Key Points
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Velopharyngeal inadequacy refers to any type of dysfunction and may be categorized as insufficiency, incompetence, or mislearning.
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“Phoneme-specific” or “sound-specific” velopharyngeal dysfunction (VPD) involves abnormal production of one or more phonemes with increased nasal airflow while other phonemes are normal. Phonemes most commonly involved with phoneme-specific VPD include /s/, /sh/, and /z/, and rarely, /f/.
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VPD is best managed by a team that includes the surgeon, speech-language pathologist, and dentist or prosthodontist if needed.
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Compensatory articulation errors may result from VPD, but oral motor exercises are not appropriate unless VPD is accompanied by oral motor weakness, which is infrequent.
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The Furlow palatoplasty reorients the levator veli palatini muscles while also thickening and lengthening the palate.
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All surgical procedures that improve VPD may lead to airway obstruction.
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A “transdisciplinary” approach with input from the otolaryngologist, speech-language pathologist, and other team members is optimal for management of VPD.
Only three phonemes in the English language involve nasal air escape for normal production: /n/, /m/, and /ng/. All other sounds are produced with oral airflow. The velopharynx is one of several articulators, as are the jaw, tongue, lips, pharynx, and larynx, which work together to produce the various sounds of speech. The normal role of the velopharynx will vary according to vowel height, consonant type, proximity of nasal sounds to oral sounds, utterance length, speaking rate, and tongue height. For vowels, velar position is higher for vowels with a high pharyngeal constriction such as /i/ and /u/ than for low-pharyngeal-constriction vowels such as /a/. The velar port generally is closed for vowels, except when the vowel is in proximity to a nasal consonant. The velopharyngeal port therefore changes between relatively open and closed states depending on the balance of oral versus nasal consonants occurring in the speech stimuli. Velar movement may vary widely in velocity and displacement according to the tasks of the particular speech, particularly the speaking rate.
If the velopharynx is not functioning correctly or if a defect in the palate allows the oral sound to resonate through the nose, speech may be perceived as abnormal. Incompetence of the velopharyngeal mechanism leads to increased hypernasality, nasal turbulence, and/or nasal emission. Conversely, nasal obstruction will result in hyponasal resonance. Speech intelligibility is determined primarily by articulation; however, abnormal speech resonance distorts speech production, impairs overall speech quality, and may adversely affect intelligibility.
Functional Anatomy
The velopharyngeal port is closed by the action of several muscles ( Table 9-1 ) that move the velum in a posterior-to-superior direction. Medial movement of the lateral pharyngeal walls and occasionally anterior movement of the posterior wall may also contribute.
| Muscle | Origination | Attachment | Function | Innervation |
|---|---|---|---|---|
| Tensor veli palatini | Vertical portion arises from the scaphoid fossa at the base of the internal pterygoid plate, from the spine of the sphenoid, and from the outer side of the cartilaginous portion of the eustachian tube | Terminates in a tendon that winds around the hamular process | Tenses the soft palate; opens the auditory tube during swallowing | Mandibular branch of the trigeminal nerve |
| Levator veli palatini | Arises from the undersurface of the apex of the petrous portion of the temporal bone and from the inner surface of the cartilaginous portion of the eustachian tube; found to occupy the intermediate 40% of the length of the soft palate * | Fibers spread out in the soft palate, where they blend with those of the opposite side | Acts as a sling when contracted to pull the velum in a posterosuperior direction ; major elevator of the velum ; positions the velum † | Pharyngeal plexus derived from the glossopharyngeal and vagus nerves and the facial nerve ‡ ; course of the facial nerve is through the greater petrosal nerve § |
| Musculus uvulae | Palatal aponeurosis in a circumscribed area posterior to the hard palate || | Inserts into the uvula | Adds bulk to the dorsal surface of the soft palate | Pharyngeal plexus; pharyngeal plexus derived from the glossopharyngeal and vagus nerves and the facial nerve ‡ |
| Palatoglossus | Has a fan-shaped attachment from the anterior surface of the soft palate ¶ | Courses through loose connective tissue within the anterior faucial pillar and has a tapering termination in the side of the tongue ¶ | Elevates the tongue upward and backward to constrict the pillars and probably lowers the velum ** ; positions the velum † | Pharyngeal plexus composed of branches from the glossopharyngeus and vagus cranial nerves and from the sympathetic trunk |
| Palatopharyngeal | Arises from the soft palate | Inserts with the stylopharyngeus into the posterior border of the thyroid cartilage | Adducts the posterior pillars, constricts the pharyngeal isthmus, narrows the velopharyngeal orifice, raises the larynx, and lowers the pharynx †† ; positions the velum † | Pharyngeal plexus |
| Superior constrictor | Arises from the lower third of the posterior margin of the internal pterygoid plate and its hamular process | Inserts into the median raphe | Medial movement of the lateral aspects of the pharyngeal walls ; high levels of activity are related to laughter ; may function to draw the velum posteriorly ; pulls the posterior wall and posterolateral angle | Pharyngeal plexus derived from the glossopharyngeal and vagus nerves and the facial nerve ‡ |
* Data from Boorman JG, Sommerlad BC: Levator palati and palatal dimples: their anatomy, relationship and clinical significance. Br J Plast Surg 1985;38:326.
