silastic), 9 N 1994 [42] 15 ML (various silastic, cartilage, Gore-Tex), 15 N 1992

[31] 4 ML (silicone), 14 IA (fat), 14 N 2002 [76] 7 ML, 12 REINN 2002

[137] 7 suture CT to LCA 1993

[138] 12 1991

Randomized clinical trials [44] 70: hylan B or bovine collagen 2002

[102] 98 ML, 96 ML + AA silastic 2001

[104] 45 ML (silastic), 23 IA (autologous fat) 2001

A. Behrman / Otolaryngol Clin N Am 37 (2004) 75–104

Medialization laryngoplasty (no group comparison)

(continued on next page) 77

Arytenoid adduction (no group comparison)

[32] 40 some with AA 2002 [80] 20 silastic 2002

[113] 6 DiHA 2001

[64] 70 1989

[114] 9 autologous fat 2000

[66] 2 1986

[79] 53 titanium 2001

[115] 10 autologous fascia 2000

[140] 5 1985

[81] 10 2001

[116] 17 collagen 1999

[65] 27 1981

[58] 12 ML, 33 ML + AA silastic 2001

[117] 18 fascia 1999

Reinnervation (no group comparison)

Voice therapy (no group comparison)

One treatment group and control normals group only

Two or more treatment groups [84] 32 ML revisions (various) 2001 [139] ML revisions, 11 ML, 12 AA, 2 IA (fat) 2001 [43] 25 Gore-Tex with AA, 19 AA 2000 [59] 30 ML, 17 untreated, 22 N 2000 [68] 7 ML, 6 IA (gelfoam), 6 VT, 5 VT + surgery (technique not specified), 1 ML + IA (gelfoam) 1999

Randomized clinical trials

A. Behrman / Otolaryngol Clin N Am 37 (2004) 75–104

Injection augmentation (no group comparison)

78

Medialization laryngoplasty (no group comparison)

[118] 20 autologous fat 1999

[103] 3 AA, 2 ML (silicone) 1999

[119] 8 autologous collagen 1999

[85] 3 silastic 2001

[120] 3 autologous fat 1998 [121] 8 transcutaneous Teflon 1998 [122] 20 Teflon 1997

[105] 28 ML, some with AA silastic 1999 [107] 19 proplast, 6 hydroxyapatite 1999 [142] 9 AA, 10 AA + REINN 1999 [143] 33 REINN + ML, 27 ML only silastic 1999 [70] 14 IA (fat) or ML (not specified), 27 VT 1997 [16] 16 ML, 10 untreated 1997

[29] 43 Montgomery system 2000 [61] 26 2000

[86] 27 2000

[123] 30 transcutaneous silicone 1996

[87] 9 ML with cricothyroid approximation 2000

[124] 21 autologous fat 1996

A. Behrman / Otolaryngol Clin N Am 37 (2004) 75–104

[82] 6 anterior + posterior technique silicone 2001 [83] 26 minifenestration 2001

(continued on next page)

79

80

Table 1 (continued ) Injection augmentation (no group comparison)

[50] 56 Montgomery system 1999 [88] 12 silastic 1998

[125] 30 transcutaneous silicone 1996 [126] 11 Teflon 1995

[89] 176 Montgomery system 1997

[127] 3 (children) 1995

[90] 29 1996

[23] 240 silicone 1995

[91] 10 ceramic 1996

[63] 53 collagen 1995

[92] 4 1996

[145] 11 autologous fat 1992 [129] 3 autologous fat 1991

[93] 9 1996

Arytenoid adduction (no group comparison)

Reinnervation (no group comparison)

Voice therapy (no group comparison)

One treatment group and control normals group only

Two or more treatment groups [97] 4 ML, 8 ML + AA 1995 [106] 49 ML (silastic), 10 AA 1995 [98] 1 AA, 1 AA + IA (Teflon), 3 AA + ML (silicone) 1994 [148] 6 ML, 4 AA, 2 IA (Teflon) 1992 [108] 18 untreated, 15 IA (silicone), 18 ML (silicone) 1991

Randomized clinical trials A. Behrman / Otolaryngol Clin N Am 37 (2004) 75–104

Medialization laryngoplasty (no group comparison)

[130] 42 silicone 1990

[131] 19 Teflon 1989 [132] 10 silicone 1988 [62] 54 collagen 1986 [133] 111 Teflon 1985 [134] 1 Teflon 1978

Within each column, studies are listed by publication year from most to least current. For each study, the first number appearing in brackets corresponds to the citation number in the references section, followed by the number of subjects. For articles in which subjects’ pathologic findings varied, only those with UVFP are included here. Subject number reflects the number of patients for whom postoperative outcome measures were available. If more than one type of treatment group is included, these are noted. When specified in the article, the type of surgical implant material is indicated. For those articles listed under the column heading ‘‘Two or More Treatment Groups,’’ it should be noted that even though a study may contain more than one type of treatment group, the outcome measures were not necessarily analyzed separately by group. All ML procedures are type 1 unless otherwise specified. Abbreviations: AA, arytenoid adduction; DiHH, dextranomers in hyaluronan; IA, injection augmentation; LCA, lateral cricoarytenoid; ML, medialization laryngoplasty; N, normal controls; REINN, reinnervation; UVFP, unilateral vocal fold paralysis; VT, voice therapy. [70] Number of subjects receiving IA with fat is an estimate; the article indicates ‘‘most but not all’’ of the subjects had fat injections. [84] ML revision procedures include types 1 through 4 and also AA, but techniques are not broken out by the subgroup of patients for whom pre- and postoperative outcomes data are reported.

A. Behrman / Otolaryngol Clin N Am 37 (2004) 75–104

[33] 50 ML type I, 2 ML type I + II, 1996 [94] 20 1996 [95] 10 1995 [96] 29 1995 [99] 21 1994 [100] 8 silicone 1992 [28] 13 Silastic 1990 [101] 11 Silastic 1986

81

82

A. Behrman / Otolaryngol Clin N Am 37 (2004) 75–104

Defining outcomes and efficacy Outcomes studies are designed to assess the broad value of treatment for individual patients by measuring change across intervention. In contrast, efficacy addresses the efficiency of the treatment and can only be assessed within a controlled experimental design in which one or more components of treatment are manipulated. Efficacy may include the extent to which components of a treatment contribute to outcome, the relative outcomes of different types of treatment, and the time and financial commitment required to achieve an optimal outcome. Efficacy studies can explain why and under what circumstances treatments succeed. Outcomes studies are designed to collect data within routine clinical care, whereas clinical efficacy studies require a commitment to the random assignment of patients to specific treatment arms. The careful selection and use of assessment measures, however, are no less important in outcomes studies than in efficacy research. In the absence of a well-conceived standardized protocol of assessment consistently applied to each patient, reporting of outcomes is reduced to clinical anecdote. Regardless of how large the series of patients on which conclusions are based, clinical anecdote is insufficient to make statements about the broad value of treatment and, worse, is often misleading because of bias and confounding factors. Good use of outcomes measures is not difficult and does not necessarily require a substantial investment in complex instrumentation or clinical time. It does require some thoughtful consideration and planning. Selection of the appropriate measures of treatment outcomes and efficacy for a broad spectrum of voice problems has received much attention [1–3]. Despite attempts to derive a unified index of vocal function, decades of seeking a unitary statistical measure of dysphonia and attempts to correlate it meaningfully with specific vocal quality features or to differentiate pathologic findings have been largely unsuccessful [4–7]. Voice is widely recognized to be a multidimensional product that cannot be reduced to a single numeric score. Nevertheless, the use of multiple measures of outcome generates its own set of problems; chief among them are the selection of a corpus of measures and inconsistencies among measures, with the latter issue solved in part by the use of a primary outcome measure. These are each considered in turn. Sorting through measures of outcome There are so many potential assessment measures of treatment outcomes that choosing among them can easily become overwhelming. It is helpful to start by organizing measures into broad categories, such as presented in the following list: Laryngeal videoendoscopy/stroboscopy Vocal function

A. Behrman / Otolaryngol Clin N Am 37 (2004) 75–104

83

Acoustic Aerodynamic Clinical assessment of vocal quality Patient self-assessment The proper ways in which to obtain these measurements, the instrumentation required, signal processing, and analyses are beyond the scope of this article, and many comprehensive sources are available that provide detailed information on these topics [2,8–10]. Rather, this discussion is intended to provide guidance in measurement selection. Laryngeal videoendoscopy/stroboscopy Diagnosis of vocal fold paralysis rests on visual examination of the larynx; yet, the surgeon should be discouraged from using visualization of vocal fold movement as the sole outcome measure to assess treatment of vocal fold paralysis. Endoscopic visualization can be limited by supraglottal hyperfunction used to compensate for the incomplete glottal closure. This often obscures the view of the true vocal folds whether a fiberoptic or rigid oral endoscope is used. Hypotonia in the denervated vocal fold can cause anterior prolapse of the arytenoid complex, further obscuring the glottal view during phonation. Additionally, the two-dimensional nature of the endoscopic image limits the information obtained. Vertical level differences can only be inferred rather than directly visualized and sometimes can be exceedingly difficult to assess. Although there have been analyses of vertical height differences of the vocal folds in cases of unilateral vocal fold paralysis [11], these judgments should be made with considerable caution. Videostroboscopy has become the gold standard of assessment of laryngeal structure and function [12]. Stroboscopy is not required to visualize the relatively slow medial and lateral movements of the vocal folds, but it is often necessary for clear visualization of phonatory glottal closure, especially in cases of small or inconsistent gap. There are some limitations of the examination, however, one being its reliance on periodic vibration. The stroboscopic image is not a true representation of the vibratory behavior of the vocal folds; rather, it provides an image that is a composite of a number of true vibratory cycles. Therefore, good imaging of mucosal wave dynamics requires synchronization of the strobe light with vocal fold vibration. Unfortunately, there can be an inverse relation between vocal dysfunction and utility of the stroboscopic examination: the greater the irregularity of vibration, the poorer is the strobe image. Important characteristics of mucosal wave movement, including amplitude of vibration, focal adynamic segments, left-right asynchrony, and subtle phonatory glottal incompetence, can be impossible to judge when vocal fold vibration is irregular. Intermittent phenomena that occur at a frequency above the strobe rate cannot be seen, such as rapid irregular oscillation of a paralyzed vocal fold with decreased tone.

