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PubMed2001

Unilateral palate paralysis in patients with nasopharyngeal carcinoma: imaging and clinical correlations.

OBJECTIVE: Neck masses, hearing impairment, and blood-tinged nasal discharges are three major clinical manifestations of nasopharyngeal carcinoma (NPC). Because of the relationship between the anatomic structures of the fossa of Rosenmüller and the levator veli palatini muscle, NPC arising in the fossa can invade the levator muscle, limiting movement or causing paralysis of the ipsilateral soft palate. It is well known that NPC originates commonly from the fossa of Rosenmüller. We therefore hypothesize that the clinical signs of unilateral palate paralysis in patients with NPC must be far more common than usually realized. This issue is, as yet, not fully addressed in the literature. STUDY DESIGN: A prospective study of all patients with newly diagnosed NPC. METHODS: Two hundred sixty-four patients with newly diagnosed NPC were studied. Clinical records included the details of their clinical presentations and the results of physical and neurological examinations. The degree of elevation of the soft palate during phonation was carefully evaluated. Magnetic resonance imaging (MRI) of the head and neck region with a particular emphasis on the levator veli palatini muscles was then performed. The degree of paralysis of the palate was correlated with the degree of invasion of the levator muscles by the tumor, as seen with imaging. The incidence of paralysis of the palate in the patients with NPC was also determined. RESULTS: At the time of diagnosis, ipsilateral paralysis of the palate was observed in 137 (52%) of the 264 patients with NPC. The results of imaging indicated that 62% (163 of 264) of the patients had radiological evidence of tumor invasion of the levator muscle. The degree of paralysis of the palate corresponded well to the extent of tumor invasion of the levator muscle. Paralysis of the palate was not evident in 26 patients with early perimuscular infiltration of the levator muscle. CONCLUSION: This study revealed that ipsilateral invasion of the levator veli palatini muscle by NPC is common and typically presents with signs of unilateral palate paralysis. This subtle sign is relatively common in patients with NPC. Consequently, we think palate function should be routinely tested when diagnosing NPC, particularly when the patient has unilateral aural symptoms or a neck lump.

Female↗

PubMed1993

Use of a free conchal cartilage graft for closure of a palatal fistula: an experimental study and clinical application.

In order to establish an operative procedure for the closure of palatal fistulas, the usefulness of free conchal cartilage grafts was confirmed through animal experiments, and a clinical application of this procedure was attempted. In the animal experiment, an oronasal penetrating fistula 10 mm in diameter was formed in the hard palate of 33 rabbits. One month later, the size of the palatal fistula decreased to 2 to 3 mm in diameter in all the rabbits. These rabbits were divided into two groups. Group 1 (n = 8) was used as a control group. In group 2 (n = 25), the palatal fistula was closed by an autograft of conchal cartilage, and the conchal cartilage graft site was observed for a period of 16 weeks. In 75 percent (6 of 8) of group 1, the palatal fistula persisted even after 1 year, but in 96 percent (24 of 25) of group 2, the palatal fistula was closed. The palatal fistula closure procedure using a conchal cartilage graft was found to be remarkably effective (chi 2c = 10.9, p < 0.001). In the clinical application, a fistula closure procedure with the use of conchal cartilage grafts was attempted in 24 patients with palatal fistulas. The procedure was modified into three types according to the size of the palatal fistula. For type I (diameter less than 2 mm) a conchal cartilage graft was created as in the animal experiment. For type II (2 to 5 mm in diameter), a palatal fistula closure procedure was used employing both a small hinge flap and a conchal cartilage graft.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1993

A comparative study of facial growth following lip and palate repair performed in sequence and simultaneously: an experimental study in beagles.

