Between the 6th and 12th weeks of fetal gestation,the left
and right sides of the face and facial skeleton fuse in the
midddle. When they do fail to do so, the result is a
craniofacial cleft. Various types of clefts may occur as
isolated condition or as part of a syndrome. Since clefts
involve the anatomy of the vocal tract, varying effects on
speech are common.
Craniofacial Abnormalities are structural defects of the
head and face. These defects may be part of a syndrome that
includes other anomalies. Consequences include structuaal and
developmentalanomalies.
Craniofacial - pertains to or involving bothe cranium
(skull) and the face.
Craniofacial Anomalies - Malformations of the cranium
and/or face
INCIDENCE OF CLEFTS
Accepted estimate of incidence of vert cleft palate not
associated with other malformations is 1 in 750 live
births.
Cleft palate without cleft lip occurs more in females (57%)
than males (43%), no significant racial differences
Cleft lip with or without cleft palate occurs twice as many
males than females.
Gender differences may be related to slight differences in
timing of embryological development.
SPEECH PRODUCTION
7 Point Man
Respiratory and laryngeal activities produce voice.
The vocal signal rises through pharynx or vocal
tract.
The process by which the nasal branch is separated from
or coupled with the rest of the vocal tract is referred as
velopharyngeal closure.
Physical characteristics and activity of velopharyngeal
region imposes feature of resonance.
Speech signal with characteristics of phonation and
resonance modified by activity of tongue and lips imposes
features of place and manner of articulation.
Neural crest theory of development holds that neural crest
cells, one type of specialized embryonic cells, give rise to
various connective and neural tissues of the skull and
face
The cells migrate at different rates to destined
locations
If the migration fails to occurs, or if there is an absence
or inadequacy of related cells, clefts and other facial
abnormalities may results.
The upper lip and premaxilla are formed by merging 3
structures:
frontonasal process
right and left nasomedial processes of the maxilla
Lip closure occurs during 5 or 6th week of embryonic
development.
Palate is formed by union of palatal shelves that develop
from the maxillary processes and close during 8th or 9th week
of gestation
Embryonic tongue sits above the mandible between 2 sides of
the palate and fusion of the 2 sections of the palate can occur
after the mandible and tongue lower of the way. When this
sequence of events is interrupted, it results in a condition
called Robin sequence.
Two mandibular
processes result in the lower jaw (mandible), lower lip,
and chin. By the end of the 4th
or 5th week, these structures are formed and fused.
At 5 weeks, maxillary
processes appear on the anterior edge of the mandibular
arches. FIG 7-2 (Smith, 1983).
Two maxillary processes form most of the face, mouth,
cheeks, and sides of the upper lip. These processes form
most of the face, mouth, cheeks, and sides of the upper
lip.
These processes evolve into most of the hard palate,
alveolar ridge, soft palate.
Nasal
Processes (lateral and medial) are prominent at 6 weeks.
FIG 7-3 (Smith, 1983).
Frontonasal
Process - develops into the nose, central part of upper
face and primary palate.
Nasolateral Process will form the alae (lateral wings of
the nostrils).
Nasomedial Process will contribute to the formation of
several structures: midportion of the nose, upper
lip, maxilla, primary palate (entire frontmost portion of
the hard palate).
The nasomedial processes (medial
nasal processes) fuses with maxillary processes by week
7.
By the end of the 7
week, the upper lip and primary palate are formed.
Development of the Internal Face
Primary Palate
Prior to 6th week of development, the primary palate
includes that portion of the upper airway that will develop
into the lip, alveolar ridge, and the hard palate segment
extending back to the incisive foramen ( a hole behind the
alveolar ridge through which passes nerve and blood supply
to the palate). During 6th week, the separation between
nasal and oral cavities occur. This early structure contains
prolabium, premaxilla and four maxillary incisor teeth.
During the sixth
to 10th
week of embryological development, the foundation for
the hard palate and the floor of the nasal cavities, the
palatine shelves, begins their migration toward the midline
of the internal face. This movement toward midline coincides
with the lowering of the tongue mass which had previously
rested within the developing nasal chambers.
Between 5.5 - 8 weeks, the primary palate and the
secondary palate (that portion formed by the joining of the
palatine shelves behind the incisive foramen) coordinate
their growth to form a single structure: the hard palate.
Failure of the shelves to unite with the primary palate or
with each other will result in a cleft of the hard palate.
Soft Palate
During the 10th
to 12th week of orofacial development, the soft palate
tissue fuses. Tissue that will form the soft palate's
muscles begins to migrate toward the midline from both sides
of the back of the mouth during the 5th to 6th week. By the
10 week this tissue has grown and moved into a horizontal
orientation along with the palatine shelves.
