Khe Hở Môi Và Vòm Miệng: Chẩn Đoán Và Quản Lý Điều Trị (Cleft Lip and Palate)

754
R.J. Shprintzen
Ka-ka-ka
/sssssss/ (sustained /s/)
Suzy
Suzy sees Sally
Stop the bus
Catch a fi sh
Jerry’s slippers
1-2-3-4-5-6-7-8-9-10 (counting to ten)
The speech sample is rehearsed with the
patient just prior to the procedure to be certain
that it is repeated correctly and in a conversa-
tional manner. Repeating this sample for three
radiographic views limits the procedure to a min-
ute or less, thus keeping radiation exposure to a
minimum. Because the neck is irradiated during
this procedure and a child’s thyroid gland is sen-
sitive to radiation, it is preferred to limit
video fl uoroscopy to a one-time evaluation, usu-
ally just prior to secondary surgical intervention.
Immediately prior to the procedure, approxi-
mately 1 ml of barium sulfate suspension is
instilled in each nostril using a dropper or pipette.
This is done with the patient supine on the
fl uoroscopic table. This allows coating of the
velum, lateral pharyngeal walls, and posterior pha-
ryngeal wall. Without barium contrast, the lateral
pharyngeal walls cannot be seen in frontal view,
and the base or Townes view will not provide an en
face view of the actual velopharyngeal valve. In
addition, even in lateral view, the barium contrast
is essential for de fi ning small gaps. If there is no
contrast used, as soft tissues converge, they blur
together and a false negative for VPI is possible.
34.10.2 Nasopharyngoscopy
Nasopharyngoscopy for the assessment of the
velopharyngeal valve was described almost
simultaneously with the advent of multi-view
video fl uoroscopy. Pigott described the use of
both fl exible and rigid instruments in 1969 (Pigott
1969 ; Pigott et al. 1969 ) . Although Pigott contin-
ued to advocate for the use of rigid endoscopes
in the years that followed (Pigott and Makepeace
1982 ) , the development of smaller caliber fl exible
instruments clearly won support for fi ber-optic
endoscopy because of the ability to examine even
very young children without signi fi cant pain or
discomfort (Miyazaki et al. 1975 ; Shprintzen
1979a, b ; Shprintzen et al. 1979 ) . Today, fi ber-optic
endoscopes have external diameters well under
3 mm, many in the 2-mm range, therefore allow-
ing easy access to the upper airway (Fig. 34.11 ).
The International Working Group recommended
fl exible fi ber-optic nasopharyngoscopy and further
recommended that the examination should include
assessment of the entire vocal tract from the tip
of the nose to the larynx (Golding-Kushner et al.
1990 ) . It was also recommended that all examina-
Fig. 34.11 Arrangement of equipment for videona-
sopharyngoscopy. Two television monitors are used to
allow both the patient and the examiner to see the exami-
nation simultaneously. This helps to fi x the attention of
the patient and allows the examiner to explain the obser-
vations while the examination is taking place

755
34 The Velopharyngeal Mechanism
tions be recorded with both video and sound for
future review (Golding-Kushner et al. 1990 ) . It
has been shown that group review of studies is the
most reliable and valid method for coming to diag-
nostic and treatment decisions because it allows
for discussion of interpretations of the procedure
(D’Antonio et al. 1989 ) .
The procedure is best done using topical anesthe-
sia, especially in young children, in order to avoid
discomfort so that an adequate speech sample is
obtained. My preference is to use topical tetracaine
hydrochloride 2 % aqueous solution (Pontocaine®)
inserted into the nose on cotton packing rather than
a spray. Lidocaine is also effective. Using a pair of
bayonet forceps, the cotton packing can be passed
deeply into the nose to numb the turbinates and sep-
tum which are the sensitive portions of the nose. The
packing is left in place for several minutes and then
removed and the endoscope inserted. Using pack-
ing, the anesthetic is kept against the nasal mucosa
for several minutes rather than a brief spray which
really has minimal effect. In addition, the spray may
reach deeper into the vocal tract and be inhaled,
whereas the packing keeps the effect limited to the
nasal mucosa. Once the endoscope is passed into the
pharynx, it should not be held stationary throughout
the examination. The advantage of a fl exible instru-
ment is its fl exibility that allows movement so that
both sides of the pharynx can be seen and it can be
passed into the nasopharynx, oropharynx, and hypo-
pharynx. The larynx, tonsils, and tongue can be seen
in this manner.
The same speech sample used for video fl uoroscopy
is utilized for nasopharyngoscopy, as well, but the
sample does not need to be limited to those sounds
and phrases. Because there is no ionizing radiation
involved, there is no need to limit the procedure to
a minute or less. If phonemic variation is seen, the
examiner is free to have the patient say more sounds
and phrases than for fl uoroscopy.
34.11 Which Direct Visualization
Procedure to Use?
Many clinicians utilize nasopharyngoscopy exclu-
sively as an assessment of VPI because they think
that the information provided is the equivalent of
video fl uoroscopic procedures. However, it has
been reported that there is an approximate 30 %
discrepancy between fi ndings using multi-view
video fl uoroscopy and nasopharyngoscopy primar-
ily in the rating of lateral pharyngeal wall motion
(Shprintzen 1995 ) . Therefore, both procedures
are essential for a complete assessment of VPI
(Golding-Kushner et al. 1990 ) . Each procedure has
its own advantages and disadvantages as follows:
Multi-view video fl uoroscopy advantages
1. Provides a direct physiologic view of all com-
ponents of velopharyngeal valving in all
dimensions (width, depth, and height).
2. The entire vocal tract can be seen at one time.
3. All articulators are seen simultaneously.
4. The forward fl oor of speech is not impeded.
5. Excellent compliance even in very young
children.
6. The procedure is painless.
Multi-view video fl uoroscopy disadvantages
1. It is not a direct anatomic view, relying on
radiographic shadows for information.
2. Ionizing radiation is used.
3. As a result of ionizing radiation, there is a time
limit to the procedure.
4. Interpretation may be dif fi cult for those inex-
perienced with the technique.
Nasopharyngoscopy advantages
1. Provides a direct anatomic view usually appre-
ciated by surgeons.
2. The entire vocal tract can be seen, but not
simultaneously.
3. The normal fl ow of speech production is not
impeded.
4. There is no time limit to the procedure so
speech can be manipulated in more detail.
5. There is no ionizing radiation.
6. The procedure should be painless when done
properly.
Nasopharyngoscopy disadvantages
1. Anatomic structures moving in front of the
endoscope may block the view of physiologi-
cal movements.
2. A lack of compliance occurs in some cases,
particularly in young children.
3. The oral articulators cannot be seen.
4. The entire vocal tract cannot be seen at the
same time.

756
R.J. Shprintzen
5. The procedure can be painful in some cases or
cause bleeding if not done properly.
34.11.1 Reporting of the Results
The International Working Group also published
guidelines for the standardized reporting of the
observations from endoscopies and fl uoroscopies
(Golding-Kushner et al. 1990 ) . A ratio scale was
developed that would assess the amount of move-
ment of a structure (the velum, right lateral pha-
ryngeal wall, left lateral pharyngeal wall, and
posterior pharyngeal wall) toward its opposing
structure. This approach was an attempt to pro-
vide a method that would communicate the degree
of movement, not the actual distances moved,
that would be more standardized than qualitative
measures such as “poor,” “fair,” “good,” or “excel-
lent.” I have used this system for more than two
decades to transmit information to surgeons per-
forming reconstructive surgery, and the ratios
provided have met with a great deal of success in
terms of the ability to communicate between cli-
nicians, especially those from diverse fi elds of
practice, such as surgeons, speech pathologists,
and otolaryngologists.
34.12 The Importance of It All
There is a common “Murphyism” (one of the
humorous attempts at expanding Murphy’s Laws)
that goes something like this, “Before ordering a
diagnostic test, determine what you will do if the
result is positive or the result is negative. If the
answer is the same for both, don’t do the test.” In
other words, the value of collecting such elegant
diagnostic information is to have it guide treat-
ment. This has been amply demonstrated in a
number of studies that have documented the
ef fi cacy of guiding surgical management based
on diagnostic information from multi-view video-
fl uoroscopy and nasopharyngoscopy (Argamaso
et al. 1994 ; Chegar et al. 2007 ; Shprintzen et al.
1979 ; Tatum et al. 2002 ) . Stated another way, it
has become obvious that there is not one single
operation that can be successful in all cases. A
velopharyngeal gap during speech is a hole that
needs to be located in three-dimensional space,
and its size relative to the total size of the phar-
ynx must be con fi rmed in order to know how to
occlude it. The listener’s ear becomes the fi nal
judge of success, just as it was the entry point
into the diagnostic protocol. With the combina-
tion of direct visualization procedures and an
understanding of how to structurally solve the
problem, the elimination of VPI should be
achieved in more than 90 % of cases (Chegar
et al. 2007 ; Shprintzen et al. 1979 ; Tatum et al.
2002 ) .
References
Argamaso RV, Levandowski GJ, Golding-Kushner KJ
et al (1994) Treatment of asymmetric velopharyngeal
insuf fi ciency with skewed pharyngeal fl aps. Cleft
Palate J 31:287–294
Arvystas M, Shprintzen RJ (1984) Craniofacial morphol-
ogy in the velo-cardio-facial syndrome. J Craniofac
Genet Dev Biol 4:39–45
Calnan JS (1954) Submucous cleft palate. Br J Plast Surg
6:164–168
Chegar BE, Shprintzen RJ, Curtis MS et al (2007)
Pharyngeal fl ap and obstructive apnea: maximizing
speech outcome while limiting complications. Arch
Facial Plast Surg 9:252–259
Croft CB, Shprintzen RJ, Daniller AI et al (1978) The
occult submucous cleft palate and the musculus uvu-
lae. Cleft Palate J 15:150–154
Croft CB, Shprintzen RJ, Ruben RJ (1981a) Hypernasal
speech following adenotonsillectomy. Otolaryngol
Head Neck Surg 89:179–188
Croft CB, Shprintzen RJ, Rakoff SJ (1981b) Patterns of
velopharyngeal valving in normal and cleft palate sub-
jects: a multi-view video fl uoroscopic and nasendo-
scopic study. Laryngoscope 91:265–271
D’Antonio LL, Marsh JL, Province MA et al (1989)
Reliability of fl exible fi beroptic nasopharyngoscopy
for evaluation of velopharyngeal function in a clinical
population. Cleft Palate J 26:217–225
Golding-Kushner KJ, Argamaso RV, Cotton RT et al
(1990) Standardization for the reporting of nasophar-
yngoscopy and multi-view video fl uoroscopy: a report
from an international working group. Cleft Palate J
27:337–347
Havkin N, Tatum SA III, Shprintzen RJ (2000)
Velophgaryngeal insuf fi ciency and articulation impair-
ment in velo-cardio-facial syndrome: the in fl uence of
adenoids on phonemic development. Int J Pediatr
Otorhinolaryngol 54:103–110
Henningsson G, Isberg A (1988) In fl uence of tonsils
on velopharyngeal movements in children with

757
34 The Velopharyngeal Mechanism
craniofacial anomalies and hypernasality. Am J Orthod
Dentofacial Orthop 94:253–261
Kaplan EN (1975) The occult submucous cleft palate.
Cleft Palate J 12:356–368
Lewin ML, Croft CB, Shprintzen RJ (1980) Velopharyngeal
insuf fi ciency due to hypoplasia of the musculus uvu-
lae and occult submucous cleft palate. Plast Reconstr
Surg 65:585–591
MacKenzie-Stepner K, Witzel MA, Stringer DA et al
(1987) Velopharyngeal insuf fi ciency due to hypertro-
phic tonsils. A report of two cases. Int J Pediatr
Otorhinolaryngol 14:57–63
Mason RM, Warren D (1980) Adenoid involution and
developing hypernasality in cleft palate. J Speech Hear
Disord 45:469–480
Miyazaki T, Matsuya T, Yamaoka M (1975) Fiberscopic
methods for assessment of velopharyngeal closure
during various activities. Cleft Palate J 12:107–114
Pigott RW (1969) The nasendoscopic appearance of the
normal palatopharyngeal valve. Plast Reconstr Surg
43:19–24
Pigott RW, Makepeace AP (1982) Some characteristics of
endoscopic and radiological systems used in elabora-
tion of the diagnosis of velopharyngeal incompetence.
Br J Plast Surg 35:19–32
Pigott RW, Bensen JF, White FD (1969) Nasendoscopy in
the diagnosis of velopharyngeal incompetence. Plast
Reconstr Surg 43:141–147
Salyer KE, Sng KW, Sperry EE (2006) Two- fl ap palato-
plasty: 20-year experience and evolution of surgical
technique. Plast Reconstr Surg 118:193–204
Shprintzen RJ (1979a) Hypernasal speech in the absence
of overt or submucous cleft palate: the mystery solved.
In: Ellis R, Flack R (eds) Diagnosis and treatment of
palato glossal malfunction. College of Speech
Therapists, London
Shprintzen
RJ
(1979b)
The
use
of
multi-view
video fl uoroscopy and fl exible fi beroptic nasopharyn-
goscopy as a predictor of success with pharyngeal fl ap
surgery. In: Ellis R, Flack R (eds) Diagnosis and treat-
ment of palato glossal malfunction. College of Speech
Therapists, London
Shprintzen RJ (1982) Palatal and pharyngeal anomalies in
craniofacial syndromes. Birth Defects Orig Artic Ser
18(1):53–78
Shprintzen RJ (1995) Instrumental assessment of velopha-
ryngeal valving. In: Shprintzen RJ, Bardach J (eds)
Cleft palate speech management: a multidisciplinary
approach. Mosby, St. Louis
Shprintzen RJ (1997) Genetics, syndromes, and commu-
nication disorders. Singular Publishing, San Diego
Shprintzen
RJ
(2000)
Velocardiofacial
syndrome.
Otolaryngol Clin North Am 33:1217–1240
Shprintzen RJ (2001) Velo-cardio-facial syndrome. In:
Cassidy SB, Allanson J (eds) Management of genetic
syndromes. Wiley, New York
Shprintzen RJ (2003) The origin of speech ease: evolution
of the human upper airway and its functional implica-
tions for obstructive sleep apnea. Sleep Med
4:171–173
Shprintzen RJ, Croft CB (1981) Abnormalities of the
Eustachian tube ori fi ce in individuals with cleft palate.
Int J Pediatr Otorhinolaryngol 3:15–23
Shprintzen RJ, Lencione RM, McCall GN et al (1974)
A three dimensional cine fl uoroscopic analysis of
velopharyngeal closure during speech and non-
speech activities in normals. Cleft Palate J 11:
412–428
Shprintzen RJ, Lewin ML, Croft CB (1979) A compre-
hensive study of pharyngeal fl ap surgery: tailor-made
fl aps. Cleft Palate J 16:46–55
Shprintzen RJ, Schwartz RH, Daniller A et al (1985a)
Morphological signi fi cance of bi fi d uvula. Pediatrics
75:553–561
Shprintzen RJ, Siegel-Sadewitz VL, Amato J et al (1985b)
Anomalies associated with cleft lip, cleft palate, or
both. Am J Med Genet 20:585–596
Shprintzen RJ, Sher AE, Croft CB (1987) Hypernasal
speech caused by hypertrophic tonsils. Int J Pediatr
Otorhinolaryngol 14:45–56
Shprintzen RJ, Singer L, Sidoti EJ et al (1992a)
Pharyngeal fl ap surgery: postoperative complications.
Int Anesthesiol Clin 30:115–124
Shprintzen RJ, Singer L, Sidoti EJ (1992b) Pharyngeal fl ap
surgery: postoperative complications. Int Anesthesiol
Clin 30:115–124
Siegel-Sadewitz
VL,
Shprintzen
RJ
(1982)
Nasopharyngoscopy of the normal velopharyngeal
sphincter: an experiment of biofeedback. Cleft Palate J 19:
194–201
Skolnick ML (1969) Video velopharyngography in
patients with nasal speech, with emphasis on lateral
pharyngeal
motion
in
velopharyngeal
closure.
Radiology 93:747–755
Skolnick ML (1970) Video fl uoroscopic examination of
the velopharyngeal portal during phonation in lateral
and base projections – a new technique for studying
the mechanics. Cleft Palate J 7:803–816
Skolnick ML, McCall GN, Barnes M (1973) The sphinc-
teric mechanism of velopharyngeal closure. Cleft
Palate J 10:286–305
Tatum SA III, Chang J, Havkin N et al (2002) Pharyngeal
fl ap and the internal carotid in velo-cardio-facial syn-
drome. Arch Facial Plast Surg 4:73–80
Williams ML, Shprintzen RJ, Rakoff SJ (1987) Adenoid
hypoplasia in the velo-cardio-facial syndrome. J
Craniofac Genet Dev Biol 7:23–26
Zim S, Schelper R, Kellman R et al (2003) Thickness
and histologic and histochemical properties of the
superior pharyngeal constrictor muscle in velocar-
diofacial syndrome. Arch Facial Plast Surg 5:
503–507

759
S. Berkowitz (ed.), Cleft Lip and Palate,
DOI 10.1007/978-3-642-30770-6_35, © Springer-Verlag Berlin Heidelberg 2013
35
The primary goal of cleft palate repair is to provide
for the development of normal speech, a goal which
is dependent upon the successful establishment
of the functional and structural integrity of the
velopharynx. It has been estimated that between
10 and 35% of patients will demonstrate persistent
velopharyngeal dysfunction (VPD) following cleft
palate repair. The velopharyngeal valve is a com-
plex, dynamic structure that serves to separate the
oral and nasal resonating chambers during speech
production. VPD typically results in a combina-
tion of hypernasal resonance, audible and inau-
dible nasal emission (with or without turbulence),
weak pressure consonants, and, in most pediatric
cases, speci fi c types of articulation errors (known
as compensatory articulation errors) (Kuehn and
Moller 2000 ) . Some patients may also develop dys-
phonia (a rough, breathy vocal quality), as a conse-
quence of vocal hyperfunction to compensate for
VPD (D’Antonio et al. 1988 ) . In infants with overt
clefts or VPD, nasal regurgitation (leakage of food
or liquid through the nasal cavity) may be pres-
ent, although this diminishes signi fi cantly after the
fi rst year of life. The perception of speech symp-
toms consistent with VPD should be con fi rmed by
instrumental assessment to con fi rm the etiology,
size, and consistency of the VP gap, as well as
the movement of the velum and pharyngeal walls
during speech.
Successful surgical management of VPD is criti-
cally dependent upon precise diagnosis and careful
selection of operative technique. In the context of
overall cleft habilitation, successful management
is also critically dependent upon functional inter-
disciplinary collaboration. Management of VPD is
best conducted in an interdisciplinary team context
due to the multifactorial nature of this disorder.
Patients with con fi rmed or suspected VPD require
a thorough clinical evaluation by a plastic surgeon,
speech-language pathologist, and, in many cases,
a geneticist. Occasionally, a maxillofacial prost-
hodontist is also part of this team if nonsurgical
treatment is required. Each of these professionals
should have training and experience in the area of
cleft palate and craniofacial anomalies.
The role of the speech-language pathologist
on this team is to conduct a comprehensive
assessment of the patient’s speech including per-
ceptual speech evaluation of intelligibility, reso-
nance, nasal emission, voice quality, articulation,
and overall speech acceptability, as well as instru-
mental evaluation of VP function for speech.
Surgical Management
of Velopharyngeal Dysfunction
Richard E. Kirschner and Adriane L. Baylis
R. E. Kirschner , M.D. (*)
Chief, Section of Plastic and Reconstructive Surgery ,
Director, Cleft Lip and Palate Center,
Nationwide Children’s Hospital , Columbus , OH , USA
Professor of Clinical Plastic Surgery and Pediatrics ,
The Ohio State University College of Medicine ,
700 Children’s Drive , Columbus , OH 43205-2664 , USA
e-mail: richard.kirschner@nationwidechildrens.org
A. L. Baylis , Ph.D., CCC-SLP
Director, Resonance Disorders Program ,
Nationwide Children’s Hospital, Columbus, OH, USA
Assistant Professor of Clinical Plastic Surgery,
Speech and Hearing Science, and Pediatrics,
The Ohio State University ,
700 Children’s Drive , Columbus , OH 43205-2664 , USA
e-mail: adriane.baylis@nationwidechildrens.org

760
R.E. Kirschner and A.L. Baylis
The speech pathologist collaborates in decision-
making regarding the presence and severity of the
VPD and in formulating a tentative hypothesis for
the etiology of the VPD. In addition, the speech
pathologist determines the impact of any articula-
tion errors on the function of the VP mechanism
and whether (1) the patient is a candidate for
imaging during speech or (2) additional speech
therapy is needed prior to imaging. When indi-
cated, the geneticist performs a physical exam and
obtains a thorough family history and medical his-
tory to determine whether speci fi c laboratory test-
ing is indicated. In many cases, VPD occurs in the
context of a broader syndrome, especially in “non-
cleft” patients (e.g., 22q11.2 deletion syndrome).
With the advent of faster, more speci fi c, and more
cost-effective genetic testing, as well as an appre-
ciation of milder phenotypes of syndromes,
genetic testing is employed prior to surgical man-
agement of VPD in a growing number of cases.
The plastic surgeon conducts a craniofacial and
oral exam, con fi rms perceptual symptoms of VPD,
obtains a thorough medical history, and evaluates
for upper airway obstruction and surgical risk fac-
tors. The surgeon participates in imaging of VP
function during speech to con fi rm the diagnosis,
extent, and nature of VPD and to select and plan
surgical intervention. The primary aim of surgical
management is to establish velopharyngeal com-
petency while avoiding the complications associ-
ated with nasal airway obstruction. The choice of
surgical procedure must be individualized, taking
into consideration the speci fi c anatomy and func-
tion of the velopharyngeal valve, as well as associ-
ated comorbid conditions. The surgical procedures
employed most commonly in the management of
VPD include the Furlow double-opposing
Z-palatoplasty, posterior pharyngeal fl ap, and
sphincter pharyngoplasty. Augmentation of the
posterior pharyngeal wall has been used less fre-
quently and will not be discussed in this chapter.
35.1
Preoperative Assessment
Careful preoperative assessment is paramount to
optimizing speech outcome while minimizing
complications. Selection of the best surgical pro-
cedure and the speci fi c technical details of its
performance requires a thorough understanding
of the anatomy and physiology of the dysfunc-
tional velopharynx. A thorough medical history
should be obtained, including an assessment of
prior surgery. The patient-family interview is an
important component of preoperative assessment,
which includes a review of:
Current concerns with speech
•
Current concerns with feeding/swallowing,
•
including leakage of food/liquid through the
nose
Primary medical diagnoses (e.g., cleft palate,
•
syndrome, other birth defects, neuromuscular
disease)
Pregnancy history, complications, medication
•
use, and any exposure to teratogens
Birth and delivery history and complications
•
History of any breastfeeding, swallowing, or
•
other feeding dif fi culties during infancy,
including leakage of food/liquid through the
nose
Developmental history
•
Speech therapy history
•
History of hearing loss or middle ear disease,
•
including history of frequent ear infections or
effusions
History of snoring, restless sleep, fatigue, or
•
symptoms consistent with sleep apnea
Surgical history including prior tonsillectomy,
•
adenoidectomy, and, if appropriate, cleft-re-
lated surgical history and timing, etc., as well
as history of any surgical-related complica-
tions or risk factors (e.g., bleeding disorders,
anesthesia reactions)
History of any past genetic testing and results
•
Family history of cleft lip/palate, nasal speech,
•
speech delay, or articulation/pronunciation
dif fi culties; hearing loss; learning disabilities;
and other medical conditions
Syndromic diagnoses and comorbid conditions
should be noted, as they may have a signi fi cant
impact both on the success of the surgical proce-
dure and on the incidence of postoperative compli-
cations. When appropriate, additional preoperative
lab testing and medical and anesthetic consultation
should be obtained. Patients with a history of upper
airway obstruction, including those with Pierre

