John E. Riski
Cleft palate (CP) is the most common cause of velopharyngeal incompetence (VPI). Hypernasality, nasal air emission, and other forms of aberrant speech mark the failed primary management of the patient with CP. Despite the best attempts, primary palatal management is successful in only 70% to 80% of individuals with CP (Morris, 1973; Riski, 1979). Significant efforts have been devoted to better understand, evaluate, and manage the problem, as well as to achieve the goal of velopharyngeal competence. However, many challenges and issues remain concerning evaluation of the velopharyngeal mechanism, physical management, and speech therapy. The purpose of this chapter is to discuss these challenges and issues by reviewing our current understanding of this area.
Issues and Challenges of Craniofacial Disorders
Specialists who routinely deal with oral clefts face several challenges that impact labeling and identification of some disorders. We must meet these challenges with education, to improve the quality of care and outcomes.
Although oral clefts are among the most common birth defects, they remain a low-incidence disorder in pediatric practice. The prevalence is approximately 1/750 to 1/1000 newborns in the Caucasian population and even higher in other populations. It is estimated that there are 4000 new cleft lip with or without palate (CL/P) cases in the United States annually. Despite the relative prevalence of oral clefts, these patients still represent a small part of the pediatric caseload outside of craniofacial centers. Hypernasality, nasal air emission, and compensatory articulation are also low-incidence speech disorders and may result from structural, neurological, or functional (learned) etiologies. The rate of hypernasality after initial CP closure is only 20% to 30% (Riski, 1979; Riski and DeLong, 1984). Low-incidence disorders such as oral clefts and hypernasality offer few educational or clinical opportunities for developing clinical expertise. We are challenged to educate other healthcare workers about appropriate identification, diagnosis, and management.
A challenge to evaluation is that the etiologies of hypernasality and nasal airflow disorders are often occult or hidden. In reviews, of patients receiving surgical correction for hypernasality, approximately 30% did not have CP (Riski et al, 1992; Riski, 1995). The etiology in these children is an anatomically deep nasopharynx, which can be diagnosed accurately only by lateral cephalometric (radiographic) assessment. Normal dimensions and growth of the velopharynx were described after cephalometric analysis by Subtelny (1957) and highlighted by Zemlin (1997). The disproportionately deep pharynx, an occult anatomical defect, was described by Calnan (1971).
An issue in speech pathology that may have its origin in the low incidence and occult nature of the disorder is that noncleft hypernasality is erroneously labeled as a voice disorder. Labeling hypernasality as a voice disorder implies that it is a disorder of the larynx and results in delayed identification, labeling, referral, and management. Because the physical defect is not recognized, ineffective speech therapies are often undertaken (Ruscello, 1997). This further delays identification and referral to specialists at craniofacial teams. A CP is identified at birth, and surgical closure is before 1 year of age (Riski, 1995). In stark contrast, the average age at referral to our center for children with noncleft hypernasality resulting from velocardiofacial syndrome (VCFS) is 9.2 years of age.
Delayed management of VPI leads to increased failure of surgical intervention and refractory speech deficits. The rate of complete success when VPI is managed before 6 years of age is 90.9%. Success rates fall to 73.9% between 6 and 12 years, 70.0% between 12 and 18 years, and 47.0% after 18 years (Riski et al., 1992).
Oral clefts and hypernasality are evaluated by specialists in craniofacial clinics. However, Public Laws 94-142 and 99-457 have mandated that speech therapy be provided through specialists in schools and developmental centers. Professionals in these settings often have limited experience with cleft-related problems because these problems usually form a very small part of their caseload. This separation of evaluation and therapy can lead to poor communication between the evaluator and the therapist. The result can be therapy plans that do not directly address the needs of the patient. There is an unmistakable need for partnerships between the evaluation centers and the settings in which the therapy is conducted.
Nasopharyngeal Anatomy and Physiology
Many surgical procedures have been devised to take advantage of the presumed function of the velopharyngeal portal. In addition, some surgical strategies and techniques have been criticized as inconsistent with the neuroanatomy and physiology of the velopharyngeal mechanism. Further, understanding of the motor control of the velopharyngeal mechanism is paramount to establishing effective speech therapy regimens. There are many excellent descriptions of normal velopharyngeal anatomy and physiology (Zemlin, 1997). The purpose of this section is to comment on the specific aspects of anatomy, physiology, and motor control which are pertinent to the evaluation and management of the velopharyngeal mechanism.
The levator veli palatini is the primary elevator of the velum for speech. The levator palatini has been implicated as the sole muscle responsible for velopharyngeal closure in speech (Bell-Berti, 1976; Fritzell, 1979). Innervation of the velum is generally conceded through the pharyngeal plexus by way of the pharyngeal branch of cranial nerve X, the vagus. However, Sedlackova (1967) proposed a two-stage theory of innervation. whereby velopharyngeal function for swallowing is innervated through the vagus but speech function is innervated through cranial nerve VII, the facial nerve. This proposal has been supported by Ibuki et al. (1978), who traced facial nerve fibers of rhesus monkeys through the greater petrosal nerve to the levator palatini.
The superior constrictor narrows the pharynx during swallowing (Bell-Berti, 1976; Fritzell, 1979.) Some have proposed that the superior constrictor is also responsible for mesial movement of the lateral pharyngeal walls for speech (Shprintzen et al., 1975; Iglesias et al., 1980). In contrast, Maue-Dickson and Dickson (1980) argued that the levator veli palatini leads to lateral pharyngeal wall motion. Niimi et al. (1982) suggested that we do not know what muscle(s) contributes to the mesial movement of the lateral pharyngeal walls. Since the fibers of the superior constrictor are divided in a pharyngeal flap pharyngoplasty, postoperative movement of the lateral pharyngeal walls has been questioned. Some have observed reduced postoperative lateral wall motion (Zwitman, 1982a,b) and some have not (Shprintzen et al., 1980).
The musculus uvulae is a paired muscle that occupies the midline of the nasal surface of the velum. Its role during speech appears to be to provide midline mass and to assist in obturating the nasopharynx. Absence of the musculus uvulae leads to a midline defect on the nasal surface of the velum (Huang et al., 1997). The tensor veli palatini is generally regarded as the primary muscle of eustachian tube dilation (Bell-Berti, 1976).
The bilateral palatopharyngeus muscles form the posterior faucial pillars; their function is to narrow the posterior oral cavity during swallowing. The muscles do not consistently function with the levator for velopharyngeal closure. The palatopharyngeus muscles are used in the sphincter pharyngoplasty. Superiorly based flaps are created and then raised from a vertical to a horizontal position and inserted into a transverse incision made into the posterior pharyngeal wall. This provides a static buttress for the elevating velum to contact. There has been speculation that active sphinctering also develops. Ysunza et al. (1999) used pre- and postoperative electromyograms of this muscle to determine that any movement of the palatopharyngeus flaps remains passive postoperatively. The bilateral palatoglossus muscles form the anterior faucial pillars. They contribute to posterior tongue elevation for the lingual-velar sounds. They are antagonistic to the levator and can lower the velum. In one isolated instance, these muscles were substituted for the palatopharyngeus in a sphincter pharyngoplasty (Graiver et al., 1992).
Kuehn and Moon (1995) have conducted a series of studies to evaluate the role and limits of velopharyngeal function. They reported that subjects with CP use a relatively high activation level for the levator muscle during speech, in relation to their total activation range, compared to subjects without CP (Kuehn and Moon, 1995); i.e., speakers with CP have less reserve palatal strength. They also found that the electromyographic response of the levator increases with increased oral pressure for blowing (Kuehn and Moon, 1994). This is consistent with frequent clinical observations that there is greater velopharyngeal function when speech sounds are aspirated with more force, i.e., increased oral pressure. Lastly, Kuehn and Moon (2000) investigated the ability of the velum to close against nasal air pressure. They found that it was possible to induce such fatigue in most subjects and that greater rates of fatigue generally occurred at the higher levels of external loading, i.e., 25 and 35 cm H2O.
Patterns of velopharyngeal function have been identified. Shprintzen et al. (1974) examined velopharyngeal function by videofluoroscopy for speech and nonspeech tasks. They observed that patterns of closure were different for pneumatic (speech) and nonpneumatic (nonspeech) tasks. Tasks involving airflow (blowing, whistling, and speech) showed focal closure of the velopharyngeal port. In contrast, nonpneumatic tasks demonstrated more complete closure of the entire pharynx. Skolnick and colleagues (Skolnick, 1970; Skolnick and McCall, 1972) first described and labeled the velopharyngeal closure patterns for speech as coronal, circular, and sagittal. A coronal pattern included active velar elevation with some simultaneous mesial movement of the lateral pharyngeal walls; closure was in the coronal plane. A circular pattern was demonstrated by relatively greater lateral wall motion than velar movement. Finally, lateral wall movement and contact with little velar elevation characterized a sagittal pattern.
Some theories of motor control have developed from research of compensatory speech in speakers with CP. These theories are an application of the theory of motor equivalence. Motor equivalence was initially described as “variability of specific muscular responses, with circumstance, in such a way as to produce a single result” (Tolman, 1932; Hebb, 1949). Motor equivalence was applied to speech production by MacNeilage (1970) to refer to the adjustment of speech motor commands to assure that individual articulators reach semi-invariant target positions. A further adaptation of motor equivalence is the pressure regulation/control theory forwarded by Warren and Hinton (1983) and Warren (1986). This theory is based on compensations to VPI in the CP population and observations of normal vocal tract function. They proposed that the vocal tract is regulated during speech to maintain pressure. Vocal tract pressure is controlled by adjusting respiratory airflow and vocal tract (e.g., laryngeal) valving.
Vocal tract adjustments during breathing or speech should require continual adjustments of laryngeal valving and respiratory support. These adjustments appear to require instantaneous knowledge of vocal tract status from receptors within the vocal tract. Morr et al. (1988) speculated that certain respiratory receptors found in the trachea, larynx, and nasopharynx may also operate in the regulation of vocal tract pressures during speech. While these receptors have not been identified, investigations in humans and laboratory animals (reported in the experimental pulmonary physiology literature) offer some possible explanations regarding the location and nature of the receptors. Possible sites include the nasopharynx (McBride and Whitelaw, 1981), bronchi (Gonzalez-Baron et al., 1989), C-fiber afferents in the extrathoracic trachea and larynx (Sant'Ambrogio et al., 1983; Szereda-Przestaszewska, 1989), pulmonary stretch receptors (Harding, 1984), receptors responding to rate of lung volume change and/or upper airway pressure (Giering and Daubenspeck, 1990), and receptors of expiratory resistive loads and changes in respiratory pattern (Insalaco et al., 1991).
