Swallowing: First Stage

The first stage of swallowing is voluntary. It begins with the selective separation of the masticated food into a specific bolus. This task is accomplished primarily by the tongue. The bolus is positioned on the dorsum of the tongue and then pressed lightly against the intact hard palate. The tip of the tongue rests on the hard palate anteriorly, just behind the incisors. The lips are sealed, and the teeth are brought together; this essentially dams off the anterior oral cavity. The presence of the bolus pressed against the mucosa of the intact hard palate initiates a reflex wave of contraction of the tongue that pushes the bolus backward. As the bolus reaches the back of the tongue and with the soft palate now occluding against the nasopharynx, the bolus is transferred into the pharynx.

Swallowing: Second Stage

When the bolus has reached the pharynx, a peristaltic wave caused by the contracture of the pharyngeal constrictor muscles carries it down the pharynx. To prevent regurgitation into the nasal cavity, the soft palate must rise and touch the posterior pharyngeal wall, thereby sealing off the nasal cavity. Simultaneously, the epiglottis must block the pharyngeal airway to the trachea to prevent the food from going into the larynx or the trachea and ending up in the lungs. This process of walling off potential openings keeps the food moving down the esophagus. During this stage of swallowing, the pharyngeal muscular activity opens the pharyngeal orifices of the eustachian tubes, which would otherwise be closed.

Swallowing: Third Stage

The third stage of swallowing describes the passing of the bolus through the length of the esophagus and into the stomach. Rapid peristaltic waves carry the bolus through the esophagus. As the bolus reaches the lower esophagus, the sphincter relaxes, thereby allowing for the entrance of the bolus into the stomach. Interestingly, in the upper portion of the esophagus, the muscles are mainly voluntary and can also be used to return the bolus into the mouth when necessary for more complete mastication. In the lower section of the esophagus, the muscles are entirely involuntary.

Evaluation of Swallowing

When a complaint about swallowing is registered, a special evaluation may be required. Such an evaluation should consist of a complete medical history, a detailed description of the complaint, and a physical examination of the peripheral deglutitory motor and sensory system, including trial swallows under observation. Diagnostic studies—including videofluorography, manometry, electromyography, and fiber-optic endoscopy—are indicated in selected cases.

• Speech initiation, during which the content of the utterance to be spoken is converted into phonemes in the brain’s language center

• The generation of commands that go from the brain’s motor center to the speech organs

• Phonation, during which the emission of air sent from the lungs moves through the vocal tract and causes the formation of the voice as it moves past the vocal folds

• Articulation, which involves movement by the oral cavity, the oral pharynx, and the hypopharynx for the production of speech via this specific set of motor commands

• Plosive/stop: Air pressure is stopped within the oral cavity at a specific location, and it is then suddenly released. Examples are /p/, /b/, /t/, /d/, /k/, and /g/.

• Fricative: Air pressure is partially blocked or obstructed within the vocal tract, thereby causing turbulent airflow. Examples are /f/, /v/, /s/, and /z/.

• Affricative: There is a sequencing of the airstream initially with complete obstruction (i.e., plosive/stop) followed by fricative (i.e., partial vocal tract obstruction) at the same location. Examples are /ch/ and /j/.

• Nasal: Air is allowed to pass freely through the nasal cavity. Examples are /m/, /n/, and /ng/.

• Substitution: when one sound is replaced by another

• Omission: when a sound is omitted from a word altogether

• Distortion: when sound is not produced appropriately but is still understood

Background

Published studies show a tendency for individuals with Angle Class I occlusions to rate better with regard to speech as compared with those individuals with malocclusions.³⁷ A review of the literature shows a significant association between misarticulation in speech and Angle Class II malocclusion (Fig. 8-10), Angle Class III malocclusion (Fig. 8-11), and anterior open-bite malocclusion (Fig. 8-12).^39,43,53,54 Studies that evaluate speech articulation in individuals with jaw deformity and malocclusion confirm that as many as 90% of affected individuals have significant misarticulation errors. Several published studies report articulation errors among all jaw deformity patients analyzed.^39,47,53

