Mechanisms of Dysphagia in Suprabulbar Palsy

With Lacunar Infarct

Cumhur Ertekin, MD; Ibrahim Aydogdu, MD; Sultan Tarlaci, MD;
A. Bulent Turman, MD, PhD; Nefati Kiylioglu, MD

Background and Purpose—The objective of the present study was to investigate the neural mechanisms of dysphagia in
suprabulbar palsy (SBP) with multiple lacunar infarct.
Methods—We evaluated the swallowing disorders of patients with SBP (n⫽34) and age-matched healthy control subjects
(n⫽35) by means of an electrophysiological method that recorded the oropharyngeal swallowing patterns. With this
method, dysphagia limit, the triggering of voluntarily initiated swallows, duration of laryngeal relocation time, and total
duration of oropharyngeal swallowing were recorded and measured. In addition, the EMG behavior of the
cricopharyngeal (CP) muscle of the upper esophageal sphincter was also assessed.
Results—In patients with SBP, the dysphagia limit in all except 1 patient was pathological with limits of ⬍20-mL bolus
volume, which is contrary to normal subjects, in whom the dysphagia limit exceeds the 20-mL bolus volume. Either
triggering of swallowing reflex was delayed (P⬍0.04), or the swallow could hardly be triggered in 7 patients on the
voluntary attempts for 3 mL water. Whenever the reflex swallowing could be triggered, it was slow and prolonged
(P⬍0.01). The CP muscle of the upper esophageal sphincter appeared to have become hyperreflexic and incoordinated
with laryngeal movements during swallowing.
Conclusions—It was proposed that the progressive involvement of the excitatory and inhibitory corticobulbar fiber systems
linked with the bulbar swallowing center is mainly responsible for the triggering difficulties of the swallowing reflex
and for the hyperreflexic/incoordinated nature of the CP sphincter. In addition, the dysfunction of the extrapyramidal
system has a specific role in the slowing of oropharyngeal swallowing and the accumulation of saliva in the mouth.
(Stroke. 2000;31:1370-1376.)
Key Words: dysphagia 䡲 electromyography 䡲 lacunar infarction 䡲 paralysis, bulbar 䡲 pharyngeal muscles
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S uprabulbar palsy (SBP) is a well known clinical syn-

drome that results from various pathologies. Multiple
lacunar infarcts are the most frequently encountered causes of
SBP.1 Problems associated with swallowing are common in
patients with SBP. The severity of dysphagia varies from
subclinical disorders to advanced clinical manifestations that
require nonoral feeding. Despite the high incidence and
long-standing course of dysphagia among patients with SBP
that result from multiple lacunar infarcts, the mechanisms of
swallowing function in these patients have scarcely been
studied. On the other hand, many aspects of dysphagia
associated with acute stroke have been well documented in
recent years.2– 8 In acute stroke with an identified location of
the infarct or hemorrhage, dysphagia can readily be evaluated
due to the restricted and solitary involvement within the
central nervous system. However, in patients with SBP with
lacunar infarcts, the multiple involvement of various ascend-
ing or descending long tracts and local neuronal circuits in the
central nervous system has made it difficult to analyze and to
understand the nature of swallowing disorders. In the present
study, the mechanisms of dysphagia in patients with SBP
with lacunar state were investigated clinically, and the elec-
trophysiological methods used to assess deglutition are
described.
Subjects and Methods
Thirty-four patients with SBP (24 men and 10 women) and 35
age-matched healthy control subjects (23 men and 12 women)
participated in the study. SBP with multiple lacunar state was
diagnosed according to the following criteria: (1) dysphagia, (2) dys-
phonia or dysarthria, (3) forced laughing/crying (emotional lability),
(4) brisk brain stem reflexes, including glabellar and mandibular
reflexes, (5) paresis of the tongue, (6) saliva accumulation in the
mouth, (7) signs of long tract involvement, (8) high blood pressure
(arterial hypertension), (9) history of previous cerebrovascular at-
tacks, and (10) CT scan or MRI with positive signs of multiple
lacunar infarcts. Although criteria 1, 7, 8, 9, and 10 were unequiv-
ocally found in all patients who were investigated, the presence of
the other criteria varied from patient to patient. The patients’ ages
ranged between 32 to 75 years, with a mean age of 61.9 years. The

