AUTHOR AND EDITOR INFORMATION

Section 1 of 9  

• Authors and Editors
• Introduction
• Clinical
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

INTRODUCTION

Section 2 of 9  

• Authors and Editors
• Introduction
• Clinical
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

Background

The activities of swallowing and speaking depend on the ability to obtain adequate closure of the velopharyngeal port. Both are complex motor skills that involve the coordination of a diverse group of muscles along the upper aerodigestive tract. Velopharyngeal movements during speaking are quite distinct from those involved in swallowing, as is clinically evident in patients who are able to obtain good closure during swallowing yet are unable to obtain adequate closure during speech.

Phonation involves the generation of a column of air pressure passing from the subglottis and into the upper airway. Inadequate velopharyngeal closure (VPC) allows air to escape through the nose during the generation of consonants requiring high oral pressure, leading to inappropriate nasal resonance and/or nasal emissions during speech production.

Causes of hypernasality and velopharyngeal dysfunction (VPD) are many and range from structural causes such as cleft palate to neuromuscular problems like those seen in velocardiofacial (VCF) syndrome. Functional etiologies also exist, including splinting of the palate after tonsillectomy, imitation of cultural or familial role models, and phoneme-specific problems.

Pathophysiology

VPC is an important part of speech. All phonemes in the English language except 3 (/m/, /n/, /ng/) are produced with oral airflow, meaning that the velopharynx should be closed. The nasal phonemes (/m/, /n/, /ng/) are produced with nasal resonance and require that the velopharynx be open during their production. With so many phonemes in English requiring oral airflow, oral resonance is important to production of intelligible speech.

In describing the problem of hypernasal speech, differentiating among velopharyngeal mislearning, velopharyngeal insufficiency, and velopharyngeal incompetency is important. Velopharyngeal mislearning is best described as incorrect closure of the velopharyngeal port as result of articulation difficulties. Inconsistent hypernasality or phoneme-specific hypernasality is typical of mislearning. In contrast, velopharyngeal insufficiency is inadequate closure of the velopharyngeal port resulting from a structural problem with the velum, including submucous cleft palate, shorted velum relative to the depth of the posterior pharyngeal wall, or overt cleft palate.

Velopharyngeal incompetency is due to a functional problem with the oral motor mechanism, as seen in paresis, apraxia, and dysarthria. The effect of the velopharyngeal mislearning, insufficiency, or incompetency on the patient's speech is usually the same. For this reason, these terms are typically used interchangeably or best referred to in general as VPD.

Oral resonance (as contrasted with nasal resonance) is obtained by means of VPC, which creates a seal between the nasopharynx and the oral cavity. Typically, VPC is accomplished by elevation of the velum and approximation of the lateral walls to close off the nasopharynx, directing airflow out of the mouth instead of the nose. VPD occurs when VPC is impaired.

The effects of VPD on a patient's speech include hypernasality, decreased speech intelligibility, and nasal emissions (ie, air escape out of the nose during speech). Several factors determine how severely a patient's speech is affected, including the amount of gap with a closed velum, the patient's articulation and oral motor ability, and compensatory strategies the patient may have developed to decrease nasal emission or hypernasality.

Common compensatory strategies include speaking with soft intensity (ie, volume) to decrease airflow through the nasal cavity, speaking with loud intensity or pushing to try to project the voice, and substituting phonemes that require less airflow. Straining to increase oral airflow often results in vocal nodules, and hoarseness is a common finding with VPD.

CLINICAL

Section 3 of 9  

• Authors and Editors
• Introduction
• Clinical
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

History

Historical factors in VPD are primarily related to problems with speech intelligibility. The voice is described as having a nasal resonance; nasal emissions (ie, air escape through the nasal passage with speech) may also be present. Compensatory articulation errors are often present, worsening speech intelligibility. Hoarseness is commonly present in children with VPD.