† Data from Finkelstein Y, Shapiro-Feinberg M, Talmi YP, et al: Axial configuration of the velopharyngeal valve and its valving mechanism. Cleft Palate Craniofac J 1995;32:299.
‡ Data from Nishio J, Matsuya T, Machida J, Miyazaki T: The motor nerve supply of the velopharyngeal muscles. Cleft Palate J 1976;13:20.
§ Data from Ibuki K, Matsuya T, Nishio J, et al: The course of facial nerve innervation for the levator veli palatini muscle. Cleft Palate Craniofac J 1978;15:209.
|| Data from Azzam NA, Kuehn DP: The morphology of musculus uvulae. Cleft Palate J 1977;14:78.
¶ Data from Kuehn DP, Azzam NA: Anatomical characteristics of palatoglossus and the anterior faucial pillar. Cleft Palate Craniofac J 1978;15:349.
** Data from McWilliams BJ, Morris HL, Shelton RL: Cleft palate speech , Philadelphia, 1990, Mosby.
†† Data from Meek MF, Coert JH, Hofer SO, et al: Short-term and long-term results of speech improvement after surgery for velopharyngeal insufficiency with pharyngeal flaps in patients younger and older than 6 years old: 10-year experience. Ann Plast Surg 2003;50:13.
The elevation and posterior motion of the velum are attributed to the levator veli palatini (LVP),the main muscle mass of the velum. Variation in the angle of insertion to the base of the skull may change the elevation. The palatoglossus and palatopharyngeus muscles pull the palate down, opposing the LVP. The action of the palatopharyngeus muscle tends to stretch the velum laterally, thereby increasing the velar area and altering the shape of the contact. The palatopharyngeus muscle may also subtly affect velar height, especially when the velum is in the elevated position. The musculus uvulae adds bulk to the dorsal side of the velum.
The mobility of the lateral walls varies from person to person and depends on speech context. The greatest movement is attributed to selective action of the uppermost fibers of the superior constrictor muscle and usually occurs below the levator eminence at the level of the full length of the velum and hard palate. The palatopharyngeus is closely related to the lateral fibers of the superior constrictor and may also contribute to lateral wall motion.
The Passavant ridge is a feature of the posterior wall observed in some persons during speech or swallow. This feature has been associated with lateral wall motion and is thought to be composed of the uppermost fibers of the superior constrictor and palatopharyngeus muscles. The Passavant ridge may contribute to velopharyngeal closure in as many as one third of patients in whom it is observed. It also contributes to muscular activity that does not assist in closure, as the activity occurs below the level of the velopharyngeal port.
Approach to Diagnosis and Management of Velopharyngeal Dysfunction
Understanding the causes of VPD is essential to accurate evaluation and diagnosis. Assessment includes a precise study of the degree and nature of velopharyngeal function and its impact on speech production. Treatment options include speech therapy, surgical intervention, and/or prosthetic obturation.
Causes of Velopharyngeal Dysfunction
Velopharyngeal dysfunction encompasses all disorders of various causes involving the velopharyngeal sphincter mechanism. Perceptually, VPD is considered a dysphonia because it affects the sound quality or resonance of the voice. In fact, 16% of 427 children evaluated for voice problems were found to have velopharyngeal rather than laryngeal dysfunction. Unfortunately, the terminology of VPD is inconsistent throughout the medical literature. In this chapter, we use the definitions summarized by D’Antonio and Crockett.