Cleft
is a separation
or space between parts that are normally joined, thus
interrupting the continuity of the structure. Although
orofacial clefts can be acquired through various traumas, the
vast majority of those of the lip and/or hard and soft palates
are due to congenital failures of the structures to join. Of
the many ways to classify types of congenital cleft (Berlin,
1971), a division into general types is convenient:
clefts of the lip
and/or alveolar process (gum ridge), the embryological
primary palate (Figures 9-4, 9-5, Hixon text), and
clefts of the hard
and/or soft palates, the embryological secondary palate
(Figure 9-6, Hixon text).
Cleft
Lip - A cleft
of the lip involves only soft tissue and extend through the
red part of the lip or vermillion border, into the upper
portion of the upper lip toward the nostril. If the cleft is
unilateral, it commonly occurs on the left side. Patient may
have a short columella, which is the strip of tissue between
the base and the tip of the nose.
Cleft
Palate - The palate
serves as the partition between the nasal and oral cavities.
The anterior two-third of the palate make up the hard palate,
commonly referred to as the roof of the mouth. The soft palate
or velum consists of the posterior one-third of the palate.
Isolated cleft palate, without cleft lip, may include all of
the hard palate posterior to the incisive foramen and the soft
palate; it may involve only a small portion of the posterior
part of the soft palate; or it may between these two extremes.
Alveolar
Ridge - A part of the prepalate, partially encircles the
hard palate and consists primarily of supporting structures for
the teeth.
Cleft of Prepalate - Median Cleft - clefts of the upper lip
is median defect extends to the nose. The missing tissue is the
problabium.
Bilateral cleft lip with absence of the prolabium or complete
median cleft lip.
Premaxilla Protrusion & Detachment
Premaxilla - intermaxillary bone
Prolabium - central prominence of lip
Submucous Cleft Palates - The palate appears to be
structurally intact, but there are both muscular and bony
deficits. The defect include a bony notch in the hard palate, a
bluish line at the midline of the soft palate, and a bifid
uvula.
Hard Palate - The bony notch can be seen or felt where
normally the posterior nasal spine is found along the
posterior border of the hard palate. The submucous cleft of
the hard palate is not functionally significant.
Soft Palate - The muscular deficit found in the soft
palate often is functionally significant. This cleft is seen
as a bluish line through the length of the soft palate. The
levator muscles in these cases are often found to be
inserted into the hard palate instead of interdigitating
(interlock as or like fingers of both hands) to form the
normal levator sling. This condition foreshortens the
functional soft palate and creates a further complexity
which may contribute to velopharyngeal incompetence
requiring surgery. The levator muscle elevates the posterior
part of the soft palate, the velum, and pulls it slightly
backward which effectively closes the nasal from the oral
pharynx.
Good place of articulation and intelligible speech in
association with nasal emission and consonant weakness
resulting from lack of intraoral breath pressure.
Compensatory Learned Behaviors - Second pattern involved
only nasal escape, but also nasal snort, glottal stops,
pharyngeal fricatives, nasal grimace, and other articulatory
sibilants.
Some speakers with VPI seem to accept their loss of
intra-oral pressure and continue to articulate as
accurately as possible,. These speakers may have weak
consonants and audible escape, but placement is accurate.
Even intelligibility may be only slightly impaired.
Sounds Most Frequently Misarticulated
Most frequently in error with VPI: /s/. In short,
velopharyngeal competence is a requirement for adequate
consonant production. The first consonant to deteriorate
will be /s/. This is the phoneme most frequently in error
in individuals with VPI of a marginal or borderline
nature. As the incompetence increases, other sibilants
and fricatives (f,v,th,sh,z,s,zh) become involved. The
symptom is decreased intraoral pressure because of loss
of air at the velopharyngeal portal. Still greater
incompetence in this critical valve will lead to reduced
intra-oral pressure in association with plosives.
Sounds Most Frequently Misarticulated - McWilliams
(1953)
/s/ - 63%
/z/ (61%)
/d/ (48%)
/ch/ - (44%)
/p/ - (11%)
/b/ - (9%)
/s/ is th espeech sound most frequently and most
consistenly misarticulated by cleft palate
individuals.
Substitutions (McWilliams Audio 10)
Generally sound substitutions are seen in speech
problems that are characteristic of young children who
are still in the process of learning speech. Some
writers have referred to the fact that speakers with
cleft palate substitute a nasal consonant for a
consonant that requires intraoral pressure (for
example, substituting /m/ for /b/). In some instances,
this response is regarded as a nasally distorted /b/
rather than the substitution of /m/. Viewed in this
context, the speech sound error clearly points to
velopharyngeal incompetence rather inappropriate
learning.