84

A. Behrman / Otolaryngol Clin N Am 37 (2004) 75–104

The second limitation of stroboscopy for treatment outcomes assessment relates to the geometry of glottal insufficiency. Phonatory glottal closure may be impaired spatially and temporally. Assessment of the spatial dimension—the geometry of the glottal gap—is the more common and easier judgment. Assessment of the temporal dimension, the duration of phonatory glottal closure, is often overlooked, however. Duration of closure is a critical factor in intensity regulation, and insufficient duration may have the potential to cause vocal handicap even in the absence of notable geometric glottal gap. Judgments of duration can be difficult, given that stroboscopy does not show each cycle of vibration. For this reason, quantifying phenomena using digital measurements, including counting the number of individual video frames as a measure of closure, is not consistently helpful. The degree to which decreased closure, in extent or duration, results in dysphonia is unknown. It likely varies across patients as well as across speaking conditions within an individual patient. Harries and Morrison [13] assessed the utility of stroboscopy in 100 patients with unilateral vocal fold paralysis. They found that a reliable image of mucosal wave vibration could be obtained only in those patients with a small phonatory glottal gap. Sercarz et al [14] assessed 20 patients with untreated unilateral vocal fold paralysis and found asymmetry of mucosa wave vibration in all cases, with greater amplitude and speed of the nonparalyzed vocal fold. In summary, endoscopic and stroboscopic assessment of laryngeal structure and function offers indispensable information regarding vocal fold mobility, phonatory glottal closure, mucosal wave oscillation, and other parameters of vocal function. Nevertheless, the surgeon and voice therapist are urged to guard against overinterpretation of the endoscopic examination as well as overreliance on a sometimes less than ideal examination. Stroboscopic findings do not explain entirely the treatment outcome; although the importance of glottal closure to phonation is well recognized, there is a range of values within which normal function exists, as in all physiologic systems. Acoustic and aerodynamic assessment Outcomes assessment of vocal physiology most commonly includes acoustic and aerodynamic analyses. Other physiologic measures, such as electroglottography, photoglottography, and videokymography, are also available. They are considerably less common, however, and require specialized instrumentation that is frequently unavailable in routine clinical practice. Because the purpose of this article is not to provide an exhaustive review of instrumental measures but rather to support and encourage the generation of outcomes data in routine clinical practice, those less frequently used instrumental measures are not addressed. The decision of which instrumental measures to use for outcomes assessment is one of the greatest sources of frustration for professionals,

A. Behrman / Otolaryngol Clin N Am 37 (2004) 75–104

85

because there is no ‘‘correct’’ set of measures but many possibilities for false interpretation. Rather than starting with the question of which measures to use, it may be more meaningful for the surgeon and voice therapist to consider first what information they want to know to judge outcome of treatment. This is a clinically driven question that any professional with sufficient expertise to treat the patient should be able to answer. Then, the next question becomes ‘‘What measures will yield that information, or if that is impossible, what measures can provide an approximate answer?’’ It is this question that requires some expertise in instrumental measures, and, frequently, the voice therapist can provide the surgeon with guidance in this area. How ‘‘objective’’ are physiologic measures? Acoustic and aerodynamic data are commonly reported in the literature as ‘‘objective’’ measures to balance subjective and perceptual assessments of vocal quality and patient opinion. This is somewhat misleading. Objective measures are those that are independent of the perceptions of the person acquiring the data, yet instrumental measures require subjective interpretation. There are two major interrelated factors that render instrumental measures less than objective. First, the instrumental measures used in the assessment of dysphonia are behavioral tests of vocal performance. As such, elicitation requires clinical guidance, cueing, and feedback. Even a simple measure, such as average fundamental frequency or intensity of a sustained vowel, can be quite sensitive to clinical instructions; whether to produce it with a deeper prephonatory inhalation or to produce it with more effort, for example. Clinical judgment is also required in the generation of the numeric measures. For example, jitter provides an objective metric of the average variability of sequential vibratory cycles. Yet, the judgment of how much of the signal to include in the jitter measures—whether to include phonation onset and offset or to exclude a pitch break or momentary diplophonic phonatory segment—is a subjective determination that has the potential to affect the numeric value substantially. Although instrumental measures themselves are objective, the ways in which they are obtained and interpreted may be highly subjective. They are independent of neither the examiner’s nor the patient’s behaviors. The second factor that unavoidably compromises the objectivity of instrumental measures is the uncertain validity and interpretation of the data in cases of irregular vocal fold vibration. The essence of the problem is the need for reliable identification of individual glottal cycles of the acoustic or aerodynamic signal. In the mathematics of signal processing, demarcating the glottal cycle in cases of incomplete glottal closure or impaired vibratory movement is not a trivial problem [9]. Addressing this somewhat intractable problem in the 1995 summary statement of the Workshop on Acoustic Voice Analysis, Titze [15] classifies acoustic signals into three types. Type 1 signals are defined as nearly periodic. Type 2 signals contain modulations, rapid qualitative changes in the signal, or strong subharmonics (frequencies that lie

86

A. Behrman / Otolaryngol Clin N Am 37 (2004) 75–104

between the harmonics). Therefore, type 2 signals contain no consistent single fundamental frequency because of such phenomena. Type 3 signals are defined as random- or chaotic-appearing and contain minimal apparent periodic structure. The summary statement recommends that although fundamental frequency and perturbation measures (eg, jitter and shimmer) are generally useful and reliable for type 1 signals, they should not be used with type 2 and 3 signals, because the measures are ambiguously determined and contain little pattern information. Graphic representations (including spectrograms) are recommended for type 2 signals, and perceptual analysis is recommended for type 3 signals. The summary statement advises that spectrograms and other cyclic parameter contours may be useful in determining the signal type. Plant et al [16], acknowledging the difficulty in assessing severely dysphonic voices, used an autocorrelation function of the pitch amplitude from the inverse filtered signal. Using linear predictive coding to analyze 16 patients before and after medialization compared with 10 patients with no surgery, the authors found that pitch amplitude and perceptual ratings correlated highly, with both showing significant improvement with surgery. Measures of habitual voice use Given these concerns of periodicity and validity of measures, an already complex selection among the plethora of potential acoustic and aerodynamic measures becomes even more overwhelming. Without offering a formulaic solution, some guidance is offered here for those interested in developing a rational approach to outcomes measurement. In keeping with the strategy of considering first what information the surgeon and voice therapist want to know to judge outcome of treatment, it may be helpful to conceptualize acoustic and aerodynamic measures in two ways related either to symptom or to type of vocal performance. Vocal performance refers to both habitual voice use and maximum performance tasks [17] and has parallels in testing other physiologic systems, particularly pulmonary function and cardiac testing. Numeric measures of habitual voice provide information about how the patient typically uses the voice production system in the presence of unilateral vocal fold paralysis. Habitual voice use is most commonly assessed using spontaneous conversation or standardized sentences. Some measures, especially subglottal pressure or spectral quantities like harmonic-to-noise ratio, are often assessed during steadystate vowel production yet inferred to represent the patient’s typical voice production. In all instances of habitual measures, the individual eliciting the sample must judge whether it is representative of the patient’s spontaneous conversational voice production so as to be valid metrics. Unfortunately, this validation step is often omitted in instrumental measurement. Measures of maximum vocal performance In contrast, maximum performance tasks, such as minimum and maximum intensity and fundamental frequency, test the physiologic

