Учебники / Voice Disorders and Their Management Freeman 2000

born with a vocal fold paralysis the condition may be undiagnosed and, in some cases, function may be recovered spontaneously. Thus the condition remains unknown. Similarly, this may occur in adults who have a paralysis of a transient nature for which services are never sought. Increased prevalence of vocal fold paralysis in the older population is related to the higher incidence of progressive neurological diseases and various non-laryngeal malignancies in this group, both of which are highly implicated in disruption of recurrent laryngeal nerve function. The effects of the primary conditions in these cases may often be more debilitating and of more urgent concern than the voice symptoms. Thus, actual diagnosis of the existence of the paralysis may be bypassed or overlooked unless aspiration is of concern. Because vocal fold paralysis is more prevalent in the older population, and because that sector of the population continues to be fast growing, it would seem reasonable to conjecture that the incidence of vocal fold paralysis may be rising.

In a review of 113 patients with vocal fold paralysis, Terris et al. (1992) reported that 74% had unilateral paralysis of which 68% involved the left vocal fold. Mean age of onset was 58 years. Percentages for specific causes of vocal fold paralysis vary to some extent. However, nonlaryngeal malignancy, primarily pulmonary, is now reported as the primary cause (Terris et al., 1992; Benninger et al., 1994a; Wippold, 1998), having overtaken thyroid surgery and iatrogenic causes. Surgical trauma occurs most frequently secondary to thyroidectomy, but thoracic, cervical spine, carotid artery and cardiac procedures may also result in damage to the recurrent laryngeal nerve. The second most common aetiology of vocal fold paralysis is trauma, surgical and nonsurgical. Included in the latter category are traumas resulting from motor vehicle accidents, intubation, penetrating injuries, or other neck injuries. Nonsurgical trauma is believed by some to be increasing as a cause of vocal fold paralysis (Tucker, 1993). Idiopathic aetiology, inflammatory causes, and central pathology occur with much less frequency. A number of progressive neurological diseases such as Parkinson’s disease, Shy-Drager syndrome, multiple sclerosis and ALS, and neuropathies such as Guillain–Barré, diabetes, etc. may have a component of vocal fold movement disability as part of the course of the disease.

It is believed by some that vocal fold paralysis is an underreported problem (Benninger et al., 1994a). As previously noted, this may be particularly true in the case of idiopathic or virus induced paralysis that may recover spontaneously within a relatively short time period, obviating the need for the individual to seek medical attention. Indeed, our understanding of the degree of recovery possible in such cases is no doubt coloured by the fact that those seeking medical attention may be the group that fails to recover.

Some conditions may result in transient vocal fold paralysis that resolves in a month or less. Postma and Shockley (1998) describe cases of myasthenia gravis, meningitis and surgical trauma in which vocal fold mobility was clearly impaired for a very short time period. In each of the cases they described, normal return of function was restored following appropriate treatment of the underlying condition.

Another way to consider aetiology of vocal fold paralysis is to examine congenital versus acquired problems. The causes noted above appear to be primarily acquired. Congenital vocal fold paralysis, which has been estimated to comprise 27% of all vocal fold paralyses (Gereau et al., 1995), can be either unior bilateral. According to Gereau et al. (1995), bilateral paralysis occurs with greater frequency (38%) and is usually secondary to central nervous system problems or as part of other congenital abnormalities. In approximately 45% of these cases recovery occurs either spontaneously or secondary to treatment of the underlying condition. Although the paralysis may occur in utero, it is often difficult to determine whether the underlying aetiology is traumatic, secondary to the birth process itself, or developmental, secondary to an embryological disturbance. In a study of 113 cases of congenital vocal fold paralysis, deGaudemar et al. (1996) reported that 61 had unilateral paralysis (41 left and 20 right) while a smaller number, 52, had bilateral paralysis. The most common aetiology for this group was idiopathic, followed in decreasing numbers by paralysis associated with neurologic disorders, associated with heart malformations and difficult birth. More than 70% of unilateral paralyses of idiopathic, neurologic or difficult birth origin recovered spontaneously. The prognosis for spontaneous recovery in bilateral paralysis was poorer.

It has been reported that 10% of all congenital laryngeal lesions are paralytic (Gereau et al., 1995); however, the diagnosis may not be made immediately as the symptoms are often non-specific. Stridor is usually present in bilateral paralyses, but rarely in unilateral involvement. Vocal fold paralysis is the second most frequent cause of congenital stridor (Manaligod and Smith, 1998). Other symptoms might include weak, breathy cry, aspiration or choking during feeding.

