Abductor Vocal Cord Paralysis Research Articles

Effective Treatments for Abductor Vocal Cord Paralysis: A Comprehensive Review.

Abductor vocal cord paralysis (AVCP) is a disabling disorder that affects the voice and the quality of life of a patient, and hence, there is importance in providing a detailed knowledge of its aetiology and management. In this review article, we offer an implicational definition of AVCP and a discussion of its background, viewed as potentially affecting voice production and health. Finally, we explore modalities of diagnosis by medical history and physical examination, visualization techniques like laryngoscopy and stroboscopy, and radiographic imaging such as computed tomography (CT) and magnetic resonance imaging (MRI) scans. The article reviews and categorizes approaches into operative and non-operative treatments, including injection laryngoplasty, voice therapy, botulinum toxin injections, and the management of Reinke's edema. Surgical approaches, like arytenoid adduction, cordotomy, and posterior cordotomy, are also scrutinized taking their indication, efficacy, and complication profile into consideration. Learning about the advantages and drawbacks of the following experimental yet promising directions like nerve-muscle pedicle implantation, nerve reinnervation, and engineering of tissues is therefore highly necessitated. In conclusion, the review details the measures that have shown to be useful in the treatment process and their impact on the future practice of clinical work, calling for a more clarified structure of the organization of diagnostic, therapeutic, and rehabilitative activities. Future research directions are outlined based on the gaps which include the development of new treatment approaches, the evaluation of treatment for long-term effects, and the need for interdisciplinary cooperation in the medical field for the benefit of the patients.

Vocal cord abductor paralysis as an early sign of multiple system atrophy

Vocal cord abductor paralysis as an early sign of multiple system atrophy

The Clinical Analysis of Patients with Bilateral Vocal Cord Abductor Paralysis as an Early Manifestation of Multiple System Atrophy

Multiple system atrophy (MSA) is a neurodegenerative disease that is associated with cerebellar symptoms, autonomic symptoms and parkinsonism as three significant signs. The prevalence of MSA is 7-10 per 100,000 population, thus, among neurodegenerative diseases, it is not a rare condition.

Two Cases of Parkinson's Disease Accompanied with Nasogastric Tube Syndrome

We report 2 cases of patients with Parkinson's disease who exhibited bilateral vocal cord paralysis induced by an indwelling nasogastric tube (N-G tube). Both patients showed abrupt inspiratory stridor after N-G tube placement. A fiberoptic laryngeal examination revealed bilateral vocal cord abductor paralysis (VCAP). After N-G tube removal, patient symptoms improved. Nasogastric tube syndrome (NGTS) is an uncommon but life-threatening syndrome that causes sore throat and bilateral VCAP following N-G tube insertion. Throat pain is considered an important early manifestation of NGTS. However, in cases of advanced Parkinson's disease, subjective symptoms of NGTS, such as throat pain, may be difficult to recognize. We here report 2 patients with parkinson's disease accompanied by NGTS with literature review and proposed that inspiratory strider is a useful objective symptom in early diagnosing of NGTS. (Received March 25, 2020; Accepted May 18, 2020; Published September 1, 2020).

A Case of Bilateral Vocal Cord Abductor Paralysis Caused by Idiopathic Non-inflammatory Myopathy Localized in the Posterior Cricoarytenoid Muscle

A Case of Bilateral Vocal Cord Abductor Paralysis Caused by Idiopathic Non-inflammatory Myopathy Localized in the Posterior Cricoarytenoid Muscle

Efficacy of NPPV for vocal cord abductor paralysis with floppy epiglottis in multiple system atrophy

Background: Multiple system atrophy (MSA) often presents as obstructive breathing disorder, vocal cord abductor paralysis (VCAP) and floppy epiglottis (FE) in an advanced stage. Noninvasive positive-pressure ventilation (NPPV) is known to be effective for VCAP. On the other hand, some reports insist that in the presence of FE, NPPV may worsen obstructive respiratory disorder.

