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Evaluation of Symptoms 79
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their beginning, time characteristics (intermittent or
constant occurrence), and influencing factors. However, it is important to know about the influence of
bolus consistency on swallowing. In neurologic
patients with impaired swallowing reflex and uncoordinated swallow, swallowing liquids is more difficult than semisolids, because they cannot be controlled
well. Patients with obstructive diseases (tumors,
strictures, webs) often report sticking of solid food,
whereas patients suffering from esophageal motility
disorders complain about swallowing problems with
both liquids and solid food. To estimate the patient’s
oral intake, a description of his meals and weight
during the last weeks may be valuable.
Furthermore, information regarding previous
illnesses andtherapies (surgery, radiation—often years
before), as well as medication, needs to be obtained.
The side effects of many drugs can impair swallowing:
psychopharmacological drugs possibly interfere with
the swallow reflex or induce xerostomia, antipsychotic
drugs can cause extrapyramidal symptoms, and
spasmolytics may weaken muscles. It has to be pointed
out that changes in voice, speech and language should
be carefully noted. Above all, the examinershould also
take into consideration the patient’s general condition,
his nutritional status (body weight), and posture, and
cognitive and emotional state. Due to the epidemiological changes, dementia will become a challenging
problem in our society, and dysphagia may be an early
or accompanying symptom. Depending on the
patient’s needs, a holistic approach, including the mini
mental status (Folstein et al. 1975) or the mini nutritional assessment MNA
can help to judge the patient’s clinical condition.
Questionnaires may help describe the impaired
quality of life due to dysphagia (e.g., The MD
Anderson dysphagia inventory, Chen et al. 2001, the
dysphagia handicap index, Silbergleit et al. 2012).
TM
(Nestlé Nutrition Services),
(with sensory testing), see also Sect. 6.2.4) has to be
performed. It is a non-invasive dynamic procedure that
delivers an immediate evaluation of pharyngeal swallowing function and directly visualizes the upper
aerodigestive tract. However, it has the following limitations: no direct visualization of the bolus on it’s
entire way from the oral cavity to the stomach, no
visualization during the swallow, novisualization of the
oral and esophageal phases and pharyngo-esophageal
segment. Therefore, a videofluoroscopic swallowing
study (Ekberg 1992;Logemann1993, 1998) has to be
carried out routinely in many cases as a complementary
dynamic diagnostic procedure.
7.3 Further Examinations
If necessary, further diagnostic methods are used
(Table 4). Depending on the results of videoendoscopic and videofluoroscopic swallowing studies, esophago-gastroscopy can eventually be performed as a
first-line diagnostic method to exclude tumorous
lesions or reveal disturbances in the esophageal phase
(see also Sect. 6.3). Scintigraphy enables the quantification of bolus transit and aspiration. For an evaluation
of neurogenic dysphagia, cranial magnetic resonance
imaging (MRI) may detect intracranial lesions
responsible for dysphagia. Impedance pH-metry represents the gold standard for diagnostics of suspected
gastroesophageal (-pharyngeal) reflux disease. To
measure the pressure in the pharynx (especially before
surgery of the pharyngo-esophageal segment) impedance manometry, which allows measurement of the
intrabolus pressures and pharyngeal contraction, is
recommended. Cervical auscultation of the pharyngeal
swallow did not gain wide acceptance.
8 Conclusion
7.2 Basic Diagnostic Procedure
The ENT examination plays an important ‘‘key’’ role in
the diagnostic work-up because it allows a direct morphological and functional analysis of the upper aerodigestive tract. Since clinical observation and palpation
of the swallow alone do not meet the diagnostic
demands, a videoendoscopic swallowing study, (FEES
(ST), fiberoptic endoscopic evaluation of swallowing
Swallowing disorder symptoms necessitate an interdisciplinary, holistic, and thorough diagnostic workup that reveals etiologic factors and pathophysiological components. The patient should be asked precise
questions relating to symptoms, and valuable information should be obtained, allowing suitable diagnostic and therapeutic measures to be taken. Above
all, the adequacy of oral nutrition and the presence or
absence of aspiration is within the focus of diagnostic

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and therapeutic interests. Due to an absent cough
reflex, aspiration may occur silently. Therefore,
diagnostic methods must enable direct visualization
of aspiration by videoendoscopy and videofluoroscopy. Aspiration cannot be diagnosed or excluded by
patient history or clinical observation alone. However, for appropriate management, the patient’s
symptoms should be carefully evaluated.
