Bilateral Vocal Fold Motion Impairment Research Articles

The Clinical Course of Idiopathic Bilateral Vocal Fold Motion Impairment in Adults: Case Series and Review of the Literature

Steps for assessment and successful management of bilateral vocal fold motion impairment (VFMI) are (1) recognition of its presence, (2) identifying the etiology and factors restricting vocal fold motion, (3) evaluation of airway patency, and (4) establishing a management plan. No large series documenting the course and outcome of adult idiopathic bilateral VFMI has been published within the past 15 years. Retrospective chart review of adult patients with idiopathic bilateral VFMI at a tertiary academic center. A diagnosis was established if history, physical examination with laryngoscopy, and initial imaging excluded a cause. Records were reviewed for demographics, clinical characteristics, surgical intervention details, and length of follow-up. Nine adult patients with idiopathic bilateral VFMI were identified. There were five males and four females with a mean age of 59.6 years. The mean follow-up period was 54.4 months (range, 6-111 months). Upon presentation to our laryngology service, three patients were advised observation, three patients were advised to undergo urgent tracheostomy, and three patients were advised to undergo elective surgery for airway management. By the end of the follow-up period, only four patients (4/9, 44.4%) were tracheostomy dependent, one of them was lost to follow-up after tracheostomy tub downsizing for decannulation. To our best knowledge, this is the largest series so far of adult patients with idiopathic bilateral VFMI. Conservative treatment can be considered as an alternative to surgery in select cases.

Vocal Fold Motion Impairment

Vocal fold motion abnormalities in children are the second most common form of laryngeal pathology seen in children, and often present in the first 24 months of life. A thorough evaluation of the aerodigestive tract will include an examination of the vocal folds, and a proper diagnosis is essential in order to decipher the etiology of swallowing, voicing and breathing abnormalities. This article reviews the workup, management options and clinical outcomes of unilateral and bilateral vocal fold motion impairment in the pediatric population.

Arytenoidcordectomy for bilateral vocal cord paralysis: Primary and revision procedure

Background: Definitive enlargement of the glottis with preservation of adequate voicing in patients with bilateral recurrent nerve paralysis remains a surgical challenge especially in patients with previous unsuccessful surgery. Study design: Report of a novel surgical technique for glottis enlargement and presentation of midterm results. Methods: Four adult patients with bilateral recurrent nerve paralysis were subjected to submucosal arytenoidcordectomy through a thyreofissure approach with ventricular folds transposition and long-term translaryngeal stenting. Two of them had had previous surgeries at the glottic level. Preoperative data as well as postoperative functional results are reviewed. Follow-up ranged from 8 to 28 months. Results: In all patients tracheostomy closure was achieved. Midterm follow-up revealed stable airway, adequate for the patients' routine physical activities. Postoperatively patients phonated with the ventricular folds and the resulting voice quality was good. Conclusions: We describe a novel approach formanagement of impaired airway because of bilateral recurrent nerve paralysis and/or stenosis. It comprises intralaryngeal soft tissue resection, enlargement of the cartilaginous framework of the larynx and long-term translaryngeal stenting. The surgical approach described here proved to be successful both in patientswith simple bilateral vocal fold motion impairment and in those, who have been already unsuccessfully treated with other surgery. Nevertheless the technique should be regarded as an option only in complicated revision cases, rather than a primary intervention in bilateral vocal fold paralysis.

Vocal fold motion impairment in multiple system atrophy

Multiple system atrophy (MSA) is a degenerative neurologic disorder that can affect vocal fold mobility. Our aim was to further elucidate the impact of vocal fold motion impairment (VFMI) in MSA. Retrospective case series. We undertook a retrospective review of all MSA patients reporting voice or respiratory symptoms from 1975 to 2010 at Mayo Clinic Rochester who also received otolaryngologic examination. Thirty-eight MSA patients demonstrated VFMI. Median duration of vocal or respiratory symptoms prior to diagnosis of MSA was 12.0 months (range, 1-60 months). Stridor was present in 25 (68%) of patients. There was bilateral VFMI in 32 (82.4%) of the patients and isolated VFMI of the left true vocal fold (TVF) in six (17.6%) of the patients. No patients had isolated right VFMI. There was isolated unilateral or bilateral paresis in 21 (55.3%) of the patients and unilateral or bilateral complete paralysis in 15 (39.5%) of the patients. One patient presented with left TVF paralysis and right TVF paresis, whereas one other patient had findings of right TVF paralysis and left TVF paresis comprising the remaining 5.2% of patients with VFMI. The median survival after diagnosis of VFMI was 51.6 months. Unilateral or bilateral TVF paralysis was statistically associated with a decreased overall survival (P = .0384). The presence of stridor was not associated with adverse prognosis. The increasing severity of VFMI negatively impacts overall survival in patients with MSA. Therefore, otolaryngologic examination is warranted at the time of MSA diagnosis.

