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FIGURE 5-1 Classification of velopharyngeal inadequacies by
etiology. AOS, apraxia of speech (acquired); CAS, childhood
apraxia of speech; CVA, cerebrovascular accident; HPCs, high
pressure consonants; TBI, traumatic brain injury. (Modified from Trost-
Cardamone JE: Coming to terms with VPI: a response to Loney and Bloem. Cleft
Palate J 26:68-70, 1989; and Peterson-Falzone SJ, Trost-Cardamone JE, Karnell MP,
Hardin-Jones MA: The clinician's guide to treating cleft palate speech. St. Louis:
Mosby, 2006.)
The third category includes cases in which the speaker has in some
way mislearned the oral versus nasal airflow feature of speech
production, as in the paerns of phoneme-specific nasal emission
(PSNE) and nasal emission that persists postoperatively despite
adequate closure ability. In both instances, the speaker intentionally
directs airflow into and through the nasal cavity. This type of
velopharyngeal mislearning is seen both in speakers with clefts and speakers
with noncleft VPI. This category also includes speakers whose use of
compensatory articulations, especially gloal stops and pharyngeal
fricatives and stops, actually prevents or interferes with velopharyngeal
closure, as first documented in imaging studies by Henningsson and
Isberg (1986, 1991). Because these gloal and pharyngeal gestures are
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produced below the VP port, they effectively ignore or bypass the port
and cause it to remain open. The oral/nasal speech errors observed in
some deaf and hearing-impaired speakers that primarily alter resonance
also are subsumed under this category of mislearning (Coulton and
Crooker, 1968, Fletcher and Daly, 1976; Fletcher et al., 1999).
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Brief Review of Normal Velopharyngeal
Closure
The impact of a cleft palate or other causes of VPI on speech is best
understood against a backdrop of normal VP closure. Before we
consider how VPI negatively affects speech resonance and articulation,
we present this short review of normal VP closure.
Normal velopharyngeal closure involves movement of the soft palate,
pharyngeal walls, or both the soft palate and pharyngeal walls
simultaneously, to seal off or separate the nasal cavity from the oral
cavity. It is a predominantly sphincteric activity in which, for most
speakers, the soft palate/velum moves up and back and the lateral
pharyngeal walls move inward. Many years ago, Croft and colleagues
(1981) described four paerns of closure seen in normal speakers, based
on the relative movement contributions of (1) the velum moving up and
back, (2) the lateral pharyngeal walls (LPWs) moving inward, and (3)
the posterior pharyngeal wall (PPW) moving forward. Their findings
changed our conceptualization of VP closure from a “trap-door”
mechanism (velum to PPW or adenoid pad) to a “sphincteric” closure
activity. Sphincteric endoscopic views of the four paerns are
illustrated in Figure 5-2. They are as follows:
1. Coronal (in which the velum is the prime mover)
2. Sagial (in which the LPWs are the prime movers)
3. Circular (in which movement contribution from the velum and LPWs
is approximately equal)
4. Circular with Passavant's ridge (in which the velum, LPWs and PPW all
make about equal contributions to closure)
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FIGURE 5-2 Velopharyngeal valving patterns. (From Croft CB,
Shprintzen RJ, Rakoff SJ: Patterns of velopharyngeal valving in normal and cleft palate
subjects: a multiview video-fluoroscopic and endoscopic study. Laryngoscope 91:265-
271, 1981.)
These paerns also have been identified in speakers with repaired
cleft palates, with coronal the most common across both groups.
Videonasendoscopy studies are done with the physician or clinician
facing the patient. However, the view in this illustration is “in reverse.”
It is as if you were standing behind the individual and looking directly
down on the velopharyngeal port, so anterior is toward the top of the
illustration, and posterior is toward the boom. The curve in the top of
each figure in the left column represents the tip of the velum; the
boom of each figure is the posterior pharyngeal wall, with the lateral
pharyngeal walls to either side. The arrows indicate relative
participation in closure; the larger the arrow, the greater the
contribution. Coronal and sagial paerns are so named because the
closure configuration follows the coronal or sagial plane of the body,
respectively.
The main muscles responsible for VP closure are the levator veli
palatini (elevates and retracts the velum), superior pharyngeal
constrictor (moves the LPWs inward or medially and the PPW forward),
uvulus or musculus uvulae (adds bulk or thickness to the dorsal surface
of the velum facilitating firm closure), and palatopharyngeus (may
narrow or constrict the VP port; has a less significant role in closure).
This is admiedly a simplistic description of the muscular intricacies of
velopharyngeal closure. Researchers have provided various forms of
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data on the role that each of these paired sets of muscles plays in the
closing and opening of the VP port. However, the levator veli palatini is
without question the prime mover in velopharyngeal closure. Figure 5-3
shows the muscles that contribute to sphincteric closure.
