Palatopharyngeus Research Articles

Pathology of the Palatal Aponeurosis in Cleft Palate

The palatal aponeurosis is a controversial structure, both in terms of its anatomy and its function. This article points out a pathologic finding in the cleft palate condition that has not been previously described.By means of surgical dissections, this study demonstrates in detail that the palatal aponeurosis exists even in cleft palates, but it is disrupted, malpositioned, and folded in two layers.This dissection method has been performed on more than 150 patients with cleft of the hard and soft palate, with or without cleft of the lip and alveolus. At the time of operation, the children were between 6 and 8 months of age.It is possible to dissect the two layers of the palatal aponeurosis, to unfold the aponeurosis, and to form a tough tendinous plane.For a functional physiologic reconstruction of the cleft palate, it is necessary not only to reconstruct the levator veli palatini and palatopharyngeus muscle slings, but also to approximate and suture the fibers of the palatal aponeurosis to the corresponding fibers of the opposite side after unfolding them in a medio-dorso-cranial direction. In this manner, a continuous palatal aponeurosis can be created, which subsequently can serve as a transmitter of the muscle forces.

Pathology of the palatal aponeurosis in cleft palate.

The palatal aponeurosis is a controversial structure, both in terms of its anatomy and its function. This article points out a pathologic finding in the cleft palate condition that has not been previously described. By means of surgical dissections, this study demonstrates in detail that the palatal aponeurosis exists even in cleft palates, but it is disrupted, malpositioned, and folded in two layers. This dissection method has been performed on more than 150 patients with cleft of the hard and soft palate, with or without cleft of the lip and alveolus. At the time of operation, the children were between 6 and 8 months of age. It is possible to dissect the two layers of the palatal aponeurosis, to unfold the aponeurosis, and to form a tough tendinous plane. For a functional physiologic reconstruction of the cleft palate, it is necessary not only to reconstruct the levator veli palatini and palatopharyngeus muscle slings, but also to approximate and suture the fibers of the palatal aponeurosis to the corresponding fibers of the opposite side after unfolding them in a medio-dorso-cranial direction. In this manner, a continuous palatal aponeurosis can be created, which subsequently can serve as a transmitter of the muscle forces.

Effect of bilateral blockade of the pharyngeal branch of the vagus nerve on soft palate function in horses

Abstract Objective To determine the effect of bilateral blockade of the pharyngeal branch of the vagus nerve on soft palate function in horses. Animals 5 Standardbreds. Procedure Peak tracheal inspiratory and expiratory pressures and airflow were measured while horses exercised at the speeds corresponding to 75 and 100% of the speed that resulted in maximal heart rate, with and without pharyngeal branch of the vagus nerve blockade. Respiratory frequency-to-stride frequency coupling ratio was measured by correlating foot fall measurements with respiratory frequency. The pharyngeal branch of the vagus nerve was blocked bilaterally as the nerve coursed through the auditory tube diverticulum (guttural pouch) across the longus capitus muscle. Results Persistent, reversible dorsal displacement of the soft palate (DDSP) occurred in all horses after nerve blockade, and lasted from 1 to 3 hours; normal nasopharyngeal function returned within 3 hours. Compared with control values, peak expiratory tracheal pressure increased (P = 0.001), expiratory impedance increased (P = 0.007), and minute ventilation decreased (P = 0.04). Respiratory frequency-to-stride frequency coupling ratio decreased (P = 0.009) so that horses took 1 breath/stride without the nerve block and, approximately, 1 breath/2 strides with the block. Conclusion DDSP creates flow-limiting expiratory obstruction and may be caused by neuromuscular dysfunction involving the pharyngeal branch of the vagus nerve. It may alter performance by causing expiratory obstruction and by altering breathing strategy in horses. Clinical Relevance A repeatable, reversible model of DDSP exists that allows further study of the disease. Dysfunction of the neuromuscular group, pharyngeal branch of the vagus nerve and palatinus and palatopharyngeus muscles, may be implicated in the pathogenesis of clinical DDSP. (Am J Vet Res 1998;59:504–508)

Histological indications of a progressive snorers disease in an upper airway muscle.