In response to Warren's pressure regulation/control theory, Netsell (1990) suggested an acoustic regulation hypothesis, which suggested that the goal of speech is to produce meaningful acoustics. A speaker with VPI valves at the larynx to generate acoustic distinctions that cannot be produced downstream from the VPI. In a test of the acoustic and pressure regulation theories, Moon and Folkins (1991) disrupted auditory feedback with noise. This yielded only small increases in oral pressure, leading the investigators to conclude that auditory regulation alone does not explain pressure maintenance. Additional study of speech compensations for various deficits may provide greater insight into speech motor control.
Speech Sound System
Articulation
Understanding the normal speech system is necessary to assess the outcome of treatment and to understand compensatory articulation. American English includes approximately 46 sounds or phonemes. The sounds are learned, beginning in the first year of life and continuing through 6 to 7 years of age. The neurologically simple sounds (vowels) are learned first and the more complex sounds (affricates, i.e., ch and dg) are learned last. Normal speech learning requires adequate hearing and a competent velopharyngeal mechanism. Both may be compromised because of a CP. The severity of articulation disorders increases with the severity of clefting (Riski, 1979; Riski and DeLong, 1984; Laitinen et al., 1998).
All vowels are voiced and described by the position of the tongue in the oral cavity. The vertical position is described as high, middle, or low. The horizontal position is described as front, mid, or back. For example, ee requires a high-front tongue position and ah requires a low-back position. A high tongue carriage offers more resistance to sound energy as it exits the oral cavity. In the presence of even a small VPI, high vowels are more susceptible to hypernasal resonance than low vowels. Two parameters are used to describe consonants. The place of articulation describes the location of articulators in the oral cavity. For example p is bilabial, t is a lingual-alveolar, and k is a lingual-velar. The manner of articulation describes the way in which the sound is produced. Stop-plosive sounds such as p, t, and k are made by a brief interruption or stop of the airstream and then a release. Fricative sounds such as s, f, and th are made by constricting the airstream. The affricate sounds ch and dg are considered combinations of stops and fricatives. There are three nasal sounds, m, n, and ng. Lastly, several sounds are labeled as glides or semivowels, including the sounds w, y, I, and r.
All vowels and the nasal and glide consonants are voiced. The stops, fricatives, and affricates exist in voiced and voiceless pairs. For example, the sound s is voiceless and made only with a constriction of the airstream between the tongue and alveolar ridge. The addition of voicing to the s creates the z. All stops, fricatives, and affricates require intraoral air pressure. Intraoral air pressure requires appropriate coordination of velopharyngeal competence with adequate respiratory pressure and oral articulatory function.
Nasal Coupling
The terminology used to describe the characteristics of nasal coupling has been described (Riski and Millard, 1979). Resonance qualities are associated with the voiced elements of speech, while nasal air emission is associated with the unvoiced elements of speech.
Oral-nasal resonance is the balance of oral and nasal acoustic (voiced) energies. It is achieved by the appropriate coupling or isolation of the nasal cavity from the remainder of the vocal tract during speech by movements of the velopharyngeal valve. Three English sounds require the nasal cavity to be coupled with the vocal tract: m, n, and ng. All other sounds require the velopharyngeal valve to isolate the nasal cavity from the vocal tract. Hypernasality is the quality perceived by the listener caused by inappropriate nasal coupling with the vocal tract during speech. It is most easily perceived on vowel sounds. In contrast, hyponasality is perceived as inadequate coupling or obstruction of the nasal tract during production of those sounds normally associated with nasal energy. The obstruction may be posterior (e.g., hypertrophied adenoids) or anterior (e.g., hypertrophied turbinates). Further, a speaker may also demonstrate a mixed hyper-hyponasality when velopharyngeal closure is incomplete but the nasal cavity is occluded anteriorly.
Nasal air emission is most easily perceived on the unvoiced consonants. Nasal air emission may be inaudible in patients with patent nasal cavities. In these patients, the air passes through the nasal cavity without creating any audible turbulence. Oral pressure is required for the frication associated with the fricative consonants (e.g., s and f) or the stop and release of pressure associated with the plosive consonants (e.g., p and t). Oral pressure is often inversely related to nasal air emission, which represents loss of pressure out of the nose. Posterior nasal frication in association with attempts at oral airflow generally represents touch velopharyngeal contact. Velopharyngeal closing force is not maintained, and the air leak through the port creates the posterior nasal frication. Air flows simultaneously through the oral and nasal cavities.
Compensatory Arficukrfion
Children born with CL/P often learn articulation compensatory to the loss of oral pressure or dental arch collapse. The classic compensatory misarticulations described are glottal stops and pharyngeal fricatives. Trost (1981) added the following:
· Pharyngeal stop, point of stop is tongue base to posterior pharyngeal wall, used as substitute for k or g.
· Midpalatal stop, point of stop is midpalate, between position of t and k, used as substitute for t, d, k, or g.
· Posterior nasal fricative, point of frication is velopharyngeal valve, tongue stops airstream and nasal airflow is the only airflow, used as a substitute for s, z, and other fricative and affricate sounds.
We might also consider the anterior nasal fricative, which is similar to the posterior nasal fricative except that the point of frication is the anterior nostrils. Nasal grimacing may accompany this substitution.
The posterior nasal fricative is often observed in speakers without CP and with normal velopharyngeal function. Other hallmarks of speech include normal oral-nasal resonance, normal aspiration of stop-plosive consonants, and ability to learn a normal oral s. For such cases, the terms sound-specific VPI and functional VPI have been coined (Riski, 1984). However, the posterior nasal fricative does not reflect anatomical or neurological dysfunction of the velopharyngeal mechanism but, rather, a unique sound substitution. The clinician's differential diagnosis of the nasal airflow associated with the posterior nasal fricative and a true VPI is critical to developing an appropriate treatment plan, the former requiring speech therapy and the latter possible surgical or prosthetic intervention.
The etiology of the posterior nasal fricative is somewhat elusive. One theory is that it develops to compensate for conductive hearing loss (Riski, 1984). The vibration produced at the velopharynx could be easily transmitted by bone conduction up the cervical vertebrae to the skull and the cochlea. The sound s may be more susceptible since it is one of the earliest learned sibilants and requires a lesser degree of hearing loss to impact perception.
Assessment of Velopharyngeal Function
Assessing velopharyngeal function may be approached as a multilevel problem. The first level should include the perceptual evaluation of oral pressure, oral-nasal resonance, nasal air escape, and articulatory precision. The trained ear is still the gold standard of the evaluation. Resonance should be neither hypernasal nor hyponasal (Riski et al., 1989). The second level is the screening of velopharyngeal closure. This step can use inexpensive tools and is underutilized by clinicians. Patients who fail these two steps should undergo the third step of objective assessment with computerized instruments for acoustic (Fletcher, 1978) and nonacoustic (Warren and DuBois, 1964; Warren and Devereux, 1966) assessment of velopharyngeal function. Finally, imaging should account for the three-dimensional nature of the velopharyngeal port. This can be achieved by some combination of flexible fiberoptic nasendoscopy (Pigott, 1974; Gilbert and Pigott, 1982; Zwitman, 1982a,b), radiography, or fluoroscopy (Skolnick, 1970, 1975; Williams, 1979; Williams and Eisenbach, 1981) during speech. Articulatory precision should be evaluated separately with special attention to any compensatory misarticulations and the age appropriateness of articulation.
Each technique has its advantages and disadvantages. No one instrument can provide all of the necessary information. An ad hoc committee of the American Cleft Palate-Craniofacial Association suggested minimal standards for the evaluation of velopharyngeal function, including a perceptual evaluation of resonance and assessment using at least one instrument during connected speech (i.e., fluoroscopy or pressure-flow) (Dalston et al., 1988). A consensus conference of 71 individuals experienced in the diagnosis and treatment of individuals with craniofacial anomalies developed the Parameters for Evaluation and Treatment of Patients with Cleft Lip/Palate or Other Craniofacial Anomalies (American Cleft Palate-Craniofacial Association, 1993).
The American Speech-Language Hearing Association (1997) has also produced a resource for evaluation of the velopharyngeal mechanism, listing procedures to assess oral, nasal, and velopharyngeal functions for speech production. It advocates perceptual and instrumental assessment.
Longitudinal study of velopharyngeal port function has demonstrated instability in children as the phonological system develops and craniofacial growth and adenoid involution occur (Van Demark and Morris, 1983; Van Demark et al., 1988). Some children develop VPI as the adenoids involute (Mason and Warren, 1980; Riski and Mason, 1994). In contrast, some children eventually resolve hypernasality, which is identified immediately following palatoplasty (Fox et al., 1988). These studies demonstrate the need for longitudinal assessment of velopharyngeal function and the need to exercise caution before performing a pharyngoplasty.
Velopharyngeal function impacts speech proficiency. However, speech proficiency is not an adequate measure of velopharyngeal function (Riski, 1979). These two areas should be evaluated separately. It is possible to have severely defective speech and a competent velopharyngeal mechanism. However, normal speech usually cannot be produced without a competent velopharyngeal mechanism.
Nasopharyngeal Patency
Aerodynamic assessment has demonstrated the requirements of adequate nasal airway patency (Warren, 1984). Nasal deformities decrease nasal patency in the CP population (Warren et al., 1969), and pharyngeal flap surgery further decreases nasal airway patency in children but not in adults (Warren et al., 1974). Both children and adults with CL/P demonstrate increased nasal resistance (15%-30%) compared to the noncleft population (Hairfield et al., 1988). Furthermore, the minimal cross-sectional area of the nose can be estimated from differential oral-nasal pressure and nasal flow measures and has been reported for individuals with and without CP (Warren et al., 1992). Surgeons have become so successful in addressing and managing hypernasality that hyponasality may now be a more frequent velopharyngeal dysfunction (Riski, 1995).
Evaluation Protocol
There are many procedures and instruments for evaluating speech and velopharyngeal function. Evaluation can take the form of a perceptual exam, clinical screening of velopharyngeal closure, computer instrumental evaluation, imaging, or diagnostic therapy. Each instrument offers advantages and disadvantages that the clinician should consider. A problem-oriented protocol can lead the clinician in the process.