Velopharyngeal inadequacy and VPD are general terms that are divided into three etiologic categories: insufficiency, incompetence, and mislearning. Velopharyngeal insufficiency encompasses structural defects that result in insufficient tissue to accomplish closure, such as cleft palate. Incompetence describes impairment of motor control secondary to neurologic dysfunction, such as paresis or paralysis. Velopharyngeal incompetence may result from skull base surgery, tumors involving the jugular foramen and vagus nerve, or central nervous system impairment from brainstem stroke. Mislearning results from factors that are independent of structural defects or neuromotor pathology.
Cleft palate is the most common congenital anatomic condition affecting velopharyngeal function. VPD may also result from a submucous cleft palate, which is identified by a bifid uvula, zona pellucidum of the soft palate, and palpable notch in the posterior hard palate. Congenital short palate, palatopharyngeal disproportion, occult submucous cleft palate (absence of the musculus uvulae), and longitudinally oriented levator muscles may also cause velopharyngeal insufficiency. Hypertrophic tonsils may occasionally interfere with closure of the velopharyngeal port. Causes of velopharyngeal incompetence include muscular dystrophies, myasthenia gravis, traumatic brain injury, Down syndrome, and velocardiofacial syndrome (22q11 deletion). Adding to the complexity of the problem, many of these disorders may manifest incompetence or insufficiency, or both.
Velopharyngeal inadequacy has been reported to occur after 1 in 1500 adenoidectomies. A large adenoid may compensate for a short or poorly mobile palate, and adenoidectomy may create or unmask VDP in these conditions. It is therefore important to identify the presence of disorders that increase the risk of postoperative VPD before considering adenoidectomy.
Assessment
Perceptual Speech Analysis
Most otolaryngologists will encounter children with VPD in their practice. In taking the history of a child referred for a voice or speech problem, the clinician should listen carefully to input from the parent or caregiver who is most familiar with the child’s speech. The child may often be shy and unlikely to speak voluntarily. Playing games or asking direct questions can stimulate the child to begin spontaneous speech. This perceptual evaluation will provide the clinician with a sense of the language level, articulation, nasal resonance, and presence or absence of nasal air emission as the child is speaking. Facial grimacing during nonnasal speech is a compensatory action used by patients to decrease nasal air emission by narrowing the external nares and may be indicative of VPD. A heightened awareness of VPD should be considered even in children referred for other concerns.
The initial assessment of VPD may be quickly and easily performed in the office setting with a reasonably cooperative patient. The nasal occlusion and mirror fogging tests may be performed while the child produces various phonemes or repeats phrases selected to provoke the symptoms. The nasalized consonants /m/, /n/, and /ng/will be altered when nasal airflow is decreased. Signs of hyponasal resonance include alteration of /m/ to sound like /b/, /n/ to sound like /d/, and /ng/ to a hard /g/ within the context of speech. If the nasal airway is obstructed, humming the /m/ sound will not change whether or not the nose is plugged and the examiner will not feel nasal vibrations. Normally, a mirror held under the nose should fog with voicing of the nasal consonants ( Fig. 9-1 ). If the resonance is the same with or without occlusion of the nose during production of nasal consonants, then nasal or nasopharyngeal obstruction is present. Hyponasal resonance results in the same quality of speech as that associated with the congestion of a common cold. Large adenoids or congested nasal turbinates are other causes of hyponasal resonance. Repetition of words or sentences that are loaded with nasal consonants will aid in documentation of this abnormality ( Table 9-2 ). The velopharynx continues to be active during production of words and phrases with nasal consonant sounds but is maintained between a relaxed and a closed state.
| Nasal Consonants | |
| Ma ma | Money |
| Na na | Monkey |
| Momma made lemon jam | Nancy is a nurse |
| Nonnasal Consonants | ||
| Pa pa pa | Daddy did it | Sustain “s” |
| Baby | Too tight | Sustain “sh” |
| Puppy | Chocolate chip cookie | Pick up the kick ball |
| Puffy | Forty-four fat fish | Baby bib |
| Daddy | Sissy saw it | Get it out |
Hypernasality or increased nasal resonance will be noted with production of nonnasal phonemes, which are the majority of vowel and consonant sounds in the English language. The early phonologic repertoire usually includes the bilabial plosives /p, b/, and lingua-alveolar phonemes /t, d/. Using words and sentences loaded with oral sounds allows the listener to assess speech resonance (normal or hypernasal). Plugging the nose while the child repeats the /p, b, t, d, s/ or /sh/ sounds during syllable repetitions or within words and sentences will result in noticeable change in resonance if there is hypernasality. The use of a mirror beneath the nose during sustained /s/ and /sh/ sounds as well as during oral-only speech tasks will assist in the detection of nasal air escape (see Fig. 9-1 ). Fogging of the mirror typically is observed only for production of nasal phonemes and nasalized vowels. Increasing the complexity of the tasks (i.e., sounds to words to phrases to sentences) may reveal deterioration of velopharyngeal competence. The degree of openness is determined by the phonetic environment. Some children have more difficulty if nasal and nonnasal phonemes are mixed, such as counting from 60 to 70 and alternating repetitions of /m/ and /p/ syllables. Repetition of tasks during a period of minutes may unmask velopharyngeal fatigue, as seen in myasthenia gravis. Velar height or elevation is most pronounced during the “high” vowels of /i/ and /u/ and the sibilant /s/, and even patients with improved velopharyngeal function may have difficulty with production of these sounds.
