Reasons for immobility of vocal folds
Most frequent reason
Lesion of recurrent nerve
Lesion of vagal nerve
Movement impairment of arytenoid cartilage/cricothyroid joint abnormalities/ankyloses
(Sub)luxation (e.g. after emergency intubation)
Interarytenoid tissue changes (fibrosis)
After trauma or surgery
Interarytenoid mucosal bridge (mucosal and cartilage)
Tumours/scars in surrounding tissue
Hypopharyngeal and/or pharyngeal tumours
Before resection by tumour infiltration
After resection by scar formation
The most common reason is unilateral vocal fold paralysis (ULVFP), predominantly an iatrogenic lesion caused by thyroid surgery as well as by other transcervical surgery approaches or tumour surgery on the neck or upper mediastinum.
The key symptom is postoperative hoarseness with changes of vocal pitch, monotonous intonation, loss of range, voice fatigue, problems with loudness and shortness of breath. Most cases of ULVFP are reversible. Other reasons are movement impairment of arytenoid cartilage, interarytenoid tissue changes and tumours and scars in surrounding tissue.
In a patient population with immobility of the vocal folds (643 unilateral and 184 bilateral), Rosenthal et al.  detected that ULVFI was predominantly caused by surgical iatrogenic injury (Fig. 4.1). The inferior laryngeal nerve was mostly damaged by thyroid surgery. However, other surgical interventions such as carotid endarterectomy or spine surgery were increasing causes of paralysis of the inferior laryngeal nerve. Injuries in the motor cortex could also lead to neurogenic immobility. Additionally, in some cases the recurrent laryngeal nerve was also damaged at the jugular foramen up to the tracheoesophageal groove. However, functional aspects and psychological impairments might also lead to vocal fold immobility.
Characteristic frequencies of the reasons of unilateral vocal fold immobility in retrospective hospital-based data sets
4.1.1 Symptoms of ULVFI
Vocal fold immobility usually becomes symptomatic through acute or gradual onset of hoarseness. Symptoms of unilateral vocal fold movement restrictions vary very heterogeneously and gradually. In vocal fold paresis, however, the voice sounds less breathy in comparison to laryngoscopic findings . Phonatory immobility, different tension and position of the paralyzed vocal fold impair the mucosal wave and lead to a loss of the normal vibration pattern of vocal folds and to roughness and biphonation.
Impaired vocal folds may vibrate at different frequencies, resulting in rough voice as well as biphonation. A falsetto voice frequently develops secondary to remaining innervations of parts of the vocalis and the cricothyroid muscle .
ULVFI with different levels of the vocal folds and/or a glottal gap result in a breathy voice. Additional symptoms are swallowing difficulties or moderate breathing problems. These symptoms are important for differential diagnosis and indicate an underlying neurogenic disease. In unilateral vocal fold paralysis, about 60% of the patients complain of dysphagia and 75% of patients report difficulties in breathing (during speaking and physical activities) . If a tumour is causative for VFI, in most cases the predominate symptom is a rough voice.
Vocal fold scars (Fig. 4.2) lead to hoarseness, an increase in fundamental frequency, a decrease of self-confidence in intonation and control of voice volume and furthermore to voice effort and vocal fatigue. If deeper layers are involved in vocal fold scars and substance is missing, vocal fold mobility may disappear. The voice is nearly aphonic.
Scar of the right aryepiglottic s and the arytenoid region secondary to laser resection of a hypopharyngeal cancer resulting in impairment of the vocal fold mobility. There is a cystic lesion of the right ventricular fold
The distinction between still mobile and totally immobile vocal folds, and between unilateral or bilateral immobility, is of crucial importance because of the impact that these factors have on the possible management of the voice disorder .
4.1.2 Vocal Fold Paresis
Vocal fold paresis is the most common reason for immobility of the vocal folds. It can be complete (paralysis) or incomplete with diminished mobility, uni- or bilateral (more on bilateral immobility and paresis in Chap. 5). Unilateral vocal fold paresis/paralysis becomes postoperatively symptomatic through hoarseness and moderate dyspnea. 25% of patients with unilateral vocal fold paralysis also develop a swallowing disorder in combination with aspiration .