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Neurology of Swallowing and Dysphagia
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Mario Prosiegel
Contents
1 Neuroanatomy and Neurophysiology .................... 83
1.1 Cerebral Hemispheres ............................................... 84
1.2 Brainstem................................................................... 85
1.3 Pseudobulbar and Bulbar Palsy ................................ 86
1.4 Upper Esophageal Sphincter..................................... 87
2 Examinations............................................................ 88
2.1 Clinical Examinations ............................................... 88
2.2 Instrumented Methods ............................................... 89
3 Diseases Associated with Neurogenic
Dysphagia.................................................................. 90
3.1 Diseases of the Central Nervous System ................. 90
3.2 Diseases of the Cranial Nerves................................. 98
3.3 Diseases of the Neuromuscular Junction.................. 98
3.4 Diseases of the Muscles ............................................ 99
3.5 Iatrogenic Causes....................................................... 101
3.6 Special Diagnostic Approaches................................. 102
3.7 Therapy ...................................................................... 102
References.......................................................................... 103
Abstract
Neurogenic dysphagia is difficulty swallowing due
to neurological diseases and compromises especially the oral and/or pharyngeal stage. The first
section of this chapter deals with the neuroanatomy
and neurophysiology of swallowing as a basis for a
better understanding of neurogenic dysphagia.
Then, diagnostic approaches are described comprising history taking, screening examinations,
clinical swallowing examination, and instrumental
methods. The third section focuses on those
neurological diseases which are frequently associated with dysphagia and ends with the description
of the problem that only a few pharmacological
and invasive therapeutic interventions against
neurogenic dysphagia exist. This expressly underlines the need for swallowing therapy and the
development of new therapeutic approaches such
as electrical pharyngeal or repetitive transcranial
magnetic stimulations.
1 Neuroanatomy
and Neurophysiology
M. Prosiegel (&)
Abteilung Neurologie, m&i-Fachklinik Bad Heilbrunn,
Wörnerweg 30, 83670 Bad Heilbrunn, Germany
e-mail: mario.prosiegel@fachklinik-bad-heilbrunn.de
O. Ekberg (ed.), Dysphagia, Medical Radiology. Diagnostic Imaging, DOI: 10.1007/174_2011_339,
Ó Springer-Verlag Berlin Heidelberg 2012
This section deals with neuroanatomical and neurophysiological basics of normal and abnormal swallowing: What role do the cerebral hemispheres and
the brainstem play in deglutition? How can the
pathogenesis of pseudobulbar as well as of bulbar
palsy be explained?
Besides such topics, one focus lies also on the
upper esophageal sphincter (UES), because opening
deficits of the UES are very frequent in neurogenic
83

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Fig. 1 Swallowing cortex, corticobulbar fibers, and lower
brainstem. Top left: Right cerebral hemisphere with the
frontoparietal operculum (closed circle) and the representational areas of the esophagus (E), pharynx (P) and oral region
(O). In this example, the right hemisphere is swallowingdominant, with more corticobulbar fibers (long thick arrows)
projecting to the ipsilateral and contralateral medulla. Top
right: Left hemisphere after removal of the operculum; the
insula with its anterior swallowing-relevant part (black area)
can therefore bee seen. Bottom: Axial view of the lower
dysphagia (for other swallowing muscles see the
chapter ‘‘Anatomy and Physiology’’ by O. Ekberg and
G. Nylander, this volume).
1.1 Cerebral Hemispheres
In their pioneering work, Penfield and Boldrey (1937)
from the Montreal Neurological Institute in Canada
performed intraoperative electrical stimulations of the
cerebral cortex in awake patients. Thereby, they
found certain sensorimotor representational areas
with the net result of the well-known sensorimotor
homunculus (the ‘‘little man inside the brain’’). With
regard to swallowing, they elicited deglutition by
stimulation of the frontoparietal operculum, i.e., the
lower portion of the precentral gyrus (primary motor
brainstem (medulla; lower part=anterior; upper part=posterior).
