1. Lecture 4 Voice Disorders Part 1: Phonotrauma and Functional Voice Disorders (Aronson and Bless, 2009; Colton et al., 2011;2013; Sapienza & Hoffman-Ruddy 2014)
CD 661OL
1. Lecture 4 Voice Disorders Part 1: Phonotrauma and Functional Voice Disorders

2. Classifications of Voice Disorders
Phonotrauma – results from misuse or abuse of the vocal mechanism
Organic – results from a disease process or may be congenital, i.e., cancer, acid reflux, laryngeal web etc.
Functional – Muscle tensions dysphonias
Psychogenic – results from an underlying psychological issue and presents no identifiable vocal pathology
Neurological – results from damage to the RLN or SLN, disease processes that affect these nerves, or brain injuries or lesions
2. Over the years, classification systems for voice disorders have varied. Even today, different textbooks use different systems of categorization. Voice disorders have been categorized as hyper- or hypo- functional, structural, or neurological, etc. However, these types of categorization systems don’t really provide you with a lot of information about the disorder. For example, a structural disorder may be due to phonotrauma or the an organic cause. The most recent system introduced by Verdalini separates voice disorder into four categories; phonotrauma, organic, functional and psychogenic and neurological disorders. Although your primary text uses a different system, we will use Verdalini’s system in this course .

3. Phonotrauma Disorders
Vocal fold nodules
Vocal fold polyps
Reinke’s Edema (vocal fold swelling)
Traumatic laryngitis
Vocal fold hemorrhage
Vocal fold cysts
3. Voice disorders that result from phonotrauma are disorders that result from trauma to the VFs from vocal misuse or abuse and include nodules, polyps, Reinke’s edema, traumatic laryngitis, hemorrhage, varices and ectasias and cysts and pseudo-cysts.

4. Vocal abuse & misuse Colon & Casper, 1994
4. Phonotrauma can be acute or chronic. For example, chronic loud talking or yelling can result in vocal fold nodules, a phonotrauma disorder that develops from long term, chronic misuse and abuse. On the other hand, a polyp or vocal hemorrhage can result from one single phonotrauma event such as a loud scream at a sporting event or concert. This is especially true if the vocal folds (VFs) are already irritated and inflamed from allergies, a cold, acid reflux or chronic abuse.
Colon & Casper, 1994

5. Vocal Fold Nodules
Caused by chronic/continuous misuse or abuse, such as
1. Excessive yelling, loud talking, or screaming, especially if for prolonged periods of time
2. Pervasive use of hard glottal attacks
3. Excessive coughing or throat clearing
4. Excessive laryngeal muscle tension
5. Incorrect singing technique
6. Excessive strain, excessive use, especially during a period of vocal fold swelling or inflammation
All of the above can result in incr. medial compression and impact force during VF vibration
5. VF nodules are caused by chronic, continuous misuse and / or abuse of the voice and result from increased medial compression and high impact stress during VF vibration. Thus, behaviors such as excessive yelling, screaming and loud talking can cause nodules. Chronic throat clearing, coughing and the use of pervasive hard glottal attacks can also cause nodules as can excessive laryngeal muscle tension if it leads to excessive medial compression. In truth, it’s typically a ‘constellation of events’ or ‘perfect storm’ if you will, that come together and cause a voice disorder.

6. Vocal fold nodules Early soft nodules Later hard nodules
6. On the left, are soft nodules. On the right, are hard nodules. The soft nodules are more gelatinous. The hard nodules have more deposition of collagen and fibronectin (scar tissue). Note the ‘hourglass’ closure exhibited by the patient with had nodules. Nodules are highly responsive to therapy, especially when they’re early or soft. Improved vocal hygiene and changes in vocal technique for speech and/or singing that decrease medial compression and facilitate healthy voice production are essential components of the voice therapy plan. Voice therapy should always, ALWAYS, be the first course of treatment. This is the current standard of care in the field of voice. Surgery should be deferred until a course of voice therapy has been completed but with inadequate results for improved phonation. Most laryngologists, ENTs that specialize in voice, will always prescribe a course of voice therapy first before resorting to surgery. This is especially true for singers and other professional voice users. There is always a risk with surgery, even in the best of hands.
Early soft nodules
Later hard nodules

