There are many different types of treatment that target voice restoration. Voice restoration surgery and voice rehabilitation surgery are therefore synonyms; however, the term voice rehabilitation implies restoration to a time before some untoward event or change; and restoration to normal is the goal of most vocal fold surgery. There are four types of procedures:

                      I. Endoscopic removal of neoplastic growths

                     II. Restoration of vocal fold layered-structure (mucosal vibrations)

                    III. Injection augmentation (for glottal closure problems) (gaps <1.5mm)

                    IV. Laryngoplastic phonosurgery aka thyroplasty and medialization laryngoplasty

This article will discuss all four of the types, but the first focus here will be on medialization laryngoplasty.

Voice Disorders Are Multifactorial: Reflux, Bowing/Paresis, and Sulci

MEDIALIZATION LARYNGOPLASTY FOR VOCAL FOLD BOWING (PARESIS &ATROPHY)

In the 1980s, medialization Laryngoplasty (ML) (also known as laryngeal framework surgery, laryngoplastic phonosurgery, and Isshiki thyroplasty) was popularized as an alternative to polytef (Teflon) vocal fold injection augmentation. Initially, ML was used exclusively for the treatment of glottal insufficiency due to unilateral vocal fold paralysis; but since that time, it has become the author’s procedure of choice for the surgical rehabilitation of other glottal closure problems such as vocal fold paresis and presbylaryngis.

ML is particularly effective for correcting vocal fold bowing because placement of permanent space-occupying material such as silastic provides predictable, semi-permanent medialization, and because both sides may be done safely at the same time. Presented herein is a comprehensive and somewhat controversial paradigm for the diagnosis and management of vocal fold paresis and atrophy.

Background

The concept of vocal fold repositioning to improve (change) the voice by altering the laryngeal framework is credited to Payr (1915).¹ In the mid 20^th century, Meurman² and Sawashima³  presented variations on the theme of laryngeal cartilage repositioning; however, it was Isshiki who in 1974 first reported thyroplasty  as an effective voice rehabilitation procedure for laryngeal paralysis.⁴ In 1986, Koufman reported a successful series of ML patients and suggested refinements in surgical tecnique.⁵   

Isshiki,^6-8 Lejeune,⁹ Tucker,^10,11 and Koufman¹² reported other laryngeal framework surgical applications and techniques other than medialization by compression. In 1989, Koufman first reported bilateral medialization laryngoplasty (BML) for the surgical correction of vocal fold bowing,¹³ and technical refinements have followed.^14-19  

Over the past two decades, the evolution of implant materials and shapes as well as  surgical technique has coincided with the development of diagnostics, such as laryngeal electromyography,^20-23 electroglottography,²⁴ and digital, high-definition, transnasal laryngoscopic instrumentation that allows assessment of laryngeal biomechanics.^25-31 Among the benefits of the technological explosion in laryngology are that patients with glottal closure symptoms due to vocal fold paresis now can be accurately diagnosed and that today vocal fold bowing/paresis can be surgically corrected.^13-19

It would be inappropriate and irresponsible to offer the reader surgical techniques (of unilateral and bilateral ML) without first providing a brief overview of the diagnostic methodology and surgical patient (and procedure) selection criteria. New clinical data are presented in this article that suggest specific diagnostic and management strategies; nevertheless, the author’s paradigm continues to evolve.

Voice Disorders Are Usually Multifactorial

The author recently reviewed the medical records of 80 unselected, consecutive of patients with laryngeal and voice disorders.³² Not surprisingly, this represented a tertiary referral population and not a representative sample of the community at large. (This was evidenced, for example, by having four subjects with subglottic stenosis, three with cricoid chondrosarcoma, and two with laryngeal amyloid in the study group.) There were 31 males and 49 females with a mean age 56 years.

By clinical and/or pH-monitoring criteria 71% (57/80) of the study group had laryngopharyngeal reflux (LPR). Of those, it was the primary diagnosis in 29% (23/80) and a secondary diagnosis in 42% (34/80).

Excluding mild, asymptomatic presbylaryngis, 55% (44/80) of the study group had neuromuscular disease, including 7 patients with spasmodic dysphonia, 6 with vocal fold paralysis, and 26 with vocal fold paresis.³² It was the primary diagnosis in 29% (23/80) and a secondary diagnosis in 26% (21/80),

Fifty percent (40/80) of the study group had histopathologic lesions including nodules, polyps, cysts, pseudocysts, papillomas, granulomas, dysplasia and carcinoma. Some of the lesions were incidental, e.g., small granulomas. Eighty-eight percent (70/80) of the study population had hyperkinetic biomechanics on transnasal flexible laryngoscopy (TFL).³²

Most of the patients had multifactorial voice disorders. The data indicate that the average patient had 2.7 diagnoses (i.e., inflammation, neuromuscular disease, neoplasm, muscle tension dysphonia); see Table 1.  In some cases, paresis, reflux, or a vocal fold lesion were the primary diagnosis, and in others, they were secondary diagnoses.