On the right side (left side of the medulla) the nucleus of
the solitary tract (NST), the nucleus ambiguus (NA), and the
hypoglossal nucleus (HN) are shown. On the left side (right side
of the medulla) the dorsomedial and ventrolateral central
pattern generators for swallowing are shown (red area and blue
area, respectively). The horizontally lined area corresponds to
the site of a dorsolateral medullary infarction with consecutive
Wallenberg’s syndrome. For details, see the text
area), of the premotor cortex, and of the postcentral
gyrus (primary sensory area)––corresponding to
Brodmann’s areas (BA) 4 (motor), 6 (premotor), and
3, 2, and 1 (sensory), respectively.
Magnetic resonance imaging (MRI) and functional
imaging of the brain, including functional MRI, positron emission tomography, and magnetoencephalography, confirmed these earlier findings and showed
that also the anterior insula (BA 14–16) is involved in
volitional swallowing (Barritt and Smithard 2009;
Hamdy et al. 1999; Humbert and Robbins 2007;
Riecker et al. 2009). Furthermore, by use of
transcranial magnetic stimulation it was found that the
esophageal, pharyngeal, and oral muscles are
discretely represented within the motor cortex in a
rostrocaudal direction, with esophageal muscles being
situated more rostrally than the pharyngeal muscles,

Neurology of Swallowing and Dysphagia 85
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which in turn are more rostral than the oral muscles
(Hamdy et al. 1996) (Fig. 1).
Functional brain imaging studies also showed that
the swallowing cortex is represented bilaterally, but
asymmetrically, i.e., it is (in most people) bigger on
one side than on the other. The bigger swallowing
cortex is called the dominant one. Swallowing domi-
nance is independent of the language-dominant side
or of handedness (Barrit and Smithard 2009; Hamdy
et al. 1999).
The fibers which project from the motoneurons of
the swallowing cortex to both sides of the brainstem
are called corticobulbar fibers and constitute the
corticobulbar (corticonuclear) tract. When the dominant swallowing cortex and/or its corticobulbar fibers
are affected, a significant hemispheric dysphagia
occurs (hemispheric dysphagia means swallowing
problems caused by cortical and/or subcortical lesions
of the left and/or the right cerebral hemisphere,
i.e., supratentorial lesions) (Fig. 1). Additionally,
right-sided cortical lesions are often associated with
‘‘neglect of swallowing,’’ ‘‘food stuffing,’’ and consecutive problems in the pharyngeal phase (Robbins
and Levin 1988), whereas left-sided lesions may
cause swallowing apraxia with corresponding problems in the oral phase (Daniels 2000). Independent of
these behavioral/neuropsychological problems, leftsided and right-sided areas of the swallowing cortex
seem to play different roles during the early and later
phase of swallowing, respectively (Teismann et al.
2009).
Besides the abovementioned swallowing areas,
other cortical and subcortical regions are involved in
swallowing function, such as the supplementary
motor area (SMA) corresponding to the medial part of
BA 6, the basal ganglia, and many others. The SMA
is responsible for the generation of the readiness
potential (Bereitschaftspotential), which arises about
1 s before a volitional motor action. It was shown that
also a swallowing potential (Schluckpotential) exists,
which is generated in the SMA too, but spreads to
both primary motor areas (whereas the readiness
potential spreads to the motor area which is contralateral to the innervated extremity) (Huckabee et al.
2003).