This study was designed to assess the effects of the commonly accepted sequence of cleft lip and palate repair on subsequent maxillofacial growth and to compare these effects with those resulting from simultaneous lip and palate repair. Using 62 eight-week-old normal beagles, we tested the hypothesis that sequential repair (lip first, palate second) of surgically induced lip and palate defects is less detrimental to maxillofacial growth than simultaneous repair of both surgically created defects. Animals were assigned to one of four groups: two control groups (unoperated and unrepaired) and two experimental groups. Defects simulating cleft of the lip, alveolus, and palate were surgically created in the unrepaired controls and in the experimental animals. In one experimental group, the lip and palate defects were repaired immediately and simultaneously. In the other experimental group--simulating current clinical practice--the lip defect was repaired first at the time that it was created, while closure of the palatal defect was delayed 4 weeks. After the animals were killed at 36 weeks of age, 11 maxillary variables were measured directly from cleaned skulls and analyzed by using univariate and multivariate techniques. Animals that had lip and palate defects closed in sequence had less severe maxillofacial aberrations than animals with simultaneously closed defects. Sequential closure of the defects also had identifiable effects on maxillofacial form. The growth aberrations observed among animals with sequential closure, however, are primarily attributable to surgical creation of the defects and not to the surgical repair. Delaying palate repair is less traumatic to the subsequent growth of the maxillary complex than simultaneous repair of lip and palate defects.

Animals↗

PubMed2006

Cleft lip and palate in mice treated with 2,3,7,8-tetrachlorodibenzo-p-dioxin: a morphological in vivo study.

It is well-known that TCDD (2,3,7,8, tetrachloridedibenzo-p-dioxin) induces cleft palates (CPs) in pregnant C57BL mice. However, it is unclear if TCDD is a possible teratogen for cleft lip. We examined maxillofacial malformations including cleft lip in three animal strains: A/J mice, C57BL/6J mice and ICR mice. The A/J mouse develops cleft lip and palate spontaneously at a 5-10% rate. TCDD was administered in olive oil on gestation day (GD) 12.5 with gastric tubes at 10 microg/kg, 20 microg/kg, or 40 microg/kg to examine the dose-response, and on a single day from GD 8.5-14.5 to examine the timing effects of TCDD administration on lip and palate formation. Furthermore, the palatal shelf movements during GD 8.5-14.5 were observed with a stereoscopic microscope. All embryos had cleft palates when the TCDD was administered just before palatogenesis (GD11.5-GD12.5). With respect to the TCDD effects, there were large differences among the strains. In the A/J mice, the difference between a lethal dose and a dose that could induce a cleft palate was close. Cleft lips were not induced, even when the TCDD was given just before labiogenesis. Morphologically, both palatal shelves contacted perfectly along their lengths, but separated and formed cleft palates. In conclusion, TCDD is a strong inducer of cleft palates, and interferes with the fusion phase of the secondary palate, but has no effect on the lip.

Abnormalities, Drug-Induced↗

PubMed1993

Length of the cervical spine as a factor in the etiology of cleft palate.

The length of the cervical spine in a series of 206 adult males with cleft lip and/or palate and 50 normal controls was measured. The patients were divided into five subgroups according to the type and extent of the cleft. The shortening of the spine was most marked in bilateral cleft lip and palate patients (complete), less marked in unilateral cleft lip and palate patients, and was slight in isolated cleft palate patients. Complete isolated cleft palate and cleft lip was not associated with a shortening of the spine. A shortening of the cervical spine in less extensive types of isolated cleft palate was suggestive of the participation of the spine in their development, while in cleft lip and palate a simultaneous exposure to a teratogenic agent or any other developmental error during early stages of embryogenesis could explain the concomitant occurrence of spine anomalies. Patients with cleft lip and palate associated with a short spine also had a shorter mandibular ramus, which could be suggestive of simultaneous damage to both structures during morphogenesis. This relationship was not demonstrated in isolated cleft palate that developed in later stages of embryogenesis. In these cases a short spine itself could not have impaired the growth potential of the mandible, yet it could have mechanically induced the development of cleft palate. These observations are in agreement with the present state of knowledge on the development of orofacial clefts as shown in experimental animals.