Table 1: Voice Disorders are Multifactorial (N = 200)

                        Inflammatory disease    (e.g., reflux and respiratory infections)         75%    

            Neuromuscular disease (e.g., paralysis, paresis, SD, tremor)            55%

                        Neoplastic growths (e.g., polyps, nodules, papillomas, cysts)           50%

                        Hyperkinetic biomechanics (e.g., abnormal laryngeal tension)           88%

                        Total                                                                                             268%*

* Thus, the average voice disorder patient has 2.7 underlying problems

Twenty-eight percent (22/80) of the subjects had glottal closure symptoms that were associated with a precipitating event; 15 had a clear history of upper respiratory infection (URI) immediately preceding or coterminous with the onset of symptoms, and another seven could date the onset to the time of endotracheal intubation or head, neck, or thyroid surgery.  None of the 80 patients was felt to have a primary behavioral voice disorder.

Vocal Decompensation

Many voice disorder patients compensate for as long as possible before presenting to a physician. Decompensation occurs when compensatory behaviors are no longer effective, and then symptoms dramatically worsen. The theoretical and practical concepts behind the multifactorial model are summarized in Table 2. The model implies that there is a period of successful compensation before collapse, but of course there are instances in which a single event can precipitate decompensation without a period of adjustment; some problems render compensatory laryngeal behavior ineffective.

Table 2: The Laws of Decompensation

                            1st Axiom: Before: The composition of a system is in dynamic balance

                1st Corollary: Conflicting elements are held together by function and purpose

                2nd Axiom: Decompensation is preceded by often ignored warning signs

                2nd Corollary: During early destabilization, imbalance is assessable

                3rd Axiom: Last straw principle: When threshold is exceeded, collapse occurs

                3rd Corollary: Recovery requires stabilization and repair of all essential elements

Most patients with voice disorders have neuromuscular and/or inflammatory diseases. Vocal fold bowing (paresis and/or atrophy) and reflux disease may have adversely synergistic consequences for the voice.²³ Either or both may follow an upper respiratory infection (URI).³³

The decompensation model helps explain why some patients complain of intermittent and recurrent “laryngitis.” The most common clinical situation is that the patient, who has long-standing vocal fold bowing/paresis, may be able to effectively compensate until the variable of inflammation (vocal fold swelling and stiffness due to URI or LPR is added. Decompensation may parallel exacerbations LPR.

Within the context of the “premorbid condition,” in the author’s experience, the most common precipitants of vocal decompensation are: (1) upper respiratory infection, (2) endotracheal intubation, (3) head and neck surgery, (4) change of occupation, (5) worsening of LPR, and (6) allergy. Such may tip the compensatory balance by altering inflammation, edema, neuromuscular function, and/or laryngeal biomechanics. 

Change of occupation is a key variable that sometimes leads to decompensation because of increased vocal demands. In the case of some performers, their problem is their own success. For example, singers who increase their performance schedule or go on tour can decompensate as a result of too many performances per week or simply due to fatigue.

Glottal Closure Problems and the Development of Striking-Zone Pathology

Many patients with voice disorders have glottal closure symptoms such as vocal fatigue, effortful phonation, and odyophonia (painful speaking) (Table 3A). Glottal closure problems are common and the differential diagnosis is shown in Table 3B. Many striking-zone lesions (e.g., nodules, hemorrhagic polyps) are the result of effortful closure with or without LPR. The paresis podule, for example, is a striking-zone lesion that develops due to effortful closure in association with vocal fold paresis.³⁵ The term “podule” is derived from its having a similar location to that of a nodule, but the appearance of a pod (pseudocyst).³⁵

In 2002, the author reviewed the medical records of 20 consecutive patients with mid-striking-zone pathology.³⁴ All had laryngeal electromyography and pH testing performed as part of their evaluations. Eighty-five percent (17/20) had vocal fold paresis, 75% (15/20) had LPR, and 65% (13/20) had both.³⁴ None of the 20 was felt to have a primary behavioral voice disorder; although many responded to voice therapy.³⁴  

Under normal circumstances, the vocal folds are strong and resilient, but when effort (particularly the use of extra-laryngeal muscles) is needed to achieve vocal fold closure, striking zone trauma due to increased sheering forces may occur. The traditional presupposition that vocal nodules are the result of vocal misuse or abuse is not being wholly rejected, rather the tissue-trauma-damage model needs to be expanded. Glottal closure problems are frequently associated with the development of secondary vocal fold pathology (Table 3C).