According to Mosier and Bereznaya (2001) one
can distinguish two swallowing networks: (1) an
‘‘insular loop’’ including the insula, the primary sensorimotor motor cortex, premotor cortex, posterior
parietal cortex, and the SMA/cingulate gyrus; (2) a
‘‘cerebellar loop’’ comprising the cerebellum, the
SMA/cingulate gyrus, the inferior frontal gyrus, the
secondary sensory cortex, the corpus callosum, and
the basal ganglia as well as the thalamus. The influence of the insula within the ‘‘insular loop’’ might be
necessary to synchronize the kinematics of the swallowing movements, whereas the ‘‘cerebellar loop’’
might optimize and modulate movements using
feedback information.
As shown by Power et al. (2007), the swallow
response time is prolonged in dysphagic patients as
compared with healthy volunteers owing to unilateral
hemispheric stroke. Interestingly enough, in these
stroke patients a sensory deficit of the faucial pillars
was found bilaterally in 66% and the duration of
laryngeal delay and the degree of the sensory deficit
were associated with the severity of predeglutitive
aspiration. Very similar results were found in a recent
study by Oommen et al. (2010): the stage transition
time duration was significantly longer in 52 poststroke patients—19 aspirators and 33 nonaspirators—
than in 12 healthy controls.
Since the cortical swallowing network comprises
many sensorimotor areas, one can speculate that
sensory input is very critical for an intact swallowing.
This view was confirmed by a recent study in decerebrate pigs: the sensory threshold for the swallowing
response was increased, since the facilitatory pathways descending from cerebral structures to the
brainstem had been lost (Thexton et al. 2007).
Therefore, important roles of the cerebral cortex in
deglutition seem to be initiation of swallowing,
ensuring a normal coupling of the oral and pharyngeal
phase (stage transition time) as well as normal
sensory properties of the oropharyngeal region,
direct modulation of swallowing, and modification
of brainstem swallowing responses—in each case
mainly dependent on sensory inputs (see also
Sect. 1.2).
1.2 Brainstem
Doty and Bosma (1956) conducted a pioneering study
on the role of the brainstem in swallowing. By electrical stimulation of the superior laryngeal nerve with
30 Hz in different animals, including monkeys,
they could elicit the complete sequential pattern of

86 M. Prosiegel
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activation or inhibition of swallowing muscles of the
pharyngeal phase. Therefore, they postulated the
existence of a swallowing center in the medulla
oblongata; this view was confirmed later (for a
review, see Jean 2001). There are four swallowing
centers—two on each side of the brainstem— for
which the term ‘‘central pattern generators’’
(CPGs) for swallowing was coined. The dorsomedial CPGs (dmCPGs) are situated close beside the
nucleus of the solitary tract (NST) and the adjacent
reticular formation; they contain so-called master
neurons/programming interneurons which generate
the temporal–spatial sequence of pharyngeal swallowing muscle activation or inhibition. This information is transmitted to ventrolateral CPGs situated
near the nucleus ambiguus (NA); switching neurons/
command interneurons of the ventrolateral CPGs
distribute the timed output to the cranial nerve
nuclei V and VII in the pons as well as to the
cranial nerve nuclei IX, X, and XII in the medulla
oblongata (Fig. 1). The functioning of the brainstem
central network can be influenced by peripheral
inputs—e.g., from oropharyngeal mucosal receptors
and muscle spindles of the tongue—as well as by
central inputs from the cortex; both inputs converge
at the NST and serve in particular to adapt the
swallowing drive to properties of the bolus to be
swallowed. The brainstem is also important for
coordinating interactions between respiration and
swallowing (Jean 2001; Miller 1993).