The clinician also may encounter “phoneme-specific” VPD, or mislearning. In this entity, one or more phonemes are produced abnormally with nasal air emission, while the rest of the speech is normal. Phoneme- or sound-specific VPD most often occurs with production of /s/, /sh/, /z/, and rarely, /f/ phonemes. A nasal fricative substitution is characteristic. Because these are predominant sounds in the English language, the patient often is believed to be globally hypernasal. It is important to assess production of other nonnasal sounds for the presence of air escape, to recognize that the velopharynx is otherwise functional. Appropriate articulation therapy is usually sufficient for correction of phoneme-specific VPD, and surgery is rarely necessary.
The diagnosis of hypernasality may be confounded by concomitant dysphonia or hyponasality. Hoarseness may distort speech production sufficiently that mild VPD may be overlooked. More than 40% of children with VPD also have dysphonia. The use of the mirror test helps separate VPD from laryngeal pathology.
Children with VPD also may have nasal or nasopharyngeal airway obstruction that affects the nasal consonants. Patients with mixed hyponasal and hypernasal resonance manifest both hyponasality and nasal air escape on production of nonnasal phonemes.
The presence of velopharyngeal insufficiency has a significant impact on the child’s and the family’s quality of life, particularly emotional and communication aspects. Parents seem to be an appropriate proxy in determining the impact of the altered speech on the child’s quality of life.
When VPD is suspected on clinical examination, further testing is indicated. A number of techniques are used for evaluation. Indirect measures to assess for VPD include nasometry and aerodynamic measurements. Imaging studies of the velopharyngeal mechanism include lateral cephalometrics, speech videofluoroscopy, and speech nasopharyngoscopy. Assessment of specific resonance-related articulation is an important component in evaluation of these patients.
Nasometry
Nasometry ( Fig. 9-2 ) is an objective standardized assessment that measures the ratio of sound intensity between the nose and the mouth. It is typically done with voicing of standard phrases and passages. Standardized values exist for specific tasks. Calculating the number of standard deviations from normative values for each phonemic set yields a measure of the severity of the nasalance pattern. Nasometry is useful in the initial evaluation to document the degree of dysfunction and to assess progress during speech therapy or following other interventions. A discrepancy may exist between nasal scores and the perceived degree of hypernasality.
Aerodynamic Assessment
Velopharyngeal function during speech may also be evaluated by measurement of pressure and airflow. The nose is covered with a small mask to permit accurate measurement of nasal airflow. A probe is placed into the mouth to measure oral pressure. In the child with normal velopharyngeal function, no nasal airflow will be detected during production of nonnasal phonemes, and the oral pressure and oral airflow will be sufficient to produce normal resonance and speech articulation. An advantage to the pressure-flow technique is the ability to determine the timing of the air escape. The pressure-flow technique also is used to calculate the cross-sectional nasopharyngeal airway area from the pressure-flow measures.
Imaging Studies
An imaging study of the velopharyngeal mechanism may be indicated when speech therapy is not progressing, if speech evaluation reveals significant hypernasality, if a diagnostic dilemma is present, and/or when surgery is under consideration. Lateral cephalometric x-ray studies are no longer commonly used, as these are limited by a sagittal plane view and do not provide information on dynamic movement of the velopharyngeal mechanism. Current methods of imaging velopharyngeal function include speech videofluoroscopy and speech nasal endoscopy. Endoscopy has largely supplanted videofluoroscopy in most clinics today. Most children older than 3 years of age will be able to cooperate with the evaluation. In order to obtain adequate speech information, the child must be able to produce appropriately articulated phonemes. The accuracy of articulation has a direct effect on the closure. Velopharyngeal closure on swallow does not yield information regarding speech. Thus, evaluation may need to be deferred in children with significant developmental delays or severe articulation disorders until they have received speech therapy.