Received October 16, 1999; final revision received March 9, 2000; accepted March 9, 2000.
From the Departments of Neurology (C.E., I.A., S.T., N.K.) and Clinical Neurophysiology (C.E., I.A.), Medical School Hospital, Ege University,
Bornova, Izmir, Turkey; and Department of Biomedical Sciences (A.B.T.), University of Sydney, Sydney, Australia.
Correspondence to Prof Dr Cumhur Ertekin, Nilhan Apt, 1357 Sok No: 1 D: 10, Alsancak, Izmir, Turkey. E-mail erteker@unimedya.net.tr or
neuron@med.ege.edu.tr
© 2000 American Heart Association, Inc.
Stroke is available at http://www.strokeaha.org

1370
 Ertekin et al
average duration of SBP since the onset of incident was 36 months
and ranged from 1 month to 9 years. Clinical symptoms and
dysphagia were stable in 13 patients, had shown some improvement
in 3, and were clinically progressive in the remaining 18 patients. In
11 patients, there was a history of only 1 previous cerebrovascular
attack, but in the remaining 23 patients, there had been 2 or more
previous attacks. The clinical signs and symptoms associated with
dysphagia are documented in Results. For the 35 age-matched
control subjects, the mean age was 59.6 and ranged from 30 to 75
years.
Clinically, the degree of dysphagia was graded9 as follows: 1
indicates no clinical signs and symptoms of dysphagia; 2, very mild
dysphagia suspected from clinical examination, but the patient never
complained of any swallowing difficulty; 3, patient had complaints
of dysphagia that were supported by other clinical signs, but nonoral
feeding was not necessary at the time of investigation; and 4, patient
had distinct clinical signs and symptoms of dysphagia, including
aspiration, and dysphagia was sufficiently severe to necessitate
nonoral feeding.
The electrophysiological methods used in the present study were
previously described in detail.10 In brief, during swallowing, the
EMG activity was recorded on an EMG apparatus (Medelec MS-20)
by means of bipolar silver-chloride EEG electrodes taped under the
chin over the mylohyoid-geniohyoid-anterior digastric muscle com-
plex (referred to as the submental EMG, or SM-EMG). The EMG
signals were filtered (band pass 100 Hz to 10 KHz), amplified,
rectified, and integrated. For the detection of laryngeal upward and
downward movements, a mechanical sensor that consisted of a
simple piezoelectric wafer with a small rubber bulge affixed to it at
its center was placed on the coniotomy region between the cricoid
and thyroid cartilages on the midline.11 The output from the sensor
was fed into a separate channel of the EMG apparatus before being
amplified and band filtered (band pass 0.01 to 20 Hz). During each
swallow, the sensor gave 2 deflections of generally opposing
polarity. The first deflection was used to trigger the delay line
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circuity of the recording apparatus, so that all signals related to
swallowing were time locked to the same instant.
In 19 patients (15 men and 4 women, age range 32 to 75 years) and
21 control subjects (10 men and 11 women, age range 30 to 75
years), in addition to the SM-EMG, the EMG activity of the
cricopharyngeal (CP) muscle of the upper esophageal sphincter was
recorded. The CP-EMG was obtained with a concentric needle
electrode (Medelec disposable needle electrode DMC-37) that was
inserted through the skin at the level of the cricoid cartilage and was
advanced laterally in the posterior medial direction until the CP
muscle was reached. The CP-EMG signals were also fed to the EMG
apparatus before being filtered, amplified, rectified, and integrated.10
Each subject sat on an examination chair and was requested to
hold his or her head in a natural upright position. The swallows were
initiated by 1 or 3 mL volume of tap water introduced through a
disposable syringe. The water was positioned on the tongue while the
tip of the tongue touched the upper incisors.12 The data collection
time during each swallow was 2 or 5 seconds, or both, with an
800-ms preswallowing time included in each sweep duration. At
least 5 successive recordings were collected for each type of
swallow, and the signals were examined from both single traces and
superimposed and averaged traces.