The most frequent cause of unilateral vocal fold paresis/paralysis is a peripheral lesion of the recurrent laryngeal nerve, but the superior laryngeal nerve may also be affected (Table 4.2). This leads to immobility of the arytenoid cartilage on the recurrent laryngeal nerve (RLN)-injured side . It may be caused by iatrogenic or traumatic lesion, postoperatively, or by tumours or viral infection. It may have toxic (allergic, infectious), cerebrovascular, or neuropathic reasons, as result of radiation therapy, but it can also be idiopathic (Table 4.2).
Aetiology of vocal fold paralysis 
Thyroid gland carcinoma
Resection of bronchial carcinoma
Endarterectomy of the carotid artery/cardiac and vascular surgery
Surgery of spinal column with anterior cervical approach
Up to 10%
Thyroid gland carcinoma
Other malignancies (e.g. neck metastasis)
Up to 19.8%
Sarcoidosis, neurotropic viruses, e.g. HSV, VZV, EBV
MS, ALS, apoplexy, poliomyelitis, polyneuropathies, brain tumours
No reason found after comprehensive diagnostic work-up
The extent, degree and prognosis of paralysis and the shape of the resulting glottal gap depend on the underlying cause. In unilateral vocal fold paresis/paralysis, a large variability of vibration behaviour can be observed. Vocal fold paralysis is very different in terms of the position and impairment of the affected vocal folds.
The position of the paralyzed vocal fold determines the form of the glottal gap during phonation: median position (full circuit possible), paramedian position (even gap) and intermediate position (larger gap with bowed vocal fold due to impairment of the cricothyroid muscle) (Figs. 4.3 and 4.4). However, this classification is not sufficient and does not include the different levels of both vocal folds secondary to loss of tension at the affected side.
Schematic representation of the normal and paralyzed left vocal fold
Three cases of left sided unilateral vocal fold paralysis (ULVFP) in different positions, resulting in different glottal gaps during phonation. [(a–c) respiration and (d–f) phonation]. All ipsilateral arytenoid cartilages are tilted in an anterior-medial position. The degree of excavation and functional decompensation increases from cases 1 to 3
Rosato et al.  measured sequelae after thyroid surgery in nearly 15,000 patients in Italy: permanent paralysis of the laryngeal recurrent nerve (LRN) (1.0%), transient palsy (2.0%), diplegia (0.4%), damaging of superior laryngeal nerve (3.7%), dysphagia (1.4%), haemorrhage (1.2%) and wound infection (0.3%).
In our own patient population (n = 156) in Magdeburg, Germany, from 1990 to 2011, we observed 76 cases (50 male and 26 female) of unilateral vocal fold paresis with an age peak of onset of 57 years on average. In ULVFI, dysphonia was the most common symptom; in bilateral VFI it was dyspnea. The predominant causes of ULVFI were thyroid surgery (37%), idiopathic origin (21%), further surgical intervention (7%) and viral infections (7%).
Damage of the vagal nerve affects the entire laryngeal muscles and the sensitivity of the laryngeal mucosa. Furthermore, pharyngeal and oesophageal muscles are involved. Impairment of all ipsilateral laryngeal muscles and a vocal fold predominantly fixed in a lateral position results in a large and three-dimensional glottal gap during phonation with severe breathiness. The affected arytenoid cartilage moves into a more anterior-medial position secondary to loss of muscle tension. Vagal damage is often combined with persistent dysphagia and hyperrhinolalia.
Neurogenic vocal fold paralysis is caused by cerebrovascular or inflammatory diseases, traumatic brain damage and degenerative diseases of the cerebellum (more on immobility of central origin in Chap. 6). Supranuclear disorders, for example, in Parkinson’s disease or myasthenia gravis, may also be accompanied by vocal fold immobility. Occasionally, it may occur in amyotrophic lateral sclerosis. In most cases, voice changes are combined with articulation and swallowing disorders. These symptoms sometimes also occur in peripheral vocal fold paralysis, which is caused by lesions of the nucleus (e.g. Wallenberg’s syndrome) or the infranuclear structure.