7. Vocal fold nodules Bilateral, occur in SLP
Soft, gelatinous at first then harden becoming fibrous
Occur at juncture of anterior 1/3 and posterior 2/3 of vocal fold
Add both mass and stiffness to vocal fold
Interfere with movement of mucosal wave
‘Hour glass’ glottic closure
Result in aperiodic vibration of vocal folds
More common in adult/adolescent women than men but more common in boys than girls
7. VF nodules are bilateral, symmetrical lesions that occur at the juncture of the anterior 1/3 and posterior 2/3 of the VFs. This juncture is referred to as the ‘strike zone’ and is the portion of the VFs that experiences the greatest collision force and impact stress during vibration. Nodules alter the VF cover (mucosa) by adding both mass and stiffness. The mucosal wave may be decreased or absent in the area of the nodules depending upon the softness or hardness of the nodule. VF closure takes on an hourglass appearance.

8. Vocal fold nodules: Perceptual, Acoustic, and Aerodynamic Characteristics
Perceptual – roughness, breathiness, decreased loudness, vocal strain or effort
Acoustic - Decreased pitch and loudness ranges, increased frequency/intensity perturbations, increased noise levels
Aerodynamic – increased airflow rates, increased subglottal pressure (Ps)
Pt complaints – vocal fatigue, sensation of something in throat, vocal effort/strain, pain if muscle tension is present
8. The perceptual characteristics of nodules include roughness and breathiness. Many people will say the voice sounds hoarse. In the field of voice, we have moved away from the term ‘hoarse’ because it’s rather vague and is considered to have qualities of both roughness and breathiness. Patients with nodules may also sound strained, especially if they have been ‘talking through’ the voice problem for some time. The hourglass closure results in unvibrated air escaping anterior and posterior to the nodules and this causes the breathy quality. Decreased intensity and pitch range are also typical of nodule patients. We also observe increased frequency and intensity perturbations. A frequency perturbation, called ‘jitter’, is a cycle to cycle variation in the period of vibration that is greater than normal. An intensity pertubation, called ‘shimmer’ is a cycle to cycle variation in the amplitude of VF vibration. Nodules also result in increased airflow due to the hourglass closure and increased Ps due to strain.

9. Vocal Fold Nodules: Stroboscopic Characteristics
Hourglass closure
Bilateral lesions at juncture of anterior 1/3 and posterior 2/3 of membranous VFs.
Decreased or absent mucosal wave in region of the nodule
Decreased amplitude of vibration
9. Vocal fold nodules show an hourglass closure, decreased or absent mucosal wave, depending on whether nodules are hard or soft, and decreased amplitude of vibration.

10. Vocal fold polyps
Caused by an isolated acute episode of vocal abuse OR a period of vocal abuse, such as
1. Screaming at a concert/sports event
2. A period of excessive yelling, screaming, or shouting, loud singing.
3. Possibility of occurrence increases if vocal folds are already irritated, inflamed, swollen, etc.
10. Polyps are typically the result of an acute episode of vocal trauma or short period of vocal abuse. The possibility of developing a polyp increases if the VFs are already irritated, inflamed and swollen from acid reflux, allergies or a cold. Whenever the VFs are in this condition, the risk of phonotrauma increases. I have seen many cases of polyps and reflux. With any phonotrauma disorder, conditions like acid reflux and allergies must be controlled and the irritation and swelling must decrease in order for the VFs to heal. Resolution of nodules or polyps in the presence of uncontrolled reflux or poorly managed allergies can be difficult if not impossible.