Perceptual Evaluation
The perceptual evaluation is the most common form of evaluating speech. The result of this evaluation is still the standard from which speech surgeries are recommended. The scale studied by Subtelny et al. (1972) is especially useful since it allows functional analysis of speech qualities associated with oral clefts. Hypernasality is often used as a standard of success. However, there are advantages to rating the aspiration or oral pressure of the pressure consonants. Van Demark (1979) demonstrated that correct production of the oral pressure bilabial consonants p and b is predictive of future velopharyngeal competence.
The advantage of perceptual evaluation is that it provides an accepted standard for speech qualities. Ratings of oral-nasal resonance, nasal air escape, oral pressure, and articulation are the standards by which surgical outcomes are evaluated. The disadvantage is that these qualities are not easily quantified and validity is difficult to establish without extensive listener training (Keunig et al., 1999). However, nasal air escape is not always audible, so some VPIs might escape detection without instrumental evaluation. The quality of voice or articulation may influence the rating of resonance. The presence of articulation disorders may negatively influence ratings of resonance, while the presence of hoarseness may preclude an accurate assessment of resonance.
Screening Velopharyngeal Closure
Numerous devices are available to screen velopharyngeal closure. Generally, anything that is sensitive to airflow can be used. Examples of these devices include the See-Scape® (Pro-Ed, Austin, TX), nasal listening tubes (Blakeley, 1972; Riski and Millard, 1979), nasal mirrors, and paper paddles. Nasal airflow is monitored during the pronunciation of words such as puppy, puppy, which should be devoid of nasal airflow. The presence of any airflow indicates some degree of velopharyngeal opening and that further objective testing is warranted.
The advantages of these devices are that they are inexpensive, portable, noninvasive, and very accurate for determining the presence or absence of nasal airflow. In addition, they require little training and clinicians with little experience can become adept users. The disadvantage is that they lack quantification.
Objective Assessment of Velopharyngeal Function
The two most common computer instruments for evaluating velopharyngeal function are pressure-flow and nasometry. Pressure-flow evaluates nonvocalic elements, and nasometry documents vocalic elements. The two measures are taken consecutively, and correlations are reported in the 0.70 range. Powerful personal computers and improved multichannel software now allow simultaneous recording of vocalic and nonvocalic elements.
Pressure Flow
Pressure-flow instrumentation measures the oral-nasal pressure differential and the volume-velocity of nasal airflow. It provides quantifiable data about velopharyngeal port function for speech. The hydrokinetic equation has been modified by Warren and Dubois (1964) for estimating velopharyngeal port orifice area. This modification of the hydrokinetic equation has withstood vigorous study (Smith and Weinberg, 1980, 1982). Pressure-flow study is an objective and reliable method for repeated, noninvasive measures of velopharyngeal port function. The palatal efficiency rating computed instantaneously-Speech Aeromechanical Research System (Perci-SARS; MicroTronics, Carrboro, NC) allows six channels of input, including two pressure channels, two flow channels, a high-speed voice channel, and a low-speed DC channel. Software is included for velopharyngeal function, nasopharyngeal airway patency, laryngeal airway resistance, and several other voice-analysis measures (Riski et al., 1995).
Advantages of pressure-flow assessment are that it quantifies oral pressure and nasal air escape. It also provides an objective estimate of the size of the velopharyngeal opening. Disadvantages are that it is relatively expensive and does not quantify the shape of the velopharyngeal opening. In addition, the speech sample is restricted to unvoiced, stop-plosive consonants (i.e., p), and measures of velopharyngeal area do not always correlate with perception of hypernasality.
Acoustic Measures
The Nasometer (Kay Elemetrics, Lincoln Park, NJ) has become a popular and useful instrument for evaluating the acoustic elements (i.e., hypernasality) of velopharyngeal function. The Nasometer provides an objective measure of nasality, termed nasalance, which is the ratio of nasal acoustic energy divided by nasal plus oral acoustic energy. Hardin et al. (1992) reported 91% agreement of nasalance with listener ratings of hypernasality. In addition, nasalance values greater than 26 were correlated with hypernasality, values between 26 and 39 were correlated with mild hypernasality, and values greater than 40 were correlated with moderate to severe hypernasality. Dalston et al. (1991a) reported sensitivity of 0.89 and specificity of 0.99 for listeners' ratings of mild hypernasality. Dalston and Warren (1986) observed that nasalance and velopharyngeal area estimates change in concert. Normative nasalance values were reported by Adams et al. (1989). A completely oral passage (“zoo passage”) yielded an average nasalance of 15.53 [standard deviation (SD) = 4.8]. A mixed oral and nasal passage (“rainbow passage”) yielded an average nasalance of 35.69 (SD = 5.20). Nasal-laden sentences yielded an average nasalance of 61.06 (SD = 6.94).
The correlation of nasalance with hyponasality has also been reported. Dalston et al. (1991b) reported sensitivity of 0.48 and specificity of 0.79. The measure may have been influenced by nasal air escape in some patients since the measures improved to 1.0 and 0.95, respectively, when patients with nasal air escape were eliminated. Hardin et al. (1992) reported that listeners' perception of hyponasality was related to nasalance scores of less than 50.
An advantage of nasometry is that it reliably quantifies oral-nasal resonance. The instrument also provides feedback in real time and, thus, is useful as a therapy tool as well as a diagnostic tool. A disadvantage is that the speech sample must be restricted to voiced sound elements. Another disadvantage is that the instrument does not discriminate between hypernasality and nasal air escape. In a study that simultaneously recorded nasalance and nasal airflow, Riski (1996) found that 33/92 (35.9%) airflow peaks had recordable nasalance. These findings supported the observation of Karnell (1995) that the combination of turbulent nasal airflow during pressure consonant productions with nasal acoustic energy during vowel productions resulted in elevated nasalance values.
Imaging
Lateral still cephalometric radiographs and videofluoroscopy have been used for some time to assess velopharyngeal function. Sphincteric function during speech has been demonstrated using multiview videofluoroscopy by Skolnick and colleagues (Skolnick, 1970, 1975; Skolnick and McCall, 1972), who described and labeled the velopharyngeal closure patterns: coronal, circular, and sagittal (see above, NASOPHARYNGEAL ANATOMY AND PHYSIOLOGY). These patterns are significant because pharyngoplasties have been designed and their success reviewed with reference to the type and amount of movement. Videofluoroscopy allows assessment of velar function in its dynamic state for connected speech. Still radiographs often misrepresent velar function because of the limited speech sample that can be employed (Williams and Eisenbach, 1981). In addition, shadows and the two-dimensional nature of the still radiograph can distort the true nature of velopharyngeal function.
Advantages of the lateral radiograph are that the image it produces provides good resolution of the velopharyngeal port and allows assessment of the ratio of nasopharyngeal depth to velar length. These measures can be compared to normative age-matched data (Subtelny, 1957). The average normal ratio of nasopharyngeal depth, measured along the palatal plane, compared to the length of the velum, measured from the posterior nasal spine to the tip of the uvula, ranges from 0.6 to 0.7. This ratio is maintained through growth and development.
Despite being two-dimensional and static, the depth: length ratio appears to have some value in predicting VPI. Wu et al. (1996) reported differences in cephalometric measures between groups of patients differentiated by velopharyngeal competence. Specifically, noncleft patients with velopharyngeal competence demonstrated a significantly smaller depthrlength ratio (0.66) compared to CP patients with VPI (1.02).
Velopharyngeal closure is achieved using adenoids in all preadolescent speakers (Gereau and Shprintzen, 1988). Lateral radiographs can assess the contribution of the adenoids to, and changes in, the depth: length ratio to velopharyngeal closure. In one reported series, 11/121 (9.1%) speakers with CP developed VPI with involution of the adenoids (Riski et al., 1996). The depth: length ratio was 0.76 when nasal air escape was first detected at an average age of 5.7 years. The ratio increased to 0.91 with adenoidal involution at an average age of 8.6 years. A matched control group with normal velopharyngeal function demonstrated a depth: length ratio of 0.75.
The relationship of attempted velopharyngeal closure to the cervical spine can be determined and is important for targeting the height of insertion of the sphincter pharyngoplasty (Riski et al., 1984b). Lateral radiographs were used to determine the height of attempted velopharyngeal contact relative to the cervical spine. The information was used by the surgeon to guide the insertion of the sphincter flaps to the height of the attempted closure. The success of resolving VPI increased from 61% to 93%. Disadvantages of lateral radiographs are that the image is static and two-dimensional and requires irradiation.
Advantages of videofluoroscopy are the same as those for lateral radiographs but also include the ability to evaluate the movements of the velopharyngeal mechanism and the mechanism in multiple views. Disadvantages include exposure to irradiation and the inability of young children to cooperate.
Fiberoptic Nasendoscopy
The flexible fiberoptic nasal endoscope is a popular tool for evaluating velopharyngeal function because there is no irradiation and it allows direct observation of the portal during connected speech. There are rigid endoscopes and flexible endoscopes. Rigid scopes provide better optics, but flexible scopes are more comfortable to the patient. Each allows recording of the image using 35 mm or videotape format.
The advantages of fiberoptic nasendoscopy include direct visualization of velopharyngeal movement and evaluation of the nasal surface of the velum for the prominence of the musculus uvulae or defects. It also allows observation of the size and shape of velopharyngeal opening and evaluation of the larynx and pharynx, which are innervated through the vagus nerve. Disadvantages include its invasive nature and the possibility that young children will not be able to comply. The vertical component may be difficult to evaluate. Another disadvantage is that, although most speech pathologists working in the field of oral clefts believe that nasendoscopy is important in the assessment of velopharyngeal function, surveys have revealed that they are not well trained in the use of a nasopharyngoscope. In a survey, 40% had no academic preparation and 20% had no clinical experience in nasopharyngoscopy (Pannbacker et al., 1993).
In summary, no single instrument can provide all of the necessary information about velopharyngeal function. A combination of instruments, each selected after assessing the advantages and disadvantages, is advocated (Van Demark et al., 1975; Hirschberg and Van Demark, 1997).
Articulation Assessment
There have been numerous studies of articulation development in the CLP population (Van Demark et al., 1979; Riski and DeLong, 1984). Articulation is a very important part of speech assessment. Analysis of an articulation test provides data for the speech clinician to develop a therapy program that is realistic and structured. Articulation tests also help clinicians evaluate the child's progress (Van Demark, 1997).