• Nasal regurgitation, especially in infants, may also be a clue to the presence of VPD. Parents may describe food and liquids coming through the nose with feeding and spitting up.
• In older children and adults, recurrent and chronic sinus infections may be a sign of nasopharyngeal reflux resultant from repeated contamination of the nasal cavity.
• Persistent otorrhea with ear grommets in place may also be due to nasopharyngeal reflux extending up the eustachian tube and through the middle ear. This problems is particularly common in children with a cleft palate or other structural defect.
• When eliciting a history from patients with VPD, look for other factors that may lead to the diagnosis of a congenital syndrome. Cleft palate, frequent infections, low muscle tone, and lower lip weakness may suggest the diagnosis of velocardiofacial syndrome.
• • Poor feeding and hypotonia in infancy may suggest the presence of a neuromuscular disorder.
  • Congenital heart defects in association with VPD are common features of velocardiofacial and kabuki syndromes.
  • A family history may reveal other affected individuals, pointing to a genetic etiology.

Causes

When describing etiologies of VPD, categories of classification include structural abnormalities of the palate, dynamic impairment of a structurally normal palate, and functional abnormalities unassociated with anatomic or dynamic palatal defects. An overview of common etiologies follows.

• Cleft palate
• • Overt cleft palate, either before or after repair, is by far the most common cause of VPD. The incidence of this condition is approximately 1 per 750 live births. VPD has been reported in as many as 30-50% of patients following palate repair.
  • A submucous cleft palate is defined by the presence of a bifid or double uvula, muscular diastasis of the soft palate, and notching of the posterior border of the hard palate. This is usually evident on examination of the oral cavity, especially with elevation of the palate when the patient pronounces the phoneme /ah/.
  • By contrast, an occult submucous cleft palate is an absence or deficiency of the musculus uvulae with a diastasis of the levator veli palatini but without the presence of a bifid uvula or grooving of the oral surface of the soft palate. An occult submucous cleft is best visualized endoscopically as the absence of the bulge on the nasal surface of the soft palate during speech.
  • Most patients with submucous cleft palate typically produce normal speech. However, because of their abnormal musculature, these patients may be predisposed to VPD from any changes to the velopharyngeal anatomy (eg, with adenoidectomy).
• Postoperative VPD
• • Transient VPD with hypernasal resonance following adenoidectomy, with or without tonsillectomy, is not uncommon. This condition may persist for several days to weeks and usually resolves spontaneously. Some nasal regurgitation of liquids may also be present during this period. The incidence of persistent VPD postadenoidectomy has been reported to range from 1 per 1,500-10,000 cases.
  • Although the adenoid pad is not essential to normal VPC, it may assist in closure in those children with structural or functional abnormalities of the soft palate. An irregular adenoid pad can also lead to VPD with nasal air escape.
  • Children at risk for developing persistent VPD after adenoidectomy can often be identified preoperatively by the presence of repaired cleft palate, submucous cleft palate, palatopharyngeal disproportion (eg, abnormally deep pharynx), palatal hypotonia, or preoperative speech and resonance problems.
• Syndromic causes
• • Patients with trisomy 21 (ie, Down syndrome) have a predisposition to VPD. The combination of oromotor and developmental delays, generalized hypotonia, and intellectual delays constitutes a significant risk factor for the development of postadenoidectomy VPD. This risk is somewhat balanced by the fact that these patients often have a narrow velopharynx and a shallow skull base; thus, the distance the palate must traverse in order to effect closure is reduced.
  • VCF syndrome is an autosomal dominant disorder linked to microdeletions in the long arm of chromosome 22. Major findings include cleft palate (overt, submucous, or occult submucous), conotruncal heart anomalies, frequent infections (as part of DiGeorge syndrome), and a characteristic facial appearance with asymmetry of the lower lip. VPD is common in patients with VCF syndrome, not only because of the presence of a cleft palate, but also because of pharyngeal hypotonia.
  • VPD is also a common feature in Kabuki syndrome (KS). Many findings of KS are similar to those of VCF syndrome, including cleft palate, cardiac abnormalities (typically coarctation of the aorta), muscular hypotonia, and characteristic facial features. As in the case of VCF, poor muscular tone of the velopharynx is a major cause of VPD in patients with KS.
  • Velopharyngeal incompetency or insufficiency may also be a feature of other syndromes, such as, neurofibromatosis, myotonic dystrophy, or any syndrome in which low muscle tone is a feature.
• Acquired VPD
• • VPD may develop in children with a stroke or head injury, especially if damage occurs to the motor centers controlling the cranial nerves responsible for pharyngeal muscle control or to higher centers controlling complex motor tasks.
  • Neurologic diseases, such as muscular dystrophy, multiple sclerosis, or brain herniation due to Arnold-Chiari malformation, may result in VPD. Traction on the lower cranial nerves results in paresis of the pharyngeal musculature.
  • Although primarily seen in adults, amyotrophic lateral sclerosis (ALS) and Parkinson disease may lead to VPD in the more advanced stages of disease.
  • Children or adults with apraxia or dysarthria may experience VPD and nasal emissions.

