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342 W. Schima et al.
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Fig. 1 a–c Normal esophageal motility. The patient is placed
in the prone oblique position. There is a peristaltic contraction
wave, which occludes the esophageal lumen, resulting in the
the patient in the Trendelenburg position, the
water-siphon test, the Valsalva maneuver, and
turning of the patient (Stewart 1981). We use only
the latter two tests, which are more physiological
than the former two. If reflux is noted during the
examination, spot-film or video recording should
be used to document it. With the invention of
picture archiving and communication systems
(PACS), an attractive alternative to storage of
examination data on videotapes or DVDs has
emerged. ‘‘Videoflurososcopic’’ examinations can
now stored directly in a PACS, which allows easy
retrieval of prior examinations for comparison.
typical inverted-V shape (arrows) of the bolus tail. Distal
propagation of the bolus is shown
4. Solid bolus with the patient in the upright position:
If the patient suffers from dysphagia for solids and
the examination with liquid barium does not reveal
the cause, a solid bolus (barium-soaked cookies,
marshmallows, tablets, etc.) may be used. Transit
of solid food may be slow in some individuals.
There is no standardized reference value for
evaluation of solid food transit (Pouderoux et al.
1999). The best indicator for the presence of a
significant stenosis (i.e., a Schatzki ring or a
malignant stricture) or a motor abnormality is the
induction of the typical symptoms of ‘‘food
sticking in the throat’’ by a retained solid bolus.
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5. Double-contrast and mucosal relief films of the
esophagus and the lower esophageal sphincter
(see the chapter on esophageal morphology).
4 Esophageal Motility Disorders
Esophageal motor disorders can be divided into two
major categories. Primary motor disorders occur
independent of other diseases and include achalasia,
diffuse esophageal spasm, nonspecific esophageal
motor disorders, and nutcracker esophagus. Secondary motor disorders include a long list of motor
abnormalities seen in conjunction with other diseases
(Table 1). Classification of motor disorders is based
on manometric findings. Diagnosis of a secondary
motor abnormality requires, in addition, the diagnosis
of an extraesophageal disorder known to affect the
esophagus. Esophageal motility disorders present
with the nonspecific symptom of dysphagia or chest
pain. Although the clinical presentation may be the
same in patients with different motor abnormalities, it
is important to characterize the abnormality precisely.
The optimal therapy is based on the specific knowledge of a manometric abnormality and may differ
considerably between different groups. However,
esophageal manometry is not widely available and in
most cases is not the first diagnostic test in patients
with dysphagia. In these patients, either endoscopy or
barium radiography is recommended in many institutions and countries (Tscholakoff et al. 2011; The
Royal College of Radiologists 2007). Radiographic
assessment, in particular videofluoroscopic recording,
has been shown to be very useful in detecting and
reliably characterizing esophageal motor abnormalities (Ott et al. 1987, 1990; Schima et al. 1992).
5 Primary Motor Disorders
5.1 Achalasia
Achalasia is the most widely known esophageal
motor disorder. It is characterized by aperistalsis in
the esophageal body and incomplete relaxation of the
lower esophageal sphincter upon swallowing (Stacher
et al. 1994; Richter 2001). The cause is not exactly
known, but histopathologic lesions have been found
in the dorsal motor nuclei of the brainstem, the vagal
Table 1 Classification of esophageal motility disorders
Primary motility disorders
Achalasia
Diffuse esophageal spasm
Nutcracker esophagus
Esophageal atresia
Nonspecific esophageal motor disorders
Secondary motility disorders
Connective tissue diseases
Progressive systemic sclerosis
Dermatomyositis
Polymyositis
Mixed connective tissue disease
Lupus erythematosus
Endocrine disease
Diabetes mellitus
Myxoedema
Hyperthyroidism
Metabolic disorders
Alcohol-induced
Amyloidosis
Infectious disorders
Chagas disease
Candida
Herpes
Chemical
Gastroesophageal reflux
Caustic agents
Muscular disorders
Myasthenia gravis
Muscle dystrophy
Neurologic diseases
Parkinson disease
Guillain–Barré syndrome
Poliomyelitis
Amyotrophic lateral sclerosis
Multiple sclerosis
Immunologic
Chronic graft-versus-host disease
Eosinophilic esophagitis
Iatrogenic
Medication (anticholinergic agents, benzodiazepines,
barbiturates, etc.)
