What if Ursula ruined Ariel's voice instead of stole it?

I have been infatuated with The Little Mermaid since I was a little boy. Well, of course, as I was growing up, I wasn't really subjected to gender expectations and was therefore given the full liberty to fall in love with whatever that comes in my way. I am impressed by the power of time, the ability of time to shift my focus from A to B. All those years back, I love the film for the eccentricity of its setting (I mean, I've always thought of residing in the darkest corners of the seven seas, singing and dancing amongst the coral reefs and prancing with crabs like Sebastian). I love the idea of liberty that is promoted in the film, the lengths that Ariel took to gain her own voice and create a future she ardently desired. However, now that I look at it, I do appreciate King Triton's (Ariel's father) feelings and worries. I think the message of the story should be, instead of praising Ariel's wits and courage, that one's parents will always be there for their children, regardless of what they've done. Regardless of their lack of gratitude, and even instances of betrayal.

More importantly, as I rewatch the film for the millionth time (it can be taken as literal), I've realised one important medical issue. What if Ursula ruined Ariel's voice instead of stole it? Lauded as one of the most significant scenes of the story, Ursula, the Sea Witch banished by King Triton due to her wicked plans, exploited Ariel's weakness and desperation to live on land. She wished to gain control of King Triton's kingdom and rule over as queen. The evil plan was executed as she forced Ariel to sign a binding contract (sort of like banks if you think about it). If Ariel failed to be kissed by the prince (the kiss 'of true love') before the sunset on the third day, she would become Ursula's property. The price paid, independent of the other conditions of the contract, was her voice. Well, in legal terms, it won't be stealing but in laymen's terms, Ariel was sort of coerced or pressurised to enter into the contract. It doesn't take much to convince us that this is equivalent to stealing in the ordinary context.

In medicine, no ordinary person can steal one's voice straight off, unless a maniac has taken the idea to extremes and resected one's entire larynx. The typical scenario is the gradual destruction of the voice. Voice here refers to the end of the road - the utterances synthesised by the sound production process. Before we delve deeper into the modern-day Ursula and her grand schemes of deviousness, let's have a summary of the sound production process.

Sound production is an interesting topic and it typically involves three separate structures: (1) the upper respiratory tract, (2) the larynx - specifically, the (true) vocal cords, and (3) the lungs and the diaphragm (they count as the core of the respiratory system, so one unitary structure in this sense). We start with breathing. We inhale and air enters our lungs. The diaphragm is flattened and the external intercostal muscles contract, leading to the increase in the negativity of intrathoracic pressure. It is easier for air to enter due to the increase in pressure gradient. Our focus then turns to exhalation.

Diagram showing the steps of sound production - extracted from: https://voicefoundation.org/wp-content/uploads/2013/09/ap_01_500.jpg.

This is a very good diagram illustrating the various steps of the process. The process, also called 'phonation' or 'voicing', refers to the conversion of air pressure from the lungs into actual vibrations. These vibrations form the sounds that we can recognise. Of course, vibration in itself is also a very good 'currency' for our body. Our ears are accustomed to converting sound waves into vibrations so that sounds can be perceived and the eardrum does precisely that. Going back to phonation, let's commence from Step 5, where both the top and bottom parts of the vocal cords are open. In this case, when the bottom part is closing up, the top part is still open. This is somehow due to the discrepancies in air pressure experienced by the two. The lungs are expunging the air out of their premises and, as a consequence, the intrathoracic pressure gets more and more negative (at the height, when they are filled with air, the intrathoracic pressure is less negative). However, as soon as the top part gets closed as well (with no air squeezing through since the bottom part is closed) (Step 10), the remaining air in the lungs, still in the process of evacuation, builds up inferiorly to the larynx. It's like one of those border checkpoints where the gates are closed but the queue is getting longer and longer. Sooner or later, this forces the bottom part to open. The vibrations travel from the bottom part to the top part and a puff of air accompanies this transmission. This is called the Bernoulli Effect.