WORKUP

Section 4 of 9  

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• Introduction
• Clinical
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

Procedures

• Voice and resonance evaluation: The speech language pathologist (SLP) can offer informative data in determining the appropriate course of treatment for VPD by completing a voice and resonance evaluation. A thorough voice and resonance evaluation for VPD includes articulation assessment, oral motor assessment, and measurement of nasal airflow.
• Articulation assessment: Measures of articulation ability, such as the Arizona Articulation Proficiency Scale, are administered at the single-word level to determine articulation errors. The patient's speech intelligibility is then rated on the basis of this scale, and the dysfunction is characterized as mild, moderate, or severe. The speech pathologist also describes the types of articulation errors, including nasal emissions, glottal stops, and nasal fricatives. The patient's response to correction regarding articulation errors, distortions, nasal emissions, and hypernasality are then assessed to determine prognosis for improvement with speech therapy.
• Oral motor assessment: A subjective oral motor assessment is completed by observing the range of motion and speed of the lips and tongue, as well as elevation of the soft palate and velum with pronunciation of the phoneme /ah/. Overall facial symmetry and muscle tone are also noted.
• Measurement of nasal airflow: The MacKay-Kummer sensory nerve action potential (SNAP) test is administered for children aged 3-9 years with the Kay Elemetrics nasometer to assess the ratio of oral airflow to nasal airflow. For individuals aged 9 and older, the Zoo Passage, Rainbow Passage, and Nasal Sentences are substituted as standard reading passages. The nasometer results are compared to normative data. A score 3 standard deviations above the mean indicates hypernasal resonance, which is defined as speaking with too much airflow and resonance in the nasal cavity. A score 3 standard deviations below the mean indicates hyponasality, which is defined as insufficient nasal resonance.
• Fiberoptic nasoendoscopy (FN): Results of the voice evaluation form the basis for determining the need for FN. Indications for FN include VPD, either consistent or inconsistent; poor oral airflow with nasal escape; and structural abnormalities of the soft palate. If none of these conditions exists and the patient presents with sufficient oral airflow for most phonemes, speech therapy is typically recommended with a periodic reevaluation prior to completion of nasoendoscopy. If indicated, FN requires the following steps:
• Sedation: Children aged 5 years and younger and older children who are uncooperative are sedated prior to the procedure. Oral midazolam (Versed) dosed 0.5 mg/kg is typically given 15 minutes prior to FN. This dosage provides adequate amnesia and sedation ,while allowing the child to perform the necessary tasks for the examination. Higher doses of Versed may result in oversedation and, thus, make the examination difficult. Midazolam administered nasally has a more rapid onset, but may interfere with the examination.
• Topical anesthesia: Prior to placement of the fiberscope, the nasal cavity is examined for any obstructions that may inhibit passage of the scope into the nasopharynx. The nose is then decongested and anesthetized with a mixture of 4% lidocaine and 0.05% oxymetazoline hydrochloride, which is sprayed into the nose with an atomizing device.
• Procedure: The fiberscope is passed through the nostril, above the inferior turbinate (through the middle meatus), to the posterior nasal choana. Passage of the scope along the floor of the nose does not position the fiberscope high enough to allow visualization of the entire velopharyngeal sphincter. With the fiberscope in place, the patient is asked to repeat a series of words and sentences loaded with phonemes that require increased oral airflow (eg, plosives, fricatives) in order to observe the velar closure pattern. The examination is recorded for later review.
• Advantages and disadvantages: Nasoendoscopy is superior to other methods of assessing VPD (ie, videofluoroscopy [VF]) in that it allows direct visualization of the velopharyngeal sphincter. This is especially important in the postsurgical patient when velopharyngeal anatomy is altered, as in after placement of a pharyngeal flap. FN is slightly more invasive than VF and requires a moderate degree of cooperation from the child in order to obtain an adequate examination.
• Videofluroscopy: This is performed by the SLP in conjunction with a radiologist. Unlike nasopharyngoscopy, VF can be used to see through tissues so that movement can be discerned at all vertical and horizontal positions within the pharynx. A 3-dimensional perspective can be gained using frontal, lateral, and base or Towne projections.
• Procedure: VF is usually performed without sedation. Using a nose dropper, barium is instilled through the nose to contrast soft tissues against the surrounding skeletal structures. Fluoroscopic views are then obtained in the lateral, anteroposterior (frontal), and base projections while the patient articulates phonemes that require increased oral airflow. The lateral view helps the examiner visualize the velum, posterior pharyngeal wall, and tongue. The frontal view enables assessment of the lateral pharyngeal walls along the entire vertical extent of the pharynx.
• Advantages and disadvantages: VF allows more precise localization of the level of VPC by measuring the level against the spine. Observation of the tongue is also important because the tongue may contribute to closure in a compensatory fashion by lifting the palate, as is seen in swallowing. This information could be missed with nasopharyngoscopy alone. VF has the obvious disadvantage of radiation exposure. In addition, when normal anatomy is altered (eg, postsurgery), interpretation of the images may be difficult.

