Dysphagia
DOI 10.1007/s00455-015-9671-9
REVIEW ARTICLE
Dysphagia in Parkinson’s Disease
Inga Suttrup1 • Tobias Warnecke1
Received: 13 June 2015 / Accepted: 2 November 2015
 Springer Science+Business Media New York 2015
Abstract More than 80 % of patients with Parkinson’s
disease (PD) develop dysphagia during the course of their
disease. Swallowing impairment reduces quality of life,
complicates medication intake and leads to malnutrition
and aspiration pneumonia, which is a major cause of death
in PD. Although the underlying pathophysiology is poorly
understood, it has been shown that dopaminergic and non-
dopaminergic mechanisms are involved in the development
of dysphagia in PD. Clinical assessment of dysphagia in
PD patients is challenging and often delivers unreliable
results. A modified water test assessing maximum swal-
lowing volume is recommended to uncover oropharyngeal
dysphagia in PD. PD-specific questionnaires may also be
useful to identify patients at risk for swallowing impair-
ment. Fiberoptic endoscopic evaluation of swallowing and
videofluoroscopic swallowing study are both considered to
be the gold standard for evaluation of PD-related dyspha-
gia. In addition, high-resolution manometry may be a
helpful tool. These instrumental methods allow a reliable
detection of aspiration events. Furthermore, typical pat-
terns of impairment during the oral, pharyngeal and/or
esophageal swallowing phase of PD patients can be iden-
tified. Therapy of dysphagia in PD consists of pharmaco-
logical interventions and swallowing treatment by speech
and language therapists (SLTs). Fluctuating dysphagia with
deterioration during the off-state should be treated by
optimizing dopaminergic medication. The methods used
& Tobias Warnecke
tobias.warnecke@ukmuenster.de
Inga Suttrup
inga.suttrup@ukmuenster.de
1
Department of Neurology, University Hospital of Muenster,
Albert-Schweitzer-Campus 1, 48149 Münster, Germany
during swallowing treatment by SLTs shall be selected
according to the individual dysphagia pattern of each PD
patient. A promising novel method is an intensive training
of expiratory muscle strength. Deep brain stimulation does
not seem to have a clinical relevant effect on swallowing
function in PD. The goal of this review is giving an
overview on current stages of epidemiology, pathophysi-
ology, diagnosis, and treatment of PD-associated dyspha-
gia, which might be helpful for neurologists, speech-
language therapists, and other clinicians in their daily work
with PD patients and associated swallowing difficulties.
Furthermore areas with an urgent need for future clinical
research are identified.
Keywords Dysphagia
Parkinson’s disease

Swallowing
Treatment
Pathophysiology
Diagnosis
Epidemiology and Clinical Relevance
Parkinson’s disease (PD) is one of the most common
neurological disorders worldwide. The global prevalence
of PD steadily increases with age from about 40 per
100,000 in 40–49-year-old subjects to approximately 1900
per 100,000 in over 80-year-old subjects [1]. Furthermore,
a continuous rise in the number of PD patients is expected
in the future. It has been estimated that in the year 2030
nearly nine million people worldwide will suffer from PD
[2].
Dysphagia is a frequent and clinically relevant symptom
in PD patients. In his first description, James Parkinson
already recognized dysphagia and associated sialorrhea as
essential symptoms of PD: ‘‘As the disease proceeds
towards its last stage, […] food is with difficulty retained in
the mouth until masticated; and then as difficulty
123

swallowed. […] the saliva fails of being directed to the
back part of the fauces, and hence is continually draining
from the mouth […]’’ [3]. Over the last 15 years, various
studies on the prevalence of dysphagia in PD were able to
confirm that the vast majority of PD patients will develop
swallowing impairment during the course of their disease
[4–8]. Sex, age, disease duration, and dementia all seem to
contribute the occurrence of swallowing disturbances [8,
9]. A subjectively reported, often severe form of dysphagia
normally appears in the advanced state of PD, on average
10–11 years after onset of motor symptoms [10]. In the so-
called ‘‘Barcelona and Lisbon cohort’’ subjectively repor-
ted dysphagia in the on-state condition was documented in
68 % of late stage PD patients (Hoehn and Yahr stages 4
and 5, mean age 74.1 ± 7.0 years, mean disease duration
17.9 ± 6.3 years) [11]. However, using instrumental tools
such as fiberoptic endoscopic evaluation of swallowing
(FEES) or videofluoroscopic swallowing study (VFSS),
swallowing dysfunction can already be detected in more
than 50 % of subjectively asymptomatic PD patients [12].
