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CME

Optimal Timing of Cleft Palate ClosureRod J. Rohrich, M.D., Edward J. Love, M.D., H. Steve Byrd, M.D., and Donnell F. Johns, Ph.D.Dallas, Texas

Learning Objectives: After studying this article, the participant should be able to: 1. Understand the speech, hearing, andgrowth implications of cleft palate repairs. 2. Understand the benefits and risks of early versus late palatal closure. 3.Formulate a plan for the timing of palatal closure. 4. Describe the long-term side effects associated with the timing ofcleft palate closure.

Treatment objectives for the cleft palate patient—nor-mal speech, normal maxillofacial growth, and normalhearing—are closely related. Controversy about the tim-ing of cleft palate surgery is directed at the need for earlypalatoplasty for improved speech and hearing versus de-layed hard palate repair for undisturbed facial growth.This controversy as to the value of early versus delayedclosure continues into the present. The authors presentan updated argument regarding this controversy alongwith a comphensive literature review. They also present alogical algorithm based on the literature and their per-sonal experience. (Plast. Reconstr. Surg. 106: 413, 2000.)

The functional goals of cleft palate surgeryare normal speech, hearing, and maxillofacialgrowth.1,2 It is generally thought that speechand hearing are improved by early cleft palaterepair (before 24 months of age)3 and thatdelayed closure (after 4 years) is associatedwith less retardation of midfacial growth.4,5 Theprimary goal in the timing of cleft palate sur-gery, therefore, is to provide adequate palatalfunction for the development of normalspeech without interfering significantly withmaxillofacial growth. This article reviews theliterature in the controversial area of cleft careand proposes one logical algorithm for treat-ing such patients.

SPEECH

Early cleft palate repair increases the likeli-hood of normal speech development.3,6 De-layed treatment may interfere less with midfa-cial growth, but speech development tends tobe poor.7 If closure of the palate is delayed past2 years and the mechanisms for speech have

already developed, the chances for normalspeech are significantly diminished.8 Oropha-ryngeal movements preliminary to speech ap-parently begin in the intrauterine period. Asreported by Oiler et al.,9 the babbling andcooing of infants may be an important preludeto normal speech development.

Because most physiologic functions are opti-mally learned at an early age, it is logical thatspeech is also best learned early.10 It is thoughtthat this occurs before 2 years. For this reason,speech pathologists recommend early palatalclosure to restore the normal velopharyngealmechanism and to enhance the chances fornormal speech.3,11–13

Kaplan suggests that the ideal age for palatalrepair is 3 to 6 months.14 This recommenda-tion is based on the theory that the palate mustbe functional when palate-related sounds arefirst learned to avoid poor speech developmentand integration. Because the repaired palatehas limited mobility for an additional 3 to 6months because of postoperative edema,Kaplan advocates palatal repair at 3 to 6months of age so that the palate can be func-tioning normally at 9 to 12 months. This wasnoted clinically by Wardill as early as 1937.15

Wardill believed that the ideal time to repairthe palate was at younger than 1 year of age.However, because of the limitations of pediat-ric anesthesia at that time, he was unable topractice this himself.

In a study by Dorf and Curtin,3 12 months ofage was used as an arbitrary dividing pointbetween early and late palatal closure. They

From the Department of Plastic Surgery, University of Texas Southwestern Medical Center. Received for publication September 1, 1999; revisedJanuary 22, 2000.

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found a 10 percent incidence of pharyngealand glottal articulation abnormalities (com-mon compensatory components in cleft palatespeech) in those children who had repairs be-fore 1 year and an 86 percent incidence ofarticulation abnormalities in those who hadrepairs after 1 year. This difference was statis-tically significant. Henningsson and Isberg16

made similar observations. The articulation er-rors were more prone to develop with latepalatal repair because the pharyngeal and glot-tal abnormalities occurred as a compensatorymechanism.17

In 1944, Schweckendiek18 advocated a two-stage repair with early closure of the soft pal-ate. The hard palate was left open with therationale that this would allow normal develop-ment of the maxilla. The oronasal fistula wasoccluded by a prosthesis until the hard palatefistula was closed at 15 years of age. Schroder,19

in the first description of the speech resultsfrom this protocol in 1966, was critical ofSchweckendiek’s procedure. Schroder statedthat most of the patients needed a pharyngo-plasty and that the delayed hard palate closuredid not prevent growth disturbances of themaxilla.

