Abductor spasmodic dysphonia
A variant of spasmodic dysphonia in which the spasms pull the vocal cords apart, causing the voice to drop out or sound weak and breathy. Abductor spasmodic dysphonia (AB-SD) is an uncommon variant of spasmodic dysphonia, comprising only about 10% of the cases. It is to be distinguished from adductor spasmodic dysphonia (AD-SD), a much more common variant in which the spasms push the vocal cords together.
In its classic variant, the abductory spasms of abductor spasmodic dysphonia are intermittent, each time pulling the vocal cords apart momentarily, so that a person’s voice drops out intermittently to a whisper or breathy sound. Hence, this classic variant of abductor spasmodic dysphonia is sometimes called intermittent whisper phonation. In its tonic variant, the abductory spasms are more constant and sustained than intermittent, so that instead of interrupting the person’s speech, the spasms produce a more constant breathy quality to the voice.
Occasionally, a person has both abductory and adductory spasms; this is called mixed AB-AD spasmodic dysphonia. For more about spasmodic dysphonia in general and the treatment options for it, see our main entry.
Photos of abductor spasmodic dysphonia:
AB-SD (1 of 4)
Prephonatory instant, with arytenoid cartilages involuntarily positioned apart. Mostly tonic position giving voice relatively constant breathiness.
AB-SD (2 of 4)
Phonatory blur, standard light. Again note the separation of the arytenoid cartilages posteriorly (upper end of the photo), and broad vibratory blur, both consistent with breathy voice.
AB-SD (3 of 4)
Occasionally, patient is able to bring posterior cords together for an instant of normal-sounding voice.
AB-SD (4 of 4)
An instant later, the vocal cords involuntarily separate due to an abductory spasm, dropping the voice again to a whispery quality.
Abductor spasmodic dysphonia patient (1 of 4)
Vocal cords in normal breathing position, in a person with abductor spasmodic dysphonia (SD). The next three photos show how the vocal cord spasms seen with SD can get worse when the person performs more cognitively loaded or involved tasks (that is, the person has to think more). This pattern is related to the widespread understanding that SD's symptoms can be task-specific.
Limited abductor spasms (2 of 4)
When making voice with guttural vocal fry or sustained creaky falsetto, this person is able to keep the vocal cords together, at least part of the time.
Increased abductor spasms (3 of 4)
When the person tries to sustain a sung tone (slightly more cognitively loaded), the vocal cords involuntarily separate, producing a very breathy voice.
Even greater abductor spasms (4 of 4)
When the person speaks (even more cognitively loaded), the vocal cords separate even further, and the voice's breathiness is pronounced.
Absent swallow reflex
When a person’s automatic swallow reflex—which normally kicks in when liquid or chewed food in the mouth reaches the base of the tongue—is entirely absent. In such cases, saliva, food, or liquid in the mouth can slip back to the base of the tongue and then downward to fill the lower part of the throat and flow into the airway without a swallow reflex ever being triggered. Such an individual should not be allowed to swallow by mouth, for fear of incurring aspiration pneumonia. He or she would require an alternate method of feeding, such as a gastrostomy tube. Compare this disorder with delayed swallow reflex.
Achalasia is the failure of a ring of muscle, such as the lower esophageal sphincter (LES), to relax appropriately at the moment that food arrives at the end of its journey down the esophagus. This muscular non-relaxation creates a functional obstruction, interfering with normal passage of food into the stomach. This term is most commonly used in relation to the LES, but may also be used in reference to the upper esophageal sphincter (UES) or even anus.
The backward flow (reflux) of acid from stomach up into the esophagus or, even further up, to the level of the laryngopharynx. Symptoms may be esophageal, laryngopharyngeal, or both. Esophageal symptoms include heartburn, indigestion, and acid belching. Laryngopharynx symptoms tend to include dry throat, husky (especially morning) voice, frequent morning throat clearing, excessive mucus, and mildly sore throat.
Sometimes acid reflux is diagnosed when it isn’t the real problem. The do-it-yourself trials in this downloadable article can help a person and his or her personal physician verify if acid reflux is the appropriate diagnosis: When Acid Reflux Treatment Takes You Down a Rabbit Trail.¹
1. Originally published in Classical Singer, April 2009. Posted with permission.
Acid reflux (1 of 2)
Open phase of vibration, strobe light, with white mucus sometimes but not always suggestive of acid reflux laryngitis.
