Anatomy and Physiology of the
Upper Esophageal Sphincter
Ivan M. Lang, DVM, PhD, Reza Shaker, MD, Milwaukee, Wisconsin
The upper esophageal sphincter (UES) is
composed of the cricopharyngeus (CP),
thyropharyngeus (TP; inferior pharyngeal
constrictor [IPC] in humans), and cranial cervical
esophagus. All 3 muscles may at times function
to maintain tone in the UES, but only the CP
contracts and relaxes in all physiologic states
consistent with the UES. The CP is a striated
muscle composed of variable-sized small (25–
35 mm) muscle fibers that are primarily type I
(slow twitch), highly oxidative, and contain
abundant (40%) endomysial elastic connective
tissue. The fibers may attach to the connective
tissue framework, forming a muscular net. In
humans and rats, but not other animals, the CP
has no median raphe. The optimum length of the
CP for development of active tension is about
1.7 times resting length; therefore, in some
respects the CP acts more like cardiac than
striated muscle. A passive tone in the CP is
present and increases through all degrees of
stretch. The high compliance of the CP allows it
to be opened by distraction of other muscles
(e.g., geniohyoideus) or increased intraluminal
pressure. The CP is innervated by branches of
the vagus nerves: pharyngoesophageal (PE),
superior laryngeal (SLN), and recurrent
laryngeal (RLN); glossopharyngeal (GPN); and
cervical sympathetics. Only the PE and SLN
provide motor fibers to the CP. The GLN may be
sensory; the sympathetics may innervate the
mucosa, blood vessels, and glands; but no
functional innervation by the RLN has been
identified. Parasympathetic ganglia and various
peptides (galanin, cGRP, VIP, neuropeptide Y,
substance P, tyrosine hydroxylase) have been
found in the CP, but their role in control of the
CP is unknown. The motoneurons of the CP are
found in the nucleus ambiguus, and the
innervation is ipsilateral for animal species in
which the CP has a median raphe. These
motoneurons are topographically organized with
From the Division of Gastroenterology and Hepatology, Department of
Medicine, Medical College of Wisconsin, Milwaukee, Wisconsin.
Requests for reprints should be addressed to Ivan M. Lang, DVM, PhD,
Dysphagia Research Laboratory, Medical College of Wisconsin, 8701
Watertown Plank Road, Milwaukee, Wisconsin 53226.
50S Q1997 by Excerpta Medica, Inc.
All rights reserved.
/ 2312 5513 Mp 50 Friday Dec 05 06:18 PM
other pharyngeal and laryngeal muscles and the
striated muscle esophagus. Pharyngeal
motoneurons often have a respiratory rhythm,
but not a spontaneous background discharge.
Therefore, the CP motoneurons may not
generate CP tone. Various reflexes control the
tone of the CP. Distension of the esophagus
causes contraction of the CP and UES, which is
mediated by a vago-vagal reflex. Pressure on
the pharyngeal mucosa contracts the CP and
UES and is mediated by a glossopharyngo-vagal
reflex. Inflation of the lungs causes contraction
of the CP and UES, which is mediated by a vago-
vagal reflex. The pharyngo-UES and pulmonary-
UES reflexes may generate the respiratory
rhythm often observed on UES pressure or
electromyographic activity. The UES or CP also
contracts with arousal or with changes in
posture. All of these reflexes and responses and
the passive elastic properties of the CP may
contribute to the generation of tone in the CP
and UES. Am J Med. 1997;103(5A):50S–55S.
Q 1997 by Excerpta Medica, Inc.
T he upper esophagus presents an organ that must
be defined both anatomically and physiologically.
DEFINITION OF THE UPPER
ESOPHAGEAL SPHINCTER
The upper esophageal sphincter (UES) is defined
as the pharyngo-esophageal segment that maintains
a closed pharyngo-esophageal junction and that
phasically opens during various physiologic states.