11. Vocal Fold Polyps Typical sessile or broad based polyp
11. On the left, is a sessile or broad based polyp on the medial aspect of the L VF. The R VF has some slight swelling due to the impact of the polyp on that side during vibration. On the right, is another broad based polyp. Some ENTs might refer to this as polypoid degeneration of the entire R VF or as Reinke’s edema. The L VF appears edematous as well. When polyps are large, or if they’re hemorrhagic or have a blood vessel feeding them, then surgery will be necessary. However, when polyps are small, they may resolve with voice therapy and good vocal hygiene. I have worked with several singers who had small, unilateral, mid fold, medial edge polyps that resolved completely over a period of 6-9 months. I specialize in singing voice rehab and often address both the singing and speaking voice. The laryngologists I work with also have a great deal of experience with singers and, unless a polyp is large or hemorrhagic or has a blood supply, they will prescribe a course of voice therapy first before surgery is considered. This is because post-surgical scarring can sometimes occur and for a singer or actor any change in VF pliability can result in changes in vocal quality, decreased pitch range and decreased vocal control. Thus, a conservative approach is always taken, if possible.
Typical sessile or broad based polyp
Sessile or broad-based polyp

12. Vocal fold polyps Soft fluid filled outgrowth of tissue in SLP
Are usually unilateral and can be sessile (broad based) or pedunculated (narrow stem or stalk)
Occur anywhere along membranous vocal fold BUT are typically in same region as nodules. Can be glottic, supraglottic, or subglottic
Can be fluid, hemorrhagic (blood filled) or fibrous (connective tissue)
Hour glass or irregular closure
If fluid filled, add mass to VFs but decreases stiffness; if hemorrhagic, stiffness is increased
12.Polyps can occur anywhere on the VFs, including the inferior medial edge or superior surface of the VFs. While typically unilateral and sessile, they can be pedunculated. They are usually fluid filled but can also be blood filled. The resultant VF closure is either hourglass or irregular. Polyps add mass to VFs but may decrease the stiffness if they are fluid filled. If they are blood filled, the VF stiffness is increased.

13. Vocal fold polyps: Perceptual, Acoustic, and Aerodynamic Characteristics
Perceptual –rough, breathy, sometimes diplophonic, strained
Acoustic – decreased pitch and loudness ranges, incr. frequency/intensity perturbations, increased noise levels
Aerodynamic – increased air flow due to hourglass or irregular closure and increased subglottal pressure
Pt. complaints similar to those with nodules
13. Perceptually, polyps share many characteristics with nodules. However, polyps may present with ‘diplophonia.’ Diplophonia is when two different pitches are produced at one time and we can hear that. I have never encountered a patient with nodules who presented with diplophonia, but have encountered many patients with polyps who are intermittently diplophonic. You will sometimes run across a patient who has been diagnosed (dx) with a unilateral nodule. I have never encountered a patient with a dx of a unilateral nodule whose dx did not change to unilateral polyp upon videostroboscopic exam. Many of these patients also presented with diplophonia.

14. 14. This slide shows a fluid filled polyp on the L and a hemorrhagic polyp on the R. You can see how the polyp is an outgrowth of the VF SLP. The bottom right shows a normal VF.
Colton et al., 2011

15. Polyps: Videostroboscopic Characteristics
Increased mass, unilateral
Incomplete closure – depends on size and type
Affected side vibrates at decreased frequency
Aperiodicity (hoarseness)
Pedunculated may not affect vibration
Mucosal wave increased or decreased
Amplitude of vibration as above
15. Polyps vary greatly in size, location and appearance. You will see in the several polyp strobe exams posted how much they vary. Often, you will see swelling and irritation developing on the opposite VF due to the constant impact of the polyp during vibration. Size, location and whether or not they are hemorrhage will determine glottic closure pattern and whether mucosal wave and amplitude are increased or decreased.