Rosenthal et al.  confirm that many patients with unilateral and bilateral immobility have spontaneous remissions, depending on the cause (Table 4.3). Inflammation, infection or iatrogenic strain of the recurrent laryngeal nerve may cause only temporary immobility. However, tumour invasion and iatrogenic dissection of the recurrent laryngeal nerve always result in permanent vocal fold paralysis. Jeannon et al.  report 9.8% temporary and 2.3% permanent vocal fold paralysis after thyroid surgery.
Occurrence of hoarseness after thyroid surgery
Onset of hoarseness
Prognosis: return of mobility
Directly after surgery
Pressure on nerve
Contusion (tweezers, clamp)
Heat of the thermal cautery
Few days after surgery and later
Nerve swelling (oedema)
4.1.3 Impaired Mobility or Fixation of the Cricoarytenoid Joint
Immobility of the arytenoid cartilage may be caused by rheumatoid arthritis, granulomatosis with polyangiitis and inflammation (capsular scarring) or a result of intubation with luxation (Fig. 4.5) of the arytenoid cartilage [9–11]. Most intubation trauma is caused by emergency intubation. Typically the left arytenoid cartilage is affected due to the right-handed approach of the anesthesiologist. Rubin has stated that external laryngeal trauma is the second most common origin of luxation of the arytenoid cartilage. Arytenoid cartilage-related vocal fold immobility may range from minor impairments of mobility with minimal voice problems to ankylosis with complete immobility of the arytenoid cartilages.
(a) Frontal view: subluxation of the left arytenoid cartilage. (b) Lateral view: subluxation of the arytenoid cartilage and paradox posterior position of the upper pole leading to a bending of the vocal cord
In this context it is worth noting that different terms like subluxation, luxation and dislocation are used to describe the types of arytenoid cartilage displacement . Luxation occurs when the joint surfaces are completely separated. In subluxation, there is still contact between the two joint surfaces.
In our opinion, the term dislocation is misleading in connection with impaired mobility even when intubation trauma may occur. As Wang  describes, considerable force is necessary to destroy structural supports leading to arytenoid dislocation. For this reason, luxation seems to us to be the most appropriate term.
Sataloff et al.  describe disruption of the cricoarytenoid joint as an uncommon disorder. In our opinion, disruption or dislocation of the arytenoid cartilage may just as easily be caused by sharp neck trauma and is not exclusively a result of intubation or endoscopy. The overall incidence of arytenoid dislocation is unclear but is reported  to occur in 0.1% of tracheal intubations.
Eckel et al.  point out that a fixation of the cricoarytenoid joint (arthrogenic dysphonia) is clinically similar to vocal fold immobility in the case of paralysis of the recurrent laryngeal nerve.
Intubation trauma leads to tearing of the joint capsule with secondary capsulitis and synovitis. Additionally, there may be hematoma in the joint space leading to impairment of the joint play.
Combined diagnosis with laryngoscopy, videostroboscopy, computed tomography (CT) and electromyography (EMG; see Chap. 1) is important for early diagnosis of arytenoid luxation. In agreement with Norris and Schweinfurth , we would like to point out that flexible laryngoscopy alone is not suitable for distinguishing arytenoid luxation from laryngeal nerve injury.
Ankylosis is a complete and irreversible fixation of the cricoarytenoid joint. It may be caused by laryngeal trauma and rheumatoid arthritis of the larynx. Already in 1959, Copeman et al. described an ankylosis of the cricoarytenoid joint. Postmortem it was completely obliterated and the site replaced by fibrofatty tissue with small collections of leucocytes .
4.1.4 Interarytenoid Scars and Bridges
On the one hand, prolonged endotracheal intubation with arytenoidal mucosal ulcerations may lead within hours to inflammation of the tissue, to ischemic ulcerations and, secondarily, to scars of the cricoarytenoid joints resulting in so-called postintubation phonatory insufficiency (PIPI) [18, 19].