The jaw deformity patterns that are most frequently associated with significant articulation errors include those with 1) Angle Class II open-bite malocclusion in association with vertical maxillary excess and mandibular deficiency (i.e., the long face growth pattern; see Chapter 21) and 2) Angle Class III negative overjet malocclusion in association with maxillary deficiency and relative mandibular excess (see Chapter 20).^46,61,157 There were less articulation errors found in patients with Angle Class II primary mandibular deficiency malocclusions (see Chapter 19) and in patients with conditions that involve jaw asymmetry without significant malocclusion (i.e., mild hemifacial microsomia; see Chapter 28).⁶⁷ Voice disorders were more frequently seen with closed-bite malocclusion as compared with open-bite malocclusion. Closed-bite jaw deformities are generally associated with adequate overjet and often with a deep overbite (i.e., the short face growth pattern; see Chapter 23).⁵⁰

Patients with Class III skeletal patterns show distinct differences with regard to the consonant fricatives (/f/ and /s/) as compared with normal controls.⁷³ Distortion type speech errors are also frequently associated with this type of malocclusion. This is especially true for patients with combined acoustic and visual errors. The speech sounds that are most commonly affected in the presence of malocclusion are sibilant sounds and bilabial (i.e., upper lip to lower lip) sounds. Errors in bilabial sounds are generally found in individuals with wide lip separation, such as those with maxillary deficiency in combination with mandibular excess or long face growth patterns (i.e., vertical maxillary excess and mandibular deficiency).⁸⁷

Class II mandibular retrusion with excess overjet is likely to produce significant bilabial errors (see Fig. 8-10). Patients with Class II mandibular retrognathia also frequently show misarticulation errors (e.g., with the sound /r/). It is known that individuals with mild to moderate Class II mandibular retrusion are frequently able to adapt by posturing their lower jaw forward (i.e., by having a dual bite) to maintain control of their speech. This compensatory jaw position mechanism tends to break down with rapid speech or when the individual is otherwise fatigued.¹³⁰ As a result of the inherent anatomic barriers, it is not possible for patients with maxillary deficiencies or mandibular excesses with significant negative overjet to posture their lower jaw posteriorly as a method of speech compensation (see Fig. 8-11).¹⁴⁷ This makes the production of the /s/ sound difficult for most individuals with Class III malocclusions.¹³³

Published reports indicate that, for a majority of the individuals studied, the orthodontic and surgical correction of the baseline jaw deformity and malocclusion either eliminates or dramatically reduces articulation errors.95,97,106,107,113,127,146 A minority of the study patients report little change and occasionally speech deterioration. This lack of success in some patients is most likely attributable to 1) initial errors in dental or jaw diagnosis; 2) the incomplete initial correction of the dental or jaw deformity 3) or long-term skeletal or dental relapse with a return of the abnormal dental or jaw position. The inability of an individual with normal neuromotor ability to favorably adapt to the corrected dental and jaw relationships is not the most common reason for a lack of speech improvement. Nevertheless, some individuals will be in need of speech articulation retraining after corrective surgery and orthodontics.

Unfortunately, many of the published studies that set out to evaluate speech aspects after the orthodontic and surgical correction of the initial jaw deformity or malocclusion include too few subjects, have inadequate controls, mix varied patterns of dental and jaw deformities, and lack a standardization of the sampling times before and after treatment.* Some of the published studies seem to lack an understanding of the expected postoperative convalescence, during which short-term speech disability is to be expected. Definitive speech evaluation should occur after adequate healing (i.e., 3 to 6 months) and with documentation of the level of success of the correction of the jaw deformity and malocclusion. As a result of these study shortcomings, there is a need for the further investigation of the speech effects of jaw and dental corrections with 1) larger samples of homogenous patterns of jaw deformity and malocclusion 2) standardized treatment protocols 3) the confirmation of the actual correction of jaw dysmorphology and malocclusion 4) the setting of agreed-upon speech sampling parameters 5) interobserver and intraobserver error testing of speech evaluations and 6) appropriate statistical analysis.