A. Behrman / Otolaryngol Clin N Am 37 (2004) 75–104

87

capabilities of the system. Minimum and maximum intensity can be elicited at the upper and lower extremes of the range or, alternatively, at a range of fundamental frequencies as would be achieved within a voice range profile [18–20]. The s/z ratio and maximum phonation time (MPT) are two maximum performance tasks that require nothing more than a stopwatch for instrumentation and have therefore had some long-standing popularity. Both of these phonatory maneuvers are used to assess integrity of phonatory glottal closure. The s/z ratio is a statistic of the relative durations of maximum phonation of the phonemes /s/ and /z/. Both fricatives are produced with the same oral articulatory occlusion, with the /z/ having increased laryngeal resistance because of voicing. The rationale is that glottal incompetence provides less aerodynamic resistance during voicing and hence skews the ratio values. MPT, as the name implies, measures the duration of a maximally sustained vowel and, for reasons similar to the s/z ratio, ought to be sensitive to impaired phonatory glottal closure. The validity of these measures is questioned [17,21], largely because a number of compensatory behavioral maneuvers can be used to achieve normal or near-normal values. Some of these compensations are beneficial, and, in fact, compensatory behaviors form the basis for much of voice therapy. Some of the behavioral maneuvers used to achieve normal values for MPT or s/z ratio are actually maladaptive for speech production, however. For example, excessive inspiratory checking (maintenance of excessive contraction of the inspiratory muscles while phonating) can be used to maintain lung expansion, decreasing expiratory flow (in lieu of the resistance to the airflow that would be offered by the adducted vocal folds in normal phonation) and thereby helping to maintain longer voicing. Alternatively, excessive constriction of the supraglottal musculature, particularly the ventricular folds, can help to achieve increased resistance to the airflow, again slowing down the rate of egressive flow and helping to maintain longer phonation. The relation of the MPT and s/z ratio to normal phonatory function is unclear. It is a common error in research studies to attribute greater meaning to correlated factors than truly exists. The fact that nondysphonic individuals can produce sustained /a/ for 20 seconds on average, for example, does not mean that it is a requisite behavior for speech. It is likely that the ability to phonate continuously for no longer than 10 seconds may be all that is required for daily communicative demands [21], and absolutely no data exist to identify target s/z ratios or MPT values for demands like loud speech or classroom teaching. Solomon et al [22] recommend removing these measures from assessment protocols, a recommendation with which this author agrees. Measures related to patient symptoms Conceptualizing acoustic and aerodynamic measures in relation to the patient’s symptoms can help to determine which measures to select. Complaints related to pitch may be correlated with mean speaking fundamental frequency, range of fundamental frequency in conversation, or the

88

A. Behrman / Otolaryngol Clin N Am 37 (2004) 75–104

maximum performance test of physiologic frequency range. Complaints of loudness limitation may be correlated with mean speaking intensity, dynamic range in conversation, and physiologic dynamic capability. Patient complaints of roughness, hoarseness, or similar qualitative changes may be indirectly quantified with the harmonic-to-noise ratio, cepstral measures, and long-term average spectra, which provide information about harmonic content relative to broadband noise generated from turbulent airflow and encompass frequency and intensity information. Complaints of breathiness can be assessed with mean and peak flow airflows. Sensation of extraneous effort or complaints of vocal fatigue can be indirectly assessed with interpolation of subglottal pressure and glottal resistance (ratio of subglottal pressure to flow). An excellent reference manual for all these measures, their calculations, the instrumentation required, and the data from normal individuals and those with a variety of pathologic findings as well as an extensive bibliography of additional readings can be found in Baken and Orlikoff’s revised text [8]. Measures reported in the literature Another common strategy to aid in selection among outcomes measures is to review the literature and identify those commonly used. Unfortunately, many studies offer an abundance of measures, each of which can be identified as meaningful with reasonable argument yet together create a complex array of information that is sometimes quite difficult to reconcile with the patient’s voice. It may be that the use of such a wide variety of statistics reflects an underlying uncertainty of which measures to use. In reviewing the treatment outcomes studies included in Table 1, acoustic and aerodynamic measures are by far the most popular of all outcomes assessments (with the exception of videoendoscopy), commonly including most or all of the values already discussed. Intensity is notable for its lack of popularity despite ease of measurement and relevance to vocal dysfunction in vocal fold paralysis, however, and warrants some special attention. Intensity Although almost three quarters of the studies listed in Table 1 use acoustic or aerodynamic assessment measures, only approximately 10% include measurement of either habitual speaking intensity or maximum physiologic dynamic range. Impaired loudness, the acoustic correlate of intensity, is a common complaint of patients with vocal fold paralysis, and untreated patients are found to have limitations in average intensity and dynamic range [23]. A brief review of the physiology of intensity regulation can highlight the relevance of intensity measures to assessment of treatment outcomes. Intensity is determined by vocal tract resonance and lung pressure combined with dynamic glottal geometry. Vocal tract postural adjustments ranging from simple movements, such as widening the opening between the lips, to complex shaping of the pharyngeal space, can maximize resonant

A. Behrman / Otolaryngol Clin N Am 37 (2004) 75–104

89

frequencies and thereby increase gain. Such adjustments are part of the compensatory strategies taught to patients in voice therapy and are basic to singing and acting technique. Increasing lung pressure is the primary means of increasing intensity, however [24]. Specifically, intensity is a function of the sequential pulses of air exiting upward from the glottis during each cycle of vibration, the ‘‘glottal volume velocity.’’ In general, increased lung pressure drives a larger volume of air through the glottis, generating greater amplitude of the glottal volume velocity, which, in turn, results in greater intensity. It is not just a matter of pushing more air through the glottis, however. The closure of the vocal folds in each vibratory cycle regulates the excitation of the column of air in the vocal tract. Faster closure generates a sharper cutoff of the airflow. All other things being equal, greater lung pressure may push the vocal folds apart more widely, generating increased buildup of restorative force within the tissues and therefore causing them to spring back to the midline faster, shutting off the airflow more quickly. In fact, voices produced with greater intensity are characterized by a steeper cutoff of the glottal volume velocity waveform [25]. Spectrally, this generates greater energy distribution to the harmonics overall. Soft or breathy voice generally contains less energy in the higher harmonics when compared with louder or less breathy voice. The strong relation between lung pressure and intensity means that the integrity of the spatial and temporal dimensions of glottal closure also specifies the intensity. Complete glottal closure is required to generate greater pressure, because a glottal gap would act as a pressure bleed valve and limit pressure buildup. Increasing lung pressure is achieved by increasing the duration of the phonatory glottal closure to allow greater buildup of pressure beneath the vocal folds. Therefore, glottal closure must be sufficiently robust to offer the requisite resistance to the increased lung pressure. Unfortunately, duration and ‘‘firmness’’ of closure are difficult to judge. Further, the speed of the glottal closure nearest to the flow minimum (eg, when the vocal folds are almost completely adducted) may be critical to the overall intensity (as discussed by Scherer and Rubin [26]); therefore, it may be that even a small glottal gap has the potential to limit intensity significantly. Hence, not only is dynamic range impaired in the presence of vocal fold paralysis, and perhaps even a small glottal gap, but the increased compensatory muscle activity used to offset the glottal incompetence can lead to a sensation of extra effort and vocal fatigue. The vocal physiology of intensity control is considerably more complex than that presented in this short discussion, and the interested reader can find a more in-depth presentation, along with additional references, in articles by Scherer and Rubin [26] and Titze [9]. Measurement of intensity requires specifying the mouth-to-microphone distance and maintaining that distance consistently within and across patients. Careful instructions to the patient regarding sample productions are essential because of the sensitive relation between intensity, pitch, and effort of production. These are not difficult obstacles to overcome, however. Further,

90

A. Behrman / Otolaryngol Clin N Am 37 (2004) 75–104

instrumentation need not be complex. ‘‘Low-tech’’ solutions are available, such as having the patient stand at a preset mark on the floor measured from a floor-stand microphone or holding a microphone a ruler’s length away from the mouth. If separate acoustic instrumentation is not available, intensity can be estimated from the digital decibel sound pressure level (SPL) display of the commonly used Kay Elemetrics RLS system (Lincoln Park, New Jersey) (after connecting a microphone, of course) or simply by borrowing an SPL meter from the audiologist and holding it a consistent distance from the patient’s mouth. Intensity is improved after medialization laryngoplasty [27–29], autologous fat injection [30], and silicone injection [23]. Although patient perception of loudness is improved after surgery, it continues to be perceived as below normal [31]. Billante et al [32] found that intensity level continued to show improvements up to 1 year after medialization laryngoplasty in 40 patients (some with concurrent arytenoid adduction); in contrast, Lu et al [33] found only slight fluctuations in the postoperative increase in intensity from the 1-month to 1-year examination in 53 patients. This discussion is not meant to imply that the relation between phonatory glottal closure and intensity is ignored in the literature on treatment outcomes in vocal fold paralysis. That is not the case. For example, Hartle et al [34] conducted a unique study of 2 patients before and after the onset of iatrogenic unilateral vocal fold paralysis after thoracic surgery. Spectral slope of lowfrequency harmonics relative to high-frequency harmonics and cepstral peak prominence were among the instrumental measures used to characterize vocal dynamics. These measures are expected to be sensitive to velocity and extent of vocal fold closure and thus would be meaningful in treatment outcomes assessment for this patient population. Nevertheless, the point here is that mean speaking intensity may be a more direct manifestation of the patient’s symptoms and therefore more likely to correlate with the patient’s self-assessment and the clinical assessment of vocal quality. Further, straightforward measures of intensity may be more readily grasped by the broader medical and therapeutic community. In summary, although acoustic and aerodynamic measures are not completely objective, they do provide unique information about the voice production system for outcomes assessment of treatment for unilateral vocal fold paralysis. The greatest weakness of these measures is that the data are only indirect evidence of vocal function. The relation between perceived vocal quality and patient perception of voice disorder is not always directly related to many of the acoustic and aerodynamic measures, and this complicates assessment of outcome. It is recommended that the surgeon and voice therapist understand clearly the purpose for each acoustic and aerodynamic measure to be used and consider the degree to which the measures relate meaningfully to the patient’s voice. Increased mathematic complexity of acoustic and aerodynamic measures does not necessarily correlate with more meaningful representation of the patient’s voice production system.

