Учебники / Operative Techniques in Laryngology Rosen 2008

 

Fig. 4.8  Polyp, left vocal fold

Fig. 4.9  Fibrous mass (subepithelial), right vocal fold

Fig. 4.10  Fibrous mass (ligament), left vocal fold

Chapter 4

25

4.4.9Reactive Lesion

A reactive lesion is a submucosal, pathologic process of the vocal fold in response to a contralateral vocal fold lesion (i. e., vocal fold cyst, vocal fold polyp, fibrous mass) (Fig. 4.11). This lesion typically has a hourglass closure pattern seen on stroboscopy and has minimally reduced or normal mucosal wave vibratory activity on stroboscopy. This lesion responds quite favorably to voice rest and voice therapy and typically will reduce in size with this treatment modality. Surgical excision of the lesion can be done if the contralateral lesion requires surgery. The surgical approach is similar to a vocal fold polyp (see Chaps. 10, “Principles of Phonomicrosurgery” and 15, “Vocal Fold Polyp”). One may also elect not to operate on the reactive lesion, to remove the risk of an adverse surgical outcome (scar) at the operative site.

4.5Miscellaneous Disorders of the Vocal Fold

4.5.1Polypoid Corditis (Reinke’s Edema)

Reinke’s edema is a pathologic condition of the vocal fold that involves an accumulation of a gelatinous type of fluid throughout the superficial aspect of the lamina propria (Fig. 4.12). Often these accumulations can be quite severe, and it may become asymmetric; however, in general the process occurs throughout the entire vocal fold and is also exclusively found bilaterally. Reinke’s edema involves a demonstrable increase in size of the mass and volume of the vocal fold, which typically lowers the pitch of the voice and causes increased vocal effort and instability. The most common etiologic factors of Reinke’s edema involve tobacco abuse (97%), laryngopharyngeal reflux disease, and phonotrauma. Each of these potential etiologic factors should be addressed in a strict and thorough fashion prior to proceeding with surgical treatment of the Reinke’s edema (see Chaps. 10, “Principles of Phonomicrosurgery” and 18, “Polyp Corditis [Reinke’s Edema]”).

4.5.2Vocal Fold Granuloma

A vocal fold granuloma is inflammatory tissue arising from the perichondrium of the arytenoid cartilage (Fig. 4.13). This is a response to trauma of the arytenoid perichondrium, often found after orotracheal intubation, or excessive hyperadduction of the arytenoid cartilage (found in some phonatory behaviors and chronic cough). LPR is thought to contribute to further inflammation and propagation of granulomatous formation. Once the etiologic trauma and irritants that initiated the vocal fold granuloma are removed, vocal fold granuloma disease will often spontaneously resolve over a matter of several months. Surgical excision of vocal fold granuloma should only be performed if there is an acute airway obstruction, a suspicion of malignancy or after all etiologic factors have been thoroughly addressed (see Chap. 19, “Vocal Process Granuloma”).

26

Pathological Conditions of the Vocal Fold

4

Fig. 4.11  Reactive lesion of the right vocal fold (asterisk)

4.5.3Rheumatologic Lesions of the Vocal Folds

A variety of rheumatological disorders (e. g., rheumatoid arthritis, systemic lupus) can cause an unusual inflammatory process and deposition of abnormal tissue within the lamina propria of the vocal fold. This tissue typically results in severe reduction of the vibratory activity of the vocal folds, as seen in stroboscopy. These lesions are often adjacent to the vocal fold ligament or can occupy the entire width of the lamina propria. They have been known to form several distinct lesions within a single vocal fold, resulting in a “bamboo” appearance of the vocal fold; thus, these lesions are often called bamboo lesions of the vocal fold (Fig. 4.14). Microflap approach to surgical excision of these lesions is warranted when there is significant dysphonia, and all attempts to control the rheumatological disease have been implemented (see Chap. 10, “Principles of Phonomicrosurgery”). Given the intense fibrotic nature of this lesion(s), the surgical dissection can be difficult and tedious, and postoperative vocal fold stiffness is common.