The electrophysiological parameters associated with laryngeal
sensor signals and the SM-EMG were measured and labeled. These
parameters are defined as follows:
(1) The onset of 2 deflections in the laryngeal sensor signal
recordings are denoted as 0 and 2. The “0-2 interval” is a time
variable that indicates the duration of laryngeal upward movement
plus the relocation time during the pharyngeal phase of swallowing.
(2) Because the submental muscles are laryngeal elevators, the
SM-EMG is thought to provide information about the onset and
duration of the oropharyngeal phase of swallowing within the period
referred to as the “A-C interval.”
(3) The third parameter denoted as the “A-0 interval” is the period
between the onset of SM-EMG (A) and the appearance of the upward
deflection (0) of the laryngeal sensor. This interval reflects the
Dysphagia in Suprabulbar Palsy 1371
initiation of the reflex phase of swallowing and therefore is presum-
ably associated with the triggering of swallowing reflex.13,14
To investigate the “piecemeal deglutition”15 and dysphagia limit,
an identical recording procedure was used9,16,17 with the sweep
duration set at 10 seconds and the delay line set at 2 seconds. All
subjects were given 1, 3, 5, 10, 15, and 20 mL water, and for each
volume, the oscilloscopic traces were initiated at the examiner’s
command to “swallow.” During these long sweeps, the laryngeal
sensor signals and the integrated SM-EMG activity were collected at
the beginning of the sweep, immediately after the command to
swallow. Normally, with volumes up to of 20 mL, all material could
be swallowed in 1 attempt, as seen in the early segments of
8-second-long traces. However, when the amount of water exceeded
20 mL, piecemeal deglutition was usually observed. Any duplication
or multiplication of a swallowing attempt with ⱕ20 mL water within
the 8-second period after the first swallow was designated as the
“dysphagia limit” and regarded as pathological.
Statistical Analysis
Levene’s F test was used for ANOVA between the patient and
control subject groups. The mean and SEM values were calculated
for all quantities measured, and the Student’s t test was performed to
assess the differences in swallowing-related variables between the
groups. The Mann-Whitney U test was used for comparison of
nonnormally distributed data. A value of P⬍0.05 was considered to
indicate a significant difference.
The study was approved by the ethics committee of our university
hospital, and an informed consent was obtained from each
participant.
Results
Clinical Findings Associated With Dysphagia
In 34 patients with SBP, clinical assessment revealed that the
degree of dysphagia varied among patients and that the signs
and symptoms could be divided into several major categories.
The most common complaints and the clinical findings
associated with dysphagia are summarized in Table 1.
Clinical assessment of patients suggested that in 7 patients
(20.6%), in whom nonoral feeding by means such as naso-
gastric cannula was necessary, the degree of dysphagia was
classified as grade 4. In 3 patients among this severely
dysphagic group, voluntarily initiated swallows could not be
accomplished at all. For the remaining 4 patients, although
small amounts of food could be swallowed from time to time,
nonoral feeding was also necessary, because they frequently
experienced aspiration. The degree of dysphagia was evalu-
ated as grade 3 in 20 patients (58.8%) and grade 2 in 7
patients (20.6%).
Dysphagia Limit
Although the grading procedure for dysphagia was useful
in clinical evaluation of the patients, the method used to
measure the dysphagia limit was more sensitive and
objective in classifying the severity of clinical problems
associated with swallowing. Only 1 patient with grade- 2
dysphagia showed a normal dysphagia limit of ⬎20 mL
water. The remainder of the patients who were investigated
displayed a dysphagia limit of ⬍20 mL, including an
additional 6 patients with grade 2 dysphagia. Figure 1
shows the dysphagia limits obtained from a patient (as-
sessed with grade 2 dysphagia) in whom the bolus was
divided into 2 or more swallows (as indicated by arrows)
while attempting to swallow 10 mL water.
 1372 Stroke June 2000