A. Behrman / Otolaryngol Clin N Am 37 (2004) 75–104

91

Measures like mean speaking intensity and dynamic range are not difficult to measure; moreover, they may be more straightforward in interpretation relative to the patient’s vocal function than many complex measures. Vocal quality assessment Clinical assessment of vocal quality is probably the oldest measure of dysphonia. Voice is, after all, an acoustic phenomenon, and its aural perception by the speaker and the listener is the primary means by which voice is judged in daily communication. Assessment of vocal quality is not without controversy, however. At the most basic level, vocal quality is a matter of personal taste, and that which is disordered to one individual is normal to another. Measurement of vocal quality is fraught with difficulty, including lack of commonly defined nomenclature for various vocal attributes and the inability to obtain consistently high interrater reliability. Kent [35], Kreiman et al [36,37], and others have discussed the many limitations of auditory perceptual measures in detail. Even among voice therapists and vocal pedagogy teachers, there is argument about the level of ear training necessary to judge vocal quality appropriately. Despite these problems, vocal quality assessment remains a fundamental component of the clinical examination. Excessive breathiness is a hallmark of incomplete glottal closure, and the sound of the voice is almost always the symptom that causes the patient to seek medical attention. Vocal quality is typically assessed along two dimensions. The first is the severity of the abnormality, such as mild, moderate, or severe. The second is one or more descriptors of quality, with hoarseness being the most generic term. More specific terms include breathiness, which corresponds to turbulent airflow, and roughness, which generally corresponds to periodicity of mucosal wave vibration [9]. Assessment of vocal quality is best performed by the voice therapist rather than the surgeon. In general, the voice therapist’s training leads to greater sensitivity to vocal attributes (eg, ‘‘ear training’’) than that of the surgeon. Of course there are exceptions, especially in the case of the surgeon with a musical background or one who has participated extensively in an interdisciplinary team. It is preferable, although not always practical, to use an independent panel of listeners to decrease potential bias of those involved in treatment of the patient. In all cases, however, consistent use of some type of standardized scaling should be used. Perhaps the most commonly used scale is the GRBAS, developed by the Committee for Phonatory Function of the Japanese Society of Logopedics and Phoniatrics [38,39]. ‘‘G’’ represents grade and indicates the overall vocal quality. ‘‘R,’’ ‘‘B,’’ ‘‘A,’’ and S stand for roughness, breathiness, asthenia (weakness), and strain, respectively. Each dimension is rated from 0 to 3: 0 represents no deficit, and 1 through 3 represent mild, moderate, and severe deficits, respectively. Recently, the American Speech-Language-Hearing Association Special Interest Division 3, Voice and Voice Disorders, created the Consensus

92

A. Behrman / Otolaryngol Clin N Am 37 (2004) 75–104

Auditory-Perceptual Evaluation–Voice (CAPE-V) [40]. Overall severity, roughness, breathiness, strain, pitch, and loudness are each rated using 100-mm visual analog scales, with the option for additional user-defined parameters. The consensus committee that developed the scales recommends that judgments be based on two sustained vowels, six standard sentences, and at least 20 seconds of spontaneous speech. The rating form and instructions are available to members of the American Speech-Language-Hearing Association at their web site in a PDF file. Although both the GRBAS and the CAPE-V scales provide conversion into numeric values, it should be remembered that the numbers represent subjective judgment. Approximately half of the articles reviewed include clinical assessment of vocal quality among their outcome measures. Approximately 50% of those studies using vocal quality judgments did so with some type of formal scaling or blinded panel of evaluators. The remainder obtained the data from chart review, or in other cases, the methodology was not specified. Morsomme et al [41] used the GRBAS scale to conduct comparative assessment of vocal quality in 28 patients with unilateral vocal fold paralysis and 12 controls. They found that grade, breathiness, and asthenia were the most sensitive parameters to paralytic dysphonia rather than roughness or strain. Billante et al [32] noted that clinical assessment of vocal quality, together with acoustic measures, continued to improve for up to 1 year after surgical medialization. Other studies [42–44] found that vocal quality improved after intervention but that not all patients achieved ‘‘normal’’-sounding voice. Inagi et al [45] noted that a number of factors influenced rating of vocal quality in these patients, including degree of vocal fold bowing, use of compensatory vocal behaviors, and vertical level of the vocal folds. In summary, despite the difficulties inherent in measuring vocal quality, these judgments should be included in assessment of treatment outcomes. The purpose of the treatment in most cases (excluding airway protection in cases of significant dysphagia), after all, is to improve symptoms of dysphonia. In most clinical discussions of patients with unilateral vocal fold paralysis, the common question arises, ‘‘How did the patient sound?’’ Use of a standardized scale, such as the GRBAS or CAPE-V, is strongly recommended to help move the field toward a common and consistent language, as far as possible, for analysis of outcomes across different patients and treatment facilities. Patient self-assessment measures Patient self-assessment measures provide outcome data from the patient’s perspective, particularly quality-of-life changes caused by the dysphonia. As with many health-related problems, patients with similar laryngeal dysfunction can perceive the resulting severity of dysphonia dissimilarly, experiencing a range of handicaps. Individuals have a broad spectrum of requirements and expectations of their voices that are not always directly correlated to

A. Behrman / Otolaryngol Clin N Am 37 (2004) 75–104

93

occupational vocal demands, age, gender, or other demographic lifestyle or health factors. For the purpose of outcomes data collection, it is insufficient to obtain patient self-assessment information from chart notes made after questioning the patient during a routine clinical visit. Significant bias is introduced in the verbal exchange and the subsequent written documentation. Ideally, a written assessment should be obtained from each patient in a consistent and standardized manner before discussion of patient history and current complaints. General quality-of-life surveys, such as the Medical Outcome Study Short Form 36-Item Health Survey (SF-36) [46], are not sufficiently sensitive to voice problems. In response to this need for a dysphonia-specific quality-of-life instrument, a number of questionnaires have been developed recently, among them the Voice Handicap Index (VHI) [47,48], Voice-Related Quality of Life (V-RQOL) [49], and Voice Outcome Survey (VOS) [50] as well as the less well-known Voice Activity and Participation Profile (VAAP) [51], Patient Questionnaire of Vocal Performance [52], and Voice Symptom Scale [53]. The complete surveys as well as details of their statistical development are described in the references cited. Additionally, Hogikyan and Rosen [54], in a project of the American Academy of Otolaryngology–Head and Neck Surgery, provide an excellent comparative review of the VHI, V-RQOL, and VOS scales. As an alternative to these scales, one or more visual analog or Likert scales can be devised to elicit patient perception. The advantage of using ‘‘off-the-shelf ’’ surveys, such as those listed previously, rather than creating a unique scale is that typically, previously published scales have already undergone statistical validity and reliability analyses. Furthermore, such scales are more likely to be used by other centers, providing easier comparison and meta-analyses. Patient perception scales are not meant to provide a numeric criterion level demarcating ‘‘normal’’ from ‘‘abnormal’’ voice. Rather, the scales are primarily within-patient measures used to clarify the patient’s concerns and to show change over time or as a result of intervention. In general, the scores of patients with untreated unilateral vocal fold paralysis tend to reveal greater perceived vocal dysfunction than dysphonia from other causes and other types of dysphonia [55]. Selection of which scale to use is largely a matter of individual preference, with each one having its own strengths and weaknesses. The VHI and V-RQOL are among the more commonly used scales and are appropriate across a variety of laryngeal disorders, including vocal fold immobility. Although the VOS was developed specifically for patients with unilateral vocal fold paralysis, it is a five-item scale and thus somewhat limited in the information it obtains. Curiously, it elicits no information about perception of breathlessness, a common vocal complaint of patients with unilateral vocal fold paralysis. In contrast, the VHI and V-RQOL include such information. Any of these written scales can be offered to patients when they register for the clinical visit, and all can be completed and scored quickly.

94

A. Behrman / Otolaryngol Clin N Am 37 (2004) 75–104

Approximately 25% of the articles contained in Table 1 include patient perception in the measurement of treatment outcome, but only approximately half of those studies use some form of standardized written scale of the patient’s perception of dysphonia, with the remainder obtaining data from chart review or omitting description of methodology. Pearl et al [56] found that VHI scores significantly improved in 14 patients after medialization with micronized acellular dermis. Rosen et al [55] also assessed 14 patients with unilateral vocal fold immobility, most of whom were treated surgically and some with adjuvant voice therapy. The authors found that this group had the highest pretreatment VHI scores when compared with groups of patients with muscle tension dysphonia or benign mucosal lesions, and the immobility group also had the greatest average numeric change after treatment. Glicklich et al [50] developed the VOS to assess 56 patients before and after medialization laryngoplasty and found the VOS to be a more sensitive measure than acoustic data or the SF-36. Spector et al [57] used the VHI and VOS in the assessment of 45 patients before and after medialization laryngoplasty and found both to be sensitive measures of change. Perie et al [31] developed a survey of approximately 50 questions in French as part of their outcomes measurement in 18 patients who underwent medialization laryngoplasty. Results showed that patients perceived improvement in breath control and phonation after surgery, although not to the levels of normal subjects. Hogikyan et al [58] used the V-RQOL to compare a group of patients before and after medialization laryngoplasty and to compare treatment results with an untreated cohort. The authors found that the treated patients perceived less impairment than the untreated group but still perceived a voice problem when compared with controls. Similar results were presented by Gray et al [42] in a study that antedated the development of the current patient-oriented surveys. The authors used their own scale of patient satisfaction to assess outcome of medialization laryngoplasty in 15 patients and found that the surgical procedure improved voice but that the patients continued to perceive a deficit after surgery when compared with controls. McCulloch et al [43] used their own seven-point scale of patient satisfaction to assess 72 patients medialized with GoreTex and arytenoid adduction. The scale was consistent with the authors’ acoustic and clinical assessment of vocal quality in that the two procedures together seemed to provide better outcome than medialization alone. In the only RCT trial, Hertegard et al [44] included 35 patients with unilateral vocal fold paralysis in a clinical trial assessing cross-linked hyaluronan derivative with bovine collagen. Visual analog scales of patient satisfaction revealed similar improvement after surgery in both treatment groups. In summary, patient perception of dysphonia provides important and unique treatment outcome data, easily obtained using any one of a number of scales. The studies reviewed here suggest that, overall, most patients perceive significant improvement in vocal function after a variety of surgical