4.5.4Vascular Lesions of the Vocal Folds

A variety of vascular lesions of the vocal fold can occur, most commonly associated with repeated phonotrauma of the vocal folds. This involves an abnormal vascular structure formation and vessel diameter of the subepithelial blood vessels of the vocal fold (Fig. 4.15). By convention, the normal subepithelial vocal fold vasculature runs parallel to the longitudinal axis of the vocal fold. Vascular abnormalities of the vocal fold typically run perpendicular to the longitudinal axis of the vocal fold and are significantly greater than one millimeter in diameter. They can present and develop in a variety of different patterns, such as vascular lakes, ectasias, and varices. The management and

Fig. 4.12  Reinke’s edema of the vocal folds, bilateral

Fig. 4.13  Arytenoid granuloma

Fig. 4.14  Rheumatological lesions of the right vocal fold (asterisks)

Chapter 4

27

Fig. 4.15  Vascular lesions of the vocal fold

Fig. 4.16  Sulcus vocalis

mation of the vocal fold epithelium onto the vocal fold ligament. Sulcus vocalis presents typically as a furrow along the free edge of the vocal fold in varying lengths and varying severity with respect to the degree of loss of the lamina propria (Fig. 4.16). Sulcus vocalis can often also have associated vocal fold pathologic entities, such as vocal fold lesions (e. g., cysts, fibrous mass, etc.) and mucosal bridges. The medical and surgical approaches to vocal fold scar and sulcus vocalis are discussed in Chaps. 23, “Sulcus Vocalis and Vocal Fold Scar,” and 48, “Gray’s Minithyrotomy for Vocal Fold Scar/Sulcus Vocalis,” respectively.

Key Points

■Most pathological conditions of the vocal folds are benign and occur within the epithelium or the lamina propria.

■Recurrent respiratory papillomatosis of the larynx occurs from a viral (HPV) infection of the epithelium (most commonly the epithelium of the vocal folds). The diffuse infection of the virus and the recurrent nature of the disease demand a conservative surgical approach.

■Premalignant changes of the epithelium and cancer of the vocal fold require careful observation/treatment to maximize treatment success and voice preservation.

■Benign midmembranous vocal fold lesions typically occur from vocal misuse/overuse. These lesions cannot be accurately diagnosed by viewing alone. Using morphology, response to voice therapy

and surgical findings, seven distinct lesions can be strictly defined: vocal nodules, fibrous mass (subepithelial or ligament), cyst (subepithelial or ligament), polyp, and reactive lesion.

■Vocal fold scar and sulcus vocalis represent severe derangement or loss of the vocal fold lamina propria (respectively).

Selected Bibliography

surgical approach to these lesions are discussed in Chap. 22,

1

“Surgical Management of Vocal Fold Vascular Lesions”.

2

4.5.5Vocal Fold Scar and Sulcus Vocalis

Vocal fold scar and sulcus vocalis represent severe abnormali-	3
ties of the lamina propria of the vocal fold. The former involves
replacement of the normal extracellular matrix proteins of the
lamina propria with abnormal scar tissue and an altered col-	4
lagen matrix structure. Sulcus vocalis is a loss or absence of
the vocal fold lamina propria, resulting in a direct approxi-

Rosen CA et al (2003) Benign midmembranous vocal fold lesion nomenclature paradigm. AAO-HNS annual meeting, Orlando, Fla., 23 September 2003

Derkay CS, Hester RP, Burke B, Carron J, Lawson L (2004) Analysis of a staging assessment system for prediction of surgical interval in recurrent respiratory papillomatosis. Int J Pediatr Otorhinolaryngol 68:1493–1498

Schweinfurth JM, Powitzky E, Ossoff RH (2001) Regression of laryngeal dysplasia after serial microflap excision. Ann Otol Rhinol Laryngol 110:811–814

Thekdi, AA, Rosen CA (2003) Surgical treatment of benign vocal fold lesions. Curr Opin Otolaryngol Head Neck Surg 10:492–496

28		Pathological Conditions of the Vocal Fold
5		Zeitels SM, Hillman RE, Bunting GW, Vaughn T (1997) Reinke's		7		Welham NV, Rousseau B, Ford CN, Bless DM (2003) Tracking
		edema: phonatory mechanisms and management strategies. Ann				outcomes after phonosurgery for sulcus vocalis: a case report. J
		Otol Rhinol Laryngol 106:533–543				Voice 17:571–578
6		Hochman I, Sataloff RT, Hillman RE, Zeitels SM (1999) Ectasias		8		Rosen CA (2000) Vocal fold scar: evaluation and treatment. Oto-
		and varices of the vocal fold: clearing the striking zone. Ann Otol				laryngol Clin North Am 33:1081–1086
		Rhinol Laryngol 108:10–16		9		Verdolini K, Rosen CA, Branski R. (2005) Classification Manual
4
						of Voice Disorders. Lawrence Erlbaum Associates, Mahwah, NJ

Chapter 5
Glottic Insufficiency: Vocal Fold	5
Paralysis, Paresis, and Atrophy

5.1Introduction

Glotticinsufficiencyisoneofthemostcommoncontributingfactors in patients who present with dysphonia. It is also one of the easiest findings to overlook in the clinical evaluation (Fig. 5.1).