However, this only explains how sounds are produced, not refined or modulated. What happens next? This part is much easier. Once the sound is made out of the vibrations of the vocal cords, the features of the upper respiratory tract up and including the structures of the mouth, like the teeth and tongue, are crucial in modulating the characteristics of the sounds. Therefore, we produce different sounds to emulate different languages and modes of communication. Moreover, pitches are modified through altering the thickness (and length) of the (true) vocal cords. This is done using the intrinsic muscles of the larynx.

Why do I keep bracketing the word 'true' in front of vocal cords? Are there not a pair of vocal folds in every human body? Well, this is kind of an issue with the nomenclature. It is not an issue with the physiology, since the (true) vocal cords are the only ones responsible for producing sounds.

<The first three diagrams displayed below are extracted from Teach Me Anatomy, retrieved from URL: https://teachmeanatomy.info/neck/viscera/larynx/ligaments-folds/>

Diagram showing the ligaments and membranes of the larynx - with the vestibular folds, also known as the 'false vocal cords', being superior to the vocal folds, also known as the 'true vocal cords', in terms of anatomical location. The vestibular folds arise from the inferior edge of the quadrangular membrane (not displayed here) and are used for protection. The vocal folds arise from the superior edge of the cricothyroid membrane.

This is an axial cross-section of the larynx, showing the vocal folds and vestibular folds. Of note, the vestibular folds are not for voicing. They are formed from mucous membranes and are fixed, therefore unable to synthesise any sounds. For the vocal folds, they are intrinsically connected to the muscles of the larynx. That's why the muscles can modulate the thickness of such folds, thereby creating sounds of varying pitches.

The diagram shows the thyrohyoid and cricothyroid membranes.

This diagram shows a different view of the larynx and labels the quadrangular membrane, which goes from the lateral edges of the epiglottis (elastic cartilage) to the anterolateral edges of the arytenoid cartilages and the posteroinferior portions of the corniculate cartilages (very small cartilages associated with the arytenoid ones). The quadrangular membrane is associated with Structures A from the diagram, which are the vestibular folds. This diagram is extracted from: https://s3.amazonaws.com/classconnection/344/flashcards/6382344/png/larynx_-_ligaments_quadrangular_membrane-1511AA0C6611DEED042.png.

Having been introduced the normal physiology, we know that whenever one of the components, i.e. larynx (true vocal cords), respiratory system, or upper respiratory tract and associated oral structures, is affected, one's voice is changed effectively. In many cases, this can be a physiological change. The best example is puberty in boys, where the pitch of the voice is substantially lowered. What if it's a pathological change? What if the voice change entails something more serious than just playground banter?

It transpires that different changes in the voice indicate different pathologies and this comes with clinical experience. Moreover, it is nearly impossible to elucidate all pathologies which can be associated with voice changes. As a general rule, if it's about the weakness of the voice, we start to think about breathing since the source 'puff of air' is not strong enough to generate robust vibrations. If the individual sounds are weird, such as blighted clarity of pronunciation (note slurring of speech) exemplified by inappropriate glottal stops, then we think about the oral structures and the upper respiratory tract. If it's anything to do with the pitch and hoarseness, we turn our attention to the larynx. In addition, never forget neurological abnormalities since patent nerve endings are crucial in the normal functioning of these structures. An abnormal voice can be graded by the GRBAS Scale, with components namely being: Grade, Roughness, Breathiness, Asthenia (weakness) and Strain. It is used by ENT Surgeons to evaluate any issues to do with the larynx and upper respiratory structures.

Any pathology related to the voice due to a non-neurological abnormality is called dysphonia. Any pathology related to the content of speech, such as comprehension and articulation, is called dysphasia (brain problem, such as but not limited to: ischaemic stroke, intracranial haemorrhage, and traumatic brain injury). Any pathology related to the voice due to a neurological abnormality is called dysarthria.

This all seems a little bit abstract and confusing. Let's illustrate this with a case study.

Case Study:

Archibald* presents to the outpatient clinic (not A&E this time) complaining of recent changes in voice, as observed by his family and colleagues, and haemoptysis (coughing of blood). He is a 23-year old male teacher.