Diagnosis

In a sizeable percentage of cases, the diagnosis of vocal fold paralysis can be made and the aetiology ascertained by history and appropriate physical examination. According to Terris et al. (1992) the primary objective in the evaluation of the patient with unilateral vocal fold paralysis is to determine the aetiology, with restoration of vocal function as the secondary objective.

This order of objectives may differ for the patient with bilateral vocal fold paralysis when the airway is compromised and its management becomes the primary focus. Aetiology of bilateral paralysis is also important to ascertain, but is perhaps more readily apparent based on history.

Patients present themselves with a number of scenarios that should raise the examiner’s index of suspicion that vocal fold immobility of some sort is present. Frequent complaints are: weak voice, inability to be heard, shortness of breath and running out of breath during speaking, instability of voice, hoarseness and choking on liquids or other foods. Many of these characteristics or signs may be noted perceptually during the interview.

Careful questioning of the patient may place the onset of the voice change in close temporal proximity to surgery involving the thyroid, the neck, the thorax, the cervical spine, the heart or a surgical procedure that required short or long-term intubation. This information strongly suggests the likelihood of recurrent laryngeal nerve injury or possible arytenoid dislocation. Indeed, in some instances it may be known that the recurrent laryngeal nerve was sacrificed during the course of the surgery. Another close tie-in may be the reporting of a viral infection preceding the voice problem. It is believed that viral infection may be implicated in causing unilateral vocal fold paralysis, particularly when no other cause can be verified.

Trauma, sufficient to cause vocal fold paralysis, is not uncommon. A thorough history should reveal the possibility of such an aetiology. Patients who present with a diagnosed neurological disorder or manifestations of such a disorder and complain of voice problems may present with vocal fold mobility problems associated with the underlying neurological disease. There are numerous other metabolic, inflammatory and autoimmune disease processes that may, on occasion, result in paralysis of the vocal folds.

It is important to rule out all other possible diagnoses through a process of differential diagnosis and to attempt to determine whether the mobility problem represents paralysis, paresis, arytenoid dislocation or ankylosis. It is also necessary to recall that the perceptual and physical findings in a patient with a psychogenically based voice disorder presenting with whispered speech may mimic a vocal fold mobility problem.

Diagnostic testing

The basic components of a competent and complete evaluation are always carried out for each patient (Colton and Casper, 1996). These components are: a complete history, a complete ear nose and throat examination (including laryngeal imaging), voice evaluations of both a subjective and

an objective nature. These components of the examination help to establish and confirm the diagnosis, are essential for documentation of findings, are critical in determining the need for and nature of additional testing and in planning treatment.

Laryngeal endoscopy

Imaging of the larynx using endoscopic procedures is essential for determining movement characteristics of the vocal folds during phonation. The performance of non-phonatory acts such as whistle, cough, throat clear and swallow should also be observed. The rigid and the flexible endoscopes provide different and valuable information and the use of both is recommended. Videotaping the examination provides the opportunity for visualizing an enlarged image, for repeated study of the image, and for documentation and future comparison.

Stroboscopic examination adds the dimension of observing vibratory behaviour that sometimes can be helpful in making the differentiation between paralysis and immobility. The loss of tone of the body of the vocal fold resulting from damage to the motor fibres of the thyroarytenoid muscle is best appreciated with stroboscopy (Benninger et al., 1994a). ‘The flaccid paretic fold opens laterally earlier in the glottal cycle and to a greater degree, but it does not have the normal undulating vibration that the normal fold exhibits’ (Benninger et al., 1994a, p. 499). Stroboscopic signs of unilateral vocal fold paralysis preand post-treatment have been reported by Colton et al. (1998) for a group of 38 patients.

When the cause of the paralysis is known, such as severing of the recurrent laryngeal nerve during a surgical procedure, further tests, beyond videoendoscopy/stroboscopy, may not be necessary. When the history and physical examination fail to identify the aetiology of the paralysis or render it uncertain, further testing is mandatory.

Chest X-ray, CT scan, magnetic resonance imaging (MRI)

Because nonlaryngeal malignancy is the primary cause of vocal fold paralysis, it is imperative that exploration of that aetiologic possibility be pursued. A chest X-ray should be the first test to be performed. Lung tumours comprise the largest number of neoplasms that are implicated in laryngeal paralysis. A negative chest X-ray, however, is insufficient data on which to rule out the possibility of a malignancy. Thus, further imaging studies, such as CT scan or MRI (magnetic resonance imaging) from the base of the skull to the aortic triangle on the left and to the thoracic outlet on the right are necessary (Terris et al., 1992; Benninger et al., 1994a; Altman and Benninger, 1997).