In 1979, Perko20 compared a group of pa-tients who underwent one-stage palatal repairwith a group who had undergone delayed hardpalate closure and stated simply that “the tem-porarily remaining cleft in the hard palate doesnot disturb speech development to a relevantdegree.” No speech data were provided onthese patients, however.

In 1984 in a long-term follow-up study,Rohrich et al.2 reported on the incidence ofspeech deficiencies in 38 patients treated withdelayed versus early closure of the hard palate.The overall speech intelligibility, articulation,and nasal escape were significantly reduced inthe delayed closure group. This study showedconclusively that, in the long-term evaluationof cleft palate patients, delayed closure of thehard palate significantly decreased the pa-tient’s chance for normal speech development.

In the same year, Henningsson et al.21 de-scribed speech intelligibility, hypernasality, na-sal air emission, and articulation in a similargroup of patients. The early closure group hadsignificantly better intelligibility and fewer ar-ticulation errors than the delayed closuregroup. The articulation problems of the de-layed closure group paralleled those found by

our group2 and included frequent glottal stops,pharyngeal fricatives, and velar substitutions.

During this same period, Witzel et al.22 re-viewed the rationale for delayed palatal closureand its effect on speech. They found that thedata for a beneficial maxillofacial growth re-sponse with delayed repair were lacking andnoted severe speech problems with delayedpalate closure methods. They also pointed outthe significance of oronasal fistulas in the de-velopment and persistence of articulation de-fects. Bzoch23 found that speech developmentwas hampered by the use of an obturator(which was advocated by Gillies and Fry4), pri-marily because of an inadequate seal. Noord-hoff et al.24 reconfirmed this observation in anindependent study.

In an attempt to link the type of operativeprocedure with its effect on speech, Trier andDreyer8 compared the results of patients un-dergoing von Langenbeck’s palatoplasty with-out reconstruction of the levator veli palatinimuscle with those of patients undergoing thesame procedure but with intravelar veloplasty.They examined a total of 43 patients, who weredivided equally between the two study groupsand who had an average follow-up of 4 yearsand 7 months. All the patients underwent thepalatoplasty at 14 to 16 months. The authorsreported better speech and superior velopha-ryngeal function after intravelar veloplasty.They recommended careful reconstruction ofthe levator sling at the time of the palate re-pair.25–27

In contrast, Holtmann and associates28 ana-lyzed the early speech results obtained fromV-Y pushback, the von Langenbeck technique,or the von Langenbeck technique with pharyn-geal flaps in 62 patients. They found no differ-ences among the treatment groups in terms oflate complications, velopharyngeal insuffi-ciency, or need for speech therapy. However,patients with the V-Y pushback required moreblood transfusions, and those who had the vonLangenbeck procedure with pharyngeal flapshad more airway obstruction. It seemed thatthe pharyngeal flap with a primary palatorrha-phy was unnecessary in 75 percent of the pa-tients. These authors recommended only thevon Langenbeck palatoplasty for primary cleftrepair. Their speech results were early, with thelatest assessment performed at 8 years.

In 1989, in a speech analysis study by Hard-ing and Campbell,29 48 patients treated withearly versus delayed hard palate surgery were

414 PLASTIC AND RECONSTRUCTIVE SURGERY, August 2000

compared. In general, delaying hard palateclosure caused more persistent, noticeable,and abnormal speech patterns until after hardpalate repair. However, both groups hadtongue displacement and airstream problems.These findings reflect those of Dorf and Cur-tin3 and Cosman and Falk.7

Speech Data Summary

The earlier the repair to the palate, thesooner the soft palate can begin to functionnormally and the sooner speech can begin in-tegrating and developing without abnormalpatterns.30 Furthermore, normal levator func-tion and concomitant optimal speech resultscan be achieved by the release and reposition-ing of the levator muscle, without resorting toa mucoperiosteal pushback.14,31,32 In 1996, along-term, multidisciplinary study33,34 de-scribed 44 patients who were similarly matchedexcept for the timing and technique of hardpalate repair. The study revealed significantlygreater speech deficiencies with delayed hardpalate closure, specifically in articulation, nasalresonance, nasal emission, and overall intelli-gibility assessment. The study is unique for itslong-term follow-up. The average age at fol-low-up in the early closure group was 17.0 yearsversus 18.2 years in the late closure group. Wenoted a persistent palatal fistula rate in the lateclosure group of 35 percent in comparisonwith 5 percent for the early closure group.Therefore, the recent data are quite conclusivethat speech integration and normal speech pat-tern development are superior with early pala-tal repair.