Patient Profile:

CHIEF COMPLAINT(S) & ASSOCIATED FEATURES:

1. Recent Changes in Voice: Progressive and persistent hoarseness in voice with no prior episodes observed; changes alerted by his family and his students - first detected three months ago; for the purposes of simplicity, let's just say that the GRBAS score is abnormal; the changes in voice are not serious enough to cause an impairment to his quality of life;

2. Coughing and Haemoptysis: haemoptysis started about a week ago, against the backdrop of chronic coughing (for about 4 months); progressive severity in coughing in terms of frequency; there have not been previous episodes of haemoptysis; in terms of the quality of haemoptysis, there is fresh blood (reddish in colour); the amount of blood coughed is described as 'minor'; no identifiable factors behind exacerbation or amelioration;

3. Neck Masses: as reported by the patient (that's why we want to examine it later on), there are progressively large masses over the left lateral aspect of the mid-portion of the neck. They are persistent in course and are first observed two weeks ago. There are no past episodes of the phenomenon.

4. Constitutional Symptoms: night sweats, unexplained weight loss (waist measure dropped from 32 to 29 in the span of two months without exercising), malaise;

5. Anaemic Symptoms: Shortness of Breath only (for the past few weeks); no other anaemic symptoms.

Review of systems returns nothing of note. Significantly, the patient does not have odynophagia, nor dysphagia.

This diagram shows the key anatomical structures of the neck. Of note, notice the distribution of lymph nodes in the head and neck region - they are divided into 6 groups, numbered by roman numerals. As clarification, Group VI lymph nodes are located at the anterior neck. In terms of drainage, there is no magic - the structures are drained by the lymph nodes closest to them. For instance, the thyroid gland is drained by Group IV lymph nodes and the tip of the tongue, Group IA. This diagram is extracted from: https://tech.snmjournals.org/content/jnmt/35/1/10/F2.large.jpg.

PAST MEDICAL & SURGICAL HISTORY:

1. Past history of vocal polyps and associated voice hoarseness; a total of two times, taking place respectively 3 and 7 years prior; both instances warranted surgical removal, although the exact reasons behind the surgical operation were unclear;

2. The patient has received, in private settings, the quadrivalent HPV Vaccine (hang in there, this is relevant);

3. No chronic diseases; nor are there any past instances of malignancy. The patient also has no history (known) of immunodeficiency problems, such as diabetes mellitus and HIV;

4. There is no history of autoimmune disorders. Nor are there any known allergies, asthma or skin problems.

FAMILY HISTORY:

1. Mother died of Stage IV cervical cancer when he was merely a child;

2. Father diagnosed squamous cell carcinoma of the tongue last year and is currently recovering from surgery (he received surgical resection of the lesion and reconstruction of the tongue).

3. No family history of any respiratory disorders or any other malignancies. No other chronic or genetic conditions known in the family.

DRUG HISTORY: Unremarkable; no drug allergies known; no chronic medication taken; no known history of recreational drug use.

SOCIAL HISTORY:

1. Heavy Smoker (sixteen cigarettes per day for the past five months, increased from an average of one to two cigarettes per week for the past six years);

2. Moderately-high alcohol consumption (exceeding 18 units of alcohol per week after calculation, for the past three month; prior to that, roughly 13 to 14 units per week, for roughly five years);

3. Living alone; life stressors identified as follows- break-up with long-term girlfriend a few months ago, persistently low-mood and anxiety issues, work pressure, family health issues, financial worries (albeit not serious);

4. Occupation as a teacher of Biology; post held for the last three years.

INFECTIOUS HISTORY: Unremarkable. The patient does not have recent travel history.

DIETARY HISTORY: Unremarkable.

At this point, we have decided to shift our focus to the head and neck region, as well as the respiratory system. The major symptoms are haemoptysis (hence also coughing), voice hoarseness, shortness of breath, neck masses and constitutional symptoms. We are concerned about malignancy (which is always a red flag and placed on the list of differential diagnoses, just in case) due to the presence of constitutional symptoms and the presence of haemoptysis (which can indicate destruction of underlying tissue through tumour invasion). The presence of neck masses may also be indicative of lymph node metastasis (or reactive lymph nodes, which are intrinsic immunological phenomena in response to the dispersion of foreign-labelled, tumour cells). However, the old maxim of 'common things come first' cannot be ignored. There might still be a possibility that the voice hoarseness is due to phonotrauma. Phonotrauma can lead to the formation of vocal nodules. It means that, as a teacher, the patient might always have to project his voice loud enough for the class to hear or basically reprimand troublemakers. The vocal folds may have incurred persistent trauma that the patient fails to notice. This explains the voice hoarseness, but not other symptoms. It can, however, be equally argued, that the other issues stem from an alternative condition, in conjunction with phonotrauma.

