Velopharyngeal dysfunction (VPD) is a disorder of the velopharyngeal (VP) sphincter or valve, which functions to separate the nasal and oral cavities during speech, swallowing, vomiting, blowing, and sucking. When the soft palate and pharyngeal walls are unable to form an effective seal, an abnormal connection between the nasal and oral cavities leads to hypernasal speech, increased nasal resonance, nasal regurgitation, nasal emission, and decreased intraoral pressure during speech. The overall result is decreased speech intelligibility and significant functional and social impairment.
Diagnosis and treatment require a multidisciplinary approach centered around speech-language pathology, otolaryngology, and plastic surgery. Velopharyngeal dysfunction is the favored nomenclature, as it denotes a deficit of the velopharyngeal closure without implying a specific cause. It can be further subdivided into velopharyngeal insufficiency, incompetence, and mislearning, which provides additional information on the causation. Velopharyngeal insufficiency suggests a structural defect, incompetent us due to neurologic dysfunction, and mislearning is due to learned errors in articulation.
Velopharyngeal dysfunction may result from incomplete closure of the velopharyngeal sphincter, which controls the airflow into the nasal cavity during speech and prevents nasal regurgitation during swallowing. VPD can occur secondary to structural deficits, neurological disorders, faulty learning, or as a syndromic finding.
An overt cleft palate occurs in approximately 1 in 650 to 750 children born annually and is the most common cause of VPD. Following primary cleft palate surgery, a deficiency persists in up to 20% to 30% of patients. VPD can also be a complication after oral surgery. The incidence of VPD after adenoidectomy ranges from 1 in 1,500 to 1 in 10,000. Postoperative palatal fistula and VPD occurs after primary cleft palate repair at a rate of 3.4% to 15%.
The most common diagnosis in patients with VPD of unknown cause is 22q11.2 deletion syndrome. The frequency of 22q11 deletion syndrome ranges from 1 in 2000 to 4000 , with 27% to 92% of diagnosed children having VPD.
The velopharyngeal sphincter consists of the soft palate (velum), levator veli palatini, tensor veli palatini, palatopharyngeus, palatoglossus, muscularis uvulae, and the superior constrictor muscles. During normal velopharyngeal closure, the levator veli palatini contracts the velum posterior-superiorly while the lateral pharyngeal walls and posterior pharyngeal wall contract medially and anteriorly, respectively. This serves to close the velopharyngeal port and separate the nasal and oral cavities during speech, swallow, vomiting, blowing, and sucking.
During normal speech, this separation allows airflow to be channeled from the vocal cords to the articulating tongue, lips, and teeth of the oral cavity. This produces the consonant (p, b, t, d, k, g, f, v, s, z, sh, ch, ge, l, r, w, y) and vowel sounds or phonemes. A phoneme is the smallest unit of sound that distinguishes one word from another (ie. the t in “bat” vs. “bag”). Furthermore, air pressure needs to build up in the oral cavity up to 5 to 7 mm Hg in order to produce oral plosives, fricatives, and affricatives. Plosives are consonant sounds created when air is stopped completely in the oral cavity and then suddenly explodes with its release such as the “p” sound. Fricatives are consonant sounds that are created by narrowing the airflow such as the “s” sound. Affricatives are plosives followed by a fricative such as the “ch” sound. Phonemes can be divided in voiced versus voiceless depending on if the vocal cords also resonate. The soft palate is relaxed and the nasal and oral cavities coupled only for three nasal consonants sounds in the English language (m, n, ng). Partition of the two cavities also prevents nasal regurgitation of liquids and solids during swallow and provides an adequate negative pressure in the oral cavity during sucking.
During VPD, there is an airflow leak into the nasal cavity secondary to anatomic, neurologic, or functional impairment. Sound produced at the vocal cords subsequently enters both the oral and nasal cavities, causing both cavities to resonate and creates an overall “nasal” sound due to excessive nasal airflow. This is also known as nasal emission or nasal escape. In severe cases, a small stricture in the nasopharynx can create a distinct, fricative sound, termed nasal turbulence.
Patients’ ability to produce consonant sounds becomes impaired and they may develop maladaptive compensatory mechanisms such as glottal stops, pharyngeal fricatives, and facial grimaces in an effort to close the anterior nares and decrease nasal airflow. Those with mild VPD may compensate for decreased oral air pressure by increasing overall laryngeal airflow and shouting to produce normal speech volume. This may eventually lead to voice hoarseness and vocal cord nodules. VPD results in decreased speech intelligibility and significant functional and social impairment.
A detailed history should include any diagnosed syndromes, history of cleft palate, history of recurrent ear infections, neurologic abnormalities, prior surgical intervention within the oral cavity or pharynx, episodes of nasal regurgitation during eating, and risk for obstructive sleep apnea.
The physical examination should focus on the oral and nasal cavities with attention to the soft palate height, mobility, and symmetry, tonsil size, tongue mobility and symmetry, oral competence, nasal mucosa, nasal turbinates, and septum. Inspection for any anatomical abnormalities such as a submucosal cleft palate, bifid uvula, zona pellucida, posterior palatal notching, or neuromuscular weakness and asymmetry is recommended. Mobility of the soft palate is inspected by asking the patient to maintain a sustained phonation of the vowel sounds “e” or “i”. The clinician should also perform an otoscopic exam to assess for otitis media with effusion or tympanic membrane retraction, as VPD can be associated with Eustachian tube dysfunction.
The diagnosis of VPD is obtained through history, physical exam, assessment of speech production, imaging, and instrumental evaluation.