A. Behrman / Otolaryngol Clin N Am 37 (2004) 75–104

95

treatments of unilateral vocal fold paralysis, although not to a level comparable to individuals with normal vocal fold movement. Identifying the primary outcome measure Unfortunately, it is a reality of clinical practice that the data from the various measures of outcome are not always consistent. The patient may report greater impairment of voice than the clinical examination findings would suggest. Alternatively, phonatory glottal closure may appear better than would be predicted from the voice quality. Some specific potential causes of such inconsistencies have been addressed in this discussion, including the inherent limitations of videoendoscopy and stroboscopy and the lack of clear correlations between patient perception, clinical assessment of vocal quality, and physiologic measurement. In sum, inconsistencies in outcomes data occur because the various measures describe parameters of vocal function that have inherent differences. Such inconsistencies confound the determination of outcome and the measurement of treatment efficacy. It is useful to establish a primary measure of treatment outcome. This does not at all imply that the other outcomes measures are ignored. The secondary measures are analyzed with the same statistical rigor as the primary measure, and the results are an important part of the discussion to explain the outcomes and to determine the ability to generalize findings to other patient samples. The primary outcome measure, however, enables one to identify the overall success or failure of the treatment. Without this, the clinical utility of an outcomes or efficacy study is lessened considerably. In the opinion of this author, the patient’s perception of the dysphonia is the strongest primary outcome measure. In the absence of dysphagia, the purpose of treatment for unilateral vocal fold paralysis is to address the symptom(s) that bother the patient, whether they relate to vocal quality, the inability to produce a loud voice, relief from the sense of breathlessness, or other problems. Murry and Rosen [59] and Benninger et al [3] provide indepth discussions of quality-of-life assessment in medicine and otolaryngology in general and specifically in the treatment of benign voice disorders. The point is well made that treatment addresses the medical disease, whereas outcome addresses the physical, mental, and social well-being of a patient. Unfortunately, the fact remains that the relation between patient perception and physiologic measures is complex and poorly understood. Even intensity, an important outcome measure that is more closely related to patient complaint and phonatory glottal gap than other acoustic measures, can only explain one facet of the patient’s perception of communicative ease. Patient perception does not explain the underlying pathophysiology of the dysphonia; hence the purpose of physiologic measures of outcome and continued basic science research. Intervention is a quality-of-life issue, however, which, in the end, can only be judged by the patient. Although patient perception is an individual phenomenon, using such data as the

96

A. Behrman / Otolaryngol Clin N Am 37 (2004) 75–104

primary measure of treatment outcome may help to inform treatment of future patients. Future challenges Significant gaps are evident from the review of the literature included in Table 1. The lack of RCTs in the treatment of the dysphonia caused by vocal fold paralysis is of considerable concern. RCTs are the gold standard of clinical research, in which there are one or more treatment groups and a no treatment or standard treatment control group. Patients are randomly assigned and followed equivalently for a specified period. These are among the most difficult, expensive, and complex types of research to perform, but they are the most resistant to bias and confounding factors and therefore provide excellent evidence for guiding clinical practice. Practical and ethical considerations prohibit the use of RCTs for all clinical questions. Nevertheless, the data from RCTs, unlike other research designs, have the potential to cause fundamental paradigm shifts in treatment. The lack of RCTs is evidence of the difficulty of clinical trials. Fung and Lore´ [60] present a helpful discussion of variations of the ‘‘classic’’ RCT, which, although not completely overcoming all these difficulties, presents some solutions that help to make this type of study more realistic to perform. There is only one RCT included in Table 1, the study by Hertegard et al [44] comparing hylan B gel with bovine collagen in injection augmentation. Although improvement was obtained with both materials, at 12 months after injection, vibratory function was maintained better in the group of patients receiving hylan B. Additional data from RCTs are clearly needed, especially data comparing different surgical procedures, such as medialization laryngoplasty and injection augmentation, for example. A number of studies assess outcome a year or more after treatment, but the data are sufficiently variable so as to warrant additional longitudinal research. Billante et al [32] found continued improvement up to 1 year after injection augmentation in 40 patients; however, Lundy et al [61] found no significant changes between 1 month and 1 year after medialization laryngoplasty in 26 patients. Ford and Bless [62], in a study of 54 patients receiving injectable collagen, found that vocal function tended to stabilize by 3 months, although a slight decrement in function over 1 year was noted. Remacle et al [63] found variable long-term outcomes in 53 patients assessed an average of 4.5 years after collagen injection. Similarly, the literature on long-term follow-up of reinnervation procedures suggests stable outcome for most but not all patients beyond 1 year [64–67]. Another gap in knowledge, particularly concerning to this author, are the minimal outcomes and efficacy data regarding voice therapy intervention for unilateral vocal fold paralysis. Kelchner et al [68] conducted a retrospective review of 25 patients who had voice therapy (n = 6), a surgical procedure (n = 13), or combined therapy and surgery (n = 5). Stroboscopic

A. Behrman / Otolaryngol Clin N Am 37 (2004) 75–104

97

examination and perceptual assessment of voice revealed comparable outcomes, although there were significant group differences before treatment in that the patients referred for voice therapy had less severe laryngeal dysfunction than those referred for surgery. Given the group differences, the finding that surgery provides greater posttreatment change is not surprising. Obviously, comparative efficacy can only be assessed with randomized assignment of patients to treatment arm so as to remove the significant confounding factor of selection bias. Xu et al [69] found voice therapy effective in 20 patients with unilateral vocal fold paralysis, although specifics of outcome measures were not identified. Heuer et al [70] conducted a retrospective study of 41 patients with unilateral vocal fold paralysis, more than half of whom elected to participate in a course of voice therapy rather than to undergo surgical procedure. Using a variety of outcomes measures, the data showed similar satisfaction in the therapy and surgery patients. Pretreatment stroboscopic, acoustic, and aerodynamic data showed some trends of differences between groups, and one has to assume that there are some potentially significant factors driving the self-selection of patients to a specific treatment modality. Again, selection bias of the treatment groups heavily obscures the results. Further, in this study, posttreatment stroboscopic, acoustic, and aerodynamic measures were not obtained. It is unknown whether phonatory physiology was significantly changed with behavioral intervention or whether the patient’s ability to cope with the deficit was improved, with the latter being an equally important outcome of treatment. Correlation of patient satisfaction measures with physiologic data after treatment would perhaps have been helpful in revealing important group differences. The role of voice therapy as a primary treatment or as an adjunct to surgery has not been well tested. There are more questions than answers regarding the efficacy of behavioral intervention. In cases of spontaneous return of neural activity, do vocal exercises contribute to the rate or extent of recovery of function? What are the relative outcomes of surgical intervention with and without postoperative voice therapy? Do patients achieve better voice after surgery if preoperative voice therapy is incorporated into the treatment plan? Can the immobile vocal fold truly ‘‘cross the midline’’ as a result of voice therapy exercises, or is that a spontaneous laryngeal adjustment? In cases where voice therapy yields improved voice, is it a result of increased phonatory glottal closure or improved compensatory techniques, such as vocal tract formant tuning? Voice therapy is generally believed to be beneficial [71], and most voice therapists (this author among them) consider voice therapy an effective primary treatment for unilateral vocal fold paralysis in some patients and strongly advisable to maximize postoperative gains, yet few data exist to support this or any other position on the utility of voice therapy. In summary, a substantial amount of information on treatment outcomes for unilateral vocal fold paralysis is available, but significant and clinically relevant questions remain unanswered. The studies included in Table 1