TREATMENT

Section 5 of 9  

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• Introduction
• Clinical
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
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Medical Care

• Speech therapy
• • Speech therapy improves velopharyngeal function in postoperative cases and when the VPD is minimal or due to articulation errors. Compensatory articulation techniques secondary to VPD can also be corrected with speech therapy.
  • In patients with a specific anatomic deficiency that precludes adequate closure of the velopharynx, speech therapy cannot replace surgery. However, speech therapy is often necessary after surgical correction to address any functional (ie, articulation) errors.
  • Upon completion of speech and voice testing, the SLP determines if the VPD and hypernasality are related to articulation errors or if they are phoneme-specific. If either is the case, the VPD is usually not related to structural abnormalities, and correction with speech therapy is most likely amenable.
  • VPD can also be a result of decreased muscle tone in the oral musculature and soft palate. This decreased muscle tone can be seen on FN when the soft palate closes inconsistently or when the closure appears slow in connected speech. A period of speech/language therapy focusing on improving overall articulation, oral motor skills, and strength and elevation of the velum may be able to correct VPD in this case.
• Visual feedback
• • In some children, especially those with hearing impairment, visual feedback can assist in therapy to improve VPD.
  • Several devices are available to assist with this method. Simple tools such as a cold mirror or paper paddle can serve to show the patient when nasal escape occurs.
  • Other devices commercially available for this purpose include the See-Scape, which is placed at the nose and causes a ball to rise when airflow is nasal rather than oral.
  • A more sophisticated method involves the use of a nasometer, which graphically displays a ratio of oral sound energy to nasal sound energy. The visual readout can help the therapist and patient develop compensatory techniques to reduce nasalance. In older children, videotaped nasopharyngoscopy has been used to achieve the same goals. The latter method has been shown to be effective in patients with VPD and cleft palate.
• Nasal continuous positive airway pressure
• • Continuous positive airway pressure (CPAP) therapy is beneficial for patients whose VPD seems related to oral motor issues or velar weakness rather than structural problems of the velum.
  • CPAP therapy is a palate-strengthening program completed 6 days a week for 8 weeks in the patient's home.
  • The CPAP equipment includes a nasal mask, which is attached to the patient before he or she repeats a series of consonant-vowel combinations and sentences designed to cause the velum to open and close against the air pressure from the nasal mask.
  • CPAP pressures are increased on a regimented schedule, producing exercises similar to a weightlifting program for the soft palate.
  • CPAP therapy is very regimented and requires cooperation and participation 6 days per week for up to 24 minutes, which is difficult for young children. Wearing the nasal mask and speaking with the nasal air pressure can also be frightening. Subsequent studies of the efficacy of CPAP for hypernasality have demonstrated variable results; however, significant reductions in hypernasality are seen in some patients undergoing therapy.
• Prosthetics
• • Prosthetics are helpful when surgery is contraindicated, when the cause of velopharyngeal insufficiency is neuromuscular in nature, or as a temporizing measure until surgery can be performed. The 2 types of prostheses available include obturators and palatal lifts. A speech appliance is not only helpful in obturation, it may also improve the function of the velopharyngeal mechanism. Obturators and lifts are attached to the teeth by metal wire or bands or osteointegrated dental implants.
  • Obturators can substitute for tissue deficiency. In certain cases, the obturator can be downsized gradually so that the native tissue, if adequate in bulk, can strengthen over time and compensate for the decreasing obturator size.
  • Palatal lifts are used when adequate palatal length exists, but the dynamic motion of the palate due to neuromuscular etiologies is poor. Palatal lifts physically reduce the distance the palate must traverse to produce adequate closure.

