5.2.1 Introduction

In recent decades, voice has assumed an important role in occupational activities. According to some studies, about one-third of the workforce relies on the voice to perform the job (Carding 2007). The increasing role of verbal communication in developing society and the heavy vocal demands associated with particular professions induce the growing risk of occupational voice disorders having a serious impact on working ability (Dejonckere 2001; Vilkman 2004; Niebudek-Bogusz and Sliwinska-Kowalska 2013).

5.2.2 Definition

Occupational voice disorders are work-related self-reported symptoms and clinical signs of dysphonia occurring in subjects whose job demands voice use as a critical aspect of the work.

5.2.3 Epidemiology

Data from the United Kingdom show that more than five million workers are routinely affected by voice impairments at an annual cost of approximately ₤200 million (Carding 2007). It has been suggested that some professional groups, such as teachers, performers and telemarketing staff, are more at risk of developing voice disorders than other voice-demanding professions. Several randomised studies proved that the prevalence of dysphonia is around two to three times higher in teachers than in controls (Roy et al. 2005; Sliwinska-Kowalska et al. 2006). Data from various countries confirm that teaching is an occupation with the greatest risk (de Jong 2010). They indicate that from about 11–38% of the investigated teachers experience current voice problems, but more than 57% of them report at least one occurrence of voice disorders during their life. Additionally, at least one in three teachers claims that teaching has a detrimental effect on his or her voice and they are sometimes even forced to change profession (Roy et al. 2005).

Another emerging group of employees with a high risk of voice disorders is that of call centre industry workers. This group has dramatically grown over the past decade. Approximately 5% of the workforce in the United States works in call centres, compared with an estimated 2% in the EU. The incidence of voice disorders is expected to grow, owing to the highly demanding vocal load in this professional group and work-related stress factors in call centres (Schneider-Stickler et al. 2012). Raising the retirement age of voice professionals is an additional factor that can contribute to the increasing number of cases of occupation-related dysphonia in some EU countries.

Thus occupational dysphonia can not only affect the quality of life and social well-being of employees but also the economic efficiency of companies.

5.2.4 Aetiology and Risk Factors for Occupational Dysphonia

Occupational voice disorders have a multifactorial aetiology. Conditions at work may affect voice, whereas individual-specific factors may influence the employees’ susceptibility to dysphonia.

According to some cross-sectional studies, lifetime vocal load, incorrect techniques of voice production and psychological predispositions constitute the major risk factors for developing occupation-related voice disorders (Sliwinska-Kowalska et al. 2006; Bermudez de Alvear et al. 2010) (see Table 5.2). The individual-specific factors that can contribute to voice disorders are multiple, including frequent infections of the upper respiratory tract, allergies, laryngopharyngeal reflux and hormonal disturbances. Moreover, some studies report a gender predisposition to occupational dysphonia. The glottal cycle dose is much higher in females than in men owing to the nearly doubled fundamental frequency F0. Moreover, the female larynx seems to be more vulnerable (Dejonckere 2001) because of the following physiological differences: (1) being subjected to lifelong hormone-mediated effects, (2) the curving shape of the vocal folds contributing to insufficient glottal closure and to the hourglass-shaped oscillation pattern (characteristic of vocal nodules) and (3) reduced lubrication of the female laryngeal mucosa causing lower levels of hyaluronic acid in mucus secretions, which interferes with vocal fold vibration and decreases resistance to vocal loading. The relation between the above-mentioned factors is complex, and the relative influence of each factor varies among individuals.

5.2.5 Diagnostic Procedures

5.2.6 The Assessment of Vocal Load Effects

A crucial issue in diagnosing occupational dysphonia is the evaluation of the influence of vocal load on the voice apparatus (Hunter and Titze 2009). The evaluation of vocal load effects may be performed by means of the following.

5.2.7 Clinical Aspects of Occupational Voice Disorders

Negative voice adaptation under conditions of chronic vocal load may result in the development of vocal fatigue and, as a consequence, reduced vocal endurance, leading to occupational voice disorders.

Occupational dysphonia may produce multiple voice symptoms, including recurrent or chronic hoarseness, sensation of dry throat or a lump in the pharynx, even pain, dry cough, loss of the singing range, voice tiredness or voicelessness (aphonia).

Types of occupationally determined voice disorder may take the form of:

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  Functional (Non-organic) Dysphonia—the most frequent form of hyperfunctional origin (see also Sect. 5.1); phonation with excessive muscular forces leads to chronic abuse syndrome, inducing vocal fatigue and reduced voice capacity. Phoniatric examination may reveal incorrect type of breathing, excessive neck muscle tension, incorrect resonator activation and ‘hard’ phonation with rough voice, accompanied by abnormal vibration parameters observed by means of videostroboscopy (e.g. diminished amplitude of vocal fold vibration, reduced mucosal wave or glottal sphincter closure with vestibular phonation). Long-lasting functional dysphonia often leads to irreversible laryngeal lesions, frequently of organic type

  
  
• 
  

  Organic Dysphonia—the most common organic outcomes of vocal hyperfunction include vocal nodules, hypertrophy of the vocal folds margin, vascular lesions of the glottis, contact ulcers and asthenia of the internal larynx muscles contributing to glottal insufficiency. Vocal nodules are considered to be the most frequent occupation-related pathology. Vocal nodules are the effect of chronic phono-trauma and occur mostly in females (in adult age), which can be explained by the sex differences described above. These organic lesions are frequently preceded by prenodules—reversible symmetric slight oedema of vocal fold edges, which accompanies functional dysphonia, with muscular tension imbalance and an hourglass-shaped vibration pattern. In cases of the chronic vocal injuries, these oedemas may change into permanent hyalinised fibrous nodules or into epithelial calluses occurring around the free edge of the vocal folds, at the anteroposterior midpoint of the membranous folds. The vocal nodules, typically, are whitish, small, generally bilateral and symmetrical (Fig. 5.1)

Females of older age, particularly teachers suffering from vocal nodules for a long time, particularly with coexisting inflammatory factor can develop polypoid hypertrophy of those lesions (like those presented in Fig. 5.2). Many other vocal fold injuries may occur in connection with chronic phono-trauma. Hypertrophy of the vocal folds secondary to vocal effort often takes the form of benign vocal fold masses, mainly polypoid or fibrovascular changes localised on the edges of the vocal folds. Signs of laryngeal impairment in voice professionals may be associated with other nonoccupational risk factors: e.g. acute laryngitis, LPR (laryngopharyngeal reflux), Reinke’s oedema, sulcus vocalis and leukoplakia. Sometimes in such cases differential diagnosis and the assessment of the main risk factors are not simple.

5.2.8 Differential Diagnosis

The main role is played by videostroboscopic imaging, which enables physicians to detect pathological alterations of the vocal folds that are a consequence of repeated movements and collisions of the vocal folds during chronic vocal overload (Rubin et al. 2014). Different types of benign vocal fold masses (BVFM) located at the vocal fold edge (e.g. nodules, chronic oedema and polypoid hypertrophy) seem especially to be secondary to vocal effort (Fig. 5.3). These pathologies are sometimes unilateral at first but, with the progress of the disease the contralateral fold, can also be affected. Occupation-related vocal fold hypertrophy should be differentiated from Reinke’s oedema, which includes major polypoid corditis changes that are causally associated with cigarette smoking.