16. Vocal fold edema and Reinke’s Edema
Edema is the natural reaction of laryngeal tissue to trauma or abuse
Reinke’s Edema is almost always related to smoking & more common in females
Edema is a build up of fluid in the superficial lamina propria layer (Reinke’s Space) of the vocal folds
Bilateral or unilateral
Increases mass of vocal folds but may decrease o increase stiffness
16. Edema is the natural reaction of any body tissue to trauma or abuse and is an accumulation of fluid and various inflammatory proteins within the SLP of the VF. Reinke’s edema is almost always related to smoking and is more common in females. Edema increases the VF mass but decreases the stiffness. In some cases, as in Reinke’s edema, the mucosal wave may be increased due to decreased stiffness. Reinke’s edema can be treated with voice therapy to a certain extent, but it is sometimes treated surgically. In either case, the patient must stop smoking if smoking is the cause.

17. Reinke’s Edema
17. Bilateral Reinke’s edema.

18. Perceptual, acoustic, and aerodynamic characteristics Reinke’s Edema
Perceptual – low fundamental frequency, roughness, vocal effort
Acoustic – loss of high pitches, decreased pitch range
Aerodynamic – increased air flow, normal Ps
Patient complaints: Vocal fatigue, low pitch, dry throat, vocal effort
18. Perceptually, Reinke’s edema results in a rough, low pitched voice. The low pitch is due to the increased VF mass. A good example of a Reinke’s edema type of vocal quality is Marge Simpson’s sisters on the animated cartoon ‘The Simpsons.’ There is always a decrease in pitch range with loss of high pitches. There is typically increased airflow and normal Ps. However, some researchers speculate that Ps may be decreased due to decreased VF stiffness.

19. 19. Bottom R shows cross section of normal vocal fold tissue
19. Bottom R shows cross section of normal vocal fold tissue. Top L shows VF cross-section for Reinke’s edema.
(Colton et al., 2011)

20. Reinke’s: Videostroboscopic Characteristics
Bilateral swelling along entire membranous length of VFs (can also be unilateral)
Glottic closure is usually complete
If unilateral, affected VF may interfere with vibration of unaffected VF
Phase asymmetry – especially if unilateral
Decreased amplitude of vibration
Mucosal wave – depends on degree of stiffness
20. VFs with Reinke’s edema have been described as looking like ‘water balloons’ due to the extreme swelling. Sometimes swelling is so severe that the airway is compromised and stridor is heard during inhalation.

21. Traumatic Laryngitis
Caused by trauma to vocal fold tissue, usually excessive yelling, screaming, or loud talking
Vocal folds are erythematous (red) and swollen.
Voice is hoarse, low pitched, and breathy
Resolves within a few days to 2 weeks
May be accompanied by vocal fold hemorrhage
Chronic Laryngitis – results if vocal abuse continues, particularly if patient w/ laryngitis is using more effort or straining to speak …what we call negative compensatory strategies
21. Traumatic laryngitis is caused by trauma to the VFs from excessive yelling or screaming. Have you ever gone to a sports event or concert and yelled and screamed so much that you became hoarse or maybe you even lost your voice ? If so, you had traumatic laryngitis. Traumatic laryngitis usually resolves in a few days or at most – if you really did a good job – 2 weeks. Chronic laryngitis develops when the vocal abuse continues.

22. Acute Laryngitis and Vocal Fold Hemorrhage
22. On the L are the VFs of child with acute traumatic laryngitis. On the R, we see a VF hemorrhage on the anterior superior portion of the R VF and there is also some redness (erythema) on the superior aspect of the VF at the midpoint.

23. VF Hemorrhage
Ruptured blood vessel in submucosal layer due to damage to the small, delicate blood vessels of the VF layers
VF tissues are damaged by the blood
Cause is usually phonotrauma or trauma to VFs during surgery or medical procedure
Use of anticoagulant medications such as aspirin, ibuprofen and Coumadin increases the risk
Increases VF stiffness and mass
23. VF hemorrhage adversely affects VF vibration. Blood within the SLP increases the stiffness of the VFs. Patient’s experience roughness, increase vocal effort, and decreased pitch and intensity ranges. Sometimes the hemorrhage will resolve with voice conservation and voice therapy, but sometimes surgery is necessary. VF hemorrhage, while usually unilateral, can also be bilateral

