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Raol N, Hartnick CJ (eds): Surgery for Pediatric Velopharyngeal Insufficiency.

Adv Otorhinolaryngol. Basel, Karger, 2015, vol 76, pp 1–6 (DOI: 10.1159/000368003)

Anatomy and Physiology of Velopharyngeal


Closure and Insufficiency
Nikhila Raol  · Christopher J. Hartnick
Fellow, Pediatric Otolaryngology, Massachusetts Eye and Ear Infirmary, Boston, Mass., USA

Abstract
The velopharynx is a complex structure that is responsible for separation of the oral and nasal cavi-
ties during speech production and swallowing. Incompetence of this mechanism can lead to hyper-
nasality, with nasal air emission and incomprehensible speech, as well as nasopharyngeal regurgita-
tion. There can be a significant social stigma associated with velopharyngeal dysfunction, and
surgical treatment can be curative in many cases. Knowledge of the normal anatomy and physiol-
ogy of the velopharyngeal complex is essential when planning for surgical repair.
© 2015 S. Karger AG, Basel

Anatomy

The velopharyngeal sphincter is bounded anteriorly by the soft palate, or velum; lat-
erally by the lateral pharyngeal walls; and posteriorly by the posterior pharyngeal wall.
It is composed of six muscle types: the levator veli palatini, tensor veli palatini, mus-
culus uvulae, palatoglossus, palatopharyngeus, and superior pharyngeal constrictor
(fig. 1). The levator veli palatini originates from the inferior surface of the petrous
portion of the temporal bone and the medial rim of the Eustachian tube. The muscles
take an anterior, inferior, and medial course to then decussate with the fibers of the
contralateral levator muscle at the palatine aponeurosis in the midline. The levator
sling makes up the majority of the muscle mass in the palate, and its orientation and
function are essential for proper velopharyngeal function.
The tensor veli palatini originates from the medial pterygoid plate and from the
lateral rim of the Eustachian tube. It runs anterior and lateral to the levator and ends
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Tensor veli palatini
Levator veli palatini
Superior
pharyngeal
constrictor

Musculus uvulae

Palatopharyngeus

Fig. 1. Velopharyngeal muscular anatomy. Reprinted with permission from Bluestone’s Pediatric
Otolaryngology, 4th edition.

in a tendon that wraps around the pterygoid hamulus of the sphenoid bone and inserts
into the palatine aponeurosis. Its primary function is to tense the soft palate and there-
by assist the levator veli palatini in uncoupling the oral and nasal cavities. The tensor
veli palatini is innervated by the medial pterygoid nerve, a branch of the mandibular
nerve, which is itself the third division of the trigeminal nerve. This makes it the only
muscle involved in the velopharyngeal mechanism that is not innervated by the vagus
nerve. Surgically, the tensor veli palatini can be important in helping with tension-free
closure in palatoplasty. In cases of Furlow palatoplasty, increased laxity can be ob-
tained for closure by infracturing the hamulus around which the tensor tendon pass-
es. The hamulus can be palpated as a bilateral symmetric bony bump that is slightly
medial to the maxillary tuberosity at the junction of the hard and soft palates. Al-
though hamulus fracture is not frequently performed, it is a good adjunct technique
to be aware of in cases of difficult palate closure.
The musculus uvulae are paired intrinsic muscles that arise from the posterior na-
sal spine of the palatine bones and from the palatine aponeurosis and insert into the
uvula. They are thought to aid in velopharyngeal closure by increasing the midline
bulk and by extending the length of the nasal aspect of the velum, thus maximizing
apposition of the soft palate to the posterior pharyngeal wall [1]. In patients with a
cleft palate or a submucosal cleft, these muscles are typically deficient [2]. The triad
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Raol N, Hartnick CJ (eds): Surgery for Pediatric Velopharyngeal Insufficiency.