Adult↗

PubMed2002

Simultaneous cortex bone plate graft with particulate marrow and cancellous bone for reliable closure of palatal fistulae associated with cleft deformities.

OBJECTIVE: The purpose of this study was to evaluate the effectiveness of simultaneous cortex bone plate (CBP) graft with particulate marrow and cancellous bone (PMCB) graft for reliable closure of palatal fistulae associated with alveolar clefts. DESIGN: Following standard secondary bone graft preparation of the cleft site, CBP harvested from the medial iliac crest was inserted into the palatal deficiency. This was followed by suturing the palatal mucosa. PMCB was then packed between the cortical bone and the reconstructed nasal floor. SETTING: Ten consecutive patients with palatal fistula were operated on at Tokyo Medical and Dental University Hospital from 1998 to 2000. Primary palatal repair was performed in 7 out of 10 patients at our center and in 3 out of 10 patients at other hospitals. PATIENTS: Ten patients (6 boys and men, 4 girls and women) with a palatal fistula associated with an alveolar cleft were studied. Ages ranged from 12 to 26 years. INTERVENTIONS: All patients underwent simultaneous CBP graft with PMCB graft for closure of palatal fistula under general anesthesia. RESULTS: Complete closure of palatal fistulae were obtained in 8 out of 10 cases. A very small asymptomatic fistula remained in one patient. Total necrosis of the labial flap with a residual palatal fistula occurred in one patient. CONCLUSIONS: Simultaneous CBP graft with PMCB graft could be more reliable than PMCB alone for closure of a cleft associated palatal fistula.

Adolescent↗

PubMed1979

Taste acuity of the human palate. II. Studies with electrogustometry on subjects in different age groups.

The electrical taste acuity on the hard and soft palate and the tip of the tongue was determined in 140 subjects aged 13-81 years using an electrogustometer constructed for the study. The possible influence of several variables including age, sex, wearing of a full upper denture, smoking as well as medical and social factors on the threshold values was also studied. Taste perception was demonstrated on the soft palate and on an area of the hard palate close to the junction of the hard and soft palate in most subjects. No perception of the electrical taste was found in eleven subjects (8%) on either the hard or the soft palate and in an additional 33 subjects (24%) on the hard palate alone and 2 subjects (1%) on the soft palate alone. The taste thresholds on the hard palate were very high compared to those on the soft palate and those on the tongue. Older subjects generally had higher thresholds than did younger subjects and the differences were greater for the thresholds on the hard and soft palate than for those on the tongue. No statistically significant differences in threshold values were found between women and men, denture wearers and non-denture wearers or smokers and non-smokers.

Adolescent↗

PubMed1975

The occult submucous cleft palate.

We have studied 41 patients with classic submucous cleft and 32 cases with occult submucous cleft. Both groups have the same anatomic abnormality that leads to velar dysfunction-the insertion of the palate muscles onto the hard palate rather than onto the midline soft palate raphe. However, the occult submucous cleft palate does not have the classic triad of bifid uvula, hard palate bony notch, and furrow in the midline of the soft palate. Characteristic facial features, cephalmetric x-rays, and cine voice studies can help make a presumptive diagnosis of occult submucous cleft palate. Surgical management includes a diagnostic palate exploration to identify muscle configuration followed by levator muscle sling reconstruction, palate pushback, and pharyngeal flap. Excellent speech results are obtained except with patients having palate paresis.

Abnormalities, Multiple↗

PubMed1976

Cleft palate and congenital palatopharyngeal incompetency in mandibulofacial dysostosis: frequency and problems in treatment.

