Decisions regarding therapeutic intervention in cases of vocal fold paralysis are guided by concerns regarding morbidity, principally from dysphagia and aspiration, and expectations and assumptions about the eventual outcome for the patient if left untreated. In turn, expectations concerning prognosis are influenced by the apparent cause of the paralysis and the time that has elapsed since onset. Electrophysiologic testing, in the form of laryngeal electromyography, has also been used to predict outcome, but a surprising amount of uncertainty regarding its utility still persists.
The ideal management strategy for unilateral vocal fold paralysis would offer timely treatment to patients whose disability is permanent, while sparing those who are likely to recover spontaneously from an unneeded surgery. As a secondary goal, it would offer effective temporary relief from dysphonia and swallowing difficulties to this second group of patients while they await improvement. Existing strategies emphasize expectant management, preferring to err on the side of delay in the treatment of patients with permanent deficits. These approaches, which have been legitimized by time, tend to assign less importance to the costs and limitations of an extended period of dysphonia, although these may be considerable. An expectant approach is appropriate if rehabilitation techniques are unsatisfactory, unpredictable, or risky, and if very little is known about prognosis.
However, advances in the understanding of laryngeal neurophysiology and the accumulation of clinical information have both yielded some insight, albeit incomplete, into mechanisms of recovery from vocal fold paralysis.
Laryngeal electromyography has matured to become a practical clinical tool which yields valuable prognostic information in many cases. Interventions for vocal fold paralysis are generally safe, most techniques not even requiring a general anesthetic. They may be tailored to each case of vocal fold paralysis to achieve significant improvement in voice and other symptoms in the majority of patients. Many are reversible or revisable without undue difficulty, and dangerous complications are uncommon. In this new context, a critical examination of the factors which inform the decision to treat unilateral vocal fold paralysis may make it possible to modify the traditional approach to better serve the needs of the patient and come closer to the ideal.
Most clinicians agree that clinically significant dysphagia in patients with vocal fold paralysis overrides concerns about unnecessary intervention and mandates early intervention. Such symptoms are usually evident and readily di-agnosable from elements of the history such as coughing with eating or drinking, weight loss and episodes of pneumonia, and examination findings such as marked glottic insufficiency and observed pooling and aspiration of secretions. The modified barium swallow and endoscopic evaluation of swallowing exist to supplement the clinical assessment of such patients and to help guide treatment.
Aspiration has been identified in 18-38% of patients with unilateral vocal fold paralysis from all causes [1-3], although troublesome aspiration is probably more likely in certain clinical situations. These include combined re current and superior laryngeal nerve injury , either by discrete distal injury of both nerves or as part of a so-called "high vagal" injury, as well as situations in which vocal fold paralysis exists alongside other cranial nerve injuries, particularly the hypoglossal. Such a scenario is especially likely after skull base surgery but may also follow carotid endarterectomy and other surgeries in the neck requiring cephalad dissection, as well as stroke and other central nervous system injury or insult. In addition, surgeries that affect pulmonary reserve, as do most thoracic procedures, appear to carry a higher risk of aspiration with vocal fold paralysis. Age may also be an independent risk factor .
Algorithms featuring prompt medialization have been proposed after skull base surgery [6, 7] and thoracic surgery [8-10]. Laryngoplasty and injection appear to be equally effective in improving swallowing dysfunction . It is worth noting that a significant proportion of patients remain troubled by aspiration even after a medialization procedure [6,11], probably a reflection of the multifactorial nature of the problem. Again, it is likely that laryngeal anesthesia from a superior laryngeal nerve injury is probably an important reason for continued dysphagia. Woodson  has suggested that the addition of arytenoid adduction and crico-pharyngeal myotomy may be of benefit in these persistent cases.