Surgical Care

The primary indications for surgical intervention include a structural defect of the velum or a functional problem that results in poor or inconsistent velar closure.

Maximum benefit can be achieved when the surgical technique takes advantage of whatever native velopharyngeal function exists in the patient. Information obtained during the objective evaluation via physical examination, nasopharyngoscopy, and/or multiview VF can greatly aid in deciding the best way to make use of remaining velopharyngeal function. Determination of a patient's predominant VPC pattern directs the surgeon to the most appropriate treatment for the patient.

Several patterns of VPC have been described based on nasoendoscopy and VF examinations. The type of closure pattern is determined by the relative contribution of the palate and lateral pharyngeal walls to closure of the velopharyngeal sphincter.

The 4 basic types of velar closure patterns are coronal, sagittal, circular, and circular with the Passavant ridge. Defining the type of closure pattern is important when considering surgical intervention for correction of VPD.

Following is an overview of the 3 main surgical approaches to velopharyngeal corrective surgery. They include pharyngoplasty, pharyngeal flap, and posterior pharyngeal wall augmentation.

• Pharyngoplasty
• • This approach is advantageous when coronal or circular closure is present and lateral pharyngeal wall motion is deficient. The goal is to develop a more functional sphincter by improving the dynamics and the bulk of the velopharyngeal tissues and by tightening and reducing the size of the velopharyngeal sphincter.
  • Hynes first described pharyngoplasty in 1950, defining it as the elevation of 2 superiorly based flaps comprising the right and left salpingopharyngeus muscles and overlying mucosa. The flaps were rotated 90° and sutured to the mucosal edges of a transverse incision made across the nasopharynx just below the level of the tori tubariae.
  • In 1968, Orticochea described a modification of the pharyngoplasty procedure using 2 superiorly based flaps comprising the posterior tonsillar pillars with the underlying palatopharyngeus muscles. A small inferiorly based posterior pharyngeal wall flap was then elevated, and the 2 lateral flaps were rotated 90° and inserted onto the posterior flap. Jackson further modified this method by sewing the lateral flaps onto a superiorly based posterior pharyngeal wall flap, allowing for higher placement of the lateral wall flaps.
  • The need for a tonsillectomy and/or adenoidectomy is determined preoperatively. Adenoidectomy is performed a minimum of 6 weeks preoperatively if the desired vertical level of the sphincter is expected to lie at or above the level of the adenoid pad. Similarly, if the tonsils are enlarged enough to cause possible difficulty in raising the palatopharyngeal flaps, they must be removed.
  • Several studies have reported the rate of correction or significant reduction in hypernasality from this procedure to be 78-100%. The incidence of hyponasality postoperatively is estimated to be 12-17%.
• Pharyngeal flap procedure
• • This is the preferred method in patients who have good lateral pharyngeal wall motion but a persistent central gap due to poor palatal motion, as is common following repair of a cleft palate.
  • The aim is to develop a central flap of tissue to obturate the midline of the pharyngeal port and decrease the degree of air escape into the nasal cavity.