There is a positive relationship between the extent of clefting and articulation deficiency. Children with any one type of cleft demonstrate heterogeneous development of articulation skills (Riski and DeLong, 1984). The type of cleft may affect early sound development. Lohmander-Agerskov et al. (1994) found that noncleft and CP only children first learned anteriorly placed sounds, e.g., bilabial, dental, and alveolar sounds. In contrast, children with cleft lip and palate first learned posteriorly placed sounds.
Under normal valving conditions, a fairly constant pressure is maintained along the vocal tract during speech articulation. The unique misarticulations associated with VPI (e.g., glottal stops and pharyngeal fricative sound substitutions) may be attempts to maintain a constant resistance in the presence of a loss of pressure through the velopharyngeal port. It has been suggested that the vocal tract functions with the use of pressure-sensing regulators (Warren, 1986). Some of the receptors needed for feedback may be in the oral mucosa (Furusawa et al., 1994).
In contrast to the errors that compensate for VPI, errors such as tat/cat, wabbit/rabbit, and teef/teeth are examples of normal developmental errors. Children are expected to outgrow these errors; however, excessive errors (given the age of the child) should be treated with speech therapy.
When compensatory errors are concomitant with VPI, the course of management is two-pronged: first, the VPI must be treated; second, the speech problem must be treated. In some cases, speech therapy can begin before the VPI is managed. In such cases, the nostrils can be occluded manually to direct the airstream orally. The child usually cannot employ newly learned sounds without holding the nose. Therapy before surgery can assist learning after surgery (Riski et al., 1984a). Speech therapy has a limited role in treating VPI. Increasing oral air pressure increases muscular activity of the levators and may increase velopharyngeal movements (Kuehn et al., 1993), and continuous positive nasal airway pressure may be used to increase velopharyngeal closure (Kuehn, 1991). With these few exceptions, a review of velopharyngeal exercises demonstrates their ineffectiveness (Ruscello, 1982, 1989).
Special Concerns and Treatment Strategies
Palatoplasty
Children who have their palate closed early (before 1 year) often develop normal speech earlier and more easily than children who have the palate closed later (after 1 year) (Dorf and Curtin, 1982). This may be especially true for early learning of oral stop-plosive sounds (O'Gara et al., 1994). The best timing of palatoplasty has not been defined, possibly because studies have controlled only for chronological age and not for language age at the time of palatoplasty (O'Gara and Logemann, 1988). The coordination of palatal closure with the development of babbling is intuitive. It is at this point in speech and language development that a child must learn to coordinate velopharyngeal function with respiratory pressure, laryngeal abduction and adduction, and oral articulation to produce consonants. In short, the child's first dada is much more complicated than it appears.
Palatoplasty successfully creates a competent velopharyngeal mechanism in 80% of children. This 80% success rate may or may not be influenced by the initial type of cleft (Riski, 1979; Riski and DeLong, 1984; Karnell and Van Demark, 1986). One report demonstrated that the dimensions of the unoperated nasopharynx vary within each type of cleft and suggested that the type and extent of palatoplasty should be tailored to the preoperative dimensions of the nasopharynx (Komatsu et al., 1982). Furlow (1986) first described the double opposing Z-plasty for primary repair of CP with good results.
Long-term follow-up of palatal surgery has been reported by Becker et al. (2000). They reported on 66 adults who had isolated CP closed by either the von Langenbeck or Wardill repair. Speech problems were primarily residual hypernasality, which was moderate or severe in seven (16%) of the patients in the von Langenbeck group and in seven (32%) in the Wardill group. Patients in the Wardill group had fewer fistulas closed and fewer velopharyngoplasties. There were no significant differences between the two methods regarding speech in adulthood.
Oronasal Fistula
Loss of air through an oronasal fistula can be detected and quantified with the assessment tools described previously. It is wise to repeat these measures once with the fistula open and a second time with the fistula temporarily occluded with dental wax (Bless et al., 1980) or chewing gum. With the fistula successfully occluded, velopharyngeal port function can also be adequately tested. Accurate assessment of airflow through the fistula is often confounded by obstructing turbinates or a deviated nasal septum. If the fistula is not patent for speech, surgical intervention may not be warranted. A patent fistula allows the loss of air for speech sounds produced anterior to its site. These are usually the p, b, f, v, and th sounds, although others may be affected, depending on the location of the fistula and the placement of the tongue. Fistulas should be managed when testing indicates air loss sufficient to undermine speech or when there is a nasal hygiene problem from nasal regurgitation. Research suggests that only larger fistulas are capable of such air loss (Shelton and Blank, 1984). Further Tachimura et al. (1997) reported that the magnitude of the effect is greater for subjects with adequate velopharyngeal function than for subjects who demonstrate VPI. Fistulas may be covered with a dental appliance or closed surgically. Surgical intervention might be delayed until after any planned maxillary arch expansion because this might reopen any fistula closed under tension.
Submucous Cleft Palate
Children with submucous CP are unique in the CP population. The frequency is reported to be between 1:10,000 and 1:20,000. Velopharyngeal incompetence is more common in the coronal closure pattern (Velasco et al., 1988). The speech of individuals with submucous CP should be monitored and management initiated only when VPI is diagnosed. A large percentage (44%) remain unsymptomatic through adulthood (McWilliams, 1991).
Heading Disabilities
Investigation of reading abilities has revealed that children with CL/P display a prevalence for reading disabilities similar to the general population (9%). In contrast, children with CP only demonstrate a much higher rate of reading disabilities (33%) (Richman et al., 1988). Ceponiene et al. (1999) explored auditory shortterm memory in children with oral clefts. A measure of detection of change in auditory input was used. They reported a deficiency in auditory short-term memory trace maintenance in cleft children and contend that this dysfunction may contribute to their language and learning disabilities.
Surgical Management of Velopharyngeal Incompetence
Posferior Pharyngeal Flap Pharyngoplasty
The concept of a surgical procedure to manage VPI was first introduced by Passavant (1862), who surgically tethered the uvula to the posterior pharyngeal wall in an attempt to restore a competent valving mechanism for speech. This was modified to the superiorly based flap by Bardenheur (1892) and Sanvenero-Rosselli (1934).
Postoperative studies of pharyngeal flap surgery using electromyographic analysis and endoscopic and videofluoroscopic imaging have suggested several methods by which the nasopharynx is obturated. The primary method of velopharyngeal closure is by active mesial movement of the lateral pharyngeal walls against the static, obturating flap (Shprintzen et al., 1980). Secondarily, circumferential scar contracture narrows the pharynx. Finally, contracture of the flap itself elevates the velum into the pharynx, diminishing the anterior-posterior dimension. Crockett et al. (1988) suggested that three variables should be controlled for successful pharyngeal flap surgery: flap width, height or level of flap, and lateral port size. Strategies have been developed to cope with these variables. The size of the lateral ports has been controlled (Hogan and Schwartz, 1977), and the width of the pharyngeal flaps have been tailored to the amount of wall motion (Shprintzen et al., 1979). Some have suggested that little strategy, if any, is needed for small VPI. Randall et al. (1978) observed that if the VPI is small, any method should have a good result.
Posterior Pharyngeal Wall Augmentation and Muscle Transposition
Augmentation of the posterior pharyngeal wall was first reported by Wardill (1928, 1933). He created a permanent ridge of fibrous tissue on the posterior pharyngeal wall by making transverse incisions through the superior constrictor at the level of Passavant's ridge. The tissue was sutured vertically, creating a ridge for the elevated velum to contact. Hynes (1951, 1953) and Orticochea (1968, 1970, 1983)advocated pharyngoplasties by muscle transposition that were similar in design but differed in their intended function. Each procedure has undergone modification and refinement (Jackson and Silverton, 1977; Huskie and Jackson, 1977; Pigott, 1993; Riski et al., 1984b, 1992; Roberts and Brown, 1983; Stratoudakis and Bambace, 1984; Moss et al., 1987; Mirrett et al., 1993).
Orticochea (1968) recommended elevating the height of insertion for the sphincter pharyngoplasty from the low insertion. Several others have recommended elevating the height of insertion as high as possible (Jackson and Silverton, 1977; Roberts and Brown, 1983). Riski et al. (1992) offered a rationale for tailoring the height of flap insertion. The height of attempted velopharyngeal contact was identified relative to the anterior tubercle of the first cervical vertebra, the atlas. The atlas was identified by palpation at the time of surgery, and the flaps were surgically inset at that predetermined height. Success improved from 61% to 93% when the height of the flaps was elevated to the level of attempted velopharyngeal contact.
Debate has continued over whether closure of the sphincter orifice is active or passive. Ysunza et al. (1999) reported the results of electromyographic analysis before and after sphincter pharyngoplasty in 25 patients. None of the patients demonstrated electromyographic activity in the palatopharyngeus muscle. In contrast, all patients showed normal electromyographic activity at the superior constrictor and the levator veli palatini muscles. Videonasopharyngoscopy demonstrated that lateral pharyngeal wall movements, which ranged from 25% to 40%, were related to strong electromyographic activity at the superior constrictor muscle. They concluded that the flaps of the sphincter pharyngoplasty do not seem to create an active diaphragm for velopharyngeal closure. Moreover, the observed sphinctering appeared to be passive, caused by contraction of the superior constrictor pharyngeus.
Sie et al. (1998) reported the results of sphincter pharyngoplasty on children with VCFS. Three (12.5%) required a revision because of residual hypernasality, and three (12.5%) were hyponasal. After revision, they reported an overall success rate of 18/24 (75.0%).
Treatment strategies are compared infrequently. Pensler and Reich (1991) compared the outcome of 75 patients undergoing pharyngeal flaps with only 10 patients undergoing sphincter pharyngoplasties. Surgeries were done over a 31-year span, from 1958 to 1989. The authors reported a failure rate of 30% for each type of surgery. They concluded that either procedure could be used with equal effectiveness, de Serres et al. (1999) evaluated speech outcomes and complications of sphincter pharyngoplasties and pharyngeal flaps. Patients who underwent sphincter pharyngoplasties had a higher rate of resolution of VPI than those who had pharyngeal flaps, although this was not statistically significant. Postoperative hyponasality and obstructive sleep symptoms were present in both groups. However, only patients who underwent pharyngeal flaps and had postoperative obstructive sleep symptoms had obstructive sleep apnea.
