For when we wish to emit voice or breath through the mouth only, which may happen in the pronunciation of the letters which I shall name explosives, we shut the passage of the nostrils, as with a valve.
—Amman, 1700
The Velopharynx in Life
The isthmus between the oral and nasal cavities must be closed during swallowing and speech or else food will be regurgitated out the nares, vowels will be excessively resonated in the nasal chambers, pressure consonants will lose their characteristic explosive and friction noises, and air will be audibly emitted through the nares. In Chapter 1, we noted that phonation was a phylogenetically recent acquisition among vertebrates and that the vital functions of the larynx were respiratory and protective of the airway. Much the same can be said about velopharyngeal function. The velopharyngeal port was not designed primarily as a means of coupling or uncoupling the oral and nasal cavities for speech. Rather, velopharyngeal closure exists primarily to:
1. Seal off the nasal from the oral cavities to isolate the oropharyngolaryngeal tract from atmospheric pressure during deglutition, producing a partial vacuum to facilitate compression of the food bolus by the tongue, cheeks, and pharynx, and thereby forcing it into the esophagus
2. Open the eustachian tube during swallowing to ventilate the middle ear
In only three phonemes of English, the nasal semivowels, is it permissible for the velopharyngeal valve to remain completely open, coupling the oral with the nasal cavities: /m/, /n/, and /η/ (as in sing). The remainder of
English phonemes are correctly produced with the velopharyngeal port closed, meaning all vowels and most consonants. If the port is left too open, voiced consonants will be excessively resonated in the nasal cavities, and intraoral air pressure for plosives, fricatives, and affricates will be reduced. In an attempt to produce them, air escapes through the nares and results in a weak, nasally distorted production of the target sound. It should also be mentioned that a certain amount of nasal resonation of vowels is both normal and desirable. The borderline between normal and pathologic hypernasality often is a matter of perceptual preference. This is most notable in different regional dialects some of which have increased nasal resonance as one of the distinguishing characteristics. Moreover, resonance balance is the focus of many voice therapy techniques designed to improve vocal quality and reduce laryngeal tension.
What must be remembered is that the nasal resonatory defect of hypernasality is not the only one produced by velopharyngeal insufficiency. Hypernasality may be the primary one. Secondary or associated defects are excess nasal airflow, nasal emission articulatory distortions owing to loss of intraoral air pressure stolen by the nasal air leak, compensatory articulatory and phonatory substitutions many of which are nonphonemic, articulatory distortions due to dental and palatal defects, and even dysphonia from compensatory vocal abuse.
In medical and speech-language pathology practice, hypernasality and nasal air emission and hyponasality have similar diagnostic medical implications as dysphonia from laryngeal disease. That is, they signify structural, neurologic, or psychiatric pathologic conditions and therefore are essential to medical differential diagnosis, as well as having developmental, educational, social, psychologic, and occupational handicaps that require treatment. The following transcript of a deposition illustrates these many factors involved in velopharyngeal insufficiency.
Case Study 4.1
Clinician: “No, this is my first.”
A: “Let me explain that a deposition is an official transcript of testimony in place of your appearance in court. We are the attorneys for Ms. Alquist, who is suing the surgeon who removed her tonsils and adenoids. She claims as a result of that surgery her speech was so impaired that she was placed on indefinite leave of absence without pay from her teaching position. She also claims that when she swallows, fluids leak out her nose. So, we are taking testimony from specialists who have independently investigated Ms. Alquist's complaints. I understand you are the speech pathologist who evaluated Ms. Alquist's speech, and that the plastic surgeon and otolaryngologist who also saw her will be following you. This is the official stenographer who will take down your testimony. You will have a chance to read the transcript and make corrections before it is put into final form. Some of the questions I will ask may seem oversimplified, but remember, this testimony will go before a jury of lay individuals who have no technical knowledge of the subject. You have already stated your full name and address. What is your occupation?”
C: “I am a speech-language pathologist.”
A: “I notice you are addressed as ‘doctor.’ Are you a medical doctor?” C: “No. I hold a Ph.D. in speech-language pathology.”
A: “Are you licensed to practice speech pathology?”
C: “In this state there are no licensure laws for speech pathologists.” A: “Will you tell the court what a speech pathologist is and does?”