Table 3: Glottal Closure Problems: Symptoms, Differential Diagnosis,

Secondary pathology, and Evaluation Methods

                                                 A. Symptoms

                                          Breathy dysphonia

                                          Air wasting

                                          Shortness of breath

                                          Effortful speaking

                                          Vocal fatigue

                                          Diplophonia

                                          Odynophonia

                                                B. Differential Diagnosis

                                         Unilateral (and sometimes bilateral) vocal fold paralysis

                                         Unilateral or bilateral vocal fold paresis

                                         Presbylaryngis and other causes of atrophy

                                         Neurological diseases (e.g., Parkinsonism)

                                         Deficient soft tissue and scarring*

                                         Mass lesions, e.g., granulomas*

                                                C. Secondary Vocal Fold Pathology

                                                     Nodules

                                                     Hemorrhages

                                         Hemorrhagic polyps

                                                     Cysts and pseudocysts

                                                     Vocal process (arytenoids) granulomas

                                                     Sulcus vergeture

                                                D. Evaluation Methods

                                         Symptoms (The Glottal Closure Index)

                                         Transnasal endoscopic videostroboscopy

                                         Acoustical analysis (e.g., electroglottography)

                                         Laryngeal electromyography

* Specifically not addressed in this article are masses and soft tissue deficiency

problems caused by phonotrauma or other forms of laryngeal scarring.

Rethinking Behavioral (“Functional”) Voice Disorders

How many people do you see out there limping because it is fun to limp or because they’re too stupid to walk right? Is that not a metaphor for behavioral voice disorders?  Voice therapy can apply in the presence or absence of vocal fold pathology; however, do we really need to learn how to speak unless there is a problem such as LPR and/or paresis? Vocal fold paresis is the single most commonly occurring glottal closure problem, and it may be occult, that is, so subtle so that a positive diagnosis may require specialized testing (Table 3D).

Patients with plica ventricularis (false vocal fold speech), for example, may fail in voice therapy as the false fold phonation may be the only alternative to aphonia in cases with severe true vocal fold paresis. Again, it should be reiterated that laryngeal biomechanics must be assessed by the transnasal route.

Voice therapy as an important diagnostic and therapeutic component of voice patient care; however, responsiveness to therapy (“noncompliance”) may occur because the underlying glottal closure problem is severe. Most patients comply with voice therapy for a while, but if the severity of the glottal closure problem (gap > 1.5 mm) outweighs the effort-benefit reward of continuing behavioral therapy, the patient will usually drop out. Nevertheless, the role of voice therapy in patients with glottal closure problems cannot be devalued, because it teaches the patient to be as efficient as possible with what they’ve got. The presumption is that patients come in loaded, is that it is synonymous with compensated.  Voice therapy helps extinguish sometimes maladaptive compensatory laryngeal behaviors and replace them with more efficient ones. Furthermore, such therapeutic manipulation is intrinsically useful as a diagnostic maneuver, the goal of which is to provide unloading, revealing the uncompensated glottal condition.

Inevitably, relatively few patients with glottal closure problems need surgery. In the author’s practice, only about 10% of vocal fold paresis patients will ever have some type of glottal closure procedure. Furthermore, most of those patients will have an endoscopic injection augmentation using fat, fascia, or an alloplastic substance.^40-42 

Diagnosis and Surgical Patient Selection Criteria

Patients with glottal closure problems usually have vocal fold paresis. It is interesting to note that most elderly patients with vocal fold atrophy (presbylaryngis) alone do not seek medical attention. Although closure may look poor in this group, they seldom complain of their voices. Usually, it is the combination of paresis and presbylaryngis that causes most older patients to seek medical attention for their voices.

History and Symptoms

Patients with glottal closure problems have characteristic symptoms (Table 3A). A simple clinical index to quantify glottal closure symptoms, the as glottal closure index (GCI) also known as the glottal function index has proved to be a useful adjunct to the routine clinical history.^18,36 (Table 4). The GCI subjectively measures effortful phonation, vocal fatigue, breathy dysphonia, and odynophonia on a four-point scale; and clinically, a score of ten or more us usually indicates a glottal closure problem.³⁶  Actually, the author has had every patient for every visit complete both the GCI and the reflux symptom index³⁷ for two decades; these indices are invaluable in quantifying symptoms before, during, and after treatment.¹⁵ The GCI is a validated outcomes instrument.