Adv Otorhinolaryngol. Basel, Karger, 2015, vol 76, pp 1–6 (DOI: 10.1159/000368003)
of a bifid uvula, palatal notching, and soft palate diastasis should alert the surgeon to
a high likelihood of a submucosal cleft, and in these cases, only superior adenoidec-
tomy should be performed. The risk of velopharyngeal insufficiency (VPI) following
adenoidectomy is approximately 1:1,500, and the risk is higher in patients with a sub-
mucosal cleft palate.
The palatoglossus, also known as the anterior tonsillar pillar, originates in the an-
terior soft palate, where it is continuous with the contralateral muscle and courses
laterally, inferiorly, and anteriorly to insert into the tongue. The palatopharyngeus, or
the posterior tonsillar pillar, originates in the soft palate as well and passes laterally,
inferiorly, and posteriorly to join the stylopharyngeus and insert into the posterior
border of the thyroid cartilage. Both of these muscles depress the palate, hence creat-
ing an opposing force to the action of the levator veli palatini. They are thought to
provide fine motor control of the soft palate position while speaking [3]. It is impor-
tant to note the impact of aggressive resection of the palatopharyngeus during a ton-
sillectomy, as scarring in this area can lead to tethering of the soft palate and subse-
quent VPI.
The superior pharyngeal constrictor is made up of four parts: pterygopharyngeal
(origin: medial pterygoid), buccopharyngeal (origin: pterygomandibular raphe), my-
lopharyngeal (origin: mandible above mylohyoid line), and glossopharyngeal (origin:
tongue) parts. Despite different origins, all of these parts join and decussate with con-
tralateral fibers to insert into the median pharyngeal raphe. The primary function of
the constrictor muscle is medial displacement of the lateral pharyngeal walls and some
anterior displacement of the posterior pharyngeal wall, thereby narrowing the velo-
pharyngeal port and allowing for improved contact between the soft palate and the
posterior pharyngeal wall [4]. From a surgical standpoint, it is important to note that
due to the significant redundancy of this muscle, the posterior pharyngeal wall can be
easily closed primarily when tissue is borrowed for a pharyngeal flap or for a sphinc-
ter pharyngoplasty.
In approximately 20% of the population, a bulge along the posterior pharyngeal
wall due to contraction of the superior pharyngeal constrictor may be seen. First de-
scribed in 1863 by Passavant and therefore termed Passavant’s ridge, it is believed by
some to aid in velopharyngeal closure, although this is controversial [5].

Normal Physiology

In individuals with a normal velopharyngeal mechanism, contraction primarily of the


levator veli palatini causes the velum to move superiorly and posteriorly, contacting
the posterior pharyngeal wall and closing the velopharyngeal port. The site and extent
of contact depend on the sound that is being produced [6, 7]. This description is rath-
er simplistic, however; the actual closure pattern is based on the variable participation
of the muscles described above.
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Anatomy and Physiology 3


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Raol N, Hartnick CJ (eds): Surgery for Pediatric Velopharyngeal Insufficiency.


Adv Otorhinolaryngol. Basel, Karger, 2015, vol 76, pp 1–6 (DOI: 10.1159/000368003)
Coronal

Sagittal

Circular

Fig. 2. Various patterns of Circular with


­velopharyngeal closure. Passavant‘s ridge
­Reprinted with permission
from WebMD.

There are four classic closure patterns: coronal, sagittal, circular, and circular with
Passavant’s ridge (fig. 2). In the coronal closure pattern, the typical closure, as described
above, is seen, with the velum contacting the posterior pharyngeal wall in an anterior-
posterior fashion and minimal to no contribution from the lateral pharyngeal walls.
This pattern is present in approximately 55% of the population. With the sagittal closure
pattern, a much greater contribution is seen from the lateral walls, as medial movement
causes narrowing of the velopharyngeal port. Approximately 16% of patients have this
closure pattern. The circular closure pattern, seen in 10% of normal patients, is a com-
bination of the coronal and sagittal patterns, with movement of the velum posteriorly
and medial movement of the lateral pharyngeal walls. An additional 19% of patients
exhibit this same pattern, with an additional contribution from the posterior pharyn-
geal wall via Passavant’s ridge, known as a circular pattern with Passavant’s ridge [8].

Physiology in Velopharyngeal Dysfunction

Because multiple etiologies may cause problems with the velopharyngeal sphincter
mechanism, the term velopharyngeal dysfunction has been used to encompass the
entire spectrum.