The etiology of upper airway collapsibility in patients with snoring and obstructive sleep apnea (OSA) remains unclear. Local muscular abnormalities, including neurogenic lesions, could be a contributory factor. The aim of this study was to histologically evaluate the hypothesis of a progressive snorers disease. Biopsies of palatopharyngeal muscle were obtained from 21 patients with habitual snoring and different degrees of upper airway obstruction (10 patients with OSA) and 10 nonsnoring control subjects. Morphological abnormalities, including neurogenic signs (e.g., type grouping), were blindly quantified. The degree of abnormality was significantly increased in patients compared with control subjects. The individual score of abnormalities was significantly correlated to the percentage periodic obstructive breathing but not to oxygen desaturation index. Analyses of the individual fiber-size spectra demonstrated a significantly increased number of hypertrophied and/or atrophied fibers in patients compared with controls. The subjects were also divided into three groups according to their type of nocturnal breathing, i.e., nonsnorers, patients with < 20%, and patients with > or = 45% obstructive breathing. These groups correlated significantly with the degree of abnormality and pathological fiber-size spectra. In conclusion, these results support the hypothesis of a progressive local neurogenic lesion, caused by the trauma of snoring, as a possible contributory factor to upper airway collapsibility.

Visualizing dolphin sonar signal generation using high-speed video endoscopy

Determining the site of the delphinid sonar signal generation has eluded cetologists for decades. Activities within the pharyngeal and nasal cavities of two bottlenose dolphins (Tursiops truncatus) were studied during sound production and echolocation. A high-speed dual-camera video system provided synchronized windows for recording two concomitant events: (1) movements visible through an endoscope and (2) oscilloscope traces of acoustic pressure at a hydrophone placed near the animal’s head. Dolphins have two tissue complexes, one located on either side, and just above, the membranous nasal septum [Cranford et al., J. Morph. 228, 223–285 (1996)]. They apparently generate acoustic pulses by pushing air across sets of internal ‘‘lips.’’ The acoustic pulse occurs coincident with one oscillatory cycle of the lips. Changes in the acoustic pulse repetition rate and the vibration cycles of the lips are simultaneous, indicating that their rates and periods are synchronous. No other structures were found to vibrate in synchrony with each acoustic pulse generation event. The palatopharyngeal muscle complex compresses air for the system. These observations settle a long-standing controversy over the site of biosonar signal generation in odontocetes and open a vista of potential avenues for future investigations. [Work supported by the Office of Naval Research.]

Palatopharyngeus has respiratory activity and responds to negative pressure in sleep apnoeics.

The intrinsic tongue muscle, genioglossus, and soft palatal muscles, tensor palatini, levator palatini and palatoglossus, are known to exhibit phasic respiratory activity and to respond reflexly to negative pressure in man, which may be important in the maintenance of upper airway patency. We hypothesized that the palatopharyngeus muscle should also have respiratory activity and increased activity in response to negative upper airway pressure. We have, therefore, examined the palatopharyngeus and the antagonist muscle, levator palatini, in eight awake sleep apnoea patients, using bipolar electromyography during nose- or mouth-breathing in different postures, and with or without application of negative pressure. Overall, palatopharyngeus and levator palatini demonstrated phasic respiratory activity. Palatopharyngeus demonstrated increased activity in the supine compared to erect posture. Analysis by route of respiration showed palatopharyngeus to be more active in the supine posture when nose-breathing compared to mouth-breathing. Graded negative pressure application caused significant increases in palatopharyngeus and levator palatini activity when applied via the mouth. Nasal negative pressure application caused a nonsignificant trend to increasing palatopharyngeus activity with increasing negative pressure compared to a significant increase for levator palatini. We conclude that palatopharyngeus and levator palatini demonstrate respiratory activity and reflex activation in response to negative pressure. Palatopharyngeus may, therefore, have a role as an upper airway dilator. The differential response of palatopharyngeus to oral and nasal negative pressure application may be important in the pathogenesis of sleep apnoea.

Laser-assisted uvulopalatoplasty: description of the technique and pre- and postoperative evaluation of subjective symptoms.