Radiation
Postvagotomy
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branches, and the myenteric plexus of the esophagus.
The primary region of damage is the esophageal
myenteric plexus (Auerbach’s plexus), including
patchy inflammatory response, loss of ganglionic
cells, and some myenteric neurofibrosis (Richter
2010). Diagnosis of achalasia should be suspected
when patients present with a long history of slowly
progressive dysphagia for solids and liquids. Regurgitation of saliva and food immediately after swallowing (in contrast to gastroesophageal reflux) is
common. Achalasia may also present as (noncardiac)
chest pain. Some patients complain of heartburn,
despite the fact that incomplete opening of the lower
esophageal sphincter is one of the key features of
achalasia (Spechler et al. 1995). Esophageal
manometry is the gold standard for the diagnosis of
achalasia. The resting pressure of the lower esophageal sphincter is either normal or high, and there is
incomplete relaxation of the sphincter upon swallowing. Aperistalsis is present in the esophageal body.
Contractions are simultaneous and sometimes even
of high amplitude (so-called vigorous achalasia)
(Goldenberg et al. 1991).
Videofluoroscopy is the best initial diagnostic test
(Richter 2010). Radiologically, there is a typical
appearance of esophageal dilatation with beaklike
narrowing of the lower esophageal sphincter
(Meshkinpour et al. 1992; Francis and Katzka 2010).
Early in the disease, the esophagus has a normal
diameter (Fig. 2). With progression of the disease, the
esophagus becomes dilated and retains food and saliva (Fig. 3). In advanced cases, esophageal dilatation
may be severe (so-called sigmoid esophagus) (Fig. 4)
(Schima et al. 1993). Barium radiography has a low
sensitivity in detecting achalasia, as alterations in
esophageal morphology are present in advanced cases
only. The radiologic staging system for achalasia
according to Brombart (1980) is based on the grade of
esophageal dilatation (less than 4 cm, 4–6 cm, more
than 6 cm in diameter), which explains the low sensitivity of single-contrast upper gastrointestinal tract
studies.
Multiphasic radiographic evaluations including
fluoroscopic assessment of esophageal motility shows
a support level of contrast material due to slowed
esophageal transit. This sign hints at the presence of
either a motor abnormality or a distal stenosis
(Fig. 2). The sensitivity of radiologic studies (either
barium radiography or videofluoroscopy) for the
detection of achalasia has been reported to be 58–95%
(Howard et al. 1992; Ott et al. 1987; Schima et al.
1992, 1998). With videofluoroscopy, diagnosis is
based not only on morphologic alterations of the
esophagus, but also on assessment of functional
abnormalities. Videofluoroscopy may reveal incomplete lower esophageal sphincter opening with
delayed transit into the stomach. The feature of a
transient support level of barium with the patient in
the upright position can be explained by variations in
examination technique and patient populations.
As described, the diagnosis is much more difficult to
make in patients with early stages of the disease when
esophageal dilatation is not yet present.
Several studies have reported a relation between
achalasia and esophageal carcinoma. Patients with
long-standing achalasia are at increased risk of
carcinoma. The exact cause is unknown, but chronic
stasis of food and saliva has been suggested. The
reported incidences range from 1.7 to 20% (Meijssen
et al. 1992). In a large prospective trial, the risk of
patients with achalasia developing cancer was found
to be increased 33-fold, for a total of 3.4 cancers per
1,000 patients per year. Close follow-up of patients
with achalasia is therefore strongly recommended
(Meijssen et al. 1992).
5.2 Pseudoachalasia (Malignancy-
Induced Achalasia)
Malignancies involving the gastroesophageal junction
can result in a clinical syndrome, pseudoachalasia,
that mimics idiopathic achalasia. Pseudoachalasia is
most often caused by adenocarcinoma of the fundus
invading the distal esophagus. Other causes are
squamous carcinoma of the distal esophagus with
predominantly submucosal spread (Park et al. 2010)
and hematogenous metastatic disease of the gastroesophageal junction (Dodds et al. 1986; Parkman and
Cohen 1993; Kahrilas et al. 1987; Paulsen et al.