Overall, a recent meta-analysis showed that the pooled
prevalence of oropharyngeal dysphagia based on subjective
outcomes in PD patients is 35 % and increases to 82 % by
taking objective measures of swallowing dysfunction into
account [4]. In rare cases, emerging dysphagia might even
be the first sign of PD [13, 14]. But typically, occurrence of
severe dysphagia in the first year after disease onset indi-
cates atypical Parkinsonism, for instance multiple system
atrophy (MSA) or progressive supranuclear palsy (PSP)
[10].
PD-related dysphagia is associated with serious clinical
complications, particularly in regard to loss of life quality,
insufficient medication intake, malnutrition, dehydration,
and aspiration with subsequent pneumonia, which is the
leading cause of death in patients with PD [15–19]. In
addition, recent studies indicate that affective symptoms
like fear and depression are more often present in PD
patients with dysphagia than in PD patients without [20].
In the following sections, we highlight current knowl-
edge of pathophysiology, diagnosis, and treatment of PD-
related dysphagia based on selected literature database
research. We also discuss possible steps of further clinical
research that may advance the understanding, early diag-
nosis and efficient treatment of dysphagia in PD.
Pathophysiology
The pathophysiology underlying PD-related dysphagia is
poorly understood [21]. However, dopaminergic as well as
non-dopaminergic mechanisms may be involved in the
development of swallowing impairment in PD. The
dopaminergic basal ganglia system, which is predominantly
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I. Suttrup, T. Warnecke: Dysphagia in Parkinson’s Disease
affected by the neuropathological process of PD, plays an
important role in the supramedullary swallowing system
[22]. By using functional magnetic resonance imaging
(fMRI), it has been shown that both, putamen and globus
pallidus, are activated bilaterally during swallowing in
healthy volunteers [23]. Therefore, lack of dopamine in the
striatum of PD patients may impair the supramedullary
swallowing network. This hypothesis is also supported by
the observation that some PD patients show a significant
improvement of swallowing function after application of
L-Dopa [24]. Furthermore, by modulating dopaminergic
pathways deep brain stimulation also seem to affect the
supramedullary swallowing network [25] (see therapy
section).
According to the Braak staging, during the course of PD
lewy bodies appear in different non-dopaminergic brain-
stem and cortical areas, which are mainly involved in the
control of swallowing, and may thereby also be involved in
the development of swallowing impairment [26]. For
example, the impairment of medullary swallowing centers
by lewy body pathology has been suggested to be
responsible for the occurrence of severe PD-related dys-
phagia [27].The Braak staging describes the progress of
alpha-synulein pathology during the cause of PD affecting
first the dorsal nucleus IX and X and locus coeruleus in the
premotor phase (St. I–II) followed by the motor phase
affecting first the substantia nigra followed by meso- and
neocortex (St. III–VI) [28]. Despite the fact that the
brainstem and the areas including the central pattern gen-
erators of swallowing are affected by the neurodegenera-
tive process early on, really severe dysphagia often
becomes apparent only in the advanced stages of PD. This
discrepancy might be caused by compensation mechanisms
on the cortical level during the first stages of the disease
[21, 29].
In fact, the clinical differentiation between the separate
stages of PD is often difficult. The Hoehn and Yahr stages
(1–5) only differentiate on the base of motor function,
which is concordant with Braak stages III–VI. Therefore,
research on early swallowing impairment and gastroin-
testinal dysfunction is limited by the inability to correctly
identify patients in the prodromal stages of PD (Braak
stages I–II). Reliable clinical tools for detecting PD
patients in the premotor phase of the disease do not exist so
far [30]. However, various studies describe PD as a whole
body disease suggesting a disease origin in the gut before
affecting brainstem areas, which often leads to gastroin-
testinal dysfunction even in the prodromal stages of the
disease. Shannon et al. found evidence for alpha-synuclein
pathology in human colonic tissues even before the
development of characteristic PD motor symptoms [31]. It
is suggested that PD-related alterations appear first in the
enteric nervous system (ENS) and the olfactoric bulb and
I. Suttrup, T. Warnecke: Dysphagia in Parkinson’s Disease
then progress into and throughout the central nervous
system (CNS) [32]. Pan-Montojo et al. used mouse models
to show the progression of environmental toxins from the
ENS to the CNS and the release promotion of alpha-
synuclein by enteric neurons. This supports the thesis that
PD is a whole body disease that likely develops in the gut
and moves in a rostral projection to medullary areas [33,
34]. Even during progression of PD gastrointestinal mani-
festations can be asserted. Sung et al. demonstrated an
impairment of the esophageal body even in the early stage
of PD (mean disease duration 11.5 ± 8.8 months) using
combined multichannel intraluminal impedance manome-
try [35]. The PRIAMO study substantiated an increase of
gastrointestinal dysfunction during disease progression [8].
