Journal of Otolaryngology Head & Neck Surgery Category: Clinical Type: Review Article

Voice Disorders Associated to Covid-19: A Theory Domain Review

Guilherme Simas Do Amaral Catani1*, Aurenzo Goncalves Mocelin2, Maria Eduarda Catani3, Alvaro João Storto Ferreira3, Gustavo De Araujo Nishimoto3 and Rogério Hamerschmidt1
1 Physician And Professor Of Otorhinolaryngology, Department At Federal University Of Paraná And Hospital De Clínicas, 285, St. Padre Camargo, Curitiba, PR Zip Cod.: 80060-240, Brazil
2 Medical Student At Federal University Of Parana, Brazil
3 Medical Student At University Center Of Brusque, Brazil

*Corresponding Author(s):
Guilherme Simas Do Amaral Catani
Physician And Professor Of Otorhinolaryngology, Department At Federal University Of Paraná And Hospital De Clínicas, 285, St. Padre Camargo, Curitiba, PR Zip Cod.: 80060-240, Brazil
Tel:+55 41 9 9181-9070,
Email:gscatani@gmail.com

Received Date: Feb 11, 2022
Accepted Date: Mar 02, 2022
Published Date: Mar 08, 2022

Abstract

The Corona Virus disease (COVID-19) was detected for the first time in December of 2019, since then many studies reported voice disorders associated with mild and severe COVID-19. These vocal disorders occur from many etiologies, such as neuronal, respiratory, or vocal fold disorders. Also, they can be a consequence of the damage caused by the endotracheal intubation and the inflammatory mediators or even a result of the psychogenic factors, which were explored in this revision. Methods: the method used in this review study was the hybrid-narrative review focusing on theories and hypotheses that could explain the relationship between COVID-19 and voice disorders. Results: the hypotheses found that the most relevant factors that could explain the voice alterations were neurotropic property evidenced on the neuronal route of infection of the Sars-Cov-2, inflammatory factor, endotracheal intubation, pulmonary function, psychogenic factor. Conclusion: the association between COVID-19 and voice disorders seems to be a multifactorial result of mechanical traumas and metabolic alterations caused by the inflammation in COVID. The major elements are trauma by endotracheal intubation, systemic inflammatory repercussion, and direct neuronal damage related to the neurotropism of the virus.

Keywords

COVID-19; Dysphonia; Multifactorial Causalities; Speech-Language Pathology; Voice Disorders

Introduction

The Corona Virus Disease (COVID-19) was detected, for the first time, in December 2019, in Wuhan city, China, and further, on March 11, 2020, it was declared by the World Health Organization (WHO) as a “public health emergency of international concern”, as it was already worldwide spread [1]. The human infection with the highly pathogenic coronavirus associated with severe acute respiratory syndrome (SARS-CoV-2) was considered the cause of many infections of the upper and lower respiratory tract infections (RTI) [1]. 

Among its most common symptoms are fever, fatigue, and dry cough. Less frequently, anorexia, dyspnea, sputum production, and myalgias are reported in more than 25% of the cases. In mild or moderate forms of the disease, it is observed to cause sore throat, rhinorrhea, headaches, nausea, and diarrhea. It is also reported that COVID-19 leads to hyposmia/anosmia and taste disturbances [2]. Despite all of those manifestations in the respiratory tract, it has been described in some studies that COVID-19 can cause vocal disorders such as dysphonia. These vocal disorders can be due to many etiologies, such as neuronal, respiratory, or vocal fold disorders, or even a consequence of the damage caused by the endotracheal intubation and the inflammatory mediators or even of the psychogenic factors, which are going to be explored in this revision. 

Production of voice

The voice, as it is heard, is a result of the airstream passing through the vocal folds, making them vibrate and originate the sound of speech, it is resounded and it is articulated in words [3]. Hence, it is exceptional that all of these processes occur reasonably well so the phonation can happen. 

To start the phonation, the vocal folds adduct and approximate, reducing or closing the glottis. The expiration muscles contract so the air can flow out the lungs and generate subglottic pressure. As soon as this subglottic pressure overcomes the glottic closing pressure the vocal folds are stimulated into a self-sustained vibration of the superficial layer of the lamina propria along with the epithelial layer. This vocal fold vibration will modulate the airflow into a pulsating jet flow, which further will develop into a turbulent flow in the vocal tract [4]. To make the harmonics, the air vibration is resounded in the pharyngeal, oral, and nasal cavities. To produce the right phonemes and words, the resounded sound will be articulated by the tongue, the upper lip, the lower lip, the upper teeth, the upper gum ridge (alveolar ridge), the hard palate, the velum (soft palate), the uvula (free-hanging end of the soft palate), the pharyngeal wall, and the glottis (space between the vocal cords) [3]. Therefore, any problem in any of these phases will result in a specific and different kind and intensity of dysphonia.