TABLE 1. Summary of Complaints and Clinical Findings in

Patients With SBP and Dysphagia
%
Complaint
Feeling of cleaning the mouth 73
Inability to sufficiently clean the throat 73
Difficulties in bolus formation and control 67
Nasal regurgitation 53
Drooling of saliva 47
Feeling of material stuck in the throat 40
Abnormal postures during swallowing 33 Figure 2. Correlation between dysphagia limit and degree of
dysphagia in patients with SBP. Three patients could not be
Clinical finding included in the calculation due to their inability to swallow vol-
Dysphagia 100 untarily (r⫽0.62, P⬍0.0001). Figures around each diamond
denote the number of patients.
Slow/weak laryngeal elevation 87
Dysphonia/dysarthria 83 swallowing signal. Overall, in patients with SBP, the degree
Saliva accumulation in mouth 80 of dysphagia was well correlated with dysphagia limits
Weak voluntary cough 73 (Figure 2). The dysphagia limit was significantly reduced as
Coughing during a swallow 70 the degree of dysphagia increased (r⫽0.62, P⬍0.0001).
Emotional lability 60 Laryngeal Movements and Submental EMG
Brisk mandibular reflex 57 During Swallowing
Wet voice 50 Figure 3 illustrates the representative traces obtained from a
Increased palatal/pharyngeal reflexes 50 normal control subject (top traces) and a dysphagic patient
Loss of weight 45
with SBP (bottom traces) during swallowing of 3 mL water.
Measurements of the 0-2 interval, which is the time between
Tongue weakness 40
the onsets of the upward and downward movement deflec-
Lung infection 13 tions of the larynx and indicates the laryngeal upward and
relocation time during a swallow, and the A-C interval, the
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total duration of SM-EMG that indicates the onset and end of

The pattern of dividing the bolus into 2 separate swallows
occurred with volumes between 3 and 20 mL. As the volume
increased, patients had to divide the bolus into even smaller
portions and to perform additional swallows to swallow the
entire amount in the mouth. This pattern was never observed
in normal subjects unless they were required to swallow
volumes exceeding 20 mL. In some cases, the dysphagia
limit, at which the patient could swallow in a single attempt,
was reduced to 1 to 3 mL. Furthermore, in some instances,
coughing, which indicates subglottal aspiration, occurred
during an attempt to swallow, and these movements were
detected as several consecutive artifactual deflections in the
oropharyngeal swallowing,10,18,19 revealed significant differ-
ences in the 2 groups studied. These parameters of swallow-
ing, particularly the duration of SM-EMG, were prolonged in
patients with SBP (Figure 3B), as shown in the statistical
results given in Table 2. The A-0 time interval between the
onset of SM-EMG and the onset of laryngeal upward deflec-
tion (shown as A-0 in Figure 3 by oblique arrows) was also
significantly prolonged in patients with SBP.
In patients with SBP with severe dysphagia, the electro-
physiological pattern of swallowing showed further differ-
ences. Three of these patients could not produce voluntarily
initiated swallows, and any swallows recorded electrophysi-

Figure 1. Dysphagia limits obtained from

a patient with SBP (left) and from a con-
trol subject (right). Arrows indicate the
second and following swallows. For this
patient, the dysphagia limit was 10 mL
water.
 Ertekin et al Dysphagia in Suprabulbar Palsy 1373

Figure 4. Averaged laryngeal sensor (top traces in each pair)