Although vocal fold immobility in patients with rheumatoid arthritis had been thought to result from fixation of the cricoarytenoid joint, Link et al. (1998) report that cervicomedullary compression secondary to destructive arthritic changes and inflammatory processes may well be the cause. They provide data on three patients demonstrating the need for imaging studies that focus on skullbase, showing subluxation of the occipito-atlanto-axial joint and/or basilar invagination with brain stem compression. With appropriate treatment, the vocal fold immobility is reversible. Thus, the need for imaging studies that explore the route of the vagus nerve is further strengthened.

Laryngeal electromyography (LEMG)

Laryngeal electromyography (LEMG) is receiving increased attention and use in the examination of patients with vocal fold mobility and swallowing disorders (Woo, 1998). It is useful in making the distinction between vocal fold paralysis and vocal fold immobility due to mechanical fixation or dislocation of the cricoarytenoid joint. When action potentials are present despite the presence of an apparently immobile vocal fold, it can be inferred that the problem is one of mechanical immobility (Terris et al., 1992). Woo (1998) makes the claim that LEMG can be used to ‘triage patients with immobile vocal folds’ (p. 473) in a cost-effective and useful manner by directing the planning of further examination procedures or treatment approaches. The distinction between superior laryngeal nerve paralysis and recurrent laryngeal nerve involvement or the denervation of both nerve branches can be clarified when LEMG is used appropriately (Rontal et al., 1993; Woo, 1998). This constitutes site of lesion testing and also serves to direct the focus of further examinations. For purposes of prognosis and treatment planning, LEMG provides information about reinnervation. Comparison of tests performed at various times in the uncertain course of idiopathic paralysis or recovery from injury, helps to determine the timing and type of intervention required. Reinnervation can be detected via LEMG before it can be visually observed. This provides a refinement of treatment planning based on objective data that is not otherwise available.

However, it must be recognized that LEMG is a tool requiring precise technique and considerable experience and skill. There are numerous limitations and concerns about its reliability and the reproducibility of test/ retest results (Benninger et al., 1994a; Ludlow et al., 1994; Ford, 1998; Woodson, 1998). Interpretation of the signal is subjective and thus reflects the skill and knowledge of the interpreter.

Airflow and air pressure studies

Although not diagnostic as such, measures of airflow and air pressure during phonation most objectively reflect the effects of paralysis on glottal closure. The results of airflow studies may add significant information that is not observable in other testing. For example, high leakage airflows (the flow during phonation) may suggest the presence of a significant posterior glottal gap that cannot be visualized due to the forward posture of the arytenoid cartilage on the paralysed side. Similarly, such a finding in the presence of fair vocal fold approximation may suggest that the vocal folds may be at different vertical levels. These measures are also useful in documenting the effects of treatment or the course of reinnervation.

Other tests

Other tests may be ordered when there is suspicion that systemic or other disease processes may be contributing to the vocal fold paralysis. These decisions must be made on an individual basis.

Diagnostic practices and cost effectiveness

There is not a standard protocol for evaluation of vocal fold paralysis that is agreed to and practised by all otolaryngologists. Indeed, Terris et al. (1992) reported a wide diversity of test procedures used, and found that those laryngologists most experienced and knowledgeable about the larynx ordered fewer tests than less experienced physicians. Cost-effective- ness questions include the relative information yield of the various diagnostic procedures and what that information adds to the diagnosis or the treatment. These authors suggest that the diagnostic tests described in the preceding section are the most productive, that they are readily obtainable, relatively inexpensive and relatively non-invasive. Tests that they report to be unnecessary in most cases include: erythrocyte sedimentation rate, VDRL, glucose level, complete blood count, urinalysis, chemistry profile, or thyroid function studies. Thyroid scans and barium swallows are also felt to be unnecessary if CT or MRI studies have been done. When aspiration is a concern and requires further definition, a modified barium swallow study (MBS) would be an appropriate consideration.

Treatment

There are a number of treatment options available for the patient with unilateral vocal fold paralysis. Figure 10.1 presents schematic flow charts describing general treatment courses. It should go without saying that decisions about patient care must be made on an individual basis. However, there are some general considerations that may help to direct the choice and timing of treatment.

Treatment Options: Unilateral Vocal Fold Paralysis

Known Permanent Aetiology

Unknown Aetiology > 9 Month Duration

Voice Therapy

Phonosurgery

Temporary or Unknown Aetiology < 9 Month Duration

After 9 mos.