Materials and Methods

The method used in this review study is the hybrid-narrative review focusing on theories and hypotheses that could explain the relationship between COVID-19 and voice disorders [5]. One embracing query was made to research all articles about this topic. The most relevant articles were selected and reviewed. All articles that had been cited as a reference that could explain any relation between COVID and voice disorders were read and reviewed. 

Protocol

This review was developed according to recommendations of research from the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) and according to the hybrid theory domain design of the study.

In this study, the main question was to evaluate what are the existing theories and hypotheses to explain the association between COVID and voice disorder. Being the primary objective "to verify which are the main studied causes of COVID-related voice disorders". 

Research strategy

The authors searched MEDLINE/PubMed, EMBASE, SciELO, and Lilacs databases for all available articles reporting data about the association between COVID and voice disorders. The string used for searching the databases was as follows, considering titles and abstracts: ('covid-19' OR 'sars-cov-2' OR 'severe acute respiratory syndrome' OR 'human coronavirus') AND ('voice' OR 'dysphonia' OR 'dyspnea' OR 'vocal function' OR 'presbyphonia' OR 'voice disorder' OR 'glottic insufficiency' OR 'speech') AND ('vagus nerve' OR 'vagal fiber' OR 'vagal nerve' OR 'peripheral nerve' OR 'nerve' OR 'neurological symptom' OR 'axonal transport' OR 'neurotropic'). 

Study selection

After the studies were searched and listed, the authors evaluated the full texts of eligible articles based on the inclusion and exclusion criteria.

The inclusion criteria were as follows:

(1) Article whose main or secondary objective was to identify and/or explore the relation between COVID and voice disorders and/or voice outcomes of COVID.

(2) Articles whereof the primary or secondary objective was to investigate mechanisms of infection and/or pathogenicity of Sars-CoV-2 that were linked to voice disorders or vocal cord and vagus nerve injury.

The following types of publications were excluded:

(1) Articles that did not investigate any pathophysiological, symptomatic, or subjective outcome that is related to COVID and voice disorder.

(2) Articles in a language other than English that does not have full text available in English.

(3) Publications where original articles were inaccessible (only abstracts were available) and/or incomplete data were provided.

(4) Duplicates. 

Collected data

The authors reviewed all relevant studies and independently extracted data. In order to qualitatively compel, the results were explained and summarized the main theory about the association of COVID and voice disorders available in the medical literature. The results of the review are summarized in the subsequence topics.

Results and Discussion

COVID-19 and Dysphonia

The first studies published didn’t consider dysphonia as one of the clinical symptoms of COVID-19, as it was very overlooked and didn’t catch the attention of the physicians and scientists who were evaluating the sample patients. However, as the researchers were developing and digging deeper, some studies started to consider and question the patients about these problems in the vocal tract, and how it concerned about the voice changes. 

A study with European patients with mild-to-moderate forms of COVID-19 showed a dysphonia prevalence of 26,8%, including a range of 3,7% of the patients with aphonia. The severity of dysphonia was significantly associated with the severity of dysphagia. A significant positive association was found between dysphonia and cough [6,7]. In another study, dysphonia was reported in 43,7% of the patients and it was positively associated with voice fatigue, dyspnea, rhinitis, and cough. In those who presented the disorder, it lasted longer than 2 weeks in 47,1% of them and longer than 1 month in 15,7%, showing the importance and the huge impact of this underestimated symptom [8]. 

Voice disorders are commons on viral infections of the upper respiratory tract and can result from several reasons, neuronal infection, inflammation of vocal folds, the deficit of pulmonary function, and complications of ventilatory support with the definitive airway [6,9-11]. Patients with COVID-19 present with significant impairments of voice particularly after prolonged intubations and tracheostomies [9]. Although, mild and moderate cases also present voice disorders, these cases are associated with a significant prevalence (> 40%) of self-evaluated dysphonia among non-hospitalized COVID-19 patients [8]. 

In this literature review, five main etiological hypotheses were explored to explain the vocal deficits associated with COVID-19. 

Neuronal route and infection

Infectious diseases have been associated with an increased risk of neurological manifestations, remarkably in influenza epidemics [12,13]. In the right conditions depending on viral and host factors, all viruses can reach the Central Nerve System (CNS) [14]. Several human respiratory viruses are neuroinvasive and neurotropic, various neurological manifestations have been reported associated with COVID-19, moreover, about one-third of COVID-19 patients present neurological symptoms during the disease including Peripheral Nervous System (PNS) manifestations such as hyposmia, anosmia, ageusia, and muscle pain [15]. The first published case series studies of COVID19 reported a significant prevalence of neurological manifestations. As with other respiratory viruses, SAR-COV-2 may infect the central nervous system through the hematogenous or retrograde neuronal route [16,17]. 