There are five crucial things which can be gleaned from the patient's history (excluding symptoms and complaints):

(a) Interactions with HPV - mother dying from cervical cancer, where HPV is a major risk factor, and the patient's having taken the quadrivalent HPV vaccine; HPV can cause voice hoarseness by operating through a pathology called 'laryngeal papillomatosis'. There are papillomas (papillary projections) over the larynx. They are caused by low-risk HPV subtypes, such as types 6 and 11. In this patient

(b) Heavy Smoking - risk factor for all sorts of cancer. We are interested in laryngeal and lung cancers. Lung cancer can contribute to all these symptoms, regardless of whether it has metastasised. If it's primary lung cancer, it can be coupled with an additional laryngeal pathology to explain the voice hoarseness. If it has already metastasised, we can say that there is a laryngeal malignant deposit leading to the symptoms. This is not that rare and also depends on the histological subtype. Remember that heavy smoking is a risk factor for both lung and laryngeal cancers.

As a side note, though less likely, voice hoarseness can be caused by a condition called Reinke's Oedema. It concerns the swelling of a layer of the vocal folds (the lamina propria) in virtue of chronic smoking (not sure if it's really a virtue though) and other risk factors. Another risk factor that stands out is prior history of gastro-oesophageal reflux. It is not observed in this patient.

(c) Heavy Drinking - risk factor for many problems, but here, we are interested in laryngeal cancer.

(d) Occupational characteristics and its correlation with possible voice-related pathologies - phonotrauma. They include vocal polyps and vocal nodules.

(e) Entanglement with vocal polyps / laryngeal polyps (they actually refer to the same issue). Due to the recurrence of vocal polyps in this patient (the major aetiology of vocal polyps is phonotrauma), there is a high chance that the patient is experiencing it once more. Vocal polyps can result in voice hoarseness but does not explain other symptoms on its own.

As a side note, there is a difference in histological subtype that differentiates primary and secondary laryngeal cancers (secondary to lung cancer, most worryingly). Primary laryngeal cancers are histologically squamous cell carcinomas. Secondary ones from the lung can still be squamous cell in subtype. However, they can also be adenocarcinomas or large cell carcinomas. The diversity in histological subtypes in lung cancers makes it easier for pathologists to differentiate between primary and secondary laryngeal carcinomas. This certainly aids clinical decision-making and improves efficiency in synthesising coherent treatment plans.

This diagram shows the two major nerves supplying the laryngeal muscles (intrinsic) which are responsible for phonation, which are respectively the recurrent laryngeal nerves (bilateral) and superior laryngeal nerves (bilateral). The left recurrent laryngeal nerve loops around the aortic arch, as displayed. Its right counterpart, in contrast, loops around the subclavian artery, which is a branch of the aortic arch. The recurrent laryngeal nerves supply all the intrinsic muscles, except the cricothyroid. The cricothyroid is supplied by the external laryngeal nerve, the motor branch of the superior laryngeal nerve. Moreover, the cricothyroid muscle is used for altering the pitch of the voice since it tenses the vocal folds. Increasing tension leads to reduced thickness of the cords, leading to a higher pitch. Therefore, if this nerve (or muscle, or both) is damaged, the patient cannot sing. This diagram is extracted from Wikipedia.

Conditions capable of causing voice hoarseness but not considered in this case:

1. Neurological Issues- as we've mentioned, neurological issues can also contribute to problems in speech, since nerve endings are everywhere. They innervate muscles. If there is anything wrong with the nerve endings themselves or the neuromuscular junctions (NMJs) which bridge the muscle and nerve, dysfunction of the muscle leads to dysphonia. However, this patient exhibits no past history of neurological disorders. There is also no relevant family history. Most important of all, the clinical picture points towards the aerodigestive tract more and there are no alternative neurological manifestations.