2010). Conventional esophageal manometry may not
differentiate between idiopathic achalasia and pseudoachalasia. However, the correct diagnosis can be
determined in most cases by the clinical history and
the radiologic features. The mean duration of dysphagia is much shorter in patients with malignant
pseudoachalasia than in patients with idiopathic
achalasia (1.9 months vs. 4.5 years) (Woodfield et al.
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Fig. 2 Achalasia—early stage. a Videofluoroscopy with the
patient in the upright position reveals a support level of contrast
material indicative of delayed transit (arrow). The esophagus is
not dilated. b With the patient in the supine position narrowing
Fig. 3 Advanced achalasia.
Barium radiography reveals
moderate esophageal
dilatation with retention of
barium and secretions. There
is the typical beaklike
narrowing of the lower
esophageal sphincter
2000) and there is pronounced weight loss over time
in malignancy-induced achalasia (Reynolds and
Parkman 1989; Tremble 1959). Radiologically, the
of the gastroesophageal junction is evident. c Radiography
confirms narrowing of the gastroesophageal junction. Subsequently, manometry revealed achalasia
Fig. 4 Long-standing
achalasia. In this patient with
a 36-year history of untreated
achalasia, there is massive
dilatation of the esophagus,
which nearly fills the right
hemithorax. (From Schima
et al. 1993)
narrowed segment is longer in pseudoachalasia (4.4
vs. 1.9 cm) and reveals nodularity and abrupt proximal borders rather than a beaklike narrowing (Fig. 5)
(Woodfield et al. 2000). The muscle-relaxing effect of
amyl nitrite inhalation can be used to help make the
correct diagnosis during barium radiography. After
administration, there is relaxation of the lower
esophageal sphincter, with a subsequent opening of
2 mm or more in sphincter diameter (Dodds et al.
1986). In pseudoachalasia with tumor infiltration, the
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Fig. 5 Pseudoachalasia due
to adenocarcinoma of the
cardia. Barium radiography
reveals moderate esophageal
dilatation similar to that seen
in achalasia. However,
narrowing of the
gastroesophageal junction
does not appear beaklike.
It is more irregular (arrow)
sphincter is unaffected by amyl nitrite. Computed
tomography (CT) is also helpful in differentiating the
two syndromes. Circumferential thickening of the
lower esophageal sphincter of less than 10 mm is
indicative of idiopathic achalasia, whereas pseudoachalasia patients have CT findings of marked or
asymmetric wall thickening or a mass (Carter et al.
1997). When pseudoachalasia is suspected on the
basis of clinical history and radiologic features, neg-
Fig. 6 Diffuse esophageal spasm. a Videofluoroscopy shows
severe nonpropulsive contractions, which give the esophagus a
corkscrew appearance. b Barium radiography shows partial
relaxation of these transient contractions. There is formation of
pseudodiverticulum-like sacculations between the contractions
ative endoscopic or biopsy findings should be viewed
with caution (Tremble 1959). Repeated biopsies,
endoscopic ultrasonography, or even surgical exploration may finally lead to the diagnosis of malignancy-induced pseudoachalasia.
2010). Differentiation between diffuse spasm and
vigorous achalasia is based on the presence of normal
relaxation of the lower sphincter in the former.
However, diffuse esophageal spasm may evolve into
vigorous achalasia or classic achalasia over time
(Hannig and Wuttge-Hannig 1987).
5.3 Diffuse Esophageal Spasm
The classic radiologic features of diffuse spasm are
the presence of severe nonpropulsive contractions
The incidence of diffuse esophageal spasm is much
lower than that of achalasia. Diffuse esophageal
spasm is characterized by substernal chest pain, dysphagia, and the manometric evidence of simultaneous
nonpropulsive contractions on more than 20% of
swallows with intermittent peristaltic contractions,
with a minimum amplitude of 30 mmHg (Richter and
Castell 1984; Konturek and Lembo 2008; Grübel
et al. 2008). It has been found that even ‘‘normal’’
peristaltic contractions of diffuse esophageal spasm
patients are more rapidly propagated than normal
swallows of a control group (Krieger-Grübel et al.
causing esophageal curling or a ‘‘corkscrew’’ or
‘‘rosary bead’’ appearance (Chen et al. 1989) (Fig. 6).