When one compares the UES intraluminal high-pres-
sure zone to the anatomic components of the phar-
yngo-esophageal segment,1 – 6 one finds an elevated
pressure encompassing the proximal cervical esoph-
agus, cricopharyngeus (CP), and inferior pharyngeal
constrictor (IPC; thyropharyngeus [TP] in animals).
Experimental evidence has been found to impli-
cate each muscular element as the UES. The proxi-
mal cervical esophagus was found to have an inner-
vation pattern histologically similar to that of other
gastrointestinal sphincters.7 Careful comparison8 of
the location of the UES high-pressure zone with the
radiographic anatomy of the laryngo-pharynx re-
vealed in most studies that the peak UES pressure
was observed at the IPC in humans3,5,9 and animals.1,2
In addition, some investigators found that the elec-
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 SYMPOSIUM ON GASTROESOPHAGEAL REFLUX DISEASE/LANG AND SHAKER
tromyographic activity of the TP (IPC) and the CP
fluctuated with UES pressure and relaxed during
swallows.2 The fact that the TP may function like the
CP or UES at times or that the TP may be capable
of generating more force than the CP (possibly due
to the abundance of elastic connective tissue in the
CP as described below) does not mean it is the pri-
mary muscle of the UES. The CP has been consid-
ered the primary muscular component of the UES by
most investigators. Some investigators have found
that the peak UES pressure does correspond with
the CP6 and that the infracricoid esophagus does not
have histologic characteristics consistent with a
sphincter.10 Most importantly, however, in most
studies using humans or animals, investigators found
that the CP but not the IPC (TP) (1) had a continual
basal tone1,11 – 16; (2) relaxed during swallowing1,12 – 17;
and (3) experienced fluctuations in electromyo-
graphic activity associated with changes in UES
pressure.1,16,18
Perhaps the UES is more complex than compris-
ing one muscle. When all studies are considered, it
appears that the muscle(s) comprising the UES de-
pends on the physiologic state. Basal tension is pro-
duced by the CP and IPC (TP) and possibly the in-
fracricoid esophagus1,2,11,13 – 18; active relaxation
during swallowing1,11,13 – 17 and belching19,20 occurs
primarily on the CP; changes in activity with respi-
ration2,17,18,21,22 occur in both the CP and IPC; UES
contraction and relaxation during retching and vom-
iting occur by the simultaneous action of the CP,
IPC, and proximal cervical esophagus13,20; UES con-
traction in response to esophageal or pharyngeal dis-
tension (i.e., the esophago-UES and pharyngo-UES
reflexes11) occurs with the CP rather than the IPC;
and contraction of the UES during coughing and
sneezing occurs in both the CP and IPC.23 Therefore,
the UES may comprise the CP, IPC, and proximal
cervical esophagus, depending on the physiologic
state, but the one muscle that functions as the UES
in all physiologic states is the CP.
ANATOMY AND CELLULAR PHYSIOLOGY
OF THE CP
In most species the CP attaches to the cricoid car-
tilage and forms a c-shaped muscular band that pro-
duces maximum tension in anteroposterior rather
than lateral directions.1,2,4 In humans, two sets of
muscle fibers have been identified: the horizontally
oriented fibers (pars fundiformis) and an oblique
band of fibers (pars obliqua), which extends from the
lateral aspect of the cricoid cartilage to the posterior
midline raphe, where they blend superiorly with the
TP.24 Unlike the TP, the pars fundiformis of the CP
has no median raphe. In most animal species the CP
forms a muscular band distinct from the TP but con-
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tains a median raphe.25,26 The CP is a striated muscle
composed of variable-sized fibers of small average
diameter (25–35 mm), which are not oriented in
strict parallel fashion as most other striated mus-
cles.24,27,28 The CP contains a large amount of endo-
mysial connective tissue (about 40%), much of which
is elastic but has no muscle spindles.27 – 30 It has been
suggested that, unlike most other striated muscles,
which insert on the skeletal framework, the muscle
fibers of the CP insert onto the connective tissue
framework, thereby forming a muscular network.29
In most species the predominant muscle fiber type
is type I (slow twitch) and highly oxidative,24,28,29 and
in all species examined, the predominant fiber type
or oxidative state of the CP is different (i.e., slower
and/or more oxidative) from surrounding pharyngeal
or laryngeal muscles.24,27 – 33 The structure and bio-
chemical properties of the CP serve its function well,
allowing the CP to stretch and accommodate large
boluses but maintaining a constant tone to form a
barrier between the esophagus and pharynx. The CP,
in all species examined, also contains type II (fast
twitch) muscle fibers, and these fast twitch fibers are
predominantly highly oxidative.24,27 – 29,31 The pres-
ence of both slow and fast twitch fibers provides an
anatomic basis for the various functions of the CP
or UES: (1) maintaining constant basal tone and (2)
rapid relaxation and contraction during swallowing,
belching, vomiting, and other reflexes.