761
35 Surgical Management of Velopharyngeal Dysfunction
Robin sequence, also require careful assessment of
the upper airway, including polysomnography.
A thorough craniofacial and intraoral exami-
nation should be completed to look for clues
regarding the type (VP insuf fi ciency vs. incom-
petency) and etiology of VPD. Features that
should be assessed include:
Symmetry of craniofacial structures
•
Symmetry and length of the soft palate at rest
•
and during elevation with phonation
Presence, size, and location of any palatal
•
fi stulae
Shape (single, wide, or bi fi d) and symmetry of
•
the uvula
Degree and consistency of velar elevation dur-
•
ing phonation
Signs of submucous cleft palate (bi fi d uvula,
•
zona pellucida, posterior notch, v-shaped tent-
ing of velum upon elevation)
Length of palate relative to depth of orophar-
•
ynx (palatopharyngeal disproportion)
Evidence of past surgical management includ-
•
ing scarring post-palatoplasty, scarring post-
tonsillectomy, pharyngeal fl ap, and sphincter
pharyngoplasty
This examination should also include a thor-
ough assessment of the type and anatomic integ-
rity of prior palatoplasty. When aerodynamically
signi fi cant fi stulae are identi fi ed (e.g., audible nasal
emission is heard during speech), these should be
repaired or obturated prior to functional assessment
of the velopharynx. Position of the levator muscles
is noted, when possible. Sagittal orientation of the
levator muscle bundles suggests absent or incom-
plete intravelar veloplasty. Patients with complete
or partial velar dehiscence should undergo palatal
repair prior to reassessment of velopharyngeal func-
tion. Tonsillar size should also be noted, as tonsillar
enlargement may increase the risk of postoperative
sleep apnea. Conversely, patients who have under-
gone prior tonsillectomy may demonstrate scarring
of the posterior tonsillar pillars that may impair the
proper construction of a sphincter pharyngoplasty.
The intraoral exam in isolation should never
determine the need for surgical treatment. The
intraoral fi ndings should be interpreted in the
context of the perceptual speech evaluation, and
subsequent instrumental and VP imaging fi ndings
in order to develop an appropriate treatment plan.
The intraoral exam often reveals fi ndings that
may correlate with the perceptual speech fi ndings;
however, the nature and severity of VPD should
be validated with direct VP imaging.
35.1.1 The Speech Evaluation
A perceptual speech evaluation should be conducted
by a certi fi ed and licensed speech- language pathol-
ogist with training and experience in the assessment
of patients with cleft palate, resonance disorders,
articulation disorders (including knowledge of com-
pensatory articulation errors), and voice disorders.
The speech pathologist should also have advanced
knowledge in anatomy and physiology of the vocal
tract and upper airway. The speech-language pathol-
ogist should conduct a clinical evaluation as out-
lined below, making speci fi c adjustments in the
assessment protocol for patient age, developmental
level, language, articulation pro fi ciency, hearing
status, and cooperation level:
1. Spontaneous speech sample (e.g., during con-
versation, picture description, or play)
2. Rote speech tasks (e.g., counting, days of the
week)
3. Sentence repetition tasks
4. Word repetition and picture-naming tasks,
including standardized articulation testing
when errors are present
5. Stimulability probes, with and without nasal
occlusion
As a patient produces this speech sample, the
speech pathologist makes auditory-perceptual judg-
ments of the patient’s articulation, resonance, voice,
intelligibility, and nasal emission (Henningsson
et al. 2008 ) . Equal-appearing interval scales are the
most popular auditory-perceptual rating tool in the
clinical setting; however, more recent studies have
led to questions regarding their validity when com-
pared to ratio-based methods (e.g., direct magni-
tude estimation and visual analog scaling) (Whitehill
and Lee 2002 ) . Regardless of which rating method
is utilized, there is strong consensus that perceptual
assessment of speech remains the gold standard for
evaluation of speech, judgment of need for treat-
ment, and judgment of outcome (Kuehn and Moller
2000 ) .

762
R.E. Kirschner and A.L. Baylis
Audio and/or video recording of the speech
tasks should be completed whenever possible.
Clinical archiving will allow for comparison
before/after treatment, outcome assessment, and
data collection for potential use in quality improve-
ment projects or future research. Patients with a
history of VPD should undergo a speech evalua-
tion at least annually and more frequently if there
are changing needs, such as when an articulation
disorder is present. If the patient undergoes surgery
for VPD, a postsurgical speech assessment should
be conducted approximately 6 months after sur-
gery and then annually thereafter until growth and
development are complet or until all other therapy
goals met and the patient is discharged.
After the perceptual speech evaluation and
intraoral examination have been completed, the
speech pathologist must determine if the patient
demonstrates a clinically signi fi cant speech dis-
order and if the patient’s speech pro fi le is consis-
tent with VPD. If VPD is suspected, the speech
pathologist must then determine whether the
patient has suf fi ciently accurate articulation to
obtain valid imaging of the VP port and whether
they are likely to provide adequate cooperation to
complete instrumental testing and/or imaging.
35.1.2 Instrumental Assessment of VP
Function for Speech
Instrumental evaluation of speech is a helpful adjunct
to the perceptual speech evaluation. This tradition-
ally includes some combination of acoustic assess-
ment, aerodynamic testing, and VP imaging.
Nasalance is an acoustic correlate of nasality and
may be measured by a variety of commercially
available tools (e.g., NasalView TM , Nasometry TM ,
Nasality Visualization System TM ). Nasometry TM is
perhaps the most widely used acoustic assessment
tool for measurement of nasality. The speech pathol-
ogist must fi rst critically evaluate whether the patient
is a good candidate for acoustic assessment based
upon their age, cooperation, articulation skills, voice
quality, and language or dialect, as well as under-
stand the risk for confounding factors that can reduce
the validity of the nasalance score (e.g., dysphonia,
nasal turbulence, compensatory articulation errors,
mixed resonance). If the patient is determined to be
an appropriate candidate for acoustic assessment of
nasality, the appropriate level and type of stimuli
should be selected for use during testing. In general,
hypernasal resonance correlates with elevated
nasalance scores on oral speech stimuli, although
perceived severity does not always demonstrate a
linear relationship with nasalance scores (Fletcher
1976 ; Hardin et al. 1992 ) . Nasalance scores are
helpful as a comparison measure pre- and posttreat-
ment, but should never be considered a substitute for
perceptual speech evaluation when making a deter-
mination of the need for surgical intervention.
Aerodynamic (pressure- fl ow) testing is another
useful tool for screening and evaluation of VP
function during speech (e.g., PERCI-SARS TM ,
Microtronics). It allows for direct measurement of
intraoral pressure, nasal air fl ow, VP closure tim-
ing, and indirect measurement of VP ori fi ce size
(Warren and DuBois 1964 ; Warren et al. 1985 ) .
The degree of speech pro fi ciency and cooperation
required for pressure- fl ow testing is similar to that
required for acoustic assessment. The word “ham-
per” is classically used as the speech stimulus for
pressure- fl ow testing because of its /mp/ sound
sequence which requires the velopharynx to open
and close rapidly (Warren and DuBois 1964 ) . An
ori fi ce of 10–20 mm 2 (or larger) during the /p/
sound of this stimulus has been shown to correlate
highly with perceptual observations of hypernasal-
ity (Warren et al. 1985 ) ; however, even smaller VP
gaps may be associated with hypernasality, espe-
cially when VP closure timing is also abnormal
(Warren et al. 1993, 1994 ; Leeper et al. 1998 ) .
After the perceptual speech evaluation, instru-
mental testing, and intraoral exam are completed,
the team of providers confers to share fi ndings and
preliminary impressions. Together, the team deter-
mines if the patient requires VP imaging and the
timing of the procedure (i.e., same visit, after addi-
tional speech therapy, after tonsillectomy, etc.).
Regardless of the fi ndings from the perceptual
speech evaluation, intraoral exam, and instrumen-
tal speech testing, direct imaging of the VP port
during speech is required for de fi nitive diagnosis
of VPD and the most accurate treatment planning.
VP imaging also provides important informa-
tion for assessing the upper airway to determine
if additional management will be required prior
to undertaking VP surgery (e.g., tonsillectomy,
adenoidectomy, or other preoperative imaging), to
minimize risks.

763
35 Surgical Management of Velopharyngeal Dysfunction
35.1.3 Imaging of the VP Mechanism
During Speech
In all cases, the diagnosis of VPD should be
con fi rmed by nasopharyngoscopy and/or multiview
video fl uoroscopy during speech (MVVF) (Figs. 35.1
and 35.2 ). Some centers have moved to the exclu-
sive use of nasopharyngoscopy to avoid the radia-
tion exposure associated with MVVF, while others
still perform both procedures as part of a standard
presurgical assessment. Nasophar yngoscopy is min-
imally invasive, can be performed in the outpatient
setting, and is well tolerated by even the youngest of
patients (typically ages 4 years and older).
Nasopharyngoscopy during speech allows for the
subjective assessment of VP gap size, VP closure
consistency, shape of the VP gap, and VP closure
pattern (Golding-Kushner et al. 1990 ) . Other upper
airway structures can also be examined (e.g., tonsils,
adenoid, larynx). The primary bene fi t of nasophar-
Fig. 35.1 Nasopharyngoscopic images of the velopharyngeal structures in a child with VPD. Left , velopharyngeal
opening at rest. Right , persistent velopharyngeal gap during production of the /s/ sound (From 2nd Ed. Fig. 35.1 )
Fig. 35.2 Lateral view video fl uoroscopic images of
the velopharyngeal mechanism in a child with VPD.
Left , velopharyngeal opening at rest. Right , persistent
velopharyngeal gap ( arrow ) during production of the
word “puppy” (From Murphy and Scambler ( 2005 ) , with
permission. From 2nd Ed. Fig. 35.2 )

764
R.E. Kirschner and A.L. Baylis
yngoscopy is the ability to directly view the VP port
in color, during connected speech. It is also more
sensitive to detecting small or asymmetric VP gaps,
VPD persisting after pharyngeal fl ap, and allows for
advanced diagnosis of muscular abnormalities such
as in cases of occult submucous cleft palate or ante-
riorly displaced levator veli palatini musculature.
To improve patient comfort with the proce-
dure, topical anesthetic and/or nasal deconges-
tant may be applied transnasally, although is
not required. Application of a simple surgical
lubricant to the external surface of the scope
(avoiding the lens) also facilitates ease of trans-
nasal insertion of the scope. Typically, nasophar-
yngoscopy is completed and/or interpreted by
the speech pathologist and surgeon together
and is videorecorded. High-resolution cameras
(larger in diameter) are now available which
offer improved image quality, magni fi cation,
fi eld of view, and slow motion or frame-by-
frame analysis; however, pediatric smaller-
diameter nasopharyngoscopes tend to be better
tolerated by younger patients. Once the scope is
inserted transnasally through the middle or
inferior meatus, the boundaries of the VP port
should be visualized (i.e., anteriorly—soft pal-
ate, posteriorly—posterior pharyngeal wall/
adenoid pad, laterally—lateral pharyngeal
walls). The patient is then asked to engage in
the production of a standard speech sample to
assess VP closure during speech. The speech
pathologist should select a speech sample
focused on the patient’s accurately articulated
words and sentences. A range of stimuli (i.e.,
different phonemic contexts, range of utterance
length, and contrasting error vs. accurate pro-
ductions) are useful for gaining an understand-
ing of the underlying pathology; however, the
most
representative
image
of
maximum
attempted VP closure will be obtained during
the accurately produced (articulated) oral pres-
sure consonants in connected speech. Images
obtained during compensatory articulation error
production (e.g., glottal stops, nasal fricatives)
have been shown to be associated with a lesser
degree of attempted VP closure than accurate
speech production (Henningsson and Isberg
1991 ) . Overall, the resulting images obtained
during speech will allow the speech pathologist
and surgeon to determine the most appropriate
type of treatment, as well as location, type, and
size
speci fi cations
for
potential
surgical
intervention to improve VP closure for speech.
Examples of speech stimuli include:
Pet a puppy.
•
Buy baby a bib.
•
Dad did it.
•
Tell Ted to try.
•
Go get a cookie for Kate.
•
Fifty- fi ve fi sh.
•
Sissy sees the sky.
•
She likes to shop for shoes.
•
Chocolate chip cookies.
•
All of the above stimuli can be shortened if
needed to adjust for patient speech pro fi ciency or
other articulation constraints. It is suggested that if
the patient is only capable of accurate articulation at
the single-word level, then multiple repetitions
should be obtained in order to mimic the timing
demands of natural VP closure (e.g., puppy-puppy-
puppy). Additional stimuli including nasal conso-
nants (e.g., My mom made muf fi ns.) may be added
to assess hyponasal speech or alternating oral-nasal
contents (e.g., hamper hamper) to assess VP closure
timing and coordination. The speech pathologist
should carefully interpret the VP images in the con-
text of the phonemic demands (i.e., oral vs. nasal,
high pressure vs. low pressure) and accuracy of the
sounds produced. Options for rating and measuring
ratios of movement from the nasopharyngoscopy
exam are outlined in Golding-Kushner et al. ( 1990 ) .
In patients who demonstrate persistent or
recurrent VPD after surgical management, care-
ful intraoral and nasopharyngoscopic examination
yields important diagnostic information. Pharyngeal
fl ap integrity, width, port size, and position relative
to the attempted level of velar closure should all
be assessed. Occasionally, velar function may be
impaired by the in fl uence of a narrow fl ap that teth-
ers the palate by virtue of being placed too low on the
posterior pharyngeal wall. In such cases, the tethering
fl ap should be surgically divided and the velophar-
ynx reassessed. Similarly, the integrity, port size, and
position of a previously constructed sphincter phar-
yngoplasty may yield important clues as to the nature
of persistent VPD after surgical management.
MVVF is a valid alternative to nasopharyngoscopy
for the assessment of VP function during speech, in

765
35 Surgical Management of Velopharyngeal Dysfunction
most cases. MVVF typically requires a radiologist
and speech pathologist to obtain and record the
exam, and the images are later reviewed with the
surgeon. Motion fl uoroscopy records the movement
of intraoral and velopharyngeal structures during
speech from multiple angles (Skolnick 1970 ) .
Advantages of MVVF include more precise data
regarding palatal length, pharyngeal depth, and rel-
ative size of upper airway anatomy, as well as infor-
mation regarding the contribution of tongue
movement to speech (or even to assisting VP clo-
sure). Image quality is best if liquid barium is
instilled into the nasal cavity during the exam to
coat the surfaces of the VP mechanism. At mini-
mum, the lateral view is obtained, followed by fron-
tal, base, and Towne’s views. Measurement and
rating procedures for interpretation of MVVF are
also reviewed in Golding-Kushner et al. ( 1990 ) .
Overall, preoperative imaging of the velophar-
ynx is essential to the accurate assessment of VPD
and therefore to surgical planning. Such imaging
serves as an essential adjunct to visual assessment
of levator muscle orientation, velar integrity and
function, and adenoid and tonsillar morphology.
Occasionally, velopharyngeal dysfunction is
found to result from attempted closure of the
velum against an irregularly shaped adenoid pad.
Similarly, marked tonsillar enlargement may also
interfere with velopharyngeal closure (MacKenzie-
Stepner et al. 1987a ; Shprintzen et al. 1987 ) . In
such cases, consideration should be given to ade-
noidectomy or tonsillectomy, respectively, prior
to reassessment of velopharyngeal function. In all
cases, the extent, pattern, symmetry, and attempted
level of velopharyngeal closure should be noted.
When gap size is small and the levators are sagit-
tal in position, Furlow palatoplasty may be
suf fi cient treatment. In patients with larger gaps
and/or transverse levator orientation, conventional
wisdom suggests that closure pattern dictates the
choice of procedure. Posterior pharyngeal fl aps
are theoretically best suited for those patients that
demonstrate good lateral pharyngeal wall motion
and sagittal closure patterns, whereas sphincter
pharyngoplasty is theoretically best suited for
those with limited lateral wall motion and coronal
closure patterns. It should be noted, however, that,
despite the intuitive basis for such an approach,
there is little clinical evidence of its soundness.
Magnetic resonance imaging should also be per-
formed preoperatively in all patients with 22q11.2
deletion syndrome. One in fi ve affected patients
will demonstrate medial displacement of one or
both internal carotid arteries (D’Antonio and Marsh
1987 ; MacKenzie-Stepner et al. 1987b ; Mitnick
et al. 1996 ; Ross et al. 1996 ) , thus increasing the
risk for arterial injury during posterior pharyngeal
fl ap surgery or sphincter pharyngoplasty (Fig. 35.3 ).
Arterial pulsations noted at the time of nasendos-
copy may be transmitted through the surrounding
Fig. 35.3 Medial deviation of the internal carotid artery ( arrow ) at the level of the nasopharynx in a child with a chro-
mosome 22q11.2 deletion (From Murphy and Scambler ( 2005 ) , with permission. From 2nd Ed. Fig. 35.3 )

766
R.E. Kirschner and A.L. Baylis
soft tissues, rendering endoscopy alone an unreli-
able means of assessing carotid anatomy. Although
some have suggested that carotid artery displace-
ment should contraindicate pharyngoplasty, others
have demonstrated that surgery can be safely per-
formed in this setting (Witt et al. 1998b ; Tatum
et al. 2002 ) . In many cases, the displaced vessel(s)
will lateralize with neck extension at the time of
surgery. When a displaced carotid artery can still be
palpated beneath the posterior pharyngeal mucosa
after positioning, the design of a pharyngeal fl ap
can be modi fi ed, skewing the fl ap away from the
displaced vessel. In all such cases, preoperative
delineation of arterial anatomy plays an important
role in surgical planning and informed consent.
35.2
Furlow Double-Opposing
Z-Palatoplasty (Fig. 35.4 )
Despite its original description as a technique for
primary repair of palatal clefts (Furlow 1978 ) ,
the Furlow double-opposing Z-palatoplasty has
increasingly become recognized as an effective
procedure for the management of VPD in selected
patients. Transposition of the posteriorly based
fl aps reorients the levator veli palatini muscle
bundles and reconstructs the levator sling. It is for
this reason, however, that the Furlow procedure
should not be employed in patients who have
already undergone complete intravelar veloplasty.
The Z-plasty design provides for velar lengthening
oral mucosal flap
nasal mucosal flap
oral
musculo-mucosal flap
nasal
musculo-mucosal flap
nasal flaps rotated
oral flaps rotated
Fig. 35.4 Furlow double-
opposing Z-palatoplasty
(From Murphy and Scambler
( 2005 ) , with permission.
From 2nd Ed. Fig. 35.6 )

767
35 Surgical Management of Velopharyngeal Dysfunction
while preventing the cicatricial shortening that
may be seen with straight-line velar repair. These
features render the Furlow repair ideally suited
for patients with VPD associated with unrepaired
submucosal clefts and those with small-gap VPD
following palate repair without intravelar velo-
plasty. The procedure should not be performed in
patients that have previously undergone recon-
struction of the levator sling.
The anatomy of the Z-plasty design is deter-
mined by the underlying palatal anatomy. The
posteriorly based fl aps of both the oral and nasal
sides comprise both muscle and mucosa, whereas
the anteriorly based fl aps comprise mucosa alone.
The Z-plasty incisions extend from the tip of the
hamulus to the posterior edge of the hard palate
at the cleft margin on one side and from the base
of the uvula at the cleft margin to the tip of the
hamulus on the other. Dissection must be carried
out laterally to the hamulus in each side in order
to ensure that the levator fi bers are completely
divided from the posterior edge of the hard pal-
ate. This is necessary for proper reconstruction
and retropositioning of the levator sling with
transposition of the posteriorly based fl aps.
Several authors have con fi rmed the ef fi cacy of
the Furlow double-opposing Z-palatoplasty in
the management of VPD. Hudson et al. ( 1995 )
reported that 85 % of patients with VPD follow-
ing primary palatoplasty achieved normal reso-
nance after Furlow conversion. Chen et al. ( 1994 )
reported gap size to be the most important factor
in determining the success of Furlow palatoplasty
in the management of VPD, with the majority of
patients with a preoperative gap of 5 mm or less
achieving velopharyngeal competence postoper-
atively. D’Antonio et al. ( 2000 ) reported normal
resonance after conversion to Furlow palatoplasty
in 75 % of selected patients with post-palato-
plasty VPD. All patients in their series demon-
strated incomplete levator retropositioning, good
velar motion, and a small velopharyngeal gap
preoperatively.
As noted above, the Furlow procedure is ide-
ally suited to those patients with nonsyndromic
submucosal cleft palate and VPD. As in patients
with repaired overt clefts, success rates appear
to depend primarily on gap size. Seagle et al.
( 1999 ) reported that 83 % of patients with VPD
associated with submucosal cleft palate demon-
strated velopharyngeal competence after Furlow
Z-plasty, with successful outcomes observed
most frequently in patients with a gap size under
8 mm. Chen et al. ( 1996 ) noted that VP com-
petence was achieved in 97 % of patients with
submucosal clefts and gaps of 5 mm or less.
Studies have con fi rmed that the Furlow Z-plasty
produces a variable degree of palatal lengthening
(D’Antonio et al. 2000 ) . As noted above, however,
the geometry of the Z-plasty incisions is deter-
mined by the underlying palatal anatomy. It
stands to reason, therefore, that the success of
the procedure is inevitably linked to gap size
and to the extent of velar lengthening that can be
achieved given the underlying palatal anatomy.
Bleeding, oronasal fi stula formation, and
upper airway obstruction have all been reported
following Furlow palatoplasty. By virtue of the
Z-plasty design, the technique achieves palatal
lengthening at the expense of velar width, thereby
creating a potential increase in tension at the
suture line. Fistula formation can be minimized,
however, by reducing tension through the liberal
use of lateral relaxing incisions. Although mild
upper airway obstruction has been documented
following Furlow palatoplasty, such has been
noted to resolve in nearly all patients within 3
months of surgery (Liao et al. 2003 ) . Moreover,
patients who have undergone Furlow palatoplasty
demonstrate a signi fi cantly lower incidence and
severity of upper airway obstruction 6 or more
months postoperatively than do those patients
who have undergone posterior pharyngeal fl ap
surgery (Liao et al. 2004 ) .
35.3
Posterior Pharyngeal Flap
(Fig. 35.5 )
In 1865, Passavant fi rst described the surgical man-
agement of VPD by attachment of the velum to the
posterior pharynx (Passavant 1865 ) . Schoenborn
described the use of an inferiorly-based posterior
pharyngeal fl ap in 1875 and of a superiorly-based
fl ap a decade later (Schoenborn 1875, 1886 ) .