Causes of glottal insufficiency include:

■Vocal fold immobility/partial immobility from one or a combination of:

■Vocal fold paralysis

■Vocal fold paresis

■Cricoarytenoid joint derangements (e. g., fixation or subluxation)

■Vocal fold atrophy/soft tissue deficiency due to:

■Deinnervation (vocal fold paralysis/paresis)

■Age-related changes (presbylaryngis)

■Tissue loss from ablative/destructive vocal fold procedures

■Vocal fold scar

■Sulcus vocalis deformity

■Myopathic disease (rare)

In clear-cut clinical settings such as unilateral vocal fold paralysis, the diagnosis of glottic insufficiency can is made through flexible laryngoscopy alone. However, videostroboscopy is essential to evaluate for glottal insufficiency when both vocal folds appear mobile, as is frequently the case with subtle vocal fold weakness, vocal fold scar and sulcus vocalis (Chap. 3, “Videostroboscopy and Dynamic Voice Evaluation with Flexible Laryngoscopy”).

The most common causes of symptomatic glottic insufficiency and the focus of this chapter are:

1.Unilateral vocal fold paralysis (UVFP)

2.Presbylaryngis/age-related changes of the larynx

3.Vocal fold paresis (unilateral and bilateral)

5.2Unilateral Vocal Fold Paralysis

5.2.1Etiology

The etiology of UVFP involves dysfunction of the brainstem nuclei, the vagus nerve, or the recurrent laryngeal nerve (RLN) supplying the involved side of the larynx. The vagus nerve exits the skull base via the jugular foramen and descends in the carotid sheath, giving off three major branches: the pharyngeal branch, the superior laryngeal nerve (SLN), and the re-

current laryngeal nerve (RLN). The SLN supplies sensation to the glottic and supraglottic larynx, as well as motor input to the cricothyroid muscle, which controls vocal fold lengthening and pitch. The RLN arises from the vagus nerve in the upper chest and loops under the aortic arch (left) or subclavian artery (right), and ascends back into the neck, traveling in the tracheoesophageal groove. The nerve enters the larynx posteriorly, adjacent to the cricothyroid joint. The RLN innervates the ipsilateral posterior cricoarytenoid (PCA), the interarytenoid (IA) (an unpaired muscle), and the lateral cricoarytenoid (LCA), and terminates in the thyroarytenoid (TA). Thus, the RLN supplies all of the intrinsic laryngeal muscles with the exception of the cricothyroid muscle. Ipsilateral RLN transection usually results in complete unilateral vocal fold immobility (the ipsilateral CT does not contribute to vocal fold adduction or abduction). It is important to remember, however, that the interarytenoid muscle is unpaired, and contralateral RLN input to the IA may lead to some adduction of the vocal fold on the paralyzed side (Fig. 5.2)

The causes of unilateral VFP are myriad, but can be broken down into categories to highlight the relevant pathophysiology. These are shown in Table 5.1.

Iatrogenic nerve injury likely represents the most common cause for otolaryngologic referral. Common iatrogenic surgical causes of UVFP include thyroidectomy/parathyroidectomy, anterior cervical disc surgery, esophagectomy, thymectomy, neck dissection, carotid endarterectomy, mediastinoscopy, and cardiothoracic surgery, including aortic surgery, coronary ar-

Fig. 5.1  Videostroboscopy image of glottic insufficiency due to a right vocal fold paralysis. The right vocal fold is lateralized and a visible glottic gap is present during phonation

30	Glottic Insufficiency

tery bypass grafting, and pulmonary lobar resection. Endotracheal intubation, prolonged nasogastric tube placement, and even esophageal stethoscope placement have been implicated as occasional causes of VFP.

Nonlaryngeal malignancies are another common cause of unilateral VFP. The most common scenario involves bronchiogenic carcinoma of the lung associated with a left RLN paralysis. The cause in these cases is usually due to mediastinal spread of the malignancy into the aortopulmonary window.

5 These paralyses rarely resolve spontaneously, and deserve early intervention. Other nonlaryngeal malignancies include thyroid, esophageal, and skull base (i. e., paraganglioma) tumors.