A new surgical approach for treating patients suffering from heavy snoring or obstructive sleep apnoea is introduced. This procedure includes the use of a laser and is called laser-assisted uvulopalatoplasty (LUPP). However, the technique described here is unlike the laser-assisted uvulopalatoplasty (LAUP) as described by Kamami in 1990. LUPP is performed under local anaesthesia and in an out-patient setting. Muscle resection is minimal and includes only the distal part of the uvula muscle and some fibres of the palatopharyngeal muscles. The LUPP procedure and the subjective results in 100 patients who have had LUPP performed are presented.

Patterns of Abnormal Myogenesis in Human Cleft Palates

To test the hypothesis that soft palate muscles are abnormal in cleft palate, we compared soft palate morphogenesis in fetuses with cleft palate (n = 4) to age-matched (n = 3) and nonmatched (n = 1) control specimens. The morphologic status of all soft palate and masticatory structures were classified into one of six stages based on the level of histogenesis. At 54 mm crown-rump length (CRL), the levator veli palatini (L), palatopharyngeus (PP), and palatoglossus (PG) in cleft subjects demonstrated mesenchymal condensation into myoblastic fields, lagging behind the control specimens (97 mm CRL), which displayed definitive fields of myoblasts and myotube formation. In the 175 mm and 225 mm cleft and the 170 mm and 192 mm control specimens, muscular morphology was similar and had reached its postnatal appearance for the tensor veli palatini (175 m only) and L, PP, PG (225 mm only). Muscle fiber directions were, however, disoriented and disorganized, especially close to the medial epithelial edge of the cleft. The levator veli palatini, could not be distinguished as a discrete muscle in the cleft specimens, and what we believed to be the PP and PG seemed "normal" at the level of light microscopy, but malpositioned in a superior direction. This preliminary study demonstrates for the first time that early myogenesis in cleft palates differs from normal.

Patterns of abnormal myogenesis in human cleft palates.

To test the hypothesis that soft palate muscles are abnormal in cleft palate, we compared soft palate morphogenesis in fetuses with cleft palate (n = 4) to age-matched (n = 3) and nonmatched (n = 1) control specimens. The morphologic status of all soft palate and masticatory structures were classified into one of six stages based on the level of histogenesis. At 54 mm crown-rump length (CRL), the levator veli palatini (L), palatopharyngeus (PP), and palatoglossus (PG) in cleft subjects demonstrated mesenchymal condensation into myoblastic fields, lagging behind the control specimens (97 mm CRL), which displayed definitive fields of myoblasts and myotube formation. In the 175 mm and 225 mm cleft and the 170 mm and 192 mm control specimens, muscular morphology was similar and had reached its postnatal appearance for the tensor veli palatini (175 m only) and L, PP, PG (225 mm only). Muscle fiber directions were, however, disoriented and disorganized, especially close to the medial epithelial edge of the cleft. The levator veli palatini, could not be distinguished as a discrete muscle in the cleft specimens, and what we believed to be the PP and PG seemed "normal" at the level of light microscopy, but malpositioned in a superior direction. This preliminary study demonstrates for the first time that early myogenesis in cleft palates differs from normal.

Coordination of velopharyngeal muscle activity during positioning of the soft palate.

The relative contributions of the levator veli palatini, palatoglossus, and palatopharyngeus muscles were assessed relative to a range of positions of the velopharynx during production of the vowels [a] and [i] by four normal adult speakers. The results indicate that velopharyngeal positioning is determined by the relative contributions of the levator veli palatini, palatoglossus, and palatopharyngeus muscles. There was an increase in coefficients of determination (i.e., amount of closure level variability explained) when activity levels of all three muscles are included in the statistical model compared to activity in any one muscle analyzed independently. Both consistent and inconsistent relations among activity levels in the three velopharyngeal muscles studied were observed across speaker and vowel produced.

Neurogenic effects on the palatopharyngeal muscle in patients with obstructive sleep apnoea: a muscle biopsy study.