Figure 3. Averaged laryngeal sensor signals and integrated
SM-EMG obtained from a normal control subject (A) and a SBP
patient with dysphagia (B) during swallowing of 3 mL water. The
prolongations of the A-0 (arrow) and A-C intervals (horizontal
line) were significant in the patient (B). Five responses were
averaged for each trace.
ologically were spontaneous/reflexive in nature. An addi-
tional group of 4 patients with grade 4 dysphagia was still
able to swallow voluntarily, but their spontaneous swallows
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and integrated SM-EMG signals (bottom traces in each pair)
obtained during voluntarily initiated (A) and spontaneous saliva
swallowing (B) in a patient with SBP. Arrows denote the A-0
interval. Note that the A-0 interval is ⬍50 ms during spontane-
ous saliva swallows.
EMG Activity of the CP During Swallowing
In 19 of 34 patients with SBP, the CP-EMG recordings were
analyzed and compared with recordings obtained from 21
control subjects. Figure 5 displays the CP-EMG traces
obtained from a control subject and a patient with dysphagia.
During a swallow, the tonic EMG activity of the CP sphincter
is normally switched off. The average pause in the EMG
activity during voluntarily initiated swallows was found to be

occurred more frequently. Figure 4 illustrates that in their

462.0⫾17.8 ms in normal subjects and 388.6⫾17.8 ms in
attempt to swallow voluntarily, dysphagic patients first dem-
dysphagic patients (Table 3). This difference represents a
onstrate a prolongation of the A-0 interval (Figure 4A), and in
significant shortening of the CP-EMG pause in patients with
the advanced stages of dysphagia, when the voluntary trig-
SBP during swallowing of 1 to 3 mL water (P⬍0.006). In 9
gering of swallows is severely reduced or lost and all
patients with SBP, there were unexpected bursts of motor unit
swallows become spontaneous or saliva swallowing, the A-0
interval is notably shortened (Figure 4B), in most cases down
to ⬍50 ms.

