Voice Disorders: Unit I & II PDF

Unit I Introduction (Area One) 1.​ A voice disorder exists when: a.​ A person’s quality, pitch, and loudness DIFFER from those of similar age, gender, cultural background, and geographic location (i.e., their voice is not representative of the speaker)...

Unit I Introduction (Area One) 1.​ A voice disorder exists when: a.​ A person’s quality, pitch, and loudness DIFFER from those of similar age, gender, cultural background, and geographic location (i.e., their voice is not representative of the speaker) b.​ When the perceptual properties of voice are so deviant that they draw attention to the speaker. c.​ When the structure and/or function of the laryngeal mechanism no longer meets the voice requirements of the speaker. 2.​ Three goals in the assessment and management of voice disorders: a.​ Evaluation of laryngeal function using auditory and visual-perceptual tasks (i.e., watching the person and listening to their voice), acoustic analysis (i.e. capturing their voice and analyzing it with a computer), and aerodynamic measures (i.e., measuring airflow dynamics). b.​ Identification and modification or elimination of functional causes that lead to the development of the voice disorder. c.​ Develop a plan that will remediate the voice disorder and return the voice to improved function. 3.​ In order to meet these goals, the speech language pathologist must: a.​ Understand the anatomy and physiology of voice production b.​ Be familiar with common vocal fold (VF) pathologies c.​ Understand etiologic factors d.​ Know appropriate diagnostic techniques e.​ Develop a bank of clinical management strategies 4.​ Early Foundations of Voice Rehabilitation evolved into several general voice management orientations: a.​ Hygienic Voice Therapy — This type of voice therapy concentrates on identifying any behavioral causes of the voice disorder. b.​ Symptomatic Voice Therapy — This type of voice therapy focuses on modifying deviant vocal symptoms that the clinician identifies, such as breathiness, low pitch, and glottal attacks. c.​ Psychogenic Voice Therapy — This type of voice therapy focuses on the emotional and psychosocial status of the patient that led to and maintained the voice disorder. d.​ Physiologic Voice Therapy — This type of voice therapy relies on direct modification of respiration, phonation, and resonance to improve the balance of laryngeal muscle effort to the supportive airflow, as well as the correct focus of the laryngeal tone.  e.​ Eclectic Approach — This is the combination of any and all of the previous voice therapy orientations. Unit II: Anatomy and Physiology (Reading: Chapter 2, Stemple, Roy, Klaben) 1.​ Introductory Comments: a.​ It connects the three subsystems — our pulmonary (lungs) air supply (respiration), the laryngeal valve (phonation), and our supraglottic (above the glottis or above the vocal folds) resonating cavities. 2.​ Three Levels of Folds (pictures = pp. 18-20) a.​ Aryepiglottic Folds i.​ Connect the epiglottis to the arytenoids and form the upper rim of the larynx structure. ii.​ When the epiglottis retroverts, these help to seal off the vestibule for airway protection. b.​ Ventricular Folds (AKA: false vocal folds) i.​ It is just superior to the true folds (above the ventricles) ii.​ They compress tightly during coughing, sneezing, and physical activities requiring a build-up of subglottic pressure (thoracic fixation). iii.​ They assist with airway protection during swallowing. iv.​ They may close during hyperfunctional phonation. v.​ We do not want the false vocal folds involved in phonation and if they are, there is a problem. c.​ True Vocal Folds i.​ Open for breathing, closed for airway protection, and vibrate to produce sound. ii.​ Close tightly for vegetative acts such as cough, throat clear, swallow, or activities requiring thoracic fixation. 3.​ Respiration a.​ Briefly review the process of active inspiration and passive expiration: i.​ In normal soft speaking voice, for active inspiration, the muscles of the thorax (upper cavity), inspiratory muscles will contract to lift the thoracic cavity forward (expanding). ii.​ For passive expiration, the muscles relax (5 restoring forces) that will create a situation where the chest goes back to their original state (gets smaller again) and air gets pushed out. b.​ 5 Restoring Forces: passive expiration to occur i.​ Relaxation of the inspiratory muscles ii.​ Gravity  iii.​ Natural elasticity of the lungs (wants to pull them back to their original position) iv.​ Visceral (Gut Organ) Pressure v.​ Torque (twisting action) of the ribs c.​ Review the Muscles of Inspiration and Muscles of Expiration (pp. 27-30) i.​ Muscles of Inspiration (located in the thoracic cavity. All are paired EXCEPT the Diaphragm) 1.