In a series of 25 cases of mandibulofacial dysostosis, 7 patients had isolated clefts of the palate, 1 had a complete unilateral cleft of the lip and palate, and 8 had congenital palatopharyngeal incompetency (CPI). The CPI appeared in four forms: (a) complete agenesis of the soft palate, (b) foreshortening of the soft palate associated with a submucous defect of the hard palate, (c) submucous defect of the hard palate with adequate palatal length but inadequate elevation in speech, and (d) lack of adequate palatal elevation in the absence of a submucous defect or reduced length of the soft palate. Inadequate velopharyngeal function, whether congenital or subsequent to palatal repair, may be masked by the presence of other speech problems in this syndrome, particularly by the "muffled" voice quality which appears to be associated with an elevated and retracted tongue posture. Both prosthetic and surgical treatment of inadequate velopharyngeal function are complicated in patients with MFD by other structural anomalies, particularly inadequate oral opening and constriction of the airway.

Cleft Palate↗

PubMed2004

[Repair of hard cleft palate with absorbable membranes made by poly-DL-lactic acid: a feasibility study].

OBJECTIVE: To investigate the feasibility and clinical results of applying poly-DL-lactic acid (PDLLA) biomembranes in cleft palate repair. METHODS: 68 cleft palate patients were divided into study group and control group. The traditional surgical method was used to control group to close the soft cleft palate, and the PDLLA biomembrane was used to study group and implanted into the surgical gap between the periosteum and bone at the hard palate, and fixed with suture. The duration, blood loss at operation, post-operative complication, wound healing and recovery were recorded and compared to conventional cleft palate repair. RESULTS: Operations were successfully completed on all 34 patients. Wound healing of soft palate and uvula was uneventful with no incidence of fistula or dehiscence. The primary healing on tissue defect of hard palate occurred in 29 patients, secondary healing occurred in 3 patients, permanent fistula between the oral cavity and the nasal cavity occurred in only one patients, and 3 patients left over fistula on alveolar process. Compared to traditional cleft palate repair, blood loss and incidence of fistula on alveolar process were decreased; the average surgical time was 89.25 minutes and was not prolonged; and there was no significant increase in post-operative complication. CONCLUSION: Hard cleft palate repair with PDLLA biomembranes is safe, simple and practical with good clinical results and is beneficial to minimize the bad influences towards the development and growth for maxilla of cleft palate patients.

Absorbable Implants↗

PubMed1985

Role of neurotransmitters in palate development and teratologic implications.

It is hypothesized that neuropharmacologic agents are more teratogenic to humans. Since many neuropharmacologic agents function through neurotransmitter mechanisms, then neurotransmitters should function to regulate embryonic development. Evidence has been obtained that neurotransmitters do indeed function as biological signals in palate development. It has been shown that palate reorientation is modulated by neurotransmitters with a wide range of diversity, similar to the CNS. Thus serotonin and acetylcholine stimulate and GABA inhibits the reorientation process. Spatial diversity is also observed: serotonin functions at the anterior and acetylcholine at the posterior end, and GABA functions more efficiently at either end in different inbred strains. Many criteria for functioning neurotransmitters have been obtained. Both serotonin and GABA have been measured in the palate and developmental changes observed. Physiologic responses to serotonin have been monitored. Serotonin has been shown to stimulate palate cell motility as well as protein carboxyl methylation and cyclic GMP. The serotonin effects on protein carboxyl methylation and cyclic GMP could function to stimulate palate reorientation by modulating cell contractility and protein secretion. Further support for the hypothesis that neuropharmacologic agents could be teratogenic by perturbation of neurotransmitter mechanisms comes from studying GABA and diazepam. Evidence has been obtained that diazepam induces cleft palate by mimicking GABA in a functional GABAergic system in palate development. A significant finding is that genetic differences in both diazepam teratogenesis and in a GABAergic system have been observed. Comparing the SWV and AJ strains, the SWV mouse showed (1) a greater sensitivity to diazepam-induced cleft palate, (2) a greater sensitivity to GABA and diazepam inhibition of palate reorientation in embryo culture, (3) a greater concentration of palatal GABA and (4) a more efficient GABA uptake system. These results are suggestive that diazepam may be more teratogenic in individuals of both the mouse and human who possess a more developed GABAergic mechanism. If such a result would obtain in the human, these genotypic differences in GABA would probably not influence the individual to a significant degree in most situations, except for the pregnant woman being at high risk when treated with diazepam.