Cause and Effect Relationships

If the upper and lower lips cannot easily close together—as is frequently observed in patients with Angle Class III negative overjet skeletal patterns (e.g., maxillary deficiency with relative mandibular excess; see Fig. 8-11) or in those with classic long face growth patterns with Class II anterior open-bite malocclusion (e.g., maxillary vertical excess with mandibular deficiency; see Fig. 8-12)—then bilabial sounds (e.g., words such as pill, baby, and man) cannot be normally formed.^{55,95,97,104,136} These sounds will then be attempted through labiodental articulation. If the lower lip cannot contact the upper incisors (e.g., long face growth pattern with Class II anterior open-bite malocclusion or maxillary deficiency with mandibular excess negative overjet), then labiodental sounds (e.g., words such as five and vein) will be affected. Compensation will be attempted with bilabial sounds. If the tongue has difficulty reaching the lingual alveolar ridge of the maxilla (e.g., with moderate to severe Class II mandibular retrognathia), if the airstream cannot be correctly directed to the edges of the incisors (e.g., with an anterior open bite), or if the tongue is too far from the anterior aspect of the lower jaw (e.g., with Class III mandibular excess), then sibilant sounds (e.g., words such as sun, zoo, ship, chair, judge, and measure) will be affected (see Fig. 8-10).

Interestingly, from a speech perspective, some individuals are able to adapt to their dental or jaw defects more effectively than others. The individual’s ability to alter the airflow over the incisors or through other articulation points is necessary to effectively compensate for anatomic variations in the teeth and jaws. Marked deformities such as severe Class III maxillary deficiency (see Fig. 8-11), severe long face growth pattern (i.e., anterior open bite with mentalis strain; see Fig. 8-12), and severe Class II mandibular retrognathia with the inability to posture the jaw forward (see Fig. 8-10) are examples of situations in which compensation is not possible and speech articulation is noticeably affected. With successful orthodontics and jaw surgery, improved positioning of the teeth, jaws, lips, tongue, and soft palate results in ease of articulation to accomplish effective speech.^{28,74,126,131,137}

It is not surprising that vowel sounds are less frequently disturbed by a jaw disproportion or malocclusion. Physiologically, the major difference between vowel sounds and consonant sounds is that consonant sounds require significant constriction of the airflow within the vocal tract, whereas vowel sounds are formed by the tongue being positioned to only partially constrict the airflow.¹⁴³ Therefore, consonant sounds are more dependent on an exact positioning of the teeth with respect to each other and the lips with respect to each other (i.e., complete valve closure). Consonant sounds are more affected by jaw deformities such as Class III maxillary deficiency; long face anterior open bite; and severe Class II mandibular retrusion. These abnormal skeletal and occlusal patterns significantly interfere with the production of speech sounds. However, each individual’s speech system has variable adaptive ability. The adaptability primarily comes from the stretching of the lips (i.e., mentalis strain); the stretching of the tongue to extended positions; the posturing of the lower jaw forward (i.e., centric relation to the centric occlusal slide); and the ability to alter the airflow force across the valves and sphincters. The ability of an individual to control these factors is also dependent on the speed of speech and the amount and length of continuous speech required.

Effects on Speech Articulation: Review of the Literature

A study by Witzel and colleagues examined the articulation of 41 individuals before and after orthognathic surgery that was carried out to improve facial aesthetics and to correct the occlusion.¹⁵⁰ The investigators found a direct relationship between the pretreatment degree of mandibular retrognathia and the confirmed speech articulation errors. Twenty-two of 29 (76%) of the study patients had documented articulation errors before surgery; these included errors in sibilant production, labiodental sounds, and bilabial sounds. After surgery, significant improvement in the mean total articulation score for each patient was documented. There was also significant improvement in the sibilant sounds for all groups and in the mean bilabial scores of patients with mandibular retrognathia. Individuals with a Class III skeletal pattern and significant negative overjet (e.g., maxillary deficiency with relative mandibular excess) achieved the maximum improvement in labiodental scores after successful orthodontic and surgical correction.

Ruscello and colleagues studied the speech characteristics of 20 individuals who were scheduled to undergo orthognathic surgery for the correction of a variety of dentofacial deformities.106,107 They underwent speech evaluation before and at intervals for up to 6 months after surgery. Speech assessment at each interval included the Templin-Darley Screening Test of Articulation, a 60-item nonsense syllable task, the Deep Test of Articulation, and the Rainbow Passage. Sixty percent of the patients with jaw deformities demonstrated preoperative articulation errors. The majority of those who were exhibiting preoperative articulation errors had documented improvements after surgery. None of the patients experienced a deterioration in their articulation after surgery at the close of the study.