768
R.E. Kirschner and A.L. Baylis
Suture in uvula
Transverse incision
in soft palate
Posterior
pharyngeal
flap
Fig. 35.5 Posterior
pharyngeal fl ap
(From Murphy and
Scambler ( 2005 ) ,
with permission.
From 2nd Ed.
Fig. 35.4 )
Pharyngeal fl ap surgery was popularized in the
United States by Padgett in the 1930s (Padgett
1930 ) . For much of the twentieth century, the pha-
ryngeal fl ap remained the workhorse of VPD sur-
gery. With the addition of several modi fi cations,
the technique remains widely popular today.
The posterior pharyngeal fl ap acts as a static
central obturator of the velopharynx, relying
upon lateral pharyngeal wall motion to close the
lateral ports during sound production. The proce-
dure is best suited, therefore, for management of
VPD in the patient with a sagittal or sphincteric
closure pattern and a persistent central gap.
Laterally based, inferiorly based, and superiorly
based fl aps have all been described, though the
last remains the most widely used design today.
Optimization of surgical outcome relies upon
careful placement of the fl ap at the attempted
level of velar contact with the posterior pharyn-
geal wall, as determined by preoperative imag-
ing. As noted above, pharyngeal fl aps that have
been designed too low or that have migrated infe-
riorly due to cicatricial changes may tether the
velum and restrict velopharyngeal closure.
Just as for fl ap position, the width of the pha-
ryngeal fl ap should be tailored to each patient’s
needs as determined by preoperative assessment.
Patients with large gaps and relatively poor lat-
eral wall motion may require wider fl aps in order
to achieve velopharyngeal competence than those
with smaller gaps and more robust lateral wall
motion. Flap width is dependent not only on the

769
35 Surgical Management of Velopharyngeal Dysfunction
breadth of the fl ap design but also on the breadth
of fl ap inset into the soft palate. Inset may be
achieved by dividing the velum in the midline or
through the use of a transverse incision across the
posterior velum, the latter technique allowing for
greater fl exibility in establishing fl ap width and,
conversely, lateral port dimension (Argamaso
1995 ) . The tendency for fl aps to narrow or “tube”
over time may be minimized by the creation of
mucosal lining fl aps from the posterior velum or
through the use of short, broad pharyngeal fl aps.
In all cases, fl ap design must be balanced against
the risk of inducing postoperative upper airway
obstruction, as wider fl aps carry a higher risk of
postoperative sleep apnea.
Careful surgical planning and individualization
of fl ap design and inset are essential to achieving
successful outcomes in pharyngeal fl ap surgery.
Canady et al. ( 2003 ) reported their 10-year experi-
ence with pharyngeal fl ap surgery at the University
of Iowa. Success, de fi ned as normal or near normal
resonance, was achieved in 78 % of patients.
Argamaso ( 1995 ) reported elimination of hyper-
nasality in 96 % of patients following pharyngeal
fl ap surgery. Similarly, borderline or normal
velopharyngeal function was observed postopera-
tively by Sullivan et al. in 97 % of patients (Sullivan
et al. 2010 ) . Studies have demonstrated the results
of pharyngeal fl ap surgery to be durable, with
stable results noted more than a decade after
surgical treatment (Cable et al. 2004 ) .
The reported complication rate for pharyngeal
fl ap surgery ranges from 6.3 to 19.5 % (Valnicek
et al. 1994 ; Fraulin et al. 1998 ; Hofer et al. 2002 ) .
The operation may be complicated by hemor-
rhage, fl ap dehiscence, hyponasality, persistent
VPD, and nasal airway obstruction. Airway
compromise has been reported to result in a small
number of deaths after posterior pharyngeal fl ap
surgery. Complications may be increased by
association with limited operator experience,
associated medical conditions, and concurrent
surgical procedures. Of all complications, upper
airway compromise is the most common. Due to
postoperative edema, nearly all patients demon-
strate some transient nasal airway obstruction
following posterior pharyngeal fl ap surgery, and
careful monitoring during the immediate postop-
erative period is therefore essential. In all but a
small percentage of patients, nocturnal airway
obstruction resolves within several months of
surgery. Syndromic patients and those with a
history of Pierre Robin sequence often present
with associated functional or anatomic airway
anomalies and may therefore be at greater risk
for persistent upper airway obstruction after sur-
gery (Wells et al. 1999 ; Abramson et al. 1997 ) .
The presence of tonsillar hypertrophy should
alert the surgeon to an increased risk of sleep
apnea following creation of a pharyngeal fl ap
(Ysunza et al. 1993 ) . In such cases, tonsillectomy
should be performed prior to velopharyngeal
imaging and subsequent pharyngeal fl ap surgery.
Persistent VPD following posterior pharyn-
geal fl ap surgery may result from inappropriate
use of the procedure (i.e., poor lateral wall
motion), from poor surgical design (i.e., a fl ap
that is too low or too narrow), or from cicatricial
alterations in fl ap location or dimension. In all
cases, the treatment team must allow adequate
time for resolution of edema and for scar matura-
tion prior to consideration of surgical revision,
usually a period of 12 months. Persistent VPD
demands the same precision in diagnosis and
management as does the initial condition. In all
cases, nasendoscopic visualization is essential to
assessment of the altered velopharyngeal valve,
and surgical management should be tailored to
the functional and anatomic needs so identi fi ed.
35.4
Sphincter Pharyngoplasty
(Fig. 35.6 )
In 1950, Hynes fi rst described the treatment of
VPD by transposition of myomucosal fl aps con-
taining the salpingopharyngeus muscles (Hynes
1950 ) . He later modi fi ed the technique, construct-
ing a sphincter containing the palatopharyngeus
muscles (Hynes 1953 ) . The procedure’s success
was attributed to narrowing of the velopharynx
and augmentation of the posterior pharyngeal wall
with bulky, often contractile fl aps (Hynes 1967 ) .
The concept of dynamic sphincter pharyngoplasty
was later championed by Orticochea ( 1968 ) .
Jackson later modi fi ed the Orticochea’s procedure

770
R.E. Kirschner and A.L. Baylis
and described the technique of sphincter pharyn-
goplasty that is widely utilized today (Jackson and
Silverton 1977 ) .
In the construction of a sphincter pharyngo-
plasty, vertical incisions are made at the junc-
tion of each posterior tonsillar pillar with the
adjacent tonsillar fossa. The longitudinally ori-
ented palatopharyngeus muscles are dissected
and included in the superiorly based fl aps in
order to maximize bulk and contractility.
Vertical incisions are then made at the junction
of the posterior pillars with the posterior pha-
ryngeal wall, the inferior aspect of each fl ap is
then divided, and the fl ap elevated. The fl aps are
then rotated medially and inset into a transverse
incision in the posterior pharyngeal mucosa that
joins the superior aspect of the medial incisions.
Riski et al. ( 1984 ) have written that the level of
inset is critical to success of the procedure and
should correspond to the attempted level of
velar contact as determined by preoperative
imaging. Central port size may be controlled by
altering the extent of fl ap overlap on the poste-
rior pharyngeal wall and should be individualized
Palatoglossal arch
Soft palate
Palatopharyngeal arch
Posterior adenoid pad
Posterior pharynx
Flaps interdigitated
Palatopharyngeus flaps
Fig. 35.6 Sphincter
pharyngoplasty
(From Murphy and
Scambler (2005),
with permission.
From 2nd Ed.
Fig. 35.5 )

771
35 Surgical Management of Velopharyngeal Dysfunction
to the anatomic and functional needs of each
patient. Several studies have shown that not all
sphincters demonstrate contractility (Kawamoto
1995 ; Witt et al. 1998a ) . Port size and fl ap bulk
may therefore play critical roles in achieving
velopharyngeal competence.
Sphincter pharyngoplasty successfully manages
VPD in the majority of carefully selected patients.
Retrospective reviews by Shewmake et al. ( 1992 )
and by Mount and Marsh ( 2002 ) showed that
velopharyngeal competence was achieved in 85
and 72 % of patients, respectively. Riski et al.
( 1992 ) reported that 78 % of 139 patients demon-
strated resolution of hypernasality and normaliza-
tion of pressure- fl ow measurements following
sphincter pharyngoplasty. Poor results were associ-
ated with improper placement of the sphincter on
the posterior pharyngeal wall. Reports by Witt et al.
( 1998c ) and Losken et al. ( 2003 ) cite pharyngo-
plasty revision rates for persistent VPD of 16 and
12.8 %, respectively. In these series, poor outcomes
were associated with dehiscence, syndromic diag-
noses, and greater preoperative nasalence scores.
There is little consensus as to the superiority
of sphincter pharyngoplasty versus posterior pha-
ryngeal fl ap surgery. Indeed, procedure selection
should be based primarily on velopharyngeal
anatomy and function. Nevertheless, Ysunza
et al. found no signi fi cant difference in speech
outcome following randomization of 50 patients
with post-palatoplasty VPD to either sphincter
pharyngoplasty or posterior pharyngeal fl ap
(Ysunza et al. 2002 ) . Abyholm et al. similarly
noted no signi fi cant difference in velopharyngeal
function 12 months following sphincter pharyn-
goplasty or posterior pharyngeal fl ap surgery in a
randomized multicenter trial (Abyholm et al.
2005 ) . Complications following sphincter phar-
yngoplasty are similar to those seen after poste-
rior pharyngeal fl ap surgery: bleeding, dehiscence,
hyponasality, persistent VPD, and nocturnal
upper airway obstruction. In Abyholm’s report,
polysomnographic evidence of obstructive sleep
apnea was rare 1 year following either procedure
(Abyholm et al. 2005 ) . Nevertheless, some have
noted that fragmentation of sleep architecture
may be observed following pharyngoplasty even
in the absence of detectable obstructive apnea
(Saint Raymond et al. 2004 ) .
35.5
Timing of Surgery
Several studies have shown that the age at pha-
ryngeal fl ap surgery may impact speech outcome
(Moll et al. 1963 ; Meek et al. 2003 ; Riski 1979 ) ;
however, many other published studies have
found little to no direct relationship between age
and outcome (Van DeMark and Hardin 1985 ;
Seyfer et al. 1988 ; Becker et al. 2004 ; Hall et al.
1991 ) . Most studies report a link between out-
come and preoperative structural or functional
indices such as severity of hypernasality and the
presence of compensatory articulation errors.
Skoog ( 1965 ) was the fi rst to report that that pha-
ryngeal fl ap surgery resulted in better speech out-
comes if performed in children before 10 years of
age; however, Whitaker et al. ( 1972 ) later reported
that speech results in children aged 13–16 were
not signi fi cantly different than that of the younger
age groups. Riski ( 1979 ) conducted a thorough
study of children pre- and post-pharyngeal fl ap
surgery and found that after pharyngeal fl ap, there
was an acceleration in the acquisition of accept-
able sound production in the year immediately
following surgery. The latter data suggested that
children who had fl aps prior to 6 years of age
made faster gains in articulation skills and reso-
nance than children who had VP surgery after
6 years of age. His fi ndings align with those of
Meek et al. ( 2003 ) , who also reported that speech
development is enhanced by early surgery. Riski
hypothesized that early surgery results in less
severe and less permanent maladaptations in
speech physiology and may clinicians continue to
adhere their practices to this theory. On the con-
trary, Becker et al. ( 2004 ) found no relationship
between age at VP surgery and amount of speech
therapy needed to achieve “normalization” of the
speech impairments secondary to VPD after sur-
gery. Other studies have also found little to no
support for the theory that earlier VP surgery is
more effective, with the exception that there is a
trend for poorer articulation outcomes in children
treated after 10 years of age (Van DeMark and
Hammerquist 1978 ; Seyfer et al. 1988 ) .
Van Demark and Hardin ( 1985 ) challenged the
fi ndings of Riski ( 1979 ) as they did not fi nd a
trend for better articulation with earlier secondary
mgmt. Their data did not support the hypothesis

772
R.E. Kirschner and A.L. Baylis
that early VP management (before age 4) results
in higher articulation pro fi ciency. Overall, they
suggested that age at pharyngeal fl ap is not
extremely critical, but differences in success may
be noted at age extremes. Based on the available
evidence, it appears prudent to consider surgical
intervention as soon as there is consensus that
VPD is present, negatively impacting speech, and
all team members (including the patient-family)
are in agreement that surgical treatment is appro-
priate and offers a signi fi cant likelihood of
improvement of the patient’s speech.
Few studies have addressed the surgical out-
comes of adults undergoing VP surgery. Hall
et al. ( 1991 ) reported outcomes for 20 adults who
underwent pharyngeal fl ap surgery and found
that 75 % demonstrated “normal” resonance post-
surgery, however, less experienced improved
speech intelligibility. This was likely due to the
presence of compensatory articulation errors in
some of the adults, which persisted in most cases.
These errors negatively impact speech intelligi-
bility and may also lead to reduced VP closure
which can subsequently affect resonance and
nasal emission as well. Compensatory articula-
tion may prevent or restrict VP motion and may
result in persisting VPD (Henningsson and Isberg
1991 ) . For adults, careful presurgical assessment
of articulation is required in order to provide the
patient with the most accurate prognosis and
anticipated outcome. The Hall et al. study also
highlighted the importance of reporting hypona-
sality as an outcome as well; as in many reports,
it is simply omitted even though it should be con-
sidered a “poorer outcome.” Many past studies
include hyponasality as a successful outcome
since the VPD was improved; however, there are
multiple well-known complications that tend to
co-occur with hyponasality including mouth
breathing, snoring, decreased dental hygiene,
dif fi culties with nasal secretion management, and
other negative impacts on quality of life.
There continues to be some debate as to
whether to recommend VP surgery prior to cor-
rection of maladaptive articulation patterns or
whether to wait until after these articulation errors
have been remediated. The rationale for earlier
surgical intervention is supported by past research,
presenting the argument that patients bene fi t from
having adequate anatomy and physiology to
achieve VP closure prior to implementing behav-
ioral speech therapy. The counterargument pro-
poses that the diagnosis of VPD may not be clear,
or the true severity of extent of VPD may not be
evident, until after compensatory misarticulations
have been eliminated. These errors have been
shown to negatively impact VP closure physiol-
ogy and will not respond solely to surgical inter-
vention. Regardless of surgery, compensatory
articulation errors will require behavioral speech
therapy for correction, although the duration and
intensity of treatment may vary depend on surgi-
cal timing. The plasticity of the VP mechanism is
likely greatest in the fi rst few years of life as
speech patterns are developing; however, with
appropriate cueing and feedback (such as that
provided by nasopharyngoscopy), later changes
in VP function for articulation are still possible
even into adulthood (Witzel et al. 1988, 1989 ;
Brunner et al. 2005 ) . Ysunza et al. ( 1992 ) also
found that VP movement is signi fi cantly improved
after correction of compensatory articulation
errors, as well as reduction in the size of the VP
gap, prior to undertaking VP surgery.
35.6
Management of Persistent VPD
Although surgical management of VPD success-
fully eliminates hypernasality in most patients,
approximately 15–20 % of patients will require
revision for persistent symptoms of VPD.
Persistent hypernasality after posterior pharyn-
geal fl ap surgery may rarely be the result of com-
plete or partial fl ap dehiscence or may occur
when lateral pharyngeal wall motion is insuf fi cient
to close the lateral ports during speech. The lat-
eral circumstance may result from improper fl ap
design, cicatricial fl ap narrowing, or poor patient
selection (i.e., poor lateral pharyngeal wall
motion) (Fig. 35.7 ). In some cases, a scarred fl ap
that is located too low on the posterior pharyn-
geal wall may restrict palatal elevation, resulting
in persistent VPD. Sphincter pharyngoplasty may
also fail as a result of fl ap dehiscence, poor
design, or poor patient selection.

773
35 Surgical Management of Velopharyngeal Dysfunction
Surgical revision for persistent VPD should be
avoided until scar maturation is complete, as grad-
ual improvement in hypernasality may be observed
for up to 12 months postoperatively. Patients that
continue to demonstrate persistent hypernasality
should undergo diagnostic imaging of the velopha-
ryngeal
port
by
nasendoscopy
and/or
video fl uoroscopy. Patients under consideration for
revisional surgery should be carefully screened for
evidence of upper airway obstruction, and revision
should only be performed in patients with a stable
airway. Management of persistent VPD should
Fig. 35.7 Persistent VPD
after posterior pharyngeal fl ap
surgery. Top , narrow
pharyngeal fl ap at rest.
Bottom , persistent pharyngeal
fl ap ( arrows ) during oral
speech production (From 2nd
Ed. Fig. 35.7 )

774
R.E. Kirschner and A.L. Baylis
then be tailored to each patient’s overall medical
condition, airway status, and speci fi c anatomic
and functional inadequacies of the velopharyngeal
valve. Posterior pharyngeal fl aps that are found to
be too narrow can be augmented by “patch” fl aps
or divided and replaced by wider fl aps or sphincter
pharyngoplasty. Flaps that are found to be too low
and that tether the velum may be repositioned
higher on the posterior pharyngeal wall by V-Y
advancement. Incomplete central port closure after
sphincter pharyngoplasty may be managed by port
tightening or by conversion to a posterior pharyn-
geal fl ap. Although elevation of a pharyngeal fl ap
from a scarred posterior pharynx has the theoreti-
cal disadvantage of poor blood supply to the fl ap,
the procedure has been demonstrated to be reliable
when performed 6–12 months following the pri-
mary procedure (Barone et al. 1994 ) .
Just as for primary surgical management of
VPD, successful secondary treatment requires care-
ful preoperative evaluation and individualized man-
agement. Barone et al. ( 1994 ) have reported on 18
patients who demonstrated incomplete lateral port
closure after posterior pharyngeal fl ap surgery that
was treated by elevation of a new, wider fl ap from
the scarred posterior pharynx. Unilateral port
insuf fi ciency in another three patients was managed
by inset of a small “patch” fl ap on the affected side.
Postoperatively, 18 patients achieved normal reso-
nance, two remained hypernasal, and one became
hyponasal. Witt et al. ( 1998c ) have reviewed the
results of salvage surgery for 13 failed pharyngeal
fl aps, noting that eight were successfully revised
with a single secondary procedure. The remaining
fi ve patients achieved velopharyngeal competence
after a second revisional procedure, but all devel-
oped hyponasal speech. In the same report, 17 of 20
failed sphincter pharyngoplasties were successfully
salvaged with a single surgical revision.
35.7
Summary
The operative timing and approach to the correction
of velopharyngeal dysfunction should represent
a balance between each patient’s speci fi c ana-
tomic and functional demands, airway stability,
and overall health status. Surgeons, speech
pathologists, and researchers should consider
multiple factors beyond resonance, such as
speech acceptability, intelligibility, naturalness,
patient and family satisfaction, as well as the
presence of upper airway obstruction and other
complications, when judging and reporting sur-
gical outcome. Speech impairment associated
with velopharyngeal dysfunction may be a
signi fi cant source of stigmatization in affected
individuals, making its diagnosis and treatment
an imperative. Proper diagnosis and management
of velopharyngeal dysfunction demands a multi-
disciplinary team approach, and surgical plan-
ning should be individualized in order to optimize
outcomes.
References
Abramson DL, Marrinan EM, Mulliken JB (1997) Robin
sequence: obstructive sleep apnea following pharyn-
geal fl ap. Cleft Palate Craniofac J 34:256–260
Abyholm F, D’Antonio L, Davidson Ward SL, Kjǿll L,
Saeed M, Shaw W, Sloan G, Whitby D, Worhington H,
Wyatt R (2005) Pharyngeal fl ap and sphincteroplasty
for velopharyngeal insuf fi ciency have equal outcome
at 1 year postoperatively: results of a randomized trial.
Cleft Palate Craniofac J 42:501–511
Argamaso RV (1995) Pharyngeal fl ap surgery for velopha-
ryngeal insuf fi ciency. In: Jurkiewicz MJ, Culbertson
JH (eds) Operative techniques in plastic and recon-
structive surgery. WB Saunders, Philadelphia
Barone CM, Shprintzen RJ, Strauch B, Sablay LB,
Argamaso RV (1994) Pharyngeal fl ap revisions: fl ap
elevation from a scarred posterior pharynx. Plast
Reconstr Surg 93:279–284
Becker DB, Grames LM, Pilgram T, Kane AA, Marsh JL
(2004) The effect of timing of surgery for velopharyngeal
dysfunction on speech. J Craniofac Surg 15:804–809
Brunner M, Stellzig-Eisenhauer A, Proschel U, Verres R,
Komposch G (2005) The effect of nasopharyngoscopic
biofeedback in patients with cleft palate and velopharyn-
geal dysfunction. Cleft Palate Craniofac J 42:649–657
Cable BB, Canady JW, Karnell MP, Karnell LH, Malick
DN (2004) Pharyngeal fl ap surgery: long-term
outcomes at the University of Iowa. Plast Reconstr
Surg 113:475–478
Canady JW, Cable BB, Karnell MP et al (2003) Pharyngeal
fl ap surgery: protocols, complications, and outcomes
at the University of Iowa. Otolaryngol Head Neck
Surg 129:321–326
Chen PK, Wu JT, Chen YR, Noordhoff MS (1994)
Correction of secondary velopharyngeal insuf fi ciency
in cleft palate patients with the Furlow palatoplasty.
Plast Reconstr Surg 94:933–941