MAXILLOFACIAL GROWTH

The timing of palatal surgery and its effecton maxillary growth are likewise controver-sial.22,35 There is no doubt that the timing ofpalatal surgery affects maxillary growth.36 How-ever, two other major factors must be consid-ered. First, operative procedures to repair theprimary palate (lip and alveolus) may be asharmful to maxillary growth as the palatal re-pair itself, causing alveolar collapse and subse-quent growth impairment.37 Second, in cleftcases, there are varying degrees of inherentmaxillary deficiency, because no one cleft issimilar to another.38,39 It is obvious that theseinherent growth deficiencies vary with the in-dividual cleft types.40,41

Several studies have suggested that severefacial growth disturbances are associated with

combined cleft lip and palate repair and notwith an isolated cleft palate closure.42,43 Thishelps to differentiate between growth impair-ment in patients with combined cleft lip andpalate and those with a cleft of the palate only.

There are three general types of maxillofa-cial growth: anteroposterior, vertical, andtransverse (alveolar arch). It is important todifferentiate these because the transverse (al-veolar arch) growth problems can usually becorrected orthodontically44 and they do notalter facial aesthetics as significantly as antero-posterior and vertical growth deficiencies,which usually must be corrected by orthog-nathic surgical techniques.

Patients with an isolated cleft palate mayhave midfacial hypoplasia, which is related tothe inherent growth limitation of the congen-ital anomaly.45 Retrusion after repair may beminimal, and it is not greater than that inpatients with unrepaired clefts of the second-ary palate or submucous clefts. The isolatedcleft palate must be considered separate fromthe cleft palate associated with the cleft lipbecause of the difference in the maxillarygrowth potential of each.9,46 Thus, facial retru-sion in an isolated secondary cleft palate, asopposed to a cleft lip and palate, is relatedprimarily to its inherent maxillofacial congen-ital deficiency and secondarily to growth im-pairment induced by the operative closure ofthe cleft palate.38

In 1921, Gillies and Fry4,47 observed narrow-ing and posterior displacement of the maxil-lary arch in patients who had surgical repair ofthe hard palate. They proposed closing onlythe soft palate and obturating the hard palatewith a prosthesis. In an interesting follow-up ofa select group of 10 patients who had repairsthat followed these recommendations, Walterand Hale48 reported that the comparison ofcephalometric findings with accepted normsand an examination of study casts showed en-couraging results for facial and occlusal devel-opment. According to the authors, the dentalarch width harmony was quite good in thissmall, select group of patients who had noorthodontic care. These findings concur with astudy by Poupard et al.,49 which reported im-proved palatal occlusion using the Gillies-Fryprotocol.

In 1925, Rayner50 concluded that, in his ex-perience with 125 cleft palate cases, the hardpalate repair in the first 2 years of life causedgreater dental arch collapse than repair at 3 or

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4 years. Hagemann,51 in 1941, on the basis ofthese studies, proposed delaying surgery untilafter the eruption of secondary dentition tominimize the degree of transverse alveolar col-lapse.

In 1944, Schweckendiek18 began early clo-sure of the soft palate and delayed closure ofthe hard palate (until 12 to 15 years) to allownormal maxillary development. He postulatedthat this method would allow for normalspeech and normal growth of the maxilla.When analyzing Schweckendiek’s results, Bar-dach et al.52 found excellent facial growth andocclusion, but 81 percent of these patients hada degree of velopharyngeal insufficiency and86 percent had glottal and pharyngeal articu-lation problems.

Jolleys,53 in 1954, found no difference inmaxillary growth in children who were oper-ated on at 2 years and those operated on be-tween the ages of 3 to 5 years. In 1974, Robert-son and Jolleys54 compared actual occlusionand facial profile in cases of early hard palateclosure at 12 to 15 months of age with thosewho had palatal closure at 5 years. They foundno differences between the two groups by 4years.

In 1983, Robertson and Jolleys55 abandonedthe delayed closure of the hard palate in favorof early closure, having demonstrated no sig-nificant differences in facial growth. This cor-related with the results of the Oxford CleftPalate Study,33,34,56 which showed no statisticaldifference between dental arch width and fa-cial growth when comparing early closure at 10months versus late closure at 48 months. Fur-thermore, a statistically increased incidence ofpersistent palatal fistula occurred in patientswith delayed palatal closure (35 percent) com-pared with those with early palatal closure (5percent).