Furthermore, the following parameters of the phonatory function should be taken into consideration: (1) the quality of the mucosal wave; (2) the regularity of vocal fold vibrations; (3) the amplitude of the vocal fold movement; and (4) the configuration of glottal closure. It is assumed that slightly insufficient posterior glottal closure should be regarded as normal, particularly in women, while other types of glottal incompleteness are considered pathological. For example, vocal nodules are characterised by hourglass-shaped glottal closure, whereas overload asthenia of the internal larynx muscles displays spindle-shaped glottal closure (Fig. 5.4). This latter voice disorder seems to be related to long-lasting vocal fatigue, which can indicate occupational hazard as a risk factor (European Economic Community Brussels 2003).

5.2.9 Management in Occupational Voice Disorders

Occupation-related voice disorders are becoming a global multifocal health problem, involving social, economic and public health aspects. The prevention and treatment of occupational dysphonia call for improving occupational safety regulations and introducing better health arrangements for professional voice users.

5.3.1 Introduction

Human voice production is accomplished through the perfect coordination of breathing, laryngeal movement and articulation. The movement patterns employed in this process are some of the more complex movements of which the human body is capable.

In general, any dysfunction of the human voice is called dysphonia. According to the underlying complex mechanisms of voice production, there are multiple causes of dysphonia. The cardinal symptom of dysphonia is hoarseness, irrespective of its aetiology. In daily clinical work, a rough classification of organ-related and organ-unrelated dysphonias has proved useful.

Organic voice dysfunctions may have an inflammatory or a traumatic origin. Other causes may be benign or malignant lesions of the vocal cords.

In the latter case, the vocal dysfunction is not a disease of the vocal organ but a symptom of the general disease (Wendler and Seidner 2005).

5.3.2 Special Issues in the Evaluation of Singers’ Voices

For the evaluation of a singer’s voice, it is mandatory for the examiner to be aware that a singer’s larynx may show visible abnormalities or deviations that do not cause any voice impairment.

Structural modifications such as asymmetries, unilateral vocal cord swelling, oedema, polyps, varices, etc. are not unusual in a professional singer’s larynx. Systematic studies in professional singers have shown that these ‘anatomical lesions’ do not necessarily affect tone production or the vocal sound; moreover, no impairment of vocal sound production and sound stability may be perceived either by the singers themselves or by the person listening to them (Traser et al. 2012). For the appropriate classification of stroboscopic images with regard to functional aspects of voice production, the sound quality of the voice, as well as the vocal capacity and singing skills, has to be considered before any decision is made about whether a treatment should be initiated and, especially for singers, what the specific treatment procedures should be.

5.3.3 Singing-Related Disorders

5.3.3.1 Acute Symptoms of Vocal ‘Overuse’

The onset of respiratory infections is often associated with acute symptoms of vocal ‘overuse’. These mostly start with a rhinitic medical condition of viral origin as an ordinary ‘cold’. Young singers in particular lose control of their singing voice when they are affected by a rhinitis. They do not only perceive a change in the sound of vocal consonants, but they also sense a kinaesthetic change.

This kinaesthetic perception is one of the essential feedback systems employed during professional singing (Mürbe et al. 2002, 2004). In the case that this control mechanism is constrained, singers often try to compensate by ‘pressing’ or ‘pushing’ the voice which, in turn, may cause an increase of the subglottal pressure as well as the mechanical strain of the vocal cords (Sundberg 1987; Jiang et al. 2000). This may result in either a swelling at the free edge of the vocal fold, oedema or even bleeding into the vocal folds (see Figs. 5.5 and 5.6).

Such haematomas require special care if acetylsalicylic acid had been taken during the infection, since acetylsalicylic acid, as well as diclofenac, enhances the disposition for bleeding.

When affected by a respiratory infection, those with a high occupational use of the voice—singers and actors—are confronted with the decision whether to sing or speak despite the infection. The answer to this depends on the individual conditions and on the expected vocal strain.

In general, three crucial questions are to be considered for the evaluation of vocal strain:

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  Is the patient hoarse?

  
  
• 
  

  Does the patient show any laryngitic symptoms?

  
  
• 
  

  How good are the patient’s vocal skills?

Singers, irrespective of their experience, should not put any strain on the voice in the case of hoarseness or any signs of inflammation in the laryngeal area. The voice must not be strained under any circumstances when the acute disease comes with hoarseness. If signs and symptoms of laryngitis are proven by an ENT or phoniatrician during careful stroboscopic examination, singers and actors should not perform at all.

A hoarse voice must also not be used for singing in a choir because the auditory sound control is hampered when singing in an ensemble. This so-called Lombard-effect is an impairment of the auditory feedback system during voice production and is due to the increased surrounding noise volume (Lombard 1911). Individuals without special vocal training or experience automatically increase their speaking or singing volume when speaking or singing in surroundings with a noise volume over 70 decibels, as is often the case in a choir. Moreover, when the singing takes place in a choir, onset of hoarseness is not immediately perceived, and, since the affected singer does not want to lose face in front of his choral associates, the singing is often continued despite increasing voice problems.

Highly experienced singers with fully developed singing skills are able to sing even when suffering from an infection—as long as there is no hoarseness or laryngitis. In general, singers have learned to use their voice without increased strain even in the case of altered auditory or kinaesthetic feedback.

5.3.4 Dysfunctions and Diseases Hampering Singing

5.4.1 Lesions of the Lamina Propria of the Vocal Folds

5.4.2 Secondary Pathological Changes of the Vocal Folds and the Larynx

5.4.2.6 Benign Neoplasia

Definition

Benign neoplasia is an uncontrolled propagation of vascular or neural cells. One may also find extracellular deposition of substances leading to vocal fold bulging and dysphonia.

Causes

The causes of benign neoplasia often cannot be determined.

Signs and Symptoms

Neurofibromas are the most common benign laryngeal tumours. They appear very similar to inclusion cysts and rarely cause symptoms. They are much firmer than inclusion cysts (Anderson 2007). Adult haemangiomas may arise from the glottis or the supraglottis. They tend to form uniform submucosal masses.

Treatment

Biopsy is needed for diagnosis, and they can generally be treated with complete surgical excision. Treatment is determined by the severity of dysphonia or airway obstruction (Hoffman et al. 2003). Asymptomatic laryngeal masses with a benign appearance can be observed without a biopsy in most cases.

Prognosis

Benign laryngeal neoplasms are rare and the course of disease cannot be predicted. Usually there is no recurrence after surgical treatment.

Case Study 5.15

A 46-year-old pastry cook who worked formerly as a kindergarten teacher had been suffering from voice impairment for 1.5 year. She is otherwise healthy and takes no medication. The video shows a markedly bulging left vocal fold. Surgery was planned under the suspicion of a laryngocele. However, it turned out to be a solid mass that was histologically diagnosed as a neurofibroma. The speaking voice is a bit higher than normal, the vocal range restricted. The voice sound is moderately hoarse (R2 B2H2).