775
35 Surgical Management of Velopharyngeal Dysfunction
Chen PK, Wu JT, Hung KF, Chen YR, Noordhoff MS
(1996) Surgical correction of submucous cleft palate
with Furlow palatoplasty. Plast Reconstr Surg
97:1136–1146
D’Antonio LL, Marsh JL (1987) Abnormal carotid arter-
ies in the velocardiofacial syndrome. Plast Reconstr
Surg 80:471–472
D’Antonio L, Muntz H, Province M, Marsh J (1988)
Laryngeal/voice fi ndings in patients with velopharyn-
geal dysfunction. Laryngoscope 98:432–488
D’Antonio LL, Eichenberg BJ, Zimmerman GJ et al
(2000) Radiographic and aerodynamic measures of
velopharyngeal anatomy and function following
Furlow Z-plasty. Plast Reconstr Surg 106:
539–549
Fletcher SG (1976) “Nasalance” vs listener judgments of
nasality. Cleft Palate J 13:31–44
Fraulin FO, Valnicek SM, Zuker RM (1998) Decreasing
the perioperative complications associated with the
superior pharyngeal fl ap operation. Plast Reconstr
Surg 102:10–18
Furlow LT (1978) Cleft palate repair: preliminary report
on lengthening and muscle transposition by z-plasty.
In: Paper presented at annul meeting of Southeastern
Society of Plastic and Reconstructive Surgeons, Boca
Raton, 1978
Golding-Kushner KJ et al (1990) Standardization for the
reporting of nasopharyngoscopy and multiview
video fl uoroscopy: a report from an international work-
ing group. Cleft Palate Craniofac J 27:337–348
Hall CD, Golding-Kushner KJ, Argamaso RV, Strauch B
(1991) Pharyngeal fl ap surgery in adults. Cleft Palate
Craniofac J 28:179–183
Hardin MA, Van Demark DR, Morris HL, Payne MM
(1992) Correspondence between nasalance scores and
listener judgments of hypernasality and hyponasality.
Cleft Palate Craniofac J 29:346–351
Henningsson G, Isberg A (1991) A cineradiographic study
of velopharyngeal movements for deviant versus non-
deviant articulation. Cleft Palate Craniofac J 28:
115–118
Henningsson G, Kuehn DP, Sell D, Sweeney T, Trost-
Cardamone JE, Whitehill TL (2008) Universal param-
eters for reporting speech outcomes in individuals
with cleft palate. Cleft Palate Craniofac J 45:1–17
Hofer SO, Dhar BK, Robinson PH, Goorhuis-Brouwer
SM, Nicolai JP (2002) A 10-year review of periopera-
tive complications in pharyngeal fl ap surgery. Plast
Reconstr Surg 110:1393–1397
Hudson DA, Grobbelaar AO, Fernandes DB, Lentin R
(1995) Treatment of velopharyngeal incompetence by
the Furlow Z-plasty. Ann Plast Surg 34:23–26
Hynes W (1950) Pharyngoplasty by muscle transplanta-
tion. Br J Plast Surg 3:128–135
Hynes W (1953) The results of pharyngoplasty by muscle
transplantation in failed “cleft palate” cases, with spe-
cial reference to the in fl uence of the pharynx on voice
production. Ann R Coll Surg Engl 13:17–35
Hynes W (1967) Observations on pharyngoplasty. Br
J Plast Surg 20:244–256
Jackson IT, Silverton JS (1977) The sphincter pharyngo-
plasty as a secondary procedure in cleft palates. Plast
Reconstr Surg 59:518–524
Kawamoto HK (1995) Pharyngoplasty revisited and
revised. In: Jurkiewicz MJ, Culbertson JH (eds)
Operative techniques in plastic and reconstructive sur-
gery. WB Saunders, Philadelphia
Kuehn DP, Moller KT (2000) Speech and language issues
in the cleft palate population: the state of the art. Cleft
Palate Craniofac J 37:348–383
Leeper HA, Tissington ML, Munhall KG (1998) Temporal
characteristics of velopharyngeal function in children.
Cleft Palate Craniofac J 35:215–221
Liao YF, Yun C, Huang CS, Chen PK, Hung KF, Chuang
ML (2003) Longitudinal follow up of obstructive sleep
apnea following Furlow palatoplasty in children with
cleft palate: a preliminary report. Cleft Palate Craniofac
J 40:269–273
Liao YF, Noordhoff MS, Huang CS, Chen PK, Chen NH,
Yun C et al (2004) Comparison of obstructive sleep
apnea syndrome in children with cleft palate following
Furlow palatoplasty or pharyngeal fl ap for velopharyn-
geal insuf fi ciency. Cleft Palate Craniofac J 41:152–156
Losken A, Williams JK, Burstein FD et al (2003) An out-
come evaluation of sphincter pharyngoplasty for the
management of velopharyngeal insuf fi ciency. Plast
Reconstr Surg 112:1755–1761
MacKenzie-Stepner K, Witzel MA, Stringer DA, Laskin
R (1987a) Velopharyngeal insuf fi ciency due to hyper-
trophic tonsils: a report of two cases. Int J Pediatr
Otorhinolaryngol 14:57–63
MacKenzie-Stepner K, Witzel MA, Stringer DA, Lindsay
WK, Munro IR, Hughes H (1987b) Abnormal carotid
arteries in the velocardiofacial syndrome: a report of
three cases. Plast Reconstr Surg 80:347–351
Meek MF, Coert JH, Hofer SO, Goorhuis-Brouwer SM,
Nicolai JP (2003) Short-term and long-term results of
speech improvement after surgery for velopharyngeal
insuf fi ciency with pharyngeal fl aps in patients younger
and older than 6 years old: 10-year experience. Ann
Plast Surg 50:13–17
Mitnick RJ, Bello JA, Golding-Kushner KJ, Argamaso
RV, Shprintzen RJ (1996) The use of magnetic reso-
nance angiography prior to pharyngeal fl ap surgery in
patients with velocardiofacial syndrome. Plast
Reconstr Surg 97:908–919
Moll KL, Huffman WC, Lierle DM, Smith JK (1963)
Factors related to the success of pharyngeal fl ap proce-
dures. Plast Reconstr Surg 32:581–588
Mount D, Marsh J (2002) Sphincter pharyngoplasty. In:
Presented at the annual meeting of the American
Association of Plastic Surgeons, Seattle, 2002
Murphy K, Scambler P (eds) (2005) Velocardiofacial
syndrome: understanding microdeletion disorders.
Cambridge University Press, Cambridge
Orticochea M (1968) Construction of a dynamic muscle
sphincter in cleft palates. Plast Reconstr Surg 41:323–327
Padgett EC (1930) The repair of cleft palates after unsuc-
cessful operations, with special reference to cases with
extensive loss of palatal tissue. Arch Surg 20:453–472

776
R.E. Kirschner and A.L. Baylis
Passavant G (1865) Ueber die Beseitigung der naeselnen
Sprache bei angeborenen Spalten des harten und weichen
Gaumens (Gaumensegel, Schlundnaht und Ruecklagerund
des Gaumensegels). Arch Klin Chir 6:333–349
Riski JE (1979) Articulation skills and oral-nasal reso-
nance in children with pharyngeal fl aps. Cleft Palate J
16:421–428
Riski JE, Sera fi n D, Riefkohl R et al (1984) A rationale
for modifying the site of insertion of the Orticochea
pharyngoplasty. Plast Reconstr Surg 73:882–894
Riski JE, Ruff GL, Georgiade GS et al (1992) Evaluation
of the sphincter pharyngoplasty. Cleft Palate Craniofac
J 29:254–261
Ross DA, Witzel MA, Armstrong DC, Thomson HG
(1996) Is pharyngoplasty a risk in velocardiofacial
syndrome? An assessment of medially displaced
carotid arteries. Plast Reconstr Surg 98:1182–1190
Saint Raymond C, Bettega G, Deschaux C et al (2004)
Sphincter pharyngoplasty as a treatment for velopha-
ryngeal incompetence in young people: a prospective
evaluation of effects on sleep structure and sleep respi-
ratory disturbances. Chest 125:864–871
Schoenborn K (1875) Ueber eine neue Methode der
Staphylorrhaphie. Verth Dtsch Ges Chir 4:235–239
Schoenborn K (1886) Vorstellung eines falle von
Staphyloplastik. Verth Dtsch Ges Chir 15:57–68
Seagle MB, Patti CS, Williams WN, Wood VD (1999)
Submucous cleft palate: a 10-year series. Ann Plast
Surg 42:142–148
Seyfer AE, Prohazka D, Leahy E (1988) The effectiveness
of the superiorly based pharyngeal fl ap in relation to
the type of palatal defect and timing of the operation.
Plast Reconstr Surg 82:760–764
Shewmake K, Elias D, Fromwiller S, Kawamoto H (1992)
Modi fi cation of the Orticochea pharyngoplasty for the cor-
rection of velopharyngeal insuf fi ciency: seven-year experi-
ence. In: Presented at the annual meeting of the American
Cleft Palate-Craniofacial Association, Portland, 1992
Shprintzen RJ, Sher AE, Croft CB (1987) Hypernasal
speech caused by tonsillar hypertrophy. Int J Pediatr
Otorhinolaryngol 14:45–56
Skolnick ML (1970) Video fl uoroscopic examination of
the velopharyngeal portal during phonation in lateral
and base projections: a new technique for studying the
mechanics of closure. Cleft Palate J 7:803–816
Skoog T (1965) The pharyngeal fl ap operation in cleft pal-
ate: a clinical study of eight-two cases. Br J Plast Surg
18:265–282
Sullivan SR, Marinan EM, Mulliken JB (2010) Pharyngeal
fl ap outcomes in nonsyndromic children with repaired
cleft palate and velopharyngeal insuf fi ciency. Plast
Reconstr Surg 125:290–298
Tatum SA, Chang J, Havkin N, Shprinzen RJ (2002)
Pharyngeal fl ap and the internal carotid in velocardio-
facial syndrome. Arch Facial Plast Surg 4:73–80
Valnicek SM, Zucker RM, Halpern LM, Roy WL (1994)
Perioperative complications of superior pharyngeal fl ap
surgery in children. Plast Reconstr Surg 93:954–958
Van DeMark DR, Hammerquist PJ (1978) Longitudinal
evaluation of articulation and velopharyngeal compe-
tency of patients with pharyngoplasties. In: Paper pre-
sented at the American Cleft Palate Association,
Atlanta, 1978
Van Demark DR, Hardin MA (1985) Longitudinal evalu-
ation of articulation and velopharyngeal competence
of patients with pharyngeal fl aps. Cleft Palate J 22:
163–172
Warren DW, DuBois AB (1964) A pressure- fl ow tech-
nique for measuring ori fi ce area during continuous
speech. Cleft Palate J 1:52–71
Warren DW, Dalston RM, Trier WC, Holder MB (1985) A
pressure- fl ow technique for quantifying temporal patterns
of palatopharyngeal closure. Cleft Palate J 22:11–19
Warren DW, Dalston RM, Mayo R (1993) Hypernasality
in the presence of “adequate” velopharyngeal closure.
Cleft Palate Craniofac J 30:150–154
Warren DW, Dalston RM, Mayo R (1994) Hypernasality
and velopharyngeal impairment. Cleft Palate Craniofac
J 31:257–262
Wells MD, Vu TA, Luce EA (1999) Incidence and seque-
lae of nocturnal respiratory obstruction following pos-
terior pharyngeal fl ap operation. Ann Plast Surg
43:252–257
Whitaker LA, Randall P, Graham WP, Hamilton RW,
Winchester R (1972) A prospective and randomized
series comparing superiorly and inferiorly based
posterior pharyngeal fl aps. Cleft Palate J 9:304–311
Whitehill TL, Lee ASY (2002) Direct magnitude estima-
tion and interval scaling of hypernasality. J Speech
Lang Hear Res 45:80–88
Witt PD, Marsh JL, Arlis H et al (1998a) Quanti fi cation of
dynamic velopharyngeal port excursion following
sphincter
pharyngoplasty.
Plast
Reconstr
Surg
101:1205–1211
Witt PW, Miller DC, Marsh JL et al (1998b) Limited value
of preoperative cervical vascular imaging in patients
with velocardiofacial syndrome. Plast Reconstr Surg
101:1184–1195
Witt PD, Myckatyn T, Marsh JL (1998c) Salvaging the
failed pharyngoplasty: intervention outcome. Cleft
Palate Craniofac J 35:447–453
Witzel MA, Tobe J, Salyer K (1988) The use of nasophar-
yngoscopy biofeedback therapy in the correction of
inconsistent velopharyngeal closure. Int J Pediatr
Otorhinolaryngol 15:137–142
Witzel MA, Tobe J, Salyer KE (1989) The use of videona-
sopharyngoscopy for biofeedback therapy in adults
after pharyngeal fl ap surgery. Cleft Palate Craniofac J
26:129–134
Ysunza A, Pamplona C, Toledo E (1992) Change in
velopharyngeal valving after speech therapy in cleft
palate patients: a videonasopharyngoscopic and
multi-view video fl uoroscopic study. Int J Pediatr
Otorhinolaryngol 24:45–54
Ysunza A, Garcia-Velasco M, Garcia-Garcia M et al (1993)
Obstructive sleep apnea secondary to surgery for
velopharyngeal insuf fi ciency. Cleft Palate Craniofac J
30:387–390
Ysunza A, Pamplona C, Ramirez E et al (2002)
Velopharyngeal surgery: a prospective randomized
study of pharyngeal fl aps and sphincter pharyngo-
plasties. Plast Reconstr Surg 110:1401–1407

777
S. Berkowitz (ed.), Cleft Lip and Palate,
DOI 10.1007/978-3-642-30770-6_36, © Springer-Verlag Berlin Heidelberg 2013
36
As with most aspects of cleft care, management
of velopharyngeal dysfunction (VPD) requires
choices among different treatment modalities,
technical variations within a speci fi c modality,
and timing of intervention. I have consolidated
my experience, as a member of an interdisciplin-
ary team managing VPD over the past 34 years,
into a series of algorithms (Marsh Figs. 36.1 ,
36.2 , 36.3 , and 36.4 ). These algorithms not only
guide my personal patient care decision making
but have proven useful in teaching others about
VPD management (Marsh 2004 ) . This chapter
presents and discusses these algorithms.
Individuals with possible VPD present to indi-
vidual members of the cleft palate team or to the
team as a whole for diagnosis and treatment.
Historically, the large majority of such individuals
had a repaired cleft palate and a small minority,
without overt cleft palate, developed VPD fol-
lowing adenoidectomy. While post-palatoplasty
patients with impaired speech still comprise the
largest group evaluated for VPD (Kummer 2007 ;
Peterson-Falzone et al. 2010 ), individuals with
velocardiofacial syndrome, neurological impair-
ment, and postobstructive sleep apnea surgery
(uvulopalatoplasty) comprise a steadily increas-
ing percentage. Whereas identi fi cation of the eti-
ology of the VPD is critical to assigning
differential management based on differential
diagnosis (Marsh 1991 ; Marsh and O’Daniel
1992 ) , the evaluation of velopharyngeal function
is the same regardless of etiology (Witt et al.
1999 ) . I shall fi rst discuss the evaluatory process
and then speci fi c managements.
36.1
Evaluation of Velopharyngeal
Function
Speech results from modulation of the pressur-
ized air stream that emerges from the lungs dur-
ing expiration. A number of structures between,
and including, the glottis and the lips (articula-
tors) modify that air stream to produce speci fi c
sounds. One of those modi fi ers is the velophar-
ynx, which normally is a dynamic sphincter.
A sphincter is an anatomic structure that can open
or close to varying degrees and speeds depend-
ing on the physiological necessity. The tissues
that comprise the velopharyngeal sphincter are
the velum (soft palate), the right and left lateral
pharyngeal walls, and the posterior pharyngeal
wall. The space enclosed by and modi fi ed by
the velopharyngeal sphincter is the velopharynx.
The velopharynx is the connection between the
nasopharynx and the oropharynx. Normally at
Velopharyngeal Dysfunction
Management Algorithms
Jeffrey L. Marsh
J. L. Marsh , M.D.
Department of Surgery, Plastic and Reconstructive ,
St. Louis University School of Medicine ,
St. Louis , MO , USA
Department of Pediatric Plastic Surgery ,
Cleft Lip/Palate and Craniofacial Deformities Center,
Mercy Children’s Hospital ,
St. Louis , MO , USA
Kids Plastic Surgery ,
621 S. New Ballas Road, Suite 260A , St. Louis ,
MO 63141 , USA
e-mail: jeffrey.marsh@mercy.net

778
J.L. Marsh
Velopharyngeal management algorithm 1
Surgical candidate
Patient requiring VP management
Not
surgical candidate
Prosthetic VP
management
Assess
upper airway
stability
Fig. 36.1 Velopharyngeal
management algorithm 1
Velopharyngeal management algorithm 2
Patient requiring VP management: surgical candidate
Upper airway stable
Upper airway unstable
Can upper airway
be stabilized?
Yes
No
Stabilize
upper airway
Status adenoids
Prosthetic VP
management
Fig. 36.2 Velopharyngeal
management algorithm 2
rest, it is a wide opening through which air fl ows
easily and secretions drain; when contracted, it
closes the nasopharynx from the oropharynx,
preventing passage of gases, fl uids, and solids
between the two cavities. Dysfunction of the
velopharyngeal sphincter impairs that separation
of the nasal and oral cavities for both deglutition
and speech to varying degrees. Outcome assess-
ment of VPD management requires consideration
of velopharyngeal function for all of the following
physiological activities: speech, breathing, swal-
lowing, handling nasal secretions, and sleep.
There is a lack of consensus on the preferred
term to describe such dysfunction: velopharyn-
geal incompetency , velopharyngeal insuf fi ciency ,
and velopharyngeal inadequacy have all been
abbreviated as VPI . I prefer the term velopha-
ryngeal dysfunction , abbreviated as VPD , since
it connotes physiological impairment without
attempting to denote etiology (Loney and Bloem

779
36 Velopharyngeal Dysfunction Management Algorithms
1987 ; Folkins 1988 ; Smith and Kuehn 2007 ) .
Regardless of the terminology, a speci fi c set of
physical fi ndings suggest VPD. These include
excessive nasal resonance during speech (hyper-
nasality), inappropriate nasal air fl ow noise (nasal
turbulence or rustling), and abnormal facial move-
ments (facial grimacing). An individual with one
or any combination of these fi ndings will be
referred for evaluation of possible VPD.
The fi rst task for the VPD team is to determine
whether the patient actually has VPD. This deter-
mination has traditionally been made solely on the
basis of a perceptual speech/language evaluation
by a speech/language pathologist with speci fi c
training and experience in velopharyngeal func-
tion (Jones 1991 ) . This evaluation includes both
spontaneous speech and a provocative speech
sample, structured to speci fi cally challenge the
velopharyngeal mechanism with increasingly
more complex tasks (Philips 1980 ; Kummer
2007; Peterson-Falzone et al. 2010). The primary
activity of this perceptual assessment is auditory,
that is, listening for the production of speci fi c
phonemes. However, observing the face for gri-
macing, watching for fogging of a mirror below
the nares, and feeling for air fl ow through the
Velopharyngeal management algorithm 3
Patient requiring VPD management: surgical candidate
Yes
No
Adenoidectomy
Surgical VP
management
Upper airway stable
Adenoids present ?
Fig. 36.3 Velopharyngeal
management algorithm 3
Velopharyngeal management algorithm 4
Instrumental assessment of VP function
status m. uvulus?
sphincter
pharyngoplasty
pharyngeal flap
notch
IVV
(Furlow)
bulge
pharyngeal flap
(Furlow)
minimal
central gap
coronal
bowtie
circular
sagittal
• large central gap
• adynamic VP
• coronal gap
• bow-tie gap
• moderate central gap
• sagittal gap
Fig. 36.4 Velopharyngeal
management algorithm 4

780
J.L. Marsh
nares with attempted pronunciation of phonemes
that require velopharyngeal function are other
perceptual assessments that assist the screening
evaluation. Some professionals now argue that
instrumental assessments of oral-nasal air fl ow
should be part of this determination process.
However, we have not yet incorporated nasalance
measurement into our initial assessment.
The auditory perceptual screening of velopha-
ryngeal function sorts the patient into one of
three groups: normal VP function, minimal
VPD without impairment of communication or
psychosocial stigmatization, or suf fi cient VPD
to interfere with speech comprehension by oth-
ers and/or stigmatize the speaker. If the assessed
individual screens normally, no further evaluation
of the velopharynx is indicated until the return
for routine follow-up or some concern regarding
speech arises. If the possible dysfunction is mini-
mal, meaning that the affected individual and his
or her parents, in the case of a child, were not
aware of a speech problem and the cleft team,
in concert, feels that the dysfunction is unlikely
to cause impairment of communication or have
psychosocial consequences, then the affected
individual will have a repeat auditory percep-
tual speech evaluation at an interval shorter
than the usual follow-up and the individual/par-
ents will be informed of the concern regarding
velopharyngeal function as well as of the signs
and symptoms of increasing dysfunction so that
they can contact the cleft team should they occur.
If, on the other hand, it is the perception of the
sophisticated observer that there is a possibility
of morbid velopharyngeal dysfunction, further
evaluation is considered.
If one accepts the principle that treatment
should be diagnosis speci fi c, and I do, then effec-
tive management of velopharyngeal dysfunc-
tion requires both recognition of the condition
and de fi nition of the responsible pathoetiology
(Jones 1991 ) . While auditory perceptual evalua-
tion can separate normal from abnormal velopha-
ryngeal function, it cannot identify the etiology
of the dysfunction. Instrumental velopharyn-
geal evaluations, in contrast, can be etiology
speci fi c (Yules and Chase 1968 ; Shprintzen and
Golding-Kushner 1989 ; Hirschberg and Van
Demark 1997 ) . Instrumental evaluations can be
divided into those that visualize the velophar-
ynx and those that indirectly assess its function
(Albery et al. 1982 ; Dalston and Warren 1986 ;
Dalston et al. 1991 ; D’Antonio et al. 1988 ;
Hardin et al. 1992 ) . Clinically useful visualiza-
tion utilizes still (lateral skull x-ray) or real-time
x-ray (speech video fl uoroscopy). Documenting
the effect of velopharyngeal sphincter function
on air fl ow air pressure or sound or light trans-
mission across the velopharyngeal port produces
indirect data about velopharyngeal function. A
multidisciplinary consensus regarding reporting
of visualization studies provides a useful means
for standardized interpretation of such stud-
ies (Golding-Kushner et al. 1990 ) . For the past
20 years, the cleft teams that I have been asso-
ciated with have used both nasendoscopic and
fl uoroscopic imaging of the velopharynx during
standardized speech tasks to evaluate velopha-
ryngeal function (Sinclair et al. 1982 ; D’Antonio
et al. 1988 ; Shprintzen and Golding-Kushner
1989 ; Stringer and Witzel 1989 ) . These evalu-
ations are audio-video recorded, previously on
magnetic tape and now digitally, in order:
1. To permit review by other members of the
cleft team who were not present during the
actual examination
2. To permit comparison of serial assessments of
the same individual
3. To permit comparative assessment of the
effects of therapeutic intervention in the same
individual
4. To facilitate cross-sectional comparison of
various interventions
These tapes are then reviewed by a subset of
the cleft palate team, which consists of represen-
tatives from the disciplines of otolaryngology,
plastic surgery, and speech/language pathology
(D’Antonio et al. 1989 ; Sell and Ma 1996 ) .
A consensus opinion regarding interpretation of
the images and preferred method of management
is then arrived at by group discussion. The
conclusions are communicated to the patient/
family for reaction and to appropriate primary
and secondary care providers, such as the patient’s
speech therapist and pediatrician/physician.
When
velopharyngeal
management,
either

781
36 Velopharyngeal Dysfunction Management Algorithms
prosthetic or surgical, is recommended and per-
formed, the velopharyngeal function is reevaluated
3 months after the intervention with auditory per-
ceptual and instrumental evaluations mirroring
those performed preoperatively.
36.2
Differential Diagnosis
of Velopharyngeal Dysfunction
For the purposes of differential management
based upon differential diagnosis, velopharyn-
geal dysfunction can be divided into four broad
etiologic categories:
1. Anatomic de fi ciency
2. Myoneural de fi ciency
3. Anatomic and myoneural de fi ciency
4. Neither anatomic nor myoneural de fi ciency
Each category has several speci fi c causes for
that de fi ciency. Anatomic de fi ciency includes
those static tissue problems that prevent ade-
quate velopharyngeal sphincteric closure, such
as an unrepaired cleft palate, a palatal fi stula, a
short velum, or a deep velopharynx. Myoneural
de fi ciency implies that there is adequate pala-
tal and velopharyngeal structural anatomy but
one or more components of the velopharyngeal
port have inadequate or absent function, such
as may occur with head trauma or degenerative
neurologic disorders. Combined anatomic and
myoneural de fi ciency may occur with repaired
cleft palate, unoperated submucous cleft palate,
or post-ablative surgery and/or radiotherapy for
oronasopharyngeal malignancy. Rarely an indi-
vidual presents who has intact velopharyngeal
anatomic structures and is myoneurally intact
but whose speech nonetheless exhibits signs and
symptoms of velopharyngeal dysfunction due to
either learned behavior, such as having a parent
with cleft VPD and living in a rural area, or
psychiatric disorder.
The initial goal of the instrumental evalua-
tion of the presumably impaired velopharynx
is to determine which of the four categories
the patient belongs to since that broadly deter-
mines the type of therapeutic intervention(s) to
be considered (see below). The combination of
visual direct and indirect (mirror, endoscope)
intraoral inspection and indirect velopharyngeal
functional inspection (nasendoscopy, multiview
fl uoroscopy) permits de fi nition of the structural
and functional impairments contributing to the
VPD. Once the category has been de fi ned, fur-
ther general health history, physical examina-
tion, and testing determine the speci fi c etiology
for that patient’s VPD.
36.3
Differential Management
of Velopharyngeal Dysfunction
The four etiologic categories enumerated above
broadly determine the differential management of
velopharyngeal dysfunction. Anatomic de fi ciency
is usually managed by restoration of the de fi ciency
by either surgical or prosthetic means (Marsh and
Wray 1980 ) (Fig. 36.1 ). Myoneural de fi ciency is
usually managed prosthetically until the neuro-
logic status has stabilized and the patient becomes
a candidate for velopharyngeal surgery, which
may or may not occur (Riski and Gordon 1979 ) .
Combined anatomic and myoneural de fi ciency is
usually managed by restoration of the de fi ciency
by either surgical or prosthetic means. Speech
therapy, often pre- and usually post-intervention,
is an essential element of management of these
three categories in addition to surgical or pros-
thetic intervention. For learned or behavioral
VPD , speech therapy with or without behavioral
management is the treatment of choice; there is no
role for surgery in such cases (Heller et al. 1974 ) .
Prosthetic management for VPD is indicated
when:
1. The patient is unsuitable for surgical velopha-
ryngeal management due to other major
medical problems, such as inoperable con-
genital cardiac disease or severe pulmonary
insuf fi ciency (if and when the other medi-
cal problem becomes resolved or stabilized
enough to minimize the anesthetic/surgical
risk, conversion to surgical velopharyngeal
management is considered).
2. The parents/legal guardians refuse to permit
surgery because of religious or emotional
considerations.