24. VF Hemorrhage Perceptual – dysphonia to aphonia; hoarseness
Acoustic – decreased pitch and loudness ranges, increased pitch and intensity perturbations
Videostroboscopic –
patchy red area on VF surface
decreased mucosal wave
decreased amplitude of vibration
non-vibratory portion at hemorrhage site
24. VF hemorrhage can result in dysphonia characterized by hoarseness or complete aphonia (lack of voice). Patients will show decreased pitch and loudness ranges and increased perturbations. The VFs will show a patchy red area. It almost looks like a bruise. The mucosal wave and amplitude of vibration will be decreased due to the increased stiffness and mass. VF hemorrhage is managed with complete voice rest to allow the VF tissues to heal. Sometimes surgical excision of the microvascular lesions will help prevent VF hemorrhages from recurring.

25. VF Varices and Ectasia There are vascular lesions –
Varices :superficial, enlarged and dilated veins
Ectasias: lesioned blood vessel, coelescent hemangiomatmous appearance
Originate in SLP at mid membranous portion
Directly related to phonotrauma, especially high pressure events such as shouting or over singing.
More prevalent in women
25. Varices and ectasias are vascular lesions due to phonotrauma They are enlarged, dilated blood vessels originating in the SLP at the mid membranous portion of the VF. More common in women, they may be related to the female hormonal cycle.

26. VF Varices and Ectasia
Decreased mucosal wave due to increasedf VF stiffness
There may or may not be perceptual symptoms
May caused decreased pitch range and some hoarseness
26. Varices and ectasias show a decreased mucosal wave due to the increased VF stiffness caused by the enlarged, dilated vessel. Some patients may present with a decreased pitch range, especially in the upper frequencies and hoarseness, while others may present no perceptual symptoms. Management of varices and ectasias require vocal rest or conservation, improved vocal hygiene and, if appropriate, voice therapy approaches to improve phonatory production. Surgery is sometimes required.

27. VF Varices and Ectasia
27. Videostill of VFs with bilateral varices.

28. Vocal Fold Cysts
Cause: May be due to blockage of mucosal glandular duct w/ subsequent retention of mucus. May occur after vocal abuse or can be congenital.
Cysts are sacs of tissue that contain either liquid (mucus) or a semisolid substance (epithelial cells)
Are usually unilateral
Occur more often in women
28. VF cysts are typically due to vocal abuse or misuse, although they are sometimes congenital. If they are due to a blockage in the mucosal glandular duct, they will be filled with mucus. If not, they may be epidermoid cysts and filled with epithelial cells. They are usually unilateral but I have seen bilateral cysts. The mucosal wave will be absent in the area of the cyst due to the cyst’s stiffness. Cysts are more common in women but I have seen then in men as well.

29. Vocal Fold Cysts
29. This slide shows a R VF cyst. Notice how well defined the cyst is. While this is often the case, some cysts are deeper in the SLP and less well defined. I have never seen a patient with a VF cyst who’s cyst resolved through voice therapy alone. Cysts usually require surgery with 3-4 session of voice therapy pre-surgery and 4-5 sessions post-surgery. I have treated patients with VF cysts (singers) for whom the laryngologist deferred surgery to see if the cyst could be ‘managed’ through improved vocal hygiene and improved speaking and singing techniques in order to avoid the risks of surgery. All these patients eventually required surgery. This is because some of them found maintaining good vocal hygiene and vocal techniques too difficult to do 24/7. Also, all it takes is a cold or flu with a cough to cause the VF and area of the cyst to swell and inflame. When this occurs, the voice is once again dysphonic.

30. 30. On the bottom right is the normal VF tissue cross-section and illustration. On the top L is a VF cross-section with a cyst. The black arrow is pointing to the cyst.