BIOPHYSICS OF THE CP
The CP is not only structurally and biochemically
different from surrounding pharyngeal and laryngeal
muscles, but its mechanical properties are different
as well. The length at which the CP reaches maxi-
mum active tension is about 1.7 times its basal (or
in situ) length,34 whereas this tension in most striated
muscles occurs at resting length.35,36 The source of
elasticity in muscle is unclear, but many investiga-
tors have proposed a model that contains both par-
allel and series elastic elements, where the parallel
elastic element is assumed by most as contributing
to the passive elastic properties of the muscle.35 – 37
Structural correlates of the parallel elastic element
include connective tissue,35 i.e., collagen and elastin;
sarcolemma; and the contractile apparatus itself,38
i.e., the contractile proteins, actin and myosin. Com-
pared with other striated muscles, the CP24,27 – 29 has
abundant (about 40%) connective tissue (especially
elastic elements) and more sarcolemma (the crico-
pharyngeus muscle fibers are smaller, about 25–35
mm, than most striated muscle fibers, about 100 mm,
which therefore have more sarcolemma). These
structural characteristics as well as the network
arrangement of muscle fibers and connective tissue
could account for the passive elastic behavior
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SYMPOSIUM ON GASTROESOPHAGEAL REFLUX DISEASE/LANG AND SHAKER
of the CP. The functional implications of the passive
tension characteristics of the CP are that (1) a basal
passive pressure is generated intraluminally at all
levels of distension (there will always be tension re-
corded intraluminally from the UES that is not due
to active contraction); (2) the tension of the sphinc-
ter increases throughout its range of distension34
similar to the Frank-Starling characteristics of car-
diac muscle (the diameter of the UES during a swal-
low of maximal volume does not exceed the optimal
length of the UES34); and (3) the UES may be opened
by increased intraluminal pressure or active distrac-
tion without active relaxation of the UES.2
NEUROPHYSIOLOGY OF THE CP
The CP receives innervation from the pharyngeal
plexus, which is supplied by 3 major nerves: vagus
nerve through the pharyngoesophageal, superior la-
ryngeal, and recurrent laryngeal branches; glosso-
pharyngeal nerve; and sympathetics through the cra-
nial cervical ganglion.34,39 – 48 Dissection techniques
are incapable of determining the particular pharyn-
geal muscles innervated by these nerves, because all
of these nerves form communicating branches with
each other. In addition, dissection techniques do not
identify the nerve terminals and, therefore, cannot
distinguish sensory from motor nerves or identify
the effector organs involved (e.g., muscle or blood
vessel). Although the anatomical architecture of the
pharyngeal plexus differs among species,34,39 – 48 the
pattern of functional innervation is quite uniform
and consistent. Functional studies have determined
that in most species the primary motor innervation
of the CP is the pharyngoesophageal nerve.2,22,39,45 – 50
Electrical stimulation of the pharyngoesophageal
nerve depleted 60% of the CP muscle fibers of gly-
cogen,39 resulted in an integrated electromyographic
response much greater than that activated by the su-
perior laryngeal nerve34 or glossopharyngeal nerve,48
and strongly contracted the CP, whereas recurrent
laryngeal nerve stimulation did not.22,46 Furthermore,
transection of the pharyngoesophageal nerve rather
than glossopharyngeal49 or superior laryngeal46,47
nerves had profound long-term deficits on swallow-
ing and resting pharyngeal pressure and produced
denervation potentials in the CP muscle.48 Although
the superior laryngeal nerve may contribute to the
motor innervation of the CP, there is no functional
evidence for a role of the glossopharyngeal nerve or
recurrent laryngeal nerve in the motor control of
the CP.