Kummer and colleagues studied 16 skeletal Class III patients before and after Le Fort I maxillary advancement.⁷¹ Seven of the 16 study patients were adolescents with repaired cleft lip and palate. Each patient underwent preoperative and postoperative speech evaluations and a multi-view videofluoroscopic speech study. Patients were evaluated before surgery as well as 3 and 6 months after surgery. The Templin-Darley Screening Test of Articulation was given, and articulation, resonance, and nasal emission were judged at each time interval. Eleven of 16 patients (69%) demonstrated articulation errors before surgery. After surgery, 7 of these 11 (64%) patients (4 without clefts and 3 with clefts) showed a decrease in the number of misarticulation speech sounds. None of the patients showed deteriorations in articulation after surgery.

Vallino studied the articulation, voice, resonance, hearing sensitivity, and middle-ear function of 34 individuals before and at intervals (i.e., at 3, 6, 9, and 12 months) after they underwent orthognathic surgery.¹²⁹ Thirty of the 34 patients (88%) exhibited articulation errors before surgery. The most frequent sibilant errors were /s/ and /z/, followed by /j/, /zh/, /ch/, and /sh/. The errors were predominantly distortions of both the visual and acoustic types. After surgery, articulation generally improved spontaneously, without the need for speech training or intervention. Most of the preoperative articulation errors were eliminated by 3 months after surgery. In a minority of the study patients, a gradual decline in some of these improvements was measured at 12 months after surgery. This could be explained by either a relapse of the initial satisfactory occlusion and jaw correction or a limited sustained adaptation of speech ability in some individuals. Interestingly, voice, resonance, and hearing sensitivity were not altered by the surgeries that were carried out.

Xue and colleagues carried out a study to compare vocal tract configuration in males with skeletal Class III malocclusion (n = 8) with that of their normally developed Class I counterparts (n = 8).¹⁵⁷ The goal of these researchers was to investigate the concomitant acoustic changes caused by any alterations in the vocal tract configuration that were identified. The findings of the study confirmed that young adolescents with Class III malocclusion had different vocal tract configurations than their counterparts with normal occlusion. The differences occurred in the oral cavity only. The individuals with Class III malocclusion had significantly longer oral length and larger oral volume than their counterparts in the control group. They surmised that the Class III dentofacial deformity restricted lip protrusion during the production of /u/, thereby contributing to the significantly higher resonating frequency (first formant or F1) of /u/ as compared with that of normal controls.

A review of these studies indicate that a majority of individuals who present with moderate or severe jaw deformity and malocclusion will demonstrate articulation errors during speech. The pattern of jaw deformity (i.e., Class II, Class III, open bite, or long face) will predict the pattern of specific articulation errors. Some individuals will have a greater ability to adapt to their dentofacial deformity to achieve relatively normal articulation.

Distortions are the most frequently reported errors, which occur in association with malpositioning of the jaws and teeth. They are of more concern than substitutions or omissions. Individuals will attempt to adapt, but their speech production will not always be within acceptable phonetic boundaries. The most frequent speech sound errors are of the /s/ speech sounds, which are sibilants produced in the alveolar part of the palate with the tongue resting in this region. This type of sibilant distortion error can occur with a spectrum of jaw deformities (e.g., mandibular retrognathic Class II).

In general, individuals who present with articulation errors caused by dentofacial deformity with malocclusion are expected to achieve improved speech function after successful jaw surgery and orthodontics. This assumes that the individual articulators are placed in sufficient proximity to each other. Published studies indicate that 80% to 90% of individuals will find positive improvement in their articulation after the vocal organs are correctly positioned. Interestingly, approximately 10% of individuals are found to be either unchanged or to show some negative effects in speech articulation after jaw surgery. Possible explanations for this small failure rate include errors in jaw or dental diagnoses; unsatisfactory surgical or dental execution; skeletal or dental relapse; effects of neurosensory deterioration; or the inability of the individual to adapt over the long term.