Owing to the role of the brainstem in swallowing,
unilateral lesions of the medullary region—such as in
Wallenberg’s syndrome caused by unilateral infarctions in the supply area of the posterior inferior cerebellar artery (Fig. 1)—affecting both ipsilateral
CPGs and the NA and the NST, cause complex
swallowing disturbances, including unilateral pharyngeal paresis (NA), impaired pharyngeal peristalsis
(NA and dmCPG), sensory deficits in the oropharyngeal region (sensory trigeminal nucleus and NST),
and secondary UES opening deficit due to impaired
hyolaryngeal excursion and/or primary UES opening
disturbance due to impaired sphincter relaxation
(dmCPG) (Prosiegel et al. 2005a). Dysphagia
may be the sole symptom in dorsolateral medullary
infarctions but is—owing to ipsilateral vagal paresis—often associated with hoarseness due to unilateral vocal cord paresis. Other symptoms belonging to
Wallenberg’s syndrome are rotatory nystagmus,
ipsilateral Horner’s syndrome, numbness of the face,
and ataxia as well as contralateral hypalgesia and
thermhypesthesia.
1.3 Pseudobulbar and Bulbar Palsy
Two frequently occurring syndromes associated with
dysphagia are pseudobulbar palsy and bulbar palsy.
Pseudobulbar palsy is caused by bilateral lesions of
the cerebral cortex and/or its corresponding corticobulbar fibers, including those passing through the
brainstem. In contrast, bulbar palsy (‘‘bulbus’’ is an
outdated term formerly used for the lower brainstem)
is due to bilateral lesions of pontine and medullary
cranial nerve nuclei or their axons or is due to bilateral lesions of the cranial nerves themselves.
1.3.1 Pseudobulbar Palsy
The motoneurons of the swallowing cortex are
called first motoneurons or upper motoneurons
(UMNs). When the swallowing cortex itself and/or
and its axons, i.e., the corticobulbar fibers, are
lesioned bilaterally, there is diminished input to the
brainstem. The consequence is severe dysphagia
which affects predominantly the volitional oral
phase. Owing to impaired cortical input, the membrane of the motoneurons in the brainstem lower
their electrical threshold with consecutive hyperreflexia (e.g., enhanced masseter reflex) and muscle
stiffness in terms of spasticity. There are no muscle
atrophies, since the second motoneurons/lower
motoneurons (LMNs) in the brainstem are intact
and, therefore, able to supply the corresponding
muscles with the transmitter acetylcholine. This
syndrome is called pseudobulbar palsy and occurs
in UMN diseases (UMNDs); examples are amyotrophic lateral sclerosis (ALS) due to bilateral
degeneration of the UMNs or bilateral subcortical
infarctions affecting the corticobulbar tracts. In most
cases of pseudobulbar palsy, besides dysphagia also
dysarthria and chewing problems occur; pathological crying or laughing is often associated with
pseudobulbar palsy too. Bilateral lesions of the
corticobulbar tract in the brainstem (e.g., in bilateral
anterior mesencephalic infarctions) may also cause
pseudobulbar palsy. Very typical for pseudobulbar
palsy is automatic–voluntary dissociation: emotional
or reflex responses are intact or enhanced, whereas

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volitional activities are disturbed e.g., enhanced
palatal reflex, but no elevation of the soft palate
during phonation of /A/ or videofluoroscopic study
of swallowing (VFSS) is also spasm of the cricopharyngeal muscle.
1.3.2 Bulbar Palsy
In contrast to pseudobulbar palsy, muscle atrophy
occurs when the cranial nerve nuclei in the brainstem
(or the motoneurons in the spinal cord)—i.e., the
LMNs—are affected. Because of diminished input to
the corresponding muscles, the muscular membrane
develops a decreased electrical threshold with consecutive pathological spontaneous activity. This can
be assessed electromyographically or seen clinically
in the form of fibrillations of the atrophic tongue
(jerks of muscle fibers) or fasciculations of the face or
body musculature (jerks of groups of muscle fibers).
Other features are weakness of the orofaciopharyngeal muscles and decreased muscle tone in terms of
hypotonia with diminished reflexes as well as bulbar
(slurred) speech. This syndrome, which is caused by
affection of the LMNs, is called bulbar palsy and
occurs in LMN diseases (LMNDs) such as ALS (ALS
is an example of a combined UMND and LMND).