Case Study 5.16

A 45-year-old pharmaceutical representative had been suffering from reduced vocal capacity and recurring hoarseness for several years. Laryngeal examination revealed a swelling of the right ventricular fold and a small oedema of the right vocal fold margin. Surgery was planned on the suspicion of a laryngeal cyst. However, during the intervention a solid mass was discovered under the surface which turned out to be bulging cartilage. Vocal range is restricted; the voice is mildly hoarse (R1 B1 H1).

Examples of benign lesions of the larynx are shown in Fig. 5.7.

5.5.1 What Is Gastro-oesophageal Reflux?

Gastro-oesophageal reflux (GER) occurs when stomach contents flow back up into the oesophagus. This reflux is a physiological phenomenon with an average of 50 episodes per day, mainly after meals. Gastro-oesophageal reflux disease (GERD) is a more serious, chronic—or long-lasting—form of GER. The backward flow of stomach acid into the oesophagus causes symptoms or oesophageal mucosal lesions. The diagnosis is based on pH monitoring studies. GERD is defined (Richter 2003) by up to 50 reflux episodes below pH 4.0 per day into the oesophagus or a time below pH 4.0 up to 1.5% of the whole time of the monitoring (24 h). Classical symptoms are heartburn (uncomfortable, upward burning feeling in the mid-chest, behind the breastbone), acid regurgitation and foul-smelling eructations. They may be absent in more than half the patients presenting with extra-digestive manifestations (Jaspersen et al. 2003). Other non-typical manifestations may involve the upper aero-digestive tract (hoarseness, cough, throat clearing, globus pharyngeus, laryngeal hyperirritability, laryngospasm, pharyngitis, otitis media, laryngitis, laryngeal pyogenic granuloma, glottal and subglottal stenosis, laryngeal carcinoma) or lungs (asthma, bronchitis, bronchiectasis, aspiration pneumonia, idiopathic fibrosis) (Galli et al. 2006; Balkissoon and Kenn 2012).

Furthermore, heavy reflux may occur with aspiration of much material (mostly during sleep) leading to laryngospasm and threatening and frightening apnoea.

5.5.2 What Is Laryngopharyngeal Reflux?

Laryngopharyngeal reflux (LPR) refers to the backflow of stomach contents into the laryngopharynx. There are numerous synonyms for LPR in the medical literature; the most accepted of these terms is extra-oesophageal reflux.

Koufman (1991, 2002) demonstrated the existence of pharyngeal reflux by a double-probe pH monitoring (oesophageal and pharyngeal) performed on an ambulatory basis over 24 h. Of the 206 otolaryngology patients with GERD undergoing diagnostic pH monitoring, 62% had abnormal oesophageal pH, and 30% demonstrated reflux into the pharynx. Pharyngeal reflux was present in 58% of patients presenting laryngeal symptoms. Its duration was shorter and it arose more frequently in a vertical position. Lower oesophageal sphincter dysfunction and oesophageal motility disorders were frequently suspected. Other studies also support a role for LPR. For example, in patients with resected benign true vocal fold lesions, the prevalence of laryngopharyngeal reflux is higher than that of pathological gastro-oesophageal reflux (Beltsis et al. 2011). The diagnosis of LPR is often missed because symptoms associated classically with reflux, such as dyspepsia and pyrosis, are frequently absent because patients with LPR either do not develop oesophagitis or do not respond to acid reflux with typical symptoms such as heartburn (Ford 2005).

Despite these arguments, controversy exists because of difficulties in making the diagnosis. An LPR event is evident when pH in the proximal sensor abruptly drops to less than 4 during or immediately after distal acid exposure (exposure near the lower oesophageal sphincter). LPR is confirmed when total acid exposure time (percentage of time during 24-h monitoring when the sensor detects pH levels <4) is more than 1% (Kawamura et al. 2004). However, there are no standardised and normative data to consider pathological versus physiological reflux. That is why the most frequently used tools are the reflux finding score (RFS) and the reflux symptom index (RSI) developed by Belafsky et al. (2001b, 2002b). Currently, the two main diagnostic tools are laryngoscopy and reflux monitoring of LPR. On laryngoscopy, the signs most commonly used to diagnose LPR are erythema and oedema of the larynx; however, these signs are not specific for LPR, may be associated with other causes and may even be found in healthy individuals. In addition, pH testing has low sensitivity in diagnosing gastro-oesophageal reflux disease-related laryngeal findings (Abou-Ismail and Vaezi 2011).

By implementation in daily use, most patients may not need examination in the first-line assessment of LPR. These examinations can be reserved for nonresponders, restricting uncontrolled prescription of PPIs (Habermann et al. 2012).

However, disagreement persists regarding optimum diagnostic techniques, criteria of normality and treatment efficacy. Because of a paucity of convincing evidence regarding techniques for establishing a definitive diagnosis and causation in individual patients, and because of a plethora of imperfect studies that have produced conflicting conclusions, LPR diagnosis and management remain controversial (Sataloff et al. 2010; Hawkshaw et al. 2013). For this reason, new approaches are being explored, such as pepsin immunohistochemical staining of the laryngeal mucosal epithelia (Jiang et al. 2011).

5.5.3 Reflux and Larynx

Traditionally, laryngeal abnormalities may be caused by direct injury or by a secondary mechanism. Direct injury is due to contact of acid and pepsin with the laryngeal mucosa, resulting in mucosal damage (Koufman 1991; Delahunty and Cherry 1968; Cherry and Margulies 1968; Lillemoe et al. 1982). Alternatively, irritation of the distal oesophagus by acid may cause a reflex mediated by the vagus nerve , resulting in chronic cough and throat clearing, which may produce traumatic injury to the laryngeal mucosa (Ramet 1994; Sacre and Vandenplas 1989). Recently, some authors have been focusing on the specific molecular aetiopathology of LPR. Researchers have considered that the failure of intrinsic defences in the larynx may cause changes in laryngeal epithelium, such as alterations in carbonic anhydrases and E-cadherin (Wood et al. 2011). Mucin expression also varies according to the severity of reflux. Moreover, they have discovered the presence of H⁺/K⁺-ATPase pumps around the submucosal glands of the human larynx. The lack of carbonic anhydrase in the epithelium of the vocal folds in cases of LPR supports the hypothesis that reflux-related damage mainly affects the glottal area. Finally, pepsin is often found on laryngeal epithelial biopsy and in sputum of patients with pH test-proven GERD and symptoms of LPR. Pepsin, at pH 7, in non-acidic refluxes causes damage by becoming reactivated inside the cell. Inhibitors of peptic activity hold promise as a new therapy for reflux (Wassenaar et al. 2011; Johnston et al. 2010). Further research is required to identify a definitive mechanism for mucosal injury.

For laryngeal disorders, the most recent evidence indicates that LPR represents a complex spectrum of abnormalities. LPR appears to be associated strongly with, or be a significant aetiological cofactor in, about half of these patients (Garrigues et al. 2003). Typical laryngoscopic findings described as diagnostic of reflux in the literature are:

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  Posterior laryngitis (Kamel et al. 1994; Garrigues et al. 2003; Ulualp et al. 1999; Ylitalo et al. 2001)

  
  
• 
  

  Subglottal stenosis (Little et al. 1985)

  
  
• 
  

  Pseudosulcus (see Fig. 5.8a and in comparison sulcus in Fig. 5.8b) and partial effacement or obliteration of the laryngeal ventricle (Belafsky et al. 2002a; Belafsky 2003; Hickson et al. 2001)

These diagnostic criteria combine the type and the localisation of the lesion. They are reported in Table 5.5 by decreasing frequency (Woisard et al. 1996).