​ Diaphragm (single) — a dome-shaped muscle attached to the inferior border of the rib cage, active in both quiet and speech breathing. When it contracts, it depresses the abdomen and increases the vertical dimensions of the lungs and the thoracic cavity. 2.​ Costal (Ribs) Elevators — muscles that contract to elevate the ribs up. 3.​ External Intercostals — A series of muscles situated between each of the ribs, originating from the inferior surface of one rib and coursing down and medially to attach to the superior face of the rib below. These muscles are active in both quiet and speech breathing; when they contract, the external intercostals elevate the rib cage and increase the transverse and anteroposterior dimensions of the thoracic cavity. 4.​ Scalene Muscles (lateral neck muscles) — These muscle pairs that originate at the cervical (C2-C7) and attach to the first and second ribs. They are active during forced inspiration; when they contract, they elevate the rib cage. 5.​ Sternocleidomastoid — A major accessory muscle of inspiration that attaches at its upper end to the mastoid process of the skull and at its lower end to the sternum and clavicle. It is active only during deep breathing. When it contracts, it elevates the sternum and rib cage. 6.​ Pectoralis Major and Minor — Two accessory muscles of inspiration. Pectoralis Major originates in the sternum and attaches to the humerus; pectoralis minor originates in the costal cartilages and attaches to the scapula. They are active only during the final phase of maximal inspiration; when they contract, they elevate the rib cage. ii.​ Muscles of Expiration (all are located in the abdomen EXCEPT the Internal Intercostals. All are paired) 1.​ Internal Obliques — An upward fan-like muscle that originates at the iliac crest and attaches to the cartilage of the lower ribs. It is  active during speech breathing; when it contracts, it lowers the rib cage. 2.​ External Obliques — A downward fan-like muscle that originates at the lower ribs and attaches at abdominal points and the iliac crest. When contracting for speech breathing, it lowers the rib cage and compresses the abdomen. 3.​ Rectus Abdominis — A long, vertical muscle that covers the central abdomen, originating at the pubis and attaching to the sternum and lower ribs. It is active during speech breathing; when it contracts, it compresses the abdomen. 4.​ Internal Intercostals — A series of muscles situated between each of the ribs, originating from the inferior surface of one rib and coursing down and laterally to attach to the superior surface of the rib below. They are active during speech breathing; when they contract, the internal intercostals depress the rib cage to reduce dimensions of the thoracic cavity. 5.​ Transverse Abdominis — A broad muscle that originates at the posterior vertebral column and fans anteriorly to attach to the abdomen at various points from the diaphragm down to the pubis. It is active during speech breathing; when it contracts, it presses the abdomen. d.​ “Checking Action” — external intercostals stay contracted a little bit as the other inspiratory muscles relax. We want the air to come out more gradually so it does not come all at once. 4.​ Resonance a.​ Sound waves are generated by the vocal folds and travel through the vestibule, pharynx, oral and nasal cavities; and across artic structures such as the velum, tongue, palate, teeth,etc. 5.​ Laryngeal Structures a.​ Framework: (You need to know these structures like the back of your hand. Be able to list them, describe them, identify them on a model, and label on photos or pictures) i.​ Hyoid Bone — described as a horse shoe shape, often described as the top of the laryngeal structure. It is the only bone in the body that is not directly attached to the bone or cartilage; “floating bone” and has two ‘horns’ (cornu). ii.​ Epiglottis — a single cartilage that is tongue-shaped or leaf-shaped. It does not have a significant role in voice BUT it is important for swallowing. It attaches to the inside of the thyroid cartilage.  iii.​ Thyroid Cartilage — a single cartilage and is the largest of the laryngeal cartilages. From the back, it looks like an “H” or described as looking like a shield. 1.​ Anterior Commissure — the vocal folds attach to the thyroid cartilage in this location. 2.​ Landmarks — Superior Cornu and Inferior Cornu, Thyroid Prominence (‘Adam’s Apple’), thyroid notch, and thyroid lamina. iv.​ Cricoid Cartilage — a single cartilage and is located at the bottom or at the base of the larynx where it attaches to the trachea. It is often described as looking like a signet ring. 1.​ Landmarks — Cricoid Arch and Cricoid Lamina. v.​ Arytenoid Cartilages — located on top of the cricoid lamina and is often described as looking like little pyramids (paired). 1.