Furthermore, the hypothesis and association of neurological manifestations and neurotropism have been studied since the first cases of COVID-19. Researchers detected SARS-CoV-2 genetic material in cerebrospinal fluid in the autopsy of infected patients, degeneration of some neurons, as well as macroscopic changes in brain tissue as edema, hyperemia [16,18-21]. Besides SARS-CoV-2 presence was detected in cerebrospinal fluid in a viral encephalitis case and was directly observed in the brain cells of deceased COVID-19 patients, confirming its neurotropic potential [22,23]. 

Interestingly, vagal neuropathies due to upper respiratory viral infections are already clinically recognized as contributors to various sequelae for infectious and post-infectious [24-26]. Some studies describe that some respiratory viruses can reach the brain by the retrograde route via sensory fibers of the vagus nerve infected by the respiratory tract [20,27,28]. 

In this scenario, vagus nerve neuropathy rises as an important hypothesis to explain an etiological factor of dysphonia in COVID-19 patients [20]. SARS-CoV-2 seems to follow no specific route into the human host, but several in parallel, going forward in different speeds, which may explain symptom progression. In this case, viral transport along vagus nerve axons is possibly moving about 2 µm/s in the retrograde direction and because of its anatomy is more likely this dysphonia etiology factor be late [29]. It is known that the vagus nerve function includes the motor, sensory, and taste, involving the pharynx and tongue [30]. The viruses can invade the vagal nucleus and respiratory control center. Therefore, is plausible to hypothesize that if SARS-CoV-2 can reach the brain through the vagus nerve it can lead to respiratory and vocal dysfunction [25,27,28,31]. 

Inflammatory factor

Infection of SARS-CoV-2 often triggers a phenomenon known as “cytokine storm”, an overproduction of pro-inflammatory cytokines which appears to be greater in severe cases [32,33]. A positive correlation of increased pro-inflammatory factor and severity of COVID-19 cases was described. High levels of IL-2R, IL-6, IL-8, and TNF-a were reported to be higher in COVID-19 patients than in healthy individuals and non-severe cases. In addition, IL-6 has been associated with neuroinflammation mediated by astrocytes and microglia during SARS-CoV-2 infection [34,35]. Curiously, there is evidence of greater levels of IL-6 in the cerebrospinal fluid of patients with COVID-19-associated neurological symptoms [36]. 

There is evidence that, in viral infections, the acute inflammatory response may also affect nerve conduction, temporarily slowing its function. During the inflammation of the central and peripheral nervous system, cytokines such as interleukins, arachidonic acid, tumor necrosis factor, and viral products released appear to interfere with the electrophysiology properties of neurons [37]. Cytokine’s flow was assumed to be one of the main causes of neurological manifestations, such as polyneuropathy, which often accompany the viral damage hypoxia-related in nervus tissues that ultimately associate to the neurotoxic pathway [38,39]. Furthermore, some authors credit to inflammation processes the major contribution portion on dysfunction nerves symptoms such as anosmia [40]. The hypothesis of viral inflammation-causing neuropathy has robust precedents [41]. 

Viral-induced inflammation is widely believed to have at least three mechanisms whereby viruses may cause neuropathy:

(1) direct infection and inflammation,

(2) by induction of nonspecific inflammatory response, and

(3) nerve injury as a result of the inflammatory cascade as well as Guillain-Barre syndrome pathophysiology is proposed [24,42]. 

Dysphonia may be associated with laryngeal involvement by the respiratory tract inflammatory process and may be caused by vocal fold edema or inflammation [10]. In addition, the vagus nerve appears that have an important immunomodulatory role in the inflammatory response and inhibition [10,43-45]. Because of that, the vagus nerve infection and damage may contribute to inflammatory factors, which could strengthen the etiology of COVID-19-related dysphonia corditis. However, more studies are necessary to understand the impact of the inflammatory factor in the genesis of COVID-19-related dysphonia. 

Endotracheal intubation

Endotracheal intubation (ETT) is part of the treatment protocol for patients with the severe acute respiratory syndrome (SARS) [46]. Since the first outbreak of the COVID-19 epidemic were reported suggestions of healthcare protocols involving endotracheal intubation for severe cases [47,48]. 