C: “We identify, describe, diagnose, and treat people who have disorders of communication, that is, voice, speech, and language disturbances from organic or psychiatric illnesses. Where I work, speech pathologists consult
to physicians of all specialties.”
A: “Thank you. Now, do you know the plaintiff, and if so on what occasion have you conferred with her?”
C: “I evaluated Ms. Alquist's speech on May 21 of last year. That evaluation took approximately one and one-half hours.”
A: “Are these the clinical notes that you wrote as a result of your evaluation?”
C: “Yes, they are.”
A: “Are these the audiotape and videotape recordings you made of the patient during your evaluation?”
C: “Yes, they are.”
A: “When you evaluate a patient's speech, doctor, what exactly do you do?”
C: “I ask the patient to perform different tasks that will provide me with an adequate sample of the patient's speech. I usually tape record the speech for more detailed analysis later. I might also make certain laboratory tests, such as aerodynamic and spectrographic assessment, that is, acoustic recordings of the patient's speech and recordings of how she uses air from her lungs for speech.”
A: “Based on your analysis of Ms. Alquist's speech, would you say her speech was abnormal?”
A: “In what way, specifically?”
C: “She had hypernasality and nasal emission.”
A: “Would you please explain the meaning of these words for the court.” C: “Hypernasality refers to excess resonation of speech sounds within the nasal chambers because of partial or complete failure of the soft palate to close off the nasal from the oral cavities, or from incomplete closure of the hard palate.”
A: “You mean like cleft palate?”
C: “Yes. But she did not have a cleft palate.”
A: “Doctor, please point out on this chart the parts of the speech mechanism you are talking about.”
C: “This is a side view of the head and neck. This plate of bone separates the oral from the nasal cavity. It is called the hard palate. This flap of tissue is called the soft palate or velum. It can lift upward and backward to contact the back wall of the throat. When it does, it seals off the oral from the nasal cavity.”
A: “And, what if it doesn't?”
C: “As I explained before, then speech will be abnormally resonated in the nasal cavities. I would add that consonants will be heard as weak or absent if the opening is very large. People would then have trouble understanding what the speaker was saying.”
A: “We will return to what you found out about the plaintiff's speech mechanism, but at this point, I would like you to explain more fully the
implications of Ms. Alquist's speech defect.”
C: “As I said, she was hypernasal and had nasal emission of the airstream as she spoke. If I may, I would like to play a videotape of the patient so that you can hear and see what I'm talking about. As you can hear from the tape, her speech has a noticeable and distracting nasal quality, and some of her words are difficult to understand. We call this reduced intelligibility. Also, you can see she has a tendency to narrow her nostrils and wrinkle her forehead on many consonant sounds. This is a kind of compensation people with palatal insufficiencies develop. It is an attempt to constrict the nostrils so that less air will pass out through them.”
A: “How would this disorder interfere with the patient's everyday life?” C: “A speech defect is a personal matter. Two people with defects of the same type and severity often react differently, depending upon their personality and the importance of speech in their daily lives.”
A: “And, how would you characterize the effect of Ms. Alquist's defect on her?”
C: “Based on the psychologic and social history portion of my examination, Ms. Alquist was devastated by her speech disorder.”
A: “What is your evidence for that statement?”
C: “She broke down several times during the examination, especially during discussions of the effects of her disorder on her professional activities. She said her speech had always been important to her; that she used her speech to favorable advantage in the classroom, that she knew she had a good voice, would often dramatize segments of the curriculum through plays and storytelling, and that she taught singing. Outside of the classroom, she was active in teachers' organizations and was known as a good public speaker and debater.”
A: “Has this changed as a result of her disorder?”
C: “It has, according to what she told me, turned her life around completely. Her students, she said, became inattentive. She began to notice derisive facial expressions of students and colleagues as she would speak. Some of the children made fun of her. Speaking tired her out—she had to exert much more effort to make herself understood.”
A: “Has her speech disorder affected her in any other ways?”
C: “According to Ms. Alquist, she was called into the principal's office and told that she would have to take a leave of absence until something was done about her speech. That was a year ago. She has not worked since. She says she has become withdrawn, has a fear of using the telephone, and has been seeing a psychiatrist for depression.”