Combined Pharyngoplasty and Primary Palatoplasty
Because the initial palatoplasty may not be completely successful, a number of investigators have incorporated a primary pharyngoplasty. The procedure remains controversial. Most report more patients with normal resonance than with palatoplasty alone (Bingham et al., 1972; Dalston and Stutteville, 1975; Dorf and Curtin, 1982) but not all (Morris, 1973). One study demonstrated that 54% of children receiving a combined procedure did not require the pharyngoplasty (Riski et al., 1987). Mazaheri and colleagues (1994) could not identify any differences in velar length or nasopharyngeal depth between one group of children with clefts who required pharyngeal flaps and a second group of children with clefts who did not. Although it is clear that some children born with CP will require a pharyngoplasty, we cannot accurately identify those children at the time of palatoplasty.
Furlow Z-Plcrsty
Chen et al. (1994) reported their results with the Furlow Z-plasty as a secondary procedure. They documented velopharyngeal closure in 16/18 patients. Furlow (1994), in a review of the series, observed that retroposition of the levator muscle sling appeared to be the chief benefit of the procedure and that any lengthening of the velum may be an incidental benefit. Gunther et al. (1998) evaluated the results of Fur low's double reversing z-plasty (Furlow, 1986) compared to intravelar veloplasty. Intravelar veloplasty patients demonstrated a 34% higher incidence of hoarseness, nasal escape, and hypernasality at 3 years of age compared to Furlow patients. These same patients likewise required significantly more secondary pharyngoplastic procedures.
Complications of Pharyngoplasty
Complications with pharyngoplasties are not uncommon. Some complications are immediate and some develop in the long term. Obstruction may be severe enough to warrant takedown of the flap (Caouette-Laberge et al., 1992). Ren et al. (1992) suggested that loss of tongue-lip balance might be one factor causing midfacial retrusion. Sturim (1974) reported hemorrhaging from pharyngeal flap surgery in two patients who previously had a Teflon injection for VPI. Zaworski (1981) reported anorexia nervosa in a 15-yearold female after pharyngeal flap surgery. Hoffman (1985) reported surgical revision followed by dilation and stenting with a dental prosthesis to prevent repeat contracture of a pharyngeal flap that stenosed. Drew et al. (1985) reported that 12/25 pharyngeal flap patients demonstrated elevated serum antidiuretic hormone levels, low serum osmolity, and hyponatremia in the postoperative period.
Obstructive Sleep Apnea
Kravath et al. (1980) reported on three patients who developed obstructive sleep apnea (OSA) immediately following pharyngeal flap surgery. Thurston et al. (1980) reported significant nasal obstruction in 8/85 patients following pharyngeal flap. Obstruction was often occult and identified only after careful questioning. Seven of the eight patients required surgical revision to relieve airway obstruction.
Orr et al. (1987) observed OSA in 9/10 patients at 2 to 3 days post-surgery. Apnea resolved in 7/9 patients by 3 months. Shprintzen (1988) identified OSA by polysomnography in 30/300 patients following pharyngeal flap surgery; OSA lasted longer than 6 months in three and resolved in the remaining patients. Narrow and wide flaps had the same incidence of OSA. They postulated that the causes of OSA were obstruction of the portals by large tonsils, contraction of the nasopharynx around the flap, postoperative nasopharyngeal edema, or a sudden change in breathing pattern. Sirois et al. (1994) reported on 14/40 (35%) patients with abnormal polysomnograms after pharyngeal flap surgery. Six had OSA, six had central sleep apnea, and two had both types. Long-term follow-up demonstrated residual central apneas. Witsell et al. (1994) showed decreased nasal patency in 5/7 patients after a pharyngeal flap.
Shprintzen et al. (1992) modified pharyngeal flaps (shorter) for less contracture below the flap, in an attempt to lessen airway obstruction. They also suggested using nasopharyngeal tubes for nasal respiration until the patient is awake and can breathe orally. The authors reported that the protocol reduced all complications: OSA was eliminated in all patients, snoring was reduced from 82% to 10.5%, and hospital stay was reduced from 7 to 3 days.
Speech Therapy
Before Palatal Closure
Parents are counseled regarding what to expect from their child's early speech attempts. Resonance will be hypernasal, and the child will be able to say correctly words with a nasal sound, such as mama, but will not correctly say words with pressure sounds, such as dada. Parents are instructed in play activities which focus on verbal interaction between parent and child and appropriate modeling of speech and language.
After Palatal Closure
Speech and language stimulation should continue with age-appropriate games, vocabulary, and syntax. Parents are now asked to monitor the sounds that the child makes. If there are no confounding developmental problems, we expect the child to begin making crisp, pressure consonants such as p, b, t, d, k, and g. Often, parents are asked to occlude the child's nose manually while playing “sound games,” such as repeating the syllable ba, ba, ba, ba. Occluding the nose prevents any nasal airflow and directs the airstream to the oral cavity.
Parents are also asked to observe any signs of velopharyngeal dysfunction or oral-nasal fistulas. These include nasal reflux while eating or drinking, nasal airflow or facial grimacing, or the continued use of nasal sounds and the lack of pressure consonants while talking.
Speech therapy for the child with CP is unique because the child may present with unique misarticulations not found in the noncleft population (Trost, 1981). Unique speech therapy strategies and facilitating postures are used to correct misarticulations in the CL/P child. Moreover, exercises are generally unsuccessful at increasing velopharyngeal movements except in some very specific situations (Ruscello, 1982, 1989). Maximizing oral pressure for pressure consonants will maximize velopharyngeal elevation and may gain velopharyngeal closure for small VPIs. Kuehn (1991) developed a unique therapy technique using continuous positive airway pressure to the nasal surface of the soft palate. Velar elevation for speech under the resistance of continuous positive airway pressure may improve velopharyngeal closure.
The importance of parental involvement in the therapeutic process has been demonstrated. Broen et al. (1993) and Pamplona et al. (1996) evaluated the effectiveness of speech therapy provided by parents and directed by a speech-language pathologist. Broen et al. (1993) reported that the mother was able to change the child's speech so that more of the child's productions were at the correct place of articulation. After structural management, nasal and glottalized productions disappeared from the child's speech but glottal stops did not (Pamplona et al., 1996). Patients accompanied by their mothers showed significantly higher linguistic advance compared to patients receiving therapy without their mothers. The results of this study support the statement that linguistic development in the CP child is strongly related to adult-child modes of interaction.
Pamplona et al. (1999) studied whether a phonological intervention may reduce the total time of speech therapy necessary for correcting compensatory articulation in CP children compared to an articulatory intervention. They demonstrated that the total time of speech intervention was significantly reduced (p < 0.001) when a phonological intervention was utilized.
Once a VPI is diagnosed as adversely affecting speech or speech development, it should be managed. Articulation skills improve immediately following management of VPI (Riski, 1979). Patients with VPI make little or no progress in speech therapy until the VPI is managed (Van Demark, 1974; Riski and DeLong, 1984; Van Demark and Hardin, 1985). When a VPI is suspected or documented, speech therapy should be considered diagnostic and short-term. Referral to a CP-craniofacial team is appropriate after no more than several weeks of ineffective speech therapy.
Special Populations
Functional or Sound-Specific Velopharyngeal Incompetence
The practicing clinician should also recognize that there are a small number of cleft (and noncleft) children with normal soft palate function who use some form of nasal air emission as a sound substitute (Peterson, 1975; Riski, 1984). This is termed a functional VPI or a sound-specific VPI. The characteristics include normal resonance, sound-specific use of some form of nasal air escape (usually a posterior nasal fricative), normal velopharyngeal function for correctly produced sounds, and the ability to correctly produce the errored sound without nasal air escape. These patients present a special diagnostic challenge, and the differential diagnosis of an organic VPI from a functional VPI is the key to appropriate management.
Velocardiofacial Syndrome
Shprintzen et al. (1978) first described VCFs. Over 100 characteristics have been reported. The most common features include facial dysmorphology, conotruncal heart defects, palatal abnormalities or hypernasality, learning disabilities, and behavioral abnormalities. Phenotypically, VCFS overlaps with DiGeorge syndrome, and both are associated with hemizygous deletion of 22qll.2. Yamagishi et al. (1999) reported that VCFs might be related to the gene Ufdl.
The incidence of VCFS is reported to be 1/4000. It is thought to be the most common form of syndromic clefting. Riski et al. (1999) demonstrated that 20% of children with VCFS at two different centers had CP. There is also a high incidence of noncleft hypernasality found in VCFS, which may vary from center to center because of referral patterns. One center, with a high rate of referral from the public schools, found hypernasality in 19/25 (76%) VCFS children without clefts. The second center, with a high rate of referral from a heart center, found hypernasality in only 5/22 (23%) VCFS children without clefts (Riski et al., 1999).
Other investigations have found a high incidence of Chiari malformation, cervical spine anomalies, and neurological deficits in a series of patients with VCFS (Hultman et al., 2000). Four of 16 (25%) children demonstrated Chiari malformation type I, 2/16 (12.5%) had occipitalization of the atlas, 1/16 (8.25%) had spina bifida occulta and subluxation on extension, and 1/16 (8.25%) had narrowing of the foramen magnum with basilar invagination of the odontoid. One patient required suboccipital craniectomy with laminectomy and decompression. Orofacial neurological deficits were identified in 14/41 (34%). Ten demonstrated velar paralysis, which was unilateral in six and bilateral in four.
Summary
The child with an oral cleft or related disorder represents a special challenge. Correct identification and labeling of occult disorders such as noncleft hypernasality requires careful imaging of the velopharynx. Successful evaluation and management of the structural and behavioral problems requires special knowledge, special tools, and most importantly close communication among professionals. While craniofacial teams pride themselves on their skills and expertise, there is an obligation to partner with the community specialist in caring for these children. The past decade has seen a marked advancement in computer and imaging instrumentation. These instruments can provide the clinician with objective measures of velopharyngeal dynamics, including the size, shape, and position of a velopharyngeal opening. Each of these instruments has specific advantages and disadvantages that should be appreciated. It appears that surgical outcome is often improved by applying information obtained from preoperative imaging to patient selection and surgical procedure. Finally, our understanding of speech motor control for the velum is improving. This is leading to a better understanding of appropriate speech therapy and to the development of new management paradigms.