Bulbar palsy may also be caused by lesions of the
fibers of the cranial nerve nuclei or of the cranial
nerves themselves.
1.4 Upper Esophageal Sphincter
The UES is defined as a high-pressure zone with a
rostrocaudal extension of 2–6 cm, which maintains a
closed pharyngoesophageal junction and opens phasically during various physiological states (Lang
and Shaker 1997). It consists of striated muscles
comprising the inferior pharyngeal constrictor, the
cricopharyngeal muscle and the upper esophageal
musculature. In contrast to the other swallowing
muscles, the UES forms a network together with
connective tissue (approximately 40%) and consists
of more than 70% of slow twitch (tonic, type I) fibers.
The number of these tonic fibers is especially high in
the horizontal part of the cricopharyngeal muscle as
compared with its oblique part as well as in the slow
inner layer as compared with the fast outer layer of
the UES. Acetylcholine is the transmitter which binds
to the nicotinic motor end plates of the muscle fibers,
but many other transmitters (mainly found in blood
vessels, glands, and the mucosa) occur in the UES,
including neuropeptide Y, calcitonin-gene-related
peptide, tyrosine hydroxylase, substance P, and
vasoactive intestinal polypeptide. The slow inner
layer is innervated by cranial nerve IX (glossopharyngeal nerve), whereas the fast outer layer is supplied by different branches of cranial nerve X (vagus
nerve) in the following manner: (1) inferior pharyngeal constrictor ––pharyngoesophageal nerve forming
the pharyngeal plexus; external superior laryngeal
nerve; (2) cricopharyngeal muscle––pharyngeal
plexus; external superior laryngeal nerve; recurrent
laryngeal nerve (RLN); (3) upper esophageal musculature––recurrent laryngeal nerve (for a review, see
Mu and Sanders 2007).
UES opening is a very complex event. Firstly,
relaxation of the UES muscles occurs (as can be shown
electromyographically). Secondly, about 100 ms later,
there is a reduction of UES pressure (as can be shown
by use of manometry). Thirdly, again about 100 ms
later, UES opening occurs caused by two forces which
have to overcomethe resistance (R)ofthe sphincter: (1)
traction forces, exerted by the suprahyoid muscles
during anterior–superior hyolaryngeal excursion,
widen the cricopharyngeal muscle, since the cricopharyngeal muscle originates from the arch of the cricoid cartilage; (2) tongue base retraction with
approximation ofthe baseof thetongue tothe posterior
pharyngeal wall generates the force responsible for the
primary pressure on the descending bolus (shortening
of the pharynx helps the bolus meet the UES). These
forces (F)/pressures (P) can be described mathematically as follows: F
Traction
? P
Intrabolus
[ R
UES
(for a
review, see Lang et al. 1991). Pharyngeal peristalsis
is also important, but its predominant role is to clear
pharyngeal bolus residuals.
Defective opening of the UES due to increased
tonicity occurs frequently in patients with dysphagia
due to medullary lesion (such as in Wallenberg’s
syndrome or Parkinson’s disease (Williams et al.
2002) and is sometimes called cervical achalasia.
Defective tonicity of the UES between swallows
(cervical chalasia) may occur in motonic dystrophy,
myasthenia gravis, during ‘‘off’’ periods of Parkinson’s
disease, and after radiotherapy of the neck; it is often
asymptomatic, but may cause aerophagia, belching,
and/or regurgitation of refluxed material (Ekberg and
Olsson 1995).

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chewing or swallowing; residuals of food in the
2 Examinations
Diagnostics in (suspected) neurogenic dysphagia
comprise history taking, clinical swallowing examination, and instrumental methods. Bedside screening
tests are only necessary in certain cases, which are
described in Sect. 2.1.2.