Velopharyngeal Insufficiency
The term VPI refers to a structural abnormality that results in inadequate closure. In
some children, VPI may be congenital, such as in patients with a cleft palate or sub-
mucosal cleft or with velopharyngeal disproportion, where the soft palate is short
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Raol N, Hartnick CJ (eds): Surgery for Pediatric Velopharyngeal Insufficiency.


Adv Otorhinolaryngol. Basel, Karger, 2015, vol 76, pp 1–6 (DOI: 10.1159/000368003)
relative to the depth of the pharynx. In patients with 22q11.2 deletion syndrome, in-
creased pharyngeal depth and flattening of the cranial base angle have been shown,
which predispose these patients to VPI without the presence of a cleft due an increase
in the depth-to-length ratio [9].
Mechanical obstruction, such as enlarged tonsils or a mass, may impair movement
of the velum [10]. In some cases, patients may develop VPI following surgery, such as
following adenoidectomy, as discussed above. Palatoplasty complicated by an orona-
sal fistula, palatal tethering, or velar shortening may also result in VPI [11]. Lastly,
trauma may also lead to acquired VPI.

Velopharyngeal Incompetence
The term velopharyngeal incompetence typically refers to a neurologic impair-
ment that causes dysfunction of the velopharyngeal mechanism. In contrast to
VPI, these patients have adequate velar length and do not have an underlying me-
chanical obstruction. In children, neurologic etiologies may include cerebrovascu-
lar accident, neuromuscular disease such as myasthenia gravis, global hypotonia,
cerebral palsy, muscular or myotonic dystrophy, demyelinating diseases, and Mo-
bius syndrome [12–14]. Other neurologic symptoms may be noted, including dys-
arthria and apraxia. In patients with apraxia, a combination of hypernasality and
hyponasality may be seen due to general difficulty with speech motor program-
ming and control [15]. Of note, these patients may also have problems with the
swallowing component of velopharyngeal function, since this is a reflexive brain-
stem function.

Velopharyngeal Mislearning
The term velopharyngeal mislearning describes those children with velopharyngeal
dysfunction that is purely functional, without evidence of anatomic or physiologic
cause for articulation errors. It is most commonly seen in those patients who have
had cleft palate repair but have persistent hypernasal speech due to compensatory
misarticulation [5]. These patients often will have nasal airflow produced as a sub-
stitute for certain consonants, and most frequently s, z, sh, and ch, but not for all
consonants [16, 17]. In addition, they may produce glottal stops that interfere with
velopharyngeal closure [17]. Intensive speech therapy is needed for treatment, as
this is not a surgical problem. In addition, it should be noted that patients may have
a combination of the above types of velopharyngeal dysfunction. For example, a
patient may have coexistent VPI and mislearning. Preoperative multidisciplinary
evaluation is therefore essential in the treatment of these patients. It should be em-
phasized to the patient that surgery will be unlikely to completely fix the articula-
tion problems and that further speech therapy will likely be needed; alternatively,
following speech therapy, there may be a role for surgery, depending on what defi-
cit remains.
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Anatomy and Physiology 5


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Raol N, Hartnick CJ (eds): Surgery for Pediatric Velopharyngeal Insufficiency.


Adv Otorhinolaryngol. Basel, Karger, 2015, vol 76, pp 1–6 (DOI: 10.1159/000368003)
Pearls and Pitfalls

Knowledge of normal velopharyngeal anatomy and closure patterns is imperative for


accurate surgical decision-making.
Velopharyngeal mislearning should be recognized early so as to prevent unneces-
sary surgery or to convey realistic expectations for surgery when multiple types of
velopharyngeal dysfunction are present.

References
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Christopher J. Hartnick, MD
Chief, Pediatric Otolaryngology
Massachusetts Eye and Ear Infirmary
243 Charles St., Boston, MA 02114 (USA)
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E-Mail christopher_hartnick@meei.harvard.edu
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Raol N, Hartnick CJ (eds): Surgery for Pediatric Velopharyngeal Insufficiency.


Adv Otorhinolaryngol. Basel, Karger, 2015, vol 76, pp 1–6 (DOI: 10.1159/000368003)