2. Surgery- iatrogenic damage to the nerves serving the larynx can also cause hoarseness. This goes back to point no. 1. We're most interested in a procedure called thyroidectomy, which basically involves making a Kocher incision traversing the midline of the neck and getting rid of the thyroid. This procedure comes with inherent risks, the most crucial of all (for our purposes here) is accidental injury inflicted upon the recurrent laryngeal nerves - the most significant nerves supplying the larynx. The superior laryngeal nerves, the other set of nerves supplying a laryngeal muscle (cricothyroid), can also be affected, although admittedly less likely. However, in this patient, the removal of vocal polyps is likely to have only involved microsurgery - where the probabilities of incurring neural damage are minimal.

3. Laryngitis- there are several subtypes of laryngitis: autoimmune, reflux, and infective. Autoimmune laryngitis is more common, needless to say, in patients with predisposing autoimmune conditions or tendencies (as displayed by allergies, early-life asthma and dermatitis). This is rejected in this patient since it's not that common anyway. As for reflux laryngitis, there are no symptoms suggestive of GORD (gastro-oesophageal reflux disease). Nor is there a history of so. It must also be rejected. Finally, for infective laryngitis, it is not that common in adults. It is usually found in children aged 6 months to 3 years, where it is part of a larger, virally-induced condition called laryngotracheobronchitis (from the construction of the term, the larynx, trachea, and bronchi are affected) (also known as croup). In this case, any possibility of its occurring in an adult entails a discussion of whether there is relevant predisposition - i.e. immunodeficiency in the most ubiquitous sense. There's no reason to suggest this patient has a viral infection due to the absence of coryzal symptoms and a relevant prodrome.

Laryngoscopy showing bilateral vocal nodules (diagram extracted from: https://app1.unmc.edu/medicine/heywood/laryngealdisease/Data/images/10avocalcordnodules.jpg)

Laryngoscopy showing a large, pedunculated vocal polyp, which is in the process of being resected (diagram extracted from: https://i.ytimg.com/vi/MCA3xqnrZmU/maxresdefault.jpg)

Having rejected the differentials above and established the cases for some of them, we move on to physical examination. This time, I've discussed the differential diagnoses before moving on to physical examination mainly because there is no physical exam relevant to throat disorders. We go straight to investigations concerning that.

Physical Examination:

Performed: Respiratory Examination, General Examination, and Neck Lump Examination. Lymph nodes are also examined in the general examination.

Major Examination Findings:

1. Tachypnoea (slight), where the patient's breathing rate reaches 22 breaths per minute;

2. Inspection of Neck Masses: The two neck masses are measured at roughly 2 cm x 3 cm. They are adjacent to each other, both over the lateral aspect of the neck at C3 (vertebral level). There are no additional neck masses, including on the other side. There are no overlying skin changes. There are no scars observable. The contours of the masses are regular, while the surfaces are smooth.

3. Palpation of Neck Masses: They are non-tender and non-pulsatile. They are firm in consistency and are not tethered to the underlying tissue. They are negative in transillumination (which might suggest cysts if positive).

4. Lymph node examination returns normal results (concerning whether there are similar masses elsewhere);

5. Respiratory examination is normal.

The neck masses are most likely enlarged lymph nodes. For more details as to how lymph nodes are examined in clinical practice, watch a demonstration by Dr Gill from the University of Warwick - URL: https://www.youtube.com/watch?v=_N89T_Yqu68&ab_channel=WarwickMedicalSchool.

Summing up the information gathered, the prevailing hypothesis is malignancy. It might not sit well with many people, due to the perceived severity and stigma attached to cancers in general. However, this is not confirmed until we've done some tests: (1) radiology, (2) laryngoscopic evaluation, and (3) neck mass aspiration for pathological examination. Laryngoscopy is the modality indicated for visualising directly the larynx. However, since there are fears of malignancy and the possibility of staging, pan-endoscopy is performed. It means that, by using the same tube and poking around, from the nasal cavity all the way down the oesophagus, we can screen for any undue lesions and biopsy material when indicated.