In two large studies by Ott et al. (1987, 1990) the
correct diagnosis of diffuse spasm was made radiologically in 55–71% of patients. Incomplete or absent
peristalsis and nonpropulsive contractions are present
in 71–76% of patients (Chen et al. 1989). However,
radiologic findings are often nonspecific and do not
allow the diagnosis of diffuse esophageal spasm to be
made; therefore, patients with otherwise unexplained
chest pain and radiologic evidence of a nonspecific
esophageal contraction abnormality should be
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referred for manometry. On CT, diffuse esophageal
spasm may appear as smooth circumferential wall
thickening of the lower esophagus in 21% of patients
(Goldberg et al. 2008) and should be included in the
differential diagnosis of esophageal wall thickening.
5.4 Nutcracker Esophagus
As more patients with noncardiac chest pain were
studied manometrically, an abnormality clearly different from diffuse spasm was recognized in 1979
(Benjamin et al. 1979). In the so-called nutcracker
esophagus, primary peristalsis is preserved, but there
are peristaltic contractions of high amplitude and long
duration. The diagnosis of nutcracker esophagus is
made by manometry.
It is known that approximately 20% of patients
admitted to cardiac care units show no abnormality in
a detailed cardiac workup (Bassotti et al. 1998). In a
large percentage of these patients with noncardiac
chest pain, nutcracker esophagus or diffuse esophageal spasms are present.
Radiologically, the diagnosis is difficult to make,
because peristalsis is preserved. Chobanian et al.
(1986) found nonspecific abnormalities of esophageal
bolus transit in 36% of patients. These findings were
confirmed in a study by Ott et al. (1990): in a series of
170 patients suffering from chest pain, nutcracker
esophagus was even more prevalent than diffuse
esophageal spasm, but a specific radiologic diagnosis
could not be made in any of the patients.
The patho-physiological of nutcracker esophagus
remains unclear. The transition of nutcracker esophagus into achalsia has been shown, suggesting that
both diseases lie within the same part of a spectrum of
motor disorders (Konturek and Lembo 2008).
peristalsis, and secondary peristaltic contractions have
lower amplitudes than those seen in normal infants
(Daum and Keuerleber 1969).
5.6 Nonspecific Esophageal Motor
Disorders
By far the most common esophageal motor disorders
are nonspecific contraction abnormalities. They may
be idiopathic (primary) or secondary to a variety of
extraesophageal diseases (Table 1). Manometrically,
contraction waves with multiple peaks, peristaltic
waves with decreased amplitude, and isolated simultaneous or spontaneous contractions may be found
(Gelfand and Botoman 1987). These contraction
abnormalities do not fit into one of the aforementioned categories of specific motor disorders.
Radiologically, incomplete or absent peristalsis
and nonpropulsive contractions can be seen. The
sensitivity of radiographic studies is only 46–73%,
because intermittent contraction abnormalities may
elude radiographic detection (Ott et al. 1987; Schima
et al. 1992). Clinically, it is important to search for
underlying diseases, such as diabetes, alcoholism,
eosinophilic esophagitis, and progressive systemic
sclerosis (PSS), which may cause esophageal motility
disorders (secondary motility disorders). In these
cases, therapy is directed at the underlying disorder.
Especially eosinophilic esophagitis may mimic all
categories of motor disorders, including nutcracker
esophagus and vigorous achalasia (Hejazi et al. 2010).
Appropriate treatment may reverse motor abnormalities to the normal state.
5.7 Presbyesophagus
5.5 Esophageal Atresia
In infants with esophageal atresia, Vogt’s classification is based on the presence and location of an esophagotracheal fistula (Hasse 1968). After esophageal
repair, swallowing difficulties are common. The most
common source of postoperative dysphagia is the
presence of strictures; however, esophageal dysfunction is also common (Auringer and Sumner 1994).