Muscle biopsies from the palatopharyngeal muscle of eight patients with obstructive sleep apnoea were performed during uvulopalatopharyngoplasty. Control biopsies were performed during tonsillectomy in seven control patients with no history of symptoms suggesting obstructive sleep apnoea. The diagnosis was based on the patient's history and a whole night recording of arterial oxygen saturation and respiration movements. The mean number of oxygen desaturations > or = 4% per sleeping hour was 39 (range 7-80) in patients with obstructive sleep apnoea. In the control patients the occurrence of muscle fibre type and size relation between type I and type II fibres were comparable to what is found in the quadriceps femoris muscle, but the mean size of the fibres was < 25% of what is found in limb muscles. All biopsies from patients with obstructive sleep apnoea showed abnormalities. Atrophy with a fascicular distribution, increased number of angulated atrophic fibres, a twin or multiple peak distribution of the fibre size spectra, and an abnormal distribution of fibre types in many muscle fascicles corresponding to "type grouping" all points to a neurogenic alteration. This neurogenic lesion may be a primary phenomenon or secondary to the trauma of repetitive and prolonged stretching of the pharyngeal structures during apnoeas. A disturbance of the function of the dilating muscles of the upper airway may be important in causing the abnormal airway collapse seen in obstructive sleep apnoea.

片側軟口蓋形成不全の３例

The authors report three cases of unilateral soft palate hypoplasia without any other major malformations.Case 1: A 9-year-old boy had a left velar defect, which consisted of unilateral hypoplasia of the levator palatini, the tensor palatini, palatoglossus, and the palatopharyngeus muscles. He manifested no signs of velopharyngeal incompetence before the age of 7 years. However, mild rhinolalia appeared at 7 years old. No articulatory disorders were found.Case 2: A 3-year-old girl had similar findings on the left side and a hamartoma at the base of the tongue. Velopharyngeal incompetence had not been manifested yet. She is under follow-up.Case 3: A 9-year-old girl had similar findings on the right side. No velopharyngeal incompetence has been manifested.

Neurogenic effects on the palatopharyngeal muscle in patients with obstructive sleep apnoea: a muscle biopsy study.

Muscle biopsies from the palatopharyngeal muscle of eight patients with obstructive sleep apnoea were performed during uvulopalatopharyngoplasty. Control biopsies were performed during tonsillectomy in seven control patients with no history of symptoms suggesting obstructive sleep apnoea. The diagnosis was based on the patient's history and a whole night recording of arterial oxygen saturation and respiration movements. The mean number of oxygen desaturations > or = 4% per sleeping hour was 39 (range 7-80) in patients with obstructive sleep apnoea. In the control patients the occurrence of muscle fibre type and size relation between type I and type II fibres were comparable to what is found in the quadriceps femoris muscle, but the mean size of the fibres was < 25% of what is found in limb muscles. All biopsies from patients with obstructive sleep apnoea showed abnormalities. Atrophy with a fascicular distribution, increased number of angulated atrophic fibres, a twin or multiple peak distribution of the fibre size spectra, and an abnormal distribution of fibre types in many muscle fascicles corresponding to "type grouping" all points to a neurogenic alteration. This neurogenic lesion may be a primary phenomenon or secondary to the trauma of repetitive and prolonged stretching of the pharyngeal structures during apnoeas. A disturbance of the function of the dilating muscles of the upper airway may be important in causing the abnormal airway collapse seen in obstructive sleep apnoea.

Patterns of Abnormal Myogenesis in Human Cleft Palates

To test the hypothesis that soft palate muscles are abnormal in cleft palate, we compared soft palate morphogenesis in fetuses with cleft palate (n=4) to age-matched (n=3) and nonmatched (n=1) control specimens. The morphologic status of all soft palate and masticatory structures were classified into one of six stages based on the level of histogenesis. At 54 mm crown-rump length (CRL), the levator vell palatini (L), palatopharyngeus (PP), and palatoglossus (PG) in cleft subjects demonstrated mesenchymal condensation into myoblastic fields, lagging behind the control specimens (97 mm CRL), which displayed definitive fields of myoblasts and myotube formation. In the 175 mm and 225 mm cleft and the 170 mm and 192 mm control specimens, muscular morphology was similar and had reached its postnatal appearance for the tensor veli palatini (175 m only) and L, PP, PG (225 mm only). Muscle fiber directions were, however, disoriented and disorganized, especially close to the medial epithelial edge of the cleft. The levator veli palatini, could not be distinguished as a discrete muscle in the cleft specimens, and what we believed to be the PP and PG seemed “normal” at the level of light microscopy, but malpositioned in a superior direction. This preliminary study demonstrates for the first time that early myogenesis in cleft palates differs from normal.