Table 5.5

Suggestive laryngeal aspects

On the other hand, oedema of the interarytenoid mucosa seen on endoscopy is related to endoscopic-positive oesophagitis (EE) and is an independent predictor of EE.

Unfortunately, laryngoscopy cannot be considered as a tool determining the diagnosis of reflux because of the poor intra- and inter-assessor agreements of the scores developed to establish the clinical laryngoscopic diagnosis (Sataloff et al. 2010; Branski et al. 2002; Welby-Gieusse et al. 2008). The diagnosis reflux laryngeal disease remains too examiner-dependent.

Moreover, the association of several factors may lead to the apparition of specific laryngeal lesion. For example, mechanical laryngeal trauma and reflux are factors provoking granuloma; reflux and inhaled corticosteroids can promote fungal laryngitis.

According to recent advances, it is assumed that the gastro-oesophageal reflux (GER) is a possible co-promoting factor for squamous cell carcinoma development in the upper parts of the gastrointestinal and respiratory systems, considering the higher frequency of acid-dependent lesions in the population suffering GER. Laryngopharyngeal reflux appears to be an important risk factor in the development of laryngeal carcinoma. Some authors have demonstrated that gastric reflux is an independent risk factor for laryngopharyngeal carcinoma (Ozlugedik et al. 2006; Mercante et al. 2003; Langevin et al. 2013; Coca-Pelaz et al. 2013), while the prevalence of Helicobacter pylori is lower than the prevalence of LPR and is not correlated with the risk of cancer (Cekin et al. 2012).

Finally, reflux dysphonia is possible without posterior laryngitis in laryngoscopy.

5.5.4 Reflux and Voice

GER is a vocal risk factor often entangled with other factors such as stress, poisoning from smoking and vocal overload. It is systematically sought in vocal disorders, but the multifactorial aspect of dysphonia makes difficult the precise determination of the role of each factor. Therefore, if the reality of a causal relationship between the GER and laryngeal symptoms is no longer discussed, highlighting it in clinical practice remains difficult.

The problems of voice affect more than 30% of the population at some period of life. The GER is also a very frequent phenomenon. Its prevalence in adults is from 30 to 40% for one episode at least monthly and from 5 to 10% for a daily episode. Prevalence of the extra-digestive symptoms is estimated at 30% (Jaspersen et al. 2003). Recently, Randhawa et al. (2009) highlighted the risk of masking of GER by other factors, such as allergy and food intolerance, that lead to overestimation of the role of the reflux. Allergy, more specifically allergic rhinitis, affects approximately 24% of the population. These authors note the very high frequency of this effect and the difficulties it presents to highlight causal relations between these various other entities.

Therefore GER and LPR cannot be considered as a disease per se within the framework of ENT manifestations. They act as cofactors and must be integrated into a multifactorial causation with regard to the symptom from which the patient suffers. Richter illustrated this construct (Fig. 5.9) by a pyramid with a decreasing prevalence of the GER in the extra-digestive manifestations. He also suggested that the need for therapeutic tests with omeprazole decreases with the decreasing specificity of the disease for GER.

Thus, in the presence of an ENT manifestation of reflux, the physician has to adopt a holistic approach, analysing the various factors contributing to the emergence of the symptom.

This situation leads to an overdiagnosis of laryngopharyngeal reflux as the cause of hoarseness (Thomas and Zubiaur 2013).

Regarding the treatment, one proposal is to plan empirical anti-reflux treatment according to the reflux index system (RSI) and reflux finding score (RFS). There is no agreement about the modalities of the therapeutic test, but some authors recommend the use of a double dose of a proton pump inhibitor for 3 months.

Proton pump inhibitors (PPIs) are medications that are ubiquitous in a gastroenterologist’s practice.

Their safety among pharmacological agents has been recognised despite the reports of potential adverse effects associated with their use. These potential interactions have ranged from alteration of the absorption of vitamins and minerals, metabolic effects on bone density, alteration of pharmacokinetics/pharmacodynamics and related drug interactions and alterations of intended effect, infection risk to hypersensitivity responses with consequent organ damage (de la Coba et al. 2016).

In the study of Naiboglu et al. (2011), anti-reflux treatment led to significantly reduced laryngopharyngeal symptoms and signs. Longer times of treatment may be needed for complete resolution of symptoms. This method seems to be effective, but the level of proof remains low because of the lack of placebo controls. Therefore, many physicians empirically prescribe reflux medication as a primary therapy, even when symptoms of gastro-oesophageal reflux disease are not present (Ruiz et al. 2014). The current management recommendation for this group of patients is empirical therapy with twice-daily PPIs for 1–3 months. In the majority of those who are unresponsive to such therapy, other causes of laryngeal irritation should be considered. Surgical fundoplication is most effective in those who are responsive to acid-suppressive therapy.

In broad outline, three situations can be met in phoniatric practice with a therapeutic proposal, as communicated here.

First Situation

Dysphonia is associated with suggestive signs of GER, but the reflux is not in the foreground. The medical history may or may not highlight a pyrosis or other digestive symptoms. The laryngeal lesions due to the reflux are limited to an erythema or oedema of the posterior margin (Fig. 5.10) more or less associated with a thickening of the interarytenoid area (Fig. 5.13).

The GER is only retained as an associated risk factor. The main factor may be dysfunctional, psychological or anatomical. The treatment is based on the hygiene and dietary measures associated with a medical treatment according to the degree of posterior inflammation of the larynx. Taking into consideration the GER in case of laryngeal surgery is important and may lead to a preventive treatment before and after the surgery.

Second Situation

GER may be the main aetiological factor of the vocal disorder. It leads to more ‘specific’ lesions. In the absence of other associated irritating factors, chronic laryngitis is observed. It is necessary to look for fungal infection in the presence of an aspect of white lesions such as leukokeratosis laryngitis (Fig. 5.11a, b).

Associated with vocal overload or with closed glottis efforts, the GER promotes contact ulcerations (Fig. 5.12), which cannot heal completely, giving a granuloma (Fig. 5.13). The concomitant association of episodes of pyrosis and closed glottis efforts can provoke painful posterior laryngitis.

Finally, in a context of intubation, reflux favours complications such as granuloma and laryngeal synechia.

Medical treatment is necessary by inhibiting the proton pump. A tri-therapy can be proposed: antacids, prokinetic and antisecretory. It is always associated with the hygiene and dietary measures and with the management of the various associated vocal risk factors, to avoid relapse upon stopping the treatment.

Third Situation

This is very rare and corresponds to an atypical laryngeal lesion in a GER context resistant to the medical treatment and may be an indication for surgery. This is an anterior granuloma or a granulomatous laryngitis (Fig. 5.14). This latter lesion involves the whole larynx and corresponds to an unspecific inflammation seen in the histology. Despite the GER treatment, the treatment remains problematic with questions about its evolution.