  • Schoenborn first reported this procedure in 1876 when he described an inferiorly based posterior wall flap sutured to the nasal surface of the soft palate. He later modified this procedure by using a superiorly based flap when he found that inferiorly based flaps tended to contract and tether the palate downwards over time, worsening the patient's velopharyngeal insufficiency (VPI).
  • Most commonly, a superiorly based flap is created, which is then inset into the nasal surface of the soft palate. This serves to obturate the deficient middle portion of the velopharynx, creating lateral openings on either side. The opening and closure of these lateral ports is what controls velopharyngeal function postoperatively.
  • One large series of 500 patients reported normalization or resolution of hypernasality in 90% of subjects. Failure to improve is related to inadequate flap width either by design or due to contracture. On the other hand, a flap that is too wide narrows the lateral ports and produces hyponasal speech. Postoperative airway obstruction is most likely to occur within the first 24 hours and, in one series, resolved within 2 days in more than 90% of subjects.
• Posterior wall augmentation
• • This approach is appropriate in the presence of a persistent gap of 1-3 mm in the central velopharyngeal port. It is also indicated when the patient can achieve touch closure that is not tight enough to prevent air escape with high oral pressure. Persistent postadenoidectomy velopharyngeal insufficiency is also an appropriate indication for this procedure. Autogenous tissue and foreign implants have both been used for this approach.
  • Another method of posterior wall augmentation involves a superiorly based pharyngeal flap incorporating the superior constrictor buckled onto itself and sutured in place. Initially good results with this method can become less favorable because the flap can atrophy with time. This procedure is recommended only for small gaps.
  • A wide variety of implantable materials have been used to augment the posterior wall. Problems with extrusion, migration, resorption, and infection have been reported. The Food and Drug Administration (FDA) has banned silicone because of a high extrusion rate. Teflon is not approved for use in the pharynx because of concerns over the risk of injection into large blood vessels. Autologous tissues such as fat or rolled dermis have been less problematic, but they tend to resorb with time.
  • While these procedures appear to be safe and relatively easy to perform, critical evaluation of procedures for posterior wall augmentation have not demonstrated significant improvements in speech following surgery. Autologous fat injections may be of some benefit in further augmentation, following either pharyngoplasty or pharyngeal flap. The use of injectable collagen materials for pharyngeal augmentation has not been reported.

MEDICATION

Section 6 of 9  

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Drug therapy currently is not a component of the standard of care for this condition. See Treatment.

FOLLOW-UP

Section 7 of 9  

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Complications

• Pharyngoplasty: The incidence of hyponasality postoperatively is estimated to be 12-17%.
• Pharyngeal flap: Failure to improve is related to inadequate flap width either by design or due to contracture; however, a flap that is too wide narrows the lateral ports and produces hyponasal speech. Postoperative airway obstruction is most likely to occur within the first 24 hours and resolved within 2 days in more than 90% of subjects in one series.
• Posterior wall augmentation: Problems with extrusion, migration, resorption, and infection have been reported.

Prognosis

• See Surgical Care.