Investigations:

1. Blood Tests: Full Blood Count, Coagulation Profile (crucial here since there's a high chance of surgical intervention), CRP, ESR, U&E, Liver and Renal Function Tests (also crucial to determine suitability of surgery), Group & Save and Crossmatching (for surgical consideration);

2. Pan-Endoscopy and Biopsy (as mentioned above);

3. Ultrasound-guided neck mass aspiration (to see about the nature of the lymphadenopathy - reactive, or metastatic);

4. Head and Neck CT for more detailed evaluation.

For staging purposes, a Chest CT will be performed in due course. This is crucial to see if there is any metastasis to the thoracic cavity. However, it is quite premature to do so before making a firm diagnosis.

Results of Investigations:

1. Slightly Anaemic, slightly high urea and potassium; normal platelet count and coagulative function; normal liver and renal function;

2. The aspirate of the neck masses is returned from the laboratory. It is determined to be free of cancerous cells. It comprises solely immune cells. The logical conclusion is that the lymphadenopathy is reactive in nature;

3. Laryngoscopy shows a whitish mass occupying the left vocal fold with supraglottic extension. The right vocal fold is spared. Subsequent pathological analysis reveals squamous cell carcinoma.

4. Head and Neck CT shows a corresponding mass on the left without bony invasion.

Laryngoscopic image showing laryngeal cancer (diagram extracted from: https://i.ytimg.com/vi/ePValVPW1YY/hqdefault.jpg)

Head and Neck CT Scan showing bulky laryngeal cancer invading the thyroid cartilage (right). The diagram is extracted from BMJ Best Practice (URL: https://bestpractice.bmj.com/topics/en-gb/1115/investigations)

Diagnosis: LARYNGEAL CANCER.

Since we've confirmed the cancer diagnosis, we now have to stage it to determine our treatment plan. We are using the TNM Staging System for laryngeal cancer. We screen for distant metastases using Chest CT and PET/CT.

Results of Systemic Radiological Evaluation: Absent systemic metastases. There is no lung mass.

Staging:

According to the clinical picture assembled, we have come up with the following deductions with regard to the stage of the cancer:

1. T (Tumour): T2 - since the tumour invades into the supraglottic region (above the vocal folds) but does not invade into the paraglottic space. Nor does it present with vocal cord fixation, and cartilage erosion.

2. N (Nodes): N0 - since the lymphadenopathy is found to be reactive instead of related to metastasis. Moreover, there are no other masses found in the neck. The lymph node examination is also unremarkable.

3. M (Distant Metastases): M0, where PET/CT and Chest CT are unremarkable.

Hence, we've got the general result of Stage 2 Laryngeal Squamous Cell Carcinoma.

With this pathological diagnosis in mind, how should we treat the patient?

Treatment:

There are generally two modalities available for patients who have Stage 2 laryngeal cancer. It is a good sign that the patient does not have any form of metastasis. Otherwise, things can get tricky. The modalities are respectively: (a) radiotherapy, and (b) surgery. Radiotherapy is usually preferred, since surgical trauma can be serious enough to lead to permanent changes in one's voice, or even impaired speech. Having said that, radiotherapy can also cause damage to the tissue adjacent to the larynx, such as the oesophagus, and can lead to problems like skin dryness and discolouration. There is also higher risk of malignant change of the tissue surrounding the larynx. A good example is hypopharyngeal cancer. The patient is also not contraindicated for surgery, owing to normal coagulative function, no history of immunodeficiency and generally tolerable health status. According to a study [11], surgery achieves better disease control. Local cancer control rates range from 86 to 98 per cent. 5-year disease-specific survival rates also range from 92 to 97 per cent.

According to a Norwegian cohort [12], the cumulative risks of recurrence in 1, 3, 5 and 10 years of follow-up are respectively 11.3 per cent, 20.5 per cent, 22.5 per cent, and 23.6 per cent. The recurrence risk at the 3-year mark for T2 cancers is 27.3 per cent. There are also substantial differences in recurrence probability owing to the treatment modality administered. Those having received radiotherapy experience an overall recurrence risk of 74 per cent. The same risk for total laryngectomy (resection of the entire larynx) is only 11 per cent.