Sleep and autonomic function: sleep related breathing disorders in Parkinson's disease and related disorders

In patients with multiple system atrophy (MSA), sleep related breathing disorders (SRBD), including obstructive and central sleep apnea, vocal cord abductor paralysis and dysrhythmic breathing pattern, are frequently observed. SRBD may have a considerable impact on variation of autonomic nervous activity during sleep. The previous studies correlated upper airway muscle dysfunction related parkinsonism with increased prevalence of SRBD in patients with Parkinson's disease (PD). However, recently, the clinical significance of SRBD and its impact on sleepiness and disease severity have been debated. In this review, we discuss sleep and autonomic function, especially, SRBD in PD and related disorders, including the previous studies from our department.

Critical vocal cord abductor paralysis as an emergency in myasthenia gravis

A 78-year-old woman was admitted for sudden-onset dyspnea, presenting with hypoxemia, stridor and pooling of saliva in the pharynx. One month earlier, she had complained of dysphagia and had been diagnosed with myasthenia gravis (MG) based on weakness of the proximal muscles, decremental response in repetitive nerve stimulation and positive anti-acetylcholine receptor antibodies (Myasthenia Gravis Foundation of America [MGFA] class IIb). Laryngoscopy disclosed severe bilateral vocal cord abductor paralysis (VCAP), which was improved to one-third of the maximum abduction by edrophonium injection (Fig. 1a, b). An emergency tracheostomy was required to avoid suffocation (MGFA class V). Immunosuppressive treatment improved symptoms including VCAP (Fig. 1c). A thymectomy was carried out and the involuted thymus was found. VCAP, a rare complication of MG, can be the first and sole manifestation of the disease.1 VCAP also occurs in patients with anti-muscle-specific receptor tyrosine kinase antibodies.2 When neurologists encounter dyspnea in MG, not only respiratory muscle weakness, but also VCAP should be considered, and indications of tracheostomy must be assessed immediately by laryngoscopy using edrophonium. The authors declare no conflicts of interests with respect to this article.

Laryngo-pharyngeal findings and sleep-related breathing disorders in patients with multiple system atrophy

Patients with multiple system atrophy (MSA) manifest a variety of sleep-related breathing disorders (SRBD). Vocal cord abductor paralysis (VCAP) is associated with respiratory failure and sudden death during sleep. To evaluate the relation between SRBD and clinical symptoms in patients with MSA, 11 patients with MSA admitted to our hospital were recruited for this study. All patients underwent detailed neurological examinations and brain imaging studies. Laryngoscopic examination and polysomnography were performed to detect SRBD and abnormal movements of the vocal cords and larynx. Ten patients (91%) showed SRBD, defined as five or more episodes of apnea and/or hypopnea per hour, with hypopnea predominant. Among the nine patients who underwent laryngoscopic examination, six (67%) showed VCAP, of whom two exhibited it only during sleep. Four patients had abnormal laryngeal movements, of whom two (33%) showed floppy arytenoid, one showed omega type, according to the classification of sleep-induced laryngomalacia in MSA, and the fourth one showed an unclassified pattern. Patients with VCAP tended to be older and have more frequent dysphagia, neurogenic bladder and severe SRBD, compared with those without VCAP. Physicians should be aware that SRBD is frequently observed in patients with MSA, and that VCAP and laryngo-pharyngeal abnormalities may be the initial or early signs of MSA.

Adult-onset Alexander disease with an R66Q mutation in GFAP presented with severe vocal cord paralysis during sleep