Despite some advances, success rates are not much better than described in reviews from more than two decades ago (Yules and Chase, 1971). This is especially disheartening given the advances in computer instrumentation and imaging during the same time. Surgeons, and possibly teams, are slow to learn from the mistakes of others and appear more content to follow their own learning curve. There appears to be greater improvement in individual results over time than there is in the collective management of hypernasality. Further, a pharyngoplasty is not without risk to the patient. The benefits of pharyngoplasty should be weighed against possible complications.
A number of clinical research challenges remain, including early identification of children who require a pharyngoplasty, development of criteria for selecting a pharyngeal flap or a sphincter pharyngoplasty in individual situations, and management of VPI without creating hyponasality and obstruction. Hyponasality has been considered more socially acceptable than hypernasality, and many consider hyponasality an improvement over hypernasality (Crockett et al., 1988).
A pharyngoplasty should have a physiological basis, and evaluation of velopharyngeal physiology has been the responsibility of the speech pathologist. The clinician is challenged to incorporate available instrumentation into the evaluation process. The clinician may be guided by experience and by documents of the American Speech-Language, Hearing Association and the American Cleft Palate-Craniofacial Association. The American Speech-Language, Hearing Association (1997) offers specific recommendations for the evaluation of nasal resonance and nasal airflow. The American Cleft Palate-Craniofacial Association (1993) offers several recommendations for evaluation and treatment, including “secondary palatal and pharyngeal surgery for velopharyngeal inadequacy should be performed only after evaluation of the velopharyngeal mechanism and review by the team.” This includes “in-depth analysis of articulatory performance, aerodynamic measures, videofluoroscopy, nasopharyngoscopy, and nasometric studies, all of which should be conducted with the participation of the team speech-language pathologist.”
References
Adams, L, Fletcher, S, McCutcheon, M (1989). Cleft palate speech assessment through oral-nasal acoustic measures. In: Communicative Disorders Related to Cleft Lip and Palate, 3rd ed., edited by K Bzoch. Boston: College Hill Press, pp. 246–257.
American Cleft Palate-Craniofacial Association (1993). Parameters for Evaluation and Treatment of Patients with Cleft Lip/Palate or Other Craniofacial Anomalies. Pittsburgh: American Cleft Palate-Craniofacial Association.
American Speech-Language, Hearing Association (1997). Preferred practice patterns for the profession of speech-language pathology. Resonance and Nasal Airflow Assessment. Rockville, MD: Author.
Bardenheur, D (1892). Vorschlage zu plastischen operationen bei chirurgischen eingriffen in der mundhohle. Arch Klin Chir 43: 32.
Becker, M, Svensson, H, Sarnas, K, Jacobsson, S (2000). Von Langenbeck or Wardill procedures for primary palatal repair in patients with isolated cleft palate: speech results. Scand J Plast Reconstr Surg Hand Surg 34: 27–32.
Bell-Berti, F (1976). An EMG study of VP function in speech. J Speech Hear Res 19: 225–240.
Bingham, HG, Suthunyara, P, Richards, S (1972). Should the pharyngeal flap be used primarily with palatoplasty? Cleft Palate J 9: 319.
Blakeley, RW (1972). The Practice of Speech Pathology: A Clinical Diary. Springfield, IL: Charles C. Thomas.
Bless, DM, Ewanowski, SJ, Dibbell, DG (1980). A technique for temporary obturation of fistulae: a clinical note. Cleft Palate J 17: 297.
Broen, PA, Doyle, SS, Bacon, CK (1993). The velopharyngeally inadequate child: phonologic change with intervention. Cleft Palate Craniofac J 30: 500–507.
Calnan, JS (1971). Permanent nasal escape after adenoidectmy. Br J Plast Surg 24: 197–204.
Caouette-Laberge, L, Egerszegi, EP, de Remont, AM, Ottenseyer, I (1992). Long-term follow-up after division of a pharyngeal flap for severe nasal obstruction. Cleft Palate Craniofac J 29: 27–31.
Ceponiene, R, Hukki, J, Cheour, M, et al. (1999). Cortical auditory dysfunction in children with oral clefts: relation with cleft type. Clin Neurophysiol 110: 1921–1926.
Chen, PK-T, Wu, JTH, Chen, YR, Noordhoff, S (1994). Correction of velopharyngeal insufficiency in cleft palate patients with the Furlow palatoplasty. Plast Reconstr Surg 94: 933–941.
Crockett, DM, Bumstead, RM, Van Demark, DR (1988). Experience with surgical management of velopharyngeal incompetence. Otolaryngol Head Neck Surg 99: 1–9.
Dalston, RM, Marsh, JL, Vig, KW, et al. (1988). Minimal standards for reporting the results of surgery on patients with cleft lip, cleft palate, or both: a proposal. Cleft Palate J 25: 3.
Dalston, RM, Stutteville, OM (1975). A clinical investigation of the efficacy of primary nasopalatal pharyngoplasty. Cleft Palate J 22: 177.
Dalston, RM, Warren, DW (1986). Comparison of Tonar II, pressure flow, and listener judgements of hypernasality in the assessment of velopharyngeal function. Cleft Palate J 23: 108.
Dalston, RM, Warren, DW, Dalston, ET (1991a). Use of nasometry as a diagnostic tool for identifying patients with velopharyngeal impairment. Cleft Palate J 28: 184.
Dalston, RM, Warren, DW, Dalston, ET (1991b). A preliminary investigation concerning the use of nasometry in identifying patients with hyponasality and/or nasal airway impairment. J Speech Hear Res 34: 11.
de Serres, LM, Deleyiannis, FW, Eblen, LE, et al. (1999). Results with sphincter pharyngoplasty and pharyngeal flap. Int J Pediatr Otorhinolaryngol 48: 17–25.
Dorf, DS, Curtin, JW (1982). Early cleft palate repair and speech outcome. Plast Reconstr Surg 70: 74.
Drew, GS, Tripathi, S, Lehman, JA, Jr (1985). The syndrome of inappropriate secretion of antidiuretic hormone in the pharyngeal flap operation. Cleft Palate J 22: 88–92.
Fletcher, SC (1978). Diagnosing Speech Disorders from Cleft Palate. New York: Grune and Stratton.
Fox, DR, Lynch, JI, Cronin, TD (1988). Change in nasal resonance over time: a clinical study. Cleft Palate J 25: 245.
Fritzell, B (1979). Electromyography in the study of velopharyngeal function: a review. Folia Phoniatr 31: 93–102.
Furlow, LT (1986). Cleft palate repair by double opposing Z-plasty. Plast Reconstr Surg 78: 724–738.
Furlow, LT (1994). Correction of velopharyngeal insufficiency in cleft palate patients with the Furlow palatoplasty. Plast Reconstr Surg 94: 942–943.
Furusawa, K, Yamaoka, M, Ichikawa, N (1994). Responsiveness of single afferents in the infraorbital nerve to oral air pressure generated by consonants. Cleft Palate J 31: 161.
Gereau, SA, Shprintzen, RJ (1988). The role of adenoids in the development of normal speech following palate repair. Laryngoscope 98: 299–303.
Giering, RW, Daubenspeck, JA (1990). Time course of laryngeal aperture response to expiratory resistance loading in humans. Respir Physiol 81: 371–379.
Gilbert, STJ, Pigott, RW (1982). The feasibility of nasal pharyngoscopy using the 70° Storz-Hopkins nasopharyngoscope. Br J Plast Surg 35: 14.
Gonzalez-Baron, S, Dawid-Milner, MS, Lara, JP, Calvijo, E (1989). Changes in laryngeal resistance and bronchial tonus. Rev Esp Fisiol 45: 191–196.
Graiver, MH, Cohen, SR, Kawamoto, HK, Fromwiller, S (1992). A new operation for velopharyngeal insufficiency: the palatoglossus myomucosal flap. Plast Reconst Surg 90: 707–710.
Gunther, E, Wisser, JR, Cohen, MA, Brown, AS (1998). Palatoplasty: Furlow's double reversing Z-plasty versus intravelar veloplasty. Cleft Palate Craniofac J 35: 546–549.
Hairfield, WM, Warren, DW, Seaton, DL (1988). Prevalence of mouthbreathing in cleft lip and palate. Cleft Palate J 25: 135.
Hardin, MA, Van Demark, DR, Morris, HL, Payne, MM (1992). Correspondence between nasalance scores and listener judgements of hypernasality and hyponasality. Cleft Palate J 29: 346.
Harding, R (1984). Function of the larynx in the fetus and newborn. Annu Rev Physiol 46: 645–659.
Hebb, DO (1949). The Organization of Behavior: A Neuropsychological Theory. New York: John Wiley and Sons.
Hirschberg, J, Van Demark, DR (1997). A proposal for standardization of speech and hearing evaluations to assess velopharyngeal function. Folia Phoniatr Logop 49: 158–167.
Hoffman, S (1985). Correction of lateral port stenosis following a pharyngeal flap operation. Cleft Palate J 22: 51–55.
Hogan, VM, Schwartz, MF (1977). Velopharyngeal incompetence. In: Converse, JM Reconstructive Plastic Surgery, 4th ed., edited by JM Converse. Philadelphia: WB Saunders, pp. 2268–2283.
Huang, MH, Lee, ST, Rajendran, K (1997). Structure of the musculus uvulae: functional and surgical implications of an anatomic study. Cleft Palate Craniofac J 34: 466–474.
Hultman, CS, Riski, JE, Cohen, SR, et al. (2000). Chiari malformation, cervical spine anomalies, and neurologic deficits in velocardiofacial syndrome. Plast Reconstr Surg 106: 16–24.
Huskie, CF, Jackson, IT (1977). The sphincter pharyngoplasty—a new approach to the speech problem of velopharyngeal incompetence. Br J Disord Commun 12: 31–35.
Hynes, W (1951). Pharyngoplasty by muscle transposition. Br J Plast Surg 3: 128–135.
Hynes, W (1953). The results of pharyngoplasty by muscle transplantation in “failed cleft palate” cases, with special reference to the influence of the pharynx on voice production. Ann R Coll Surg Engl 13: 17–35.
Ibuki, K, Matsuya, T, Nishio, J, et al. (1978). The course of the facial nerve for the levator veli palatini muscle. Cleft Palate J 25: 209.
Iglesias, A, Kuehn, DP, Morris, HL (1980). Simultaneous assessment of pharyngeal wall and velar displacement for selected speech sounds. J Speech Hear Res 23: 429.
