Surgical Speech Disorders

Most speech disorders of childhood are treated with speech therapy. However, two conditions, ankyloglossia and velopharyngeal dysfunction, may be amenable to surgical intervention. It is important for surgeons to work with experienced speech language pathologists to diagnose the speech disorder. Children with articulation disorders related to ankyloglossia may benefit from frenuloplasty. Children with velopharyngeal dysfunction should have standardized clinical evaluation and instrumental asseessment of velopharyngeal function. Surgeons should develop a treatment protocol to optimize speechoutcomes while mnimizing morbidity.

Key points

  • Frenotomy is a common procedure treating ankyloglossia in infants with thin frenulum.

  • The incision needs to be carried posteriorly until the tongue is sufficiently released before closing with interrupted sutures.

  • Complete clinical history, including speech, communication, swallowing, airway, and sleep symptoms, is important in velopharyngeal insufficiency management.

  • A team using a standardized approach should evaluate the patient and perceptual speech assessment should be conducted by a qualified speech pathologist to provide speech differential diagnosis.

  • Furlow palatoplasty can optimize the levator veli palatini (LVP) muscular function and increase the length of the palate, and sphincter pharyngoplasty is best suited for patients with transverse orientation of LVP and poor lateral wall movement.


Speech is one of the main forms of communication. Speech production is a complex motor activity that requires generation of air pressure (respiratory control), vocal function (phonation), articulation, motor planning, and velopharyngeal (VP) function. Coordination of these components is needed to produce intelligible speech. Most speech delays, such as dysfluency, articulation errors, and childhood apraxia of speech, are treated with speech therapy. However, 2 conditions, ankyloglossia and VP dysfunction (VPD), may require surgical intervention for their associated speech symptoms. This article discusses the surgical management of ankyloglossia and VPD.


Speech is one of the main forms of communication. Speech production is a complex motor activity that requires generation of air pressure (respiratory control), vocal function (phonation), articulation, motor planning, and velopharyngeal (VP) function. Coordination of these components is needed to produce intelligible speech. Most speech delays, such as dysfluency, articulation errors, and childhood apraxia of speech, are treated with speech therapy. However, 2 conditions, ankyloglossia and VP dysfunction (VPD), may require surgical intervention for their associated speech symptoms. This article discusses the surgical management of ankyloglossia and VPD.


There are several important structures required for correct articulation. The most important active articulator is the tongue. Ankyloglossia is a condition associated with a shortened lingual frenulum that restricts movement of the tongue tip. The clinical phenotypes vary from mild abnormalities to complete ankyloglossia in which the tongue is fused to the floor of the mouth ( Fig. 1 ).

Fig. 1

Ankyloglossia with thick frenulum that requires frenuloplasty.

( From Anatomy & Physiology for Speech, Language, and Hearing by J. A. Seikel, D. King, & D. Drumright, 2010, 4E. Copyright © 2010 Delmar Learning, a part of Cengage Learning, Inc. Reproduced with permission.)

Symptoms of ankyloglossia may include breastfeeding difficulties, speech disorders, or problems with deglutition and dentition. Any of these symptoms may be an indication for surgical management. During infancy breastfeeding may be the most salient symptom. Ankyloglossia in infants is associated with a 25% to 60% incidence of difficulties with breastfeeding, including failure to thrive and maternal breast pain. Studies have shown that, for every day of maternal pain during the initial 3 weeks of breastfeeding, there is a 10% to 26% risk of cessation of breastfeeding.

Speech production is another common indication for surgery. The effect of ankyloglossia on speech has been a subject of debate. Some children with tongue-tie are able to develop normal speech without treatment, whereas others have articulation difficulties. The speech problems associated with ankyloglossia are typically the production of lingual dental sounds (such as t, d) and sibilants (such as z, s, th). Up to one-half of young children with ankyloglossia referred for otolaryngology evaluation have articulation difficulties. The 2 main surgical approaches are frenotomy and frenuloplasty.


The most common treatment of ankyloglossia in infants is frenotomy by incising a few millimeters into the lingual frenulum when it is thin. Frenotomy can be performed at the bedside or in the clinic with or without topical anesthesia. In general, the discomfort associated with release of thin frenulum is very brief. If desired, oral sucrose solution may be given a few minutes before the procedure to provide short-term analgesia.