Perhaps the most significant impediment to efficient management of vocal fold paralysis has been a lack of clear information regarding prognosis. There is no equivalent of Pieters-en's landmark studies [13,14] of facial palsy to clarify the natural history of the paralyzed vocal fold. Clearly, the potential for spontaneous improvement varies from clinical scenario to clinical scenario, but even reports addressing vocal fold paralysis from the same cause can be difficult to reconcile with one another because of important differences in data collection and reporting. These differences consist principally of:
1. heterogeneity in clinical series resulting from differences in the time elapsed from the onset of the paralysis to examination.
2. variable definitions of recovery.
3. an oversimplified, "all-or-none" concept of paralysis and paralytic dysphonia presented in many reports.
The first difficulty arises from the clinical nature of vocal fold paralysis. A comparison with facial palsy, another peripheral cranial mono-neuropathy which may result from surgery, medical disease, or unknown etiology, is instructive. Facial hemiplegia is immediately evident and alarming, and affected patients typically rush to seek medical attention. Vocal fold paralysis, however, is not always so obvious, symptoms being proportional to the degree of glottic insufficiency; an immobile vocal fold resting close to the midline may not generate significant dysphonia. Even when patients are severely dysphonic, they are capable of dismissing symptoms as "laryngitis" for weeks, if not months, before seeing a physician.
The time which has elapsed from onset to examination has an impact on observations. Prompt examination is likely to reveal a higher rate of paralysis than an examination performed weeks or months later, as well as a higher rate of recovery. Conversely, delayed examination yields a lower rate of paralysis, as some cases will have already improved, and a lower rate of recovery, as only the more profound neuropathies will have persisted to be identified. This is borne out in studies regarding vocal fold paralysis following carotid endarterectomy presented in Chap.3 (see Table 9): systematic immediate examination revealed a rate of paralysis of 27%, far higher than the more typically reported rate of 1-6%. This same effect is probably also present to some extent after nonsurgical vocal fold paralysis, as short-lived vocal fold paralysis has been identified in several clinical contexts . To date, only reports in which all patients undergo laryngeal examination after a surgery which puts the vocal fold at risk have succeeded in controlling this variable. Many other studies do not even report information regarding the relation of the time of examination to the onset of the complaint.
Another important point of confusion stems from the fact that, in some cases, acceptable voice returns in the absence of vocal fold motion. Studies suggest that this is due to maintenance or restoration of vocal fold muscular tone and bulk, and thus adequate glottic closure in adduction, by reinnervation which is not sufficient or specific enough to restore motion [16,17]. Vocal fold motion and voice function are, therefore, not entirely synonymous. Reports usually assess recovery in terms of either motion or voice quality, but only rarely both. Most articles in the otolaryngology literature consider "recovery" to mean a return of vocal fold motion, and make only passing mention of voice quality. These articles probably understate the rate of clinical recovery, although the information regarding physiologic reinnervation is accurate. Others, usually in the general surgery or medicine literature, declare outcome favorable if voice has returned, but do not systematically assess vocal fold motion in these cases. It is possible to argue convincingly that this second group of studies, which effectively categorize nonmobile but well-apposed vocal folds as favorable outcomes, provide more clinically useful information, since, as of this writing, surgical interventions can offer no better result.
Finally, vocal fold motion and voice function are often treated strictly as all-or-none phenomena: either the vocal fold is paralyzed or it is not, and either the voice has returned to normal or it has not. However, it is probably correct to view neural compromise of glottic function as a continuum of disability. It is clear that both partial paralysis (paresis) and incomplete recovery of complete paralysis are possible, as is a wide variability in the extent of phonatory dysfunction. While the potential for partial recovery is generally acknowledged, it is rarely incorporated into tabulations and discussions of nontreated outcomes of cases of vocal fold paralysis. This cannot be attributed to a lack of means of measuring voice quality. Reports of voice improvement following surgical treatment are detailed, typically featuring a number of qualitative and quantitative means of voice assessment. In comparison, data regarding voice in cases of vocal fold paralysis allowed to evolve naturally are crude. Considerable detail, and possibly some insight into mechanisms of recovery, are lost as a result. At the very least, this compromises our ability to compare spontaneous evolution with the effects of treatment.