TABLE 2. Summary of Electrophysiological Findings of

Patients and Normal Subjects During 3 mL Water Swallowing
Patients With
SBP With Normal Control
Dysphagia Subjects
Swallowing Parameters (n⫽31)* (n⫽35) P
0 –2 Laryngeal relocation 640.1⫾20.4 581.1⫾129.0 0.01
time, ms 111.6 74.0
360–925 420–702
Submental EMG duration 1188.0⫾103.2 924⫾24.5 0.02
(A-C interval), ms 565.5 140.5
500–3440 674–1250
A-0 interval, ms 423.5⫾64.6 279.2⫾19.4 0.04
353.6 111.7
18–1440 40–480
Figure 5. Superimposed laryngeal sensor signals (top traces in
Submental EMG 68.1⫾4.8 57.3⫾4.1 NS each pair) and CP-EMG traces (bottom traces in each pair) rec-
amplitude, ␮V 26.4 23.4 orded from a patient with SBP with dysphagia (top) and from a
26–133 22–103 control subject (bottom) during swallowing of 3 mL water. In the
patient, the duration of CP-EMG pause is shorter and indicates
Values are given as mean⫾SEM, SD, and range. a premature closure of the sphincter. Note the unexpected
*In 3 patients, voluntarily initiated swallows could not be performed. bursts of motor unit potentials (MUP; arrow).
 1374 Stroke June 2000
TABLE 3. CP-EMG Parameters of the Cricopharyngeal Muscle of Upper
Esophageal Sphincter During Voluntarily Initiated Swallowing of 3 mL Water
Patients With SBP
With Dysphagia
Parameter
CP sphincter EMG pause, ms
Time from onset of laryngeal upward
movement to onset of CP-EMG pause, ms
Time from end of CP-EMG pause to onset
of laryngeal downward movement, ms
Values are given as mean⫾SEM, SD, and range.
potentials (MUP in Figure 5) throughout the pause period of
the CP-EMG. The average time from the onset of laryngeal
upward movement to the onset of CP-EMG pause did not
differ in the 2 groups studied. However, in patients with SBP
the CP sphincter closed prematurely during the upward
relocation of the larynx, as indicated by the statistically
significant difference (P⬍0.006) in the duration measured
from the end of CP-EMG pause to the onset of laryngeal
downward movement between patients and control subjects
(Table 3). Indeed, in 5 patients, this period exceeded the
maximum measurement of 190 ms obtained in normal
subjects.
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Overall, in patients with SBP, either the triggering of
swallowing reflex was delayed or the swallow could hardly
be triggered at all. Furthermore, whenever the reflex swal-
lowing could be triggered, it was slow and prolonged. In
addition, the CP muscles of the upper esophageal sphincter
appeared to have become hyperreflexic, resulting in incoor-
dination, especially between slow laryngeal movements and
short and incomplete relaxation time of CP sphincter during
swallowing. None of these patients were referred for myot-
omy surgery.
Discussion
In SBP with multiple lacunar state, dysphagia is a very
common disorder, and for many patients, this causes serious
management problems. This was also reflected in our sample,
because 79.4% of 34 patients with SBP who were included in
the study had severe dysphagia and 20.6% required nonoral
feeding. Another important point was that in the majority of
patients, dysphagia persisted for weeks to months without any
improvement. Thus, dysphagia is common, severe, and per-
sistent in majority of patients with SBP. This is probably due
to the presence of lesions in multiple loci, including the brain
stem and both cerebral hemispheres. Furthermore, the basal
ganglia and associated neural pathways should also play a
role in the pathogenesis of dysphagia, as in most cases the
involvement of these structures was demonstrated by MRI.
In the present study, some clinical findings were frequently
associated with dysphagia. Among these were the weak or
slow elevation of larynx during swallows (87%), dysphonia
and dysarthria (83%), and saliva accumulation in the mouth
Normal
Control Subjects
(n⫽19) (n⫽21) P
388.6⫾17.8 462.0⫾17.8 0.006
77.8 81.8
250–600 300–630
137.9⫾23.2 113.1⫾17.7 NS
92.9 70.8
20–380 36–256
166.5⫾15.7 100.4⫾19.0 0.006
56.8 60.1
60–232 18–190
(80%). Dysarthria/dysphonia are reported to be common
clinical characteristics of stroke patients with dysphagia and
aspiration.7,20 –24 However, in previous stroke studies, the
weak or slow elevation of larynx and saliva accumulation in
the mouth either have not been found in a significant
proportion of patients or were not mentioned at all. Never-
theless, according to our clinical experience, these findings
also appear to be frequently associated with dysphagia of
patients with SBP.
With the electrophysiological tests described in our earlier
studies for the evaluation of oropharyngeal swallow,10,13,15,16
the dysphagia limit in all except 1 patient with SBP was
found to be pathological, with limits of ⬍20-mL bolus
volume. On the other hand, in all normal subjects, the
dysphagia limit exceeded the 20-mL bolus volume. Further-
more, the measurements of dysphagia limit also correlated
with the degree of clinical dysphagia in these patients (Figure
2). Therefore, the measurement of dysphagia limit is a
sensitive method for the assessment of neurogenic dyspha-
gia,16 and as a simple, quick, reproducible, and cost-effective
method, it can readily be used in patients with SBP and the
time course of dysphagia can be followed objectively.
In addition to dysphagia limit assessment, other electro-