Definitive Phonosurgery

Figure 10.1 Flow chart of treatment options and course of treatment for patients with unilateral vocal fold paralysis. Dotted lines suggest possible options depending on individual patient needs while the unbroken lines suggest the typical course of treatment.

The first of these is an understanding of the patient’s health status including the presence or absence of aspiration. Patients whose vocal fold paralysis results from the effects of a nonlaryngeal malignancy may be quite ill and debilitated, as may also be true of patients with other aetiologies. Aspiration is the primary concern for many. In such instances immediate intervention is required and should take the least aggressive, least invasive course possible. It is most likely that there will be improvement in the voice secondary to whatever procedure is done to control the aspiration. The presence of significant aspiration in any patient with vocal fold paralysis is of concern and demands prompt attention. However, if the patient is otherwise healthy, the choice of treatment to manage the aspiration may be different from that for the seriously ill patient. Assessment of the degree and severity of the aspiration relative to the time that the condition has been present is essential. Some patients may experience aspiration immediately following the onset of paralysis but may readily learn to control it through behavioural approaches. These approaches should be tried before other procedures are undertaken, particularly in an otherwise healthy person.

The second consideration is the certainty regarding the permanent vs. transient nature of the paralysis and the length of time since onset. As noted in previous sections of this chapter, knowledge of the aetiology of the paralysis will help to determine whether return of function or nerve regeneration is a possibility. If it is known that the nerve has been severed, it is usually a certainty that there will not be any spontaneous recovery of function. This knowledge will influence the choice and timing of treatment. There would be no need to postpone definitive procedures. However, if the paralysis is idiopathic in nature, some degree of functional recovery is possible for up to a year from onset. Thus, it is usually unwise to pursue a definitive treatment plan that might be incompatible with spontaneous recovery before at least nine months have elapsed.

The third consideration is the acceptability of the patient’s voice. Although there are some ‘typical’ characteristics of voice in the presence of a paralysed vocal fold, the severity of the effects varies from individual to individual. In addition, there are varied personal vocal needs: the need to be heard easily, the need to be able to talk at length, the need to speak above noise, the need to have a pleasing voice, the need to communicate with the public, etc. The patient is the final arbiter of the adequacy of his or her voice to meet those needs. This assessment must be accepted by the professionals and must be taken into consideration in the planning of the timing and nature of treatment.

The available treatment options and indications for their use will be described in the following sections.

Voice therapy

Voice therapy is a non-invasive, behavioural treatment option that typically has no negative effects. Thus, a period of voice therapy has the potential of helping the patient even to the point of regaining functional voice, while doing no harm. When voice therapy fails to produce an acceptable degree of improvement, all other treatment options remain open and the only thing that may have been lost in some instances is a bit of time. Attempts have been made to devise a method of determining which patients would be most likely to benefit from a course of voice therapy and which would be better served by early surgical intervention (Woo et al., 1991; Heuer et al., 1997). Some authors simply state that patients who exhibit large glottal gaps are appropriate surgical candidates. However, such statements fail to specify at what point in the course of the paralysis the judgement relative to glottal gap size is made. We have seen patients whose initially large glottal gaps gradually reduced in size over the course of recovery of function. A functional staging approach was described by Woo et al., based on clinical symptoms and selected objective measures. The findings resulted from the study of 55 patients. Patients for whom surgery was felt to be the treatment of choice were those rated as having severe dysphonia, with significantly elevated airflow rates and decreased loudness and phonation times. The added presence of severe aspiration increased the need for surgical intervention. On the other hand, patients with mild dysphonia and no aspiration tended to respond well to voice therapy. It was determined that there is no clear-cut statement that can be made for the group in the middle, those with moderate symptoms and moderate dysphonia. Treatment decisions for those patients must be made on an individual basis. This study also found that objective measures of certain vocal functions are more sensitive to changes than are visible stroboscopic signs.

None of the proposed prognostic plans has assured a high enough level of accuracy to be universally accepted. However, numerous authors have reported very positive results for many patients following a course of voice therapy (Woo et al., 1991; Colton et al., 1992; Benninger et al., 1994a; Casper et al., 1996; Heuer et al., 1997). Casper et al. reported a significant decrease in mean severity of dysphonia rating from 6.06 at the initiation of voice therapy for 17 patients with unilateral vocal fold paralysis to a mean rating of 1.67 at the conclusion of therapy six to eight weeks later. The potential benefit of a period of voice therapy is given support in the following statement by the Committee on Speech, Voice and Swallowing Disorders of the American Academy of Otolaryngology Head and Neck Surgery (Benninger et al., 1994a)