Sensory Information
The glossopharyngeal nerve and sympathetics
may provide important sensory information from the
CP, underlying pharyngeal mucosa, or blood vessels,
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but the role of these nerves is unclear. Some early
investigators found that peripheral electrical stimu-
lation of the cervical sympathetics caused changes
in CP motor activity,51 but these results have not
been corroborated.46,50 Considering the large amount
of branching among the nervous inputs to the CP, it
is possible that some of these effects may have been
due to stimulation of vagal pathways. The glosso-
pharyngeal nerve may mediate the afferent limb of
pharyngeal mucosal reflexes, because transection of
the glossopharyngeal nerve blocked the pharyngo-
UES contractile reflex without affecting the eso-
phago-UES contractile reflex.11 This sensory role for
the glossopharyngeal nerve may explain some of the
deficits in swallowing observed after transection of
the glossopharyngeal nerve.48
Neurotransmitters
The neurotransmitters involved in the control of
the CP include acetylcholine as well as various neu-
ropeptides. The following peptides have been
found52 within the CP using immunohistochemistry:
calcitonin gene related peptide, neuropeptide Y, ty-
rosine hydroxylase, substance P, vasoactive intesti-
nal polypeptide, and galanin. The calcitonin gene re-
lated peptide is also found in other pharyngeal and
laryngeal muscles and the striated muscle esopha-
gus.53,54 The CP has significantly less calcitonin gene
related peptide than the TP, but the functional sig-
nificance of this difference is unknown. These neu-
ropeptides may simply represent the autonomic in-
nervation of the muscle, because calcitonin gene
related peptide, neuropeptide Y, and tyrosine hy-
droxylase are found in sympathetic nerves and sub-
stance P, vasoactive intestinal polypeptide, and gal-
anin are found in parasympathetic nerves.
Interestingly, the sympathetic peptides were more
abundant than the parasympathetic peptides. Clus-
ters of neurons, i.e., ganglia, were found in the CP
rather than the TP, and these contained mostly para-
sympathetic peptides, suggesting that these were
parasympathetic ganglia.52 The role of either the
sympathetic or parasympathetic innervation and
peptides are unknown, but control of blood vessels,
glands, and pharyngeal mucosa are the most likely
functions.
Motor Neurons
The motor neurons controlling the CP are found
primarily within the semi-compact and rostral com-
pact portions of the nucleus ambiguus (NA)55 – 62 and
the innervation is mostly (ú95%) ipsilateral58,61 in
those species with a median raphe. The CP motor
neurons are topographically organized with the
other muscles of the pharynx and esophagus, al-
though there is considerable overlap.56,60,61 The ipsi-
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lateral innervation pattern of the CP by the NA is
consistent with swallowing studies, which found
that half of the brainstem controls the ipsilateral half
of the CP during swallowing.63 In contrast, reflex ac-
tivation of the CP requires both halves of the brain-
stem64; and electrical stimulation of the nucleus trac-
tus solitarius (NTS), the primary afferent nucleus of
the vagus, causes activation of the CP bilaterally.48,49
These results suggest that control of the CP differs
with different functions. The neurons of the NA have
extensive dendritic arborization to the adjacent re-
ticular formation55 and ultrastructural studies indi-
cate the synapses on these neurons are both exci-
tatory as well as inhibitory.65 These findings provide
an anatomic basis for numerous excitatory and in-
hibitory reflexes and responses by the CP. Pharyn-
geal premotor neurons of the NA have been identi-
fied in the interstitial and intermediate subnuclei of
the NTS,57 and this pathway is distinct from the
esophageal swallowing circuit. This circuit may me-
diate nonswallowing reflex responses of the UES,
such as the pharyngo-UES contractile reflex.11 Many
pharyngeal motoneurons of the NA exhibit a respi-
ratory rhythm, some units were in phase, but others
were out of phase with inspiration but have no spon-
taneous background discharge.62 These results sug-
gest that the pharyngeal motoneurons do not gen-
erate the basal tone observed in the CP or UES.