​ They have two important processes — (1) muscular process (where muscles attach) and (2) vocal process (where vocal folds attach). vi.​ Cuneiform Cartilages — little cartilages give the edge some structure and stability so that they can stay put. vii.​ Corniculate Cartilages — sitting on top of the arytenoid cartilages and are fused to the arytenoids. They do not really do anything. b.​ Laryngeal Joint — the joints are named for the 2 structures involved. i.​ Cricoarytenoid Joint — purpose is to allow for adduction and abduction of the vocal folds. A ball and socket joint that connects the cricoid and arytenoid cartilages. It allows for gliding and rotation to open/close the folds ii.​ Cricothyroid Joint — purpose is for pitch adjustment. This joint allows for the thyroid cartilage to move back and forth. It connects the thyroid and cricoid cartilages. As it moves back and forth, it will stretch out the vocal folds and raise the pitch. c.​ Laryngeal Muscles i.​ Extrinsic Muscles (see Table 2-1 on p.32) 1.​ Suprahyoid Muscles — Pulls the larynx up/Elevators a.​ Stylohyoid b.​ Digastric M. c.​ Geniohyoid M. d.​ Mylohyoid M. 2.​ Infrahyoid Muscles — Pulls the larynx down/Depressors a.​ Omohyoid b.​ Sternohyoid  c.​ Sternothyroid d.​ Thyrohyoid ii.​ Intrinsic Muscles (See Table 2-2 on p.33) All muscles innervated by the Vagus nerve EXCEPT Cricothyroid Muscle. 1.​ Cricothyroid Muscle — Pulls the larynx down and forward. An adductor muscle. Its main job is pitch adjustment, because it is working with the cricothyroid joint to stretch the vocal folds. a.​ The ONLY muscle innervated by the Superior Laryngeal External Branch of the Vagus X nerve. 2.​ Thyroarytenoid Muscle — this muscle goes from the thyroid cartilage to the arytenoid cartilages (thyroid and arytenoid muscles — vocal folds) AKA makes up the body of the vocal folds. This is an adductor muscle. 3.​ Posterior Cricoarytenoid Muscle — When it contracts, the arytenoids will fold in and rotate. It will open the vocal folds. a.​ This is the ONLY abductor muscle. 4.​ Lateral Cricoarytenoid Muscle — works in opposition to the posterior Cricoarytenoid muscle. This muscle pulls the vocal folds back and are closed. Adductor muscle. 5.​ Interarytenoids (Oblique Arytenoids and Transverse Arytenoids) — this muscle adducts the arytenoids. Transverse is horizontal and the oblique is in the shape of an ‘X’. d.​ Anatomy of the Vocal Folds (Vocal Fold Microstructure): (see picture p.43) i.​ The adult vocal folds have 5 distinct layers. 1.​ Epithelium — most external layer of the true vocal folds. Most mucosal, thinnest, compliant. a.​ Basement Membrane Zone (BMZ) — It is a well-defined microcellular transition region between the epithelium and the superficial lamina. It is made up of anchoring fibers that allow tissue in the vocal fold mucosa to shift and glide. 2.​ Superficial Layer of the Lamina Propria a.​ Reinke's Space is located here. When this place swells with fluid, it is called Reinke’s Edema. b.​ Second layer, it will vibrate significantly during phonation. There are not as many collagen fibers here, but it is very loose and flexible. 3.​ Intermediate Layer of the Lamina Propria a.​ Third layer, with mostly elastic fibers with few collagen fibers. There is more mass than the previous layer, but still vibrates during phonation.  4.​ Deep Layer of the Lamina Propria a.​ Fourth layer, mostly collagen fibers with only a few elastic fibers, which makes it more dense, but still vibrates. b.​ Vocal Ligament — intermediate layer + deep layer. 5.​ Vocalis Muscle a.​ Innermost layer. It is part of the cricoarytenoid muscle and makes up the body of the vocal folds. It provides tone, mass, and stability of the vocal folds. The tissue is very dense. It is the only part of the tissue that is active and capable of contracting and relaxing. 6.​ Neurology a.​ Afferent (sensory) i.​ Sensory messages from sensory receptors in the laryngeal mucosa and the respiratory passages send afferent messages to the central nervous system (CNS) via the internal branch of the Superior Laryngeal Nerve (branch of the Vagus Nerve X) and terminate in the medulla at the nucleus tractus solitaries (NTS). b.​ Efferent (motor) i.​ Motor commands for voice production originate in the precentral gyrus of the cortex. ii.​ Both pyramidal and extrapyramidal motor pathways are involved in laryngeal control. iii.​ The nucleus ambiguous contains central origins of the laryngeal motoneurons for all intrinsic muscles — motoneurons for esophageal and respiratory control are also located here. The nucleus ambiguous is located in the reticular formation. c.​ Peripheral Innervation of the Larynx = VAGUS NERVE (X) i.​ 2 branches of the Vagus Nerve (picture = p.48) 1.​ Superior Laryngeal Nerve (SLN) — more likely to impact pitch. a.​ Internal Branch — provides sensory information from the larynx b.