Omissions (McWilliams Audio 11)
Could delete final consonants as a means of
avoiding nasal emission, because sounds lacking normal
oral air pressure could be interpreetedd as omissions
even though some energy marked the final
consonants.
Compensatory Strategies for VPI (McWilliams Audio 12,14)
Some speakers with VPI seem to accept their loss of
intra-oral pressure and continue to articulate as accurately
as possible,. These speakers may have weak consonants and
audible escape, but placement is accurate. Even
intelligibility may be only slightly impaired.
Others attempt to compensate for their valving deficits
by seeking new approaches to consonant articulation. These
individuals discover that it is easier to produce a
sibilant-like consonant lingua-palatal or pharyngeally than
it is to produce it in the front of the mouth and that
plosives created glottaly are unaffected by the defective
valve.They adopt gross articulation errors, which are
referred to as pharyngeal fricative and glottal stops. These
compensations are rarely accompanied by nasal escape because
that critical valve is bypassed.
Stop plosives, fricatives, affricates misarticulated cannot
manage airstream for development and maintenance of high oral
air pressure. Therefore, leading to deterioration of sound
(Hixon, 372).
Hypernasal resonance, nasal air emission, and weak
pressure consonants cause phonetic distortions, compensatory
gestures cause phonetic substitutions.
Individuals with clefts tend to substitute non English
sounds for English phonemes. Substitute glottal stop
(whispered cough) for stop-plosives (p, t, k, b, d, g).
Glottal stops are made by closing the glottis, building up
pressure within the trachea, and then suddenly reopening the
glottis to release a transient puff of air. Substitute
pharyngeal fricatives for fricative consonants. Pharyngeal
fricatives are produced by positioning the tongue close to
the back wall of the throat or by decreasing the side to
side diameter of the throat by moving the walls of the
pharynx inward. Air is then forced through the constricted
pharyngeal airway to produce a turbulent sound.
Substitution of Glottal Stops - GO BACK TO WITZEL VIDEO
Speakers with VPI problems demonstrate glottal
articulation for plosives, typically back plosives. The
interruption of the air stream at the level of the
glottis results in a cough-like speech sound that has
been labeled the glottal stop /?/.
Substitution of Pharyngeal Fricative - GO BACK TO
WITZEL VIDEO
Typically, fricatives and affricates are the result
of a constriction of the air stream in the anterior
portion of the oral cavity (lips, tongue, teeth).
Speakers with velopharyngeal incompetence are not
able to produce the friction noise because the air
pressure escapes from the oral cavity through the
velopharyngeal opening. Such speakers sometimes distort
fricatives and affricates in order to create the friction
noise by constriction between the tongue and pharyngeal
wall or perhaps by constriction of the pharyngeal
tube.
Distortion by Nasal Emission (McWilliams Audio 13,3,4)
Description -The type of error sometimes referred to as
the distortion-nasal is typical of what most listeners
regard as "cleft palate speech" and is demonstrated by many
cleft palate speakers. The air pressure is emitted through
the nostrils during the production of the pressure
consonants. If the escape is sufficient in quantity, the
nasal emission of air pressure is audible and distorts the
acoustic signal of the speech sound.
Nasal air escape associated with production of
consonants requiring high oral pressure. It occurs when air
is forced through an incompletely closed velopharyngeal
port. Nasal emission may be audible or not.
RESONANCE
Hypernasality
that occur supraglottally is referred to as "resonance
disorders."
Voice disorders refers to a problem that occurs at the
level of the larynx, a disorder of phonation.
Hypernasality is not a voice problem that implies
phonation.
Resonance is the vibratory response of a body or
air-filled cavity to a freqeuency imposed upon it. (Wood,
1971).
Individuals with velopharyngeal incompetence have
traditionally been described in the literature as having an
hypernasal voice quality. In actuality, hypernasality is
not a problem associated with phonation. It is the result
of alterations that occur when the oral and nasal cavities
are coupled when they should be separated by action of the
velopharyngeal mechanism.
Definition - The perception of excessive nasal resonance
during the production of vowels. This results from
inappropriate coupling of the oral and nasal caviities. Low
vowels and vowels in nasal consonant contexts are normally
somewhat nasalized.
Factors Responsible for Hypernasality
Results form inadequate closure of the VP valve
during speech, but it may caused by entrance of air into
nasal cavity through an open cleft palate or fistula in
hard or soft palate.