FIGURE 5-3 Muscles of velopharyngeal closure. (Modified from
Kummer AW: Cleft palate and craniofacial anomalies: effects on speech and
resonance, ed 2, Clifton Park, NJ, 2008, Thomson Delmar Learning, p. 14.)
In young children, “velopharyngeal” closure is often “veloadenoidal”
closure. The adenoid pad typically reaches its maximum size sometime
between 7 and 10 years of age and then begins to involute (gradually
disappear). In youngsters with normal velar length and mobility, the
disappearance of the pad is of no consequence. However, the loss of the
adenoid pad may uncover a previously undetected physical problem
such as a short or hypotonic velum. Similarly, youngsters with
submucous cleft palates and no visible intraoral signs may be
asymptomatic until their adenoid pad disappears and their speech
reveals the problem. Of course, adenoid tissue can also cause a problem
if it is large enough (in any child) to obstruct the airway.
Although forward movement of the PPW in speech is often found in
normal speakers, it is worth noting that a shelflike projection of the
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PPW toward the velum often is seen in speakers with repaired palates
or congenitally short palates during aempted VP closure. This is
termed “Passavant's ridge” or “Passavant's pad” (Fig. 5-4). Historically,
researchers in the 1970s argued about whether this was the action of the
superior pharyngeal constrictor or the result of a pulling action
performed by the levator that creates this shelf. For many decades
Passavant's ridge was considered to be a compensatory action
employed by speakers with clefts, but the truth is that we do not know
how often it may occur in speakers with normal velopharyngeal
anatomy.
FIGURE 5-4 Passavant's ridge (PR) as a primary source of
velopharyngeal narrowing or closure. A, Velar eminence to
Passavant' s ridge. B, Vertical portion of velum to Passavant' s
ridge. C, Uvula to Passavant' s ridge. (From Glaser ER, Skolnick ML,
McWilliams BJ, Shprintzen RJ: The dynamics of Passavant' s ridge in subjects with
and without velopharyngeal insufficiency: a multiview video fluoroscopic study. Cleft
Palate J 16:24, 1979.)
No inferences about VP function during speech can be made from VP
function in swallowing. Uninformed clinicians (and radiologists) should
not be misled if dynamic imaging studies of swallow show VP closure
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y g g
during this vegetative, nonspeech activity. Swallowing and speech are
programmed differently in human neuromotor function. See Chapter 9
on instrumental assessment of VP function.
See the Evolve site for a brief PowerPoint presentation on normal VP
closure.
For those readers who may need to refresh the details of speech
anatomy and physiology, you may also want to revisit more detailed
material on velopharyngeal closure for speech. You may also find these
resources, listed in the References to this chapter, helpful: Jones (2012);
Zemlin (1998).
Impact of VPI on Speech Resonance
By definition, VPI/VPD causes abnormal coupling of oral and nasal
cavities, and this results in excessive nasal resonance, or hypernasality,
on vowels and vocalic consonants, the oral sonorants.
Definition of Resonance
In this discussion, resonance is used to describe both the perceptual and
physical aributes of speech, although the reader should understand
that resonance actually reflects a physical phenomenon (Peterson-
Falzone, et al., 2010, p. 221). Physically, speech resonance is the result of
the vocal tract's transfer function of the tone produced at the larynx.
The vocal tract functions as a selective filter for the complex tone
generated by the vocal folds, thus enhancing some harmonics in this
tone, ignoring others, and actively suppressing others. The acceptable
product is one that is perceived to have an adequate balance of oral and
nasal resonance. Although this adequate balance varies across
languages, most speech resonance for English vowels and vocalic
consonants is predominantly oral (produced with oral cavity energy
enhancement) with some contribution of nasal resonance. Resonance is
a speech parameter that has a range of acceptability and is perceived
along a continuum. It therefore eludes a singular reference point that
can be designated as “normal.” On the other hand, as you well know,
our ears do alert us to resonance deviations or abnormalities along this
continuum.
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Hypernasality
Too much nasal resonance results in hypernasal speech. There is
excessive nasal energy enhancement of vowels, the glides /w, j/ and the
liquids /l, r/. Collectively, glides and liquids comprise the low-oralpressure consonants of English and also are referred to as oral
sonorants or approximants. The high long vowels /u/ and /i/ are
especially vulnerable to becoming hypernasalized when there is VPI.
Hypernasality is transcribed with the diacritic /~/ placed above the
affected target, as in /
/ or /ũ/. As severity of hypernasality increases,
we may hear nasalized voiced consonants, and in its more severe form,
the distinctiveness between oral pressure consonants (especially the
voiced oral stops, /b, d, g/) and their nasal counterparts is lost (e.g., b
sounds like m, d sounds like n). Most hypernasality in speakers with
repaired clefts is obligatory; it has a physical, as opposed to a learned,
basis.