31. Perceptual, acoustic,& aerodynamic characteristics of VF cysts
Perceptual: Rough, breathy, might be low pitched, decreased loudness
Acoustic: Decreased pitch range, aperiodicity, increased noise levels
Aerodynamic: incr. airflow (little data)
Patient complaints: hoarseness, vocal effort/strain, vocal fatigue
31. Perceptual characteristics of cysts are similar to those for nodules and polyps. There is little acoustic and aerodynamic data for cysts. Patients I’ve seen have presented with decreased pitch and intensity ranges, increased frequency and intensity perturbations and increased noise levels.

32. Videostroboscopic Characteristics of Cysts
Absent or decreased mucosal wave
Decreased amplitude of vibration
Increase VF mass/stiffness of VF cover
Irregular or hourglass closure
32. The mucosal wave may be absent or decreased in the area of the cyst and amplitude of vibration will also be decreased. Glottal closure may be irregular or hourglass.

33. Pseudo-cysts
Localized collections of serous fluid without a true cyst lining or capsule
Occur mid fold in strike zone
Changes in BMZ, vascular abnormality, more fibrin (Hantzakos et al., 2008)
May resolve or improve with voice therapy but sometimes require surgical excision
Koufman (2001) pseudo-cyst histopathology is poorly understood. Appears to b a localized area of Reinke’s edema
33. Pseudocysts are poorly understood VF lesions of the SLP. They are different from true cysts in that they do not have a true capsule. A recent study by Koufman (2001) stated they are a localized area of Reinke’s edema. A study comparing lesion descriptions by surgeons and pathologists by Hantzakos et al reported changes in the BMZ and vascuscular abnormalities in pseudocysts. I have had a number of patients dx’d with pseudocysts. While voice therapy seems to help, vocal hygiene must be impeccable and patient compliance high to get positive results.

34. FUNCTIONAL AND PSYCHOGENIC VOICE DISORDERS
34. Functional and psychogenic voice disorders are nonorganic voice disorders that are not characterized by a change in VF structure or laryngeal anatomy and are not due to a neurological cause. Functional disorders are caused by musculoskeletal tension or of pyschoemotional origin.

35. Muscle Tension Dysphonia
Can be caused by
1) Excessive extrinsic laryngeal muscle tension, including tension in supra- and infrahyoid muscles and neck muscles
2) Excessive internal/supraglottic laryngeal muscle tension
Can occur by itself or secondary to a primary vocal pathology as a negative compensatory strategy
35. According to Aronson (2009), the intrinsic and extrinsic laryngeal muscles are highly sensitive to emotional stress and hyper contraction of the muscles is a common denominator behind the dysphonia and aphonia observed in functional and some psychogenic voice disorders. Although muscle tension dysphonia (MTD) is often a primary voice disorder, it may also occur secondary to a primary disorder such as VF paralysis or VF nodules as a compensatory strategy.
Persons exhibiting muscle tension show visible signs of increased head and neck muscle activity. In most cases, no single cause can be identified as the primary cause of the laryngeal muscle tension. However, many patients’ responses on case history forms often relate to the occurrence of stress, anxiety, depression, high vocal demand, and issues w/ time management along with physical and emotional overload. Deitrich et al. (2008) cited depression and stress as the two main features in a cohort of patients w/ MTD seen in their clinic.
In a chart review of over 150 MTD patients, Altman et al. (2005) found that 49% had gastroesophageal reflux, 63% reported excessive voice use, and 18% reported excessive stress.

36. Muscle Tension Dysphonia (MTD)
Clinical signs of extrinsic laryngeal MTD on laryngeal palpation include
1. Elevated laryngeal height
2. Narrow, tense thyrohyoid space
3. Tension in suprahyoid muscles
4. Tense, tight thyrohyoid muscles
5. Inability to lateralize larynx (rock left to right)
6. Tense tight floor of mouth
7. Base of tongue tension
36. Musculoskeletal tension can be detected manually by the clinician during laryngeal palpation. The excessive laryngeal tension often causes elevation of the larynx and hyoid bone, but may also result in a tense and narrow thyrohyoid space, tension in the suprahyoid muscles with a tense floor of mouth, base of tongue tension, tense thyrohyoid muscles and an inability to lateralize or ‘rock’ the larynx from side to side due to excessive tension in the strap muscles and / or pharyngeal constrictors.