There is absence of swallow-induced primary
Soergel et al. (1964) reported a high incidence of
esophageal motor abnormalities in elderly individuals, for which they coined the term ‘‘presbyesophagus.’’ In their study on nonagenarians, nonpropulsive
contractions were prevalent in ten of 15 patients.
However, the existence of such a clinical entity has
been much disputed. In another study (Hollis and
Castell 1974), esophageal peristalsis was not found to
be abnormal in elderly healthy individuals. It has been
suggested that the increased prevalence of esophageal
motor abnormalities is likely a function of an
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Fig. 7 Progressive systemic sclerosis: early stage. a Videoflu-
oroscopy with the patient in the prone oblique position shows
normal peristaltic contraction in the proximal, striated muscle
part of the esophagus. b The peristaltic wave subsides in the
middle third of the esophagus with massive retention of barium,
increased prevalence of underlying diseases, such as
diabetes and neuromuscular disorders, which can
affect esophageal motility (Ekberg and Feinberg
1991; Price and Castell 1978). It is most important in
elderly individuals with newly developed dysphagia
to rule out the presence of a tumor or a stricture
before making the diagnosis of a motor disorder.
6 Secondary Motility Disorders
6.1 Progressive Systemic Sclerosis
and Other Connective Tissue
Diseases
Esophageal dysmotility is a well-known feature of
PSS (or scleroderma) (Campbell and Schultz 1986)
and other connective tissue diseases. PSS often affects
the gastrointestinal tract, especially the esophagus and
the small bowel, resulting in fibrosis and atrophy of
smooth muscle. Esophageal involvement in PSS
where the smooth muscle segment is affected results
in hypomotility of the distal esophagus with absence
of peristalsis and a patulous lower esophageal
indicative of hypomotility. c There is no evidence of narrowing
of the gastroesophageal junction. Together with the clinical
history, this is typical of esophageal involvement in progressive
systemic sclerosis
because of the incompetent sphincter, and refluxed
acidic gastric contents are not readily cleared from the
esophagus by secondary peristalsis. Esophageal
symptoms, especially heartburn and dysphagia, are
common in PSS. Such symptoms are found in up to
50% of patients (Sprung and Gibb 1985).
In the early stages of esophageal involvement, there
is weak peristalsis in the distal esophagus (Montesi
et al. 1991). Radiographically, the esophagus may be
air-distended for a prolonged period after swallowing,
without exhibiting the typical swallowing-induced
collapse of the lumen due to a peristaltic contraction.
In the prone oblique position,hypomotility is presentin
the distal esophagus with retention of barium (Fig. 7).
With more advanced disease, esophageal dilatation
and apatulous lower esophageal sphincter are apparent
(Fig. 8). With the patient in the prone oblique position,
complete aperistalsis with severe retention of barium
(and saliva) will be found. Oropharyngeal dysfunction,
including pharyngeal retention and aspiration, is found
in 26% of patients (Montesi et al. 1991). Patients with
an oropharyngeal disorder have a higher incidence of
PSS-related pulmonary disease.
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Esophageal dysmotility has also been reported to
occur in patients with dermatomyositis/polymyositis
and mixed connective tissue disease. Radiographic
findings are nonspecific, including low-amplitude
peristalsis, aperistalsis, and delayed esophageal
emptying on scintigraphy (Marshall et al. 1990;
Horowitz et al. 1986).
6.2 Diabetes Mellitus
Esophageal symptoms are common in patients with
diabetes, and the likelihood of dysphagia is more than
threefold higher than in nondiabetic controls (Bytzer
et al. 2001). Esophageal motor dysfunction has been
demonstrated, characterized by weak peristalsis and
increased frequency of nonpropulsive contractions
(Hollis et al. 1977; Holloway et al. 1999). Not
surprisingly, a relation between the presence of
Fig. 8 Progressive systemic sclerosis: advanced disease.
a Barium radiography demonstrates esophageal dilatation
and a widely patent gastroesophageal junction (arrows). b
In another patient, there is obvious distal fold thickening
indicative of reflux esophagitis. Barium radiography also shows
a slight peptic stricture in the distal esophagus (arrow)
As esophageal dysmotility progresses, gastroesophageal reflux and its sequelae will predominate.