Special diagnostic approaches such as laboratory
examination and MRI are dealt with in Sect. 3.6.
mouth after swallowing; nasal regurgitation of food or
liquids; feeling of ‘‘food sticking’’ (where?); need for
repetitive swallowing in order to remove all residuals;
breathing problems; prior or current disease such as
chronic pulmonary obstructive disease; prior surgery/
medical therapy such as anterior cervical surgery,
carotid endarterectomy, or radiochemotherapy for
head and neck cancer; current status such as dependence on a percutaneous endoscopic gastrostomy
(PEG) tube, nasogastric tube or tracheal cannula;
prior and current medication.
2.1 Clinical Examinations
2.1.2 Bedside Screening Examinations
2.1.1 History Taking: Signs and Symptoms
in Neurogenic Dysphagia
In many textbooks or articles one can find the statement that dysphagia for liquids is typical for neurogenic dysphagia. Although it often occurs, it is,
however, not a pathognomonic symptom for dysphagia of neurogenic origin. In reality, there is a
broad range of different signs and symptoms occurring in patients with neurogenic dysphagia. During
history taking it is helpful to use a checklist of
questions and to ask the patient and his/her relatives
to try to answer them as accurately as possible.
Interestingly enough, in many cases the relatives may
observe, e.g., disturbances of feeding behavior or
postural changes which are not or not to the same
extent realized by the patients themselves.
Some of the most important signs and symptoms
are listed in the following: abrupt or gradual beginning of swallowing problems; difficulty with control
of saliva; problems with liquids and/or thick consistencies; problems with warm, hot, or cold liquids and/
or food; involuntary weight loss; eating and/or
drinking more slowly than in the time before symptom onset; eating and/or drinking smaller portions
than in the time before symptom onset; unexplained
fever and/or pneumonia; coughing and/or choking
and/or voice change (e.g., wet, hoarse, nasal) after
eating and/or drinking; drooling and/or sialorrhea;
increase of secretions; dry mouth; articulation problems (e.g., slurred speech); feeling of a ‘‘lump in the
throat’’; fear of swallowing; pain during swallowing
(where?); change of head or trunk posture during
swallowing; chewing problems; problems to propel
the bolus from the mouth backwards into the pharynx;
problems to hold the bolus in the mouth during
Bedside screening examinations should predict the
presence or absence of dysphagia or aspiration with
sufficient sensitivity and specificity (more than 70%)
(Doggett et al. 2002). A bedside screening examination seems to be especially helpful in acute illnesses
such as stroke; rapid therapeutic decisions have to be
made in those situations with regard to oral administration of food and water versus nil by mouth,
because there is often not enough time to perform a
clinical swallowing examination or instrumental
methods within 72 h. Bedside screening examinations
can, however, never replace an accurate clinical
swallowing examination or an instrumental method
such as flexible endoscopic evaluation of swallowing
(FEES) or VFSS (see Sect. 2.2), since the latter ones
are necessary for the assessment of the individual
swallowing disturbance patterns and thus for applying
the corresponding therapeutic interventions.
With regard to acute stroke, Hinchey et al. (2005)
convincingly demonstrated the importance of an early
screening procedure, which is reflected by the title of
their article: ‘‘Formal dysphagia screening protocols
prevent pneumonia.’’ Indeed, the most dangerous
complication of dysphagia is aspiration pneumonia;
but also malnutrition—defined as a body mass index
of less than 18.5 kg/m
elderly persons)—is an important variable, since its
occurrence during the acute stroke phase correlates
with a poor clinical outcome and with a prolonged
length of stay in the hospital (Finestone et al. 1996;
Gariballa et al. 1998).
The Standardized Swallowing Assessment was
developed for use by nurses within the first 24 h after
stroke; the sensitivity and specificity for detection of
dysphagia were 97% and 90%, respectively; a kappa
2
(or less than 20 kg/m2in

Neurology of Swallowing and Dysphagia 89
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value of 0.88 indicated good agreement with summative clinical judgment of swallow function (Perry
2001a, b). The Standardized Swallowing Assessment
consists of a preswallow screening checklist comprising seven questions/symptoms concerning level of
consciousness, ability to sit upright, volitional cough,
control of saliva, licking of the lips, breathing, and
voice; thereafter, a swallow screen consisting of a
water test is performed with consecutive recommendations for interventions (e.g., in the case of problems
such as coughing or choking after administration
of a teaspoonful of water, the recommendation is
‘‘patient nil by mouth,’’ ‘‘refer to speech and language
therapist’’).