Acid reflux (1 of 4)
This man has obvious clinical symptoms of acid reflux such as heartburn, excessive morning mucus, husky morning voice. Note classic interarytenoid pachyderma, diffuse pinkness.
Prominent capillaries and mucus (2 of 4)
Here we see loss of color differential between true and false cords. Capillaries are prominent (like bloodshot eyes) on the true cords. There is also adherent mucus.
Redness and inflammation (4 of 4)
Even the upper trachea shows evidence of redness and inflammation. This is not seen that often except with truly severe nocturnal acid reflux/ LPR.
Acoustic analysis of voice
The measurement or graphing of acoustic (sound) information about the voice. This acoustic analysis includes such voice measures as fundamental frequency, formant pattern and energies, decibel level (a physical measure of sound pressure level that roughly correlates to perception of loudness), signal-to-noise ratio, jitter, and shimmer.
At present it is difficult to find unique diagnostic information from any set of acoustic measures. Hence, acoustic analysis is arguably justified for now in the realm of voice research and when used as a feedback tool in the therapy room. Although this may change in the future, at present acoustic analysis is superfluous to the diagnostic process, and specifically to the integrative diagnostic model.
Addition of loudness
Refers to the ability to increase the loudness of the voice. An individual may, either apparently or due to physical limitation, be unable to add loudness because of vocal cord paralysis, a nonorganic disorder, or vocal cord bowing – though when three individuals representing these three diagnoses try to add loudness, the phenomenology observed differs markedly.
Adductor spasmodic dysphonia
A variant of spasmodic dysphonia in which the spasms push the vocal cords together, choking off or straining the voice. Adductor spasmodic dysphonia (AD-SD), also called strain-strangle phonation, is the most common variant of spasmodic dysphonia, comprising about 90% of the cases. It is to be distinguished from abductor spasmodic dysphonia (AB-SD), a variant in which the spasms pull the vocal cords apart.
In its classic variant, the adductory spasms of adductor spasmodic dysphonia are intermittent, each time clamping the vocal cords together momentarily, so that words or syllables in a person’s speech are intermittently choked out. In its tonic variant, the adductory spasms are more constant and sustained than intermittent, so that instead of interrupting the person’s speech, the spasms cause a constant strained or “tight” vocal quality.
Occasionally, a person has both abductory and adductory spasms; this is called mixed AB-AD spasmodic dysphonia. For more about spasmodic dysphonia in general and the treatment options for it, see our main entry.
AD-SD (1 of 2)
Sustained, clear phonation, standard light. Note vibratory blur of the vocal cord margins. The false vocal cords (lines) are in normal relation to the true vocal cords.
AD-SD (2 of 2)
Involuntary adductory spasm. Note that the false vocal cords suddenly over-close (arrows) as a result of the adductory spasm, and voice momentarily stops (along with vibratory blur).
Adductory spasm (1 of 2)
Continuous phonation, standard light. Note the position of the false cords in relation to each other, and also the distance between the anterior face of the arytenoids and the petiole of the epiglottis.
Adductory spasm (2 of 2)
A moment later, an adductory spasm occurs. The spasm may momentarily stop the voice (phonatory arrest). Note the inward squeezing of the entire supraglottis (false cords, arytenoids, and petiole).
Pure AD-SD tonic only, moderate severity:
Aerodynamic analysis of voice
Instrument analysis of the power supply for voice pulmonary air. Aerodynamic analysis of voice can include spirometry, which assesses various capacities and capabilities of the respiratory system, apart from phonation. It also allows determination of the pressure and flow through the vocal folds during phonation.
Our clinicians believe that aerodynamic analysis of voice has yet to earn a place as part of the routine diagnostic workup (see the integrative diagnostic model). Aerodynamic analysis of voice, however, may be of interest for voice research, and when the equipment is used as a biofeedback tool in the therapy room.