Obligatory speech errors must be distinguished from those that are
more optional and learned (Golding-Kushner, 2001; Trost-Cardamone,
1990). Cleft palate speech includes both obligatory errors and
optional/learned errors. Obligatory errors are physically based; they result
from structural problems such as VP insufficiency and fistulas or they
may be neurogenic, and both etiologies require physical management.
Optional/learned errors are habituated errors that are the result of early
speech mislearning and persist in the context of adequate
velopharyngeal closure, and they require speech remediation.
Obligatory errors are also characterized as passive errors because they
are the unavoidable result or natural consequence of velopharyngeal
inadequacy. By contrast, learned errors are characterized as active errors
because they are understood to be strategies developed to overcome
the impact of velopharyngeal inadequacy on speech sound production
(Huers and Bronsted, 1987; Harding and Grunwell, 1998; Sell et al.,
1994, 1999; among others).
Although most hypernasality is caused by (persisting) VPI, a
sufficiently large fistula can also be the source (Henningsson and Isberg,
1987; Shelton and Blank, 1984). Fistulas also can contribute to
velopharyngeal dysfunction or can increase existing VPI and therefore
aggravate the hypernasality (Henningsson and Isberg, 1987; Isberg and
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Henningsson, 1987; Karling et al., 1993). In addition, mouth opening,
tongue height and front-to-back position tend to influence perceived
hypernasality (Cullinan and Counihan, 1971; Falk and Kopp, 1968;
McDonald and Baker, 1951). A more closed mouth and a higher more
backed tongue posture all tend to aggravate hypernasality.
Audio examples of hypernasal speakers are provided in Audio 5-1,
Audio 5-2, and Audio 5-3. Video 5-1
shows a school-age child with a
repaired cleft and pervasive hypernasality, passive nasal fricatives, and
consistent nasal grimacing. Nevertheless, except for the nasal fricatives,
he exhibits good articulation skills.
Other Resonance Deviations
Individuals with repaired cleft palate may present with resonance
deviations other than hypernasality. These include hyponasality, mixed
nasality, and cul-de-sac resonance.
Hyponasality
Too lile nasal resonance results in hyponasal speech affecting vowels,
sonorants/liquids and glides and also in denasalized nasal consonants,
making them perceptually similar to their oral stop counterparts /b, d,
g/. Hyponasality results when the nasal airway itself is partially
blocked, as with a deviated septum, or when the posterior entrance to
the airway is partially blocked, as with a large adenoid. Hyponasality is
indicated by the diacritic /
/ placed above the affected target; for
example, /
/ or / /. In clinical practice, the terms hyponasality and
denasality are used interchangeably. Technically speaking, however, if
blockage is complete, denasality results, with similar but more severe
impact on speech resonance. For example, the nasal consonant targets
become indistinguishable from their homorganic oral stops.
The important clinical issue here is that hyponasal or denasal
resonance can perceptually mask any underlying VPI. Once the
causative condition (e.g., head cold, allergy, hypertrophied adenoid)
clears, the VPI may be revealed. As the clinician treating the child, you
do not want to make an incorrect judgment regarding velopharyngeal
status. This is why it may not be possible to make a reliable perceptual
judgment on resonance if the child has a cold or allergy, and so forth, at
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the time of a visit. It also why it is helpful to obtain various types of
instrumental assessments: radiographic films, imaging studies (e.g.,
nasopharyngoscopy, videofluoroscopy), and more objective
aerodynamic and acoustic data and why it is so important that children
with cleft palate are followed regularly by a team of specialists so that
both change and stability can be documented and treatment planned
accordingly.
Video 5-2
shows a child with a repaired cleft lip and palate who has
hyponasality caused by adenoid hypertrophy. As you will hear, he also
uses gloal stops.
Mixed Nasality
Mixed nasality in speech is “… resonance characterized by elements of
both hypernasality and hyponasality” (Peterson-Falzone, et al., 2010, p.
222). In individuals with cleft palate, mixed nasality is often heard in
speakers with pharyngeal flaps or in those who wear a speech appliance
(a rare occurrence at this time). In most instances, mixed nasality results
when increased nasal resistance affects, but does not eliminate, nasal
resonance on vowels or nasal consonants.
Cul-de-Sac Resonance
This variation of hyponasality differs in place of obstruction and impact
on speech. The term “cul-de-sac” comes from the French, meaning
“blind pouch.” Speech sounds muffled. You can simulate this by
repeating “mi mi mi mi” or “nu nu nu nu” first with nostrils open and
then with nostrils pinched closed. The sound is trapped by the anterior
nasal cavity constriction. A common cause of cul-de-sac resonance is a
markedly deviated septum.
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