782
J.L. Marsh
3. The patient has a complex speech/language
problem, and it is not clear that velopharyngeal
management will signi fi cantly improve speech
intelligibility (if the trial of a speech prosthe-
sis demonstrates signi fi cant improvement
in intelligibility, then conversion to surgical
velopharyngeal management is considered).
4. The patient has a neurological condition that
includes VPD, and it is not clear whether the
neurological de fi cit has stabilized and/or that
velopharyngeal management will signi fi cantly
improve speech intelligibility (if the trial of
a speech prosthesis demonstrates signi fi cant
improvement in intelligibility and the neuro-
logical status has stabilized and the patient is
not a signi fi cant anesthetic risk due to the neu-
rological pathology, then conversion to surgical
velopharyngeal management is considered).
5. The patient has an unstable upper airway that
cannot be stabilized (Fig. 36.2 ) and VPD (this
was the major indication for prosthetic
velopharyngeal management at our cleft cen-
ter prior to the introduction of mandibular dis-
traction osteogenesis for stabilization of the
upper airway in individuals with mandibular
microretrognathia).
When a prosthesis is used to manage VPD, the
type of prosthesis depends on the amount and
quality of palatal tissue and the fi ndings on nasen-
doscopic velopharyngeal functional assessment
(Turner and Williams 1991 ; Witt et al. 1995b ) :
1. When there is adequate velar tissue (a long,
unscarred velum), a palatal lift is prescribed.
2. When the velar tissue is de fi cient (a short,
scarred velum with a deep pharynx), a velopha-
ryngeal obturator is prescribed.
3. When the velum is long but the pharynx is
deep or a palatal lift fails to achieve complete
velopharyngeal closure, a combined lift and
obturator, “liftorator,” is prescribed.
Surgical VP management is recommended
for all other individuals with VPD who do not
meet one of the criterion listed above for pros-
thetic management. Several types of surgical
alteration of components of the velopharynx are
possible:
1. Velar lengthening (palatal pushback, Furlow
double-opposing Z-veloplasty)
2. Intravelar muscular reconstruction
3. Pharyngoplasties (pharyngeal fl ap, sphincter
pharyngoplasty)
4. Posterior pharyngeal wall augmentation
Each type of surgical alteration of velopharyn-
geal structures has its advocates. Although some
comparisons of two or more methods of VPD
management have been reported, they fail to meet
rigorous scienti fi c criteria for discriminating
among therapeutic options (Pensler and Reich
1991 ; de Serres et al. 1999 ; Sloan 2000 ; Seagle
et al. 2002 ; Ysunza et al. 2002 ) .
Both types of velar operations and posterior
wall augmentation procedures are fundamentally
different from, and theoretically more physiologic
than, the pharyngoplasties in that they do not cre-
ate a permanent subtotal obstruction of the
velopharyngeal port. Nasal physiology is less
likely to be impaired with velar and posterior pha-
ryngeal wall procedures than with pharyngo-
plasties. The challenge for the velopharyngeal
surgeon is to provide the patient with the means to
achieve velopharyngeal closure without obstruct-
ing the nasal airway for breathing, secretion con-
trol, and passage of air into the nose during speech
for those sounds that require nasal resonance. For
this reason, when either a pharyngeal fl ap or a
sphincter pharyngoplasty is elected, an adenoidec-
tomy is performed at least 3 months prior to the
velopharyngeal procedure so that hypertrophic
lymphoid tissue cannot obstruct the surgically
diminished velopharyngeal port(s) and to facili-
tate the performance of the pharyngoplasty.
[Previously, we also had tonsillectomy performed
synchronous with the adenoidectomy. However,
the tonsillectomy often resulted in fusion of the
anterior and posterior tonsillar pillars into a single
rigid scar that precluded an effective sphincter
pharyngoplasty. Therefore, since 2008, we have
only had adenoidectomy performed prior to
de fi nitive surgical velopharyngeal management.]
So how does the surgeon choose among these
options for intervention? In collaboration with my
colleagues on the multidisciplinary velopharyngeal

783
36 Velopharyngeal Dysfunction Management Algorithms
team, I choose among the therapeutic options
based upon the anatomy and function of the
velopharynx as documented by nasendoscopic
and multiview fl uoroscopic visualization of the
velopharynx (Croft et al. 1981 ) , performing both
spontaneous speech and standardized speech
tasks. The selection process follows an algorithm
that has been in use, with minor modi fi cation, over
the past 14 years (Marsh Fig. 36.4 ). My rationale
for pairing of the residual velopharyngeal gap on
attempted complete velopharyngeal closure with
speci fi c interventions follows:
Small midline gap – Management of a small
midline gap on attempted complete VP closure
depends on the status of the intravelar muscula-
ture. If the patient has not had an intravelar velo-
plasty or did not have a “radical” (method of either
Sommerlad or Cutting) intravelar veloplasty, a
radical IVV is recommended. The patient/family
is informed that there is about an 80 % change
of correction of the VPD with such an interven-
tion, in my experience, with no expected airway
morbidity. They are also informed that either a
narrow, lined, superiorly based pharyngeal fl ap or
a sphincter pharyngoplasty could be performed
with an almost 100 % correction of VPD but with
some risk of impairment of the upper airway, pri-
marily intranasal retention of nasal secretions, and
to a lesser degree nasal airway obstruction or the
rare case of obstructive sleep apnea. If the radi-
cal IVV fails to suf fi ciently correct the VPD, then
a pharyngeal fl ap or sphincter pharyngoplasty is
offered with the caveats listed above. Some fami-
lies prefer to avoid nasal obstruction even if there
is a 20 % chance of needing a second operation
while others prefer more certainty of resolution
of the VPD regardless of airway compromise.
[Rearrangement of the velar soft tissues includ-
ing the muscle via the Furlow double-opposing
Z-plasty is an alternative to radical IVV for the
patient with a small midline gap on attempted
complete VP closure. I am unaware of a prospec-
tive comparison of the ef fi cacy and morbidity of
these two approaches for equivalent VPD situ-
ations. The choice then between the two opera-
tions currently is surgeon’s preference. I have no
personal experience with the Furlow, but several
of my associates, current and past, use it for this
indication as well as several cleft surgeons whose
technical skill and reporting honesty I respect.]
Between 2003 and 2011, I performed four intra-
velar veloplasties to manage symptomatic VPD.
Of these, two subsequently underwent sphincter
pharyngoplasty for persistent or recurrent VPD:
one 1 year later and one 4 years later. None of
the IVV patients had sleep apnea or symptomatic
nasal secretion retention following the IVV.
Sagittal gap with active to moderately active
lateral pharyngeal wall motion – I reserve the pha-
ryngeal fl ap operation for VPD due to a sagittal gap
with active to moderately active lateral pharyngeal
wall motion. Because of this restriction, I only per-
form narrow or moderately wide, superiorly based,
lined pharyngeal fl aps. [I stopped performing wide
obstructive pharyngeal fl aps in 1989, when sphinc-
ter pharyngoplasty entered our therapeutic reper-
toire, due to the consistent morbidity of wide
obstructive pharyngeal fl aps with respect to the
upper airway: intranasal retention of nasal secre-
tions, obstruction of the nasal airway with obliga-
tory mouth breathing, hyponasal resonance, and
obstructive sleep apnea as well as death (Kravath
et al. 1980 ) .] A review of 71 patients, who under-
went a pharyngeal fl ap operation at our cleft center
between 1982 and 2000 and had adequate preop-
erative and 3-month postoperative perceptual and
instrumental velopharyngeal speech function eval-
uations and a 12-month postoperative perceptual
velopharyngeal speech evaluation, was conducted
in 2001. This study documented satisfactory nasal
resonance in 74 % of patients so selected and
treated. Of the remainder, surgical tightening of the
one or both lateral ports with incomplete closure,
as documented on post-pharyngeal fl ap nasendos-
copy, increased the resolution of symptomatic VPD
to 92 %. Postoperative complications included
obstructive sleep apnea in fi ve patients, symptom-
atic nasal secretions in seven patients, and obligate
mouth breathing in fi ve patients. Denasality (hypo-
nasal nasal resonance ) was noted in 21 % of patients
at 3 months postoperatively but had diminished to
only 6 % at 12 months postoperatively. Of the

784
J.L. Marsh
patients receiving a pharyngeal fl ap, 3/4 had cleft
palate+/−cleft lip, 1/4 were non-cleft VPD, and 1/5
of the patients were syndromic. Postoperative nasal
resonance was not affected by the presence or
absence of cleft palate ( p = 0.7) or the presence or
absence of a syndrome ( p = 0.2) (Sabry and Marsh
2003 ) . Between 2003 and 2011, I performed 12
pharyngeal fl aps. Of these, 100 % had resolution of
symptomatic VPD following the operation. None
of these had sleep apnea or symptomatic nasal
secretion retention.
Hypodynamic or adynamic velopharyngeal
sphincter – I utilize the sphincter pharyngoplasty
(Jackson modi fi cation of the Hynes procedure
with “crossed arms” overlapping posterior ton-
sillar pillar myomucosal fl aps) for all cases of
VPD secondary to a hypodynamic or adynamic
velopharyngeal sphincter (Witt et al. 1995a,
b ) . Preoperative speci fi cation of the locus for
insertion of the myomucosal fl aps on the pos-
terior pharyngeal wall is based on the level of
maximum attempted velopharyngeal closure,
as documented on the lateral fl uoroscopic VP
evaluation (Riski et al. 1984 ) . A review of our
sphincter pharyngoplasties in 2000 (Mount and
Marsh 2002 ) documented resolution of symp-
tomatic VPD in 72 % of 162 patients so selected
and treated. Of the remainder, surgical tightening
or reconstruction of the central port with incom-
plete closure, as documented on post- pharyngeal
fl ap nasendoscopy, increased the resolution of
symptomatic VPD to 85 %. For the 11 residually
symptomatic patients, a third tightening was per-
formed or a narrow pharyngeal fl ap was placed
in the center of the residual sphincter pharyngo-
plasty port. Signi fi cant hyponasality was noted in
only 10 % of patients. Between 2003 and 2011,
I performed 78 sphincter pharyngoplasties. Of
these, 91 % had resolution of symptomatic VPD
following the operation; the remaining 9 %
had VPD resolution following sphincter port
tightening. Of note, however, was the occur-
rence of either sleep apnea and/or symptomatic
nasal secretion retention in 10 of the success-
fully managed patients. Initially managed with
CPAP or BiPAP, 5 underwent subsequent port
enlargement, 3 uvulectomy, and 2 combined port
enlargement with uvulectomy for resolution of
the symptomatology in all but 1 who required
continued BiPAP.
Conclusion
Differential diagnosis of velopharyngeal dys-
function, using instrumental visualization of
velopharyngeal function, allows for differential
therapeutic management (Peat et al. 1994 ;
Seagle et al. 2002 ) . The objective of such
management is to optimize the function of the
velopharynx for speech tasks while minimiz-
ing the morbidity of the intervention upon the
upper airway. My experience with such an
approach over the past 34 years validates the
assumption that differential management of
velopharyngeal dysfunction based upon differ-
ential diagnosis can achieve this goal.
References
Albery EH, Bennett JA et al (1982) The results of 100
operations for velopharyngeal incompetence – selected
on the fi ndings of endoscopic and radiological exami-
nation. Br J Plast Surg 35:118–126
Croft CB, Shprintzen RJ et al (1981) Patterns of velopha-
ryngeal valving in normal and cleft palate subjects: a
multi-view video fl uoroscopic and nasendoscopic
study. Laryngoscope 91:265–271
D’Antonio LL, Muntz HR et al (1988) Practical applica-
tion of fl exible fi beroptic nasopharyngoscopy for eval-
uating velopharyngeal function. Plast Reconstr Surg
82:611–618
D’Antonio LL, Marsh JL et al (1989) Reliability of
fl exible fi beroptic nasopharyngoscopy for evaluation
of velopharyngeal function in a clinical population.
Cleft Palate J 26:217–225
Dalston RM, Warren DW (1986) Comparison of Tonar II,
pressure- fl ow, and listener judgments of hypernasality
in the assessment of velopharyngeal function. Cleft
Palate J 23:108–115
Dalston RM, Warren DW et al (1991) The identi fi cation of
nasal obstruction through clinical judgments of hypo-
nasality and nasometric assessment of speech acous-
tics. Am J Orthod Dentofacial Orthop 100:59–65
de Serres LM, Deleyiannis FW et al (1999) Results with
sphincter pharyngoplasty and pharyngeal fl ap. Int
J Pediat Otorhinolaryngol 48:17–25
Folkins JW (1988) Velopharyngeal nomenclature: incom-
petence, inadequacy, insuf fi ciency, and dysfunction.
Cleft Palate J 25:413–416
Golding-Kushner KJ, Argamaso RV et al (1990)
Standardization for the reporting of nasopharyngoscopy
and multiview video fl uoroscopy: a report from an
International Working Group. Cleft Palate J 27:337–347

785
36 Velopharyngeal Dysfunction Management Algorithms
Hardin MA, Van Demark DR et al (1992) Correspondence
between nasalance scores and listener judgments of
hypernasality and hyponasality. Cleft Palate Craniofac
J 29:346–351
Heller JC, Gens GW et al (1974) Velopharyngeal
insuf fi ciency in patients with neurologic, emotional, and
mental disorders. J Speech Hear Disord 39:350–359
Hirschberg J, Van Demark DR (1997) A proposal for stan-
dardization of speech and hearing evaluations to assess
velopharyngeal function. Folia Phoniatr Logop 49:
158–167
Jones DL (1991) Velopharyngeal function and dysfunc-
tion. Clin Commun Disord 1:19–25
Kravath RE, Pollak CP et al (1980) Obstructive sleep
apnea and death associated with surgical correction of
velopharyngeal incompetence. J Pediatr 96:645–648
Kummer AW (2007) Cleft palate and craniofacial anoma-
lies: effects on speech and resonance, 2nd edn.
Thompson Delmar Learning, Clifton Park
Loney RW, Bloem TJ (1987) Velopharyngeal dysfunc-
tion: recommendations for use of nomenclature. Cleft
Palate J 24:334–335
Marsh JL (1991) Cleft palate and velopharyngeal dys-
function. Clin Commun Disord 1:29–34
Marsh JL (2004) The evaluation and management of velopha-
ryngeal dysfunction. Clin Plast Surg 31:261–270
Marsh JL, O’Daniel TG (1992) Management of velopha-
ryngeal dysfunction: a surgeon’s viewpoint. Probl
Plast Reconstr Surg 2:86–111
Marsh JL, Wray RC (1980) Speech prosthesis ver-
sus pharyngeal fl ap: a randomized evaluation of the
management of velopharyngeal incompetency. Plast
Reconstr Surg 65:592–594
Mount D, Marsh JL (2002) Outcome of sphincter pharyn-
goplasty. American Association of Plastic Surgeons,
Charleston
Peat BG, Albery EH et al (1994) Tailoring velopharyngeal
surgery: the in fl uence of etiology and type of opera-
tion. Plast Reconstr Surg 93:948–953
Pensler JM, Reich DS (1991) A comparison of speech
results after the pharyngeal fl ap and the dynamic sphinc-
teroplasty procedures. Ann Plast Surg 26:441–443
Peterson-Falzone S, Hardin-Jones M et al (2010) Cleft
palate speech. Mosby/Elsevier, St. Louis
Philips BJ (1980) Perceptual evaluation of velopharyngeal
competency. Ann Otol Rhinol Laryngol Suppl 89:
153–157
Riski JE, Gordon D (1979) Prosthetic management of
neurogenic velopharyngeal incompetency. N C Dent J
62:24–26
Riski JE, Sera fi n D et al (1984) A rationale for modifying
the site of insertion of the Orticochea pharyngoplasty.
Plast Reconstr Surg 73:882–894
Sabry MZ, Marsh JL (2003) The ef fi cacy of pharyngeal
fl ap in the management of velopharyngeal dysfunc-
tion. American Cleft Palate-Craniofacial Association,
Asheville
Seagle MB, Mazaheri MK et al (2002) Evaluation and treat-
ment of velopharyngeal insuf fi ciency: the University of
Florida experience. Ann Plast Surg 48:464–470
Sell D, Ma L (1996) A model of practice for the manage-
ment of velopharyngeal dysfunction [comment]. Br
J Oral Maxillofac Surg 34:357–363
Shprintzen RJ, Golding-Kushner KJ (1989) Evaluation of
velopharyngeal insuf fi ciency. Otolaryngol Clin North
Am 22:519–536
Sinclair SW, Davies DM et al (1982) Comparative reli-
ability of nasal pharyngoscopy and video fl uorography
in the assessment of velopharyngeal incompetence. Br
J Plast Surg 35:113–117
Sloan GM (2000) Posterior pharyngeal fl ap and sphincter
pharyngoplasty: the state of the art. Cleft Palate
Craniofac J 37:112–122
Smith BE, Kuehn DP (2007) Speech evaluation of velopha-
ryngeal dysfunction. J Craniofac Surg 18:251–261
Stringer DA, Witzel MA (1989) Comparison of multi-
view video fl uoroscopy and nasopharyngoscopy in the
assessment of velopharyngeal insuf fi ciency. Cleft
Palate J 26:88–92
Turner GE, Williams WN (1991) Fluoroscopy and nasoen-
doscopy in designing palatal lift prostheses. J Prosthet
Dent 66:63–71
Witt PD, Marsh JL et al (1995a) Management of the hypo-
dynamic velopharynx. Cleft Palate Craniofac J 32:
179–187
Witt PD, Rozelle AA et al (1995b) Do palatal lift prosthe-
ses stimulate velopharyngeal neuromuscular activity?
Cleft Palate Craniofac J 32:469–475
Witt PD, Cohen D et al (1999) Sphincter pharyngoplasty
for the surgical management of speech dysfunction
associated with velocardiofacial syndrome. Br J Plast
Surg 52:613–618
Ysunza A, Pamplona C et al (2002) Velopharyngeal sur-
gery: a prospective randomized study of pharyngeal
fl aps and sphincter pharyngoplasties. Plast Reconstr
Surg 110:1401–1407
Yules RB, Chase RA (1968) Quantitative cine evaluation
of palate and pharyngeal wall mobility in normal pal-
ates, in cleft palates, and in velopharyngeal incompe-
tency. Plast Reconstr Surg 41:124–134

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S. Berkowitz (ed.), Cleft Lip and Palate,
DOI 10.1007/978-3-642-30770-6_37, © Springer-Verlag Berlin Heidelberg 2013
37
Surgeons, speech pathologists, and other members
of cleft palate/craniofacial teams have been try-
ing for decades to gain some kind of “sure grip”
on the relationship between age at palatoplasty
and the child’s speech development . I have reviewed
the literature on this topic four times in the last
15 years: 1996 (Peterson-Falzone 1996 ) , 2001
(Peterson-Falzone et al. 2001 ) , in concert with my
coauthors in 2004 (Peterson-Falzone 2004 ) , and
again with my coauthors in 2010 (Peterson-
Falzone et al. 2010 ) . All four of those reviews
pointed out the differences between unveri fi ed
clinical commentary (e.g., “Our speech results
were good.”) and scienti fi c proof of investigators’
conclusions about speech and language develop-
ment. Much of the literature consisted of undocu-
mented clinical insight, although there were many
data-based reports as well. The reliance upon clin-
ical insight and upon case reports that lack inde-
pendent documentation of results still prevails as
of this writing. On the one hand, one must com-
mend the continuing and, indeed, zealous pursuit
of this critical question. On the other hand, we
must ask if there is a way to increase the relative
proportion of reliable, valid data and decrease the
dependence upon undocumented opinions.
37.1
Why Is It So Dif fi cult to Answer
This Question?
Clinical research is inherently hazardous because
so many factors affect the outcome of a study.
The investigator(s) cannot control all the factors
the way they would in a laboratory study. Far too
often, however, the professionals who have tried
to determine the optimum timing for closure of a
cleft palate have not fully recognized the possible
contaminating factors, such as:
1. Patients with varying types and extents of
clefts, heterogeneous socioeconomic back-
grounds, and varying health status and health-
care history (adequacy of pediatric care,
otologic history, and documentation of hearing
status; adequacy of early feeding and growth;
adequacy of stimulation in the home).
2. Multiple surgeons presumably performing the
same surgical procedure.
3. Children undergoing the same physical proce-
dure but at different times in their chronologi-
cal and developmental ages.
4. Children whose pre- and post-palatoplasty care
may or may not have included regular follow-up
evaluations by the cleft palate/craniofacial team
(see recommendations from the American Cleft
Palate-Craniofacial Association) (American
Cleft Palate-Craniofacial 2009 ) .
5. Children whose pre-and post-palatoplasty
interventions may or may not have included
early childhood stimulation programs.
Optimal Age for Palatoplasty
to Facilitate Normal Speech
Development: What Is the Evidence?
Sally J. Peterson-Falzone
S. J. Peterson-Falzone , Ph.D., CCC-Sp, FASHLA
Clinical Professor Emerita,
University of California ,
San Francisco , CA , USA
e-mail: spf222@comcast.net