The infant is positioned directly in front of the surgeon. Fingers or a groove retractor is placed on either side of the frenulum, and the ventral surface of the tongue is exposed. A hemostat is used to clamp the frenulum in order to reduce bleeding. Iris scissors are used to divide the frenulum. Care is taken to avoid injury to the submandibular ducts. Two or more sequential cuts may be needed to accomplish a complete release. The incision does not require sutures. Feeding is allowed immediately after the procedure. Bleeding is generally scant and controlled with pressure or breastfeeding. Complications associated with this procedure are usually negligible.


In older children, frenuloplasty with sutures is generally performed to allow a more complete release. Local anesthesia in clinic may be considered for cooperative older children. If surgery is deferred until the child is more than 1 year old or the frenulum is thick, general anesthesia is normally preferred. When general anesthesia is used, intermittent mask ventilation is usually sufficient. Local anesthetic with epinephrine can be infiltrated at the surgical site to improve hemostasis and postprocedure pain. The tongue is retracted superiorly with a groove retractor or a penetrating clamp to expose the frenulum. The frenulum is sharply divided in a horizontal fashion to the level of ventral tongue. This division creates a diamond-shaped defect. The incision needs to be carried posteriorly until the tongue is sufficiently released to allow protrusion. Hemostasis is obtained with electrical cautery. The defect is then closed in a vertical fashion with interrupted absorbable sutures. For more severe ankyloglossia, Z-plasty reconstruction of the floor of the mouth may be considered. Prophylactic antibiotics are not prescribed because infection is rare.


VPD results in failure of the VP port to close appropriately during speech production. It is characterized by hypernasal resonance and nasal air emissions. VPD includes VP incompetence, VP mislearning, and VP insufficiency (VPI).

VP incompetence is caused by poor motor speech function despite adequate anatomy. Patients with VP incompetence are likely to improve with speech therapy. VP mislearning includes disordered speech behaviors such as compensatory misarticulations in spite of normal VP anatomy and function. VPI is caused by incomplete closure of the VP port during speech production.

Cleft palate is the most common congenital anomaly associated with VPI. Unrepaired cleft palate predictably results in VPI. Speech production is the main indication for cleft palate repair. Patients who undergo cleft palate repair remain at risk for developing VPI, particularly if the misaligned soft palate musculature is not addressed, resulting in a situation similar to submucous cleft palate. The estimated frequency of VPI after cleft palate repair ranges from 10% to 40%. Increased palatal cleft width may be associated with a higher risk of VPI after palate repair.

Submucous cleft palate can also cause VPI. Submucous cleft palate is defined by the presence of bifid uvula, a bony notch at the caudal edge of the hard palate, and a translucent zone in the midline of the soft palate caused by the sagittal orientation of the LVP muscles. The abnormal insertion of levator palatini muscles may be associated with inadequate elevation of the soft palate during speech, which results in incomplete VP closure. The estimated frequency of VPI in patients with submucous cleft palate is around 25%. Speech symptoms are the main indicators for repair of submucous cleft palate.

VP anatomy and physiology

It is important to understand the normal anatomy and physiology of VP closure when treating patients with VPD. The soft palate and pharyngeal muscle play an important role in normal speech production. Complete VP closure is required to direct the airflow to oral articulation muscles during production of nonnasal sounds.

The 5 major muscles that comprise the palatal apparatus are levator veli palatini (LVP), tensor veli palatini (TVP), palatoglossus, palatopharyngeus (PP), and muscularis uvulae. Other muscles, including the salpingopharyngeus and superior pharyngeal constrictors (SPC), also contribute to the lateral and posterior pharyngeal wall movements ( Fig. 2 ).

Fig. 2

Muscles of the VP mechanism: the 5 major muscles that comprise the palatal apparatus are LVP, TVP, palatoglossus, PP, and uvulae.

( From David LJ. The basics of velopharyngeal function: a brief review for the practicing clinician. Perspect Speech Sci Orofac Disord 2012;22:28; with permission.)

The LVP muscle is one of the most important muscles for VP closure. It originates from the eustachian tube and inserts into the midline palatal aponeurosis at an oblique angle. The fibers of LVP muscles create a dynamic sling in order to suspend the velum from the skull base. Its force of contraction pulls the velum both posteriorly and laterally.

