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Incidence of Velopharyngeal Insufficiency with Submucous Cleft

Robert Mason Dmd, Ph.D

December 21, 2009

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Question

Are there any statistics on the number of children with a submucous cleft who correspondingly have velopharyngeal insufficiency (VPI)? How many submucous cleft chlidren have absolutely no issue with speech?

Answer

While about 48% of those with submucous cleft palate (SMCP) may have velopharyngeal competence (that is, no hypernasality) the figure is expected to change over time.

There are many forms of submucous clefts, or underlying clefts of bone or muscle tissues covered with connective tissue from birth onward. In all instances of SMCP of the soft palate, there is a lack of muscle continuity across the midline of the soft palate (or velum). In most instances of SMCP, there is also a bony submucous cleft of the hard palate taking the form of an inverted "V". So it is possible to have a SMCP involving both hard and soft palate, or soft palate alone. A split or bifid uvula is also typically seen as an accompaniment of SMCP. As a result, while the overall length of the soft palate may be normal, the functional length, that is, the amount of soft palate tissue used in velopharyngeal closure, is reduced. This is because the muscles of the soft palate, which normally meet and interdigitate at the midline of the velum, course forward to find an attachment onto the hard palate aponeurosis (connective tissue sheet). With a SMCP of the hard palate, the aponeurosis is displaced forward along the margins of the cleft, resulting in a V-shaped configuration of hard and soft palate. When the soft palate elevates for speech and swallowing under these circumstances, a lesser amount of the velum is available to make a contact with the posterior wall of the pharynx.

A simple way of perceiving this is to liken the soft palate as a door, and the phaynx to a doorway. If the door is hinged in the wrong place, the door cannot appropriately close off the doorway.

When one looks in the mouth of an individual while they are saying "ah", it will be noted, normally, that the uvula hangs pendant and that there is a dimple or buckling of the velum occurring a few mm above the uvula. As measured from the posterior border of the hard palate to the uvula, this buckling occurs about 80% of the way back on the palate. A person with SMCP will show a buckling point farther forward on the palate - like 50 -60 % of overall length. This is referred to anterior displacement of velar muscles within the velum. For such patients who have normal nasal voice quality, the adenoid pad on the posterior and lateral walls of the pharynx acts as a target for velopharyngeal closure.

The adenoids, however, have a growth cycle. They are seen to be large by around age 3, and remain large until around age 12, when they undergo a normal process referred to as involution (atrophy) of the adenoids. That is, they waste away and are usually gone by around age 20. For normal speakers without SMCP, the palate is overbuilt and adapts nicely by stretching (the phenomenon of velar stretch) to this change in the increase in diameter of the pharynx. For individuals with SMCP, it has been noted that the involution process can begin earlier than age 12 - with a lot of variability, and that the soft palate is often unable to adapt to the increased size of the pharynx. This produces hypernasality, or excessive flow of air through the nose and a "nasal" quality in the speaking voice.

It is possible to predict which individuals with SMCP will likely develop hypernasality over time. The predictions are done using lateral radiographic studies of the pharynx, and/or airflow studies which are sensitive to changes in nasal flow.

There is a caveat in medicine that every ENT knows and every physician should know; that you would never do a total adenoidectomy on a patient with SMCP, as this dramatically changes the size of the nasopharynx and will almost always lead to severe hypernasality that would require a pharyngoplastic operative procedure. In instances where the adenoids are impinging on the Eustachian tubes, a lateral (also known as a partial or peritubal) adenoidectomy can be done.

I mentioned a pharyngoplasty above. There are several forms of this operation. One is called a pharyngeal flap; another is a sphincter pharyngoplasty. Still another option is a Furlow palatal lengthening procedure. Injecting substances into the posterior wall to decrease the depth of the pharynx has been attempted and discarded many times over the past 40 years. Currently, injections do not offer a consistent and predictable option. All surgical procedures except injections into the posterior pharyngeal wall require general anesthesia.

The use of a speech appliance is not usually a viable treatment, or at least should be only regarded as a temporary fix, while in contrast, surgery is permanent. I have made many speech appliances in my career - some are obturators which fill the gap while others are palatal lifts - holding the soft palate up. I'm not a big fan, although for a variety of reasons, an appliance may the procedure of choice if the patient is not a candidate for surgery. Appliances can work well, but a permanent surgical solution is preferred.

I have published articles on predicting hypernasality where there are intraoral findings consistent with SMCP, and as well, articles on palatal stretch, the adenoid mass and its significance to this condition. I am happy to provide references if any interested reader may desire more details. My email address is oitsbob@sc.rr.com.

The bottom line here is that statistics do not matter, since a child with SMCP and normal speech may become hypernasal over time as the pharynx grows and as the adenoids undergo the natural process of involution.

Please visit our eLearning Library to view courses on this topic and a variety of other courses.

Robert M. Mason, DMD, Ph.D. is a speech-language pathologist (CCC-ASHA Fellow), a dentist, and orthodontist. He is a Past President of the American Cleft Palate-Craniofacial Association, a professional, interdisciplinary organization specializing in problems associated with facial and oral deformities. Dr. Mason has studied and written extensively about orofacial examination, developmental problems related to the tongue, and the anatomy and physiology of the speech and hearing mechanisms. His reports have appeared in speech, dental, medical, and plastic surgical journals and texts. He is considered to be an expert in tongue thrusting, tongue tie, and other problems related to tongue functions and speech.


Robert Mason Dmd, Ph.D


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