Air-wasting dysphonia is a kind of hoarseness that refers to the breathiness (see breathy dysphonia) that one is hearing. Typically, the length of time a person can sustain voice without taking a new breath (maximum phonation time) is decreased. The voice may be described as whispery or foggy or fuzzy. Among other things, possible causes include vocal fold paralysis or paresis, vocal fold bowing and atrophy, or functional (especially nonorganic) voice problems.
A condition in which abnormal proteins (called amyloids) become deposited in the spaces between cells. In some cases, the cause of amyloidosis is a systemic disorder in which the body over-produces proteins–for example, multiple myeloma, a blood disease; in these cases, the amyloid deposits can be dispersed widely across the body. In other cases, the amyloid deposits do not seem to reflect systemic disease, and in such cases, the amyloid deposits can be more organ-specific.
Amyloidosis in the larynx:
In laryngeal amyloidosis, the deposits seem to be localized either just to the larynx, or to the larynx and pharynx. One sees what looks like yellowish candle wax within the tissues. The amyloid deposits are quite firm, and when biopsied, there is little bleeding.
Treatment for laryngeal amyloidosis:
Because of their infiltrative nature, amyloid deposits typically cannot all be dissected out of the larynx; instead, then, an operating physician will aim to debulk the deposits in areas where they impair breathing or the voice. That is, when deposits are widespread in the larynx, there does not seem to be any point in removing them except in locations where removal will improve function. Often, repeated procedures are required over many years’ time, though occasionally the condition seems to stop progressing.
Amyloidosis, before debulking (1 of 4)
Panoramic view. Submucosal amyloid deposits in pharyngeal walls and epiglottis, with examples at arrows.
Amyloidosis, before debulking (2 of 4)
View of anterior subglottis shows diffuse infiltration of yellowish, submucosal amyloid.
Amyloidosis, before debulking (3 of 4)
Phonation under strobe light shows deposit at anterior commissure tethering upper surface of left vocal cord, and resultant vibratory asymmetry.
Amyloidosis, after debulking (4 of 4)
Some months later, after laser debulking at short arrow, showing improvement of vibratory closure after tethering reduced. Note increase of nearby supraglottic amyloid deposit does not need to be addressed because it has no functional consequence to the patient, who has other asymptomatic deposits in subglottis, epiglottis, and nasopharynx.
Amyloidosis (1 of 1)
Amyloid deposits (arrows) at the carina, where trachea splits into right and left mainstem bronchi, as well as a few centimeters down the left mainstem bronchus (smaller arrow). The deposits appear yellowish and widen or project from the tissues they infiltrate.
Amyloidosis, before debulking (1 of 8)
Panoramic view of a large spherical mass of amyloid material bulging submucosally (contour at dotted line) in the false and aryepiglottic cords. The patient has only a harsh stage whisper, and glottic voice only with inspiratory (inhaling) phonation. The posterior vocal cord and ventricle of the opposite side (left of photo) are visible, but the amyloid mass obscures all but a few millimeters of the posterior cord on its side.
Amyloidosis, before debulking (3 of 8)
View yet further down, showing the upper trachea (top-center of photo), the posterior end of one of the vocal cords (left of photo), and the edge of the amyloid mass (bottom-right of photo, again marked by a dotted line). The mass is again obscuring a view of the vocal cord on its side; in fact, it is pressing the cord downward, which affects the voice.
Amyloidosis, before debulking (4 of 8)
Phonation, while attempting to see the vocal cords beyond the large overhanging mass. The vocal cords are each marked with an F, one of the posterior ventricles with a V, and the amyloid mass with an A. This mass actually overlies most of both vocal cords and presses them both downward.
Amyloidosis, after debulking (6 of 8)
Looking into the deepest recess of the dissection. The parallel lines indicate the upper border of the thyroid cartilage.
Amyloidosis, after debulking (7 of 8)
After debulking, both vocal cords are now visible from this angle (compare with photo 2). Remaining swollen overhanging tissue did not appear to be infiltrated with amyloid deposition.
Complete healing (8 of 8)
Many months after debulking, and with complete healing, the voice can pass for normal, and the laryngeal vestibule is no longer filled with the enormous bulk of amyloid. The nubbin at anterior false cord would only need removal if it became large enough to interfere with voice.