Given these limitations, it should come as no surprise that information about the natural history of vocal fold paralysis is approximate. Prognosis for both vocal fold motion and voice following paralysis due to mediastinal nerve compression by malignancy is so poor that it is taken as a matter of course that these patients do not recover. The same is generally true of nerve section. Lest the latter observation seem too self-evident, it is useful to recall that experience with recurrent nerve section for spasmodic dysphonia has shown that the vocal fold has a robust tendency for reinnervation, even when a sizable length of nerve is removed. A surprising number of these cases show evidence of reinnervation (without return of vocal fold motion), and in fact, this may account for treatment failure in the majority of cases [18, 19]. However, the general clinical impression of poor prognosis remains valid.
Prognosis following various types of surgical injury is highly variable and no doubt affected by differences in the definition of recovery, as described above. A review of recent series of vocal fold paralysis following thyroidectomy show that 46-100% of paralyses identified after surgery recover, although most reports fall into the range of 65-85% (see Chap. 3, Table 7). In vocal fold paralysis after cervical spine surgery via an anterior approach, 18-90% recovered [20-23], the rate exceeding 60% in most reports. Injury during carotid endarterectomy improves in 0-86% (see Chap. 3, Table 9), and early reports indicate that recovery occurs in most cases which follow implantation of the vagal nerve stimulator. A similar pattern appears to follow vocal fold paralysis ascribed to intubation [24, 25], as might be expected in a case of neurapraxic injury. The rate of recovery following intrathoracic surgery is not well documented but may well be lower, in part because of the need to sacrifice the nerve during pneumonectomy for oncologic reasons. Recov ery following skull base surgery is generally deemed to be poor .
The natural evolution of idiopathic vocal fold paralysis has been of considerable interest, and outcomes are generally reported more scrupulously and in somewhat more detail than for other clinical scenarios. In most series, 2040% of patients regain vocal fold mobility and an additional number recover voice without motion, so that 25-50% of patients (see Chap. 3, Table 10) experience substantial improvement evident 1-9 months following the onset of the problem, although recovery has been reported as late as 18 months . Selected studies report higher rates of recovery, either of voice  or vocal fold motion , but no factor to account for the discrepancy is obvious.
Thus, apart from vocal fold paralysis from malignancy and nerve section, prognosis for vocal fold paralysis remains variable and difficult to extrapolate except in the broadest way from the clinical scenario in which it occurs. It is this uncertainty that probably accounts for the persistence of the traditional delay of 6-12 months prior to intervention. A review of the literature reveals that the evidence supporting these intervals is limited and subject to all of the ambiguities reviewed above. Most otolaryngologists who have treated patients with vocal fold paralysis can recall cases that have not conformed to these expectations.
In the absence of conclusive information about prognosis and time required for recovery, clinical neurophysiologic testing may be especially useful. Laryngeal electromyography measures electrical activity in muscle by means of needle electrodes. Technical aspects and findings are described in Chap. 5. Laryngeal electromyography is able to identify normal innervation, absence of innervation, reinnervation, and even synkinetic reinnervation by virtue of characteristic electrical signals. Criteria for assignment of prognosis in vocal fold paralysis can vary, but generally, preservation of normal motor unit waveforms, activation of motor units during appropriate voluntary tasks, and pres ervation of a brisk degree of recruitment have been considered indicative of good prognosis. The presence of spontaneous activity and the absence of normal motor unit waveforms and recruitment are signs of poor prognosis. Time is also a highly relevant factor. The earlier favorable signs are identified, the more likely it is that spontaneous recovery will take place, although extremely early electromyographic assessment may exaggerate the degree of injury [30, 31]. Beyond 6months, electromyography seems to be of limited use, as the potential for recoveryis uniformlypoor [32-34].