37. Muscle Tension Dysphonia
Videoendoscopic signs of supraglottic & intrinsic muscle tension :
1. Anterior –posterior compression
2. Mediolateral compression (may or may not involve medialization of FVFs)
3. VF hyperadduction and foreshortening
4. Supraglottic squeezing
5. Incomplete glottic closure, anterior gap or bowing
37. On endoscopic evaluation, the VFs may appear normal, slightly inflamed, show incomplete adduction, anterior gap or bowing, and /or appear foreshortened due to excessive TA muscle activity. There may be anterior-posterior compression of the supraglottic structures including the AC’s and epiglottis. There may be medial compression of the TVFs and FVFs. There may also be supraglottic squeezing which is a sphincter-like closure of the entire supraglottic area w/ posterior tongue carriage and contraction of pharyngeal constrictors. The amplitude of VF vibration may also be decreased.

38. Severe Supraglottic Squeezing
Arytenoid Cartilages
38. Videostill of severe supraglottic squeezing or ‘sphinctering.’
Base of epiglottis

39. Muscle Tension Dysphonia (MTD)
Perceptual characteristics – harsh, rough, or breathy; tense/tight, effortful, pitch and /or phonation breaks ; normal pitch or elevated pitch; whisper, aphonia
Patient complaints: vocal fatigue, tight, tense throat, laryngeal pain/discomfort
39. Vocal quality in MTD can vary by patient. Patients will often report vocal fatigue and pain or laryngeal discomfort. During a voice evaluation, we always ask about laryngeal pain. If pain is present, we ask where the pain is , what type of pain and when it occurs. MTD is managed with therapy techniques such as circumlaryngeal massage and laryngeal digital manipulation. If the tension is intrinsic, supraglottic relaxation exercises will be helpful to stop excesive medialization and compression. In the case of floor of mouth (FOM) tension and base of tongue tension, specific exercises are performed to release the tongue and FOM muscles. Is it not unusual to also teach neck and shoulder relaxation stretches.

40. Ventricular Phonation
Adduction and use of the false or ‘ventricular’ vocal folds for phonation .
Can be a primary or secondary disorder
Secondary – seen in pts. with a primary underlying voice disorder that results in decreased glottic closure and increased air flow (vocal fold paralysis/paresis, large vocal fold lesions, etc.)
Pt. increases laryngeal muscle tension to compensate for air wastage, inability to build Ps, and decreased loudness.
40. Also called plica ventricularis, ventricular phonation occurs when the source of vibration is the false or ventricular folds. It’s etiology is often unclear. However, because it is often seen in muscularly tense people and is an extreme form of hyperfunction, it is best classified as a musculoskeletal disorder. It can be both a primary or secondary disorder. It may occur secondary to a hypofunctional voice disorder (voice disorder characterized by incomplete glottic closure).

41. Ventricular Phonation
Adducted FVFs overlap true VFs and ‘load’ them, causing them to vibrate in an abnormal manner.
FVF vibration may also cause‘ diplophonia’
Voice is rough and harsh, low pitched due to the mass of FVF or combined mass of true and false folds, breathy, monotone, decreased pitch range
Patient complaints: vocal effort/strain, possibly pain/discomfort
41. FVF phonation is quite distinct and typically sounds rough and low pitch. Diplophonia is also often observed. Ventricular phonation is managed with voice therapy.

42. Psychogenic Voice Disorders
Types of psychogenic dysphonias:
1. Puberphonia or mutational falsetto
2. Conversion Dysphonia / Aphonia
Have no underlying organic or physical cause, i.e., no identifiable disease or pathology
42. Psychogenic voice disorders are disorders for which there is no underlying organic or physical pathology. These disorders are purely psychogenic.