Abnormalities, Drug-Induced↗

PubMed1980

Delayed hard palate repair and speech deficiencies: a cautionary report.

In the management of patients with complete palatal clefts early repair of the soft palate (before 1 year of age) and delayed repair of the hard palate (after five or six years of age) has been advocated on the basis that good speech will develop following soft palate closure and that avoidance of trauma to the hard palate will obviate maxillary growth disturbance. In addition, it is said that many of the remaining hard palate fistulas will close spontaneously and that residual hard palate openings will be easy to close. Thirty-two cases treated in this way are reviewed, and a decade of experience with this technique is presented. A majority of cases failed to develop acceptable speech spontaneously. A very high percentage suffered both anterior and posterior air escape and a strikingly high proportion required pharyngeal flaps. Spontaneous complete closure of the hard palate was infrequent. The hard palate openings were not easy to close. The speech deficiencies associated with this technique are clear. The method's possible advantages in relationship to maxillofacial growth remain difficult to prove and were not specifically investigated in this study.

Child↗

PubMed1997

Developmental alterations in casein kinase 2 activity during the morphogenesis of quail secondary palate.

BACKGROUND: During the progression of avian secondary palate morphogenesis, the rate of cell proliferation declines, whereas the production and accumulation of extracellular matrices increases. To investigate the regulation of these events, we examined the quail secondary palate for the activity of casein kinase 2 (CK 2), a pleiotropic serine/threonine second messenger independent enzyme implicated in cell growth and differentiation. METHODS: Quail palatal shelves were dissected between days 5 and 9 of incubation, which is the period of palate morphogenesis in quail, and prepared either for light microscopic observations or homogenized, cleared by ultracentrifugation, and then subjected to fractionation on a MonoQ column by fast protein liquid chromatography and Western immunoblotting. RESULTS: Histological examination showed that the palatal shelves appeared on day 5 of incubation and approximated by day 8 of incubation. Fractionation of palate extract using a Mono-Q column revealed the presence of a major peak of phosvitin phosphotransferase activity which eluted with 0.5 M NaCl. This activity peak coincided with the presence of a 42 kDa subunit of CK 2 as determined by Western blotting with a CK 2 specific antibody. The CK 2 activity towards phosvitin was elevated on days 5 and 6 and then rapidly declined by day 9. The decrease in CK 2 activity did not correlate with a decrease in CK 2 protein during palate development indicating that the differential activity of the CK 2 enzyme observed during quail palate development may be due to post-translational modifications of the enzyme. A high positive correlation was found between the CK 2 phosphotransferase activity and both the proliferation index and DNA synthesis during palate development. CONCLUSION: On the basis of literature analysis and the results of the present study, it was suggested that the activity of CK 2 may be regulated along with protein kinase A to coordinate cell proliferation and the synthesis of extracellular matrices during palate development in quail.

Animals↗

PubMed1988

Chondrodystrophic mice with coincidental agnathia: evidence for the tongue obstruction hypothesis in cleft palate.