Another aspect of the question is the physiological interaction of speech or singing with reflux. Vocal load without singing is probably not an important aetiological factor for laryngopharyngeal reflux. However, the increase of intra-abdominal pressure and stress appears to increase GER in singers (Cammarota et al. 2007), and some authors have described that laryngopharyngeal reflux affects choristers more often than teachers or control subjects without vocal load at work (Hočevar-Boltežar et al. 2012). These results suggest that singing as the main professional activity can notably contribute to the development of the reflux.

5.5.5 Conclusion

It can be assumed that reflux that reaches the larynx can damage it. Because the symptoms possibly related to LPR can be linked to other causes, a careful consideration of the patient’s medical history is of utmost importance, followed by mandatory laryngoscopy. Several laryngeal and vocal risk factors are often present in voice disorders, highlighting a frequent multifactorial context. This level of complexity explains the poor level of scientific proof and why the role of GER remains a ‘myth’ fed by practical clinical observations. The search for the different factors involved and their organisation into a hierarchy allow the determination of a strategy of care, by ranking the various therapeutic options.

Diagnostic procedures, such as the trial administration of proton pump inhibitors or long-term pH measurement, should be used selectively. Depending on the individual symptoms, lifestyle changes, breathing or voice therapy or PPI therapy might be useful.

5.6.1 Introduction

This section focuses on central neurological issues. For further information on the peripheral neurological system, please see Sects. 1.​2 and 5.​7.

In the twenty-first century, voice remains the primary means of human communication, in spite of the massive increase in the use of electronic devices. With the advent of Skype and telemedicine communications, it is the authors’ opinion that an increasing number of currently non-verbal teletextual types of electronic communication will incorporate the human voice owing to the richness of the signal that it includes.

Sound signals are used to communicate intellectual content, linguistic and paralinguistic content and emotional content. There is little doubt that the voice and the vocal tract are interlinked to emotions and feelings. It is a common experience that the phone will ring, the listener will hear a sound (that is frequently frequency-limited) and within a matter of moments, even if the speaker has not been heard from in many months or years, the listener will be able to both recognise the listener, the paralinguistic as well as the linguistic message, and respond. This response may well be influenced by a sudden change in the listener’s autonomic system as well as central nervous system. How can this occur?

In an attempt to respond to the question posed above, we need to go back to basics. The brain has approximately 100 billion neurons. These include nerve cells and glial (support) cells. The neurons, in essence, act as ‘on-off’ switches. When ‘on’ they transmit nerve signals-electrical signals/current. Neurons are made up of a cell body (soma), nucleus, dendrites (that can branch multiple times and communicate with other cells) and axons (that can be very long (metres)). Synapses connect the neurons; they are found between somas and dendrites of nerve fibres or axonal terminals. Each neuron has between 1000 and 10,000 synapses. When an action potential reaches a synapse, it triggers the release of tiny amounts (quanta) of neurotransmitter causing depolarisation of the postsynaptic region. There are hundreds of neurotransmitters, both excitatory and inhibitory. Well-known ones include dopamine, serotonin, acetylcholine, noradrenaline and gamma aminobutyric acid (GABA). Whether or not an action potential is generated in the target neuron will depend on a variety of factors, including the integration and summation of inhibitory and excitatory synaptic inputs to that cell. Thus the heart of neural function is part electrical part chemical.

Information tends to reach the brain via neural networks. A typical, rather simple, but powerful neural network is that of the laryngeal adductor reflex. As an example, imagine that the readers were eating crisps at the time they were reading this section and a crisp accidently irritated one side of the epiglottis or lateral pharyngeal wall. This irritation would elicit neurons to fire, via the internal branch of the superior laryngeal nerve, and neural activity will go up to the nodose ganglion and then to the ipsilateral nucleus tractus solitarius. At this point there would be interneural connections to both nucleus ambiguus. This would effect a bilateral motor response to the internal laryngeal muscles with a resultant glottal closure reflex. This reflex arc is very fast, the conduction velocity in the extracranial nerves being approximately 60 m/s, leading to a glottal closure response in less than 60 ms from the stimulating event. Had the stimulating event been at the glottis or subglottal level, the effector would have been via the recurrent rather than the superior laryngeal nerve.

The surface of the brain is grey-brown, the colour of the neuronal cell bodies (grey matter) and the neuropil (dendrites and unmyelinated axons). Grey matter regions are typically involved in muscle control and sensory perception. They can be thought of as the Chief Executive Officers and Trustees, performing executive functions of the brain, processing information. Deep to this lie the axon layers with white sheath (myelinated). This is the white matter and can perhaps be thought of as the personal administrators and middle managers—white matter tends to carry information.

Historically the brain was anatomically divided into separate lobes that were functionally distinct, whereby the frontal lobe is involved in speech planning and reason and contains the primary and supplementary motor cortices; the parietal lobe in sensory perception and praxis, with sensory feedback from the body; the temporal lobe with speech perception, some memory and hearing; the occipital lobe with the visual cortex; the cerebellum with movement and balance; and the brainstem with breathing and swallowing. The brain also has two hemispheres connected by the corpus callosum. In general the right hemisphere is said to deal with visual activities. It is more ‘intuitive’ than the left hemisphere and can be thought of as putting information together, grouping it. For example, if a car is viewed, the right hemisphere activity might be to note ‘I recognise that, it is a car’. The left hemisphere is said to be dominant in 95% of the population. It is more analytical than the right hemisphere, analysing the information collected by the right hemisphere. It also tends to deal more with language, understanding and expression.

5.6.2 Language

In terms of language, the left temporal and frontal areas are dominant in 95% of individuals for language. Please see Figs. 1.​47 and 1.​48 in Sect. 1.​2, demonstrating areas active in language on the brain surface (Fig. 1.​47) and functional anatomy of language processing (Fig. 1.​48). The right side is somewhat equivalent for environmental noise, spatial skills and prosody (Nasreddine et al. 1999). Wernicke’s area is one of the two parts of the cerebral cortex that have been linked to speech since the nineteenth century. It is located in the posterior section of the superior temporal gyrus in the left (or dominant) cerebral hemisphere and encircles the auditory cortex on the Sylvian fissure. It is neuroanatomically described as being in the posterior part of Brodmann’s area (BA 22). Wernicke’s area is the site that on functional MRI studies is most consistently implicated in understanding of written and spoken language/word recognition (DeWitt and Rauschecker 2012). Broca’s area is the other classically recognised speech-related area. It is a region of the frontal lobe of the left hemisphere usually identified as the pars opercularis and pars triangularis of the inferior frontal gyrus, neuroanatomically as Brodmann’s area 44 and 45 (BA 44, 45). It abuts on and instructs the motor cortex regarding articulation and speech.

Previously it was believed that information passed from Wernicke’s to Broca’s area through the arcuate fasciculus, a band of white matter deep to the supramarginal gyrus connecting both language areas, but this is in dispute. Broca’s area initiates a motor plan that is transmitted to the primary motor cortex (Brodmann’s area 4) to pronounce the words. The motor cortex, in coordination with the supplementary motor area, basal ganglia and cerebellum, sends corticobulbar fibres to implement speech sounds (Nasreddine et al. 1999). More recent functional imaging has supported a larger range of processing areas for speech reception and language processing, and the last word has certainly not been written on this subject (Newman et al. 2010).