It is known that endotracheal intubation and tracheostomy may cause laryngeal injury, mainly ulcerative lesions that can lead to granuloma formation, vocal fold scarring, and laryngeal stenosis [49-53]. Moreover, functional impact on voice outcomes was a recognized complication of prolonged endotracheal intubation [11,54,55]. Another complication, although uncommon, is the true vocal cord paralysis resulting from peripheral nerve damage caused by nerve compression between an inflated endotracheal tube cuff and the overlying thyroid cartilage [56]. 

In the COVID-19 pandemic, there were reported increased cases of complications following prolonged intubation and tracheostomy [57]. Hence, tracheal intubation seems to be an important cause of voice disorders COVID-19-related in severe cases. Sequels and short-term effects on voice are associated with endotracheal intubation [58-60]. This cause appears to be the most strongly associated with a vocal deficit in severe cases of COVID-19, however, it does not clarify the voice alterations present in mild and moderate cases that did not require ETT [9]. On the other hand, the direct lesions caused by endotracheal intubation do not explain all about voice alterations on postintubation patients, mainly on short-time intubations. Furthermore, objective measures point out that this speech disorder caused by intubation also is probably multifactorial [61]. Other possible causes to explain vocal fold immobility after prolonged intubation are laryngeal intrinsic muscle myopathy/myositis or arytenoid dislocation and inflammation of the cricoarytenoid joint, despite its lower prevalence could also explain some cases of voice disorders [62,63]. 

House et al. found that the size of the endotracheal tube and increased duration of intubation (µ = 9.7 days) were not significantly associated with worse laryngeal injury scores. Shinn, however, concludes on a cohort study that an endotracheal tube greater than size 7.0, diabetes, and larger body habitus may predispose to injury [11]. On the other hand, Santos set forth a significant correlation between increasing duration of intubation and degree of laryngeal injury (µ = 9 days). As a consequence, additional studies are required to further elucidate the real impact and mechanism of each variable linked to the patient who needs intubation that can affect the voice. 

Pulmonary function

Voice sound production is a complex and delicate process in which the respiratory muscles, lungs, and airflow represent essential factors. Especially subglottal pressure and the glottal airflow are responsible for the voice production [4,64]. Phonation requires considerable respiratory function in terms of expiratory flow and expiratory excursions in lung volume [65]. Patients with airway obstructions or pulmonary function deficits may experience difficulty sustaining minimum expiratory flow during phonation [66,67]. Thus, dyspnea is a common manifestation in the acute phase of COVID-19 infection but also a persistent symptom and pulmonary damage are important features able to justify voice disorders [68-71]. Since were reported impaired respiratory muscle strength and abnormalities were reported in pulmonary function tests of COVID-19 patients [72]. Thus, it is possible to compare and propose an association between the prevalence of dyspnea and voice changes during and after viral infection. Nevertheless, there may be confounding biases that can be clarified with further future studies. 

In addition, surprisingly, the vagus nerve may also be associated with this pulmonary etiology once the upper airway receptors stimulated by the dynamic airway compression distortion and collapse may afford vagal afferent impulses contributing to dyspnea [67,73-75]. However, more researches are necessary to assess the exact significance of this association. 

Psychogenic dysphonia

It has been recently established that the SARS-CoV-2 infection may be related to the onset of psychosis, mood disorders, post-traumatic stress depression (PTSD), and even suicide if we consider how self-isolation, physical distancing, and other factors may affect one’s mental health [76]. 

In this matter, such psychological precipitants may also be related to the increase of symptomatology, leading to a special concern over the vulnerability of COVID-19 patients with pre-existent psychiatric conditions, especially those affected by Somatic Syndrome Disorders [77]. 

Psychogenic dysphonia, by itself, is defined as the onset of voice disorders in the absence of primary organic changes in the larynx [78]. Emotional conditions can directly influence the process of phonation, being connected to the functioning of respiratory, phonatory, and articulation mechanisms of voice production [79]. 

It is frequently observed in patients between 30 and 50 years of age with emotional dysfunctions, with a mild predominance on the female sex [80]. Those emotional issues may also affect a wide spectrum of aspects, such as vocal intensity, vocal resonance, vocal range, frequency, among others, and it is well established that anxiety, stress, depression, and social problems are important risk factors of this disorder [81]. 

When it comes to COVID-19, Buseli et al reported a case of a 50-year-old nurse that experienced persistent dysphonia after the resolution of the infection, with no evidence of laryngeal structural dysfunction. Besides the trauma of the disease, this may also be explained by the fact that healthcare professionals are more exposed to moral dilemmas, suffering, and ethical issues, which may contribute to the increase of such symptoms, especially during a worldwide pandemic [79]. 