A: “Have any attempts been made to correct, treat, or rehabilitate her speech?”
C: “Not to my knowledge. No one recommended speech therapy in her locality.”
A: “Doctor, let's get back to the physical examination of the plaintiff. What, in your opinion, was the reason she developed this disorder at this time in her life? Why would anyone whose speech had been not only normal, but who was in fact a skilled speaker, suddenly acquire this kind of defect?”
C: “I would feel more comfortable if you asked the plastic surgeon and otolaryngologist that question, although I think we agree, having discussed the case in private, on the cause of the disorder.”
witness in your field, you are justified in commenting on the physical aspects of the case.”
C: “Well, we have photographs of the patient's mouth and x-ray motion pictures of her soft palate during speech. These lateral motion picture studies clearly show that, although the soft palate is able to lift up, it is too short to make closure contact against the back wall of the throat; it elevates, but there is a considerable gap left between it and the posterior pharyngeal wall. During our examination, although the hard and soft palate looked all right when the patient opened her mouth, when we explored her hard palate we felt a notch at the back where the soft and hard palate join. This notch is called a submucous cleft. We also noticed, and we almost missed this because it was so subtle, that the little pendulum of tissue that hangs down from the middle of the soft palate, the uvula, was almost invisibly split; you could separate it with a tongue depressor, but most of the time the two halves stuck together so that it looked like solid tissue. You can see the split on this photograph.”
A: “Would you give us the implications of all this?”
C: “We think Ms. Alquist has had a lifelong condition of submucous cleft palate, a cleft in the bone and muscular tissue that is hidden under the mucosal tissue. In her case, a speech disorder was not evident because she was able to attain adequate closure by contacting her soft palate against her adenoids. In other words, the adenoids were serving as an anatomic structure on the back wall of the throat and were helping to effect complete closure; when they were removed, the space created was too great for her soft palate to bridge. The adenoid removal unmasked the submucous cleft.”
A: “Is this condition remediable?”
C: “A prosthetic device called a palatal lift would partially close the gap. More permanent would be a surgical procedure, a pharyngeal flap operation, in which a flap of tissue raised from the pharyngeal wall is sutured to the soft palate, or a sphincter pharyngoplasty.”
A: “We want to thank you for your testimony. If we have any further questions, we'll arrange another appointment through your secretary.”
As this testimony illustrates, although hypernasality and nasal emission are only aesthetically displeasing when mild, when excessive, they diminish or even destroy intelligibility, producing serious occupational and psychologic disturbances. When hard palate or velopharyngeal port defects are left untreated in infancy or early childhood, they may impede speech and language production development and negatively influence the self- concept. Even when they occur for the first time in adulthood, as in the case just presented, they can produce profound psychologic and occupational maladjustments. One might ask, “Which would be more devastating: aphonia (whispered speech) from laryngeal disease or severe hypernasality and nasal emission from velopharyngeal or palatal insufficiencies?” Our first impulse might be to answer that the aphonia would have more profound consequences. In actual fact, loss of normal velopharyngeal closure can be much more serious, because without adequate intraoral pressure, most consonants lose their identity. This fact is amply illustrated in isolated paralyses of the soft palate; respiration, phonation, and articulation are normal, yet, speech is unintelligible solely on the basis of diminished resonance balance. When there is a leak of air into the nasal cavity, it is difficult to build up intraoral pressure and to maintain speech motor coordination necessary for intelligible speech.
Nasal Resonatory Disorders
Classification and Definition of Nasal Resonatory Disorders
Nasal resonatory disorders can be classified into four main auditory- perceptual types:
1. Hypernasality and nasal air emission
a . Hypernasality Synonyms are rhinolalia aperta, hyperrhinolalia, and open nasality. Defined as excess resonance of vowels and voiced consonants within the nasal cavities. The anatomic-physiologic basis is open coupling between the oral and nasal cavities due to incomplete closure of the hard palate and/or velopharyngeal sphincter.
b. Nasal air emission Defined as abnormal flow of air from the nares during the production of high-pressure consonants, it is measurable biophysically via airflow (aerodynamic) techniques. It is heard as friction noise accompanying or replacing the target consonant and may have a “gurgling” quality if there is coexisting nasal congestion. It is sometimes referred to as a nasal rustle.
c. Nasal and/or facial grimacing Defined as occlusion of the nares by contracting the alae of the nose, with associated wrinkling of the forehead, during consonant production, a compensatory action in an attempt to restrict the nasal flow of air.