In a large series of 2000 patients, Koberg andKoblin57 noted no statistical difference in theseverity of growth retardation after surgery upto 8 years. Early palatal surgery before 1 year ofage did not cause greater maxillary growth in-hibition than surgery at any other age. Inter-estingly, most midfacial retrusion occurredfrom palatal surgery during the second phaseof maxillary growth at 8 to 15 years. The au-thors concluded that, for hard palate surgerynot to affect maxillary growth, the operationshould be delayed until after age 15.

Koberg and Koblin57 further compared max-illofacial growth relationships in 1033 patients.

They noted the greatest growth disturbancescame from the Veau pushback method, fol-lowed by the von Langenbeck relaxing inci-sions method. The least amount of facial retru-sion was noted in the two-stage operation ofsoft palate repair at 1 to 2 years and hard palaterepair after age 12. Studies by Jolleys53 andPalmer et al.58 confirmed the deleterious ef-fects of the pushback technique; however,Aduss59 and Bishara et al.38,60 found no differ-ence in facial growth when the V-Y pushbackwas used.

The proposed advantage of V-Y pushback isto lengthen the palate and to achieve betterspeech; this supposed advantage has not beensubstantiated.60–62 This technique cannot bejustified routinely because of the higher risk ofmidfacial retrusion, arch collapse, and palatalfistula. More importantly, there seems to be nospeech benefit. The benefit of the pushbackmethod is derived more from the release of theabnormal attachments of the levator and pala-topharyngeal muscles and the reconstitution ofthe levator sling than from an increase in ac-tual length.61,63,64 Braithwaite and Maurice63

first suggested this repair of the levator velipalatini as an adjunct to palatal repair. Softpalate muscle release, retropositioning, and re-construction of the muscle sling without a hardpalate pushback obtain this functional length-ening. This results in good velar function andbetter speech development, without thegrowth inhibition caused by the anterior scarof the pushback.

It does not seem that the timing of the cleftpalate repair is the major deterrent to facialgrowth interference; instead, the surgery itselfmay cause the deformity. The most severe de-formities are seen in children who had theirpalates repaired between the ages of 8 to 12years, which is the most rapid phase of maxil-lary growth.57

HEARING

Conductive hearing loss in patients with cleftpalate has been known to occur for more thana century; eustachian tube dysfunction is theprimary cause of middle-ear disease.65–67 In1978, Bluestone68 reported an incidence ofhearing loss in the cleft palate population rang-ing from 0 to 90 percent; the average was 50percent. In addition, Paradise69 noted that oti-tis media in the cleft palate patient is almostuniversal. The incidence of hearing loss is re-duced if the palate is closed early.70–72


Hearing has long been neglected in the con-troversy surrounding the timing of palatal clo-sure. Yet a child’s ability to learn a languageand to articulate intelligently depends primar-ily on his or her hearing capacity.73,74 A signif-icant hearing loss, even one that is short-lived,during the active period of child developmentmay have permanent and irreversible effects atthe level of the brain stem.10

According to Chaudhuri and Bowen-Jones,70

children who had palatal repair before 1 yearhad a 10 percent incidence of hearing loss,compared with 60 percent for those who hadsurgery at an older age. Although it is acceptedthat these children have middle-ear effusion, itis not known at what stage middle-ear malfunc-tion occurs. The child with a cleft palate mayhave a malfunction at birth.

Yules75 concluded that approximately 50 per-cent of the cleft palate population sufferedsome hearing loss and that 94 percent have eardiseases arising from early serous otitis media.Middle-ear disease remains a problem well intolater life.

Too-Chung71 conducted an interesting studyusing tympanometry in infants to assess mid-dle-ear function. He found that all cleft palatechildren had normal aeration of the middleear at birth and that this remained normaluntil 17 weeks of age. Closure of the cleft pal-ate at or before 4 months of age decreasedmiddle-ear complications.

In 1986, Watson et al.72 found that, in thelong-term follow-up of patients with early ver-sus late closure of the hard palate, those withlate closure had a significantly higher inci-dence of otitis media or of the number ofventilation tubes inserted. They concluded thatthe late closure of the hard palate had anadverse long-term effect on hearing and sug-gested frequent follow-up of these patientsthroughout adolescence and adulthood to as-sess their otologic status. This is in agreementwith an earlier study by Bennett76 on hearingloss in the older cleft palate patient.