Oral Cavity constriction during speech may increase
hypernasal resonance by forcing more sound waves into the
nasal cavity. This constriction may be the result of :
restricting mouth opening during speech,
posterior or superior positioning of the dorsum
(upper surface) of the tongue during articulation of
some sounds,
or abnormal positioning or tension of the
pharynx.
Hyponasality is the speech characteristic associated with a
reduction in nasal resonance with /m,n,ng/ approaching but not
matching /b,d/g/.
a reduction in normal nasal resonance usually resulting
form blockage or partial blockage of the nasal airway by any
number of causess, including upper respiratory tract
infection and a wide obstructiing pharyngeal flap, and
moderately large adenoids were present.
If the nasal airways were completely occluded, speech
would be denasal, meaning that nasal air flow associated
with /m, n, ng/ would be eliminated and the sound wave
altered; the nasal consonants would approach but not match
/b, d, and g/.
VOICE DISORDERS
Hoarseness
Hamlet (1973) speculated that glottal tightness might
contribute to vocal abuse which would lead to hoarseness,
harshness, and vocal nodules secondary to hypernasality.
This conclusion appears reasonable in view of the clinical
evidence of patients who attempt to control hypernasality by
tightening both the respiratory muscles and laryngeal
muscles to control air flow before it reaches the crucial
velopharyngeal valve.
Soft Voice Syndrome
Because of loss of air through the velopharyngeal port,
some cleft patient shave difficulty creating a voice that is
of sufficient loudness to serve them well in communication
or they use reduced loudness as a compensatory strategy.
Patients who adopt this voice pattern may have little nasal
escape, although their velopharyngeal valving mechanisms are
usually deficient. In order to increase loudness, their
subglottic pressures must be higher than normal, and there
is air loss leading to an increase in nasal emission,
together with alterations in the perception of
hypernasality. This problem is identified on the basis of
clinical experience.
Reduced loudness
General characteristic of client with repaired cleft
palate is the reduced loudness. Aerodynamic and acoustical
factors contributes to the reduced loudness rather reduced
self confidence or self consciousness.
For vowels, diphthongs, and many voiced consonants, the
problem is related to incomplete velopharyngeal mechanism
which allows sounds produced at the larynx to pass through
the nasal segment of the upper airway.
For many consonant sounds of speech, an incompetent
velopharyngeal mechanism precludes the adequate buildup
of oral air pressure that is required behind airway
occlusions and obstructions to generate normal speech sounds
(Subtelny, Worth, and Sakuda, 1966). This means that sounds
like voiceless stop-plosives, fricatives, and affricates
will fail to their normal crispness when produced.
Consequently, they are perceived as being too soft. Trying
to generate sounds orally in the face of velopharyngeal
incompetence is like trying to blow up a tire that has a
leak in it.
Monotone
Often accompanying the soft-voice syndrome is the
monotonous voice with little pitch variation. Patients with
problem are often unable to demonstrate pitch variations of
more than 3 or 4 tones. This problem is identified on the
basis of clinical experience.
Strangled Voice
This problem is not one of the more common phonation
disorders found inpatients with valving problems, but is
encountered often enough to warrant mention here. Strangled
voice quality appears to be associated with an attempt to be
non-nasal in the presence of VPI. Phonation is associated
with extreme tension in the abdominal, diaphragmatic,
thoracic, laryngeal, and supraglottal muscles. It is almost
as if the person were trying to hold his breath and talk at
the same time. The introduction of relaxation results in an
increase in hypernasality.
DELAYED LANGUAGE
Research suggests that there may a lag in language
acquisition during early years of development for many children
with orofacial clefts, but as the individual gets older the gap
closes. By adulthood, no significant language differences
remain.
Disruption in early experience disruption of oral
touch-pressure sensation, oral cavity exploration, perceptual
motor deprivation, prolonged deprivation during formative
language period and reduced hearing sensitivity.
Insufficient language stimulation due to low expectations
for verbal responsiveness given child's physical problem.
Negative reactions of listeners cause child to limit the
frequency and elaboration of speech language attempts.
HEARING DISORDERS
Hearing disorders are prevalent among individuals with
orofacial clefts. These disorders are a result of middle ear
dysfunction, involving both ears. Exist in all infants with
unrepaired clefts of palate under the age of 2, 70 to 80% with
repaired clefts of older children
Prevalence is due to a disease called otitis media involves
an inflammation and/or infection of middle ear system and
presence of liquid in middle ear root of otitis media problem
is eustachian tube dysfunction muscle to open ET are cleft and
do not function normally consequently ET remains closed,
pressure and liquid builds up in ME inflammation and infection
occurs middle ear sound transmission system is impaired
conductive type of loss occurs