Although there is not enough evidence in the scientific literature over COVID-19’s impacts on people’s mental conditions, it is safe to recognize that traumatic experiences, fear, and insecurity are, in general, strongly related to somatic disorders and increases the experience of symptoms and physical health [82].

Conclusion

The association between COVID-19 and voice disorders seems to be a multifactorial result of mechanical traumas and metabolic alterations caused by the inflammation in COVID. The treatment for COVID can lead to vocal cord trauma when endotracheal intubation is necessary. Furthermore, non-intubated patients might undergo vocal cord trauma because a severe cough can change the voice quality. The mechanical ventilation with endotracheal intubation was found as the most important factor associated with a vocal alteration. Moreover, the neurotropic behavior of Sars-CoV-2 was pointed out as a possible explanation of this association. The role of inflammatory cytokines, the psychogenic hypothesis, and the pulmonary function were evaluated as possible factors that could be involved in the pathophysiology of voice disorder COVID-related. Nonetheless, its impact on voice dysfunction is unclear.

Declaration of Competing Interests

The authors do not have any financial interests or conflicts of interest.

References

  1. Habas K, Nganwuchu C, Shahzad F, Gopalan R, Haque M, et al. (2020) Resolution of coronavirus disease 2019 (COVID-19). Expert Rev Anti Infect Ther 18: 1201-1211.
  2. Krajewska J, Krajewski W, Zub K, Zato?ski T (2020) COVID-19 in otolaryngologist practice: a review of current knowledge. Eur Arch Oto-Rhino-Laryngology 277: 1885-1897.
  3. https://www.britannica.com/topic/articulation-speech
  4. Zhang Z (2016) Mechanics of human voice production and control. J Acoust Soc Am 140: 2614-2635.
  5. Paul J, Criado AR (2020) The art of writing a literature review: What do we know and what do we need to know? Int Bus Rev 29: 101717.
  6. Lechien JR, Chiesa-Estomba CM, Cabaraux P, Mat Q, Huet K, et al. (2020) Features of mild-to-moderate COVID-19 patients with dysphonia. J Voice.
  7. Lechien JR, Chiesa-Estomba CM, Place S, Van Laethem Y, Cabaraux P, et al. (2020) Clinical and epidemiological characteristics of 1420 European patients with mild-to-moderate coronavirus disease 2019. J Intern Med 288: 335-344.
  8. Cantarella G, Aldè M, Consonni D, Zuccotti G, Berardino F Di, et al. (2021) Prevalence of dysphonia in non-hospitalized patients with covid-19 in Lombardy, the Italian epicenter of the pandemic. J Voice 1997: 00108-00109
  9. Archer SK, Iezzi CM, Gilpin L (2021) Swallowing and voice outcomes in patients hospitalized with COVID-19: an observational cohort study. Arch Phys Med Rehabil 102: 1084-1090.
  10. Johnston GR, Webster NR (2009) Cytokines and the immunomodulatory function of the vagus nerve. Br J Anaesth 102: 453-462.
  11. Shinn JR, Kimura KS, Campbell BR, Sun Lowery A, Wootten CT, et al. (2019) Incidence and Outcomes of Acute Laryngeal Injury After Prolonged Mechanical Ventilation. Crit Care Med 47: 1699-1706.
  12. Gialluisi A, de Gaetano G, Iacoviello L (2020) New challenges from Covid-19 pandemic: an unexpected opportunity to enlighten the link between viral infections and brain disorders? Neurol Sci 41: 1349-1350.
  13. Henry J, Smeyne RJ, Jang H, Miller B, Okun MS (2010) Parkinsonism and neurological manifestations of influenza throughout the 20th and 21st centuries. Parkinsonism Relat Disord 16: 566-571.
  14. Koyuncu OO, Hogue IB, Enquist LW (2013) Virus infections in the nervous system. Cell Host Microbe 13: 379-393.
  15. Niazkar HR, Zibaee B, Nasim A, Bahri N (2020) The neurological manifestations of COVID-19. Prat Neurol – FMC 11: 145-146.
  16. Mao L, Jin H, Wang M, Hu Y, Chen S, et al. (2020) Neurologic manifestations of hospitalized patients with coronavirus disease 2019 in Wuhan, China. JAMA Neurol 77: 683-690.