Adult-onset Alexander disease (AOAD) is clinically characterized by slowly progressive bulbar palsy, pyramidal signs, spastic paresis and cerebellar ataxia with atrophy of the medulla oblongata and upper cervical cord, and the glial fibrillary acidic protein (GFAP) gene has been identified to be the causative gene for Alexander disease [3]. So far, some reports have mentioned that AOAD presents with sleep apnea [1, 4, 5, 8–10, 12], but the apnea mechanism is not sufficiently known. Here, we report an AOAD patient presented with vocal cord paralysis during sleep. This is the first report indicating that AOAD presented with vocal cord abductor paralysis, followed by the rapid progression of vocal cord dysfunction. A 61-year-old woman was admitted to our hospital because of gait disturbance over a 4-year period. She has been described as ‘‘round shouldered’’ since childhood and would snore loudly while sleeping since her early 30 s. Her family history revealed that even her mother snored loudly and died because of unknown reason at 54 years of age. The patient had a short neck and cervical kyphosis. Neurological examination revealed slurred speech, spasticities of all extremities, and bilateral extensor Babinski signs. MRI findings revealed atrophy of the upper cervical cord and medulla oblongata. Axial imaging of the medulla oblongata showed multiple T2-weighted high-intensity lesions. Her cerebral blood flow on ECD-SPECT was reported previously [7]. Mutational analysis revealed a previously reported heterozygous missense mutation at exon 1 of GFAP, c.197G[A, which involved the substitution of glutamine for arginine at the 66th codon (R66Q) (Fig. 1a) [11]. We confirmed the diagnosis of AOAD. Polysomnography revealed obstructive sleep apnea syndrome with 292 apneic episodes at night (245 obstructivetype and 47 mixed-type). Although her mean percutaneous oxygen saturation during wakefulness was 94 %, her mean saturation during sleep was 84 %. Her apnea–hypopnea index (AHI) was 52.2/h indicating severe apnea syndrome. To investigate the mechanism of her apnea, we examined her laryngeal movement during wakefulness and sleep induced by intravenous administration of diazepam [6]. Awake-laryngofiberscopy showed mild vocal cord abduction restriction during inspiration. After intravenous diazepam administration (5 mg), the vocal cords showed paradoxical movement with obstruction during inspiration. To avoid fatal outcome Electronic supplementary material The online version of this article (doi:10.1007/s00415-012-6540-4) contains supplementary material, which is available to authorized users.

Bilateral vocal cord abductor paralysis associated with primary herpes simplex infection: A case report

To report a case of bilateral vocal cord abductor paralysis in the context of primary herpes simplex infection. A 63-year-old man was urgently admitted to hospital with laryngeal dyspnoea associated with dysphagia but without dysphonia. Physical examination demonstrated the vocal cords in a paramedian position with paralysis of abduction. The patient reported primary herpes simplex infection two weeks prior to this episode. HSV serology indicated recent infection and lumbar puncture demonstrated the presence of herpes simplex virus type 1 in the cerebrospinal fluid. Complete resolution of respiratory symptoms was observed after 21 days of treatment with intravenous aciclovir. Gerhardt syndrome comprises inspiratory dyspnoea without dysphonia. It used to be mainly due to syphilis, but is now mostly observed in the setting of neurodegenerative disease. The authors report a case of Gerhardt syndrome occurring after an episode of primary herpes simplex infection with the presence of herpes simplex virus in the CSF. Treatment by intravenous antiviral drugs allowed rapid resolution of the symptoms. The pathophysiology of Gerhardt syndrome remains unexplained, but the possible role of herpes simplex infection should be considered in cases of laryngeal palsy.

The close relationship between life-threatening breathing disorders and urine storage dysfunction in multiple system atrophy

Survival of multiple system atrophy (MSA) depends on whether a variety of sleep-related breathing problems as well as autonomic failure (AF) occur. Since the brainstem lesions that cause respiratory and autonomic dysfunction overlap with each other, these critical manifestations might get worse in parallel. If so, the detection of AF, which is comparatively easy, might be predictive of a latent life-threatening breathing disorder. In 15 patients with MSA, we performed autonomic function tests composed of postural challenges and administered a questionnaire on bladder condition, as well as polysomnography and laryngoscopy during wakefulness and under anesthesia. Polysomnographic variables such as the apnea-hypopnea index (AHI) and oxygen saturation (SpO(2)) and the findings of laryngoscopy were compared with the degree of cardiac and urinary autonomic dysfunction. AHI, mean SpO(2) and the lowest SpO(2) showed significant correlations with urine storage dysfunction. In addition, patients with vocal cord abductor paralysis (VCAP) or central sleep apnea (CSA) contributing to nocturnal sudden death had more severe storage disorders than those without. On the other hand, no significant relationship between polysomnographic variables and orthostatic hypotension was observed except in the case of mean SpO(2). These results indicate that life-threatening breathing disorders have a close relationship with AF, and especially urine storage dysfunction. Therefore, longitudinal assessment of deterioration of the storage function might be useful for predicting the latent progress of VCAP and CSA.