Effects on Velopharyngeal Function: Review of the Literature

Velopharyngeal insufficiency (VPI) is the hallmark sign of the negative speech effects among individuals who are born with cleft palates.7,12,22,52,76,91 The basic etiology of VPI in the repaired or unrepaired cleft palate is dysfunction of the soft palate (Fig. 8-13).^{13,19,20,51,101,111} The muscular anatomy that is affected by clefting includes both the elevators of the soft palate (i.e., the musculus uvulus and the levator veli palatini) and the antagonists to the elevators (i.e., the palatoglossus and the palatopharyngeus).^{56,69,70,116–118,145,160} VPI involves the inadequate closure of the velum to the pharyngeal walls while speaking.^{78,108,141,142} VPI results in increased nasal air escape with increased nasal resonance that can be heard.^72,88,159 Resonance disorders include both hypernasality and hyponasality.⁷⁷ When there is improper control of airflow across the velopharyngeal (VP) sphincter, hypernasality can occur, with increased nasal resonance occurring during the production of vowel sounds.^84,153,154 Hyponasality is defined as a reduction in normal nasal resonance as a result of the blockage of airflow within the nasal cavity.^92,104 A review of the literature is helpful to better understand the effects of Le Fort I osteotomy with advancement on VP function.*

In 1969, Jabaley and Edgerton were the first to report about the potential for changes in the spatial relationship of the soft palate to the pharyngeal wall as a result of maxillary Le Fort I advancement.⁶³ They described an 18-year-old patient without clefting who underwent a Le Fort I osteotomy with advancement. They stated that there was “no adverse alteration of velopharyngeal function accompanying the maxillary advancement.”⁶³

In 1976, Schwarz and Gruner reported about 40 patients who were undergoing Le Fort I osteotomy with repositioning (31 out of 40 with repaired cleft palate).¹¹³ The authors concluded that the “subjective evaluation of velopharyngeal function and nasality in the cleft palate patients showed no relationship between the degree of hypernasality before or after the Le Fort I advancement.”¹¹³

Witzel and Munro discussed a 16-year-old patient with a repaired unilateral cleft lip and palate who presented to them with maxillary hypoplasia and malocclusion.¹⁴⁹ Before surgery, this patient’s VP valving mechanism showed only touch closure of the soft palate against the posterior pharyngeal wall. Two months after Le Fort I osteotomy (10 mm of advancement and 4 mm of vertical lengthening), his speech evaluation revealed marked hypernasality throughout connected discourse. The authors concluded that “maxillary advancement may have a disastrous effect on the velopharyngeal valving mechanism.”¹⁴⁹ They recommended that “all patients undergoing this procedure should have detailed clinical investigation of speech and velopharyngeal function pre- and postoperatively.”¹⁴⁹

Epker and Wolford observed that adolescent patients with repaired clefts, maxillary deficiency, and preoperative VPI became worse after Le Fort I advancement.²⁹ The authors stated that individuals with only borderline VP closure may demonstrate notable VPI after maxillary osteotomy, particularly if the advancement exceeds 10 mm. Bralley and Schoeny reported about a 19-year-old patient with a submucous cleft palate and maxillary deficiency who showed no change in nasality after Le Fort I advancement.⁹ Schendel and colleagues evaluated 21 patients without clefts before and after maxillary Le Fort I osteotomy to assess VP closure.¹¹⁰ They did this through speech evaluation, lateral cephalometric radiography, and nasopharyngoscopy, and they found no change in VP competence after Le Fort I advancement.

Witzel described a sample of 41 patients without cleft palate and 50 patients with repaired cleft palate (bilateral, unilateral, or isolated) who underwent Le Fort I maxillary advancement.¹⁵² The results indicated that patients without cleft palate have a very low risk of deterioration of VP function. Patients with a repaired cleft palate who had adequate VP function before Le Fort I advancement were also at lower risk. However, 11 of 15 of the study patients with a repaired cleft palate and a preoperative rating of borderline VP closure acquired surgically induced symptomatic VPI after Le Fort I advancement. Patients who were considered to have inadequate VP closure before surgery remained so after surgery. For most patients, the extent of preoperative competence of the VP sphincter before Le Fort I advancement predicted the competence of the VP sphincter after surgery (as documented by videofluoroscopy and nasoendoscopy).

