Welcome to Module 3, Changes in Vocal Effort and Vocal Quality. Our educational objectives for this module are to relate an understanding of vocal fold physiology to our patient complaints of changes in vocal effort and quality, to describe how inefficient speaking and singing techniques can result in vocal trauma, and to be able to assess how laryngeal lesions affect vocal fold vibration. Benign laryngeal lesions are a response to injury. The most common source of that injury is trauma from voice production with inappropriate laryngeal closure to produce excess laryngeal volume. This excess volume results in shear in the cover of the vocal fold that vibrates. Reflux and infection may predispose the laryngeal cover to the effects of shear. However, they're not the primary cause. The primary cause is the inefficient voice use patterns. Essentially, shear equals tangential stress. Remember from modules 1 and 3, we regulate tension in the thyroarytenoid muscle and the vocal ligament and cover through interaction of the thyroarytenoid muscle primarily and interaction of the cricothyroid muscle. Remember also from a module 2, that in order to be heard, we want volume. So to get volume, this tissue has to vibrate and has to vibrate rapidly and close quickly if we tense the thyroarytenoid muscle inappropriately to get volume, to squeeze the vocal folds shut. Then we're going to add more tangential stress in this region, more shear. That shear will lead to micro trauma within this region, which leads to the buildup of proteins or scar tissue. This creates the benign laryngeal lesions. These lesions are a build up of scar tissue or proteins. They're acellular. Because they're acellular, we refer to them as non-neoplastic lesions. They're not cancerous. They're non-cancerous. And clinically, these are nodules, polyps, and cysts and sometimes something called polyploid corditis. Just to be complete neoplastic lesions are cellular lesions. They're are lesions that develop within the epithelial cells as a response to viral infections, such as papilloma, and then as a response to mutations, such as cancer. These non-neoplastic lesions are traumatically induced. Excess shear through inefficient vibratory patterns creates trauma in the superficial layer of the lamina propria that results in nodule, polyp, or cyst formation. Viral infections produce papilloma and cancers are produced by mutations within the genes that cause cells of the skin or epithelial surface to grow. There may be some interaction between trauma and viral expression. However, this is not completely understood. Why are benign laryngeal lesions important? These lesions are important because they cause disphonia or difficulty voicing because they disrupt laryngeal vibration. They develop within the superficial lamina propria as a benign response to trauma. Specifically, the superficial lamina propria is a portion of the cover to cover vibrates. If we over tense the vocalis muscle or the thyroarytenoid muscle as the cover vibrates, there will be increased shear in the vibratory portion. These lesions then develop just beneath the epithelium in the superficial lamina propria. They cause dysphonia by disrupting laryngeal vibration either through alterations in the viscosity of the cover by interfering with the body cover relationship, not allowing it to separate as freely as it should or by distorting the pre-phonatory glottic configuration. Remember from module 1, we need to get our vocal folds into a nearly closed efficient position for vibration to begin. Lesions that alter cover viscosity are clinically determined nodules or very small sessile polyps. As you can see, these lesions are not going to significantly alter the pre-phonatory glottic configuration but they will change the viscosity, the thickness or the thinness, of this cover that needs to vibrate. Remember, the thickness or thinness of the cover is important because that determines the cover pliability. Cover pliability is important because that determines how rapidly the vocal folds will shut. How rapidly the vocal folds shut is important because that determines the volume of voice. In a similar manner, polyps will do the same thing as something we call nodules. Lastly, a lesion, which we haven't talked about before, is a sulcus vocalis. This is actually a groove within the vocal fold in which the superficial layer of the lamina propria is missing in portions. Other lesions that alter cover viscosity are the interepithelial neoplasia or precancerous lesions. You can see they increase the weight of the epithelium. The epithelium is part of the cover. Similarly, papilloma does the same thing. It's a virus in the epithelium and getting its roots from the superficial lamina propria but it increases the overall viscosity of the cover. Lesions that actually interfere with the body cover relationship or don't allow the body to separate from the cover of during vibration are squamous inclusions cysts and invasive cancer. Perhaps the most easily understood process is a cancer that starts in the epithelial cells and then grows directly into the vocal ligament. We can clearly see how this type of a lesion would prevent the vocal fold from vibrating normally. Cysts within