Mice homozygous for either of two mutations, chondrodysplasia (cho) or cartilage matrix deficiency (cmd), have short-limbed chondrodystrophy. This phenotype includes retrognathia, relative macroglossia, and cleft palate. It has been postulated that the cleft palate in these mice is the result of tongue obstruction during palatogenesis. Agnathia associated with microglossia is an independent spontaneously occurring defect in the strains bearing these mutations. The coincidental occurrence of agnathia-microglossia with chondrodystrophy lends itself to the study of the mechanism of cleft palate formation. We examined approximate midsagittal histological sections of normal and chondrodystrophic newborn mice, both with and without agnathia. Mandibular measurements and examinations of palate closure and tongue structure were made from photographic prints. Typical chondrodystrophic mutants with cleft palates had a mean mandibular length that was 66% of normal and a tongue that appeared large relative to the shortened mandible. Chondrodystrophic mutants with agnathia and microglossia had a mean mandibular length that was further reduced to 30% of normal, yet had a closed palate. We also observed two nonagnathic chondrodystrophic mutants that had slightly decreased mandibular lengths, microglossia, and closed palates. These observations suggest that tongue obstruction during palatogenesis is the pathogenetic mechanism of cleft palate in chondrodystrophic mice. A similar tongue obstruction hypothesis has been proposed as the mechanism of cleft palate formation in the human Pierre Robin sequence, which consists of retrognathia, glossoptosis, and cleft palate. This mechanistic hypothesis has been challenged, but our findings support the tongue obstruction hypothesis in the Robin cleft.

Abnormalities, Multiple↗

PubMed1991

TCDD exposure of human embryonic palatal shelves in organ culture alters the differentiation of medial epithelial cells.

The highly toxic, polychlorinated aromatic compound 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) occurs as a contaminant throughout the environment. Epidemiology studies of populations accidentally exposed to TCDD have failed to identify TCDD as a human teratogen, but these studies are limited by the small numbers of exposed pregnancies and imprecise estimates of exposure. TCDD is highly teratogenic in mice, inducing cleft palate and hydronephrosis. TCDD exposure in vivo of embryonic mice alters the differentiation and expression of growth factors in the medial epithelial palatal cells. These alterations also occur in rat and mouse palates exposed to TCDD in organ culture. In the present study, human embryonic palatal shelves were cultured in the rodent organ culture system. In order to achieve in vitro the developmental stage at which fusion would normally occur, GD 52 shelves were cultured for 4 days, GD 53 shelves were cultured for 3 days, and GD 54 shelves were cultured for 3 days. Three of four palatal shelves exposed to 5 x 10(-11) M TCDD were identical to their homologous controls (right shelf cultured with control medium; left shelf cultured with TCDD-containing medium). TCDD at 1 x 10(-7) M produced cytotoxicity detected by transmission electron microscopy (TEM). Exposure to 1 x 10(-8) M TCDD resulted in continued incorporation of thymidine ([3H]-TdR detected autoradiographically) by palatal medial cells, failure of the medial peridermal cells to degenerate as observed by scanning electron microscopy (SEM), and differentiation into a stratified, squamous epithelium. These alterations are identical to those induced by TCDD in vitro in rat and mouse palatal cells. The main difference between these species is the level of TCDD required to elicit the responses. Cultured mouse palates respond to 5 x 10(-11) M TCDD with altered medial cell differentiation, and 1 x 10(-10) M TCDD is cytotoxic. The rat shelves respond with altered differentiation at 1 x 10(-8) M and cytotoxicity at 1 x 10(-7) M. All the human shelves respond at 1 x 10(-8) M TCDD with altered differentiation, 1 out of 4 responded at 5 x 10(-11) M, and cytotoxicity occurred at 1 x 10(-7) M. The present data suggest human embryonic palates are less sensitive than those of the C57BL/6N mouse, and that exposure to high levels of TCDD would be required to elicit altered differentiation in the palatal shelf.

Analysis of Variance↗

PubMed1991

Development of the lung in mice with bromodeoxyuridine-induced cleft palate.