On the other hand, it may result in decreased mobility of the arytenoid through the development of granuloma at the contact points and secondary scarring (Fig. 4.6). The pressure of the endotracheal tube on the posterior and medial portions of the glottis can be more than 100 mmHg. The ulceration leads to fibrosis (Fig. 4.7), to scarring and bridges (Fig. 4.8a,b) and thus to immobility of the vocal folds .
Intubation granulomas after long-term intubation
Interarytenoid fibrosis after long-term intubation
Two cases of interarytenoid bridges: (a) fibrous and (b) bony
4.1.5 Immobility of the Vocal Folds Caused by Tumours and Scars
Predominantly malignant tumours may impair the mobility of the vocal folds because of their size, shape and/or localization. Tumours involving more than one fourth of the thyroarytenoid muscle lead to impairment of the vocal fold. Especially tumours growing at the arytenoid cartilage may hinder the movement of the vocal fold by invading the joint capsule or the joint itself . Brasnu et al.  describe the immobility of the vocal fold secondary to the weight of the tumour located at the top of the arytenoid cartilage without any tumour extension of the cricoarytenoid muscles. Fixation is a criteria of the TNM classification, which classifies tumours T3 or higher.
On the other hand, tumour resections of the larynx and/or hypopharynx involving the area of the arytenoid may lead to scar development resulting in restricted mobility of the vocal folds (Fig. 4.9).
A 47-year-old male with recurrent HPV-associated cancerization of both vocal folds after several microlaryngoscopies resulting in a posterior web formation occluding the glottic lumen and scar formation impairing the mobility of the right arytenoid cartilage
4.2 Diagnostics in ULVFI
Since the etiology and symptomatology of vocal fold immobility are heterogeneous, wide-ranging diagnostics have to be carried out based on the ELS basic protocol for voice diagnostics [22, 23]. Vocal performance, aerodynamic aspects and the individual voice handicap of patients has to be quantified.
Essential tools for the assessment of impaired movement, immobility of the vocal folds, are patient-reported symptoms, endoscopic and stroboscopic examination of the vocal folds and EMG assessment for establishing neural damage.
4.2.1 Patient-Reported Symptoms
Wide-ranging symptoms, many anamnestic details, functional and patient-related aspects like the individual impairment, social or occupational role of the voice and the overall health situation, as well as prognostic information all play a major role in the differential diagnosis and the development of treatment options.
The impaired movement of one vocal fold may be well compensated by the contralateral vocal fold (depending on origin and severity). Acute respiratory distress may lead to serious life-threatening situations, e.g. in the case of bilateral vocal fold paralysis. Thus, the main symptom of unilateral vocal fold immobility is hoarseness, not so much difficulties in breathing. Other complaints are problems with getting loud, monotone intonation, problems with singing and discomfort during speaking.
4.2.2 Endoscopic Findings
Routinely performed rigid as well as flexible laryngoscopy gives a precise impression of the extent of the immobility of the vocal fold. Due to the lack of an evaluable fundamental frequency, laryngostroboscopy can usually not be performed in cases of complete vocal fold paralysis.
Possible endoscopic and stroboscopic findings in patients with vocal fold immobility are a glottal gap, asymmetric left- and right-sided mucosal wave, impaired mobility of the arytenoid cartilage, forward-tilted arytenoid cartilage, different levels of the vocal folds, vocal fold bowing, signs of reflux, granulomas and signs of swallowing disorders.
Whether computer tomographic scans (CT) make sense is controversial. CT seems to detect (malignant) diseases of idiopathic paralysis. Other findings suggest that CT has a low yield for occult neck and mediastinal pathology in patients with idiopathic vocal fold paresis .
Magnetic resonance imaging (MRI) is the most appropriate imaging technique in patients with vocal fold paralysis. The pathology is likely to be located in the neck or at the skull base or the brain stem. MRI is preferable to CT due to its better soft tissue resolution at the skull base or in the case of intracranial diseases. MRI offers excellent visualization of the morphologic soft tissue structures at and below the skull base [24, 25].