2 . Hyponasality Synonyms are denasality, rhinolalia clausa, and closed nasality. Defined as diminution or absence of normal nasal resonance of the nasal semivowels /m/, /n/, /η/ and loss of normal assimilation nasality. Its physical basis is over closure of the portal or obstruction between the oral and nasal cavities owing to space-occupying lesions within the nasopharynx or nasal cavities. Two subtypes are recognized:
a . Rhinolalia clausa, posterior A type of closed nasality in which the nasal semivowels lose their normal resonance because of an obstruction in the posterior region of the nasal cavities or the nasopharynx. The nasal phonemes /m/, /n/, and /η/ are heard as oral stops /b/, /d/, and /g/.
b. Rhinolalia clausa, anterior A type of closed nasality in which all the vowels and nasals are produced with a hollow-sounding resonance owing to obstruction in the anterior region of the nasal cavities. It is also called cul- de-sac resonation.
velopharyngeal insufficiency and nasal obstruction resulting in a hollow resonation of all vowels and voiced consonants.
4. Resonance imbalance Resonance imbalance is most often exhibited in persons with hyperfunctional voice disorders. Perceptually, they may sound neither hypr-o-nor hypernasal. Voice quality is most likely to sound throaty, tight, and thin. Stroboscopic recordings of the vocal folds often reveal a long, closed phase and considerable medial or anteroposterior (A-P) constrictions of the larynx.
Etiology of Nasal Resonatory Disorders
The etiologies of nasal resonatory disorders are outlined in Table 4.1. Their causes can be subdivided into organic and psychogenic. Organic causes of hypernasality and nasal emission are anatomic defects, such as clefts of the hard and soft palate, obstructive tonsils, nasal structural deviations; iatrogenic from surgical removal of some portion of the palate; and neurologic disease producing paresis or paralysis of the velopharyngeal musculature. Nonorganic causes of hypernasality and nasal emission are conversion reaction, immature personality development, poor motivation, and imitation. Hypernasality is also common in persons with severe, congenital sensorineural hearing loss owing to poor auditory feedback. Velopharyngeal incompetence is associated with genetic conditions and identifiable syndromes (Shprintzen, 2000a, b). Thus, velopharyngeal incompetence may result from an isolated cause or may be multifactorial in origin resulting from learning, reduced sensory feedback, poor motor control, and/or morphologic deviations in the speech structures.
Table 4.1 Etiology of Nasal Resonatory Disorders Hypernasality and nasal emission
Organic Anatomic
Overt cleft palate with or without cleft lip Submucous cleft palate
Congenitally short soft palate or large nasopharynx Traumatic structural damage
Neurologic (dysarthria)
Lower motor neuron (flaccid)
Unilateral upper motor neuron (“flaccid”) Bilateral upper motor neuron (spastic)
Mixed lower-upper motor neuron (flaccid-spastic) Hyperkinetic (dystonic-choreic) Psychogenic Conversion reaction Immature personality Poor motivation Imitative Hyponasality Organic Hypertrophied adenoids Tumors Inflammations Postsurgical repair Patulous eustachian tube Nasal deformity
Mixed nasality
Combinations of organic etiologies of hypernasality and hyponasality
Causes of hyponasality are primarily organic: space-occupying lesions, such as tumors, inflammations, nasal polyps, and hypertrophied adenoid tissue, and structural deformities, such as deviated nasal septum.
Mixed nasality is caused by coexisting velopharyngeal insufficiency and obstruction of the nasal passageways.
Anatomy and Physiology of the Velopharyngeal Mechanism
The anatomy that pertains to normal and abnormal nasal resonatory functions consists of the oral, nasal, and pharyngeal cavities bounded by muscles and their bony attachments. The x-ray in Fig. 4.1 illustrates the separation of the oral from the nasal chambers by the bony hard palate. Suspended from its posterior edge is the resting soft palate, or velum.