According to Jürgens and colleagues, in many mammals there is a visceromotor subcortical network of brain regions dedicated to phonatory species-specific calls. In a sense the peri-acqueductal grey can be considered at the core, regulating neurons of the lower brainstem via the reticular formation from the lateral pontomedullary- and limbic-related regions. There are cortical laryngeal projections from the anterior cingulate gyrus (Jürgens 2002a, b, 2009). In humans, some aspects of emotive voicing exploit this older pathway. However, for linguistic and paralinguistic speech, there are more direct corticobulbar projections to the reticular formation in effect bypassing the limbic system. Temporal lobe activity is critical for auditory self-regulation. The time from a thought to sound is approximately 130 ms.

In the mammalian brainstem the nucleus ambiguus and retroambiguus are of particular importance from an effector standpoint for laryngeal and expiratory muscle control. The midbrain and cerebellum are substantially involved in feedback and timing (Benninger et al. 2006; Jürgens 2002a, b, 2009; Kuypers 1958).

5.6.3 Neurolaryngology History-Taking

History taking in neurological voice disorders is of paramount importance (Woodson 2008). Temporal development of the disorder, symptom description, associated features, handedness, associated intercurrent or past medical disease, past psychiatric history and family history have all been highlighted as integral to the neurological history (Nasreddine et al. 1999). We also feel that emphasis should be placed on aspects relating to the psychosocial history, as this is often the key to successful management and rehabilitation.

Vocal fatigue, vocal weakness, pain when speaking, increased effort relating to speech, glottal tightness, pitch breaks and tremor all point towards a neurological cause of the disorder (Woodson 2008). Changes in normal vocal quality (strain/strangle, harshness), vocal effort (range, breathiness, fatigue), vocal pitch (monopitch, loss of stability of pitch with yodelling or pitch breaks, etc.) and vocal tremor should all be ascertained and may point to problems at the level of the vocal folds. Speech-related problems such as articulatory issues, slurred or unintelligible speech, velopharyngeal insufficiency with hypernasality point towards bulbar or suprabulbar pathology. Woodson (2008) notes that hoarseness in isolation is far less likely to point to a neurological cause than when associated with dysphagia. Again the history is crucial.

5.6.4 The Clinical Examination: General

When evaluating a patient with a suspected neurological voice (or swallow) disorder, the patient will often come in with the diagnosis already substantiated. None the less, the first assessment by the ENT surgeon/phoniatrician should be global rather than ENT-specific; otherwise it is easy to miss a critical clue to diagnosis and management. In particular affect, gait, posture and coordination, movement (spontaneous, tremor, etc.), reflexes and tone all need reviewing, before the more-focused ENT/phoniatric examination. Let us review these.

As part of the ENT/phoniatric examination all of the cranial nerves should be tested. The ears should be examined to make certain that cerumen impaction or middle ear pathology is not impacting upon the patient’s ability to hear. ‘Glue’ ear may also be indicative of pathology of the Eustachian tube, post nasal space, nose or the soft palate. The mouth and oropharynx are of particular importance as many patients with neurological disorders present with dysarthrophonia. The lips should be evaluated for adequate ability to seal the tongue for fasciculations (often a sign of neurodegenerative pathology such as motor neuron disease) and for fullness of movement. Skull base lesions could lead to hypoglossal nerve (XII cranial nerve) dysfunction. Subtle tongue dysfunction, particularly after repeated movement could ‘unmask’ a neuromuscular junction pathology such as myasthenia gravis. Tongue dysfunction is a not infrequent sequela of stroke. The soft palate should be looked at for evidence of clonus (such as seen in myoclonus). Assessment of voluntary function is also necessary. Loss of such function is not uncommon in stroke or severe head injury and can be associated with velopharyngeal dysfunction as well as speech issues. Soft palate, tongue and facial muscle problems can lead to dysphagia as well as speech disorders.

The key ENT/phoniatric examination in anyone suspected of neurological voice, speech or swallow disturbance is flexible nasendoscopy, preferably in combination with stroboscopy (Woodson et al. 1991). En route to the larynx the nose, post nasal space and soft palate can be comprehensively studied for altered anatomical and physiological function. The degree of closure of the soft palate against Passavant’s ridge can be assessed and the integrity of the velum confirmed.

The larynx should be observed at rest as well as in function. At rest, clonic or other spontaneous activity can be looked for. In function, gentle adduction, sphincteric closure, cough, quiet breathing and vigorous abduction are all reviewed. The larynx is ‘stressed’ by repeated counting and repeated ‘e-sniff’ manoeuvres. This permits the examiner to look for laryngeal muscular fatigue or incompetence or both related to work, a sign of neuromuscular junction pathology. Asymmetry of abduction or adduction over time may be a subtle sign for vocal fold paralysis or paresis. General laryngeal incoordination may be a sign of suprabulbar pathology. The use of stroboscopy allows routine qualitative assessment. Of particular importance from the standpoint of management is identification of bowing or incompetent valving/closure of the glottis. This can be addressed with speech therapy intervention or surgical augmentation.

Laryngeal EMG is of great importance. It can help determine if functional recovery is feasible or if there is ongoing neuronal degeneration. It can also assist in determining which nerves have been injured. In certain forms of myopathy and motor neuron disorders, it can be diagnostic. If botulinum toxin is being considered for a spastic or spasmodic condition, EMG will assist the surgeon in locating the tip of the injecting needle (Sulica et al. 2006; Blitzer et al. 1985; Brin et al. 1992).

5.6.5 Neurological Speech and Voice Disorder Terms

As we begin to discuss specific disorders, certain terms are helpful. Dysphasia or aphasia is a partial or complete impairment of the ability to communicate, resulting from brain injury, usually brought on by damage to the cortex. Aphasia types include, amongst others, expressive aphasia, receptive aphasia, conduction aphasia, anomic aphasia, global aphasia and primary progressive aphasias. In essence expressive (Broca’s) aphasia is associated with the expressive difficulty in word finding and putting words together. Patients with expressive aphasia have lesions to the medial insular cortex (Dronkers et al. 2007; Masdeu 2000). Receptive (Wernicke’s/sensory) aphasia is associated with the inability to comprehend meanings. It is associated with damage to the medial temporal lobe and underlying white matter (Kolb et al. 2003).

Verbal apraxia or dyspraxia is an oro-motor speech disorder characterised by the inability to speak correctly and consistently. It is not due to weakness or paralysis of the speech musculature individually; conversely, it affects the purposeful control of the movements necessary for speech. Verbal dyspraxia may occur in children, and thus it is also known as developmental articulatory dyspraxia.

Ataxia is loss of muscular coordination. Ataxia-phasia is the inability to form connected sentences—only single intelligible words. Dysarthria signifies a disturbance of articulation generally due to paralysis, incoordination or spasticity of the muscles used for creating spoken language. Dysarthrophonia is a speech dysfunction that affects respiration, phonation, articulation and prosody of speech.