Insalaco, G, Kuna, ST, Costanza, BM, et al. (1991). Thyroarytenoid muscle activity during loaded and nonloaded breathing in adult humans. J Appl Physiol 70: 2410–2416.
Jackson, IT, Silverton, JS (1977). The sphincter pharyngoplasty as a secondary procedure in cleft palates. Plast Reconstr Surg 59: 518–524.
Karnell, MP (1995). Nasometric discrimination of hypernasality and turbulent nasal airflow. Cleft Palate Craniofac J 32: 145–148.
Karnell, MP, Van Demark, DR (1986). Longitudinal speech performance in patients with cleft palate: comparisons based on secondary management. Cleft Palate J 23: 278.
Keuning, KH, Wieneke, GH, Dejonckere, PH (1999). The intrajudge reliability of the perceptual rating of cleft palate speech before and after pharyngeal flap surgery: the effect of judges and speech samples. Cleft Palate Craniofac J 36: 328–333.
Komatsu, Y, Genba, R, Kohama, G (1982). Morphological studies of the velopharyngeal orifice in cleft palate. Cleft Palate J 29: 275.
Kravath, RE, Pollak, CP, Borowiecki, B, Weitzman, ED (1980). Obstructive sleep apnea and death associated with surgical correction of velopharyngeal incompetence. J Pediatr 96: 645–648.
Kuehn, DP (1991). New therapy for treating hypernasal speech using continuous positive airway pressure (CPAP). Plast Reconstr Surg 88: 959-966.
Kuehn, DP, Moon, JB (1994). Levator veli palatini muscle activity in relation to intraoral air pressure variation. J Speech Hear Res 37: 1260–1270.
Kuehn, DP, Moon, JB (1995). Levator veli palatini muscle activity in relation to intraoral air pressure variation in cleft palate subjects. Cleft Palate Craniofac J 32: 376–381.
Kuehn, DP, Moon, JB (2000). Induced fatigue effects on velopharyngeal closure force. J Speech Lang Hear Res 43: 486–500.
Kuehn, DP, Moon, JB, Folkins, JW (1993). Levator veli palatini muscle activity in relation to intranasal air pressure variation. Cleft Palate J 30: 361.
Laitnen, J, Haapanen, ML, Paaso, M, et al. (1998). Occurrence of dental consonant misarticulations in different cleft types. Folia Phoniatr Logop 50: 92–100.
Lohmander-Agerskov, A, Söderpalm, E, Friede, H, et al. (1994). Prespeech in children with cleft lip and palate or cleft palate only: phonetic analysis related to morphologic and functional factors. Cleft Palate J 31:271.
MacNeilage, PF (1970). Motor control of serial ordering of speech. Psychol Rev 77: 182–196.
Mason, RM, Warren, DW (1980). Adenoid involution and developing hypernasality in cleft palate. J Speech Hear Dis 45: 469.
Maue-Dickson, W, Dickson, DR (1980). Anatomy and physiology related to cleft palate: current research and clinical implications. Plast Reconstr Surg 65: 83.
Mazaheri, M, Athanasiou, AE, Long, RE (1994). Comparison of velopharyngeal growth between cleft lip and/or palate patients requiring or not requiring pharyngeal flap surgery. Cleft Palate J 31: 452–460.
McBride, B, Whitelaw, WA (1981). A physiologic stimulus to upper airway receptors in humans. J Appl Physiol 51: 1179.
McWilliams, BJ (1991). Submucous clefts of the palate: how likely are they to be symptomatic? Cleft Palate J 28: 247–248.
Mirrett, P, Georgiade, GS, Riski, JE (1993). Tailoring the Sphincter Pharyngoplasty Presented at the April 22 annual meeting of the American Cleft Palate-Craniofacial Association, Pittsburgh, Pennsylvania,
Moon, J, Folkins, JW (1991). The effects of auditory feedback on intraoral air pressure during speech. J Acoust Soc Am 90: 2992–2999.
Morr, KE, Warren, DW, Dalston, RM, et al. (1988). Intraoral pressure measures after experimental loss of velar resistance. Folia Phoniatr 40: 284–289.
Morris, HL (1973). Velopharyngeal competence and primary cleft palate surgery, 1960-1971: a critical review. Cleft Plate J 10: 62.
Moss, AL, Pigott, RW, Albery, EH (1987). Hynes pharyngoplasty revisited. Plast Reconstr Surg 79: 346–355.
Netsell, R (1990). Commentary on maintaining speech pressures in the presence of velopharyngeal impairment regulation. Cleft Palate J 27: 58–60.
Niimi, S, Bell-Berti, F, Harris, KS (1982). Dynamic aspects of velopharyngeal closure. Folia Phoniatr 34: 246.
O'Gara, MM, Logemann, JA (1988). Phonetic analyses of the speech development of babies with cleft palate. Cleft Palate J 25: 122.
O'Gara, MM, Logemann, JA, Rademaker, AW (1994). Phonetic features by babies with unilateral cleft lip and palate. Cleft Palate Craniofac J 6: 446–451.
Orr, WC, Levine, NS, Buchanan, RT (1987). Effect of cleft palate repair and pharyngeal flap surgery on upper airway obstruction during sleep. Plast Reconstr Surg 80: 226–232.
Orticochea, M (1968). Construction of a dynamic muscle sphincter in cleft palates. Plast Reconstr Surg 41: 323–327.
Orticochea, M (1970). Results of the dynamic muscle sphincter operation in cleft palates. Br J Plast Surg 23: 108–114.
Orticochea, M (1983). A review of 236 cleft palate patients treated with dynamic muscle sphincter. Plast Reconstr Surg 71: 180–188.
Pamplona, MC, Ysunza, A, Espinosa, J (1999). A comparative trial of two modalities of speech intervention for compensatory articulation in cleft palate children, phonologic approach versus articulatory approach. Int J Pediatr Otorhinolaryngol 49: 21–26.
Pamplona, MC, Ysunza, A, Uriostegui, C (1996). Linguistic interaction: the active role of parents in speech therapy for cleft palate patients. Int J Pediatr Otorhinolaryngol 37: 17–27.
Pannbacker, MD, Lass, NJ, Hansen, GG, et al. (1993). Survey of speech-language pathologists' training, experience, and opinions on nasopharyngoscopy. Cleft Palate Craniofac J 30: 40–45.
Passavant, G (1862). Ueber die operation der angeborenen spalten des harten gaumens und der damit complicirten hasenscharten. Arch Ohr Mas Kehlkopfheilk 3: 193.
Pensler, JM, Reich, DS (1991). A comparison of speech results after the pharyngeal flap and the dynamic sphincteroplasty procedures. Ann Plast Surg 26: 441–443.
Peterson, SJ (1975). Nasal emission as a component of the misarticulation of sibilants and affricates. J Speech Hear Disord 40: 106.
Pigott, RW (1974). The results of nasopharyngoscopic assessment of pharyngoplasty. Scand J Plast Surg 8: 148.
Pigott, RW (1993). The results of pharyngoplasty by muscle transplantation by Wilfred Hynes. Br J Plast Surg 46: 440–442.
Randall, P, Whitaker, LA, Noone, RB, Jones, WD (1978). The case for the inferiorly-based posterior pharyngeal flap. Cleft Palate J IS: 262–265.
Ren, YF, Isberg, A, Henningsson, G, Larson, O (1992). Tongue posture in cleft palate patients with a pharyngeal flap. Scand J Plast Reconstr Surg Hand Surg 26: 307–312.
Richman, LC, Eliason, MJ, Lindgren, SD (1988). Reading disability in children with clefts. Cleft Palate J 25: 21.
Riski, JE (1979). Articulation skills and oral-nasal resonance in children with pharyngeal flaps. Cleft Palate J 16: 421–428.
Riski, JE (1984). Functional velopharyngeal incompetence: diagnoses and management. In: Treating Articulation Disorders: For Clinicians by Clinicians, edited by H Winitz. Baltimore: University Park Press, pp. 224–234.
Riski, JE (1995). Assessment of speech in adolescents with cleft palate. Cleft Palate J 32: 109–113.
Riski, JE (1996). The relationship of nasal air turbulence and nasalance in speakers with VPI. Presented at the annual meeting of the American Cleft Palate-Craniofacial Association, San Diego, California, April 26.
Riski, JE, DeLong, E (1984). Articulation development in children with cleft lip/palate. Cleft Palate J 21: 57–64.
Riski, JE, Millard, RT (1979). The process of speech evaluation and treatment. In: Cleft palate and cleft lip: A team approach to clinical management and rehabilitation of the patient, edited by HK Cooper, RL Harding, WM Krogman, et al. Philadelphia: WB Saunders, pp. 431–484.
Riski, JE, Cohen, SR, Burstein, F, et al. (1999). Pressure flow and nasometric evaluation of velopharyngeal function in velo-cardiofacial syndrome at two centers. Presented at the annual meeting of the American Cleft Palate-Craniofacial Association, Scottsdale, Arizona, April 16.
Riski, JE, Georgiade, NG, Serafin, D, et al. (1987). The Orticochea pharyngoplasty and primary palatoplasty: an evaluation. Ann Plast Surg 18: 303–309.
Riski, JE, Hoke, JA, Dolan, EA (1989). The role of pressure-flow and endoscopic assessment in successful palatal obturator revision. Cleft Palate J 26: 1.
Riski, JE, Kunze, LH, Mann, J, Nailling, KR (1984a). Speech patterns and disturbances associated with clefts and craniofacial anomalies. In: Pediatric Plastic Surgery, edited by D Serafin and NG Georgiade. St. Louis: Mosby, p. 246–258.
Riski, JE, Mason, RM (1994). Adenoid involution as a cause of velopharyngeal incompetence in children with cleft palate. Presented at the annual meeting of the American Cleft Palate- Craniofacial Association, Toronto, Canada.
Riski, JE, Ruff, GL, Georgiade, GS, et al. (1992). Evaluation of the sphincter pharyngoplasty. Cleft Palate Craniofac J 29: 254–261.
Riski, JE, Serafin, D, Riefkohl, R, et al. (1984b). A rationale for modifying the site of insertion of the Orticochea pharyngoplasty. Plast Reconstr Surg 73: 882–894.
Riski, JE, Stewart, M, Mason, R, Simms, C (1996). Analysis of the craniofacial skeleton in cleft palate children with and without adenoids. Program of the annual meeting of the American Cleft Palate-Craniofacial Association, San Diego, California.