physiological methods, namely recordings of laryngeal move-
ment, submental EMG, and CP-EMG of the upper esophageal
sphincter, also provided valuable findings in patients with
dysphagia. These additional findings can be summarized as
follows:
(1) In patients, the triggering of a voluntarily initiated
swallow was delayed compared with control subjects, as
demonstrated by the prolongation of the A-0 interval (see
Figure 3), which is the time difference between the onset of
SM-EMG and the onset of upward movement of the larynx13
and provides indirect information about the voluntary trig-
gering of swallowing reflex.14
(2) The laryngeal upward movement and relocation time of
the larynx during swallowing were significantly prolonged in
patients with SBP, as revealed by the prolongation of 0-2 time
interval, which reflects the pharyngeal phase of swallowing
reflex.9,10,16,17
(3) During swallowing, the duration of activation of
submental suprahyoid muscles was longer in patients than in
 Ertekin et al
control subjects. These muscles have 2 principal roles in
swallowing: the protection of the larynx by elevation, and the
transportation of bolus by providing a secondary support to
the tongue for its pumping action.18,25,26 Therefore, the
duration of the SM-EMG is a parameter that provides
considerable information about the duration of the pharyngeal
phase of swallowing that was prolonged in dysphagic patients
with SBP with lacunar state.
(4) The CP-EMG recordings made during swallowing
revealed that the striated sphincter muscle of the upper
esophageal sphincter was hyperreflexic and presumably dys-
inhibited like other brain stem reflexes, such as mandibular
and palatopharyngeal reflexes. The emotional lability ob-
served in these patients may also have been associated with
dysinhibition at the brain stem level. The hyperreflexic nature
of CP sphincter was apparent in the shorter EMG pause
period during swallowing and its premature closure before
the larynx descended.9,14
Three pathophysiological mechanisms can be proposed for
the manifestation of dysphagia in SBP with multiple lacunar
state:
Because corticobulbar fibers are involved in the triggering
of voluntarily initiated swallows and have facilitatory effects
on the bulbar swallowing center,26 –29 in SBP, the extreme
prolongation of excitation of the submental muscles for
triggering of the swallowing reflex observed with the A-0
interval should be associated with the involvement of the
corticobulbar fiber system. In the advanced stages of corti-
cobulbar descending motor system involvement, a voluntary
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swallow cannot be initiated, and therefore it would be
impossible for a patient with SBP to swallow voluntarily,
although reflex swallowing can still be performed with the
bulbar swallowing center.26 These reflex swallows can be
detected clinically as well as electrophysiologically9,14 (Fig-
ure 4).
The second mechanism affected in swallowing disorders
may be associated with suprasegmental inhibitory influences
on the bulbar center. These influences appear to have been
removed through some peculiar pathological involvement of
corticobulbar fibers. The abnormal EMG patterns recorded
from the CP sphincter is similar to those obtained from
patients with amyotrophic lateral sclerosis with corticobulbar
involvement.9 There is further evidence in the literature for
the presence of such pyramidal inhibition on the swallowing
reflex.30 Therefore, it appears that the involvement of corti-
cobulbar pathways in SBP not only alters the direct excitatory
influences but also results in dysinhibition by affecting the
inhibitory neural circuits. Consequently, the swallowing re-
flex, particularly the CP sphincter reflex pattern, is dysinhib-
ited (ie, released from inhibitory control). Further support for
this mechanism comes from observations in our patients of
increased mandibular and palatopharyngeal reflexes and
emotional lability. Likewise, it has also been suggested that in
amyotrophic lateral sclerosis, the possible involvement of
suprabulbar inhibitor control may be accountable, through a
release from inhibitory influences, for the increase in brain
stem reflexes.9,14,31–33
Because the bulbar swallowing center is presumed to be
intact in patients with SBP, it is difficult to explain the
Dysphagia in Suprabulbar Palsy 1375
prolongation of the laryngeal relocation time of the swallow-
ing reflex as measured with the 0-2 time interval. Further-
more, the duration of submental muscle contraction was also
prolonged, as demonstrated by prolongation of the A-C
interval. These findings may indicate that the extrapyramidal
influences on the bulbar center have somehow been affected.
This assumption is based on similar findings observed in
patients with Parkinson’s disease with dysphagia.14 Similarly,
in patients with SBP, the accumulation of saliva in the mouth
and drooling may also be related to the involvement of the
extrapyramidal system, in addition to the disturbance associ-
ated with the corticobulbar system.
Acknowledgments
This work was supported by a grant from the Turkish Scientific and Tech-
nological Research Council (TÜBITAK) (project SBAG-1739).
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