5.6.6 Clinical Approach

In our Neurological Voice Clinic at the National Hospital for Neurology and Neurosurgery, we find it helpful to consider voice disorders from the standpoint of their effects at the level of the larynx (and speech disorders from the standpoint of their effects on the vocal tract especially the articulators). To that end we use a modified version of the Ramig classification (Smith and Ramig 2006). From a laryngeal standpoint, we look at vocal fold adduction/abduction. In this portion of the section, we shall focus on certain disorders with hypo-adduction, hyper-adduction and mal-adduction.

5.6.7 Summary

This section has reviewed central neurological disorders. It introduced the subject by reviewing some basic aspects of brain function and of language. It then presented the neuro-laryngological history and physical examination, emphasising ENT/phoniatric manifestations.

Specific central neurological disorders were then described, using the context of the effect at a voice (laryngeal) level and speech (articulatory) level. Parkinson’s disease, closed head trauma, motor neuron disease, spasmodic dysphonia and tremor were reviewed in some detail.

5.7.1 Introduction

Physiological positions of vocal folds are ‘median’ during phonation and ‘lateral’ during respiration. In cases of vocal fold paralysis, the impaired adduction and abduction of vocal folds lead to different positions between ‘median’ and ‘lateral’.

For the majority of textbooks, vocal fold mobility impairments are classified by their ‘paramedian’ or ‘intermediate’ position. Additionally ‘cadaveric’ positions are described with a bowed vocal fold in a most lateral position.

This common classification does not consider further variables (e.g. time course, functional deficits) and does not entirely meet the high variability of laryngoscopic and videostroboscopic findings.

Paralyses have to be identified and characterised in order to indicate necessary diagnostics and to arrange obligatory or facultative therapies. Therefore the knowledge of laryngeal innervation, possible reasons for their dysfunction and options for recreation or rehabilitation are essential.

This section will give the anatomical and physiological background and intends to be a useful guide for clinical tasks.

5.7.2 Brief Historical Review

Because a historical review is not common in textbooks, I would like to offer this to interested readers. There is an ongoing discussion about laryngeal innervation, and the readers’ own clinical experience can be compared with current theories and classifications.

Since the first studies of vocal fold paralyses (Gerhardt 1863), the aim was to conclude the site of nerve lesion from the position of paralysed vocal folds. ‘Semon’s law’ (Clerf and Baltzell 1953) and the ‘Wagner-Grossmann-Theory’ (Grossmann 1897) have to be mentioned first in this context. Early contradictory publications came from Lemére (1933), Clerf and Baltzell (1953) and Tschiassny (1957) who suspected that different affected nerve branches were responsible for vocal fold position. More recent publications from Crumley (1989), Sanders et al. (1994), Sanudo et al. (1999) and Olthoff et al. (2007) have illustrated an ongoing discussion about the laryngeal motoric system.

Trying to incorporate all different kinds of vocal fold impairment under the generic term ‘paralysis of the recurrent nerve’ implies an indissoluble problem: in our human motoric system, competing abductors and adductors (e.g. flexors and tensors in our extremities) are innervated by different nerves. Transferring this fact to the laryngeal motoric system, the only opener of the larynx (the posterior cricoarytenoid muscle) should have an exclusive innervation. Hence, the recurrent laryngeal nerve must be ‘more than one’ and needs further analysis to reveal whether at least separated fibres allow the innervation of antagonistic muscles. The different theories that were intended to show separate innervation of laryngeal adductors and the sole abductor will be briefly highlighted.

The main intent of all authors has been to interpret the cause of ‘paramedian’ positions of paralysed vocal folds. Semon (Clerf and Baltzell 1953) found a separation of the recurrent laryngeal nerve into abductor and adductor fibres and stated that a higher vulnerability of abductor fibres led to ‘paramedian’ vocal fold positions. In case of recurrent laryngeal nerve lesion, Wagner-Grossmann (Grossmann 1897) defined the external branch of the superior laryngeal nerve as the only competing nerve that enables a ‘paramedian’ vocal fold position resulting from the exclusive innervation of the adductory cricothyroid muscle. Even though this theory was rejected by other authors (Woodson 1993; Koufman et al. 1995), it became consensus in the European literature. Lemére (1933) supported Semon’s aspect of fibre separation, and later Miehlke et al. (1973) used this aspect for reinnervation procedures. Lemére (1933) additionally suspected that the only unpaired muscle of the larynx, the interarytenoid muscle, was responsible for ‘paramedian’ findings owing to its adductor competence and bilateral innervation. The unaffected opposite nerve could cause the adduction and paramedian position. To explain bilateral ‘paramedian’ paralyses, Clerf and Baltzell (1953) and Tschiassny (1957) implicated motoric fibres in the internal branch of the superior laryngeal nerve that run to the interarytenoid muscle. In case of recurrent laryngeal nerve lesion, the preserved adductory fibres from the superior laryngeal nerve would lead to bilateral ‘paramedian’ vocal fold positions. This theory was supported later from Sanders et al. (1994) who visualised these fibres with a special staining technique. The existence of motoric fibres in internal branches that run into the interarytenoid muscle could not be proved by histochemical analyses (Olthoff and Ehrlich 2010). Lemére (1933) and Rueger (1972) demonstrated these fibres running through the interarytenoid muscle without motoric but with sensory endings in the laryngeal mucosa. Other studies with retrograde tracers also proved that fibres from the internal branch of the superior laryngeal nerve run to the posterior cricoarytenoid muscle with motoric projection to the rostral ambiguous nucleus. A collateral reinnervation and neuromuscular sprouting of these fibres in the case of recurrent laryngeal nerve lesions were interpreted as evidence for motoric reinnervation (Hydman and Mattsson 2008).

Apart from vagal innervation and all mentioned laryngeal muscles, Réthi (1952) described a ‘stylopharyngeal muscle system’ in order to interpret ventricular phonation and dystonic voice disorders. The involved stylopharyngeal muscle is innervated from the glossopharyngeal nerve, and its insertion into the supraglottal area might enable some supraglottal adduction in the case of vagal nerve paralyses.

In later studies the aspect of spontaneous or surgical reinnervation was emphasised as the main reason for ‘paramedian’ vocal fold positions caused by increased adductor muscle tension (Crumley 1989). The fixation of vocal folds was interpreted by concurrent innervation of antagonistic muscles (‘synkinesis’) that causes an ‘autoparalysis’ that was first described for facial innervation (Stennert 1982). But as the regeneration of nerve fibres needs time (several months), the idea of ‘reinnervation’ could not explain immediate bilateral paramedian vocal fold paralysis after thyroid surgery.

More recent macroscopic studies have revealed new findings of very vulnerable recurrent laryngeal nerve fibres running to the posterior cricoarytenoid muscle. These fibres are highly endangered in, for example, thyroid surgery, and their injury is potentially responsible for ‘paramedian’ paralyses (Olthoff et al. 2007). Additionally, a branch that runs from the external branch of the superior laryngeal nerve into the endolarynx might support a ‘paramedian’ vocal fold position and may redirect the discussion of the ‘Wagner-Grossmann-Theory’ (Wu et al. 1994; Olthoff et al. 2007).