Clinical and laboratory observations show that denial of free communication between the amniotic fluid and lung fluid results in pulmonary hypoplasia. Thus, cleft palate resulting from tongue obstruction to palatal shelf elevation might be associated with disturbed lung development. This association exists in the Pena-Shokeir phenotype. The goal of these experiments was to see what effect bromodeoxyuridine (BUdR)-induced cleft palate had on lung development. LACA mice were injected with 500 mg/kg BUdR on E11 or E11 and E12 of gestation, a treatment known to produce a 25% and 50% incidence of cleft palate, respectively. BUdR had a direct retarding effect on lung growth but, when cleft palate occurred as well, the lungs were more severely affected. Morphometry showed that lungs from fetuses with cleft palate had only one-half the saccular volume of controls or of treated fetuses with normal palates. Although hypoplastic, lungs associated with cleft palate had type I and type II pneumocytes, and the latter were shown by electron microscopy to be capable of producing surfactant. Hence, cellular differentiation had not been affected by the treatment. Fetuses with cleft palate had less amniotic fluid than controls but significantly more than those with normal palates after treatment. Thus, the pattern of abnormalities in this animal model bears some resemblance to that of the human Pena-Shokeir phenotype.

Animals↗

PubMed2000

Linguistic development in cleft palate patients with and without compensatory articulation disorder.

INTRODUCTION: Cleft palate patients frequently show compensatory articulation disorder (CAD). CAD severely affects speech intelligibility and requires a prolonged period of speech intervention. CAD has been considered a phonologic disorder. Thus, it seems necessary to explore the relationship between CAD and language development. OBJECTIVE: To study the relationship between language development and the presence of CAD in cleft palate patients. MATERIALS AND METHODS: Cleft palate children with residual velopharyngeal insufficiency (VPI) after palatal closure, with and without CAD were studied. Only patients with an age ranging from 3 to 8 years were included in the study group. Twenty-nine cleft palate patients with residual VPI and CAD were included in the first group (active). The second group was assembled with 29 cleft palate patients with residual VPI without CAD, matched by age and sex (control). For evaluating language development, all patients were analyzed using the Situational-Discourse-Semantic (SDS) Model [13]. This Model is a valuable tool for conducting naturalistic observation and descriptive assessment of language development. The SDS Model provides a detailed description of three contexts (situational, discourse, and semantic) in ten levels of cognitive and linguistic organization. RESULTS: In all contexts considered by the model of cognitive and linguistic organization used for this study, i.e. SDS, a Fischer exact test demonstrated that patients with CAD showed a significantly higher frequency of language delay as compared with patients without CAD. None of the patients present with CAD showed an adequate level of language development. The degree of language delay was greater in the situational context as compared to the semantic and discourse contexts. CONCLUSIONS: Cleft palate patients present with CAD, demonstrated a significantly higher frequency of delay in language development as compared with cleft palate patients present with VPI without CAD. From the results of this paper, it seems that a detailed evaluation of all aspects of cognitive and linguistic organization should be performed in cleft palate patients, especially in patients present with CAD. Moreover, it seems that speech intervention in cleft palate patients with CAD should address not only the articulation process, but also specific aspects of language development.

Adaptation, Physiological↗

PubMed2003

Evaluation of palatal snoring surgery in an animal model.

OBJECTIVE: We introduce an animal model to reproduce and measure palatal snoring and to assess the effectiveness of cautery-assisted palatal stiffening operation and injection snoreplasty versus a control (no palatal intervention) on treatment of palatal flutter snoring. Study design and setting An anesthetized laboratory canine model uses 2 simultaneous temporary tracheotomies. An inferior tracheotomy is cannulated with an endotracheal tube for ventilation. A superior tracheotomy is cannulated with a tube passed cephalad and seated in the hypopharynx. Negative pressure applied to the upper tube leads to partial collapse of the upper airway with palatal fluttering, and the anesthetized dog snores. Videostroboscopy records palatal flutter frequency before and after surgical intervention. Preoperative and postoperative palatal assessments are made on 15 beagles. RESULTS: Cautery-assisted palatal stiffening operation and injection snoreplasty objectively stiffen the canine soft palate with diminished snoring compared with controls. Conclusion and significance We provide a reproducible animal model to experimentally measure new interventions to treat palatal flutter snoring.

Animals↗