Laryngeal electromyography has been criticized as being "subjective." While this is true of certain aspects, particularly judgments regarding the integrity or impairment of recruitment with voluntary activity, most electromyographic findings - such as fibrillations, positive sharp waves, and polyphasic motor unit potentials -are clear, both in appearance and significance. Electromyography might be more properly described as qualitative rather than subjective: electromyographic findings require interpretation by a knowledgeable physician. In this regard it does not differ from laryngoscopy and stroboscopy, for example, except inasmuch as training and familiarity allows otolaryngologists to use these studies routinely and comfortably in daily practice. Strictly speaking, in fact, electromyography exceeds both of these in its ability to definitively - and objectively
- diagnose vocal fold paralysis, as opposed to immobility.
The practical clinical difficulty has been that laryngeal electromyography appears to be unreliable in predicting recovery. That is, the appearance of unambiguous signs of reinnervation does not always lead to return of function. In fact, both animal and human studies have shown that a paralyzed vocal fold is only sometimes a denervated fold [16, 36, 37]. In many
- perhaps most - cases, vocal fold muscles are reinnervated, but that reinnervation is often dysfunctional. This includes not only misdirected adductor and abductor innervation but also changes in neural organization peripherally and centrally (see Chap. 2). The complex, highly specialized nature of the laryngeal neuromotor system probably leaves many ways in which reinnervation may miscarry. Laryngeal electromyography is not able to reveal all of these subtleties, so that electromyographic evidence of nerve regrowth is not synonymous with vocal fold motion. Probably for this reason, laryngeal electromyography continues to occupy an indeterminate position in the evaluation of vocal fold paralysis in the minds of some practitioners.
The power of electromyography in revealing the failure of reinnervation is often overlooked in the eagerness to predict recovery. In this context, there are no physiologic ambiguities, and electromyographic findings reflect glottic function more reliably. Over time, the resting potential of a muscle cell that receives no neural input falls to near the depolarization threshold. From time to time, it crosses this threshold, and the single cell fires, depolarizes, and then repeats this cycle. On electromyography, this manifests as fibrillation potentials or positive sharp waves which occur spontaneously. These characteristic electrical features of denervation leave little to be misinterpreted and strongly suggest that (a) the initial injury is profound, and (b) there is little reinnervation of any sort. The more time that elapses from injury, the more definitive the finding becomes. Although potentially misleading very early in the course of the paralysis , spontaneous activity, with absent or scant voluntary motor unit activation, appears to be a highly accurate predictor of nonrecovery significantly earlier than 6 months [35, 38, 39, 40, 41]. A review of comparable studies of electromyographic assessment of vocal fold paralysis of less than
6 months duration (Table 6.1) reveals that accurate prediction of recovery does not exceed 80%, and has been reported to be as low as 13% when strict criteria for recovery of full range of motion are used. However, when determination of poor prognosis rests on the presence of spontaneous activity and absence (or scant presence) of motor units, laryngeal electromyography is an accurate predictor of the failure of recovery (75-100%).
This is clinically useful information that can be used to identify patients for early definitive intervention, eliminating a several-month wait for a vocally disabled person, or eliminating the need for a temporary intervention when a definitive one is likely to be ultimately necessary. At our centers, failure of reinnervation as demonstrated by electromyography has been a reliable finding as early as 3 months. Appropriately designed studies are needed to refine this observation further and determine more precisely how early such findings may be deemed to be significant.
The means of treating unilateral vocal fold paralysis are usually divided into temporary and definitive techniques. Temporary medialization is nearly synonymous with injection augmentation, as injectable substances do not persist reliably in the vocal fold. Polytetrafluo-roethylene polymer (Teflon, Polytef), which has fallen into disfavor because of adverse tissue response, and calcium hydroxylapatite
Number of Cases
Accurate predition of recovery (%) of no/limited
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