  17. Briguglio M, Bona A, Porta M, Dell’Osso B, Pregliasco FE, et al. (2020) Disentangling the Hypothesis of Host Dysosmia and SARS-CoV-2: The Bait Symptom That Hides Neglected Neurophysiological Routes. Front Physiol 11: 1-13.
  18. https://journals.lww.com/cmj/Fulltext/2020/05050/Diagnosis_and_Treatment_Protocol_for_Novel.13.aspx
  19. Desforges M, Le Coupanec A, Brison É, Meessen-Pinard M, Talbot PJ (2014) Human respiratory coronaviruses: neuroinvasive, neurotropic and potentially neurovirulent pathogens. Virol (Montrouge, Fr 18: 5-16.
  20. Yachou Y, El Idrissi A, Belapasov V, Ait Benali S (2020) Neuroinvasion, neurotropic, and neuroinflammatory events of SARS-CoV-2: understanding the neurological manifestations in COVID-19 patients. Neurol Sci 41: 2657-2669.
  21. Lau KK, Yu WC, Chu CM, Lau ST, Sheng B, et al. (2004) Possible Central Nervous System Infection by SARS Coronavirus. Emerg Infect Dis J 10: 342.
  22. Moriguchi T, Harii N, Goto J, Harada D, Sugawara H, et al. (2020) A first case of meningitis/encephalitis associated with SARS-Coronavirus-2. Int J Infect Dis 94: 55-58.
  23. Paniz-Mondolfi A, Bryce C, Grimes Z, Gordon RE, Reidy J, et al. (2020) Central nervous system involvement by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). J Med Virol 92: 699-702.
  24. Amin MR, Koufman JA (2001) Vagal neuropathy after upper respiratory infection: A viral etiology? Am J Otolaryngol 22: 251-256.
  25. Rees CJ, Henderson AH, Belafsky PC (2009) Postviral vagal neuropathy. Ann Otol Rhinol Laryngol 118: 247-252.
  26. Niimi A, Chung KF (2015) Evidence for neuropathic processes in chronic cough. Pulm Pharmacol Ther 35: 100-104.
  27. Bohmwald K, Espinoza JA, González PA, Bueno SM, Riedel CA, et al. (2014) Central nervous system alterations caused by infection with the human respiratory syncytial virus. Rev Med Virol 24: 407-419.
  28. Driessen AK, Farrell MJ, Mazzone SB, McGovern AE (2016) Multiple neural circuits mediating airway sensations: Recent advances in the neurobiology of the urge-to-cough. Respir Physiol Neurobiol 226: 115-120.
  29. Bearer EL, Breakefield XO, Schuback D, Reese TS, LaVail JH (2000) Retrograde axonal transport of herpes simplex virus: Evidence for a single mechanism and a role for tegument. Proc Natl Acad Sci 97: 8146-8150.
  30. https://www.ncbi.nlm.nih.gov/books/NBK545209/
  31. Ikeda K, Kawakami K, Onimaru H, Okada Y, Yokota S, et al. (2017) The respiratory control mechanisms in the brainstem and spinal cord: integrative views of the neuroanatomy and neurophysiology. J Physiol Sci 67: 45-62.
  32. Mahallawi WH, Khabour OF, Zhang Q, Makhdoum HM, Suliman BA (2018) MERS-CoV infection in humans is associated with a pro-inflammatory Th1 and Th17 cytokine profile. Cytokine 104: 8-13.
  33. Wong CK, Lam CWK, Wu AKL, Ip WK, Lee NLS, et al. (2004) Plasma inflammatory cytokines and chemokines in severe acute respiratory syndrome. Clin Exp Immunol 136: 95-103.
  34. Han H, Ma Q, Li C, Liu R, Zhao L, et al. (2020) Profiling serum cytokines in COVID-19 patients reveals IL-6 and IL-10 are disease severity predictors. Emerg Microbes Infect 9: 1123-1130.
  35. Qin C, Zhou L, Hu Z, Zhang S, Yang S, et al. (2020) Dysregulation of immune response in patients with Coronavirus 2019 (COVID-19) in Wuhan, China. Clin Infect Dis 71: 762-768.
  36. Benameur K, Agarwal A, Auld SC, Butters MP, Webster AS, et al. (2021) Encephalopathy and encephalitis associated with cerebrospinal fluid cytokine alterations and coronavirus disease, Atlanta, Georgia, USA, 2020. Emerg Infect Dis 26: 2016-2021.
  37. Köller H, Siebler M, Hartung H-P (1997) Immunologically induced electrophysiological dysfunction: implications for inflammatory diseases of the cns and pns. Prog Neurobiol 52: 1-26.
  38. Stainsby B, Howitt S, Porr J (2011) Neuromusculoskeletal disorders following SARS: a case series. J Can Chiropr Assoc 55: 32-39.
  39. De Chiara G, Marcocci ME, Sgarbanti R, Civitelli L, Ripoli C, et al. (2012) Infectious agents and neurodegeneration. Mol Neurobiol 46: 614-638.