43. Puberphonia (mutational falsetto)
Definition: Persistence of a child-like voice quality after puberty
Learned or psychogenic in nature
Voice is high pitched, possibly hoarse and breathy, decr. loudness; pitch often lowers when they shout or do heavy lifting
Incomplete glottic closure, stiff VFs, decreased amplitude
Dx must rule out laryngeal structural defects, endocrine disorder & diseases that might affect the larynx
43. Several causes of puberphonia have been proposed and most include a psychological basis such as difficulty accepting the new male voice, social immaturity or male identity problems. Endoscopy typically reveals a normal male adult larynx size, incomplete glottic closure, stiff VFs, and decreased amplitude of vibration. In some cases, hyperfunction may be present and evidenced by a high laryngeal position or FVF compression.
Puberphonia is managed with voice therapy to lower the higher than normal habitual pitch and eliminate hyperfunction.

44. Conversion Aphonia
Complete loss of voice (aphonia) with no underlying physical cause
Nonphonatory VF movements are normal. On phonation, VF movement is irregular & adduction inadequate to produce vibration
Onset is sudden or preceded by periods of voice loss or dysphonia
Onset of aphonia is associated with fear, stress, or traumatic event
Non-speech / vegetative functions such as throat clearing, coughing, laughing etc show normal VF movement and vibration
44. Conversion aphonia is believed to relate to a manifestation of anxiety, severe stress, or depression. The onset is sudden and may be associated with a traumatic event. There is no apparent laryngeal pathology, disease or structural abnormality. On endoscopy, nonphonatory VF movements are normal, but when phonation is attempted, the VFs move irregularly and adduction is not sufficient to produce vibration. Neck pain is sometimes reported and extrinsic muscle tension is sometimes evident during phonation attempts. Management includes a thorough physical examination to rule out physical or neurological causes. If the dx is conversion aphonia, treatment may include psychological counseling and therapy in isolation or in conjunction with voice therapy. Many times, restoration of the voice is quick. However, if the underlying psycho emotional issues are not resolved or managed, the voice problem may re-emerge.

45. Idiopathic Voice Disorders

46. Paradoxical Vocal Cord Movement (PVCM)
Characterized by adduction of VFs during quiet breathing
Causes stridor, shortness of breath
No known cause– may be learned, maybe due to hyperactivity of the airway, a neurological problem, a psychological problem, or unspecified medical problem (Bless &Swift, 1995)
Often confused with asthma or exercise induced bronchospasms
Concerns are non-vocal. Primary concern is ability to breathe
46. PVCM is characterized by VF adduction during inhalation. Many times these patients have a history of many visits to the ER for asthma attacks that are in fact episodes of PVFM. There is no known cause. The primary concern is not voice or voice quality but the ability to breathe.

47. Paradoxical Vocal Fold Movement (PVFM)
Termed ‘Episodic Paroxysmal Laryngospasm ’
Vocal fold adduction occurs during inhalation
Unknown cause but may be related to stress, performance anxiety, reflux, allergies, brainstem or vagal disturbances, or have a psychological component.
Often seen in athletes – most common in adolescent athletes and in women ages y/o.
47. Although PVFM is a complex disorder of unknown etiology, it may be related to stress or vagal disturbances. During an episode of PVFM, the posterior 2/3 ‘s of the VFs adduct during inhalation. The attacks recur periodically. Once the episode has begun, it often carries over into expiration as well. The condition is most common in adolescent athletes and woman ages

48. Paradoxical Vocal Fold Movement
Patients complain of throat tightness, chest/neck tightness. Intermittent or chronic cough, shortness of breath
Stridor, wheezing, irregular breathing pattern
Voice may be hoarse, weak, breathy, strain-strangled
Larynx is normal w/ normal VF function when there is no event; during an episode, inspiratory adduction of anterior 2/3 of VFs w/ posterior gap is observed.
48. An episode of PVFM is a frightening event. In addition, for athletes, the stress of the competition plus the stress from the fear of a PVFM episode increases the likelihood of a PVFM event. PVFM is managed with voice therapy and respiratory training. Andrianopoulis et al. (1999) has described a 3 phase treatment approach which we will discuss in our Voice Therapy lecture.