98

A. Behrman / Otolaryngol Clin N Am 37 (2004) 75–104

reveal that pre- and postoperative assessments of a single treatment modality are the most common, likely because of the ease with which they can be accomplished. Comparative assessment of different modalities of intervention, surgical techniques, and voice therapy approaches would most certainly provide the strongest contribution to guide clinical treatment, however. References [1] Dejonckere PH. Perceptual and laboratory assessment of dysphonia. Otol Clin North Am 2000;33:731–50. [2] Hirano M. Objective evaluation of the human voice: clinical aspects. Folia Phoniatr (Basel) 1989;41:89–144. [3] Benninger MS, Gardner GM, Jacobson BH, Grywalski C. New dimensions in measuring voice treatment outcomes. In: Sataloff RT, editor. Professional voice: the science and art of clinical care. 2nd edition. San Diego: Singular Publishing; 1997. p. 789–94. [4] Eskanazi L, Childers DG, Hicks DM. Acoustic correlates of vocal quality. J Speech Hear Res 1990;33:298–306. [5] Hammarberg B, Fritzell B, Gauffin J, et al. Perceptual and acoustic correlates of abnormal voice qualities. Acta Otolaryngol (Stockh) 1980;90:441–51. [6] Klich R. Relationship of vowel characteristics to listener ratings of breathiness. J Speech Hear Res 1982;25:574–80. [7] Ludlow CL, Bassich C, Connor NP, et al. The validity of using phonatory jitter and shimmer to detect laryngeal pathology. In: Bear T, Sasaki C, Harris K, editors. Laryngeal function in phonation and respiration. Boston: College-Hill Press; 1987. p. 292–308. [8] Baken RJ, Orlikoff Robert F. Clinical measurement of speech and voice. 2nd edition. San Diego: Singular Thomson Learning; 2000. [9] Titze Ingo R. Principles of voice production. Englewood Cliffs, NJ: Prentice Hall; 1994. [10] Hirano M. Clinical examination of voice. Vienna: Springer-Verlag; 1981. [11] Hong KH, Jung KS. Arytenoid appearance and vertical level difference between the paralyzed and innervated vocal cords. Laryngoscope 2001;111(2):227–32. [12] Woo P. Quantification of videostroboscopic findings—measurements of the normal glottal cycle. Laryngoscope 1996;106(Suppl 79):1–20. [13] Harries ML, Morrison M. The role of stroboscopy in the management of a patient with unilateral vocal fold paralysis. J Laryngol Otol 1996;110(2):141–3. [14] Sercarz JA, Berke GS, Ming Y, Gerratt BR, Natividad M. Videostroboscopy of human vocal fold paralysis. Ann Otol Rhinol Laryngol 1992;101(7):567–77. [15] Titze IR. Workshop on acoustic voice analysis: summary statement. National Center for Voice and Speech, Iowa City, IA: The University of Iowa, 1995. [16] Plant RL, Hillel AD, Waugh PF. Analysis of voice changes after thyroplasty using linear predictive coding. Laryngoscope 1997;107(6):703–9. [17] Kent RD, Kent J, Rosenbek J. Maximum performance tests of speech production. J Speech Hear Res 1987;52:367–87. [18] Titze IR. Acoustic interpretation of the voice range profile (phonetogram). J Speech Hear Res 1992;35(1):21–34. [19] Sulter AM, Wit HP, Schutte HK, et al. A structured approach to voice range profile (phonetogram) analysis. J Speech Hear Res 1994;37(5):1076–85. [20] Behrman A, Agresti CJ, Blumstein E, et al. Meaningful features of voice range profiles from patients with organic vocal fold pathology: a preliminary study. J Voice 1996;10(3): 269–83. [21] Kent RD. Reference manual for communicative sciences and disorders. Austin: Pro-Ed; 1994. p 121.

A. Behrman / Otolaryngol Clin N Am 37 (2004) 75–104

99

[22] Solomon NP, Garlitz SJ, Milbrath RL. Respiratory and laryngeal contributions to maximum phonation time. J Voice 2000;14(3):331–40. [23] Hirano M, Mori K, Tanaka S, Fujita M. Vocal function in patients with unilateral vocal fold paralysis before and after silicone injection. Acta Otolaryngol (Stockh) 1995;115: 553–9. [24] Isshiki N. Regulatory mechanisms of voice intensity variation. J Speech Hear Res 1964;7: 17–29. [25] Berke GS, Hanson DG, Gerratt BR. The effect of air flow and medial adductory compression on vocal efficiency and glottal vibration. Otolaryngol Head Neck Surg 1990; 102:212–8. [26] Scherer RC, Rubin JS. Laryngeal physiology: normal and disordered. In: Benninger M, editor. Benign disorders of the voice. Alexandria: American Academy of Otolaryngology– Head and Neck Surgery Foundation; 2002. p. 29–44. [27] Leder SB, Sasaki CT. Long-term changes in vocal quality following Isshiki thyroplasty type I. Laryngoscope 1994;104:275–7. [28] Sasaki CT, Leder SB, Petcu L, Friedman CD. Longitudinal voice quality changes following Isshiki thyroplasty type I: the Yale experience. Laryngoscope 1990;100:849–52. [29] McClean-Muse A, Montgomery WW, Hillman RE, Varvares M, Bunting G, Doyle P, et al. Montgomery thyroplasty implant for vocal fold immobility: phonatory outcomes. Ann Otol Rhinol Laryngol 2000;109(4):393–400. [30] Brandenburg JH, Kirkham W, Koschkee D. Vocal cord augmentation with autogenous fat. Laryngoscope 1992;102(5):495–500. [31] Perie S, Roubeau B, Liesenfelt I, Chaigneau-Debono G, Bruel M, St Guily JL. Role of medialization in the improvement of breath control in unilateral vocal fold paralysis. Ann Otol Rhinol Laryngol 2002;111:1026–33. [32] Billante CR, Clary J, Childs P, Netterville JL. Voice gains following thyroplasty may improve over time. Clin Otolaryngol 2002;27:89–94. [33] Lu FL, Casiano RR, Lundy DS, Xue JW. Longitudinal evaluation of vocal function after thyroplasty type I in the treatment of unilateral vocal paralysis. Laryngoscope 1996;106: 573–7. [34] Hartl DM, Hans S, Vaissier J, Riquet M, Brasnu DF. Objective voice quality analysis before and after onset of unilateral vocal fold paralysis. J Voice 2001;15(3):351–61. [35] Kent RD. Hearing and believing: some limits to the auditory-perceptual assessment of speech and voice disorders. Am J Speech Lang Pathol 1995;5(3):7–23. [36] Kreiman J, Gerratt BR, Berke GS. The multidimensional nature of pathologic vocal quality. J Acoust Soc Am 1994;96:1291–313. [37] Kreiman J, Gerratt BR, Precoda K. Listener experience and perception of vocal quality. J Speech Hear Res 1990;33:103–15. [38] Imaizumi S. Acoustic measure of roughness in pathological voice. J Phonetics 1986;14: 457–62. [39] Wendler J, Rauhut A, Kruger H. Classification of voice qualities. J Phonetics 1986;14: 483–8. [40] American Speech-Language-Hearing Association Special Interest Division 3, Voice and Voice Disorders. Consensus auditory-perceptual evaluation of voice (CAPE-V). 2003. Available at: http://www.asha.org. [41] Morsomme D, Jamart J, Wery C, Giovanni A, Remacle M. Comparison between the GIRBAS Scale and the acoustic and aerodynamic measures provided by EVA for the assessment of dysphonia following unilateral vocal fold paralysis. Folia Phoniatr Logop 2001;53(6):317–25. [42] Gray SD, Barkmeier J, Jones D, Titze I, Druker D. Vocal evaluation of thyroplastic surgery in the treatment of unilateral vocal fold paralysis. Laryngoscope 1992;102:415–21. [43] McCulloch TM, Hoffman HT, Andrews BT, Karnell MP. Arytenoid adduction combined with Gore-Tex medialization thyroplasty. Laryngoscope 2000;110:1306–11.

100

A. Behrman / Otolaryngol Clin N Am 37 (2004) 75–104

[44] Hertegard S, Hallen L, Laurent C, Lindstrom E, Olofsson K, Testad P, Dahlqvist A. Cross-linked hyaluronan used as augmentation substance for treatment of glottal insufficiency: safety aspects and vocal fold function. Laryngoscope 2002;112:221–9. [45] Inagi K, Khidr AA, Ford CN, Bless DM, Heisey DM. Correlation between vocal functions and glottal measurements in patients with unilateral vocal fold paralysis. Laryngoscope 1997;107(6):782–91. [46] Ware JE Jr, Sherbourne CD. The MOS 36 item Short Form Health Survey (SF-36), I: conceptual framework and item selection. Med Care 1993;30:473–83. [47] Jacobson GH, Johnson A, Grywalski C, et al. The Voice Handicap Index (VHI): development and validation. Am J Speech Lang Pathol 1997;6(3):66–70. [48] Benninger MS, Ahuja AS, Gardner G, Grywalski C. Assessing outcomes for dysphonic patients. J Voice 1998;12(4):540–50. [49] Hogikyan ND, Sethuraman G. Validation of an instrument to measure voice-related quality of life (V-RQOL). J Voice 1999;13:557–69. [50] Glicklich RE, Glovsky RM, Montgomery WM. Validation of a voice outcome survey for unilateral vocal cord paralysis. Otolaryngol Head Neck Surg 1999;120:153–8. [51] Ma EP-M, Yiu EM-L. Voice activity and participation profile: assessing the impact of voice disorders on daily living. J Speech Lang Hear Res 2001;44(3):511–24. [52] Carding PN, Horsley IA, Docherty GD. Measuring the effectiveness of voice therapy in a group of forty-five patients with non-organic dysphonia. J Voice 1999;13: 76–113. [53] Deary IJ, Wilson JA, Carding PN, et al. VoiSS, a patient-derived voice symptom scale. J Psychosom Res 2003;54:483–9. [54] Hogikyan ND, Rosen CA. A review of outcome measurements for voice disorders. Otol Head Neck Surg 2002;126(5):562–72. [55] Rosen CA, Murry T, Zinn A, Zullo T, Sonbolian M. Voice handicap index change following treatment of voice disorders. J Voice 2001;14:619–23. [56] Pearl AW, Woo P, Ostrowski R, Mojica J, Mandell DL, Costantino P. A preliminary report on micronized AlloDerm injection laryngoplasty. Laryngoscope 2002;112: 990–6. [57] Spector BC, Netterville JL, Billante C, Clary J, Reinisch L, Smith TL. Quality-of-life assessment in patients with unilateral vocal cord paralysis. Otolaryngol Head Neck Surg 2001;125:176–82. [58] Hogikyan ND, Wodchis WP, Terrell JE, Bradford CR, Esclamado RM. Voice-related quality of life (V-RQOL) following type I thyroplasty for unilateral vocal fold paralysis. J Voice 2000;14:378–86. [59] Murry T, Rosen CA. Outcome measurements and quality of life in voice disorders. Otol Clin North Am 2000;33:905–16. [60] Fung EK, Lore´ JM Jr. Randomized controlled trials for evaluating surgical questions. Arch Otolaryngol Head Neck Surg 2002;128:631–4. [61] Lundy DS, Casiano RR, Xue JW, Lu FL. Thyroplasty type I: short- versus long-term results. Otolaryngol Head Neck Surg 2000;122:533–6. [62] Ford CN, Bless DM. Clinical experience with injectable collagen for vocal fold augmentation. Laryngoscope 1986;96:863–9. [63] Remacle M, Dujardin JM, Lawson G. Treatment of vocal fold immobility by glutaraldehyde-cross-linked collagen injection: long-term results. Ann Otol Rhinol Laryngol 1995;104(6):437–41. [64] Tucker HM. Long-term results of nerve-muscle pedicle reinnervation for laryngeal paralysis. Ann Otol Rhinol Laryngol 1989;98:674–6. [65] Tucker HM, Rusnov M. Laryngeal reinnervation for unilateral vocal cord paralysis: longterm results. Ann Otol Rhinol Laryngol 1981;90:457–9. [66] Crumley RL, Izdebski K. Voice quality following laryngeal reinnervation by ansa hypoglossi transfer. Laryngoscope 1986;96:611–6.