The neurologic event most commonly associated with unilateral VFP is stroke, usually of the brainstem. However, in these patients, other neurologic symptoms (such as paraplegia) or additional cranial nerve involvement are the rule, and isolated UVFP in this setting is highly unlikely. Many of these patients have severe dysphagia and aspiration due to ipsilateral laryngopharyngeal sensory and motor deficits.

Idiopathic UVFP is also seen frequently. A small number of case reports suggest that “idiopathic” UVFP may be due to her-

Fig. 5.2  Diagram depicting the dual innervation (from both the right and left RLN) of the interarytenoid muscle

Table 5.1  Unilateral vocal fold immobility: causes

Cause (%)

Malignancy—nonlaryngeal (24.7)

Iatrogenic—surgical trauma (23.9)

Idiopathic (19.6)

Nonsurgical trauma (11.1)

Intubation (7.5)

Neurologic (7.9)

Thoracic aortic aneurysm (4.3)

Pulmonary or mediastinal TB (1.1)

Adapted from: Benninger MS, Gillen JB, Altman JS (1998) Changing etiology of vocal fold immobility. Laryngoscope 108:1346–1349

 

pes simplex infection (HSV1) of the vagus nerve or its branches. The injury is presumed to be an inflammatory neuropathy, similar to the cranial neuritis observed with Bell’s palsy. Although this theory is widely regarded as true, little scientific data have been published to demonstrate that HSV neuritis is the causative agent in “idiopathic” UVFP. In addition, no studies exist that evaluate the benefit of systemic corticosteroids and/or antivirals in the treatment of this condition. Idiopathic UVFP is a diagnosis of exclusion, only after a detailed history and appropriate imaging studies fail to demonstrate a cause.

Medications such as the vinca alkaloids (vincristine and vinblastine), and cisplatinum, are known to cause neurotoxicity of the RLN (unilateral or bilateral). Fortunately, the VFP associated with the vinca alkaloids is dose related, and usually resolves over a 4- to 6-week period after stopping or adjusting the dose of the medication

Systemic diseases can (rarely) cause vocal fold immobility, due to either paralysis or joint fixation. Such diseases include gout, sarcoidosis, tuberculosis, rheumatoid arthritis, and hypothyroidism (only in cases of myxedema). These systemic diseases would be expected to have myriad symptoms in addition to unilateral vocal fold immobility, and these conditions should not be suspected in cases of isolated VFP.

In the case of endotracheal intubation leading to unilateral vocal fold mobility, one must be careful to rule out the possibility of arytenoid dislocation or subluxation as the true cause of an immobile vocal fold, although this scenario is probably quite rare. Laryngeal electromyography is helpful in these situations, as indicated below. Other traumatic causes of VFP include blunt or penetrating injuries to the neck.

5.3Surgical Indications and Contraindications

5.3.1Vocal Quality and Swallowing

The primary symptom of UVFP is dysphonia. The voice can vary from simple vocal fatigue in mild or well-compensated cases, to almost complete aphonia in severe cases. Much of the quality of the voice is determined by the muscular tone and position of the affected vocal fold and each patient’s unique laryngeal compensatory strategy. An atrophic and poorly compensated vocal fold paralysis typically presents with a breathy, weak voice due to air escape. The voice may also have a watery or “gurgle-y” quality to it if secretions are retained in the pyriform sinus, as is typical in high vagal injuries. With time, some patients will eventually progress to a stronger voice, using various compensatory strategies. Supraglottic hyperfunctional compensation is common. These patients constrict the supraglottic tract either laterally, apposing the false folds, and/ or in an anterior posterior dimension, apposing the epiglottis to the arytenoids. This hyperfunctional muscular contraction leads to a characteristic rough, pitch-locked, low-frequency voice. This voice can sound quite similar to a patient with primary muscular tension dysphonia, and the diagnosis of vocal fold paralysis may not be suspected. “Unloading” of the voice, as described later in this chapter, is used to help analyze these patients. In contrast, other patients, often females, may

Chapter 5

31

develop an unnaturally high-pitched voice that is breathy in quality. This has been referred to as a “paralytic falsetto,” and is characterized by a mean increase in fundamental frequency 85 Hz above “natural” pitch. This condition is thought caused by compensatory contraction of the ipsilateral cricothyroid (CT) muscle, which remains innervated in isolated RLN paralysis.