​ External Branch — motor innervations to the Cricothyroid Muscle. i.​ Located in the front. All muscles shorten when they contract. ii.​ If you have damage to the superior laryngeal nerve, how would that impact the voice? ​ Less pitch variation, reduced pitch range, monotone/monopitch, difficulty getting to the high pitches, etc.  2.​ Recurrent Laryngeal Nerve (RLN) a.​ Extends to the thorax, where it forms long loops through the heart before coursing superiorly back up under the thyroid gland and onto the larynx. The pattern of ‘recurrence’ is different on the right and left sides of the body. These nerves (especially to the left) are susceptible to injury. b.​ Supplies all sensory information below the vocal folds. c.​ Supplies all motor innervations to the posterior cricoarytenoid, thyroarytenoid, and oblique/transverse interarytenoid muscles. d.​ If there is damage to the recurrent laryngeal nerve, how would it impact vocal fold movement? They would not be able to adduct and abduct properly depending on the extent of the injury and how it is impacting the muscles; vocal fold paralysis. i.​ Bilateral Vocal Paralysis ii.​ Paramedian Vocal Paralysis iii.​ Fully Open Position — aspiration can be a risk because not closed off for swallowing. iv.​ To observe paralysis, look at which arytenoids are not moving in the video. d.​ Laryngeal Reflexes i.​ Laryngeal Adductor Response (closes reflexively) — tight sphincter closure to protect the airway from foreign materials or aspiration by closing off the trachea and lungs (via sensory receptors in the mucosal tissue, joints, and muscles) ii.​ Laryngospasm — extreme glottis clossue in response to stimulants that irritate the vocal fold mucosa. 1.​ Irritable Laryngeal Syndrome a.​ This irritation can be triggered by chemicals (e.g. farm chemicals). Some may be sensitive and can react to household chemicals, perfumes, etc. 2.​ It can become a problem when the larynx becomes hypersensitive because the larynx will close when it should not. 7.​ Developmental Changes (summary chart p.50) a.​ Babies i.​ Larynx sits high in the neck and is at the C3 or C4 level (fourth cervical vertebrae). ii.​ Larynx is close/compact. Everything is high and compact in the neck.  ​ For example, if a baby cries, you may see the epiglottis pop out. b.​ Childhood i.​ The larynx begins to descend lower in the neck. ii.​ The length of the vocal folds in boys and girls are about the same UNTIL 10 years of age. Their voices are not very different as children. c.​ Puberty i.​ From 10 years of age and forward, there is a gradual but significant difference in the growth patterns between boys and girls. ii.​ By puberty, the larynx has descended down to about C6 or C7 (significant difference lower in the neck). iii.​ In males, testosterone increase stimulates growth on the thyroid prominence (i.e., ‘adam’s apple’ becomes more prominent). iv.​ 5 layers of vocal folds are not fully developed until puberty. d.​ Adulthood i.​ The female vocal fold length is about (varies depending on the size of the person) 11 to 15 millimeters. ii.​ For males, it is about 17 to 21 millimeters. e.​ Old Age (geriatric folds) i.​ We see changes in the larynx (Presby Laryngeus — aging of the larynx). ii.​ Vocal folds become thinner and they take on bowing of the vocal folds. The voice starts to become weaker, breathier, and fatigues more easily as we age. iii.​ They will lose some pitch and loudness range. iv.​ As we age, we start to lose elastin and collagen (e.g. sags, wrinkles) in our vocal folds — tissues losing flexibility and tension = stiffer vocal folds and do not move as easily. 8.​ Physiology a.​ Myoelastic Aerodynamic Theory (Vandenberg) i.​ Pre-Phonation Phase 1.​ Exhalation is occurring (no phonation yet). When we are relaxed breathing, our vocal folds are open. Air is coming out (exhaling), but we want to initiate phonation. 2.​ Vocal folds begin to approximate (come together) / adduct due to innervation of the adductor muscles (there is no voice yet!). As the vocal folds are coming together, the glottis (opening) becomes smaller. We are trying to push the same amount of air through a smaller space. There will be a lot of pressure starting to build up. The subglottic pressure (pressure below those folds) is building. STILL NO PHONATION because we have not blown the folds apart yet.  ii.​ Phonation Phase 1.​ Subglottic pressure builds until it overcomes the resistance of the vocal folds and they blow open. This is the initiation of phonation. 2.​ When the vocal folds are blown open, there is a sudden instantaneous release of high velocity air through the glottis. a.​ Bernoulli Principle — airflow velocity and air pressure have an inverse relationship. As one goes up, the other goes down. This refers to the movement of air through the glottis. 3.