多系統萎縮症患者の睡眠時呼吸障害―覚醒時および睡眠時の喉頭所見―

多系統萎縮症患者の睡眠時呼吸障害―覚醒時および睡眠時の喉頭所見―

Neuromuscular junctions of the posterior cricoarytenoid muscle in multiple system atrophy: a case study

Conclusion: The present study showed a variety of stages of neurogenic degeneration of the muscle fibers and the neuromuscular junctions (NMJs) of the posterior cricoarytenoid (PCA) muscle in multiple system atrophy (MSA). These findings coincide with abductor paralysis of vocal cords. Ultrastructural features of the NMJs of the PCA muscle in MSA were different from those of previous studies on experimental resection of recurrent nerve and amyotrophic lateral sclerosis (ALS). Objectives: MSA may influence various respiratory functions. Upper airway tracts including larynx are affected without exception during its clinical course. Morphological changes of NMJs of the intrinsic laryngeal muscle in MSA were examined ultrastructurally. Patient and methods: The patient was a 68-year-old male complaining of recurrent aspiration pneumonia, dysphagia, respiratory disturbance, and abductor paralysis of vocal cords. The motor nerve terminals of the PCA muscle in a patient with MSA were investigated electron microscopically. Results: The NMJs showed varying degrees of ultrastructural changes by motor nerve degeneration. They were seen in the pre- and post-synaptic regions. Muscle fibers losing nerve terminals showed severe damage in their cytoplasm.

Sleep and breathing in multiple system atrophy

Sleep disorders are common manifestations in multiple system atrophy (MSA) and include reduced and fragmented sleep, excessive daytime sleepiness, rapid eye movement (REM) sleep behavior disorder (RBD), stridor, and sleep-disordered breathing. RBD and nocturnal stridor are considered red flags and may be the first symptoms of the disease. RBD occurs in 90% to 100% of the patients, indicating severe and widespread pathologic impairment in the brain structures that regulate REM sleep. In 50% of the patients, RBD precedes the onset of waking motor symptoms and autonomic failure by several years. Sleep-disordered breathing manifests as 1) central hypoventilation that reflects impaired automatic control of ventilation secondary to degeneration of the pontomedullary respiratory centers; and, more commonly, as 2) stridor and obstructive sleep apnea due to larynx narrowing secondary to combined vocal cord abductor paralysis and excessive adductor activation during inspiration. Nocturnal stridor is a life-threatening condition in MSA associated with respiratory failure and sudden death during sleep. Long-term treatment with continuous positive airway pressure (CPAP) eliminates nocturnal stridor. Tracheostomy is advised when CPAP is not tolerated and stridor occurs during wakefulness.

Daytime Hypoxemia, Sleep-Disordered Breathing, and Laryngopharyngeal Findings in Multiple System Atrophy

The mechanism underlying nocturnal sudden death in patients with MSA remains unclear. It may be explained by upper airway obstruction, such as vocal cord abductor paralysis; an impairment of the respiratory center, such as Cheyne-Stokes respiration; or an impaired hypoxemic ventilatory response. To investigate the mechanism of sleep-disordered breathing in multiple system atrophy (MSA). We recruited 21 patients with probable MSA who were admitted sequentially to our hospital, and performed daytime blood gas analysis, pulmonary function tests, polysomnography, and fiberoptic laryngoscopy during wakefulness and with the patient under anesthesia. A decrease in arterial oxygen pressure and an increase in alveolar-arterial oxygen gradient significantly correlated with disease duration (P = .045 and .046, respectively). Polysomnography demonstrated Cheyne-Stokes respiration in 3 (15%) of 20 patients. Fiberoptic laryngoscopy during wakefulness showed that 3 (14%) of the 21 patients exhibited vocal cord abductor paralysis, and laryngoscopy under anesthesia showed that 9 (45%) of 20 patients exhibited vocal cord abductor paralysis. Laryngoscopy under anesthesia also revealed that 11 (55%) of 20 patients showed upper airway obstruction in places other than the vocal cords, including obstruction at the base of the tongue or soft palate. In addition, it demonstrated novel laryngopharyngeal findings, such as floppy epiglottis and airway obstruction at the arytenoid. We observed daytime hypoxemia with an increased alveolar-arterial oxygen gradient, Cheyne-Stokes respiration, and novel abnormal laryngopharyngeal movements in patients with MSA. We also found that laryngoscopy under anesthesia might be useful for evaluating upper airway obstruction. The significance of these findings to the mechanism of sudden death in those with MSA needs to be examined.