Immobility and fusion of a joint due to disease, injury, or a surgical procedure. Ankylosis of the cricoarytenoid joint may be seen after traumatic dislocation, or in rare instances of the disease rheumatoid arthritis.
Photos of Ankylosis:
Paralysis or vocal cord fixation? (1 of 2)
Right vocal cord (left of photo) immobility in young woman who was intubated more than 20 years earlier, at 5 months of age. Voice has been weak and air-wasting ever since. Both vocal cord paralysis and vocal cord fixation are potential complications of intubation: In this case, which is it? In this distant view, one can already see a “divot” in the right posterior cord (left of photo) that is not seen with any of the permutations of vocal cord paralysis or paresis. The area of shading also suggests an area of scarring where the tube traversed the medial arytenoid cartilage.
Scarring seen, no flaccidity (2 of 2)
Under strobe light at closer range. As the cords begin to oscillate, one can again see the scarring of the posterior right cord and arytenoid face. In addition, there is no flaccidity of the right cord (left of photo) such as would be seen with a neurogenic cause. The problem is vocal cord fixation, not paralysis.
Toward the front side of a person’s body. For example: the toes are anterior to the heel. The opposite of posterior.
Anterior commissure microweb
A tiny webbing between the vocal cords at the anterior commissure, where the two cords meet. Some think that an anterior commissure microweb can help to cause vocal nodules, but we do not see any such relationship.
The aryepiglottic cord is the membranous sheet of tissue that stretches from the lateral edge of the epiglottis to the arytenoid cartilage. The upper edge of the aryepiglottic cord is like the gunwale of a boat, so that liquid or saliva can pool in the pyriform sinus without immediately spilling over into the laryngeal entrance.
A pair of small triangular cartilages in the larynx that help to move the vocal cords. The arytenoid cartilages sit on the upper surface of the cricoid cartilage ring’s posterior section. Each arytenoid has a body, apex, muscular process, and vocal process. The vocal process is the only part of the arytenoid cartilage that is sometimes clearly visible when viewing the larynx endoscopically, such as in the photos provided on this site (see the photo below), since the vocal process projects into the posterior part of the vocal cord with thin enough soft tissue covering it that it may “shine through.”
Attachments of the arytenoid cartilages:
The arytenoid cartilages help to move the vocal cords because the vocal cords are attached to them and because several muscles also attach to the arytenoids and can move them around. The joint capsule (tiny ligaments and fibrous tissue) attaches the arytenoid cartilage to the cricoid cartilage; the vocal cord (comprised mostly of the thyroarytenoid, or TA, muscle) attaches to the arytenoid cartilage at its vocal process. The PCA and LCA muscles attach to the arytenoid at what is called the muscular process, which points more laterally, at 90 degrees from the vocal process. The interarytenoid muscle (IA) attaches to the arytenoid on the concave posterior surface of each arytenoid’s body; the IA muscle also connects the arytenoids to each other.
Movement of the arytenoid cartilages:
The IA muscle pulls the arytenoid cartilages together for coughing, voicing, and so forth. The PCA muscles move the arytenoids apart simultaneously to open the larynx widely for breathing. The LCA muscles can move the arytenoids, and especially the vocal processes, toward each other, and can also rock the arytenoids anteriorly.
As the arytenoids move in all these different ways, the vocal cords—being attached to the arytenoids—move along with them. Thus, via the arytenoid cartilages, these muscles cause the vocal cords to separate (abduct) for breathing or come together (adduct) for voicing, throat clearing, coughing, and so forth. There are also other muscles that affect the vocal cords, but apart from the involvement of the arytenoids: the TA muscle that makes up most of the bulk of each cord can isometrically contract and affect the tension of the cords, for varying the quality and (somewhat) the pitch of the voice, and an external muscle, the cricothyroid, has a major role for creating high pitches.
Vocal process of the arytenoid, artificially highlighted
Strobe light, as the vocal cords are just coming into contact for phonation. The vocal process of each arytenoid is brightly highlighted; the extension of each vocal process back into the arytenoid is moderately highlighted.
Vocal processes, accentuated by vocal cord atrophy (1 of 4)
The vocal processes in this patient are extremely visible because the rest of the vocal cord on each side is atrophic and bowed.