Reflexes Involving UES
Numerous reflexes control the function of the
UES. Slow balloon or bolus distension of the esoph-
agus — proximal is more sensitive than distal—
causes increased UES pressure or CP electromyo-
graphic activity mediated by vagal afferent fi-
bers.11,12,66 – 68 The receptors mediating this reflex may
be slow adapting mechanoreceptors of the muscular
wall.69 Some investigators have found that slow acid
infusion into the esophagus causes increased UES
tone,67,70,71 but these results have not been corrobo-
rated by more recent studies,72,73 and in addition,
esophageal pH was found not to correlate with UES
tone.73 The increased UES tone after acid infusion
may have been due to nonphysiologic concentra-
tions of acid, activation of esophageal distension re-
flex, or the pull-through technique of measuring UES
tone. Pharyngeal stimulation was also found to
cause increase in UES tone74 and CP but not TP elec-
tromyographic activity.11 The afferent limb of this re-
flex is the glossopharyngeal nerve, and the efferent
is the pharyngoesophageal branch of the vagus. The
physiologic stimulus (i.e., air or fluid) for this reflex
is unknown; therefore, the function of this reflex in
unclear. This reflex may close the esophagus during
inspiration to prevent reflux aerophagia, or it may
close the esophagus to prevent reflux aspiration. It
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has been observed for a long time that UES pressure
fluctuates with respiration, but it may be in or out of
phase with inspiration, and it may be associated with
contraction of the CP or TP.1,18,21,55,75 This rhythm
may be generated centrally by brainstem respiratory
centers or peripherally by reflex mechanisms. One
reflex that may account for this respiratory rhythm
is the pharyngo–UES contractile reflex, but a pul-
monary–UES contractile reflex has also been
found.21 The magnitude of tidal volume correlated
positively with CP electromyographic activity, and
lung distension by positive pressure ventilation or
hyperventilation caused strong contraction of the
CP. The pulmonary–UES reflex was mediated by va-
gal afferents and may be part of the Hering-Breuer
reflexes. In some situations inspiration is associated
with contraction of the TP rather than the CP,2,21 sug-
gesting that other reflexes or mechanisms may con-
trol respiratory rhythm of the UES.
Generation of Tone
Perhaps the most significant function of the UES
as a sphincter is the generation of tone. The me-
chanical properties of the CP ensure that tone will
develop in the muscle at any degree of stretch with-
out active contraction. Many sphincters have a con-
stant basal tone generated by the neural input or in-
trinsic properties of the muscle. However, the UES
or CP do not appear to exhibit a significant constant
active basal tone. The CP electromyography of
chronically instrumented awake and unanesthetized
dogs experiences periods of very low activity when
the animal is calm, supine, and resting its head, but
awake.23 Tone of the CP of animals or UES of people
falls to very low states during anesthesia18 or sleep.76
On the other hand, changes in posture8 or arousal1,76
can cause very large increases in activity. Moreover,
pharyngeal motoneurons found in decerebrate and
paralyzed cats did not exhibit a basal constant dis-
charge.62 These results suggest that much of the tone
of the UES or CP may be generated by various re-
flexes, responses, and muscle mechanics rather than
a specific tone-generating circuitry of the brainstem.
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