Kummer and colleagues reported on VP function in two different patient groups: those with repaired clefts and those without clefts who underwent maxillary Le Fort I advancement with or without vertical change.⁷¹ The measured change in VP function was not clinically significant. They concluded that “Le Fort I maxillary osteotomy has a negligible effect on velopharyngeal function in both cleft and non-cleft cases.”⁷¹

Vallino discussed 34 patients without clefts before and at intervals after orthognathic surgery that included Le Fort I osteotomy.¹²⁹ The VP port area was measured in the study patients before and at intervals (i.e., 3, 6, 9, and 12 months) after Le Fort I osteotomy. The estimation of the size of the VP port area was obtained with the pressure-flow technique described by Warren and Dubois.¹³⁹ All study patients demonstrated VP port areas that measured between 0 and 0.49 cm² both before and after surgery across all speech tasks, which indicated adequate VP competence. The author concluded that the Le Fort I osteotomies carried out in patients without clefts did not alter the VP valve or cause hypernasal speech.

Watzke and colleagues evaluated VP function with the use of aerodynamic testing before and at least 1 year after Le Fort I maxillary advancement in 24 adolescents with repaired cleft palates.¹⁴⁴ Five of these patients (23%) demonstrated VP deterioration, whereas another five (23%) showed improvement after Le Fort I advancement. Interestingly, those patients with a pharyngeal flap in place had a higher incidence of improved VP function after surgery. Of the five (23%) that showed VP deterioration, four had adequate VP function and one had borderline VP function preoperatively. Fourteen (46%) of the patients with clefts showed no significant change in VP function as a result of Le Fort I advancement.

Janulewicz and colleagues completed a retrospective study that evaluated VP function in patients with repaired cleft lips and palates (N = 54) who underwent maxillary Le Fort I advancement.⁶⁴ The authors documented a significant deterioration of VP function in many of the patients with clefts after Le Fort I advancement. There was also an increase in hypernasality, which further supported the findings of VP deterioration in a subgroup of the patients with repaired clefts after Le Fort I advancement. The authors also found improvements in hyponasality as compared with in preoperative values, which was attributed to a decrease in nasal airflow obstruction after maxillary advancement.

Velopharyngeal Evaluation Among Individuals with Repaired Cleft Palates and Maxillary Deficiencies Undergoing Le Fort I Advancement

A variety of methods for the assessment of VP function have been described.57,62,86,89,90,93,94,99,100,105,115,119,140,152 A protocol for the evaluation of patients undergoing orthognathic surgery has been advanced by the American Cleft Palate-Craniofacial Association in Parameters for Evaluation and Treatment of Patients with Cleft Lip/Palate or Other Craniofacial Anomalies (American Cleft Palate-Craniofacial Association, Revised edition 2009 www.acpa-cpf.org).

Witzel also developed a protocol for the evaluation of VP function in adolescents and adults after palate repair to anticipate alterations in the VP sphincter after maxillary Le Fort I osteotomy.¹⁵⁴ She recommends a routine speech assessment that includes instrumentation evaluation of VP function, preferably with nasoendoscopy or, as a second choice, videofluoroscopy. After surgery and sufficient time for healing (i.e., 6 to 12 months), a final assessment of articulation and VP function can be carried out. At that time, if VP function is inadequate, definitive management can go forward (e.g., pharyngeal flap surgery or the revision of a flap that is already in place).

Both before and after Le Fort I osteotomy, VP function is rated as adequate, borderline, or inadequate:

Patients without clefting and those with repaired cleft palates who present with maxillary deficiency and adequate preoperative VP closure seem to have enough adaptability in the pharyngeal and soft palate muscles to maintain VP closure after Le Fort I advancement. In general, patients with either a repaired cleft palate or those who have undergone uvulopalatopharyngoplasty and who have only borderline VP closure do not have the same adaptability of the soft palate musculature to achieve valve closure after Le Fort I advancement. Thus, they are at higher risk for the development of clinical VPI. Patients with repaired cleft palates and maxillary deficiency or those with obstructive sleep apnea who have undergone uvulopalatopharyngoplasty and who are considered to have inadequate VP closure before Le Fort I advancement are expected to have the same degree of poor closure after surgery.

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