Vocal processes, accentuated by vocal cord atrophy (2 of 4)
The vocal cords approach each other for voicing. Note the evident asymmetry between the vocal processes. The left vocal process (right of image) projects further anteriorly than does the opposite process. It is also at a higher (more cephalad) level.
Vocal processes, accentuated by vocal cord atrophy (3 of 4)
Phonation, closed phase of vibration, under strobe lighting. Note the overlap (scissoring) of the left vocal process (right of image) on top of the other process.
Vocal processes, accentuated by vocal cord atrophy (4 of 4)
Phonation, at a higher pitch, at which the scissoring of the left vocal process (right of image) on top of the other becomes even more evident.
Arytenoid chondritis / perichondritis
An infectious or inflammatory response with ongoing ulceration or granulation on the superstructure of the arytenoid cartilage. Here we are talking of the arytenoid cartilage and/ or its thin “envelope” of fibrous tissue called perichondrium. The root chondr- refers to cartilage.
A similar and much more common disorder, contact granuloma or contact ulcer, occurs on the medial surface of the arytenoid cartilage, but low and at the level of the vocal process. When arytenoid chondritis or perichondritis occurs, it causes significant chronic pain (in contrast to contact granuloma, which can be pain-free or bring only minor discomfort). We have never diagnosed the underlying cause. Treatment tends to require definitive removal of the area of cartilage involved (not the entire arytenoid, of course), and then typically the area will heal, though often only after a time of re-granulation.
Arytenoid chondritis (1 of 5)
Festering arytenoid chondritis of over a year's duration. Several biopsies done elsewhere showed only inflammation.
Arytenoid chondritis, removed (2 of 5)
Two weeks after aggressive partial arytenoid superstructure excision, in an attempt to get down to healthy cartilage.
Arytenoid chondritis, removed and healed (3 of 5)
After complete healing. Note loss of anterior arytenoid prominence on the operated side as compared with the unoperated side.
Arytenoid chondritis, removed and healed (4 of 5)
At this point, patient is entirely symptom-free. Notice resolution of the lesion and inflammation. The arytenoid mound is a little lower on right (left of image) than on left (right of image), due to surgical removal of part of the superstructure of the arytenoid.
Arytenoid chondritis, removed and healed (5 of 5)
The area of festering chondritis has completely healed. The arrow shows center of where the lesion was.
Arytenoid chondritis (1 of 3)
This person has twinges of pain every time she swallows, like “ground glass” or “razor blades.” She locates the sensation by pointing precisely to the upper part of the thyroid cartilage on the left. The exam reveals an arytenoid ulcer (upper right of image), with surrounding erythema.
Arytenoid chondritis (2 of 3)
A closer view shows more clearly the central depression and rolled border of the lesion.
Arytenoid chondritis (1 of 1)
Small ulcer with surrounding erythema, right arytenoid superstructure.
2 weeks post dilation (1 of 3)
Two weeks after dilation of this inflammatory subglottic stenosis. Treatment elsewhere with esomeprazole for 2 years had not resolved this. This is likely forme fruste Wegener’s-type stenosis, which in this patient has required dilation every few years, with marked resolution of shortness of breath/ noisy breathing.
Ulcer not caused by tube or reflux (2 of 3)
There was no postoperative pain at all until on the 4th postoperative day, when she developed left throat pain radiating to the left ear. Note within dotted line a flat ulcer with surrounding redness, resembling an apthous ulcer more than endotracheal tube injury or acid reflux. Observation was counseled, and even discontinuation or reduction of her esomeprazole.
3 months later, ulcer is gone (3 of 3)
Within a few weeks, the pain resolved. Here, 3 months later, the ulcer and erythema are gone. Dotted lines indicate where the ulcer would be if still present. Compare with photo 2.
Arytenoid perichondritis (1 of 5)
Singer with constant right throat pain and vocal impairment, worsened by singing and speaking. Examination finding: arytenoid perichondritis. Note the erosion exposing the arytenoid cartilage, and the associated swelling.
Pseudopolyp (2 of 5)
Swelling creates a “pseudopolyp” (at arrow) that interferes with vocal cord closure and vibration.