Severe reflux esophagitis, strictures, and Barrett
esophagus develops (Fig. 8). In the early advanced
stages of the disease, differentiation between PSS and
achalasia can be made with a high level of certainty.
Although aperistalsis and esophageal dilatation are
present in both diseases, the shape of the gastroesophageal junction is markedly different. However,
the development of distal peptic strictures in PSS may
be confusing, although these strictures almost never
have the bird-beak-like appearance seen in achalasia.
PSS patients with severe reflux esophagitis are at
increased risk of developing Barrett esophagus and,
subsequently, adenocarcinoma (Sprung and Gibb
1985). Although barium radiography and videofluo-
roscopy are very sensitive (67–100%) for the detection of motor dysfunction in PSS (Campbell and
Schultz 1986; Schima et al. 1992), these tests are not
very accurate in the detection of peptic complications.
For this reason, close endoscopic surveillance of PSS
patients with reflux esophagitis and peptic strictures is
recommended.
esophageal dysmotility and diabetic neuropathy has
also been reported (Mandelstam et al. 1969; Hollis
et al. 1977). It has been suggested that autonomic
neuropathy of the vagal nerve supplying the esophagus plays a major role in the development of diabetic
dysmotility (Holloway et al. 1999). Radiographically,
weak peristalsis or nonpropulsive contractions can be
observed (Borgström et al. 1988).
6.3 Chagas Disease
Chagas disease (South American trypanosomiasis) is
caused by infection with the protozoon Trypanosoma
cruzi (Dantas et al. 1999). In the chronic phase, the
disease most often involves the heart, esophagus,
and colon, causing cardiomegaly, megaesophagus,
and megacolon. Chagas disease and achalasia share
the same histopathologic lesion and the loss of
ganglion cells within the esophageal myenteric
plexus (Dantas et al. 2001), which are destroyed by
the infectious organism in Chagas disease. The
clinical and radiological appearance of achalasia and
Chagas disease may be identical (Fig. 9). Manometry may help to differentiate the two by identifying a
higher resting pressure of the lower esophageal
sphincter pressure in Chagas disease. The geographic
origin of the patient may also provide a clue to the
right diagnosis, and proof of Chagas disease is based
on serologic testing.
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Fig. 9 Megaesophagus in a
14-year-old boy with Chagas
disease. Barium radiography
reveals esophageal dilation
with tapering of the sphincter
indistinguishable from
idiopathic achalasia.
(Courtesy of Roberto Dantas,
Ribeirão Preto, Brazil)
7 Esophageal Diverticula Associated
with Motility Disorders
Esophageal diverticula are included in this chapter
because they are associated with an esophageal
motility disorder in the vast majority of cases.
Classification is based in the location: Zenker’s
diverticulum above the pharyngoesophageal sphincter
(i.e., a pharyngeal diverticulum that will not be
covered in this chapter), midesophageal diverticulum
just inferior to the level of the aortic arch, and epiphrenic diverticulum just above the diaphragm.
7.1 Midesophageal Diverticula
In the past, midesophageal diverticula were widely
considered to be traction-type diverticula of no clinical
significance (Schmidt et al. 1991). Recently, this view
has been questioned by some studies, which have shown
that these diverticula resemble more the pulsion-type
diverticula (Borrie and Wilson 1980; Evander et al.
1986). Kaye (1974) reported on associated esophageal
motor disorders found by manometry. In a series of 12
patients, diffuse spasms and nonspecific contraction
abnormalities were the most common findings.
6.4 Other Secondary Motility
Disorders
There are a variety of other diseases and clinical
conditions that may affect the esophagus and cause a
secondary motility disorder (Table 1), including
amyloidosis (Rubinow et al. 1983; Lefkowitz et al.
1989; Burakoff et al. 1985), alcoholism (Grande et al.