A. Behrman / Otolaryngol Clin N Am 37 (2004) 75–104

101

[67] Paniello RC. Laryngeal reinnervation with the hypoglossal nerve: II. Clinical evaluation and early patient experience. Laryngoscope 2000;110:739–48 [comment appears in Laryngoscope 2001;111:1113–4]. [68] Kelchner LN, Stemple JC, Gerdeman E, Le Borgne W, Adam S. Etiology, pathophysiology, treatment choices, and voice results for unilateral adductor vocal fold paralysis: a 3-year retrospective. J Voice 1999;13:592–601. [69] Xu JH, Ikeda Y, Komiyama S. Bio-feedback and the yawning breath pattern in voice therapy: a clinical trial. Auris Nasus Larynx 1991;18:67–77. [70] Heuer RJ, Sataloff RT, Emerich K, Rulnick R, Baroody M, Spiegel JR, et al. Unilateral recurrent laryngeal nerve paralysis: the importance of ‘‘preoperative’’ voice therapy. J Voice 1997;11:88–94. [71] Isshiki N. Mechanical and dynamic aspects of voice production as related to voice therapy and phonosurgery. J Voice 1998;12:125–37. [72] Olson DE, Goding GS, Michael DD. Acoustic and perceptual evaluation of laryngeal reinnervation by ansa cervicalis transfer. Laryngoscope 1998;108:1767–72. [73] Schneider B, Denk DM, Bigenzahn W. Acoustic assessment of the voice quality before and after medialization thyroplasty using the titanium vocal fold medialization implant (TVFMI). Otolaryngol Head Neck Surg 2003;128(6):815–22. [74] Zeitels SM, Mauri M, Dailey SH. Medialization laryngoplasty with Gore-Tex for voice restoration secondary to glottal incompetence: indications and observations. Ann Otol Rhinol Laryngol 2003;112(2):180–4. [75] Selber J, Sataloff R, Spiegel J, Heman-Ackah Y. Gore-Tex medialization thyroplasty: objective and subjective evaluation. J Voice 2003;17(1):88–95. [76] Heman-Ackah YD, Michael DD, Goding GS Jr. The relationship between cepstral peak prominence and selected parameters of dysphonia. J Voice 2002;16:20–7. [77] Billante CR, Clary J, Sullican C, Netterville JL. Voice outcome following thyroplasty in patients with longstanding vocal fold immobility. Auris Nasus Larynx 2002;29(4): 341–5. [78] Abraham MT, Bains MS, Downey RJ, Korst RJ, Kraus DH. Type I thyroplasty for acute unilateral vocal fold paralysis following intrathoracic surgery. Ann Otol Rhinol Laryngol 2002;111:667–71. [79] Dean CM, Ahmarani C, Bettez M, Heuer RJ. The adjustable laryngeal implant. J Voice 2001;15:141–50. [80] Shin JE, Nam SY, Yoo SJ, Kim SY. Analysis of voice and quantitative measurement of glottal gap after thyroplasty type I in the treatment of unilateral vocal paralysis. J Voice 2002;16:136–42. [81] Kumar VP, Reddy SR. Medialisation laryngoplasty: a new surgical frontier in the management of vocal cord paralysis. J Indian Med Assoc 2001;99:638–9. [82] Hong KH, Kim JH, Kim HK. Anterior and posterior medialization (APM) thyroplasty. Laryngoscope 2001;111:1406–12. [83] Stasney CR, Beaver ME, Rodriguez M. Minifenestration type I thyroplasty using an expanded polytetrafluoroethylene implant. J Voice 2001;15(1):151–7. [84] Maragos NE. Revision thyroplasty. Ann Otol Rhinol Laryngol 2001;110(12):1087–92. [85] Safak MA, Gocmen H, Korkmaz H, Kilic R. Computerized tomographic alignment of silastic implant in type 1 thyroplasty. Am J Otolaryngol 2000;21:179–83. [86] Hajioff D, Rattenbury H, Carrie S, Carding P, Wilson J. The effect of Isshiki type 1 thyroplasty on quality of life and vocal performance. Clin Otolaryngol 2000;25(5): 418–22. [87] Nasseri SS, Maragos NE. Combination thyroplasty and the ‘‘twisted larynx:’’ combined type IV and type I thyroplasty for superior laryngeal nerve weakness. J Voice 2000;14(1): 104–11. [88] Abdel-Aziz MF, el-Hak NA, Carding PN. Thyroplasty for functional rehabilitation of the incompetent larynx. J Laryngol Otol 1998;112(12):1172–5.

102

A. Behrman / Otolaryngol Clin N Am 37 (2004) 75–104

[89] Montgomery WW, Montgomery SK. Montgomery thyroplasty implant system. Ann Otol Rhinol Laryngol 1997;170(Suppl):1–16. [90] Ramadan HH. Medialization laryngoplasty for the treatment of unilateral vocal cord paralysis. WV Med J 1996;92:268–70. [91] Sakai N, Nishizawa N, Matsushima J, Kurihara H, Kokubun T, Koichi K, et al. Thyroplasty type I with ceramic shim. Artif Organs 1996;20:951–4. [92] Bryant NJ, Gracco LC, Sasaki CT, Vining E. MRI evaluation of vocal fold paralysis before and after type I thyroplasty. Laryngoscope 1996;106:1386–92 [erratum appears in Laryngoscope 1997;107:148]. [93] Adams SG, Irish JC, Durkin LC, Wong DL, Brown DH. Evaluation of vocal function in unilateral vocal fold paralysis following thyroplastic surgery. J Otolaryngol 1996;25: 165–70. [94] Omori K, Slavit DH, Kacher A, Blaugrund SM. Quantitative criteria for predicting thyroplasty type I outcome. Laryngoscope 1996;106(6):689–93. [95] Harries ML, Morrison M. Short-term results of laryngeal framework surgery—thyroplasty type 1: a pilot study. J Otolaryngol 1995;24:281–7 [comment in: J Otolaryngol 1996;25(5):363]. [96] Rosingh HJ, Dikkers FG. Thyroplasty to improve the voice in patients with a unilateral vocal fold paralysis. Clin Otolaryngol 1995;20:124–6. [97] Thompson DM, Maragos NE, Edwards BW. The study of vocal fold vibratory patterns before and after type I thyroplasty. Laryngoscope 1995;105:481–6 [erratum appears in Laryngoscope 1995;105:1148]. [98] Slavit DH, Maragos NE. Arytenoid adduction and type I thyroplasty in the treatment of aphonia. J Voice 1994;8:84–91. [99] Mori K, Blaugrund SM, Yu JD. The turbulent noise ratio: an estimation of noise power of the breathy voice using PARCOR analysis. Laryngoscope 1994;104(2):153–8. [100] LaBlance GR, Maves MD. Acoustic characteristics of post-thyroplasty patients. Otolaryngol Head Neck Surg 1992;107:558–63. [101] Koufman JA. Laryngoplasty for vocal cord medialization: an alternative to Teflon. Laryngoscope 1986;96:726–31. [102] Abraham MT, Gonen M, Kraus DH. Complications of type I thyroplasty and arytenoid adduction. Laryngoscope 2001;111:1322–9. [103] Yumoto E, Sanuki T, Hyodo M. Three-dimensional endoscopic images of vocal fold paralysis by computed tomography. Arch Otolaryngol Head Neck Surg 1999;125: 883–90. [104] Shaw GY, Searl JP. Electroglottographic and acoustic changes following type I thyroplasty or autologous fat injection. Ann Otol Rhinol Laryngol 2001;110(11):1000–6. [105] Kraus DH, Orlikoff RF, Rizk SS, Rosenberg DB. Arytenoid adduction as an adjunct to type I thyroplasty for unilateral vocal cord paralysis. Head Neck 1999;21:52–9. [106] Bielamowicz S, Berke GS, Gerratt BR. A comparison of type I thyroplasty and arytenoid adduction. J Voice 1995;9(4):146–72. [107] Dulguerov P, Schweizer V, Caumel I, Esteve F. Medialization laryngoplasty. Otolaryngol Head Neck Surg 1999;120:275–8. [108] Tsuzuki T, Fukuda H, Fujioka T, Takayama E, Kawaida M. Voice prognosis after liquid and solid silicone injection. Am J Otolaryngol 1991;12:165–9. [109] Laccourreye O, Papon JF, Kania R, Crevier-Buchman L, Brasnu D, Hans S. Intracordal injection of autologous fat in patients with unilateral laryngeal nerve paralysis: long-term results from the patient’s perspective. Laryngoscope 2003;113(3):541–5. [110] Hoffman H, McCabe D, McCulloch T, Jin SM, Karnell M. Laryngeal collagen injection as an adjunct to medialization laryngoplasty. Laryngoscope 2002;112:1407–13. [111] McCulloch TM, Andrews BT, Hoffman HT, Graham SM, Karnell MP, Minnick C. Long-term follow-up of fat injection laryngoplasty for unilateral vocal cord paralysis. Laryngoscope 2002;112:1235–8.