Two weeks post treatment (4 of 5)
Two weeks after antibiotic treatment. He has intermittent mild discomfort only when singing, and his voice is much improved. Minimal residual erosion (see arrow), with mild inflammatory changes.
Normal voice (5 of 5)
Pseudopolyp has resolved and no longer interferes with voice. At follow-up 6 weeks later, his voice is entirely normal and he has no pain.
Inflammation (1 of 2)
Spontaneous onset of sore throat, laryngitis, without any other URI symptoms approximately 6 months earlier. Biopsy elsewhere showed 'acute and chronic inflammation.' Note the inflamed, rolled border outlined by dotted line, and a sense of central excavation.
Surgery likely (2 of 2)
At closer range. The solution here will likely be to remove the lesion to include a central "festering" area of perichondrium, as for the other cases on this page. Cause of this kind of lesion is always unknown.
Throat pain (1 of 4)
Very localized throat pain, left mid-neck, has been present for about 5 months with no sign of improvement despite trials of antibiotics, and fluconazole elsewhere. The location of pain correlates well to the lesion (bold arrow). The pain is very troublesome, fluctuating between 5 and 7 on a ten-point scale, worse with talking and tending to increase as the day progresses. The patient was also experiencing frequent laryngospasm. The patient was offered further observation vs. excision at her option.
1 week post removal (2 of 4)
After waiting an additional month, the patient became motivated to have the lesion removed. This examination is one week after excision of perichondrium and a small amount of cartilage, seeking to remove the “festering point.” The surgical wound is indicated by small dotted line on the left (right of photo). The patient’s pain is already much reduced, in spite of this wound, but peculiarly, she now has just a slight similar pain on the right. Note the small lesion indicated by the arrow, and visible in retrospect, in photo 1.
5 weeks post removal (3 of 4)
Five weeks after surgical removal, left-sided pain is still gone, and after a course of antibiotics and steroids, right sided lesion (arrow) and pain are nearly gone. It is not known whether healing was spontaneous or the result of steroid and antibiotic. This is because treatment of longstanding lesions often fails, and early, minimal lesions like this one sometimes heal without treatment.
3 months post removal (4 of 4)
Now 3 months after surgical excision, the larynx is entirely healed; pain and laryngospasm are gone.
The entry of foreign material, such as saliva, ingested liquid or food, or gastric contents refluxed up to the level of the throat, into the airway below the vocal cords. If this foreign material only enters the laryngeal vestibule but does not descend below the vocal cords, this is not considered aspiration, but instead laryngeal penetration. Significant or recurring aspiration puts a person at risk of pneumonia; laryngeal penetration alone does not, though a person with laryngeal penetration is more likely to aspirate trace amounts than is the person with completely normal swallowing function.
Aspiration can occur before, during, or after the act of swallowing. Aspiration before the swallow means that liquid or food in the mouth dribbles or spills down into the larynx and beyond before the swallow is initiated. This is seen most commonly when there is a neurological disorder, such as after a cerebrovascular accident (stroke).
Aspiration during swallowing happens when, as the swallowed material travels from the base of the tongue toward the entrance to the esophagus (in the pharyngeal phase of swallowing), some of that material drops into the larynx and straight down through it to enter the airway. This kind of aspiration can happen because a person’s vocal cords don’t close properly, due to paralysis, paresis, or tissue loss such as after a partial laryngectomy.
Aspiration after swallowing happens when some of the ingested liquid or solid remains pooled in the lower throat after the swallow is complete, and when the patient takes the first post-swallow breath, it enters the airway. To try to prevent aspiration after swallowing, the supraglottic swallow technique can help.
Aspiration (1 of 1)
After patient swallows blue-stained applesauce, some enters the trachea. Vigorous coughing can clear this away so that even chronic aspiration of this sort does not necessarily cause pneumonia.
Trachea, aspiration (2 of 2)
The patient aspirates a drip of saliva. If this were a larger amount of food material, and if it frequently descended much lower, to the level of the air sacs, this person would develop pneumonia.
Aspiration (1 of 7)
Panoramic laryngopharynx view. The patient is holding a sip of liquid in his mouth and preparing to swallow it.