MULTIMEDIA

Section 8 of 9  

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Media file 1:  Child born with velocardiofacial syndrome. Characteristic clinical findings included unilateral lower lip palsy, heart murmur, small external ear canals, and submucous cleft palate.
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Media file 2:  Pharyngeal closure patterns: (A) coronal, (B) sagittal, (C) circular, and (D) circular with the Passavant ridge.
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Media file 3:  Coronal closure noted. Primary movement is the palate contacting the posterior pharyngeal wall, with minimal or no movement of the lateral pharyngeal walls. Notice air escape along the lateral margins as the palate contacts the adenoid pad.
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Media file 4:  Sagittal closure demonstrated. The soft palate moves little, with most of the closure achieved by movement of the lateral pharyngeal walls. Notice the notching of the soft palate consistent with a submucous cleft palate.
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Media file 5:  Example of circular closure with contributions from the palate and lateral pharyngeal walls. Patient underwent recent adenoidectomy as evidenced by nasopharyngeal eschar.
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Media file 6:  Circular closure with Passavant's ridge demonstrated. Note elevation of ridge on posterior pharyngeal wall contributing to closure.
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Media file 7:  Case study of patient status post cleft palate repair. Child presents with hypernasal speech, especially with /s/. No history of nasopharyngeal reflux. Intraoral examination demonstrates the repair to be intact except for the posterior most portion (a bifid uvula is noted). Nasopharyngoscopy demonstrates notching of the soft palate (arrow) and an enlarged adenoid pad (asterisk).
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Media file 8:  Same patient as in picture 7. Velar closure noted as patient pronounces /s/. Circular closure pattern is noted with central defect and air escape. Palate closure is noted with swallow in the middle portion of the frame.
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Media file 9:  Same patient as in picture 7. Palate closure noted against the adenoid pad as the patient speaks /p/. Phoneme specific velopharyngeal dysfunction (VPD) is diagnosed and speech therapy is recommended to improve articulation. Adenoidectomy in this patient would most likely result in structural velopharyngeal insufficiency (VPI).
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REFERENCES

Section 9 of 9

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• Workup
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• Follow-up
• Multimedia
• References

• Brunner M, Stellzig-Eisenhauer A, Proschel U, et al. The effect of nasopharyngoscopic biofeedback in patients with cleft palate and velopharyngeal dysfunction. Cleft Palate Craniofac J. Nov 2005;42(6):649-57. [Medline].
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• Mitnick RJ, Bello JA, Golding-Kushner KJ, et al. The use of magnetic resonance angiography prior to pharyngeal flap surgery in patients with velocardiofacial syndrome. Plast Reconstr Surg. Apr 1996;97(5):908-19. [Medline].
• Orticochea M. The timing and management of dynamic muscular pharyngeal sphincter construction in velopharyngeal incompetence. Br J Plast Surg. Mar 1999;52(2):85-7. [Medline].
• Parton MJ, Jones AS. Hypernasality following adenoidectomy: a significant and avoidable complication. Clin Otolaryngol. Feb 1998;23(1):18-9. [Medline].
• Shprintzen RJ, Golding-Kushner KJ. Evaluation of velopharyngeal insufficiency. Otolaryngol Clin North Am. Jun 1989;22(3):519-36. [Medline].
• Sie KC, Tampakopoulou DA, de Serres LM, et al. Sphincter pharyngoplasty: speech outcome and complications. Laryngoscope. Aug 1998;108(8 Pt 1):1211-7. [Medline].
• Tachimura T, Nohara K, Hara H, Wada T. Effect of placement of a speech appliance on levator veli palatini muscle activity during blowing. Cleft Palate Craniofac J. May 1999;36(3):224-32. [Medline].
• Vantrappen G, Rommel N, Cremers CW, et al. The velo-cardio-facial syndrome: the otorhinolaryngeal manifestations and implications. Int J Pediatr Otorhinolaryngol. Oct 2 1998;45(2):133-41. [Medline].
• Witt PD, O''Daniel TG, Marsh JL, et al. Surgical management of velopharyngeal dysfunction: outcome analysis of autogenous posterior pharyngeal wall augmentation. Plast Reconstr Surg. Apr 1997;99(5):1287-96; discussion 1297-300. [Medline].
• Witt PD, Marsh JL, Arlis H, et al. Quantification of dynamic velopharyngeal port excursion following sphincter pharyngoplasty. Plast Reconstr Surg. Apr 1998;101(5):1205-11. [Medline].

Article Last Updated: Jun 28, 2006