Eventually, Archibald has opted for radiotherapy. He also received post-operative speech rehabilitation to get used to changes in his voice. Disease control is effectively acquired and he has been disease-free for 1-year now. However, we have recommended counselling services for his personal issues which have taken their toll on his mental health. We have also advised him against smoking and alcoholism. After all, these are major risk factors of laryngeal cancer. The recurrence rate for smokers after being treated for laryngeal cancer is found to be 55.26 per cent, as compared to 28.7 per cent in non-smokers. The mortality rate for continuing smokers post-treatment is also significantly higher, at 52.63 per cent, than non-smokers, at 28.69 per cent. [13]

Concluding Remarks: Laryngeal Cancer remains a disease of high morbidity and mortality. It is a significant cause of voice hoarseness and possibly, is the modern reincarnation of Ursula herself. Ursula might have failed in depriving people of their voices immediately. She has, however, devised a more devilish way of making people pay - eating away their voices ounce by ounce, until they can no longer speak properly. What's more, the larynx problem grows to become a systemic issue, engulfing the rest of the body and stealing the victim's last breath. I guess Ariel would have had a much poorer time adapting and coping with the torture, had Ursula ruined her voice instead of stolen it.

*Again, seeing my name choices, this is another case study I've written to prove a point. No patient details are used and all materials referred to are contained in the section below.

References and Further Reading:

[1] Mehanna H, Paleri V, West C, Nutting C. Head and neck cancer--Part 1: Epidemiology, presentation, and prevention. BMJ. 2010;341(sep20 1):c4684-c4684. doi:10.1136/bmj.c4684.

[2] Barnes L. Pathology of the Larynx,. Archives of Otolaryngology - Head and Neck Surgery. 1986;112(11):1214-1215. doi:10.1001/archotol.1986.03780110090019.

[3] Vokes E, Stenson K. Therapeutic Options for Laryngeal Cancer. New England Journal of Medicine. 2003;349(22):2087-2089. doi:10.1056/nejmp038171.

[4] Zhang Z. Mechanics of human voice production and control. J Acoust Soc Am. 2016;140(4):2614. doi:10.1121/1.4964509.

[5] Vocal Sound Production. Hyperphysics.phy-astr.gsu.edu. http://hyperphysics.phy-astr.gsu.edu/hbase/Music/voice.html. Published 2020. Accessed December 18, 2020.

[6] Laryngeal Ligaments and Folds - Vocal - Vestibular - TeachMeAnatomy. Teachmeanatomy.info. https://teachmeanatomy.info/neck/viscera/larynx/ligaments-folds/. Published 2020. Accessed December 18, 2020.

[7] Wood JM, Athanasiadis T, Allen J. Laryngitis. BMJ. 2014;349:g5827. Published 2014 Oct 9. doi:10.1136/bmj.g5827.

[8] Vasconcelos D, Gomes AOC, Araújo CMT. Vocal Fold Polyps: Literature Review. Int Arch Otorhinolaryngol. 2019;23(1):116-124. doi:10.1055/s-0038-1675391.

[9] Marcotullio D, Magliulo G, Pezone T. Reinke's edema and risk factors: clinical and histopathologic aspects. Am J Otolaryngol. 2002;23(2):81-84. doi:10.1053/ajot.2002.30961.

[10] Jardine D, Bhutta O, Inglis A. Specific Diseases of the Respiratory System. Pediatric Critical Care. 2011:561-574. doi:10.1016/b978-0-323-07307-3.10044-8.

[11] Agrawal N, Ha PK. Management of early-stage laryngeal cancer. Otolaryngol Clin North Am. 2008 Aug;41(4):757-69, vi-vii.

[12] Brandstorp-Boesen J, Sørum Falk R, Folkvard Evensen J, Boysen M, Brøndbo K. Risk of Recurrence in Laryngeal Cancer. PLoS One. 2016;11(10):e0164068. Published 2016 Oct 7. doi:10.1371/journal.pone.0164068.

[13] Kikidis D, Vlastarakos PV, Manolopoulos L, Yiotakis I. Continuation of smoking after treatment of laryngeal cancer: an independent prognostic factor?. ORL J Otorhinolaryngol Relat Spec. 2012;74(5):250-254. doi:10.1159/000342685.