Учебники / Voice Disorders and Their Management Freeman 2000

Indeed, under good guidance, therapy sometimes produces astonishingly rapid improvements in voice quality despite persistence of the neurologic deficit. In any case, initial assessment is worthwhile to document vocal condition before surgery is considered and to get an estimate of how much the patient’s voice can be improved without surgery.

We cannot ignore the contribution of spontaneous nerve regeneration in improvement of voice. There are no data available to prove that voice therapy speeds the rate of recovery or otherwise affects the recovery course in those patients with idiopathic paralysis. Certainly voice therapy cannot claim to restore nerve function. Nevertheless, we are strong advocates for initiating a course of voice therapy as soon as the paralysis is diagnosed. It is our belief that through voice therapy patients learn to use the mechanism to the best of its capability without adopting maladaptive compensatory behaviours. Thus, as spontaneous recovery occurs, they are able to gain greatest benefit from it through the manner of voice production they have been taught. A course of voice therapy in most settings today does not exceed weekly sessions for a 6–8 week period. The course of spontaneous recovery may last up to a year. Providing a course of therapy is helpful to patients in knowing that they have exercises they can do and continue to do throughout the ‘waiting period’. Serial measures of vocal function taken over time are extremely important to track progress.

Another benefit of voice therapy for patients with vocal fold paralysis is an educational one. Patients learn about phonation and about the effects of a paralysis on the normal process. They gain an understanding of the nature of their specific problem and have more opportunity to explore and understand the various treatment options. It has been our experience that patients who understand their problem are better able to handle it, have higher motivation for improvement, and have more realistic goals.

The goal of voice therapy, and thus the techniques employed, must be decided on an individual basis. It is well known that when a body part becomes non-functional a variety of compensatory behaviours may arise. This is certainly the case when a vocal fold ceases to function. The classical description of the compensatory behaviour typical of patients with unilateral paralysis is that the remaining intact vocal fold overworks and crosses the midline in an attempt to contact the paralysed, nonmedialized fold. There has been some controversy as to whether this, in fact, takes place. Although we have observed occasional evidence of this behaviour, it does not happen in all cases, and indeed, even when it appears to happen it may not be sufficient to produce an adequate voice. Furthermore, there are numerous other attempted compensatory behaviours that are observed with some frequency and need to be recognized.

Excessive medialization of the ventricular folds – unilaterally on the affected side or bilaterally – is not uncommonly seen. It is not difficult to understand the mechanism for the development of this compensatory behaviour as the individual attempts to modulate the exiting airflow and produce the loudest sound possible. The presence of unilateral ventricular fold medialization does not usually present a problem. However, when seen bilaterally the entire laryngeal mechanism is being ‘squeezed’ in a hyperfunctional posture. This is a maladaptive compensatory behaviour (often referred to as ventricular phonation) producing a voice that is often unpleasant and fatiguing. Furthermore, this pattern can become so habitualized that it may persist even when the true vocal folds are increasingly capable of movement or when a surgical procedure has corrected the glottal incompetence. Thus, when bilateral ventricular fold medialization is observed, the goals of voice therapy should be to eradicate this hyperfunctional behaviour and teach a more gentle form of voice production.

Excessively high airflow and pressure measures are helpful in identifying those patients who are overworking the respiratory system and increasing air pressure in an attempt to better drive the phonatory system. In the absence of the bilateral vocal fold tensions and activity required to close the glottis and resist airflow, the increased pressure serves no useful purpose. Indeed, patients who engage in this behaviour complain of shortness of breath and an inability to speak more than a word or two per breath. This is very fatiguing. In such instances, the goal of voice therapy is to reduce the effort being expended to ‘force’ sound. Usually the resulting voice quality will be improved, the length of utterance capability will also improve and the element of fatigue will be significantly reduced. After this is accomplished the second goal of establishing the best voice of which the patient is capable becomes the focus of therapy.

Occasionally a patient may adopt the use of a high pitch as a compensatory behaviour. The use of a high pitch often results in a louder and clearer voice. Patients who do this have recurrent nerve involvement but the superior laryngeal nerve, which innervates the cricothyroid muscle and is most active in pitch regulation, is intact. When the intact motor units are brought into play, the tension of the vocal fold is increased allowing perhaps for slightly improved adduction and thus a stronger voice. If the ‘new voice’ is acceptable there is no need to suggest a change. However, an excessively high-pitched voice may be irritating and out of character for the individual. In such instances, the focus of voice therapy will be to lower the pitch while maintaining the best acceptable voice.