Surgical management of bilateral abductor paralysis by extralaryngeal approach.

Paralysis of the abductors of both vocal cords causes the vocal cords to lie in the midline or paramedian position. This compromises the airways and causes respiratory distress which may often be acute necessitating tracheostomy. A lateralisation of the vocal cord is required to provide adequate airway without significantly affecting speech. Extralaryngeal approach is our preferred approach. This article reports a study of eight cases who underwent arytenoid abduction by an extralaryngeal approach for bilateral abductor paralysis of vocal cords.

A Variant Form of Nasogastric Tube Syndrome

Nasogastric tube syndrome named by Sofferman et al in 1981 is a laryngeal complication presenting with life-threatening vocal cord abductor paralysis derived from peroforation of the NG tube-induced esophageal ulcer. As compared with the previously reported cases of this syndrome, our 4 autopsied patients were so peculiar in the following two points that vocal cord abductor paralysis developed repeatedly and no esophageal ulcer was present in spite of the presence of the laryngeal abductor muscle injury. We hypothesized that the etiology of such a variant form was circulatory injury of the laryngeal abductor muscle which was caused by the compression of the postcricoid blood vessels perfusing this muscle. Nasogastric tube syndrome, which is treatable by decannulation, cannot be ruled out even if no esophageal ulcer is detected by fiberoptic laryngoscopy.

Vocal cord abductor paralysis evaluated by laryngoscopy in multiple system atrophy

Objectives: Multiple system atrophy (MSA) is a chronic neurological disorder characterized by atypical parkinsonism and autonomic dysfunction. Sudden death during sleep is common among MSA patients. Sleep laryngoscopy demonstrates the restriction of abduction of vocal cords with a markedly reduced size of the glottic chink. Vocal cord abductor paralysis (VCAP) is considered to be an important predisposing factor of sudden death in MSA. The aim of this study was to elucidate the effects of VCAP on sleep and the utility of awake and sleep laryngoscopy in MSA. Methods: We recruited 14 patients with MSA presenting with snoring (4 men and 10 women; mean age, 54.6 years; disease duration, 4.2 years; International Cooperative Ataxia Rating Scale [ICARS], 46.9). After performing arterial blood gas analysis, spirometry, and polysomnography (PSG), awake and sleep laryngoscopy were performed. Results: Sleep laryngoscopy revealed that 7 patients exhibited VCAP and 7 patients did not. Between these 2 groups, there were no significant difference in the following findings: sex, disease duration, ICARS, findings of daytime blood gas analysis and PSG findings (mean SpO2 during sleep, AI, AHI and arousal index). Five of 7 patients who exhibited VCAP also showed bilateral arytenoidal tremor on awake laryngoscopy. Conclusion: These findings suggest that MSA should be followed by sleep laryngoscopy, however, it is difficult to perform sleep laryngoscopy as a routine evaluation. Since early diagnosis of VCAP is difficult to make on awake laryngoscopy, arytenoidal tremor may be useful as a sign to predict VCAP.

多系統萎縮症に起因した声帯麻痺による睡眠時呼吸障害

Bilateral vocal cord abductor paralysis (VCAP) is frequently associated with multiple system atrophy (MSA). The early clinical manifestation of VCAP is nocturnal inspiratory stridor simulating heavy snoring that is observed in patients with obstructive sleep apnea syndrome. We have observed two cases of respiratory disturbance during sleep due to VCAP caused by MSA. Using laryngofibroptic examination, vocal cord movements were analyzed during wakefulness as well as during sleep induced by intravenous administration of diazepam. In case 1, VCAP was observed not only during wakefulness but also during sleep. In case 2, although VCAP was observed only during sleep, the vocal cords' movement in breathing at rest was normal in the course of wakefulness. As a treatment, continuous positive airway pressure (CPAP) was applied for the respiratory disturbance during sleep. In case 1, apnea-hypopnea index (AHI) as well as the sleep architecture completely recovered and daytime sleepiness improved. In case 2, the sleep architecture became worse despite improvement of the AHI; as a result, treatment by CPAP was given up. These results indicate that CPAP should initially be applied toward the respiratory disturbance during sleep in MSA.