Patients with bona fide glottal closure problems such as paresis have a constellation of symptoms and findings that are consistent with their diagnosis. The diagnostic testing is virtually always congruent with the history and the symptoms. An important element of the medical history taking is to identify the pattern and the nature of the symptom onset. The history may give the most likely diagnosis. A significant proportion of paresis patients will tell you when it happened if you ask. Paresis may result from a post-viral vagal neuropathy (analogous to Bell’s palsy of the larynx)³³ or to an iatrogenic cause, e.g., carotid endarterectomy, thyroidectomy or endotracheal intubations.²³

Laryngoscopy: Assessment of Laryngeal Biomechanics

Patients with glottal closure problems experience glottal closure symptoms because in most cases they have bowed vocal folds that do not contact well without effort. Bowing is associated with hyperkinetic laryngeal behaviors, the most common of which appear to be side-to-side compression of the false vocal folds (whether or not they touch) and partial antero-posterior contraction (vocal fold foreshortening).^26-30

Four laryngeal postures or muscle tension patterns (MTPs) have been previously described.^28-30 Supraglottic contraction (MTP II and III) are characteristic. If secondary vocal fold pathology can result from glottal closure problems, and if glottal closure problems are common, then hyperkinetic biomechanics are frequently compensatory. Therefore, although voice therapy is useful in helping the patient extinguish maladaptive compensatory patterns, by itself, it cannot correct the underlying problem. In some cases, a surgical procedure is needed to help the patient achieve relatively effortless closure.

This conceptual framework, that striking zone pathology is secondary to squeezed vocal laryngeal behavior, does not portend the demise of behavioral voice disorders; however, it suggests that voice disorder patients should be routinely evaluated for inflammatory and neuromuscular disease before assuming that vocal abuse, misuse, or overuse accounts for vocal fold pathology.  Vocal fold paresis and LPR alone and in combination are the reason that most adult voice disorder patients present to voice clinics for (diagnosis and) treatment. The next section will reveal that glottal closure problems are not necessarily difficult to diagnose with state-of-the-art testing, and that some patients can dramatically benefit from ML surgery.

The technique of laryngeal examination (videostroboscopy) is important in the clinician’s ability to assess laryngeal biomechanics. Per oral examination methods alter laryngeal biomechanics to a degree that one cannot appreciate subtle degrees of bowing, paresis, atrophy.³⁰  The findings of vocal fold paresis on transnasal flexible laryngoscopy (TFL) are: (1) unilateral vocal fold (arytenoid) hypomobility; (2) vocal fold foreshortening with or without an anteriorly displaced arytenoid; (3) unilateral or bilateral vocal fold bowing in a patient under 40 years of age; (4) laryngeal tilt and/or axial rotation on high-pitched phonation; and (5) increased amplitude on stroboscopy, “floppiness,” (suggesting decreased tone). A glottal closure index, incomplete glottal closure on electroglottography (Figure 1) and laryngeal findings of paresis on TFL are indications for laryngeal electromyography.²³

Acoustical Analysis and Electroglottography

The diagnosis of vocal fold paresis or other glottal closure problems is associated with symptoms and findings of hyperkinetic compensatory laryngeal behaviors. The underlying glottal condition (for which compensation is needed), however, is incomplete vocal fold closure. Effortful speaking and vocal fatigue symptoms are manifestations of the glottal squeeze that occurs using extra-laryngeal muscles.

Electroglottography (EGG) and photoglottography effectively approximate the open- and the closed-phase (technically contact-time) of the vocal-fold vibratory cycle. The former does it by impedance and the latter by grading light. With either method, compensatory, hyperkinetic muscle tension dysphonia patterns are associated with vocal fold over-closing (over-contact). In our laboratory using EGG, the normal closed phase is 45%± 2%.^REF

At presentation when patients are still “loaded,” the EGG may be typically be between 45% and 55%; however, with unloading -- the process of temporarily removing compensatory laryngeal behaviors to assess the underlying glottal condition – the closed-phase measurement of the EGG in bilateral vocal fold paresis will typically drop by 5% or more (range 5%-25%). If the closed phase is much below 28%; the case example in Figure 2 shows a 17% drop in the EGGs (from 50% loaded to 33% unloaded).

The EGG is the most sensitive measure of a subtle glottal closure problem; however, with moderate to severe glottal closure insufficiency, there are other useful objective measures such as abnormally high perturbation (jitter and shimmer), spectral noise, and disturbed aerodynamics (high-airflow-low-resistance or reduced-airflow-high-resistance).  