The most typical observation is incomplete glottal closure without effective compensatory behaviour. The goals of voice therapy are: (1) to help the patient identify the best voice he or she is capable of producing

by exploring effects of pitch change, attending to respiratory dynamics, manipulating head position; (2) to begin to exercise the vocal folds using such activities as pitch extension exercises and trill (lip or tongue); (3) to increase the resonance characteristics of the voice which increases loudness without added laryngeal effort. The traditional ‘pushing techniques’ and effort closure of the glottis techniques should be undertaken with great care. Those techniques usually result in squeezing of all laryngeal structures, as they are incapable of isolating the true vocal folds alone. Thus, they may encourage the maladaptive ventricular phonation or other hyperfunctional behaviours (Casper et al., 1985). If these techniques are to be used, it is recommended that their physiological effect be assessed under endoscopic visualization to ensure that hyperfunction of an unproductive type is not being introduced and reinforced.

A very short course of voice therapy may be indicated for patients who undergo a phonosurgical procedure to ensure that the patient is attaining the best voice possible with the least effort. Despite the changed anatomy, patients may retain learned maladaptive compensatory behaviours or may not adjust phonatory behaviour to the changed structure.

Many of the techniques mentioned in this section and rationales for their use are more fully described in Colton and Casper (1996).

Phonosurgery

The term phonosurgery is used to refer to all of the various surgical techniques that are primarily used to preserve or improve voice (see Chapter 17). This area has been the focus of much research and much growth over the past twenty years with constant improvement in techniques and results. The purpose of phonosurgery in the presence of unilateral vocal fold paralysis is to change the shape and/or position of the paralysed vocal fold, bringing it to the midline. There are two goals in doing this, i.e. to improve voice by allowing the intact vocal fold to come into contact with the impaired vocal fold, and to improve swallowing function by the same mechanism that provides greater protection of the airway. Injection procedures that augment the size of the affected fold or framework surgical procedures that either augment by surgical technique or surgically move the affected fold medially, or a combination of both, may attain these goals.

Intrafold injection procedures

These procedures began to be performed regularly in the 1970s with the reporting of intracordal injection of Teflon in 135 patients by Dedo et al. (1973). The use of Teflon has since gone out of favour because it has been

shown to result in foreign body reactions with formation of Teflon granulomas. Teflon hardens, interfering with vocal fold vibratory behaviour and it tends to migrate, altering its position within the fold and moving to adjacent structures. However, there are several other materials that have been used to ‘bulk up’ the vocal fold: silicone, collagen, autologous fat and Gore-Tex (Wexler et al., 1989; Ford et al., 1992a). Gelfoam is another material that is used, but primarily for purposes of temporary augmentation of the vocal fold, as it is a substance that dissolves spontaneously over a relatively short period of time. The materials most commonly used at present are autologous fat (Shaw et al., 1997) and autologous collagen. Both substances may be partially resorbed following injection, sometimes requiring repeated procedures. The method of managing these materials is constantly undergoing study and improvement in anticipation of a more predictable and stable outcome. The use of Gore-Tex is relatively recent, with no long-term reports available at this time relative to its efficacy.

Intrafold injection is used most commonly to correct the glottal incompetence that results from unilateral paralysis. However, it is also used for vocal fold bowing, to correct sulcus vocalis defects or those caused by other surgery, trauma or scar tissue.

There are various methods of injection. Transoral injection using indirect laryngeal mirror visualization is possible with selected patients. The patient is seated in an examination chair and following topical anaesthetization of the laryngeal and pharyngeal mucosa, a curved needle is used to administer the substance into the fold. Visual and auditory monitoring is possible as the injection proceeds. Transoral injection under direct laryngoscopic visualization using a microscope requires at least the use of local anaesthesia. If this is possible, auditory monitoring of vocal changes during the procedure is possible. However, general anaesthesia may be required, which eliminates the possibility of auditory monitoring of the voice. Transcutaneous injection through the cricothyroid space requires that the patient is supine and progress can be monitored visually via a flexible nasendoscope and auditorily as well. Flint and Cummings (1998) describe a ‘lateral percutaneous approach through the thyroid ala at the level of the vocal fold’ (p. 2075).

For correction of glottal incompetence due to paralysis, the material is injected lateral to the thyroarytenoid muscle and/or in the space between the thyroid lamina and the thyroarytenoid muscle. Fat is injected into the thyroarytenoid muscle. It is essential that the material not be injected into the mucosa overlying the vocal fold. The mucosa of the vocal fold must maintain its elasticity in order to ensure that vibratory behaviour will occur. The search is ongoing for a substance that will match the viscosity of the material in the normal vocal fold so that the resulting voice will be

improved. Although these procedures correct the glottal defect, they do not necessarily restore ‘normal’ or pre-paralysis voice.