The role of botulinum toxin in the management of airway compromise due to bilateral vocal fold paralysis

The management of a patient with bilateral vocal fold motion impairment (BVFMI) can be challenging for the otolaryngologist. The treatment traditionally involves tracheotomy, which can be very distressful for some patients. Alternatively, there are endoscopic procedures, which irreversibly sacrifice voice in order to improve airway. The optimal treatment of BVFMI still eludes us. The purpose of this review is to highlight an alternate management strategy for bilateral vocal fold paralysis using botulinum toxin (BTX). This procedure is predicated on the premise that vocal fold immobility is related to synkinetic reinnervation of the vocal fold. Eliminating any thyroarytenoid/lateral cricoarytenoid (LCA) activity during respiratory gestures should allow greater unopposed posterior cricoarytenoid abduction. There have been several case reports and series, the largest of which involved 11 patients, describing the successful use of BTX for this application. The best candidates for this adductor chemical denervation are those patients who have undergone trauma to the recurrent laryngeal nerve without evidence of cricoarytenoid joint fixation. Patients should have evidence of voluntary thyroarytenoid/LCA laryngeal electromyography activity, though true synkinesis cannot always be reliably identified. The procedure can be another management option for patients with BVFMI.

Botulinum toxin injections for new onset bilateral vocal fold motion impairment in adults

Review of clinical experience and results using botulinum toxin type A (BTX) for the management of adult patients with respiratory compromise due to new onset bilateral vocal fold motion impairment (BVFMI). Retrospective case series. The records of 11 patients from two institutions with respiratory compromise due to bilateral vocal fold motion impairment were reviewed. Age, sex, etiology of motion impairment, subjective response to BTX injections, changes in pulmonary function studies pre- and postinjection when available, the dosage of botulinum toxin required to achieve response, the number of injections per patient, and complications were reported. All patients were over 18 years old. There were three male and eight female subjects. The etiology of BVFMI was due to previous anterior cervical surgery in nine patients and prolonged intubation in two. Ten patients reported symptomatic improvement and returned for an average of nine injections over the 10-year period of study. The most common interval between injections was 3 months. In all patients the dose required to achieve symptomatic improvement was at least 2.5 mouse units injected into each vocal fold. One patient without relief of symptoms had bilateral cricoarytenoid joint fixation. Complications were limited to moderate dysphagia in one patient and breathy dysphonia in all patients. BTX injection into the vocal folds provides temporary relief of symptoms in airway obstruction in adult patients with BVFMI. Patients require an average of 2.5 units of botulinum injection into each vocal fold and have an average length of response of 3 months. BTX injection may be used as a form of temporary relief of airway obstruction in patients wishing to avoid ablative surgery or tracheotomy.