Swallowing difficulties are often encountered, specifically aspiration of liquids, along with a weak and ineffective cough. Some dysphagia for solids may also be present, especially in brainstem or high vagal injuries, due to the concomitant denervation of the pharyngeal constrictors. Risk of aspiration is heightened in these instances as well, due to the loss of ipsilateral laryngeal sensation from SLN involvement.

It is important to obtain a vocal inventory of the patient’s voice responsibilities (both work related and social). Vocal professionals rely on a serviceable voice for their livelihood, and these patients should be questioned regarding their upcoming work schedule to help determine the urgency of early surgical intervention. Most professional voice users will opt for temporizing vocal augmentation (Chap. 14, “Principles of Vocal Fold Augmentation”) so that they may return to work as soon as possible. A validated instrument, such as the VHI-10 is very useful for understanding the perceived severity of the patient’s vocal disability.

5.4Unilateral Vocal Fold Paralysis: Physical Examination

5.4.1General

Examination of the neck for adenopathy and thyroid masses should be performed. Cranial nerve X neural compression and infiltration by a neck or thyroid neoplastic process can lead to VFP in advanced cases. Palatal movement when phonating /a/ should be observed. Palatal paralysis in combination with ipsilateral VFP may indicate a “high” vagal lesion. In the case of palatal paralysis, the palate retracts toward the uninvolved “good” side (e. g., in a left vagal paralysis, the palate retracts to the right). A complete cranial nerve exam should evaluate for other involved nerves, especially CN XI and XII due to the close proximity these have to CN X at the skull base. Involvement of these adjacent cranial nerves warrants a thorough radiographic evaluation of the base of the skull.

5.4.2Laryngeal

The appropriate evaluation for VFP starts with the recognition of unilateral vocal fold immobility on examination. Indirect (mirror) laryngoscopy and rigid 70 or 90° laryngoscopy are helpful but do not replace flexible laryngoscopy. It is important to obtain an unencumbered, extended viewing period of the vocal folds during a variety of tasks. Flexible laryngoscopy is the only method to view vocal fold mobility in its natural state (refer to Chap. 3, “Videostroboscopy and Dynamic Voice Evaluation with Flexible Laryngoscopy”). When evaluating for suspected UVF paralysis/paresis, a useful task is to ask the

patient to perform an “ee-sniff” maneuver, where the patient alternates between phonating an “e” vowel and sniffing vigorously. This causes the vocal folds to alternately adduct and abduct maximally and is an excellent way to judge the degree of paresis/paralysis. Any purposeful and appropriate abduction of the affected vocal fold suggests incomplete paralysis (paresis). It is important not to falsely attribute a small amount of ad- duction of the affected vocal fold as representing evidence of partial innervation. RLN sectioning leads to paralysis of the ipsilateral thyroarytenoid, posterior cricoarytenoid, and lateral cricoarytenoid, but not the interarytenoid. The interarytenoid is a midline muscle, and has dual innervation from both RLNs; therefore, some residual adduction may be present in complete unilateral VFP, due to innervation from the contralateral RLN.

A paralyzed vocal fold can occupy a variety of positions, including lateral (cadaveric), paramedian, and median. It was once thought that the position of the paralyzed vocal fold had some topognostic significance (for example, that lateral vocal fold position indicated complete CN X paralysis due to RLN and SLN involvement). This theory was later disproven by both Woodson and Koufman. The final position of the vocal fold after nerve injury is now thought to be due entirely to the degree of reinnervation and synkinesis present.

It is important to focus on the vocal fold movement itself, rather than the arytenoid position, in determining vocal fold immobility. In some cases of vocal fold immobility, however, an overhanging arytenoid obscures the observation of the underlying vocal fold, making it impossible to ignore its position. This overhanging, anteriorly displaced arytenoid is sometimes mistaken for an arytenoid dislocation; however, this finding is usually caused by complete denervation or poor reinnervation of the PCA muscle

In some patients with UVFP, compensatory supraglottic contractions (i. e., “plica ventricularis”) obscure vocal fold movement. In these cases, the author advocates that the patient phonate with an easy onset such as a “sigh,” or be instructed to “hum through the nose.” This technique, described by Koufman as “unloading,” is useful for removing unwanted compensatory supraglottic hyperfunction that obscures vocal fold visualization. This technique is invaluable in many cases of longstanding VFP that have been misdiagnosed as primary muscle tension dysphonia, or plica ventricularis.