Treatment modalities for VPD include speech therapy, prosthetics, and surgery.
Due to the varying etiological causes for VPD, a thorough evaluation must be first be performed. Patients with hypernasal speech secondary to faulty learning, phonologic disorder, or language impairment without anatomic or neurological deficits should be treated with speech therapy.
Instrumentation can assist in surgical planning by determining the location of the VP closure, size of VP gap, mobility of VP structures, and pattern of VP closure (coronal, sagittal, or circular) as well as an underlying occult cleft palate. In patients with neurological deficits or those who are poor surgical candidates, evaluation by a prosthodontist for oral prosthetics is recommended.
VPD secondary to anatomic abnormality is most commonly caused by a cleft palate. Delayed primary cleft palate repair after 18 months is associated with a higher incidence of speech impairment and VPD. However, the timing of VPD surgery has not been shown to affect long-term speech outcomes. Pamplona et al showed that earlier surgical treatment of VPD did not affect postoperative speech therapy. Studies have shown that the success of VPD surgery and speech therapy is influenced mainly by the quality of speech therapy as opposed to the timing of the surgery. Thus, older patients should not be denied surgery with the belief that they might not benefit due to their age. Neither speech therapy nor surgery alone can resolve the poor articulation from VPD and patients often require a combination of speech therapy and surgical interventions.
Several studies note a successful reduction in hypernasality with pharyngoplasty up to 85%. Failure after VPD surgery can present in 4% to 12% of patients who may require additional or revision surgery. Several studies did not find gender, age, palatal defects, prior adenoidectomy, or IQ, to be predictors of postoperative speech outcomes.
In a systematic review for patients with 22q11 microdeletion syndrome and VPD, there was no significant difference in speech outcome or morbidity between the different types of pharyngeal flaps. Rates of failures from primary pharyngeal flap and sphincter pharyngoplasty have been equal, with both techniques being amenable to salvage through revision surgery.
Complications from surgical intervention involve obstruction of nasal airflow, hyponasal speech, persistent hypernasal speech, and obstructive sleep apnea (OSA). The pharyngeal flap has been associated with lateral port stenosis, hyponasal voice secondary to over-obturation of the nasopharynx, and postoperative OSA in up to 20% of patients. Native mucosa should be used to cover any exposed muscle during flap elevation to prevent tissue contraction and suboptimal obturation of the VP port. An increased risk of postoperative OSA has been found with sphincter pharyngoplasty requiring flap revision.
Risks of posterior pharyngeal wall augmentation include migration or extrusion of injected material, foreign body reaction, and fat embolism. Persistent VP gap and hypernasal speech can be treated with a combined surgical approach using both sphincter pharyngoplasty and Furlow palatoplasty. This combination approach requires significantly less surgical revision compared to pharyngeal flap or sphincter pharyngoplasty alone.
Postoperatively, patients are admitted overnight and monitored for oxygen desaturations, snoring, hyponasal speech, and OSA. They are discharged once tolerating adequate oral intake. Patients with concern for sleep apnea should undergo formal polysomnography to evaluate for OSA and be considered for continuous positive airway pressure in the short term. Persistent sleep apnea, airflow obstruction, and hyponasal speech may require flap revision or takedown in the long term. Speech therapy should continue after surgical repair to enhance speech outcomes and address poor compensatory behaviors used by patients prior to surgery.
Collaboration among the otolaryngologist, oral maxillary facial surgeon, plastic surgeon, speech-language pathologist, and the prosthodontist is essential for the diagnosis and treatment of velopharyngeal dysfunction. Close partnership with the cleft lip and palate team at hospitals is also beneficial due to the frequent association of VPD with cleft palate.
The speech therapist is responsible for the perceptual analysis of speech production and interpretation of findings on nasal endoscopy and videofluoroscopy. A multidisciplinary review of endoscopic and radiographic images has been shown to increase the reliability of interpretations.
Patient education on velopharyngeal dysfunction can be challenging due to the heterogeneous causes and need for multidisciplinary management. An early introduction to a speech-language pathologist is key for the diagnosis and alleviation of any inappropriate compensatory behaviors. Patients and their families should be counseled on the different methods of evaluation such as perceptual speech analysis, video nasal endoscopy, videofluoroscopy, and nasometry. Findings on testing and imaging should be shared and a discussion held regarding the best approach for treatment. Prior to any surgical intervention, patients and parents should be educated on the risks of surgery such as airway obstruction, sleep apnea, and need for additional surgical revisions.
Patients with velopharyngeal dysfunction should be managed by a multidisciplinary team of otolaryngologists, oral maxillary facial surgeons, plastic surgeons, neurologists, speech-language pathologists, prosthodontists, radiologists, primary care physicians, pediatricians, and geneticists. Early diagnosis and treatment of VPD are essential for long-term speech fluency and social function. Children with poor speech development and signs of VPD such as hypernasal speech and nasal regurgitation should be referred by their pediatricians to speech therapy for first-line treatment. A genetic workup should also be performed in collaboration with a geneticist.
Patients with associated neurological weakness should be evaluated by neurology. If anatomical abnormalities such as submucosal or occult cleft palate are diagnosed on instrumentation, a referral should be sent to an otolaryngologist or plastic surgeon specializing in velopharyngeal surgery. Speech therapy should continue even after surgical repair to enhance speech outcomes and address poor compensatory behaviors used by patients prior to surgery. Finally, patients may develop social anxiety and avoidance due to the intelligibility of their speech, especially in school and work settings. Formal peer support groups with parents and patients who share the diagnosis can aid patients in addressing their concerns.
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