As an ‘up-to-date hypothesis’, we could state that synkinesis will be crucial for paramedian vocal fold positions in paralyses older than 3–6 months.

Paramedian vocal fold positions in earlier stages will be caused by injuries of abductor fibres owing to incomplete lesions of the recurrent trunk fibres. In incomplete lesions the superior number of adductor fibres will cause paramedian positions.

Thus, a paramedian vocal fold position is based on an imbalance between adductor and abductor muscle activities for the reasons above. A more lateral (‘intermediate’) position will consequently indicate an additional lesion of adductor fibres or refer to a more complete lesion of the recurrent trunk.

This knowledge was the basis for the current advantage in laryngeal pacing. The first target of stimulation was the laryngeal abductor muscle (posterior cricoarytenoid muscle) to free patients with bilateral paramedian vocal fold paralysis from dyspnoea (Li et al. 2013). Because the bilateral paramedian vocal folds’ position implies imbalanced adductor muscle activity, the stimulation of the laryngeal opener tends to restore the muscular balance.

5.7.3 Anatomy and Physiology

The efferent laryngeal vagal nerve fibres (cranial nerve X) derive from the nucleus ambiguus and run together with fibres from the spinal nuclei of the accessory nerve (cranial nerve XI) through the jugular foramen. Afferent laryngeal fibres run back to the nuclei of the solitary tract (Sasaki et al. 2001). Because muscle spindles are proven to be in laryngeal muscles (Baken and Noback 1971; Malannino 1974; Tellis et al. 2004), a reflex motoric system can be stated following the general principles of our human motoric system. Afferent proprioceptive fibres will run with the internal branch of the superior laryngeal nerve (Lemére 1933; Sanudo et al. 1999; Sasaki et al. 2001).

Owing to the cortical representation of laryngeal muscles, functional magnetic resonance imaging techniques have given new insights and revealed a more medial area than traditionally known from Penfield’s ‘homunculus’ (Olthoff et al. 2008; Brown et al. 2008). The site is located adjacent to the lateral hand area. Transcranial magnetic stimulations were optimal in the same site and confirmed these findings (Rödel et al. 2004) (Fig. 5.15).

5.7.4 Laryngeal Innervation

After passage of the jugular foramen the superior laryngeal nerve separates from the vagus nerve and sends one internal sensoric branch through the hyothyroid membrane into the larynx and one external motoric branch to the cricothyroid muscle. Deriving from the external nerve, a branch runs into the larynx that was first called ‘communicating nerve’ and later ‘ventricular branch’ owing to its course into the ventricular muscle (Wu et al. 1994, Olthoff et al. 2007).

After parting from the vagal nerve, the right recurrent nerve curves around the brachiocephalic trunk, and the left recurrent nerve around the aortic arch, before running upwards to the larynx. The recurrent laryngeal nerves pass close to the trachea and reach the larynx from the rear laterally. Before entering the larynx, the ansa galeni leaves the recurrent nerve and joins the internal branch of the superior laryngeal nerve. Directly before the dorsal entrance into the larynx, very thin and vulnerable fibres leave the recurrent nerve and enter the posterior cricoarytenoid muscle, which is the only opener of the larynx (posticus). These extralaryngeal fibres (Rr. postici) are highly endangered in surgical treatment, such as thyroid surgery, even by just moving the recurrent nerve.

After the laryngeal entrance, and covered by the posterior cricoarytenoid muscle, the posterior ramus runs to the interarytenoid muscle. The anterior ramus supplies the medial and lateral thyroarytenoid and the lateral cricoarytenoid muscle, which are synergistic adductors of the vocal fold (Fig. 5.16). Over the course of more than 100 years, the anatomical nomenclature of the posterior ramus changed in anatomical textbooks. In contrast to our classification that was based on fundamental studies from Lang et al. (1986), the posterior branch is sometimes seen as the branch that turns to the ansa galeni (Mattsson et al. 2015). This fact is mentioned to prevent misunderstandings.

Apart from their vagal innervation, the stylopharyngeal muscles insert bilaterally into the supraglottis and are also innervated from the glossopharyngeal nerve. They are still discussed as supporting the elevation of the larynx during swallowing. Owing to their supraglottal insertion, they might be able to induce some supraglottal adductions.

5.7.5 Laryngeal Motoric System

Except for the posterior cricoarytenoid muscle, every laryngeal muscle tends to narrow the laryngeal lumen. The exclusive opener of the larynx enables an abduction of vocal folds exceeding the cadaveric position that is caused by the elastic laryngeal tissues.

The adduction of vocal and ventricular folds, combined with the approach of the arytenoids against the caudal part of the epiglottis, leads to a complete sphincteric closure of the larynx that is essential for airway protection during swallowing. More differentiated adduction is present in throat clearing, coughing and phonation.

This might explain the presence of various adductors that in concert are able to perform the different adductor tasks. Laryngeal opening is a comparatively simple but essential function. Therefore only one abductor muscle, namely, the posterior cricoarytenoid muscle, proves to be sufficient.

In detail the adductors are the lateral cricoarytenoid muscle, the strongest adductor of the ligaments of the vocal folds, owing to its insertion to the anterior part of the muscular process of the arytenoid cartilage (opposite and antagonistic to the posterior cricoarytenoid muscle, which inserts on the posterior surface). The interarytenoid muscle is responsible for the closure of the cartilaginous part of the glottis by narrowing the arytenoid bodies to the midline. Transverse and oblique fibres work in a synergistic manner (Schiel et al. 2004). The internal and external thyroarytenoid muscles are responsible for the fine-tuning of vocal fold tension. An increased vocal fold tension tends to support adduction. The cricothyroid muscles narrow the cricoid against the thyroid cartilage anteriorly. Owing to the dorsal articulation between both cartilages, this approximation leads to a tension and consequently adductory support of the vocal folds. This effect depends on a sufficient tension of the thyroarytenoid muscles.

The origins and insertions are shown in a figure that serves as a crib using hands and fingers (‘rule of thumb’) (Fig. 5.17).

The above-mentioned ‘stylopharyngeal muscle system’ (Réthi 1952) might enable some supraglottal (ventricular) adductions owing to its insertion, away from all mentioned laryngeal muscles, into the supraglottis.

5.7.6 Laryngeal Tasks and Function

The distinctive feature of the aerodigestive tract is the common use of one anatomical area (the larynx) for two essential but incompatible functions: breathing and swallowing. Even if textbooks, anatomical atlases and clinical diagnostics, such as videofluoroscopies, show sagittal views as the most common aspect of our aerodigestive tract, they give the wrong impression of a digestive hose behind a ventilation tube. For the correct impression, we have to look at the axial view: the airway is combined with and surrounded by our digestive tract. Irrespective of the separation of mouth and nose, the division of our aerodigestive tract starts with the larynx. In newborns we can clearly see the anatomical position of the larynx in the centre of the digestive tract: a high-riding epiglottis, the aryepiglottic folds and the posterior commissure form a protecting ‘tube’ against aspiration. In adults this aspect becomes less explicit, and the protection of our airway depends essentially on an adequate sphincteric closure of glottal and supraglottal structures (described above) (Fig. 5.18).

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