A well-known instrument for assessing the risk of
aspiration in the acute stroke phase was developed by
Daniels et al. (1997), often referred to as the Daniels
test. In their study on 59 patients (within 5 days of
admission), the authors determined whether risk factors detected in the clinical examination approximated
the VFSS in identification of dysphagia severity. They
found that occurrence of two or more of the following
variables predicted aspiration with a sensitivity of
92.3% and a specificity of 66.7%, respectively:
dysarthria, dysphonia, abnormal (decreased or absent)
gag reflex, abnormal volitional cough, cough after
swallow, and voice change after swallow. The last
two items were assessed by use of a water test in
the following manner: patient in sitting position;
5-ml liquid bolus administered from a cup or straw,
progressed to 10- and 20-ml volumes; phonation of
/Ah/ (change in vocal quality?); all volumes administered twice, i.e., a total of 70 ml; termination of the
test in the case of cough or voice change immediately
after swallowing or within 1 min after ingestion of the
liquid.
With regard to aspiration risk and feeding recommendations, the clinical utility of the 3-oz water
swallow test was examined by Suiter and Leder
(2008) in 3,000 patients. The diagnostic categories
comprised 850 neurological disorders (most frequently stroke) and 232 neurosurgical disorders. The
patients were required to drink 3 oz (90 ml) of water
without interruption; the criteria for referral for further assessment of swallowing included inability to
complete the task, coughing, choking, or a wet-hoarse
vocal quality exhibited either during or within 1 min
of test completion. The sensitivity and specificity for
assessing the risk of aspiration were 96.5% and
48.7%, respectively. Owing to a high negative predictive value of 98.3%, passing the 3-oz water swallow test was a good predictor for the ability to tolerate
oral diet without further dysphagia testing. Failing the
test is, however, not a good predictor for unsuccessful
swallowing of water, since the false-positive rate is
very high. Because of the large amount of water, this
test should not be used in patients with compromised
medical status, e.g., in frail elderly persons, patients
in the acute stroke phase, or persons with severe
bulbar type of ALS.
2.1.3 Clinical Swallowing Examination
The clinical swallowing examination aims at detecting disturbances of specific swallowing components
as a basis for adequate therapeutic interventions. It
comprises—in descending order of cranial nerves—
the following examinations: decreased strength of
chewing muscles, asymmetry of the mandible, and
sensory impairment of the facial and oral region—
cranial nerve V; decreased strength and/or motility of
facial muscles, fasciculations of the facial musculature, and hypogeusia of the anterior two thirds of the
tongue—cranial nerve VII; decreased or absent palatal and pharyngeal reflex, unilateral pharyngeal wall
paresis (paralyzed side moving towards the healthy
side, also called ‘‘Vernet’s mouvement de rideau’’),
sensory impairment of the pharyngeal mucosa,
impaired phonation (e.g., wet, hoarse, nasal), disturbed breathing, e.g., stridor, impaired volitional
cough, and hypogeusia of the posterior third of the
tongue—cranial nerves IX and X; fibrillations and/or
atrophy of the tongue, decreased strength and/or
motility, and asymmetry of the tongue during rest (to
the healthy side) and protrusion (to the affected
side)—cranial nerve XII.
Other findings may include dyskinesia or dystonia
of the face, jaw, head, and neck; dysarthria; buccofacial apraxia; neglect; attention or memory deficits;
and impaired vigilance. Of special importance are
pseudobulbar and bulbar signs (see Sect. 1.3).
2.2 Instrumented Methods
The two most important instrumental methods are
FEES and VFSS. FEES is dealt with in the chapter
‘‘Endoscopy of the Pharynx and Esophagus’’ by
D.-M. Denk and R. Schöfl (this volume). Therefore,
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