Aspiration (2 of 7)
Before he initiates the swallow, a small drip of liquid "escapes" and drips downward into the pharynx. The patient does not yet suspect this. There are only a few drops of liquid, even though it looks like a larger amount due to the close-up view.
Aspiration (3 of 7)
A few milliseconds later yet, the tiny drip has fallen halfway down the length of the pharynx. One can see that the patient is not aware of this drip, as he has not fully closed the vocal cords.
Aspiration (4 of 7)
A few milliseconds later, the drop is arriving at the left (right of image) pyriform sinus. The patient is still not aware of this swallowing "mistake". The vocal cords remain open, so if this liquid had dripped instead into the laryngeal opening, it would have entered the airway and made him cough.
Aspiration (5 of 7)
With a second sip of faintly blue-stained water, a small trickle escapes "early" before the swallow. One can see the leading edge of water flowing onto the epiglottis (indicated by the dotted line).
Aspiration (6 of 7)
The leading edge of the water has advanced and continues to flow downwards. This is indicated by the dotted line and arrows.
Aspiration (7 of 7)
The leading edge of the water has again advanced and continues to flow downwards into the laryngeal vestibule and through the open vocal cords. This time, the patient coughs.
Pneumonia, or an infection of the lungs, that has resulted from aspiration—that is, from passage of food, liquid, saliva, or vomited stomach contents down into the larynx, trachea, and air sacs of the lungs. Aspiration pneumonia can occur in individuals who have chronic swallowing deficits (e.g., presbyphagia), or can be a result of intoxication, seizure, loss of consciousness, etc.
Atypical spasmodic dysphonia
A benign neurological voice disorder caused by laryngeal dystonia. Atypical cases of spasmodic dysphonia (SD) may be challenging to diagnose, even by clinicians with some experience with the disorder. Examples of reasons that this may be so: In the atypical case, contrary to what is usually seen, singing may be more affected than talking; falsetto/head voice may be more affected than chest voice, and so forth. There may also be no phonatory arrests in the less common tonic variant spasmodic dysphonia.
Auditory perceptual evaluation of voice
The sense of hearing applied to assessment of the voice. In some locations, auditory perceptual evaluation of voice refers primarily to characteristics of the patient’s spontaneous speaking voice, and sometimes very basic additional elicitations.
However, in clinics where the integrative diagnostic model has been mastered, the clinician’s auditory perception has been informed by extensive knowledge and experience of normal and abnormal vocal capabilities and vocal limitations. This knowledge, along with his or her own voice used for modeling and elicitation, are the tools used when conducting the vocal capability battery. It is auditory perceptual evaluation of elicited vocalizations at the extremes of normal capability that provide powerful diagnostic information about the voice, as distinct from the larynx.
Inflammation of the vocal cords, especially of the layer just beneath the mucosa, caused by an auto-immune disorder. Auto-immune disorders that can potentially cause laryngitis (albeit infrequently) include rheumatoid arthritis, lupus erythematosus, Wegener’s granulomatosis, and combined auto-immune disorder. Some individuals develop an inflammatory picture of capillary prominence and mucosal edema which is unrelated to vibratory trauma; that is, these individuals do not have the profile of the “vocal overdoer.” Others form rheumatoid nodules of the vocal cords, aka “bamboo nodes.”
Average/anchor frequency is a term used at our practice to designate the pitch (and by extension, fundamental frequency) that an individual is using during spontaneous, running speech, as determined via auditory perception. We use both “average” and “anchor” together, because some persons speak in a perceptually monotone voice, at which point we consider the pitch extracted via auditory perception to be virtually synonymous with “average” fundamental frequency (proven to be the case in informal study comparing Fo extracted by auditory perception vs. by machine measures).
Other individuals speak with a great deal of pitch inflection. In these cases, we listen for the lowest common pitch to which the voice seems to be “anchored.” When highly inflected speakers become generally fatigued or “depressed,” they tend to default to this pitch, which then becomes more of an “average” pitch for them. Of course, using machine measures of fundamental frequency (primarily using equipment for acoustic analysis), a formal average fundamental frequency can be determined. The ability to determine average/anchor pitch via auditory perception during the vocal capability battery can be learned by clinicians with good pitch perception.