After early repair of the palatal defect, eusta-chian function may still be abnormal, andhearing impairment may result.77 Subtelny12,78

found that, anatomically, cleft palate patientshave a wider intertuberous distance and corre-sponding decrease in the height of the naso-pharynx, which affects the angle of inclinationto the eustachian tube and the action of thetensor tympani dilator muscle. This was recon-firmed by Maue-Dickson et al.79

The cartilaginous portion of the eustachiantube may also be poorly developed, as shown byRood and Stool.80 The pressure differential be-tween the nasopharynx and the tympanic cavitymay reduce ventilation and drainage of themiddle ear. This may initiate an inflammatoryresponse from the regurgitation of food thatsubsequently affects the ciliary activity of themucus-lined tube. The nasopharyngeal orificeis opened by the action of the tensor palatimuscle, and failure of this action leads to eu-stachian tube obstruction.

Bluestone81 has demonstrated that increasedmiddle-ear secretions occur if the viscosity ofthe secretions is high. Interruption of this cycleat an early age by the installation of a ventilat-ing grommet may alter this viscosity and breakthis vicious cycle concomitant with early palatalclosure. This can prevent recurring otitis me-dia, subsequent middle-ear infections, andlong-term hearing loss.82

The prophylactic insertion of ventilatinggrommets at the time of the closure of the cleftpalate not only saves the patient an anesthetic,but also significantly decreases the chances ofrecurrent middle-ear infection and subsequentlong-term hearing loss. This also allows for bet-ter speech and language development at thisearly, critical developmental age.

DISCUSSION

On the basis of our own long-term studies inthis area2,33,34,72 and a comprehensive review ofthe literature, we have created a goal-oriented,pragmatic approach for the management ofthe cleft palate patient that has evolved overthe past 15 years. The ultimate goals in eachcleft palate child are normal speech, maxillo-facial growth, and hearing.

An early, two-stage palate repair is advocatedin the management of patients with cleft lipand palate (Table I). The recommended se-quence involves closure of the soft palate at 3to 6 months of age, with secondary closure ofthe residual hard palate at 15 to 18 months ofage. This sequence takes advantage of the earlyphysiology and growth that occurs in the softpalate, which is vital in the development ofspeech. Furthermore, it avoids the potentialpitfalls of growth disturbance related to earlyperiosteal undermining of palatal and vomer-ine tissue. This repair sequence also providestotal palatal closure before connected speechevolves.83 If the soft palate is repaired at the


time of lip repair, an additional anesthetic isavoided.

The complete release of the levator mecha-nism from the palatal aponeurosis extendinglaterally beyond the insertion of the tensortympani tendon and the stripping away of alltethering muscle fibers from both the liningand the posterior margin of the bone are es-sential. This extensive release of the muscleallows retrodisplacement within a lining of oraland nasal mucosa. This sequence results in thedevelopment of normal speech in approxi-mately 75 percent of patients. Another 10 per-cent develop mobile but short palates, whereasthe remaining 15 percent have neurogenic pal-ates. Those children with mobile but short pal-ates are considered treatment failures; how-ever, neurogenic palates are thought to be aconsequence of the clefting rather than a fail-ure of technique. A similar subgroup of chil-dren with neurogenic palates has been identi-fied in a group of children requiringpharyngeal flaps after one-stage, pushback pal-atal repair. From these observations, we thinkthat a near-ideal palatal closure would result innormal speech in approximately 85 percent ofpatients.

In an effort to identify shortfalls of thisprocedure, children with short, mobile velawere identified, and their maxillary arch con-figurations were evaluated. In this study,there was a direct correlation between in-competent speech and the magnitude of thecleft.84 This correlation pertains to the mag-nitude of the clefting in the secondary palateand relates specifically to the occurrence ofbilaterality. A paucity of lining is thought torestrict the development of normal velarlength. From these observations, our treat-ment sequence has evolved. The cleft lip andthe soft palate are closed at 3 to 6 months ofage. We realize that the lip repair can causemaxillary retrusion; however, facial retrusionfrom lip surgery can occur, regardless of theage of the patient at surgery. With recon-

struction of the anterior palatal arch throughthe cleft lip repair and posterior maxillaryarches through the soft palate repair, there isa molding effect, with alveolar arch align-ment. We perform an intravelar veloplastywith release and retropositioning of the leva-tor veli palatini muscles. As previously de-scribed, all surfaces, including the nasal mu-cosa and mucoperiosteum, remain intact,and there are no raw surfaces. We avoid anymucoperiosteal undermining at this age.85

A major benefit of the simultaneous closureof the lip and soft palate at an early age is thatit narrows the hard palate gap so that lessextensive hard palate surgery is required lat-er.86 Dental casts are made at the time of therepair of the cleft lip and soft palate and againat the time of repair of the hard palate. Thepatient is monitored at 3-month intervals toassess the narrowing of the hard palate gap.