The TVP muscle originates from the medial pterygoid palate and the lateral eustachian tube. It inserts into the palatal aponeurosis and the horizontal plate of the palatine bone. Its contraction tenses the palate. Because TVP is an important muscle in equilibrating the middle ear pressure, patients with VPD frequently have eustachian tube dysfunction caused by the abnormal insertion of TVP.

The PP muscle originates from the velum and inserts into the thyroid cartilage. It defines the posterior tonsillar pillar. Contraction of PP and SPC muscles pulls the lateral pharyngeal wall medially. The SPC muscle forms a hemisphincter that is closely associated with the PP muscle at the VP isthmus. Its contraction pulls the lateral and posterior pharyngeal walls both medially and anteriorly.

Patient assessment

The initial patient evaluation starts with complete clinical history, focusing on speech and communication. Information about a child’s ability to communicate in the setting of school and home can be acquired through family members. Important areas of discussion include the degree of speech intelligibility and the ability to communicate. Patients and their families should be queried about difficulties in socializing with peers caused by the speech issue. Other nonspeech symptoms, such as nasal regurgitation, nasal congestion, and rhinosinusitis, should also be discussed.

In some older patients, the speech may be normal. However, the ability to sustain intraoral pressure for activities like playing wind or brass instruments is compromised. Patients may also describe difficulties in blowing out candles and may not be able to whistle. This condition is called stress VP incompetence, because playing wind or brass instruments takes up to 30 times the average intraoral pressure of normal phonation. More than 30% of student musicians report symptoms of nasal air escape while playing wind instruments.

In addition to speech and swallowing issues, airway and sleep symptoms should be explored. If the patient has a clinical history equivocal for obstructive sleep apnea, an overnight sleep study may help to determine the severity of the sleep problems. The patients and their families should understand that the VPI management might make obstructive symptoms worse. Medical intervention or surgical management of obstructive symptoms should be addressed before the intervention for VPI.

Other important medical history, such as previous cleft palate repair or adenoidectomy, may also elucidate risks for VPI. All unrepaired cleft palates have VPD. The main reason to repair cleft palate is to optimize VP function. Even after cleft palate repair, these patients remain at risk for postoperative VPI. Adenoidectomy has also been associated with the development of VPI, especially in patients with unrecognized submucous cleft palate. The incidence of speech alteration after adenoidectomy has been reported to be 1 in 1200.

The medical history may also help identify previously undiagnosed syndromes. The most common genetic syndrome associated with VPD is 22q11.2 deletion or velocardiofacial syndrome (VCFS), which is associated with deletion or duplication of a variable portion of the long arm of chromosome 22. Patients with VCFS often have palatal abnormalities, heart defects, characteristic facial appearance, and learning disabilities. It has been estimated that 75% of patients with VCFS have some degree of VPD.

A compete head and neck examination should be a part of the initial physical assessment. Intraoral examination provides information on the LVP muscle movement, tonsil size, palate function, tongue mobility, dentition, and occlusion. The status of both primary and secondary palate should be assessed. Patient should be examined for submucous cleft palate. The caudal margin of the bony palate should be palpated for the notch. Tongue movement should be checked for ankyloglossia or neuromuscular disorder.

Instrumental assessment

The diagnosis of VPI can be difficult. Surgeons should ideally collaborate with skilled speech-language pathologists when assessing and managing children with speech disorders. Perceptual speech assessment should be conducted by a qualified speech-language pathologist, focusing on judgments of articulation, speech intelligibility, nasal resonance, and nasal emission. Speech pathologists help to provide speech differential diagnosis, including speech mislearning or compensatory misarticulations that are unrelated to VP function. Short phrases loaded with pressure consonants such as “Go get a cookie” and “Suzy sees the scissors” are used to detect nasal air emission. In the presence of hyponasal resonance, nasal consonants such as “Mama made some mittens” may become nonnasalized. For example, “Mama” would sound more like “Baba.”