  40. Lorenzo Villalba N, Maouche Y, Alonso Ortiz MB, Cordoba Sosa Z, Chahbazian JB, et al. (2020) Anosmia and dysgeusia in the absence of other respiratory diseases: should covid-19 infection be considered? Eur J case reports Intern Med 7: 001641.
  41. Achar A, Ghosh C (2020) COVID-19-associated neurological disorders: the potential route of cns invasion and blood-brain relevance. Cells 9: 2360.
  42. Giovannoni G, Hartung HP (1996) The immunopathogenesis of multiple sclerosis and Guillain-Barré syndrome. Curr Opin Neurol 9: 165-177.
  43. Pavlov VA, Tracey KJ (2012) The vagus nerve and the inflammatory reflex—linking immunity and metabolism. Nat Rev Endocrinol 8: 743-754.
  44. Kox M, Pompe JC, Pickkers P, Hoedemaekers CW, van Vugt AB, et al. (2008) Increased vagal tone accounts for the observed immune paralysis in patients with traumatic brain injury. Neurology 70: 480-485.
  45. JM H (2012) The vagus nerve and the inflammatory reflex: wandering on a new treatment paradigm for systemic inflammation and sepsis. Surg Infect 13: 187-193.
  46. Fan E, Brodie D, Slutsky AS (2018) Acute respiratory distress syndrome: advances in diagnosis and treatment. JAMA 319: 698-710.
  47. Xia H, Huang S, Xiao W, Lin Y, Hu X, et al. (2020) Practical workflow recommendations for emergency endotracheal intubation in critically ill patients with COVID-19 based on the experience of Wuhan Union Hospital. J Clin Anesth 66: 109940.
  48. Pisano A, Yavorovskiy A, Verniero L, Landoni G (2020) Indications for tracheal intubation in patients with coronavirus disease 2019 (COVID-19). J Cardiothorac Vasc Anesth 35: 1276-1280.
  49. Schweiger C, Manica D. Estenose da Laringe. (2015) In: Piltcher OB, Costa SS da, Maahs GS, Kuhl G, editors. Rotinas em Otorrinolaringologia. Porto Alegre: Artmed; pp. 380-386.
  50. Jorgensen J, Wei JL, Sykes KJ, Klem SA, Weatherly RA, et al. (2007) Incidence of and risk factors for airway complications following endotracheal intubation for bronchiolitis. Otolaryngol Head Neck Surg 137: 394-399.
  51. House JC, Noordzij JP, Murgia B, Langmore S (2012) Laryngeal injury from prolonged intubation: a prospective analysis of contributing factors. Laryngoscope 121: 596-600.
  52. Bertone F, Robiolio E, Gervasio CF (2020) Vocal cord ulcer following endotracheal intubation for mechanical ventilation in COVID-19 pneumonia: A case report from northern Italy. Am J Case Rep 21: 1-4.
  53. Jackson C (1953) Contact ulcer granuloma and other laryngeal complications of endotracheal anesthesia. Anesthesiology 14: 425-436.
  54. Benninger MS, Alessi D, Archer S, Bastian R, Ford C, et al. (1996) Vocal Fold Scarring: Current Concepts and Management. Otolaryngol Neck Surg 115: 474-482.
  55. Brodsky MB, Levy MJ, Jedlanek E, Pandian V, Blackford B, et al. (2018) Laryngeal injury and upper airway symptoms after oral endotracheal intubation with mechanical ventilation during critical care: A systematic review. Crit Care Med 46: 2010-2017.
  56. Cavo JW (1985) True vocal cord paralysis following intubation. Vol. 95, Laryngoscope pp. 1352-1359.
  57. Rouhani MJ, Clunie G, Thong G, Lovell L, Roe J, et al. (2021) A Prospective Study of voice, swallow, and airway outcomes following tracheostomy for COVID-19. Laryngoscope 131: E1918-E1925.
  58. Hamdan AL, Sibai A, Rameh C, Kanazeh G (2007) Short-term effects of endotracheal intubation on voice. J Voice 21: 762-768.
  59. Sørensen MK, Durck TT, Bork KH, Rasmussen N (2016) Normative values and interrelationship of mdvp voice analysis parameters before and after endotracheal intubation. J Voice 30: 626-630.
  60. Bastian RW, Richardson BE (2001) Postintubation phonatory insufficiency: An elusive diagnosis. Otolaryngol Head Neck Surg 124: 625-633.
  61. Mayo R, Beckford NS, Wilkinson III A, Tierney M (1990) Effects of short-term endotracheal intubation on vocal function. Laryngoscope 100: 331-336.
  62. Yin SS, Qiu WW, Stucker FJ (1996) Value of electromyography in differential diagnosis of laryngeal joint injuries after intubation. Ann Otol Rhinol Laryngol 105: 446-451.