Laryngeal framework surgery

There are a number of framework surgeries that are done for various reasons. The particular ones that are appropriate for correction of vocal fold paralysis are those that medialize the affected fold.

The Isshiki Type 1 thyroplasty (Isshiki et al., 1975) is the most commonly performed procedure and one demonstrated to be effective in reducing glottal incompetence (Sasaki et al., 1990; Ford et al., 1992b; Gray et al., 1992; LaBlance and Maves, 1993; Netterville et al., 1993; Leder and Sasaki, 1994; Kieff and Zeitels, 1996). This procedure, performed externally through the neck, requires that the patient be able to respond and vocalize during the procedure. Thus, it is carried out under local anaesthesia with sedation. A window is prepared in the thyroid lamina lateral to the vocal fold through which a synthetic prosthesis (often a silicone wedge) is inserted, medializing and supporting the paralysed vocal fold. This procedure has several advantages including:

1.the ability to be performed under local anaesthesia;

2.preservation of the structural integrity of the vocal fold;

3.the individualization possible in customizing prosthesis size;

4.the reversibility of the procedure;

5.the minimal morbidity associated with it intraand postoperatively;

6.the relative immediacy of the result;

7.the benefits that extend beyond voice to swallowing function, reduction of dyspnea and improvement of pulmonary toilet in sick patients allowing them to generate an improved cough.

Arytenoid adduction is another medialization procedure that can be done in conjunction with a Type 1 thyroplasty, or as a secondary procedure if the benefits of the initial thyroplasty were limited (Isshiki et al., 1978; Slavit and Maragos, 1994). It can also be done following intrafold injection, again to improve further on glottal closure and thus on voice production. The thyroplasty and injection medialization techniques are often incapable of providing adequate posterior glottic closure or in addressing differences in vertical level of the folds. In addition to improving posterior glottal closure, it is claimed that this procedure also makes it possible to adjust the vertical height of the paralysed fold and its length. However, Zeitels et al. (1998) have introduced a new procedure, adduction arytenopexy, in which the arytenoid is affixed on the cricoid facet. In animal studies and then in a series of patients this procedure resulted in a

consistently significant increase in vocal fold length (2.1 mm) and a more normally contoured arytenoid in an optimal position for posterior glottal closure. Preand postsurgical comparisons of vocal function measures revealed improvement in all parameters following this procedure. These types of surgical refinements continue to improve the final vocal result for the patient.

Reinnervation techniques

The intent of these techniques is to correct the neuromuscular deficit by implanting adjacent functioning muscles. Tucker (1978), who is their primary proponent, provides the best description of these techniques. The techniques have not met with widespread acceptance or use.

Future direction

Neurolaryngology, an emerging field of increased research and interest, will probably provide improved understanding of vocal fold paralysis and improved methods for its treatment. We are just beginning to learn about the possibilities of electrical laryngeal pacing via implantable electrodes (Zealear et al., 1996). This holds much promise for future development.

Bilateral vocal fold paralysis

Bilateral impairment of vocal fold movement is much less prevalent than unilateral impairment. Improved surgical procedures for conditions affecting the thyroid and reduction in the need for that surgery due to improved medical treatment have reduced the frequency with which damage is iatrogenically done to the recurrent laryngeal nerve. Societal changes, on the other hand, have been responsible for increased incidence of laryngeal trauma as a result of mechanical injuries and perhaps injuries from violent confrontations. These types of trauma may result in bilateral vocal fold involvement. Increased survival of patients who suffer major head and neck traumas may also increase the numbers of patients seen with vocal fold paralysis, either unilateral or bilateral. Prolonged intubation often results in laryngeal trauma, with vocal fold immobility not an uncommon sequela. The cause of the immobility, whether dislocation of the arytenoids or posterior glottic scarring or paralysis, often presents a diagnostic challenge. Certain neurologic diseases may present with laryngeal findings. The presence of bilateral vocal fold paralysis in Shy-Drager syndrome and multiple system atrophy, for example, has been recognized as an early finding in some patients with these diseases, although still often overlooked (Williams et al., 1979; Wu et al., 1996; Hughes et al., 1998). Lack of recognition of the problem can be life threatening.

Bilateral impairment may involve both abductor and adductor function, with one or the other being predominant. When the impairment is primarily of the adductor type the patient’s voice will be very weak and breathy, respiration will be unimpaired, but aspiration may be the most serious concern. Due to the potentially life-threatening concerns of intractable aspiration these patients require early intervention. Pou et al. (1998) report that of the patients they studied who presented with aspiration following high vagal injuries, 94% experienced improvement following medialization procedures, 79% who had required tracheotomy were decannulated and 90% were found to have subjective improvement in voice postoperatively. However, when the medialization procedures are not successful other surgical procedures may be required. In some instances patients have required total laryngectomy which is very effective in preventing aspiration but results in the loss of laryngeal function for voice production.