Exit, pursued by a bear

In August, 2004, a 71-year-old man was admitted to our hospital, with a hoarse voice and “noisy sleep”. His medical history was essentially uneventful: mild hypertension, for which he took valsartan; and a brief episode of laryngitis in the early 1980s. He had dysphonia, and persistent nocturnal inspiratory stridor, but no diurnal dyspnoea or stridor. Neurological examination revealed slight diffi culty with tandem gait, which we considered normal, given the patient’s age. Blood tests, CT of the chest, and MRI of the brain and cervical spine showed nothing of note. Laryngoscopy revealed bilateral vocalfold motion impairment: we diagnosed idiopathic bilateral recurrent-laryngeal-nerve palsy. The patient was discharged 8 days after admission. 4 months later, the patient was admitted again, with unsteadiness. His stridor was less severe than before. On detailed questioning, the patient reported erectile dysfunction, urinary urgency, and a recurring nightmare of being chased by a bear, during which he had hit his wife. Examination showed dysphonia and cerebellar dysfunction (dysdiadochokinesia and ataxia). We found retropulsion, consistent with Parkinsonism, but no tremor, rigidity, or bradykinesia. We noted asymptomatic postural hypotension (systolic blood pressure dropped from 130 mm Hg to 98 mm Hg). We found no other abnormalities, other than brisk knee jerks. Lumbar puncture, and electromyography of the anal sphincter, showed no abnormality. We diagnosed multiple system atrophy. Videopolysomnography, with sound recording, revealed prominent inspiratory stridor and obstructive sleep apnoea (34 events per h, causing oxygen saturations to decrease transiently to 75%). During REM sleep, tonic muscle activity remained, and the patient spoke and pointed with his right arm, confi rming that he could move during his nightmares: he had REM sleep behaviour disorder. We prescribed clonazepam (250 μg) for the sleep disorder, and treated sleep apnoea with bilevel positive airway pressure, which was shown by polysomnography to be highly eff ective. However, as expected, the patient’s underlying condition has continued to worsen. When he was last seen, in April, 2007, his ataxia had worsened; he fell often when trying to walk unaided. His postural hypotension had become symptomatic. Nonetheless, he slept well, and was not sleepy in the daytime. He had not dreamt of the bear for several months. Multiple system atrophy is a term used to describe syndromes formerly known as Shy-Drager syndrome, striatonigral degeneration, and olivoponto cerebellar atrophy. It is a neurodegenerative disease—which, like Parkinson’s disease and Lewy-body dementia, is characterised histopathologically by cytoplasmic accumu la tion of α-synuclein. Patients with multiple system atrophy have motor and autonomic dysfunction. In 80% of patients, motor features are mainly parkinsonian; other patients have cerebellar dysfunction. Electro myography of the anal sphincter often gives abnormal results, but is not required for diagnosis. Manifestations of autonomic dysfunction include postural hypotension, urinary urgency, and erectile dysfunction. REM sleep behaviour disorder has been found in over half of patients with multiple system atrophy. Vocal-fold motion impairment develops in around 30% of patients; it was thought to be caused by impaired abduction of the vocal cords, attributable to degeneration of the nucleus ambiguus and recurrent laryn geal nerve. However, such a mechanism is diffi cult to reconcile with the spontaneous improvement in our patient’s stridor, and with the worsening of symptoms at night. Recent work supports a diff erent mech an ism: dystonia of the laryngeal muscles during sleep, ie, inappropriate adduction of the cords. Since ventilatory support was introduced as a treatment, tracheostomy is rarely required.

Laryngologic management of infants with the Chiari II syndrome

As a part of a prospective multi-disciplinary study, all children born with a Chiari II malformation within the Uppsala region during a 3-year period were evaluated for any difficulties in breathing or swallowing. The evaluation was repeated at regular intervals during their first 18 months. Direct laryngoscopies were performed using flexible fiberscopes. Four out of 22 children were found to have disturbed breathing. Among those, two suffered from central apnoeic spells as well as bilateral vocal fold motion impairment, one from apnoeic spells only and one from bilateral vocal fold motion impairment only. All four also had dysphagia with aspiration. Three of the children developed respiratory symptoms within the first 3 months and the symptoms of the fourth begun within the first 6 months. One infant with severe symptoms expired at the age of 3 months. The vocal fold paralysis, apnoeic spells and swallowing difficulties of another infant resolved following active neurosurgical management. The conclusion that laryngologic issues are prominent in the severe Chiari II syndrome was further supported by a review of four more cases managed in recent years. Laryngologic assessment in the neonatal period can help to raise the issue of early neurosurgical intervention as well as identify some of the infants who will need extensive habilitation. Screening of laryngeal function by means of flexible fiberoptic laryngoscopy is recommended.

Bilateral Vocal Fold Motion Impairment: Pathophysiology and Management by Transverse Cordotomy

Although bilateral vocal fold paralysis (BVFP) is an uncommon disorder, bilateral vocal fold motion impairment (BVFMI) resulting from a variety of laryngeal derangements is encountered with increasing frequency. Moreover, pure BVFP accounts for only a small proportion of BVFMI. When antecedent factors associated with BVFP are absent, recognition of BVFMI is often delayed and frequently overlooked. The requirements for assessment and successful management of BVFMI are 1) recognition of its presence, 2) identification of the constituent factors restricting vocal fold motion, 3) objective assessment of airway patency, and 4) selection of a reliable management plan. More often than not, two or more BVFMI-causing factors are present; only rarely is BVFMI attributable to a single vocal fold motion-limiting cause. The clinical and endoscopic examinations should evaluate the relative contributions of vocal fold paralysis, cricoarytenoid joint fixation, infiltrative disorders, and webs and synechiae that cause restricted vocal fold motion. The flow-volume loop examination documents airflow rate and volume and the site, nature, and severity of the obstructing lesion(s). This presentation describes the evaluation and rationale for management in BVFMI. The surgical techniques currently used to address BVFMI are compared to determine their respective merits and drawbacks, depending upon the constituent factors causing vocal fold motion limitation.