Speech Videofluoroscopy
Videofluoroscopic evaluation has been a standard tool in assessment of the speech mechanism. Generally, a speech-language pathologist attends this examination with a radiologist in the hospital imaging department, as is done for modified barium swallow studies. A small amount of barium is introduced through the nose to coat the velopharynx and improve visualization. While under fluoroscopy, the child repeats or reads a set of phoneme-specific speech tasks. Because the velopharyngeal sphincter functions in several planes of movement, accurate analysis requires at least two and preferably three views. The lateral view demonstrates the length, thickness, and anterior-posterior and superior motion of the palate, as well as the anterior movements of the posterior pharyngeal wall (Passavant ridge). The anterior-posterior view assesses the lateral wall motion. The en face view (e.g., Towne or submental vertex view) is focused along the plane of the velopharyngeal port and demonstrates movement of the lateral walls, velum, and posterior wall.
The limitations of videofluoroscopy include the need for a cooperative patient and for radiation exposure, which may limit the length of the speech sample that can be obtained. The examining team must include both a radiologist and a speech pathologist with experience in analysis of these images. Videofluoroscopy is useful to define closure patterns and assess the level of the Passavant ridge and its participation in closure. Nevertheless, this assessment may still miss small fistulas and intermittent closure patterns. In addition, it is difficult to evaluate postsurgical changes. For these reasons, most teams use endoscopy as the standard first-line assessment tool.
Speech Endoscopy
Speech endoscopy is increasingly considered the standard first-line assessment tool, and many otolaryngologists and some speech-language pathologists are experienced in its use. Ideally, the test is performed in the presence of both the physician and speech-language pathologist. Alternatively, the examination may be video recorded for later review. After topical anesthesia of the nose, a flexible nasopharyngoscope is introduced into the velopharynx.
The scope should be positioned higher in the nasopharynx to reduce parallax and fish-eye distortions. This is best accomplished by passing the flexible scope in the middle meatus region rather than along the floor of the nose. As with speech videofluoroscopy, the patient repeats a series of words, phrases, and sentences while the endoscopic images are recorded. It is important to use a microphone and record the voice as well as the video images. Endoscopy allows assessment of the static anatomy such as the nasal septum, eustachian tube orifice, and adenoid pad. The structure of the musculus uvulae should be evaluated to rule out occult submucous clefting ( Fig. 9-3 ).
The examiner observes velar and lateral wall motion and looks for contributions from the Passavant ridge during speech tasks. Incomplete closure may be documented by viewing the unclosed port or bubbling of mucus in the velopharynx. Contribution of the adenoid pad to closure, adenoid or posterior wall irregularities, and interference by the tonsils may also be seen. Speech videofluoroscopy imposes no constraints on the duration of the speech sample, other than the child’s ability to cooperate. Both structure and function are readily and specifically assessed.
Figure 9-4 depicts the four primary velopharyngeal closure patterns that may be observed on endoscopy or speech videofluoroscopy. These patterns differ in terms of the orientation of the residual gap resulting from incomplete closure of the velopharynx.
The coronal closure pattern is seen in 55% of the population and results in a coronally oriented gap. The palate (velum) moves posteriorly with minimal contribution from the lateral walls and posterior wall. The sagittal closure pattern (seen in 10% to 15% of the population) leaves a gap oriented in a sagittal plane, because the major contribution to closure is from the lateral walls. The circular closure pattern involves significant motion of the velum and the lateral walls, leaving a circular central gap (seen in 10% to 20% of the population). The circular with Passavant ridge pattern results from motion of the velum and lateral walls with additional presence of the Passavant ridge (seen in 15% to 20% of the population). It is important to recognize that the Passavant ridge may be present without contributing to closure.
Identification of the closure pattern may assist in prescribing surgical or prosthetic intervention; knowing the location of the “gap” allows the clinician to decide how best to obturate that gap.
Magnetic Resonance Imaging
Recently, magnetic resonance imaging of the velopharynx has been investigated as an assessment tool for VPD. This noninvasive imaging modality avoids ionizing radiation and may be helpful in the uncooperative child. Magnetic resonance imaging allows delineation of soft tissue planes in multiple views. Unfortunately, cost and the inability to correlate dynamic velopharyngeal function with the audio signal (speech sample) have limited the applications of this imaging modality.
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