  63. Sataloff RT, Bough ID, Spiegel JR (1994) Arytenoid dislocation: diagnosis and treatment. Laryngoscope 104: 1353-1361.
  64. Erath BD, Peterson SD, Zañartu M, Wodicka GR, Plesniak MW (2011) A theoretical model of the pressure field arising from asymmetric intraglottal flows applied to a two-mass model of the vocal folds. J Acoust Soc Am 130: 389-403.
  65. Binazzi B, Lanini B, Bianchi R, Romagnoli I, Nerini M, et al. (2006) Breathing pattern and kinematics in normal subjects during speech, singing and loud whispering. Acta Physiol 186: 233-246.
  66. Hyatt RE (1961) The interrelationships of pressure, flow, and volume during various respiratory maneuvers in normal and emphysematous subjects. Am Rev Respir Dis 83: 676-683.
  67. O’Donnell DE, Revill SM, Webb KA (2001) Dynamic hyperinflation and exercise intolerance in chronic obstructive pulmonary disease. Am J Respir Crit Care Med 164: 770-777.
  68. Carfì A, Bernabei R, Landi F (2020) Persistent symptoms in patients after acute COVID-19. JAMA 324: 603-605.
  69. Xiong Q, Xu M, Li J, Liu Y, Zhang J, et al. (2021) Clinical sequelae of COVID-19 survivors in Wuhan, China: a single-centre longitudinal study. Clin Microbiol Infect 27: 89-95.
  70. De Lorenzo R, Conte C, Lanzani C, Benedetti F, Roveri L, et al. (2020) Residual clinical damage after COVID-19: A retrospective and prospective observational cohort study. PLoS One 15: e0239570.
  71. Cortés-Telles A, López-Romero S, Figueroa-Hurtado E, Pou-Aguilar YN, Wong AW, et al. (2021) Pulmonary function and functional capacity in COVID-19 survivors with persistent dyspnoea. Respir Physiol Neurobiol 288: 103644.
  72. Huang Y, Tan C, Wu J, Chen M, Wang Z, et al. (2020) Impact of coronavirus disease 2019 on pulmonary function in early convalescence phase. Respir Res 21: 163.
  73. Eltayara L, Becklake MR, Volta CA, Milic-Emili J (1996) Relationship between chronic dyspnea and expiratory flow limitation in patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med 154: 1726-1734.
  74. Burki NK, Lee LY (2010) Mechanisms of dyspnea. Chest 138: 1196-1201.
  75. Burki NK, Lee LY (2010) Blockade of airway sensory nerves and dyspnea in humans. Pulm Pharmacol Ther 23: 279-282.
  76. Gunnell D, Appleby L, Arensman E, Hawton K, John A, et al. (2020) Suicide risk and prevention during the COVID-19 pandemic. The Lancet Psychiatry 7: 468-471.
  77. Colizzi M, Bortoletto R, Silvestri M, Mondini F, Puttini E, et al. (2020) Medically unexplained symptoms in the times of COVID-19 pandemic: A case-report. Brain Behav Immun Health 5: 100073.
  78. Koszty?a-Hojna B, Moskal-Jasi?ska D, Kraszewska A, ?obaczuk-Sitnik A, Zdrojkowski M, et al. (2019) Verbal communication disorders in psychogenic dysphonia. Otolaryngol Pol 73: 1-5.
  79. Buselli R, Corsi M, Necciari G, Pistolesi P, Baldanzi S, et al. (2020) Sudden and persistent dysphonia within the framework of COVID-19: The case report of a nurse. Brain Behav Immun Health 9: 100160.
  80. Baker J (2003) Psychogenic voice disorders and traumatic stress experience: A discussion paper with two case reports. J Voice 17: 308-318.
  81. Martins RHG, Tavares ELM, Ranalli PF, Branco A, Pessin ABB (2014) Psychogenic dysphonia: Diversity of clinical and vocal manifestations in a case series. Braz J Otorhinolaryngol 80: 497-502.
  82. Morina N, Kuenburg A, Schnyder U, Bryant RA, Nickerson A, et al. (2018) The association of post-traumatic and postmigration stress with pain and other somatic symptoms: An explorative analysis in traumatized refugees and asylum seekers. Pain Med 19: 50-59.

Citation: Catani GSA, Mocelin AG, Catani ME, Ferreira AJS, Nishimoto GA, et al. (2022) Voice Disorders Associated to Covid-19: A Theory Domain Review. J Otolaryng Head Neck Surg 8: 68

Copyright: © 2022  Guilherme Simas do Amaral Catani, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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