1996), myxedema (Wright and Penner 1981), hyper-
thyroidism, parkinsonism (Leopold and Kagel 1997),
graft-versus-host disease (Schima et al. 1994),
Sjögren syndrome (Kjellén et al. 1986; Palma et al.
1994), and eosinophilic esophagitis (Hejazi et al.
2010). In all these diseases, except PSS and Chagas
disease, which have a typical radiographic appearance, nonspecific esophageal function abnormalities
have been found. Therefore, in all patients with an
otherwise unexplained dysphagia and a nonspecific
esophageal contraction abnormality, the search should
be directed toward the detection of and therapy for an
underlying disease.
On the basis of radiographic findings, Rivkin et al.
(1984) pointed out that midesophageal diverticula are
likely of the pulsion type. The pear-shaped configuration of most diverticula and their movement on swallowing resembles the appearance of Zenker’s and
epiphrenic diverticula. In our study including 30
patients with 33 midesophageal diverticula, 80% were
diagnosed as propulsion-typediverticula on thebasis of
radiographic findings. Diverticula were classified as
pulsion-type when they were pear-shaped, when the
size and shapechanged during bolus passage, and when
there was upward and downward movement of the
diverticulum of at least 2 cm upon swallowing
(Fig. 10) (Schima et al. 1997). In this study, 88% of
patients with a pulsion diverticulum suffered from an
esophageal motor disorder,and six of 20patients (30%)
were diagnosed as having achalasia as evidenced by
videofluoroscopy and manometry (Schima et al. 1997).
In conclusion, midesophageal diverticula in symptomatic patients are primarily of the pulsion type and
tend to be associated with esophageal motor disorders.
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Fig. 10 Midesophageal
propulsion diverticulum in a
patient with nonspecific motor
disorder. a The spot film of
the esophagus taken during
deglutition is normal.
b Another spot film taken
approximately 2 s later shows
outpouching of a propulsion
diverticulum in the
midesophagus (arrow).
A nonspecific motor disorder
was found by
videofluoroscopy
7.2 Epiphrenic Diverticula
Epiphrenic diverticula are generally associated with
and probably caused by an underlying esophageal
motor dysfunction. Approximately two thirds of
patients will have specific motor disorders, with
achalasia the most common (Bruggeman and Seaman
1973; Debas et al. 1980) (Fig. 11). The high per-
centage of motor abnormalities in association with
epiphrenic diverticula determines the therapeutic and
especially the surgical approach. Patients should
always be referred for manometry to search for a
curable manometric disorder before surgical resection
of a ‘‘symptomatic’’ midesophageal diverticulum
(Fig. 10). In these cases, diverticulectomy alone carries the risk of postoperative suture breakdown and
predisposes the patient to recurrence of the diverticulum (Rivkin et al. 1984). Myotomy of the lower
esophageal sphincter is now a routine part of the
operation (Evander et al. 1986).
8 Gastroesophageal Reflux Disease
and Esophageal Function
The term ‘‘Gastroesophageal reflux disease’’ (GERD)
covers the entire spectrum of clinical conditions and
histologic esophageal alterations that result from
gastroesophageal reflux (Dodds 1988). GERD is by
far the most common cause of esophagitis in the
general population. In the last 15–20 years, our
knowledge of the cause and pathogenesis of gastroesophageal reflux and the development of esophagitis
has considerably broadened. The pathogenesis is
multifactorial and the factors believed to be important
include (1) inadequate antireflux mechanisms, (2)
chemical consistency of refluxed material, (3) esophageal clearance of refluxed material, (4) esophageal
mucosal resistance, and (5) volume of gastric contents
and efficacy of gastric emptying (Dodds et al. 1981;
Dodds 1988).
8.1 Hiatal Hernia and Reflux
In the past, the finding of a hiatal hernia was considered the most important predisposing factor for the
development of reflux. The exact prevalence of hiatal
hernia in the general population remains unknown,
largely because of the differences in examination
techniques and diagnostic criteria (Fransson et al.
1989; Ott et al. 1985; Kahrilas et al. 1999). The
relationship between the presence of a hiatal hernia
and reflux disease remains controversial. Several
studies have found that a hiatal hernia is much more
common in patients with symptomatic reflux or
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