Laryngeal Electromyography (LEMG)

Clinical LEMG provides essential information about the neuromuscular status of the larynx that no other test can provide. The test is uncomfortable, but tolerable, and it takes only a few minutes. Monopolar needle electrodes are used, and the right and left cricothyoroid (CT) and thyroarytenoid (TA) muscles are routinely tested. The author has previously reported her technique;^20-23 however, it is important to point out some of the key elements of technique and interpretation, as well as the limitations and pitfalls of LEMG; see Table 5.

References

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 8. Isshiki N: Phonosurgery‹Theory and Practice. Tokyo, Springer-Verlag, 1989

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10. Tucker HM: Anterior commissure laryngoplasty for adjustment of vocal fold tension. Ann Otol Rhinol Laryngol 1985;94:547-49.

11. Tucker HM: Laryngeal framework surgery in the management of spasmodic dysphonia. Preliminary report. Ann Otol Rhinol Laryngol 1989;98:52-54.

12. Koufman JA: Laryngoplastic phonosurgery. In Johnson JT, Blitzer A, Ossoff R, Thomas JR (eds): Instructional Courses, Volume I, American Academy of Otolaryngology-Head and Neck Surgery. St. Louis, CV Mosby Co., 1988

13. Koufman JA.  Surgical correction of dysphonia due to bowing of the vocal cords. Annals Otol Rhinol Laryngol 1989;98:41-45.

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19. Statloff (personal communication)

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24. Blalock DP, Kemp ES, Belafsky PC, Clyne S, Postma GN, Koufman JA. Utility of electroglottography (EGG) with unloading in the diagnosis of vocal fold paresis. Presented at the annual meeting of the American Academy of Otolaryngology-Head and Neck Surgery, Denver, CO, 2001.

25. Koufman JA, Blalock PD.  A classification and approach to patients with functional voice disorders. Ann Otol Rhinol Laryngol 1982;91:372-77. 

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28. Koufman JA.  Approach to the patient with a voice disorder.  In:  Koufman JA, Isaacson G, eds. Voice Disorders.  Otolaryngol Clin N Amer 1991;24:989-98.

29. Koufman JA, Radomski TA, Joharji GM, Russell GB, Pillsbury DC. Laryngeal biomechanics of the singing voice. Otolaryngol Head Neck Surg 1996; 115:527-37.

30. Koufman JA.  Evaluation of Laryngeal Biomechanics by Fiberoptic Laryngoscopy. In Gould WJ, Rubin JS, Korovin G, Sataloff R, eds.  Diagnosis and Treatment of Voice Disorders. Igaku-Shoin Publishers, New York, 1997.

31. Belafsky P, Postma G, Reulbach T, Holland B, Koufman J.. Muscle tension dysphonia as a sign of underlying glottal insufficiency. Otolaryngol Head Neck Surg 2002:127:448-51.

32. Koufman JA. Voice disorders are usually multifactorial. (Unpublished data 2006)

33. Amin MR, Koufman JA.  Vagal neuropathy after upper respiratory infection: a viral etiology? Am J Otolaryngol 2001;22:251-56.

34. Koufman JA. Occult vocal fold paresis and things that go bump on the vocal fold Presented at the Annual Meeting of the Voice Foundation. Philadelphia, PA.  June 8, 2002.

35. Koufman JA, Belafsky PC.  Unilateral or localized Reinke’s edema (pseudocyst) as a manifestation of vocal fold paresis: The paresis podule.  Laryngoscope 2001;111:576-80.

36. Bach KK, Belafsky PC, Wasylik K, Postma GN, Koufman JA. Validity and reliability of the glottal function index. Arch Otolaryngol Head Neck Surg 2005;131:961-964.

37. Belafsky PC, Postma GN, Koufman JA.  Validity and reliability of the reflux symptom Index (RSI). J Voice 2002;16:274-77.

38. Isshiki N, Tanabe M, Sawada M: Arytenoid adduction for unilateral vocal cord paralysis. Arch Otolaryngol 1978;104:555-58.

39. Maves MD, McCabe BF, Gray S: Phonosurgery: Indications and pitfalls. Ann Otol Rhinol Laryngol 1989;98:577-80.

40. Halum SL, Postma GN, Koufman JA.  Endoscopic Management of Extruding Medialization Laryngoplasty Implants. Laryngoscope 2005;115:1051-54.

41. Mikus JL, Koufman JA, Kilpatrick SE. Fate of liposuctioned and purified autologous fat injections in the canine vocal fold. Laryngoscope 1995;105:17-22.

42. Duke SG, Salmon J, Blalock PD, Postma GN, Koufman JA.  Fascia augmentation of the Vocal fold: graft yield in the canine and preliminary clinical experience. Laryngoscope 2001;111:759-64.