the vocal fold affect vibration in a similar way. The cyst develops commonly as a response to trauma or possibly as a birth defect, and the cyst fills up the superficial layer of the lamina propria. It can be filled with skin cells or it can be filled with mucus called a mucous retention cyst. Either one of these two fill up the superficial regional lamina propria not allowing the cover to separate from the body during vibration. Finally, large lesions such as polyps that are pedunculated, interdigitate or stick between the vocal folds. Because of that, the larynx is too wide and initiation of phonation, the pre-phonatory glottic configuration that we talked about is the aerodynamic portion of the aerodynamic myoelastic theory of vocal fold vibration can not occur efficiently because the polyp is too large to let the vocal folds adapt an efficient position. In summary then, we see these different benign lesions that result in dysphonia because they affect the larynx's ability to vibrate either through making the cover too stiff or distorting the pre-phonatory glottic configuration. Laryngeal vibration cannot be witnessed by the human eye. As we've said earlier, vocal folds vibrate roughly between 100 and 1,000 times each second. A cycle per second is referred to as a Hertz. Our visual system, our eye, our retina, our brain that processes the visual image can only resolve about five images each second. For this reason, when we view laryngeal vibration with a continuous light, the vocal fold skin itself actually appears slightly blurred. We can see in this demonstration here, at rest, there's no motion and we can see fine detail in the vocal fold vasculature. This patient had a small cancer removed from his left vocal fold using continuous light endoscopy. When he inhales, we can see the fine vasculature in the left vocal fold that has developed in response to his surgery and surgical healing. However, because we're using a continuous light, once he begins to speak, that fine vascular, which has such a nice resolution with this high definition photography, no longer can be seen in detail and the image appears blurred. Laryngeal stroboscopy relies on a brief flash of light. That light is in the range of microseconds. Originally, xenon light technology was developed to study airplane engine rotation. The xenon light flashes a very bright flash of light for approximately 100 microseconds. That illumination produces an image which we process in our brain. The same effect can be done with a computer system which turns a continuous light source such as a halogen light source on and off very rapidly. However, it can be as rapid with today's computer systems as Xenon light technology. Lastly, LED light technology is also a flashing light and can be used to produce stroboscopy. Many of the images you'll see in this course are produced with LED stroboscopic technology. Regardless of the flashing light principle you use though, the images are created and then pieced back together to provide an apparent slow motion image of vocal fold vibration. There is clinical utility when stroboscopy is performed at multiple pitches and multiple loudness levels to see how changing pitch and changing volume affects the way the vocal folds vibrate. Here is our same patient, now viewed with a stroboscopic light source. You can see that once the strobe light triggers the resolution we have under his still image when he breathes in is the same as the resolution we have while we watch vocal fold vibration. You can see here also that his right vocal fold on the left side of the screen is vibrating relatively normally, whereas the operated vocal fold on the right side of the screen, the left vocal fold is stiff and doesn't vibrate as dynamically as the opposite side vocal fold. So, how do we the images? We have two different ways. We can either use a Rod-lens telescope which is a rigid telescope that is placed to the patient's mouth or a flexible telescope that bends and is placed to the patient's nose. The Rod-lens telescope developed by Harold Hopkins in the middle part of the 20th century uses a series of rod lenses placed in serial configuration and is transmitted sequentially to each different lens and then eventually out to the human eye. We can combine this with a prism at one end so that the visual path can be angled down to view the larynx. Alternatively, we can use a flexible telescope and pass it through the patient's nose. These telescopes were originally produced with fiber optic rods, tiny glass rods slightly larger than human hairs were placed in a bundle and packaged in the scope. They needed to be kept in parallel configurations so that the image wasn't distorted. Today, most of our telescopes used distal chip technology or a miniature camera at one end. That miniature camera then picks up the image at the end of the scope and transmits it back to a series of wires to a camera or the human eye at the other end. When obtaining these images clinically, it's important to try to capture at least three to five vibratory cycles at each pitch that we choose to examine our patients. We can look at the vibratory cycles and compare the left vocal fold to the right vocal fold in terms of symmetry and