Unilateral hypoplasia of the soft palate

A case of unilateral hypoplasia of the soft palate with aplasia of the palatoglossus and palatopharyngeus muscles in a child of one year of age and a modification of an existing technique for the repair of hypoplasia of the soft palate is presented.

Refinements of intravelar veloplasty.

Between 1981 and 1985 115 children from 11 to 20 months of age underwent palatal reconstruction with an intravelar veloplasty. The operative technique is described with, in our opinion, some important refinements. These relatively limited surgical procedures consist of careful separation of the muscles from the posterior edge of the palatal bone, posterior movement of the muscles, nasal layer closure, reconstruction not only of the levator muscle, but also of the palatopharyngeus and uvularis muscle. A preliminary evaluation of 28 children who ranged in age from two to five years showed high rates of intelligible speech, normal articulation and resonance.

Phonosurgery (combined approach palatopharyngoplasty--CAP).

A new surgical approach (CAP--Combined Approach Palatopharyngoplasty) is described for the correction of speech defects in palatopharyngeal incompetence. In palatopharyngeal incompetence the spatial relationships between the various components of the palatopharyngeal mechanism are disturbed. This combined approach brings about near-normal relationships (viz. intrapalatal and palatopharyngeal), as well as providing a competent palatopharyngeal sphincter, thus offering a remarkable improvement in speech. The operation comprises a two-stage procedure: stage I:--(a) submucosal transplantation of the levator palati muscles posteriorly to the region of the uvula and (b) 'crossed' palatopharyngoplasty; isolation of the palatopharyngeus muscles (posterior pillars) with their bases superiorly placed at their junctions with the soft palate, and transplantation of the lower free ends into the transverse retropharyngeal musculo-fascial pockets on the opposite side, the flaps thus crossing each other in the midline: stage II:--'check-valve' palatopharyngoplasty; elevation of a superiorly based posterior pharyngeal flap with anastomosis to the soft palate. The dynamics which are responsible for the improvement in speech are: (a) elevation of the palate to about the level of the atlas; (b) statico-dynamic constriction of the pharyngeal phonetic passage at the following levels: (i) at the newly placed levator eminence, (ii) at the newly constructed dynamic sphincter situated between the above-mentioned crossing and the free margin of the soft palate, and (iii) at the junction of the check-valve flap with the posterior pharyngeal wall; (c) increase in the effective length of the soft palate. The phonetic stream is prevented from entering the nasal chambers during the utterance of non-nasal pressure sounds by the newly constructed three-tier protective mechanism. This is identical with, but a 'reverse' representation of, the normal three-tier protective mechanism of the larynx, which prevents food from entering the tracheo-broncheal tree during deglutition. The operation has been performed in eight cases and the results are satisfactory, in so far as improvement in the quality of speech is better than that observed following other operations. In conclusion, the principles of phonosurgery may well be diagrammatically represented in Fig. 7.