A. Behrman / Otolaryngol Clin N Am 37 (2004) 75–104

103

[112] Reijonen P, Lehikoinen-Soderlund S, Rihkanen H. Results of fascial augmentation in unilateral vocal fold paralysis. Ann Otol Rhinol Laryngol 2002;111:523–9. [113] Hallen L, Testad P, Sederholm E, Dahlqvist A, Laurent C. DiHA (dextranomers in hyaluronan) injections for treatment of insufficient closure of the vocal folds: early clinical experiences. Laryngoscope 2001;111:1063–7. [114] Hsiung MW, Woo P, Minasian A, Schaefer Mojica J. Fat augmentation for glottis insufficiency. Laryngoscope 2000;110(6):1026–33. [115] Saarinen A, Rihkanen H, Lehikoinen-Soderlund S, Sovijarvi AR. Airway flow dynamics and voice acoustics after autologous fascia augmentation of paralyzed vocal fold. Ann Otol Rhinol Laryngol 2000;109:563–7. [116] Sagawa M, Sato M, Fujimura S, et al. Vocal fold injection of collagen for unilateral vocal fold paralysis caused by chest diseases. J Cardiovasc Surg 1999;40:603–5. [117] Rihkanen H, Lehikoinen-Soderlund S, Reijonen P. Voice acoustics after autologous fascia injection for vocal fold paralysis. Laryngoscope 1999;109:1854–8. [118] Laccourreye O, Paczona R, Ageel M, Hans S, Brasnu D, Crevier-Buchman L. Intracordal autologous fat injection for aspiration after recurrent laryngeal nerve paralysis. Eur Arch Otorhinolaryngol 1999;256(9):458–61. [119] Remacle M, Lawson G, Delos M, Jamart J. Correcting vocal fold immobility by autologous collagen injection for voice rehabilitation. A short-term study. Ann Otol Rhinol Laryngol 1999;108(8):788–93. [120] Laccourreye O, Crevier-Buchman L, Le Pimpec-Barthes F, et al. Recovery of function after intracordal autologous fat injection for unilateral recurrent laryngeal nerve paralysis. J Laryngol Otol 1998;112:1082–4. [121] Harries ML, Morrison M. Management of unilateral vocal cord paralysis by injection medialization with Teflon paste. Quantitative results. Ann Otol Rhinol Laryngol 1998; 107:332–6. [122] Chu PY, Chang SY. Transoral Teflon injection under flexible laryngovideostroboscopy for unilateral vocal fold paralysis. Ann Otol Rhinol Laryngol 1997;106:783–6. [123] Iwatake H, Iida J, Minami S, Sugano S, Hoshikawa T, Takeyama I. Transcutaneous intracordal silicon injection for unilateral vocal cord paralysis. Acta Otolaryngol Suppl (Stockh) 1996;522:133–7. [124] Shindo ML, Zaretsky LS, Rice DH. Autologous fat injection for unilateral vocal fold paralysis. Ann Otol Rhinol Laryngol 1996;105:602–6. [125] Iwatake H, Iida J, Minami S, Sugano S, Hoshikawa T, Takeyama I. Transcutaneous intracordal silicon injection for unilateral vocal cord paralysis. Acta Otolaryngol Suppl (Stockh) 1996;522:133–7. [126] Varvares MA, Montgomery WW, Hillman RE. Teflon granuloma of the larynx: etiology, pathophysiology, and management. Ann Otol Rhinol Laryngol 1995;104:511–5. [127] Levine BA, Jacobs IN, Wetmore RF, Handler SD. Vocal cord injection in children with unilateral vocal cord paralysis. Arch Otolaryngol Head Neck Surg 1995;121:116–9. [128] Su CY, Lui CC, Lin HC, Chiu JF, Cheng CA. A new paramedian approach to arytenoid adduction and strap muscle transposition for vocal fold medialization. Laryngoscope 2002;112(2):342–50. [129] Mikaelian DO, Lowry LD, Sataloff RT. Lipoinjection for unilateral vocal cord paralysis. Laryngoscope 1991;101:465–8 [comment in Laryngoscope 1991;101:1385]. [130] Hirano M, Tanaka S, Tanaka Y, Hibi S. Transcutaneous intrafold injection for unilateral vocal fold paralysis: functional results. Ann Otol Rhinol Laryngol 1990;99:598–604. [131] McCaffrey TB, Lipton R. Transcutaneous Teflon injection for paralytic dysphonia. Laryngoscope 1989;99:497–9. [132] Hirano M, Hibi S, Yoshida T, Hirade Y, Kasuya H, Kikuchi Y. Acoustic analysis of pathological voice. Some results of clinical application. Acta Otolaryngol 1988;105:432–8. [133] Weber RS, Neumayer L, Alford BR, Weber SC. Clinical restoration of voice function after loss of the vagus nerve. Head Neck Surg 1985;7:448–57.

104

A. Behrman / Otolaryngol Clin N Am 37 (2004) 75–104

[134] Reich AR, Lerman JW. Teflon laryngoplasty: an acoustical and perceptual study. J Speech Hear Disord 1978;43:496–505. [135] Tucker HM. Combined surgical medialization and nerve-muscle pedicle reinnervation for unilateral vocal fold paralysis: improved functional results and prevention of long-term deterioration of voice. J Voice 1997;11:474–8. [136] Zheng H, Li Z, Zhou S, Cuan Y, Wen W. Update: laryngeal reinnervation for unilateral vocal cord paralysis with the ansa cervicalis. Laryngoscope 1996;106:1522–7. [137] Nonomura M, Kojima H, Omori K, Kanaji M, Honjo I. Anticus-lateralis muscle suturing. Treatment of recurrent nerve paralysis. Arch Otolaryngol Head Neck Surg 1993;119:343–6. [138] Crumley RL. Update: ansa cervicalis to recurrent laryngeal nerve anastomosis for unilateral laryngeal paralysis. Laryngoscope 1991;101:384–8. [139] Woo P, Pearl AW, Hsiung MW, Som P. Failed medialization laryngoplasty: management by revision surgery. Otolaryngol Head Neck Surg 2001;124(6):615–21. [140] Sato F, Saito H. Functional reconstruction for unilateral recurrent laryngeal nerve paralysis caused by thyroid cancer. Auris Nasus Larynx 1985;12(Suppl 2):S210–16. [141] Chou FF, Su CY, Jeng SF, Hsu KL, Lu KY. Neurorrhaphy of the recurrent laryngeal nerve. J Am Coll Surg 2003;197(1):52–7. [142] Chhetri DK, Gerratt BR, Kreiman J, Berke GS. Combined arytenoid adduction and laryngeal reinnervation in the treatment of vocal fold paralysis. Laryngoscope 1999;109: 1928–36. [143] Tucker HM. Long-term preservation of voice improvement following surgical medialization and reinnervation for unilateral vocal fold paralysis. J Voice 1999;13:251–6. [144] Bielamowicz S, Gupta A, Sekhar LN. Early arytenoid adduction for vagal paralysis after skull base surgery. Laryngoscope 2000;110(3 Part 1):346–51. [145] Brandenburg JH, Kirkham W, Koschkee D. Vocal cord augmentation with autogenous fat. Laryngoscope 1992;102(5):495–500. [146] Zeitels SM, Hochman I, Hillman RE. Adduction arytenopexy: a new procedure for paralytic dysphonia with implications for implant medialization. Ann Otol Rhinol Laryngol Suppl 1998;173:2–24. [147] Woodson GE, Murray T. Glottic configuration after arytenoid adduction. Laryngoscope 1994;104(8 Part 1):965–9. [148] Slavit DH, Maragos NE. Physiologic assessment of arytenoid adduction. Ann Otol Rhinol Laryngol 1992;101(4):321–7.