height or amplitude of vibration and how periodically the vocal or regularly the vocal folds vibrate together. We can look at the specific vibratory parameters of each vocal fold often referred to as the mucosal wave which travels along the medial surface and the superior surface and then we can evaluate how well the vocal folds close or how completely the vocal folds close. Let's review some clinical examples on how stroboscopy is useful. Our first patient demonstrates how it is important to understand the vocal requirements of our patient and how it's important to evaluate them through the ranges where their vocal complaints are. The first patient is a male tenor. In order to adequately evaluate this patient, we as clinicians need to understand the range of what a male tenor needs to sing. This patient also complains of difficulty only in his upper head voice or the highest end of his singing voice. We therefore need to understand what the upper end of a male tenor's singing voice would be and how he produces that. The patient states that he can't reach notes in the range of A above middle C to C above middle C. That's the upper end of a male tenor. It's important that I then evaluate him through these different ranges. The patient has no complaints in the speaking voice. We can see the frequency of his voice right here. His vocal folds are vibrating slightly higher than a normal speaking voice range for a male tenor and we can see that they're vibrating relatively symmetrically, relatively equally. They're certainly periodic. We can see, however, as he goes up in pitch that his left vocal fold on the right side of the screen here becomes stiffer than his right vocal fold. We also noticed that the closure, the air or blacks slit between the vocal folds doesn't go away complete. Because of that we can understand why this male tenor then would have difficulty in this pitch range of his voice. Our second patient, complains of difficulty in speaking over background noise. Specifically, he states then talking in crowds or in trying to talk to his family in the car, he can't be heard. As his vocal folds vibrate here, we can see that they're attempting to vibrate but both vocal folds are so stiff that as the air passes through them, the patient is having difficulty in training them into vibration. Even when he lowers his pitch while the left vocal fold appears to be vibrating relatively normal with a good upper and lower lip or mass formation, the right vocal fold upper region never vibrates completely to the midline. Why is this important? Well, he has an air gap there or a gap that allows air to leak out. Remember volume is produced by the degree and rapidity of vocal fold closure. If the vocal folds are not vibrating to closure completely and rapidly then the source of spectrum is altered. We get better volume by closing our larynx completely and rapidly. This patient can't do that. Our third example is that of a professional actor. This patient performs on the stage mostly in speaking roles but she is required to sing at times. She notes that the mid portion of her range is difficult. In general, she complains of increased effort to produce voice even at low and high pitches but at certain points her voice will just crack on her and often become too toned. This has limited her acting to character roles and really reduces the amount of singing she can reliably perform. When we evaluate her through laryngeal stroboscopy, bump or a diffuse bump in her right vocal fold. We can see how at certain pitches that bump actually stops vibration and the right vocal fold breaks into two vibratory segments. She can't produce a good sound source. She has no harmonic spectrum or a reduced harmonic spectrum to present to that supraglottic vocal tract. In summary of module three, benign vocal fold lesions are a response to trauma, not the type of trauma you think about with a car accident or some sort of strangulation injury, but rather trauma from inefficient vocal fold vibration that produces tangential stress known as shear in the superficial region of the lamina propria that leads to micro injury which leads to the buildup of proteins. The proteins form the nodules and the polyps. The nodules or polyps stiffen the vocal fold cover, making it less able to vibrate freely. The larynx then doesn't close rapidly, volume is reduced, the overall strength of the harmonic sound source is reduced, and patients just can't speak loudly and don't have a good harmonic sound source to present to the supraglottic vocal tract. Benign vocal fold lesions develop in the superficial layer of the lamina propria as a response to this vocal trauma and are called nodules, polyps and cysts. These lesions affect voice because they disrupt vocal fold vibration. Either they make the cover too stiff, not supple enough to vibrate freely and to close freely and rapidly during vibration. They don't allow that cover to separate from the body to allow us to blend different modes of vibration and they can actually distort the pre-phonatory glottic configuration that allows us to have that aerodynamic configuration necessary to vibrate the vocal folds freely. Thank you very much and I look forward to seeing you on module four.