咽頭弁手術による鼻咽腔機能と形態の変化に関する研究

A follow-up research, before and during 2 years after pharyngeal flap surgery, of 30 patients was undertaken in order to investigate the auditory changes, nasal air escape and the roentgenographical changes in velopharyngeal function and shape. The results were as follows ; 1. Both nasality and nasal air escape disappeared during about the same period. 50% of the subjects showed disappearance of nasality and nasal air escape at 2 months after operation, and 83.7% of them showed disappearance within a year after operation. All of the other subjects, with the exception of those who could not accept the follow-up research, also showed disappearance of nasality and nasal air escape within 18 months after operation, indicating remarkable improvement. The effectiveness of pharyngeal flap surgery was reaffirmed from this. 2. After the pharyngeal flap surgery, the velar length showed an increase but the tendency to constriction was not recognized. However, the velar elevational angle on phonation showed relatively lower degree until 3 months after operation than before operation. 3. The greatest change in the velopharyngeal function and shape, before and after pharyngeal flap surgery, was the reduction of the minimal velopharyngeal distance at the time of rest and phonation. 4. Within a month after operation, the depth of the posterior pharyngeal wall revealed the maximum constriction (forward protrusion) in the area of middle and lower pharynx, and later, within 6 months after operation, revealed the tendency to returning to the pre-operative shape. Coincident with this period of extention, nasality, nasal air escape and "snore" after operation disappeared or reduced, though the upper pharynx above the level of the palatal plane showed no change or a tendency to constriction, which was supposed to be the change caused by existence and growth of adenoid. 5. Pharyngeal flap base showed a tendency to descending until 9 months after operation. The average distance of descending was about 5 mm. The area of flap attached to soft palate also showed much the same tendency to descending until 6 months after operation. 6. Contrary to the descending of the flap base, the elevational mobility of the flap base showed an increase until 9 months after operation, but no striking change was recognized after that. This elevational movement was closely connected with the velar elevation. The coopertive movement between M. constrictor pharyngis superior and M. levator veli palatini was considered with much importance. 7. It seems proper that judgement of results after operation should be done later than 9 months after operation, since, as mentioned above, the velopharyngeal function and shape revealed considerable changes until 9 months after pharyngeal flap surgery. These changes in function and shape are considered to be affected most by the scar tissue. 8. Analysis of the manner of velopharyngeal closure and the improvement after pharyngeal flap surgery showed that pharyngeal flap base should be placed at the level of the palatal plane and in the area containing Passavant's ridge, and that it is difficult to expect successful results if the pharyngeal flap base is placed above the palatal plane. 9. Age, speech training, function of velopharyngeal muscle and shape of upper pharynx were pointed out as factors on improvement of results after pharyngeal flap surgery. In other words, successful results will be obtained regardless of surgical technique in younger patients with pre-operative speech training, Passavant's ridge as well as fairly good function of palatopharyngeal muscle, smaller palatopharyngeal distance, parallel type of nasal air escape and smaller velopharyngeal area as well as "non box-shaped" upper pharynx.

An Electromyographic Study of Velopharyngeal Function in Speech

Electromyographic (EMG) recordings were obtained from the levator palatini, superior pharyngeal constrictor, middle pharyngeal constrictor, palatoglossus, and palatopharyngeus muscles of three talkers of American English. Bipolar hooked-wire electrodes were used. Each subject read nonsense words composed of three vowels (/i, a, u/), six stop consonants (/p, b, t, d, k, g/), and two nasal consonants (/m, n/) to form various stop-nasal and nasal-stop contrasts. Multiple repetitions of each utterance type were recorded and subsequently processed by computer. The levator palatini was found to be the primary muscle of velopharyngeal closure for each of the subjects. The palatopharyngeus also showed consistent oralization activity for each of the subjects, although the activity of this muscle was strongly affected by vowel environment. Two subjects showed pharyngeal constrictor muscle activity related to oral articulation, but pharyngeal constrictor activity for the third subject was related to vowel quality. Nasal articulation was accomplished by suppression of oral articulation for each subject. Vowel quality affected the strength of EMG signals for lateral and posterior pharyngeal wall muscles. In those cases where activity was different for the three vowels, activity was greatest for /a/.

Disorders of Pharyngeal and Upper Esophageal Sphincter Motor Function

Buccopharyngeal motor disorders causing difficulties in swallowing are frequently encountered in clinical medicine. Affected patients manifest distinctive clinical features and pose special problems in their management. We summarize the pathogenesis, consequences, evaluation, and treatment of the motor disorders of buccopharyngeal swallowing. We also describe some selected clinical conditions that are associated with buccopharyngeal dysphagia. <h3>MALFUNCTION OF DIFFERENT COMPONENTS OF BUCCOPHARYNGEAL SWALLOWING</h3><h3>Disorders of Buccal Phase of Swallowing</h3> In the initial stages, before active deglutition, the oral cavity prepares the bolus for deglutition. The oral cavity makes room for the bolus by initial depression and grooving of the tongue, elevation of soft palate, and relaxation of the palatoglossus and palatopharyngeus muscles.¹The bolus is then pumped into the oropharynx by the progressive anteroposterior contractile sequence of the tongue. The oral phase is under voluntary control.^2,3 Weakness of buccal muscles, which are supplied by the seventh cranial nerve, may lead to