Videostroboscopy is a helpful part of the workup of vocal fold movement abnormalities, demonstrating the degree of incomplete closure present. In many cases of VFP, however, the paralyzed vocal fold shows increased amplitude of vibration due to the atrophic, “floppy” nature of the denervated vocalis muscle. In cases of mild or moderate vocal fold paresis, the increased amplitude seen on stroboscopy, or an asynchronous “chasing wave” may be the only signs of vocal fold weakness. Stroboscopy may also provide information regarding vocal fold height differences and the status of vocal process contact during phonation. These parameters help determine the need for arytenoid adduction, when evaluating patients for laryngeal framework surgery.

A simple test to evaluate the degree of vocal disability and glottic incompetence is measuring the patient’s maximal phonation time (MPT). This is done by simply instructing the patient to take a deep breath and phonate an “ee” vowel for as long as possible. Normal MPT for a healthy adult is approx-

32	Glottic Insufficiency

imately 25 seconds. In cases of VFP, the MPT is reduced to 10 seconds or less, typically. Shorter MPT values indicate more severe glottic incompetence, worse voice, and increased vocal fatigue. MPT values of 5 seconds or less indicate severe, uncompensated VFP that may need arytenoid adduction in addition to medialization laryngoplasty. Poor pulmonary reserve from asthma or chronic obstructive pulmonary disease may reduce MPT significantly, so results need to be taken in context of the patient’s pulmonary status. MPT should be expected to

5 improve (i. e., increase) after successful medialization surgery for VFP.

5.5Unilateral Vocal Fold Paralysis: Workup

It should be noted that unilateral vocal fold immobility is a physical finding, and not a diagnosis. One must determine the cause of the immobility. In the vast majority of cases of unilateral vocal fold immobility, VFP is the cause. Therefore, the bulk of the evaluation pertains to UVFP. In a small number of cases, the etiology may be cricoarytenoid (CA) joint arthritis (rheumatoid arthritis, gout), cricoarytenoid joint effusion/subluxation/dislocation (external trauma/ traumatic endotracheal intubation), or neoplastic infiltration (“occult” carcinoma in the ventricle/paraglottic space). In general, the history will suggest whether CA joint derangements are the culprit, and careful flexible laryngoscopy combined with CT scan will reveal neoplastic infiltration as the cause of vocal fold immobility. In cases where one cannot confidently exclude the CA joint involvement or neoplasm as the cause of unilateral vocal fold immobility, laryngeal electromyography and a laryngoscopy with palpation for passive mobility of the vocal folds is warranted.

5.5.1Serology

There is little yield from ordering screening laboratory tests such as chemistry panel, complete blood count, urinalysis, VDRL/FTA-ABS, thyroid function tests, autoimmune panels, or erythrocyte sedimentation rate. If additional elements of the history and physical exam point towards a systemic process as the cause of unilateral vocal fold immobility, directed serology tests may be indicated. However, in general, a “shotgun” approach to the workup of uncomplicated UVFP is unnecessary and wasteful.

5.5.2Imaging Studies

As screening tools, barium swallow and thyroid scans have virtually no yield in determining the etiology of VFP and are not advocated in the diagnostic workup. In contrast, a modified barium swallow or functional endoscopic evaluation of swallowing to evaluate swallowing and aspiration risk is frequently helpful in managing patients with dysphagia in the workup of VFP.

 

In cases where a clear-cut temporal relation exists between surgical iatrogenic trauma and VFP, no additional radiologic workup is necessary. In cases where no cause can be found for the VFP, imaging studies are essential. Most investigators agree that a CT (with contrast) or MRI encompassing the base of skull through the upper chest is adequate. Laryngeal electromyography (LEMG) undoubtedly has a place in the work up of unilateral vocal fold immobility; its role is still yet to be determined. LEMG can provide definitive diagnosis and prognostic information on the possibility for spontaneous recovery of VFP.

Useful information from LEMG is obtained between 1 and 6 months after the onset of VFP. Evaluation outside of these parameters can render the information misleading (early), or of limited usefulness (late).

5.6Unilateral Vocal Fold Paralysis: Treatment

The treatment of VFP can be broken into three management strategies:

1.Observation for 9–12 months, reserving treatment for patients with continued dysphonia

2.Referral to speech pathology for voice strengthening or swallow therapy, as indicated

3.Early surgical intervention:

a)Temporary: injection augmentation

b)Permanent: laryngeal framework surgery, injection augmentation

Obviously, these treatment strategies may overlap or may be employed simultaneously, but a management plan should be developed and followed as soon as all of the important diagnostic information is gathered. Several factors should be considered when determining the best course of action, and treatment must be individualized for each patient. A treatment algorithm is not advocated, as each patient’s expectations and vocal needs are unique.