788
S.J. Peterson-Falzone
6. Highly variable documentation of the status of
velopharyngeal closure post-palatoplasty. The
substance of postoperative evaluation contin-
ues to vary widely. The low end of the spec-
trum consists of non-data-based statements
such as “the palate appeared to move well
after surgery” or “speech was signi fi cantly
improved.” The upper end consists of well-
documented objective measures in combina-
tion with perceptual assessment of speech.
7. One-time postoperative assessment versus
longitudinal data (kids grow, adenoids usually
go away, maturity eventually kicks in, etc.).
8. Children who have undergone primary velo-
plasty (at varying ages), with inconsistent use
of interim obturating plates (for varying lengths
of time and typically with very little documen-
tation of that use) and later surgical closure of
the hard palate (again, at ages that vary from
less 1 year to the early teenage years). 1
Thus, the clinician who is trying to gather
information on this topic must examine each
report for the fl aws that may have led to false
conclusions.
37.2
Why Do Speech-Language
Pathologists Worry So Much
About Early Development?
One concept that may seem foreign to practitio-
ners whose primary focus is the physical status of
the child’s palate, teeth, or oropharyngeal mecha-
nism is that what an adult hears as normal speech
(or speech development) in a toddler is not simply
the result of that toddler echoing what he hears
around him. Normal communication development
depends upon many factors: normal hearing, nor-
mal oral and pharyngeal structures, adequate stim-
ulation from the environment, and reinforcement
from that environment for communication efforts.
A child who experiences communication failure
on a consistent basis will simply give up (uncon-
sciously) and settle for the simplest signals he can
produce (grunts, whines, cries, etc.) in order to
make the world pay attention. Try to envision an
otherwise normally developing child at the age of
1 year who is walking (or nearly ready to do so),
smiling, and vocalizing but whose fi rst attempts
at words consist of only nasal consonants, grunts,
and vowels. “Mama” will be produced normally
(the consonant/m/does not require velopharyn-
geal closure), but any attempt at “dada” or “baba“
(bottle) will sound like “uh uh.” By contrast,
a 12-month old who can produce “b,” “d,” “g,”
plus some of the consonants that do not require
velopharyngeal closure (the nasal consonants
/h/, /w/, and “y”) will probably be producing ten
recognizable (if simplistic) words. (Please see
Fig. 37.1 ) His parents will reward these efforts
with smiles and expanded inputs, e.g., “Da?! Do
you want Daddy?” The child who cannot produce
these speech patterns at this very young age will
quickly recognize that his communication attempts
are useless. He cannot convey much about what he
wants, needs, or feels and will conclude that those
around him do not care, “so why bother?” These
early failed communication attempts have a long-
term impact not only on language development
but the child’s overall cognitive and psychoedu-
cational development. Communication success
versus communication failure at 12–18 months
of age will inevitably become either wonder-
ful or disastrous well before the age of 3 years.
The potentially dismal long-term outlook for the
child’s well-being thus becomes the concern of all
his caregivers, including all members of the cleft
palate/craniofacial team.
37.3
What Constitutes Scienti fi c
Evidence in Clinical Research?
The strongest evidence that a particular treat-
ment protocol is better than another comes from
prospective clinical trials that include study not
only of the “treatment group” but of a carefully
matched control group over the same period
of time (American Speech-Language-Hearing
1 The topic of primary veloplasty is a particularly dif fi cult
one to pursue in any scienti fi c endeavor to answer the
question of how early (or late) de fi nitive palatal closure
should be accomplished and will therefore be discussed in
a separate section of this chapter (Sect. 37.6).

789
37 Optimal Age for Palatoplasty
2003 ; Friedman et al. 1996 ) . Prospective studies
with a study group and a control group are also
termed “cohort studies” (Wissow and Pascoe
1990 ) . This is in contrast to “case control stud-
ies,” which are usually retrospective in that they
compare current cases with controls from the
past (perhaps consisting of untreated cases or
cases treated by an older method). Prospective
clinical trials are the most dif fi cult to execute.
In fact, Wissow and Pascoe (Wissow and Pascoe
1990 , p. 63) warned,
Clinical trials are poorly suited to studies of (1)
multiple therapeutic modalities (because too many
subjects are needed to evaluate the many possible
therapeutic combinations); (2) small changes in a
therapeutic plan (the effort it takes to do the study
may outweigh the potential signi fi cance of the out-
come); (3) therapies that may be changed during
the course of the study so that the results are at risk
for becoming obsolete before the study is com-
pleted; and (4) treatments with only rare outcomes
or outcomes that will be observable at a time far
distance in the future.
Note how strongly # 1, 2, 3, and the second
half of #4 pertain to the study of the best timing
for palatoplasty.
Shprintzen ( 1991 ) made several observations
that should be kept in mind by anyone engaged
in clinical research and certainly by those who
would study the question of the optimum timing
of palatoplasty. He pointed out that most research
is guided by a speci fi c motive, usually a vested
interest of the investigator, meaning the individ-
ual has an a priori bias regarding the outcome.
With regard to sample selection, he pointed out
the necessity of acknowledging the heteroge-
neous etiology of clefting and the in fl uence this
variation may have on development. He stated
(p. 137), “…if a unilateral cleft lip and palate
occurs because of an intrinsic hypoplasia of one
maxillary process, it would be anticipated that
the intrinsic hypoplasia would remain a factor
throughout postnatal growth....If a major source
of variability [in post-surgical growth] is intrin-
sic differences in facial growth potential related
to population heterogeneity, then the subject
population must be made as homogeneous as
possible.” He observed that, while investigators
may have tried to eliminate all syndromic cases
in their studies of this issue, none of the stud-
ies published up to the date of his commentary
had held constant all the variables that could
in fl uence treatment outcome. At the same time,
he warned (p. 138), “Holding all variables con-
stant in patients with multiple problems is not
only dif fi cult, but the ethics of withholding treat-
ment for the purposes of determining research
outcome might have some dif fi culty passing an
Institutional Review Board.”
10−12 months
0
200
400
600
800
1,000
1,200
18 months
2 years
3 years
Fig. 37.1 Vocabulary
development within the fi rst
3 years of life. The number
of words used at
10–12 months of age is not
“0” but usually 2–10 words.
By 18 months, most
children have at least 50
words, and in the next
6 months that number
quadruples to 200. By the
age of 3 years, most normal
children have speaking
vocabularies of about
1,000 words

790
S.J. Peterson-Falzone
Table 37.1 rank-orders research designs by
the strength of the evidence they can provide. In
a simpler form, we may segregate the aspects of
research design that weaken a study’s conclu-
sions versus those that lead to stronger support-
ive evidence for a particular treatment approach
into “undesirable” versus “desirable”:
Undesirable
Desirable
Investigator
undertakes the study
to prove that his
treatment protocol is
better than another
Investigator has no prior bias as
to outcome of the study
Results recoded only
by the investigator
without independent
observations by
unbiased judges
Unbiased observers/recorders of
results
Single recorder/
observer
Multiple independent observers/
recorders, with measurement of
intra- and inter-observer
reliability
One-time assessment
of results
Longitudinal observation of
results
Retrospective review
of records
Prospective study
Single group of
patients, treated
according to one
protocol, no control
group
Cohort studies, comparing two
or more groups of homogeneous
patients, one treated according
to the protocol under study, the
other untreated or treated by a
standard, accepted protocol
No attempt to
control for the
multiple variables
that may in fl uence
results
Control, or at least careful
independent documentation, of
all variables (e.g., absence of
associated anomalies, type and
extent of cleft, health history, ear
disease and hearing loss,
socioeconomic factors including
parental nurturing and
stimulation)
The summary to both Table 37.1 and the com-
ments above might be “If you want to prove that
a given surgical protocol produces better speech
results in nonsyndromic children with clefts, you
need to plan a prospective, randomized study with
matched controls; two or more surgeons perform-
ing the same procedure (to prove that it is not the
surgeon’s technique that is making the differ-
ence); all independent variables matched across
patient pairs; large numbers of patients in each
treatment group; results recorded by independent
observers on standardized forms (not just anec-
dotal comments) and recorded over time rather
than in a single post-treatment observation.”
Obviously, this description is one of a utopia
that one can only keep in vision, not plan on
reaching. The clinical researcher is therefore
charged with the task of trying to come as close
to this as possible and being very careful in the
interpretation of the results, taking into account
all the factors that could not be controlled.
37.4
A General Warning: “A” Does
Not Cause “B”
Because we clinicians are so anxious to answer
the question that is the focus of this chapter, we
are very prone to jump to conclusions about cause
and effect. The most common trap is assuming
that because “B” is strongly associated with “A,”
even if “B” always follows “A,” that “A” causes
“B.” Friedman et al. ( 1996 ) termed this “causal
inference.” A widely used analogy points out that
Tuesday always follows Monday, but does that
mean Monday causes Tuesday? Even if we were
to see that maxillary arch collapse is present in
100 % of children with cleft lip and palate fol-
lowing palatoplasty at 12 months of age, that
does not mean that either the palatoplasty tech-
nique or the age at palatoplasty caused the arch
collapse. 2 Cleft palate is not just a rearrangement
or “disarrangement” of structures, but an inherent
de fi ciency of tissue. The mere performance of
palatoplasty, the particular surgical procedure
employed, or the age at which it is performed
thus cannot be blamed for subsequent arch
collapse. On the other side of the argument, none
of these three factors alone or in concert can be
held responsible for either normal or abnormal
subsequent development of communication
development. If we were to segregate the physi-
cal variables from the nonphysical variables that
2 Shprintzen ( 1991 , pp. 137–138) made this same point:
“Basing cause and effect relationships on the correlation
of two factors is scienti fi cally unsound, yet is undoubtedly
the most common error made in research design and
interpretation.”

791
37 Optimal Age for Palatoplasty
Table 37.1 Levels of evidence in clinical practice, ranked from weakest to strongest and what each type of evidence would require in a study attempting to relate age of palato-
plasty to speech outcome
Source of evidence
What is involved
What would add strength to the evidence
Comments regarding the value of this form of
evidence
A. “Expert opinion” or
“clinical insight”
Minimally, one person’s opinion on what
works best
Agreement by other “experts,” each with
appropriate experience
Relatively easy to fi nd; most vulnerable to dispute
a B. Retrospective case
studies; all information taken
from archived records (with
or without historical
controls)
Independent non-biased personnel who
examine a pre-determined set of data
recorded in a uniform format
Demonstration of intra- and interclinician
reliability; historical controls would be
patients with the same types and extents of
clefts, non-syndromic, treated by some
other surgical protocol
Probably the most common source of data on this
question; subject to bias, especially if one or more
of the investigators has a predetermined opinion;
most dif fi cult aspect is controlling for the myriad
independent variables (e.g., hearing loss, overall
health, socioeconomic factors, etc.) that affect
outcome
a C. Retrospective case
studies (archived
information) combined with
current clinical assessments
As in (B), above, plus current assessment
of outcomes by independent, non-biased
personnel using the same assessment
protocol with all patients
Demonstration of intra- and interclinician
reliability; control group(s) treated by other
surgical protocols
Case histories + clinical assessments are very
common, but, as in (B) above, investigator bias is
frequently built into the research and control of
independent variables is dif fi cult
a D. Cohort studies
(retrospective)
Investigator pairs each patient treated by
Method X with a patient treated by Method
Y. Each of the pair must match for the
independent variables that could in fl uence
outcome
Demonstration of intra- and inter-clinician
reliability; the larger the number of patients
in each treatment group, and the longer the
period of observation, the stronger the
evidence
Currently a favored approach in studying this
question, but extremely dif fi cult to control for all
the independent variables
a E. Cohort studies
(prospective)
Investigator establishes the matched groups
of patients before any treatment is rendered
Strength of study depends upon the
investigator’s ability to hold everything
constant for each pair in the matched
groups except for outcome; longitudinal
follow-up of outcome strengthens the study
Very dif fi cult to execute due to demands of
matching patients on all independent variables;
also, in longitudinal studies, patient populations
change over time (growth, health factors,
relocation, etc.)
a F. Prospective randomized
trials
Investigator randomly assigns treatment
protocols (i.e., X, Y, Z) to patients who are
matched for type and extent of cleft, age,
sex, other health factors (ear disease, etc.)
As in (E), above
Randomizing treatments raises serious ethical
issues; patient consent is a must. Hospital IRB
approval dif fi cult to obtain. Strongest level of
evidence, but rarely achieved
Designs “B” through “F” would require IRB (Institutional Review Board) review. Please see comments regarding HIPAA (the Health Insurance and Accountability Act of 1996)
following this table
a The HIPAA (Health Insurance and Accountability Act of 1996) prohibits research personnel in health-care facilities from combing patient records unless permission has been
granted by the patients themselves. The only person who can recruit the patients is the physician (clinician) who provided the care to the patient. This has an obvious impact in
cleft palate/craniofacial care, where the preferred approach to care is through a multidisciplinary team (American Cleft Palate-Craniofacial Association 2000) and not by a single
health-care professional. Historically, permission for examination of records or the sharing of information from patient records has not usually been obtained in the form cur-
rently required by HIPAA, rendering most retrospective studies impossible if they must meet HIPAA requirements. Information on HIPAA is available on the web at:
hhs.gov/ocr/hipaa/

792
S.J. Peterson-Falzone
determine outcome from palatoplasty, we would
be looking at the following:
Physical factors
Nonphysical factors
Type and extent of
original cleft
Developmental level
(chronological age compared
to cognitive and communica-
tion development)
Presence/absence of
associated anomalies,
syndromes, etc.
Parent-infant bonding,
parental stimulation
Overall health history
(particularly with
regard to infant feeding
and otologic health)
Other psychosocial issues
affecting the family
Adequacy of pediatric
care both before and
after surgery
Adequacy of relationship
between surgeon (or team)
and the family both before
and after surgery
37.5
An Updated Review
of the Literature
The main points made in the review of 2004
(Peterson-Falzone 1996 ) were as follows:
1. There was a very wide range in what clini-
cians considered to be “early” palatal surgery,
e.g., the fi rst 28 days of life (Denk and Magee
1996 ; Sandberg et al. 2002 ) , 9–25 weeks
(Copeland 1990 ) , and up to 2–3 years (Koberg
and Koblin 1973 ) .
2. Judgment as to whether or not palatoplasty had
in fact provided an intact palate often consisted
of only visual observation of the oral cavity 3
(and sometimes only on a one-time basis),
sometimes combined with rather pathetic
“objective” measures, e.g., fogging on a mirror
held beneath the child’s nose during speech
(Blijdorp and Muller 1984 ) . At the other end of
the continuum, many studies combined com-
paratively rigorous perceptual data with a full
armamentarium of instrumental assessments.
3. The increased knowledge gained in the 1980s
and 1990s regarding the effects of early struc-
tural constraints on pre-speech vocalizations and
on later speech development in children with
clefts could constitute a very good reason to per-
form palatal closure early, e.g., before the child
reaches the milestone of producing his fi rst
meaningful words (Chapman 2011 ; Chapman
et al. 2008 ; Estrem and Broen 1989 ; Grunwell
and Russell 1987, 1988 ; Jones et al. 2003 ;
O’Gara and Logemann 1988 ; O’Gara et al.
1994 ) . Chapman ( 1991 ) found, as had previous
researchers, that the process of phonologic
acquisition in youngsters with clefts was “…
slower, perhaps due to lingering or past articula-
tory and/or structural constraints on the speech
mechanism.”
What Is New Relative to This Point : The closer
we look at the effects of early structural con-
straints on communication development, the
more trouble we fi nd. For example, Chapman
( 1993 ) found that school-age children with
repaired clefts who had persistent speech and
language problems were also more likely to
have reading problems in comparison to chil-
dren with clefts whose speech and language
skills were within normal limits. Of course, we
have long known that children and adults with
clefts are at increased risk for reading prob-
lems and other learning disabilities [please see
Peterson-Falzone et al. ( 2010 , pp. 380–384)].
A 2006 study on infant vocalizations (Thom
et al. 2006 ) provided acoustic and nasal pres-
sure data showing that normal infants show
gradual acquisition of velopharyngeal clo-
sure in their syllable utterances in the fi rst 6
months of life. This process is not complete by
the age of 6 months but is well under way. The
authors conjectured that knowledge of this
developmental process might help determine
optimal timing for palate repair. These results
fi t in well with the theoretical framework pro-
posed by Kemp-Fincham et al. ( 1990 ) . The
latter authors, reviewing the literature on the
development of speech motor control and
phonetic development in infants, concluded
3 The examiner may be able to tell from the intraoral view
alone whether or not the repaired palate is intact, but the
velopharyngeal system is not visible because VP closure
is the closure of the upper (nasal) surface of the velum
against the posterior pharyngeal wall. Visualization of VP
closure requires radiographic (usually fl uoroscopic) or
endoscopic instrumentation. Magnetic resonance imaging
of the velopharyngeal system is also gaining a following,
but is still too expensive to be a routine clinical tool.

793
37 Optimal Age for Palatoplasty
that there is a particularly sensitive period or
state of readiness between the ages of 4 and
6 months. Perhaps palatal closure before or
during this time frame is important if we are
to avoid the development of the maladaptive
compensatory articulations that are so delete-
rious to speech intelligibility.
A 2008 study by Scherer and colleagues ( 2008 )
gave further validation to previous studies demon-
strating the effects of early structural constraints
(open clefts) on babbling at 12 months and sub-
sequent size of consonant inventory when the
children became toddlers. These authors found
persistent vocalization and vocabulary de fi cits
well beyond the time of palate closure, which in
this study was 11–12 months. Note that this age is
well within the time frame for palatal closure sug-
gested by the American Cleft Palate-Craniofacial
Association ( 2009 ) . In comparison to a matched
group of children without clefts, the children
with clefts showed signi fi cant differences in fre-
quency of babbling and “mean babbling level” at
12 months and de fi cits in speech sound accuracy
and vocabulary production at 30 months of age.
Scherer and colleagues ( 2008 ) recommended
early intervention programs for babies with clefts
to enhance speech and language development in
babies with clefts.
4. A much-cited earlier claim by Dorf and Curtin
( 1982, 1990 ) that the chronological age of
12 months for completion of palatal closure was
a cutoff line for preventing the development of
maladaptive compensatory misarticulations in
children with clefts was not supported by subse-
quent studies (Dalston 1992 ; Peterson-Falzone
1990 ) in which an attempt was made to verify
that cutoff age. In addition, Dalston ( 1992 )
and Peterson-Falzone ( 1990 ) pointed out the
critical information, such as age at the time of
assessment, that was missing from the Dorf and
Curtin publications. Unfortunately, 12 months
is still often cited as a magical goal line for the
performance of palatoplasty, ignoring problems
in the methodology of Dorf and Curtin.
5. Despite the fact that their results could not
be replicated in subsequent studies, Dorf
and Curtin ( 1982 ) had made one very impor-
tant point that was largely ignored by other
investigators, namely, that the child’s “articu-
lation age” (level of phonologic and phonemic
development ), not his chronologic age, should
be a prime consideration when trying to plan
the best timing for surgery. That is, speech and
language development vary among children:
Some are attempting to produce 10–12 mean-
ingful words at that age, while others are just
beginning to use “mama.” The more sounds
and words the child is trying to produce, the
more urgent the need for an intact palate and
velopharyngeal system.
What Is New Relative to This Point : In a 2008
publication by Chapman and colleagues
( 2008 ) , the authors tracked speech outcome in
two matched groups of children with nonsyn-
dromic clefts. One group was less lexically
advanced (meaning that they were using fewer
than fi ve words) and younger (mean age of
11 months) when palate surgery was done.
The second group was more lexically advanced
(using fi ve or more words) and a little older
(mean age of 15 months) at the time of sur-
gery. The children were assessed for 11 speech
outcome measures between the ages of 33 and
42 months. The children in the fi rst group had
better articulation and less hypernasality than
the children in the second group.
The authors pointed out that lexical difference
between the two groups at the time of surgery
would be expected because expressive vocabu-
lary increases with age. They also pointed out
that the children who were older and had larger
vocabularies prior to surgery did not produce
maladaptive compensatory misarticulations at
a greater rate than children who were younger
and had less advanced vocabularies; they sim-
ply exhibited poorer speech in general
(Chapman and Hardin 1992 ) . The authors did
not have an explanation for the results, but sug-
gested that future studies should compare chil-
dren undergoing surgery by 6 months of age or
prior to onset of babbling with children receiv-
ing surgery at approximately 12 months.
Interestingly, they did not speci fi cally cite the
results of Ysunza et al. ( 1988 ) who compared
speech outcomes between groups of children
operated at these exact ages.

794
S.J. Peterson-Falzone
6. Clinical surveys in the 1960s, 1970s, 1980s,
and 1990s awakened us to the fact that associ-
ated anomalies, sequences, associations, and
syndromes were probably affecting develop-
ment in at least 50 % of children with clefts
(Jones 1988 ; Shprintzen et al. 1985a, b ;
Womersley and Stone 1987 ) . It is very easy
for anyone other than an experienced dysmor-
phologist to miss subtle signs of other con-
genital defects in children with clefts.
Furthermore, it is easy to miss signs of cogni-
tive delays, hearing loss, and other threats to
development, particularly if a child is not eval-
uated by an interdisciplinary team. Mixing
surgical results from normally developing
children with results from syndromic, multi-
ply involved, or cognitively delayed children
seriously impairs our ability to make decisions
about the effects of any speci fi c treatment.
7. Studies published during the 1990s on the
ostensible relationship between timing of pal-
atal surgery and subsequent speech develop-
ment tended to support performance of surgery
in the fi rst 12–18 months of life, the exception
to this general trend being the studies on pri-
mary veloplasty (reviewed in Sect. 37.6 ). 4
(a) Although
their
report
was
entitled
“Correlation Between the Age at Repair and
Speech Outcomes in Patients with Isolated
Cleft Palate,” Haapanen and Rantala ( 1992 )
did little to clarify the -age-at-surgery question
because they had only small, uneven numbers
of subjects; none were operated before the age
of 1 year; and speech results consisted only
of general categorizations based on one-time
perceptual judgments without independent
or objective documentation. These authors
reported better speech in children whose pal-
ates had been closed between the ages of 16
and 20 months, as opposed to those whose
surgeries had taken place either earlier (12–
15 months) or later (21–24 months). They
came to this conclusion because none of the
children in the middle group (16–20 months
at closure) had developed compensatory
articulations. However, the number of chil-
dren in this group was less than half the num-
ber in each of the other two groups. This fact,
plus the one-time-only assessment with no
longitudinal data, rendered the conclusion
tenuous at best.
(b) Marrinan et al. ( 1998 ) segregated 228
patients with four types of clefts (soft pal-
ate only, clefts of the hard and soft palate,
unilateral cleft lip and palate, bilateral cleft
lip and palate) into four groups based on
age at closure: 8–10, 11–13, 14–16, and
over 16 months. They found that sec-
ondary management for postoperative
velopharyngeal inadequacy was neces-
sary in 11 % of the 8–10 month group,
14 % of the 11–13 month group, 19 % of
the 14–16 month group, and 32 % of the
16+ month group. This linear relationship
between age at palate repair and need for a
pharyngeal fl ap was reported to be statisti-
cally signi fi cant at the p = 0.025 level. The
likelihood of need for a pharyngeal fl ap was
much greater in those children with clefts
of the hard and soft palate (no lip cleft) or
BCLP in comparison to those with clefts of
the soft palate only or UCLP. In fact, in the
latter two groups, age at palate repair was
not statistically signi fi cant (ranging from
10 % need for pharyngeal fl aps in the earli-
est repair up to 18 % in those repaired over
the age of 16 months). The authors attrib-
uted this difference to the size of the cleft,
since the vomer bone was attached in these
two groups, whereas the need for second-
ary surgery in children with an unattached
vomer (complete clefts of hard and soft
palate or bilateral clefts) ranged from 12 %
in the earliest repair group up to 50 % in
those repaired over the age of 16 months.
4 All experienced clinicians realize that “timing isn’t
everything” in palatal surgery. Extent of the defect
(inversely related to the amount of available tissue), surgi-
cal technique, and experience of the surgeon all play a
critical role. In 2001, Timmons and coauthors ( 2001 )
reported on speech results in 54 children. Twenty-seven
had isolated cleft palate and were repaired by intravelar
veloplasty at an average age of 9.6 months; 17 had unilat-
eral clefts and were repaired by the same procedure at an
average age of 8.9 months. When their speech was
assessed between the ages of 5 and 7 years, “cleft-type
speech characteristics” were present in 20/54 = 37 %. For
these surgeons, operating below the age of 12 months was
no guarantee of success.