​ Due to the Bernoulli Effect, when there is a sudden increase in airflow velocity, there is a sudden decrease in pressure (suction) in the glottis, which brings the folds back together. 4.​ The natural elasticity of the vocal folds also helps to bring the folds back together. 5.​ With the vocal folds closed/come back together, subglottis pressure builds up again until they blow apart. This will keep repeating itself. iii.​ For every single phonation, it is due to Bernoulli Principle. b.​ Hirano’s Body-Cover Theory i.​ Hirano re-groups the 5 layers (epithelium, 3 layers of lamina propria, muscle tissue-vocalis) into 3 distinct vibratory divisions, based on their unique vibratory properties: 1.​ Cover = epithelium + superficial layer of lamina propria 2.​ Transition = intermediate + deep layers of lamina propria 3.​ Body = vocalis muscle ii.​ Mucosal Wave — the flexible and compliant layers of the lamina propria and epithelium oscillate over the mass and stability of the vocalis muscle and deeper layers of the lamina propria to create an undulating or oscillating motion — a ripple effect or complex waveform that moves across the vocal folds. Horizontal, vertical, and longitudinal movements are present. c.​ Pitch Control (Fundamental Frequency) i.​ Determined by — vocal length and tension ii.​ To increase pitch — the cricothyroid contract to lengthen and stretch the vocal folds so they vibrate faster. Faster vibration is changing the rate. Vocal folds have to vibrate faster; the cricothyroid contracts, vocal folds elongate and get more tense then vibrate faster.  iii.​ To decrease/lower pitch — cricothyroid relaxes, thyroarytenoid (vocal folds) involved in moving the thyroid back and fourth (relax as well), the folds will shorten and pitch decreases and they vibrate more slowly. iv.​ Changes in subglottis pressure — we need more subglottic pressure to have a louder voice, but sometimes we increase subglottic pressure to have a higher pressure. It can be manipulated a little bit for pitch but the key thing is loudness. 1.​ Amplitude of the movement (how far apart are the folds blowing) — in order to increase amplitude, usually take a deeper breath and when our vocal folds are opening and closing, it has a slightly closed phase and in between more air and more closure, we build up more subglottic pressure, which blows the folds further apart. You need to increase your subglottic pressure and having a longer closed fold phase to increase the amplitude. v.​ Changes in vibratory amplitude — if you have changes in your loudness, it will affect your pitch. If you have changes in your pitch, then it will affect loudness. 1.​ The higher the pitch, the smaller the vibratory amplitude; amplitude increases as pitch decreases. d.​ Intensity Control (Loudness) i.​ Determined by: subglottal pressure, vocal fold vibratory closure, transglottal flow, and supraglottic vocal tract tuning. e.​ Vocal Quality Control i.​ Affected by: 1.​ Compliant and symmetric biomechanical properties of the vocal folds 2.​ Adequate and consistent subglottic pressure and flow source 3.​ Appropriate vocal tract tuning characteristics 4.​ The shape of the glottis (nice and closed glottis) 5.​ Tissue deformity will impact the quality of the voice. 6.​ Degree of glottal constriction (how tight the vocal folds are closed) ii.​ Deviations or cycle-to-cycle variations: 1.​ Shimmer — cycle to cycle variations in loudness. 250 cycles per second. We do not want each of those cycles to be changing their amplitude → it should be consistent, smooth, and symmetrical. 2.​ Jitter — cycle to cycle variations in pitch. The rate of vibration is changing when it should not. a.​ We cannot hear these with our naked ears. We can measure using the CSL or other medical equipment. If it is happening at a certain point, you may hear a roughness in  the voice, no smoothness in the voice, noise in the voice, etc. This becomes a quality issue at a certain point. iii.​ Registers: 1.​ Falsetto (loft) — characteristic pattern of vocal fold vibration. Upper limits of our pitch range, the cricothyroid is strongly retracted, the folds are so tight that most of the vibrations are happening only right on those edges and you have a lot of subglottic pressure (because you are pushing through tense folds). 2.​ Modal (chest) — middle of our frequency range/ normal voice. The voice we most often use in our normal speaking, the folds should be relatively relaxed, etc. 3.​ Glottal Fry (pulse) — it is the low end of our frequency range. It has a very pulsing irregularity vibration. The vocal folds have to be relaxed, low low pitch, and very little air flow. If a person is hyperfunctional, they won’t be able to do it. This is often used during an assessment as a measure of vocal fold tension --- can they produce glottal fry? It slows down their air.