Classical teaching for the treatment of VFP advocates a watchful waiting period of 9–12 months before surgical intervention is considered. This management strategy was developed in the 1970s, when the only viable treatment option for VFP was injection augmentation with Teflon. As Teflon injection is irreversible and sometimes associated with an unfavorable vocal outcome, early surgical intervention was ill advised during this era. LEMG and laryngeal framework techniques, along with an arsenal of injectable substances, have made early surgical intervention an excellent option in the treatment of VFP.

In patients with clear-cut aspiration due to VFP, early surgical intervention is indicated, either with injection augmentation of the vocal fold, or medialization laryngoplasty (ML). Evidence of severe denervation injury on LEMG may also lead to early surgical intervention. Clinical experience has shown that RLN paralysis due to carcinoma (lung, esophagus, thyroid, …) rarely recovers, and patients are counseled to consider early surgical intervention in these cases. Patients with VFP and high-level vocal demands (salespersons, clergy, teachers,

 

attorneys) often have difficulty continuing their work-related duties. In these cases, it may be necessary to intervene early (prior to 9 or 12 months) to get the patient back on the job. Temporary surgical procedures such as injection augmentation of the vocal fold should be considered in this population.

The medical health of the patient occasionally comes into play. Patients with significant cardiopulmonary and other medical comorbidities may not be candidates for a general anesthetic (i. e., for microlaryngoscopy with vocal fold injection augmentation), yet may be perfectly suitable for ML or injection augmentation performed under local anesthesia. In most cases, the patient should be counseled regarding the different treatment options, including the advantages and disadvantages of the three main strategies of treatment. In this way, the patient can actively participate in the decision-making process. When LEMG is available, it can serve as a crucial guide to the patient and surgeon regarding (1) treatment or observation and (2) temporary versus permanent treatment.

5.7Unilateral/Bilateral Vocal Fold Paresis

5.7.1Etiology

As is the case with vocal fold paralysis, incomplete paralysis or paresis can be due to iatrogenic, neoplastic, neurologic, and idiopathic causes outlined in section 5.2. Idiopathic causes are much more common with vocal fold paresis, and may represent a viral neuropathic process. A high index of suspicion for an underlying progressive neurologic disease (e. g., amyotrophic lateral sclerosis, postpolio syndrome) must be maintained as well.

5.7.2History

In contrast to patients presenting with UVFP, the presenting symptoms of a patient with vocal fold paresis can be very subtle. While the patient may complain of a breathy, weak voice, more subtle forms of dysphonia are often present. These symptoms include:

■Loss of volume/projection

■Vocal fatigue

■Loss of voice after extended use

■Odynophonia

■Loss of a portion of the vocal range (especially upper end of the register)

■Problems with stamina/quality of the singing voice

Vocal fatigue is usually present in patients with vocal fold paresis, and is a cardinal symptom of glottic insufficiency. The temporal course of the presenting vocal complaints can vary from sudden in onset, to gradually progressive, and even in some cases intermittent in nature.

Chapter 5

33

5.7.3Physical Examination

Flexible laryngoscopy and videostroboscopy, as outlined for UVFP in the previous sections is essential in the examination of the patient with suspected vocal fold paresis. The “ee-sniff” maneuver should be performed, using slow-motion review to evaluate for motion asymmetries in abduction and adduction of the vocal folds. Compensatory muscle tension disorders are common with vocal fold paresis; therefore, “unloading” techniques are useful as described previously.

■Videostroboscopy plays a pivotal role in the evaluation of suspected paresis. Subtle clues include:

■Mild bowing of the vocal fold(s)

■Incomplete glottic closure

■Prolonged “open phase” of vibratory cycle

■Increased vibratory amplitude in the paretic vocal fold (see Chap. 3, Fig 3.3)

■“Chasing”/asynchronous mucosal wave propagation

5.7.4Diagnostic Workup

Is the same as for UVFP, with the following notable exceptions:

■LEMG is critical to confirming the diagnosis, and establishing the “sidedness” of the vocal fold paresis (left, right, or bilateral). Findings are typically limited to reduced recruitment of motor units in the RLN or SLN distribution.