795
37 Optimal Age for Palatoplasty
(c) Ysunza et al. ( 1988 ) compared speech
results in one group of children ( N = 41)
whose clefts were closed at 12 months
of age to another group ( N = 35) who
were operated on at 6 months. This was
a multifaceted study in which the post-
operative evaluations included standard-
ized perceptual evaluation of speech,
video fl uoroscopy, and nasopharyngoscopy.
Somewhat surprisingly, early phonologic
development was signi fi cantly better in
the second group than in the fi rst. In addi-
tion, none of the 6-month group showed
subsequent development of maladaptive
compensatory articulations, even though
6/35 (17 %) of them showed evidence of
postoperative velopharyngeal inadequacy.
By contrast, in the 8/41 (19 %) of the
12-month group that had VPI, 5 of these
(62 %) developed compensatory articula-
tions. There was no difference between
the two groups in terms of degree of max-
illary collapse when the patients were
examined at 4 years of age. None had had
either preoperative or postoperative ortho-
pedic treatment. The authors concluded
(p. 678), “Because maxillofacial growth
was not signi fi cantly different in [the two]
groups of patients, it seems that cleft pal-
ate closure at 6 months of age is a safe and
reliable procedure for correcting velopha-
ryngeal function in cleft palate patients.”
It is interesting that Ysunza et al. ( 1988 ) ,
using a full range of perceptual and objec-
tive tests, found a signi fi cant difference
between children whose palates were
repaired at 6 months of age and those
repaired at 12 months. 5 As pointed out in
Peterson-Falzone et al. ( 2001, 2010 ) , these
results may speak to the value of the theoret-
ical framework proposed by Kemp-Fincham
et al. in 1990 (Kemp-Fincham et al. 1990 ) .
(d) A few surgeons in the 1990s were performing
very early palatal closure (often simultane-
ous with lip closure) in the fi rst weeks of
life (Copeland 1990 ; Denk and Magee
1996 ; Sandberg et al. 2002 ) . However,
despite the fact that these papers were pub-
lished 22 and 16 years ago, respectively,
there have been no data on speech develop-
ment in the babies so treated, nor has there
been any independent substantiation of any
of the early physical results of the surgery.
Thus, these publications still constitute
studies without results.
37.6
Primary Veloplasty: A Solution
or a Problem?
Two-stage closure of the palate, with soft palate
closure (often combined with lip closure) taking
place in the fi rst few months of life and closure
of the hard palate delayed for variable periods of
time (often until age 7 or beyond), continues to
be the preferred treatment plan in many treatment
centers. Those who prefer this approach state that
closure of the lip and velum promotes a decrease
in size of the hard palate cleft, making it easier to
close at a later date with a less traumatic effect
on the growing maxilla than would be the case
with a complete surgical closure of the hard and
soft palate in a single procedure. The timing of
both the primary veloplasty and the later closure
of the residual hard palate cleft has varied greatly
both among treatment centers and in single cen-
ters that have changed their treatment regimen
over time. Age at the time of soft palate closure
has ranged from the fi rst few weeks of life, 3, 6–8,
12–18 months, and up to the late age of 2 years and
6 months; age for closure of the hard palate has
run the gamut from 12 months up to an extreme
of 11–13 years (Bardach et al. 1984 ; Cosman
and Falk 1980 ; DeLuke et al. 1997 ; Dingman
and Argenta 1985 ; Friede et al. 1980, 1991 ;
Greminger 1981 ; Harding and Campbell 1989 ;
5 These authors were not the fi rst to note a difference in
speech outcome apparently related to differences in age at
closure within the fi rst year of life. Desai ( 1983 ) and
Copeland ( 1990 ) , in companion reports on the same
groups of patients, reported differential effects of age at
palatal surgery compared across 3 months, 4 months,
5 months, and 6 months of age. However, there were very
uneven numbers of children in the four groups, and the
short times separating the ages at surgery plus the rather
questionable nature of the speech data (reportedly col-
lected 5 years after palatal surgery but with an age range
of the patients from “3.8 to 6.3 years”) signaled the need
for skepticism in interpreting the results.

796
S.J. Peterson-Falzone
Hotz et al. 1978 ; Jackson et al. 1983 ; Kramer et al.
1996 ; Lohmander-Agerskov 1998 ; Lohmander-
Agerskov and Soderpalm 1993 ; Lohmander-
Agerskov et al. 1993, 1994, 1995, 1996a, b, 1997,
1998 ; Meijer and Cohen 1990 ; Noordhoff et al.
1987 ; Noverraz et al. 1993 ; Poupard et al. 1983 ;
Rohrich and Gosman 2004 ; Schweckendiek and
Kruse 1990 ; Tanino et al. 1997 ; Van Demark et al.
1989 ; Vedung 1995 ; Wu et al. 1988 ) . 6 7
In addition to the variability in timing and
techniques of eventual hard palate closure in the
regimen of primary veloplasty, interpretation of
results of many clinical studies was complicated
by (1) use of infant orthopedics in some clinic
populations, primarily in Europe (Gnoinski 1982 ;
Hotz et al. 1978, 1984 ; Hotz and Gnoinski 1979 ;
Konst et al. 1999, 2000, 2003a, b, c, 2004 ) , and
by (2) sporadic, inconsistent use of obturating
plates while the hard palate remained open. In
fact, in reviewing these studies, it is very dif fi cult
to differentiate the information given about infant
obturating plates from that pertaining to infant
presurgical orthopedics. For example, in the
patient population of Hotz et al. ( 1979, 1984 ) ,
intraoral devices were designed both to mold
palatal segments and to at least partially obturate
the cleft. The “Hotz” plate (a passive plate) was
also used in the series of studies by Konst et al.
( 1999, 2000, 2003a, b, c, 2004 ) . Interestingly,
when Konst et al. ( 2003c ) analyzed the cost-
effectiveness of their infant orthopedic treatment,
they reported that treatment produced an average
improvement in speech of 1.34 points on a
10-point scale, at a cost of approximately 1,041
Euro dollars.
As early as 1998, Lohmander-Agerskov
( 1998 ) concluded that the use of an intraoral plate
had not proved to enhance articulatory develop-
ment in her patients. 8 She remarked that use of
the plate had been very inconsistent. Not all
patients with open residual clefts had been fi tted
with plates, and consistency of use by any single
patient could not be fully documented. A year
later, Konst et al. ( 2004 ) reported the results of a
prospective clinical trial that compared the prel-
exical (babbling stage) development of babies
with unilateral clefts randomly assigned to either
a presurgical infant orthopedic (PIO) group or a
nonorthopedic group after birth. The “PIO” was
a “Hotz” plate. At 12 months of age, the babies
with plates were using more alveolar articulations
than the non-plate group, but by 18 months of age,
this difference was no longer apparent. In 2002,
Hardin-Jones et al. ( 2002 ) similarly reported
essentially no bene fi t of obturating plates on size
of consonant inventory or place and manner of
consonant production. In fact, there was a trend
for the babies in the obturated group to produce
more glottal consonants than the babies in the
unobturated group.
The point should be made here that the obtu-
rating plates that have been used in babies to pro-
mote speech development have not been
constructed to reach the posterior pharyngeal
wall. Remember that very young infants are obli-
gate nasal breathers, and to completely close off
the nasopharynx would deprive them of an air-
way. Apparently, plates made to cover only the
more anterior portions of the clefts are not enough
to promote appropriate development of anterior
consonants. As the baby grows, oral or oro-nasal
breathing becomes possible, but perhaps the older
the child becomes, the more likely he or she
6 In the 2003 study by Lehner et al. ( 2003 ) , hard palate clo-
sure was performed fi rst, between 4 and 5 months of age,
with later closure of the soft palate at 10–17 months. The
authors concluded (p. 126), “There was no signi fi cant dif-
ference in terms of anterior and posterior maxillary width
between early and delayed closure of [the] hard palate….”
However, the timing of “delayed” hard palate closure was
in no way comparable to what that term connotes in the
rest of the literature.
7 The clinical appeal of primary veloplasty was not
enhanced by the article by Henkel et al. ( 2004 ) in which
speech results were inexplicably determined before the
hard palate had been closed and the open cleft was not
obturated. The “test” for velopharyngeal closure consisted
of whether or not the speech pathologist heard a “sound
difference” between open-nose and closed-nose condi-
tions. It is not surprising that “disordered articulation”
(whatever that term meant) was present in half the popula-
tion of 24 children.
8 Although Dorf and coworkers ( 1985 ) promoted the use of
an “articulation development prosthesis” for infants with
clefts, their caseload consisted of just one child. No
untreated children were studied for comparison regarding
speech sound development.

797
37 Optimal Age for Palatoplasty
rejects the device, dislodging it or just fussing so
much that the parents are reluctant to reinsert it. 9
One also wonders if some babies actively (but
unconsciously) try to avoid tongue contact with
the foreign acrylic invader in their mouths. The
fi ndings of Hardin-Jones et al. ( 2002 ) particularly
suggest this.
What Is New Relative to This Issue : Although
the use of presurgical orthopedics is still part of
the regimen in some treatment centers (Rohrich
et al. 1996, 2000 ; Rohrich and Gosman 2004 ) ,
several studies have been published in the last
12 years showing little bene fi t. 10 Six years after
Lohmander-Agerskov concluded that intraoral
obturating plates were not bene fi cial to speech
development (Lohmander-Agerskov et al. 1993 ) ,
she and her colleagues reported that intraoral pre-
surgical orthopedics did not enhance articulation
development (Lohmander et al. 2004 ) .
Konst and coworkers ( 1999, 2000, 2003a, b, c,
2004 ) felt that their studies demonstrated a
bene fi cial effect of presurgical infant orthopedics
at an acceptable cost, but the size of their treat-
ment groups was small (e.g., fi ve children or
less). In addition, their cost analysis did not
include the costs to families in terms of number
of treatment visits, time off work, transportation
costs, or effects on family life.
The center in Gothenburg, Sweden, continues
to produce the largest amount of data on patients
undergoing primary veloplasty (Friede et al. 1991 ;
Lohmander-Agerskov 1998 ; Lohmander-Agerskov
and Soderpalm 1993 ; Lohmander-Agerskov et al.
1993, 1994, 1995, 1996a, b, 1997, 1998 ;
Lohmander et al. 2002, 2004 ) . In some of their
later work, they began carrying the initial palatal
surgery (veloplasty) further forward, providing
more extensive surgical closure of the cleft and
hoping to promote more postoperative spontane-
ous closure of the residual cleft. 11 They have also
moved the timing of closure of the residual cleft
forward to somewhat earlier ages than was the
case in their original protocol.
In each of the Lohmander- Agerskov studies
(Lohmander-Agerskov 1998 ; Lohmander-Agerskov
and Soderpalm 1993 ; Lohmander-Agerskov et al.
1993, 1994, 1995, 1996a, b, 1997, 1998 ; Lohmander
et al. 2002, 2004 ) , perceptual speech outcomes
were rigorously documented. Overall, these studies
have shown a remarkably low incidence of mal-
adaptive compensatory misarticulations (glottal
stops, pharyngeal fricatives, etc.) both prior to and
following full palatal closure, far less than one
would expect when a child has reached school age
with an open residual cleft. Perhaps this was the
result of early intervention (speech therapy). Prior
to de fi nitive palatal closure, the children undergo-
ing primary veloplasty have shown the expected
hypernasal resonance and nasal air loss, but the
articulatory problems have primarily been retracted
placement of dental and dento-alveolar consonants
to palatal and velar placements.
In 1993, Lohmander-Agerskov and Soderpalm
( 1994 ) stated that they had changed their clini-
cal routine to include “early intervention pro-
grams, evaluation of speech development, and
early speech therapy if necessary.” However,
in their 1998 paper (Lohmander et al. 2002 ) ,
Lohmander-Agerskov and colleagues noted that
speech therapy had only a “marginal effect” on
the misarticulations (retracted oral consonants)
found in 5-year-olds with large residual clefts.
Other studies by the same group (Lohmander-
Agerskov et al. 1995, 1996a, b ; Lohmander et al.
2004 ) con fi rmed that adverse effects of an open
cleft were evident in babbling and continued to
have an effect on speech sound acquisition in the
toddler, preschool, and school-age years.
9 Maintaining the plate in place by pin retention avoids this
problem, but has the potential of interfering with maxil-
lary growth. In addition, constant apposition of the acrylic
to the oral mucosa has deleterious effects on the tissue. In
fact, when Holland et al. ( 2007 ) reported that “delayed
closure of the hard palate leads to speech problems and
deleterious maxillary growth,” they were reporting results
from a 5-year clinical period during which they were
using pin-retained plates to cover the residual cleft after
primary veloplasty. The poor results with regard to maxil-
lary growth are not a surprise.
10 The topic of presurgical orthopedics is discussed else-
where in this book.
11 The treatment groups in both Sweden and Texas (Rohrich
et al. 1996, 2000 ; Rohrich and Gosman 2004 ) have
reported instances of complete spontaneous closure of the
residual cleft after primary veloplasty.

798
S.J. Peterson-Falzone
Other clinicians studying effects of the pri-
mary veloplasty regimen have also reported poor
speech results (Bardach et al. 1984 ; Cosman and
Falk 1980 ; Jackson et al. 1983 ; Noordhoff et al.
1987 ; Rohrich et al. 1996, 2000 ; Rohrich and
Gosman 2004 ; Witzel et al. 1980 ) . Rohrich and
Gosman ( 2004 ) closed the hard palate simultane-
ously with the soft palate in 21 children at a mean
age of 10.8 months (range 6–18 months). Another
set of 23 children had primary veloplasty at a
mean age of 11.4 months (range 6–22 months)
and hard palate closure at an average age of
48.6 months (range 30–57 months). 12 They con-
cluded (p. 236), “Our data suggest that delaying
had palate closure results in signi fi cant speech
impairment with a bene fi cial maxillofacial growth
response.” In a later publication, Rohrich et al.
( 1996 ) advocated a protocol of (1) presurgical
orthopedics begun at 1–2 weeks of age, (2) lip
closure and velar repair at 3–6 months of age, and
closure of the residual hard palate cleft at
15–18 months.
It is pertinent here to point out that some
other studies on growth have also cast doubt
on the effects of delayed hard palate closure
on maxillofacial growth. Noverraz et al. ( 1993 )
studied dental arch relationships in 88 children
with unilateral clefts who underwent primary
veloplasty at a mean age of 1.1 years and who
were segregated into four groups depending
upon timing of hard palate closure (modi fi ed
von Langenbeck in all cases): 1.5, 4.6, 9.4 years,
and unclosed by the age of 10 years. All of these
children had received presurgical orthopedic
treatment according to the method of Hotz (Hotz
et al. 1978, 1984 ; Hotz and Gnoinski 1979 ) , but
only until the time of soft palate closure. These
authors found no differences in the dental arch
relationships among the four groups. Thus, age
at hard palate closure, at least within the range of
1.5 up to 9.4 years, did not differentially affect
maxillofacial growth. Gaggi et al. ( 2003 ) exam-
ined maxillofacial growth in 30 individuals with
unilateral cleft lip and palate whose palates had
been closed in a single procedure between 11 and
14 months, compared to 30 who had had velo-
plasty between 18 and 24 months and hard pal-
ate closure at 6 years. At 18 years of age, those
patients in the delayed hard palate repair group
had a more severe impairment in growth of the
maxilla than those who had had a single proce-
dure. This study did not include data on speech,
but one can only imagine the devastating effect
on speech sound development in those children
whose palates were left completely open until the
age of 18–24 months. By 24 months of age, most
children are using at least two-word sentences.
Van Demark ( 1995 ) pointed out that advocates
of primary veloplasty have ignored the fi nancial
and psychosocial costs of the increased number
of surgical procedures (two palatal surgeries
instead of one), the clinic visits for the fi tting and
maintenance of plates, and the intensive speech
therapy such as implemented in the Zurich treat-
ment center (Gnoinski 1982 ; Hotz et al. 1978,
1984 ; Hotz and Gnoinski 1979 ; Van Demark
et al. 1989 ) . These remarks may have particular
pertinence in the USA, where third-party payers
(insurance companies, HMOs) continue to cut
services to the bare bones, meaning that families
who need more team visits and more surgeries
are apt to be paying out of pocket. To be blunt, a
treatment protocol of primary veloplasty, which
tends to be both care intensive and could be cost
intensive, may be preferred in treatment centers
functioning in countries in which medical care is
fully socialized (such as Sweden), but it is less
likely to gain a large following in countries such
as the United States where medical care is largely
pay-as-you-go.
There is little doubt that those centers that
have devoted so much effort to studying and
improving treatment outcomes using primary
veloplasty will continue to do so. However,
speech-language pathologists remain skeptical,
especially when the provision of a fully repaired
palate during the crucial time for speech sound
acquisition can prevent the stigmata of “cleft
palate speech.”
12 The large range of ages at surgery, both in the early
complete closure and in the delayed closure groups, weakens
the strength of this study.

799
37 Optimal Age for Palatoplasty
Conclusions
Given the fact that innovations in palatal sur-
gery are constantly being pursued in the effort
to reduce trauma to tissue and minimize scar-
ring [e.g., (Karsten et al. 2003 ; Mendoza et al.
1994 ) ], there is reason to be optimistic that cli-
nicians will come closer to making reasonable
decisions about the best timing for palatal sur-
gery, without the old argument of speech ver-
sus growth. For example, we no longer have to
rely on such scar-inducing procedures as the
Wardill-Kilner pushback (Ishikawa et al. 1998 )
or the infamous “island fl ap” (Greminger
1981 ) . Surgeons can now produce better mor-
phologic and physiologic results so that ortho-
dontists do not have to fret about iatrogenic
effects on maxillary growth. Signi fi cant palatal
scarring and its subsequent effects on growth
are not inevitable consequences just because
palatal surgery is carried out early enough to
facilitate normal communication development.
Multicenter studies of all aspects of treatment
outcomes (e.g., ScanCleft, DutchCleft, and
AmeriCleft) are trying to iron out inconsisten-
cies, particularly with regard to approaches to
assessment of speech and craniofacial growth.
A large part of the program of the next
International Congress on Cleft Palate and
Craniofacial Anomalies (Orlando, FL, 2013)
will be devoted to progress reports on these
issues.
Speech pathologists have continued to doc-
ument the deleterious effects of an open palate
on babbling in 6-month-olds and the subse-
quent effects on speech as the child reaches
toddlerhood. There is no question that normal
speech depends upon velopharyngeal closure
being provided when it is needed, 13 which is
long before full maxillary growth has been
achieved. The expectation for every otherwise-
normal child with a cleft should be normal
speech development.
References
American Cleft Palate-Craniofacial Association (2009)
Parameters for the evaluation and treatment of patients
with cleft lip/palate or other craniofacial anomalies.
. Accessed 10 Nov 2011
American Speech-Language-Hearing Association (2003)
Evidence-based
practice:
practice
guidelines
http//:professional.asha.og/communityslp/evidence_
guidelines.cfm . Accessed 10 Nov 2011
Bardach J, Morris HL, Olin WH (1984) Late results of
primary veloplasty: the Marburg project. Plast
Reconstr Surg 73:207–215
Berkowitz S (2004) Timing of cleft palate closure should
be based on the ratio of the area of the cleft to that of
the palatal segments and not on age alone: Chap. 17.
In: Berkowitz S (ed) Cleft lip and palate: diagnosis and
management, 2nd edn. Springer, Berlin/Heidelberg
Blijdorp P, Muller H (1984) The in fl uence of the age at
which the palate is closed on speech in the adult cleft
palate patient. J Maxillofac Surg 12:239–246
Chapman KL (1991) Vocalizations of toddlers with cleft
palate. Cleft Palate Craniofac J 28:172–178
Chapman KL (1993) Phonologic processes in chil-
dren with cleft palate. Cleft Palate Craniofac J 30:
64–72
Chapman KL (2011) The relationship between early read-
ing skills and speech and language performance in
young children with cleft lip and palate. Cleft Palate
Craniofac J 48:301–311
Chapman KL, Hardin MA (1992) Phonetic and phono-
logic skills of two-year-olds with cleft palate. Cleft
Palate Craniofac J 29:435–443
Chapman KL, Hardin-Jones MA, Goldstein JA, Halte
MS, Havlik J, Schulte J (2008) Timing of palatal sur-
gery and speech outcome. Cleft Palate Craniofac J
45:297–308
Copeland M (1990) The effects of very early palate repair
on speech. Br J Plast Surg 43:676–682
Cosman B, Falk AS (1980) Delayed hard palate repair and
speech de fi ciencies: a cautionary report. Cleft Palate J
17:27–33
Dalston RM (1992) Timing of cleft palate repair: a speech
pathologist’s vewpoint. Probl Plast Reconstr Surg
Cleft Palate Surg 2:30–38
DeLuke DM, Marchand A, Robles EC, Fox P (1997)
Facial growth and the need for orthognathic surgery
after cleft palate repair. J Oral Maxillofac Surg
55:694–697
Denk MJ, Magee WP (1996) Cleft palate closure in the
neonate: preliminary report. Cleft Palate Craniofac J
33:57–61
Desai S (1983) Early cleft palate repair completed before
the age of 16 weeks: observations on a personal series
of 100 children. Br J Plast Surg 36:300–304
Dingman R, Argenta L (1985) The correction of cleft pal-
ate with primary veloplasty and delayed repair of the
hard palate. Clin Plast Surg 12:677–684
13 Berkowitz ( 2004 ) was concerned about speech patholo-
gists seeking palatal surgery for children with clefts based
on age of the child. It is not the age but the developmental
level of the child. See Chapman and Hardin ( 1992 ) .