4.2.4 Individual Handicap
The Voice Handicap Index (VHI) , the Voice-related Quality of Life (VrQoL) measurement , the Voice Outcome Survey (VOS) developed for unilateral laryngeal paralysis  and the Voice Activity and Participation Profile (VAPP)  are all excellent instruments for measuring the individual handicap in patients with unilateral vocal immobility.
4.2.5 Functional Findings
So far, functional and performance tests of voice quality, such as voice range profile, or the calculation of the dysphonia severity index , only have a descriptive function. But they do provide information about the vocal fold losses caused by ULVFI. This is of importance for the recognition of the personal handicap and thus for the therapeutic strategy.
In cases of vocal fold immobility, all voice-related aerodynamic measurements are relevant and meaningful diagnostic parameters, such as maximum phonation time (on the sustained [a:]), vital capacity with the help of a spirometric test system, calculation of phonation quotient (=vital capacity in ml/maximum phonation time on [a:] in s) and calculation of s/z ratio (fortis [s]/lenis [z]) ([31, 32]).
4.2.6 Electromyography of the Larynx (Details in Chap. 1)
Sittel et al. [33, 34] evaluate electromyography of the larynx (LEMG) as an important examination in the case of paralysis of the recurrent laryngeal nerve. LEMG is able to detect 94.4% of possible defect healing. It does not allow prediction of long-term voice quality, e.g. in vocal fold paralysis in paramedian or median position, where, in spite of pathologic LEMG results, a good voice may be present . But unilateral vocal fold paresis (ULVFP) can be defined in terms of results from EMG assessment, and LEMG provides additional information about the functional status of voice-related muscles .
4.3 Treatment of ULVFI
The goal of any therapy in unilateral vocal fold immobility is the activation of the paralyzed vocal fold and improvement of the glottic closure. Phonosurgical procedures are used to change the vocal fold position (vertical and horizontal), the vocal fold volume (e.g. by grafting and implant placement), the adduction and abduction (e.g. by arytenoid adduction) as well as the tension of the vocal folds (e.g. by reinnervation). Maintenance or optimization of the vocal fold vibration, especially the mucosal wave of the vocal fold, is an additional purpose of the therapy. The three-dimensionality of the vocal fold movement must be considered when selecting the surgical procedure.
This aims to improve the quality of voice, vocal performance and control of airflow with special consideration of best synchronized oscillation frequencies and phases of the vocal folds. It also focusses on the conservation and restoration of abdominal pressure ability and cough effectiveness.
In analogy to Friedrich’s remarks on endolaryngeal phonosurgery , conservative voice therapy (vocal exercises/voice techniques) is an important component of the holistic treatment concept. This is due to the inherent multidimensional pathogenesis of immobility of vocal folds. The choice of the optimal treatment method should be based on an interdisciplinary assessment and decision made by otolaryngologists, phoniatricians, voice therapists and other involved professions, such as psychologists.
4.3.1 Conservative Voice Therapy (Vocal Function Exercises)
Conservative voice therapy with voice function exercises for the treatment of ULRP may already be sufficient but may only achieve satisfactory results in cases of minor glottal gap . Sittel et al. noticed a regained satisfactory-to-usable vocal performance in 75–90% of patients with ULVFP, although a complete recovery of vocal fold mobility was observed only in 10–40%. Voice function exercises may facilitate glottal compensation and should be prescribed generously . Conservative voice therapy should begin when wound healing is completed.
Aims of voice function exercises are stimulating the nerve, preventing atrophy, improving glottal closure and supporting the unimpaired vocal fold to cross the middle line for better glottal closure.
As an interim solution, glottal closure can be improved by lateral manual pressure (thumb or index finger and middle finger) on the contralateral outside of the thyroid cartilage or by rotation of the head and neck in the direction of the paralyzed vocal fold .
Selection of the optimal voice therapy method depends on the symptoms, etiology and pathogenesis of vocal fold immobility. Voice function exercises should focus on vocal fold physiology as a part of the inspiratory sphincter system, because all muscle groups involved in respiration are determined by body posture and body movement. To improve glottal closure, the inspiration-related sphincter should be activated, for example, through pull-ups [39, 40]. In the case of unilateral vocal fold paralysis, a combination with an electrical stimulation therapy may prove successful .