Riski, JE, Warren, DW, Lutz, RL, Zajac, D (1995). Application of Perci-SARS for speech evaluation. Study session at the annual meeting of the American Cleft Palate-Craniofacial Association, Tampa, Florida.
Roberts, TMF, Brown, BSJ (1983). Evaluation of a modified sphincter pharyngoplasty in the treatment of speech problems due to palatal insufficiency. Ann Plast Surg 10: 209–213.
Ruscello, DM (1982). A selected review of palatal training procedures. Cleft Palate J 19:181.
Ruscello, DM (1989). Modifying velopharyngeal closure through training procedures. In: Communicative Disorders Related to Cleft Lip and Palate, 3rd ed., edited by K Bzoch. Austin, TX: Pro-Ed, pp. 338–349.
Ruscello, DM (1997). Considerations for behavioral management for velopharyngeal closure for speech. In: Communicative Disorders Related to Cleft Lip and Palate, 4th ed., edited by KR Bzoch. Austin, TX: Pro-Ed, pp. 509–528.
Sant'Ambrogio, G, Matthew, OP, Fisher, JT, Sant'Ambrogio, FB (1983). Laryngeal receptors responding to transmural pressure, airflow and local muscle activity. Respir Physiol 54: 317.
Sanvenero-Rosselli, G (1934). Divisione palatina e sua cura chirugica. Rome: Casa Editrice Luigi Pozzi.
Sedlackova, E (1967). The syndrome of the congenitally shortened velum. The dual innervation of the soft palate. Folia Phoniatr 19: 441–450.
Shelton, RL, Blank, JL (1984). Oronasal fistulas, intraoral air pressure, and nasal air flow during speech. Cleft Palate J 21: 91.
Shprintzen, RJ (1988). Pharyngeal flap surgery and the pediatric upper airway. Int Anesthesiol Clin 26: 79–88.
Shprintzen, RJ, Lencione, RM, McCall, GN, Skolnick, ML (1974). A three dimensional cinefluoroscopic analysis of velopharyngeal closure during speech and nonspeech activities in normals. Cleft Palate J 11: 412–428.
Shprintzen, RJ, Lewin, ML, Croft, CB, et al. (1979). A comprehensive study of pharyngeal flap surgery: tailor-made flaps. Cleft Palate J 16:46-55.
Shprintzen, RJ, McCall, GN, Skolnick, ML (1980). The effect of pharyngeal flap surgery on the movements of the lateral pharyngeal walls. Plast Reconstr Surg 66: 570–573.
Shprintzen, RJ, McCall, GN, Skolnick, ML, Lencione, RM (1975). Selective movement of the lateral aspects of the pharyngeal walls during velopharyngeal closure for speech, blowing, and whistling in normals. Cleft Palate J 12: 51.
Shprintzen, R, Goldberg, R, Lewin, M, et al. (1978). A new syndrome involving cleft palate, cardiac anomalies, typical facies, and learning disabilities. Cleft Palate J 5: 56–62.
Shprintzen, RJ, Singer, L, Sidoti, EJ, Argamaso, RV (1992). Pharyngeal flap surgery: postoperative complications. Int Anesthesiol Clin 30: 115–124.
Sie, KC, Tampakopoulou, DA, de Serres, LM, et al. (1998). Sphincter pharyngoplasty: speech outcome and complications. Laryngoscope 108: 1211–1217.
Sirois, M, Caouette-Laberge, L, Spier, S, et al. (1994). Sleep apnea following pharyngeal flap: a feared complication. Plast Reconstr Surg 93: 943–947.
Skolnick, ML (1970). Videofluoroscopic examination of the velopharyngeal portal during phonation in lateral and base projections— a new technique for studying the mechanics of closure. Cleft Palate J 7: 803–816.
Skolnick, ML (1975). Velopharyngeal function in cleft palate. Clin Plast Surg 2: 285.
Skolnick, ML, McCall, GN (1972). Velopharyngeal competence and incompetence following pharyngeal flap surgery: videofluoroscopic study in multiple projections. Cleft Palate J 9: 1–12.
Smith, BE, Weinberg, B (1980). Prediction of velopharyngeal orifice size: a re-examination of model experimentation. Cleft Palate J 27:277.
Smith, BE, Weinberg, B (1982). Prediction of modeled velopharyngeal orifice areas during steady flow conditions and during aerodynamic stimulation of voiceless stop consonants. Cleft Palate J 19: 172.
Stratoudakis, AC, Bambace, C (1984). Sphincter pharyngoplasty for correction velopharyngeal incompetence. Ann Plast Surg 12: 243–248.
Sturim, HS (1974). Bleeding complications with pharyngeal flap construction in humans following Teflon pharyngoplasty. Cleft Palate J 11: 292–294.
Subtelny, JD (1957). A cephalometric study of the growth of the soft palate. J Plast Reconstr Surg 19: 49–62.
Subtelny, JD, Van Hattum, RJ, Myers, BB (1972). Ratings and measures of cleft palate speech. Cleft Palate J 9; 18–27.
Szereda-Przestaszewska, M (1989). Effects of serotonin on laryngeal resistance and respiratory timing in lung denervated rabbits. Mater Med Pol 21: 297–300.
Tachimura, T, Hara, H, Koh, H, Wada, T (1997). Effect of temporary closure of oronasal fistulae on levator veli palatini muscle activity. Cleft Palate Craniofac J 34: 505–511.
Thurston, JB, Larson, DL, Shanks, JC, et al. (1980). Nasal obstruction as a complication of pharyngeal flap surgery. Cleft Palate J 17: 148–154.
Tolman, EC (1932). Purposive Behavior in Animals and Men. New York: Century.
Trost, JE (1981). Articulatory additions to the classical description of the speech of persons with cleft palate. Cleft Palate J 18: 193.
Van Demark, DR (1974). A comparison of articulation abilities and velopharyngeal competence between Danish and Iowa children with cleft palate. Cleft Plate J 11: 463.
Van Demark, DR (1979). Predictability of velopharyngeal competency. Cleft Palate J 16: 429.
Van Demark, DR (1997). Diagnostic value of articulation tests with individuals having clefts. Folia Phoniatr Logop 49: 147–157.
Van Demark, DR, Hardin, MA (1985). Longitudinal evaluation of articulation and velopharyngeal competence of patients with pharyngeal flaps. Cleft Palate J 22: 163–172.
Van Demark, DR, Hardin, MA, Morris, HL (1988). Assessment of velopharyngeal competence: a long-term process. Cleft Palate J 25: 362.
Van Demark, RV, Kuehn, DP, Tharp, RF (1975). Prediction of velopharyngeal competency. Cleft Palate J 12: 5–11.
Van Demark, DR, Morris, HL (1983). Stability of velopharyngeal competency. Cleft Palate J 20: 18.
Van Demark, DR, Morris, HL, VandeHaar, C (1979). Patterns of articulation abilities in speakers with cleft palate. Cleft Palate J 16:230.
Velasco, MG, Ysunza, A, Hernandez, X, et al. (1988). Diagnosis and treatment of submucous cleft palate: a review of 108 cases. Cleft Palate J 25: 171.
Wardill, WEM (1928). Results of operation for cleft palate. Br J Surg 16: 127.
Wardill, WEM (1933). Cleft palate. Br J Surg 21: 347.
Warren, DW (1984). A quantitative technique for assessing nasal airway impairment. Am J Orthod 86: 306.
Warren, DW (1986). Compensatory speech behaviors in individuals with cleft palate: a regulation/control phenomenon? Cleft Palate J 23: 251–260.
Warren, DW, Devereux, JL (1966). An analog study of cleft palate speech. Cleft Palate J 3: 103.
Warren, DW, Drake, AF, Davis, JU (1992). Nasal airway in breathing and speech. Cleft Palate Craniofac J 29: 511–519.
Warren, DW, Duany, LF, Fischer, ND (1969). Nasal pathway resistance in normal and cleft lip and cleft palate subjects. Cleft Palate J 6: 134.
Warren, DW, DuBois, AB (1964). A pressure flow technique for measuring velopharyngeal orifice area during continuous speech. Cleft Palate J 1: 52.
Warren, DW, Hinton, VA (1983). Compensatory speech behaviors in cleft palate: a regulation/control phenomenon? ASHA 25: 107.
Warren, DW, Trier, WC, Bevin, AG (1974). Effect of restorative procedures on the nasopharyngeal airway in cleft palate. Cleft Palate J 13:367.
Williams, WN (1979). Radiological measures of abnormal speech physiology. In: Communicative Disorders Related to Cleft Lip and Palate, edited by KR Bzoch. Boston: Little, Brown, pp. 249–262.
Williams, WN, Eisenbach, OR (1981). Assessing VP function: the lateral still technique vs. cinefluorography. Cleft Palate J 18: 45.
Witsell, DL, Drake, AF, Warren, DW (1994). Preliminary data on the effect of pharyngeal flaps on the upper airway in children with velopharyngeal inadequacy. Laryngoscope 104: 12–15.
Wu, JT, Huang, G, Huang, CS, Noordhoff, MS (1996). Nasopharyngoscopic evaluation of cephalometric analysis of velopharynx in normal and cleft palate patients. Ann Plast Surg 36: 117–123.
Yamagishi, H, Garg, V, Matsuoka, R, et al. (1999). A molecular pathway revealing a genetic basis for human cardiac and craniofacial defects. Science 283: 1158–1161.
Ysunza, A, Pamplona, MC, Molina, F, et al. (1999). Velopharyngeal motion after sphincter pharyngoplasty: a videonasopharyngoscopic and electromyographic study. Plast Reconstr Surg 104: 905–910.
Yules, RB, Chase, RA (1971). Secondary techniques for correction of palatopharyngeal incompetence. In: Cleft Lip and Palate, edited by K Bzoch, Grabb, Rosenstein. Boston: Little, Brown.
Zaworski, RE (1981). Anorexia nervosa following a pharyngeal flap operation. Cleft Palate J 18: 223–224.
Zemlin, WR (1997). Speech and Hearing Science: Anatomy and Physiology, 4th ed. New York: Prentice-Hall.
Zwitman, DH (1982a). Velopharyngeal physiology after pharyngeal flap surgery as assessed by oral endoscopy. Cleft Palate J 19: 36–39.
Zwitman, DH (1982b). Oral endoscopic comparison of velopharyngeal closure before and after pharyngeal flap. Cleft Palate J 19: 40–46.