The hard palate is repaired at 15 to 18months of age. Because the width of the hardpalate cleft diminishes significantly, a muchless extensive procedure must be performed.In many cases, only paring of the medialpalatal edges with elevation of enough nasaland palatal mucosa to attain a tension-free,two-layer closure is done. Lateral or anteriorincisions or mucoperiosteal elevations areavoided if possible. If mucoperiosteal eleva-tion is needed, the von Langenbeck proce-dure is preferred over palatal pushback pro-cedures.31

It can be argued that a two-stage approach inthe isolated cleft palate necessitates a secondanesthetic that can be avoided with a one-stagerepair. To obtain comparable velar lengthen-ing, this repair would need to be done before 1year of age. Until growth has been docu-mented through the development of both theprimary and secondary dentition, with one-stage repairs before 1 year of age, it should beconsidered that these early, one-stage repairsplace the child at greater risk for the distur-

TABLE ITwo-Staged Early Cleft Palate Repair Sequence

Birth 3 to 6 Months 15 to 18 Months

Begin active orthopedic applianceapplication for maxillary alveolar archalignment

Repair of cleft lip and intravelar veloplasty(closure of anterior and posterior palatalarches)

Repair of residual hard palate cleft using lesssubperiosteal undermining

Continue possible appliance application*

* After the lip is closed, the active phase of treatment is complete, and a small obturator appliance is used to retain alignment and to provide a more normal tongueposition. Keeping the tongue out of the cleft may allow further closure of the residual cleft palate.


bance of both transverse and anteroposteriormaxillary arch development.

This approach is in concert with the primarygoals of normal speech, retaining normal max-illofacial growth, and decreasing the incidenceof otitis media and subsequent long-term hear-ing loss in these patients.

Rod J. Rohrich, M.D.Department of Plastic SurgeryUT Southwestern Medical Center5323 Harry Hines BoulevardDallas, Texas [email protected]

ACKNOWLEDGMENT

We very gratefully acknowledge the assistance and exper-tise of Cheryl K. Anderson, D.D.S., Dallas, Texas.

REFERENCES

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4. Gillies, H. D., and Fry, W. K. A new principle in thesurgical treatment of “congenital cleft palate” and itsmechanical counterpart. Br. Med. J. 1: 335, 1921.

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32. Keith, R. W. Middle ear function in neonates. Arch.Otolaryngol. 101: 376, 1975.

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Self-Assessment Examination follows onpage 422.


Self-Assessment Examination

Optimal Timing of Cleft Palate Closureby Rod J. Rohrich, M.D., Edward J. Love, M.D., H. Steve Byrd, M.D., and Donnell F. Johns, Ph.D.

1. THE ULTIMATE GOAL IN THE TIMING OF CLEFT PALATE SURGERY IS TO MAINTAIN SPEECH WITHOUTINTERFERING WITH MAXILLOFACIAL GROWTH.A) TrueB) False

2. THE ULTIMATE GOAL IN EACH CLEFT PALATE CHILD IS:A) Normal speechB) Maxillofacial growthC) HearingD) All of the above

3. RANDOMIZED CONTROLLED STUDIES HAVE SHOWN A GREATER RISK FOR POOR SPEECHDEVELOPMENT IF THE PALATE IS CLOSED AFTER 2 YEARS OF AGE.A) TrueB) False

4. CONDUCTIVE HEARING LOSS IN CLEFT PALATE PATIENTS IS DUE TO DYSFUNCTION OF:A) Tympanic membraneB) Levator palatiniC) Eustachian tube

5. LOSS OF HEARING FOR SHORT PERIODS OF TIME HAS NO EFFECT ON A CHILD’S ABILITY TO DEVELOPNORMAL SPEECH.A) TrueB) False

To complete the examination for CME credit, turn to page 528 for instructions and the response form.

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