■Imaging studies are not generally obtained to evaluate the course of the vagus/RLN in cases of long-standing, stable vocal fold paresis. If vocal fold paresis progressively worsens or the affected vocal fold becomes immobile, then radiologic evaluation is indicated.

■Some consideration should be given to the possibility that the paretic vocal fold is a manifestation of a

progressive neurological disorder (if no clear etiology is identified). Neurologic consultation may be indicated. Possible conditions include:

■ALS

■Postpolio syndrome

■Pseudobulbar palsy

5.7.5Treatment

As with UVFP, treatment options include observation, voice therapy with a speech language pathologist, or surgical management either with injection augmentation of the vocal fold(s) or laryngeal framework surgery. In general, a less aggressive approach is used in the treatment of vocal fold paresis, as compared to UVFP. Voice therapy is more likely to be successful, and injection augmentation (lipoinjection, Radiesse) may be preferred over laryngeal framework surgery. If the diagnosis of vocal fold paresis is suspected, but cannot be confirmed, then

34

Glottic Insufficiency

a “diagnostic” injection augmentation using a temporary filler can be done. Improvement in the voice after injection augmentation suggests that glottic insufficiency is present. Long-term strategies can then be employed after the effects of the injection wear off.

5.8 Presbylaryngis/Age-Related

Changes in the Larynx

5

5.8.1General Considerations

It is a common misconception to use the term vocal fold bowing synonymously with presbylaryngis. Vocal fold bowing is not a diagnosis, but a physical finding indicating an elliptical or scalloped contour to the membranous vocal fold (Fig. 5.3). Bowing can be due to vocal fold atrophy, vocal fold paresis/ paralysis, age-related changes (presbylaryngis), vocal fold softtissue loss/scarring, and sulcus vocalis.

5.8.2Etiology, History, and Physical Findings

Presbylaryngis is the condition caused by senescent changes in the larynx, which generally present in the fifth decade of life or later. Typically, the patient complains of mild/moderate dysphonia, lack of volume/projection, and vocal fatigue, especially at the end of the day. Bilateral vocal fold bowing is the typical laryngoscopic feature on physical examination. Videostroboscopic exam often reveals mild/moderate degrees of glottal insufficiency/incomplete closure. However, unlike vo-

Fig. 5.3  Videostroboscopy image of bilateral vocal fold bowing due to presbylaryngis

cal fold muscular atrophy due to deinnervation, presbylaryngis is a more global process that involves not only loss of muscle bulk, but also degeneration/loss of the layers of the lamina propria, as well as CA joint changes. For this reason, the vocal dysfunction related to presbylaryngis is usually addressed incompletely when “medialization” framework surgery is used to correct the glottal gap.

5.8.3Workup

A diagnostic workup for suspected presbylaryngis is usually not necessary in most cases of elderly patients with a finding of vocal fold bowing on laryngeal examination. However, it should be noted that Parkinson’s disease (PD) often has an identical clinical presentation to that of presbylaryngis. Patients with PD, however, are more likely to have vocal tremor and monotone pitch in addition. The clinical distinction is important, as PD patients are generally poor surgical candidates for treatment of glottic insufficiency, due to the global bradykinetic nature of their vocal dysfunction. Lee-Silverman voice therapy (see Chap. 7, “Medical Treatment of Voice Disorders”) is the preferred primary method of treatment for dysphonia due to PD. Injection augmentation and laryngeal framework surgery are reserved as an adjunctive treatment in select cases.

Key Points

■Glottic insufficiency is one of the most common contributing factors in patients who present with dysphonia and one of the easiest findings to overlook in the clinical evaluation.

■The most common causes of symptomatic glottic insufficiency are unilateral vocal fold paralysis, unilateral or bilateral vocal fold paresis, and presbylaryngis.

■Treatment of “early” unilateral vocal fold paralysis is individualized for each patient, and takes into account the patient’s risk of aspiration, vocal demands, nature of neural injury, and LEMG findings.

■Videostroboscopy plays a pivotal role in the evaluation of suspected vocal fold paresis. Subtle clues include:

■Mild bowing of the vocal fold(s)

■Incomplete glottic closure

■Prolonged “open phase” of vibratory cycle (see Chap. 2, “Principles of Clinical Evaluation for Voice Disorders”)

■Increased vibratory amplitude in the paretic vocal fold

■Chasing/asynchronous mucosal wave propagation

■Loss of vocal projection and voice fatigue with extended use are classic symptoms of vocal fold paresis and can easily be missed in the history.