Nasoendoscopy is regularly used to assess VP function by examining the nasal aspect of the soft palate and pharynx during speech production. In general, children more than 3 years old are able to cooperate with the examination. In order to provide a bird’s-eye view of the VP port, the endoscope should be passed through the middle meatus ( Box 1 ). Then the patient is asked to repeat oral and nasal loaded speech samples to assess VP function. During nasoendoscopy, the presence of a Passavant ridge and the size of the adenoid pad can be observed. The presence of a notch or a groove on the nasal surface of the palate is an indication for the sagittal orientation of the LVP musculature, as in a submucous cleft palate. Nasoendoscopy helps to verify the presence of VPI, to assess the status of LVP musculature, and to characterize the degree of lateral pharyngeal wall and palatal motions.

Box 1

  • 1.

    In general, how would you say your child’s speaking voice is?

    • Excellent

    • Good

    • Adequate

    • Poor or inadequate

    • My child has no voice

  • The following items ask about activities that your child might do in a given day.

  • 2.

    To what extent does your child’s voice limit his or her ability to be understood in a noisy area?

    • Limited a lot

    • Limited a little

    • Not limited at all

  • 3.

    During the past 2 weeks, to what extent has your child’s voice interfered with his or her normal social activities or with his or her school?

    • Not at all

    • Slightly

    • Moderately

    • Quite a bit

    • Extremely

  • 4.

    Do you find your child straining to speak because of his or her voice problem?

    • Not at all

    • A little bit

    • Moderately

    • Quite a bit

    • Extremely

Pediatric Voice Outcome Survey

The estimation of the degree of VP closure is important to optimize surgical outcome ( Fig. 3 ). A universal, standardized reporting system for VP function was proposed. The lateral wall and palatal movement during the nasoendoscopy can be classified using the International Working Group Scale as described by Golding-Kushner and colleagues. This scale has good intrarater and inter-rater reliability. For lateral wall movement, 0 indicates no movement, and 0.5 means movement to the midline. For palatal movement, 0 signifies no movement, and 1.0 indicates movement to the posterior pharyngeal wall. The posterior wall movement is described with the same scale from 0 to 1.0, with 1.0 signifying the movement to meet the soft palate.

Fig. 3

Nasoendoscopy provides a bird’s-eye view of the VP port. ( A ) Small VP gap and prominent adenoid pad. ( B ) Deep dorsal palatal notch ( arrow ). The presence of a notch on the nasal surface of the palate is an indication for the sagittal orientation of the LVP musculature.

After initial nasoendoscopy to determine the VP port closure, videofluoroscopy may be helpful to determine the surgical approach. During the videofluoroscopy, barium drops are placed into the nose, then the anterior-posterior and lateral images are recorded. The speech pathologist at our institution rates the lateral wall motion on the anterior-posterior projection. The lateral view can show the level of attempted palatal closure. In addition to anatomic information, videofluoroscopy also helps to diagnose abnormal speech patterns, such as tongue backing instead of active palate elevation.

Information provided by nasoendoscopy and videofluoroscopy can be complementary. Sometimes videofluoroscopy may show adequate VP closure on lateral images, but patients with clinical VPI may have nasoendoscopy evidence of VP gap. The correlation in findings of these two examinations has been shown to be between 70% and 75%. The information from both nasoendoscopy and videofluoroscopy can be used to plan the surgical approach. If patients have persistent VPI after speech surgery, instrumental assessment is repeated.

Nonvisualizing assessments include nasometry. Nasometry is designed to measure the aerodynamic characteristics of VP function. The ratio of nasal to oral energy during the production of oral and nasal loaded speech samples is reported as a nasalance score. Increased nasal energy results in a higher nasalance score. It may be useful in assessing the degrees of improvement after the VPI surgery.

Another indirect evaluation of VP function is to measure the extent of nasal airflow during speech with pressure-flow device. Measurements are obtained during the production of high-pressure oral consonants with repeated words or blowing tasks for younger children. There is normally no nasal airflow during the production of nonnasal phonemes. The presence of nasal airflow produces detectable changes in intraoral pressures. VP orifice area can be calculated in millimeters squared.

A combination of these assessments can define the extent of VPI in order to guide the type of intervention needed to correct it. The clinical variables, perceptual speech assessment, and instrumental assessments can help to optimize speech outcomes and minimize risks.

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Aug 26, 2017 | Posted by in General Surgery | Comments Off on Surgical Speech Disorders
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