800
S.J. Peterson-Falzone
Dorf DS, Curtin J (1982) Early cleft palate repair and
speech outcome. Plast Reconstr Surg 68:135–157
Dorf DS, Curtin J (1990) Early cleft palate repair and
speech outcome: a ten-year experience. In: Bardach J,
Morris HL (eds) Multidisciplinary management of
cleft lip and palate. WB Saunders, Philadelphia, pp
341–348
Dorf DS, Reisbeg DJ, Gold HO (1985) Early prosthetic
management of cleft palate: articulation development
prosthesis: a preliminary report. J Prosthet Dent 53:
222–226
Estrem T, Broen PA (1989) Early speech production of
children with cleft palate. J Speech Hear Res 32:
12–23
Friede H, Lilja J, Johanson B (1980) Cleft lip and palate
treatment with delayed closure of the hard palate.
Scand J Plast Reconstr Surg 14:49–53
Friede H, Enemark H, Semb G, Paulin G, Abyholm F,
Bolund S, Lilja J, Ostrup L (1991) Craniofacial and
occlusal characteristics in unilateral cleft lip and pal-
ate patients from four Scandinavian centres. Scand J
Plast Reconstr Surg Hand Surg 25:269–276
Friedman LM, Furberg CD, DeMets DL (1996)
Fundamentals of clinical trials, 3rd edn. Mosby, St.
Louis
Gaggl A, Feichtinger M, Shultes G, Santler G, Pichlmaier
M, Mossbock R, Karcher H (2003) Cephalometric and
occlusal outcome in adults with unilateral cleft lip,
palate, and alveolus after two different surgical proce-
dures. Cleft Palate Craniofac J 40:249–255
Gnoinski WM (1982) Early maxillary orthopedics as a
supplement to conventional primary surgery in com-
plete cleft lip and palate patients. J Maxillofac Surg
10:165–172
Greminger R (1981) Island soft palatoplasty for early
reconstruction of the posterior muscular ring. Plast
Reconstr Surg 68:871–877
Grunwell P, Russell J (1987) Vocalizations before and
after cleft palate surgery: a pilot study. Br J Disord
Commun 22:1–17
Grunwell P, Russell J (1988) Phonological development
in children with cleft lip and palate. Clin Linguist
Phon 2:75–95
Haapanen M-L, Rantala S-L (1992) Correlation between
the age at repair and speech outcome in patients with
isolated cleft palate. Scand J Plast Reconstr Surg Hand
Surg 26:71–78
Harding A, Campbell RC (1989) A comparison of the
speech results after early and delayed hard palate
closure: a preliminary report. Br J Plast Surg 42:
187–192
Hardin-Jones MA, Chapman KL, Wright J, Halter KA,
Schulte J, Dean JA, Havlik RJ, Goldstein J (2002) The
impact of early palatal obturation on consonant devel-
opment in babies with unrepaired cleft palate. Cleft
Palate Craniofac J 39:157–163
Henkel K-O, Dieckmann A, Dieckmann O, Lenz J-H,
Gundlach KKH (2004) Veloplasty using the wave-line
technique versus classic intravelar veloplasty. Cleft
Palate Craniofac J 41:1–4
Holland S, Gabbay JS, Helie JB, O’Hara C, Huwitz D,
Ford MD, Suade AS, Bradley JP (2007) Delayed clo-
sure of the hard palate leads to speech problems and
deleterious maxillary growth. Plast Reconstr Surg
119:1302–1310
Hotz M, Gnoinski WM (1979) Effects of early maxil-
lary orthopaedics in coordination with delayed sur-
gery for cleft lip and palate. J Maxillofac Surg 7:
201–210
Hotz M, Gnoinski WM, Nussbaumer H, Kistler E (1978)
Early maxillary orthopedics in CLP cases: guidelines
for surgery. Cleft Palate J 15:405–411
Hotz M, Gnoinski WM, Perko M, Nussbaumer H, Hof E,
Haubensak R (eds) (1984) Early treatment of cleft lip
and palate. Hans Huber, Bern
Ishikawa H, Nakamura S, Misaki K, Kudoh M, Fukuda H,
Yoshida S (1998) Scar tissue distribution on palates
and its relation to maxillary dental arch form. Cleft
Palate Craniofac J 35:313–319
Jackson IT, McLennan G, Scheker L (1983) Primary velo-
plasty or primary palatoplasty some preliminary
fi ndings. Plast Reconstr Surg 72:153–157
Jones MC (1988) Etiology of facial clefts: prospective
evaluation of 428 patients. Cleft Palate J 25:16–20
Jones CE, Chapman KL, Hardin-Jones MA (2003) Speech
development of children with cleft palate before and
after palatal surgery. Cleft Palate Craniofac J 40:
19–31
Karsten A, Larson M, Larson O (2003) Dental occlusion
after Veau-Wardill-Kilner versus minimal incision
technique repair of isolated clefts of the hard and soft
palate. Cleft Palate Craniofac J 40:504–510
Kemp-Fincham SI, Kuehn DP, Trost-Cardamone JE (1990)
Speech development and the timing of primary palato-
plasty. In: Bardach J, Morris HL (eds) Multidisciplinary
management of cleft lip and palate. WB Saunders,
Philadelphia, pp 736–745
Koberg WR, Koblin I (1973) Speech development and
maxillary growth in relation to technique and timing
of palatoplasty. J Maxillofac Surg 1:44–50
Konst EM, Weersink-Braks H, Rietvelt T, Peters H (1999)
Prelexical development of unilateral cleft lip and pal-
ate babies with reference to presurgical infant orthope-
dics: a randomized prospective clinical trial. Clin
Linguist Phon 13:395–407
Konst EM, Weersink-Braks H, Rietveld T, Peters H (2000)
An intelligibility assessment of toddlers with cleft lip
and palate who received and did not receive presurgi-
cal infant orthopedic treatment. J Commun Disord
33:483–499
Konst EM, Rietveld T, Peters HFM, Kuijpers-Jagtman
AM (2003a) Language skills of young children with
unilateral cleft lip and palate following infant orthope-
dics: a randomized clinical trial. Cleft Palate Craniofac
J 40:356–362
Konst EM, Rietveld T, Peters HF, Weersink-Braks H
(2003b) Use of a perceptual evaluation instrument to
assess the effects of infant orthopedics on the speech
of toddlers with cleft lip and palate. Cleft Palate
Craniofac J 40:597–605

801
37 Optimal Age for Palatoplasty
Konst EM, Rietveld T, Peters HF, Prahl-Andersen B
(2003c) Phonological development of toddlers with
unilateral cleft lip and palate who were treated with
and without infant orthopedics: a randomized clinical
trial. Cleft Palate Craniofac J 40:32–39
Konst EM, Prahl C, Weersink-Braks H, De Boo T, Prahl-
Andersen G, Kuijpers-Jagtman AM, Severens JL
(2004) Cost-effectiveness of infant orthopedic treat-
ment regarding speech in patients with complete uni-
lateral cleft lip and palate: a randomized three-center
trial in the Netherlands (Dutchcraft). Cleft Palate
Craniofac J 41:71–77
Kramer GJC, Hoeksma JB, Prahl-Andersen B (1996)
Early palatal changes after initial palatal surgery in
children with cleft lip and palate. Cleft Palate Craniofac
J 33:104–111
Lehner B, Wiltfang J, Strobel-Schwarthoff K, Benz M,
Hirschfelder U, Neukam F-W (2003) In fl uence of
early hard palate closure in unilateral and bilateral
cleft lip and palate on maxillary transverse growth
during the fi rst four years of age. Cleft Palate Craniofac
J 40:126–130
Lohmander A, Persson E-C, Owman-Moll P (2002)
Unrepaired clefts in the hard palate: speech de fi cits at
the ages of 5 and 7 years and their relationship to size
of the cleft. Scand J Plast Reconstr Surg Hand Surg
36:332–339
Lohmander A, Lillvik M, Friede H (2004) The impact of
early infant jaw-orthopaedics on early speech produc-
tion in toddlers with unilateral cleft lip and palate. Clin
Linguist Phon 18:259–284
Lohmander-Agerskov A (1998) Speech outcome after
cleft palate surgery with the Goteborg regimen includ-
ing delayed hard palate closure. Scand J Plast Reconstr
Surg Hand Surg 32:63–80
Lohmander-Agerskov A, Soderpalm E (1993) Evaluation
of speech after completed late closure of the hard pal-
ate. Folia Phoniatr 45:25–30
Lohmander-Agerskov A, Havstam C, Soderpalm E, Lilja
J, Friede H, Persson E-C (1993) Assessment of speech
in children after repair of isolated cleft palate. Scand J
Plast Reconstr Surg Hand Surg 27:307–310
Lohmander-Agerskov A, Soderpalm E, Friede H, Persson
E-C, Lilja J (1994) Pre-speech in children with cleft
lip and palate or cleft palate only: phonetic analysis
related to morphologic and functional factors. Cleft
Palate Craniofac J 31:271–279
Lohmander-Agerskov A, Soderpalm E, Friede H, Lilja J
(1995) A longitudinal study of speech in 15 children
with cleft lip and palate treated by late repair of the
hard palate. Scand J Plast Reconstr Surg Hand Surg
29:21–31
Lohmander-Agerskov A, Dotevall H, Lith A, Soderpalm
E (1996a) Speech and velopharyngeal function in chil-
dren with an open residual cleft in the hard palate, and
the in fl uence of temporary covering. Cleft Palate
Craniofac J 33:324–332
Lohmander-Agerskov A, Friede H, Lilja J, Soderpalm E
(1996b) Delayed closure of the hard palate: a compari-
son of speech in children with open and functionally
closed residual clefts. Scand J Plast Reconstr Surg
30:121–127
Lohmander-Agerskov A, Friede H, Soderpalm E, Lilja J
(1997) Residual clefts in the hard palate: correlation
between cleft size and speech. Cleft Palate Craniofac J
34:122–128
Lohmander-Agerskov A, Soderpalm E, Friede H, Lilja J
(1998) A comparison of babbling and speech at pre-
speech level, 3 and 5 years of age in children with cleft
lip and palate treated with delayed hard palate closure.
Folia Phoniatr Logop 50:320–334
Marrinan EM, LaBrie RA, Mulliken JB (1998)
Velopharyngeal function in nonsyndromic cleft palate:
relevance of surgical technique, age at repair, and cleft
type. Cleft Palate Craniofac J 35:95–100
Meijer R, Cohen S (1990) Two-stage palatoplasty and
evaluation of speech results. In: Bardach J, Morris
HL (eds) Multidisciplinary management of cleft
lip and palate. WB Saunders, Philadelphia, pp
321–327
Mendoza M, Molina F, Azzolini C, Ysunza Rivera A
(1994) Minimal incision palatopharyngoplasty. Scand
J Plast Reconstr Surg Hand Surg 28:199–205
Noordhoff MS, Juo J, Wang F, Wuang H, Witzel MA
(1987) Development of articulation before delayed
hard palate closure in children with cleft palate: a
cross-sectional study. Plast Reconstr Surg 80:518–524
Noverraz AEM, Kuijpers-Jagtman AM, Mars M, Van’t
Hof MA (1993) Timing of hard palate closure and
dental arch relationships in unilateral cleft and palate
patients: a mixed-longitudinal study. Cleft Palate
Craniofac J 30:391–396
O’Gara MM, Logemann JA (1988) Phonetic analysis of
the speech development of babies with cleft palate.
Cleft Palate J 25:122–134
O’Gara MM, Logemann JA, Rademaker AW (1994)
Phonetic features by babies with unilateral cleft lip
and palate. Cleft Palate Craniofac J 31:446–451
Peterson-Falzone SJ (1990) A cross-sectional analysis of
speech results following palatal closure. In: Bardach J,
Morris HL (eds) Multidisciplinary management of
cleft lip and palate. WB Saunders, Philadelphia, pp
750–757
Peterson-Falzone SJ (1996) The relationship between
timing of cleft palate surgery and speech outcome:
what have we learned, and where do we stand in the
1990s? Semin Orthod 2:185–191
Peterson-Falzone SJ (2004) Optimal age for palatoplasty to
facilitate normal speech development: what is the evi-
dence? In: Berkowitz S (ed) Cleft lip and palate: diag-
nosis and management. Springer, Berlin/Heidelberg
Peterson-Falzone SJ, Hardin-Jones MA, Karnell MP
(2001) Cleft palate speech, 3rd edn. Mosby, St. Louis
Peterson-Falzone SJ, Hardin-Jones MA, Karnell MP
(2010) Cleft palate speech, 4th edn. Mosby, St. Louis
Poupard B, Coornaert H, Cebare P, Treanton A (1983)
Cleft lip and palate. Can the hard palate be left
open? A study of sixty-two cases with a follow-
up of six years or more. Ann Chir Plast Esthet 28:
325–336

802
S.J. Peterson-Falzone
Rohrich RJ, Gosman AA (2004) An update on the timing
of had palate closure: a critical long-term analysis.
Plast Reconstr Surg 113:350–352
Rohrich RJ, Rowsell AR, Johns DF, Drury MA, Grieg G,
Watson DJ, Godfrey AM, Poole MD (1996) Timing of
hard palate closure: a critical long-term analysis. Plast
Reconstr Surg 98:236–246
Rohrich RJ, Love EJ, Byrd S, Johns DF (2000) Optimal
timing of cleft palate closure. Plast Reconstr Surg
106:413–421
Sandberg DJ, Magee WP, Denk MJ (2002) Neonatal cleft
lip and cleft palate repair. AORN J 75:490–498
Scherer NJ, Williams AL, Proctor-Williams K (2008) Early
and later vocalization skills in children with and without
cleft palate. Int J Pediatr Otolaryngol 72:827–840
Schweckendiek W, Kruse E (1990) Two stage palatoplasty:
Schweckendiek technique. In: Bardach J, Morris HL
(eds) Multidisciplinary management of cleft lip and
palate. WB Saunders, Philadelphia, pp 315–320
Shprintzen RJ (1991) Fallibility of clinical research. Cleft
Palate Craniofac J 28:136–140
Shprintzen
RJ,
Siegel-Sadewitz
VL,
Amato
J,
Goldberg RB (1985a) Anomalies associated with
cleft lip, cleft palate, or both. Am J Med Genet 20:
585–595
Shprintzen RJ, Siegel-Sadewitz VL, Amato J, Goldberg
RB (1985b) Retrospective diagnoses of previously
missed syndromic disorders among 1000 patients with
cleft lip, cleft palate, or both. Birth Defects Orig Artic
Ser 21:85–92
Tanino R, Akamatsu T, Nishimura M, Miyasaka M, Osada
M (1997) The in fl uence of different types of hard-
palate closure in two-stage palatoplasty on maxillary
growth: cephalometric analyses and long-term fol-
low-up. Ann Plast Surg 39:245–254
Thom SA, Hoit JD, Hixon TJ, Smith AE (2006)
Velopharyngeal function during vocalization in infants.
Cleft Palate Craniofac J 43:539–546
Timmons MJ, Wyatt A, Murphy T (2001) Speech after
repair of isolated cleft palate and cleft lip and palate.
Br J Plast Surg 54:377–384
Van Demark DR (1995) Commentary on Vedung S:
Pharyngeal fl aps after one- and two-stage repair of the
cleft palate: a 25-year review of 520 patients. Cleft
Palate Craniofac J 22:216
Van Demark DR, Gnoinski W, Hotz MM, Perko M,
Nussbaumer H (1989) Speech results of the Zurich
approach in the treatment of unilateral cleft lip and
palate. Plast Reconstr Surg 83:605–613
Vedung S (1995) Pharyngeal fl aps after one- and two-
stage repair of the cleft palate: a 25-year review of 520
patients. Cleft Palate Craniofac J 32:206–215
Wissow L, Pascoe J (1990) Types of research models and
methods. In: De Angelis C (ed) An introduction to
clinical research. Oxford Press, New York, pp
38–74
Witzel MA, Salyer KE, Ross RB (1980) Delayed hard
palate closure: the philosophy revisited. Cleft Palate J
21:263–269
Womersley J, Stone DH (1987) Epidemiology of facial
clefts. Arch Dis Child 62:717–720
Wu J, Chen YR, Noordhoff MS (1988) Articulation
pro fi ciency and error pattern of cleft palate children
with delayed hard palate closure. Ann Acad Med
Singapore 17:384–387
Ysunza A, Pamplona C, Mendoze M, Garcia-Velasco M,
Guerrero ME (1988) Speech outcome and maxillary
growth in patients with unilateral complete cleft lip/
palate operated on at 6 versus 12 months of age. Plast
Reconstr Surg 102:675–679

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DOI 10.1007/978-3-642-30770-6_38, © Springer-Verlag Berlin Heidelberg 2013
38
38.1
Introduction
One of the goals of cleft care is to establish normal
speech. As providers, we attempt to achieve this
goal in the face of the structural de fi cits of the
cleft palate, a changing velopharyngeal environ-
ment, a developing dentofacial structure, and a
propensity for hearing loss. We attempt to do this
understanding that velopharyngeal competence is
essential to normal speech learning. We are also
working within a “speech readiness” period. If
normal speech is not established or if maladaptive
speech is not extinguished during this “readiness
period,” results can be less than optimal. This
chapter will review the challenges and factors that
in fl uence the outcome of managing speech, lan-
guage, and velopharyngeal dysfunction through-
out the life of an individual with cleft palate.
38.2
Challenges
Despite the advances in surgical technique and
procedures and the sophistication of instrumental
assessment and imaging, there is little consensus
on an optimal treatment protocol. A contributing
factor might be the great variability in craniofa-
cial morphology and the response to treatment
in patients who have exactly the same cleft lip
and palate diagnosis (Molsted 1999 ) . While we
have not been able to develop a consensus on
management, we are developing a clearer under-
standing of factors that in fl uence our treatment.
Although there is no consensus on a management
program, the American Cleft Palate-Craniofacial
Association has published recommended param-
eters of practice for the care of individuals with
congenital craniofacial anomalies (American
Cleft Palate-Craniofacial Association 1993 ) . The
consensus conference participants who developed
the document espoused several fundamental prin-
ciples of optimal care including the importance
of team care, parent/caregiver involvement, and
longitudinal follow-up.
Hypernasality, nasal air emission, and aber-
rant articulation mark the failed primary man-
agement of the patient with cleft palate. Despite
best attempts, primary palatal management is
only successful in 70–80 % of individuals with
cleft palate ( Morris 1973 ; Riski 1979 ) . That
is, 20–30 % of children born with cleft pal-
ate will require secondary palate and manage-
ment. Despite advances in instrumentation used
to evaluate velopharyngeal function, we still
have no way of predicting or identifying, at the
time of initial palatal surgery, which 20–30 %
of children will bene fi t from a pharyngoplasty.
The speech pathologist must monitor emerging
speech and language for any signs of nasal air
Speech, Language,
and Velopharyngeal Dysfunction:
Management Throughout the Life
of an Individual with Cleft Palate
John E. Riski
J. E. Riski , Ph.D., CCC-S, FASHA
Speech Pathology Laboratory , Center for Craniofacial
Disorders, Children’s Healthcare of Atlanta ,
5455 Meridian Mark Road, NE, Suite 200 ,
Atlanta , GA 30342 , USA
e-mail: john.riski@choa.org

804
J.E. Riski
escape, hypernasality, or aberrant misarticula-
tion in order to identify children who have had an
unsuccessful initial surgery and which children
are candidates for secondary surgery.
In the last 40 years, great progress has been
made toward a better understanding of many
aspects of the cleft lip and palate defect, but con-
siderable study remains before there is agreement
on the optimal treatment procedures. Molsted
( 1999 ) provides an excellent review of the topic.
Primary closure of the palate may fall into two
main schools of thought. One advocates early
closure of the lip and palate in order achieve nor-
mal speech function. The other recommends
delayed closure of the hard palate in order to
achieve maximum growth of the maxilla. A num-
ber of intercenter and multicenter studies have
been carried out recently in an effort to investi-
gate which procedures give the best result, both
esthetically and functionally. The results are
ambiguous, and this has led a number of research-
ers to suggest that a randomized clinical trial is
the only way to resolve the ambiguity. The fact
that it has proved dif fi cult to identify the optimal
procedures in the fi eld of cleft lip and palate treat-
ment may not only be due to a less than optimal
research design. Another contributory factor
might also be the great variability in craniofacial
morphology and in the response to treatment in
patients who have exactly the same cleft lip and
palate diagnosis. Intensive research has made it
possible to state categorically that clefts occur
due to many different factors in an interplay
between genetics and environment. Therefore, it
is not likely that a single gene can be responsible
for clefting.
Further complicating the discussion is the
topic of fetal surgery. Since scar tissue presents
many problems – for instance, impairment of
growth – the reduction or prevention of scar for-
mation has long been a desirable goal. The dis-
covery that a fetus can heal without scar formation
has led to many animal experiments. The timing
of the surgical intervention on fetuses is critical,
since late-gestation fetuses heal with adult-like
scarring. There are still many unsolved problems
connected with fetal surgery, and at present, pre-
natal surgery for repair of cleft lip and palate is
not ethically defensible in humans. On the other
hand, it appears that there are considerable pos-
sibilities for the reduction of human scarring after
surgery with the introduction of various wound-
healing medications.
Although oral clefts are among the most com-
mon birth defects, they remain a low-incidence
disorder in pediatric practice. The prevalence is
approximately 1:750–1:1,000 newborns in the
Caucasian population and is even higher in other
populations. It is estimated that there are 6,000
new CL/P cases in the United States annually.
Despite the relative prevalence of oral clefts,
these patients still represent a small part of the
pediatric caseload outside craniofacial centers.
Hypernasality, nasal air emission, and compensa-
tory articulation are also low-incidence speech
disorders and may result from structural, neuro-
logical, or functional (learned) etiologies. The
rate of hypernasality after initial cleft palate clo-
sure is only 20–30 % (Riski 1979 ; Riski and
DeLong 1984 ) . Low-incidence disorders such as
oral clefts and hypernasality offer few educa-
tional or clinical opportunities for developing
clinical expertise. We are challenged to educate
other healthcare workers about appropriate
identi fi cation, diagnosis, and management.
A challenge to evaluation is that the etiologies
of hypernasality and nasal air fl ow disorders are
often occult or hidden. In recent reviews of
patients receiving surgical correction for hyper-
nasality, approximately 30 % did not have a cleft
palate (Riski et al. 1992 ; Riski 1995 ) . The etiol-
ogy in these children is an anatomically deep
nasopharynx that can be diagnosed accurately
only by radiographic assessment. Normal
velopharyngeal dimensions were described by
Subtelny ( 1957 ) and highlighted by Zemlin
( 1997 ) . Further, the anatomic defect of a dispro-
portionately deep pharynx was described by
Calnan ( 1971 ) .
An issue in speech pathology that may have its
origin in the low incidence and occult nature of
the disorder is that noncleft hypernasality is erro-
neously labeled as a “voice disorder.” Labeling
hypernasality a “voice disorder” is ambiguous
and often has dire consequences for the child and
successful management of the disorder. Labeling