When abductor impairment is predominant, the vocal folds remain in a midline-adducted posture resulting in restriction of the airway, but good vocal function and no aspiration. Airway needs are of primary concern. The treatment for this condition is problematic. A tracheotomy may be required to provide an adequate airway while maintaining voicing capability by occluding the stoma. Phonosurgical procedures designed to improve the airway are somewhat successful in doing so, but often at the expense of the voice. Many of the procedures are surgically difficult and result in other problems. However, a laser cordotomy procedure described by Dennis and Kashima (1989) and Kashima (1991) holds promise. The procedure creates a wedge-shaped widening of the posterior glottis which adequately increases airway yet minimizes the dysphonia. Arytenoidectomy is another surgical option. There are reports on nerve anastamosis as a means of repairing the recurrent laryngeal nerve (Crumley, 1990) and also on proposed muscle transfer, specifically phrenic omohyoid transfer (Crumley, 1991), as a means of restoring abductory function. These procedures may hold promise for future development but have not been widely adopted.

Summary

Unilateral vocal fold paralysis is not, in and of itself, a life-threatening disability. However, we have come to understand that the impact of disease is not only physical, but also emotional, social and vocational. Smith et al. (1998b) studied three groups, patients with spasmodic dysphonia, patients with vocal fold paralysis and a control group, to determine what effect the voice disorder had on self–image and on work life

demands. Of the group with vocal fold paralysis, 65% reported that their dysphonia had a moderately severe effect on their ability to advance in their careers and on future job options. Individuals reported a loss of selfesteem associated with their inability to perform up to expectations on the job. More than 50% of the vocal fold paralysis group reported moderate to extreme problems in communication particularly in noisy situations and on the phone.

Although we may have anticipated these results and understood them intuitively, the data validate the concerns and support the need for all forms of rehabilitation and treatment for these patients. An acceptable voice is a necessity in our society that is so heavily dependent on communication. As has been discussed in this chapter, the effects of the dysphonia that results from vocal fold paralysis can be treated effectively in a number of ways to restore acceptable vocal function. It is imperative therefore, that patients be examined early in thc course of the problem, that they receive a complete and appropriate examination, that the diagnosis be correct and that an appropriate treatment course be initiated.

only occasionally by more normal voicing. The listener is also aware of the effort that the patient is putting into forcing voice through a restricted glottis. These vocal symptoms are often accompanied by visible signs of struggle such as grimaces, eye blinking and contraction of thoracic and abdominal muscles. Patients, without exception, confirm the effort and fatigue that comes from extended speaking (Stoicheff, 1991).

Background

The condition was first described by Traube, in 1871, who suggested that spasmodic dysphonia was an hysterical illness. Others also regarded it as a hysterical conversion disorder (Heaver, 1959; Bloch,1965; Brodnitz, 1976). For over fifty years it was viewed by many as a psychiatric disorder (Beck, 1918; Berendes, 1938; Heaver, 1959; Bloch, 1965; Kiml, 1965; Brodnitz, 1976). A physical cause of SD was first proposed in 1874 and 1885 by Schnitzler (1885) who described two patients with ‘cramping of the vocal cords and forced voice’. These patients were noted to have synkinesis of the facial muscles and abnormal movements of the arms and legs. Schnitzler called the entity ‘spastic aphonia’. Gowers (1893) saw the condition as a functional laryngeal spasm, whereby the vocal cords were brought together too forcibly while speaking. In 1939 Critchley, a neurologist, described two patients with a vocal disorder who had neurological signs and concluded that the site of the pathology was likely to be the cerebellum or the basal ganglia. The vocal disorder was then described by Critchley as ‘inspiratory speech’.

Current thoughts

Critchley’s observation influenced the search for an organic cause for SD. Neurophysiological investigations have demonstrated some evidence for a neurological basis for the disorder. These have included abnormal electroencephalograms(EEG)(Robe et al., 1960), abnormal responses to vagal stimuli (Feldman et al., 1984), altered evoked potentials (Shaefer et al., 1983; Finitzo and Freeman, 1989), hypersensitive blink reflex (Cohen et al., 1989) and deviant vocal reaction times (Reich and Till, 1983; Ludlow et al., 1987).

Redefinition of SD

More recent studies of spasmodic dysphonia have linked SD with dystonia. Oppenheim (1911) introduced the term dystonia to indicate that muscle tone was hypertonic on one occasion and in tonic spasm on another, usually, but not exclusively elicited upon volitional movements. It was the association of SD with Meige’s syndrome which led to the disorder