In addition, there is also growing evidence for an
involvement of peripheral mechanisms in PD-related dys-
phagia. Mu et al. showed in post-mortem studies of PD
patients that alpha-synuclein is present in peripheral sen-
sory nerves as well as motor nerves innervating pharyngeal
muscles with greater affection in PD patients with dys-
phagia than without [36, 37]. Furthermore, alterations in
pharyngeal muscles of PD patients had been described
showing a higher percentage of atrophic myofibers in PD
patients with dysphagia [38]. This might indicate that PD-
related dysphagia is not only linked to a reduction in basal
ganglia dopamine activity or other neurotransmitter sys-
tems, but that peripheral mechanisms related to disease-
induced neuromuscular alterations are involved as well
[38]. Unfortunately, a description containing detailed
clinical and apparative pattern findings of dysphagia is
missing in these studies. Therefore, the real impact of
alpha-synuclein in peripheral tissue for clinical manifes-
tation of dysphagia cannot be determined.
Next to these insights into pathophysiology from studies
on PD patients and/or healthy volunteers, recent animal
studies assessing the underlying mechanisms of PD-related
dysphagia have been published during the last years [39–42].
These studies also confirm that next to dopaminergic even
non-dopaminergic pathways play an important role in the
development of PD-related dysphagia. Ciucci et al. showed
that targeted exercise can improve tongue force and timing
deficits in PD rat models indicating the involvement of both
central and peripheral mechanisms which might be not
related to sparing of striatal dopamine content [40]. As an
interesting new finding, in a rodent study, videofluoroscopy
was used for comparing deglutition patterns in parkinsonian
rats to young and aged rats showing impairment in oral
processing in parkinsonian rats and reduction of bolus
transport speeds and mastication rate in aged rats [41]. Thus,
videofluoroscopy is also able to be used in rat models for
evaluation and visualization of clinical dysphagia. Other
animal models have been used for examination of oromotor
function evaluating pathophysiology of dopamine
denervation and experience-dependent plasticity in the ner-
vous system as a result of sensorimotor training in unilateral
(hemi-parkinson) dopamine depletion models [42–44].
Interestingly, a reduction of substance P concentration
may represent an additional pathological factor in dys-
phagic PD patients. Substance P stimulates cough and
swallowing reflexes in healthy persons. In advanced stages
of PD, a reduced concentration of substance P, found in the
sputum of patients, probably results in disturbance of
protective reflexes, i.e., cough and swallowing reflex, and
consecutively silent aspiration [45, 46].
Finally, there is growing evidence of PD-specific
adaptive cortical changes in swallowing processing. A
recent neuroimaging study using whole-head magnetoen-
zephalography (MEG) demonstrated that cortical swal-
lowing processing in non-dysphagic PD patients is
characterized by a pronounced shift of peak activation
toward lateral parts of the premotor, motor, and inferolat-
eral parietal cortex with reduced activation of the supple-
mentary motor area. This pattern was not found in
dysphagic PD patients indicating an adaptive strategy to
prevent swallowing impairment. The over-activated brain
areas in the group of non-dysphagic PD patients are part of
the alternative cerebellar-parietal premotor loop for motor
execution responsible for externally or sensory cued
movements. A recruitment of this better preserved parallel
motor loop driven by sensory afferent input may be able to
maintain swallowing function in PD until progressing
neurodegeneration exceeds beyond the means of this
adaptive strategy, resulting in clinical manifestation of
dysphagia [29].
Diagnosis
Not more than 20–40 % of PD patients are aware of their
swallowing dysfunction, and less than 10 % of PD patients
report spontaneously about dysphagia [47, 48]. Therefore,
dysphagia has to be particularly addressed by the neurol-
ogist during consultation of a PD patient [49]. To bring
swallowing problems into focus, an advisable first step is a
self-report questionnaire. Two standardized PD-specific
questionnaires have been published for this purpose: The
swallowing disturbance questionnaire (SDQ) and the
Munich Dysphagia test-Parkinson’s disease (MDT-PD). By
using one of these specific questionnaires, PD-related
dysphagia is identified with a sensitivity of 80.5 and
81.3 %, and a specificity of 82 and 71 %, respectively [50,
51]. Whereas the SDQ evaluation is more basic and easier
to apply, the MDT-PD is able to detect milder or even
beginning forms of oropharyngeal dysphagia without any
aspiration risk. Additionally, the dysphagia-specific quality
of life questionnaire (SWAL-QOL) has been designed for
123

assessing dysphagia-related impact in patients. It has been
tested clinimetrically in broad dysphagia populations and
performed robustly in most clinical testing, but has not
been specifically validated in the PD population [52–54].
The well-known non-motor symptoms questionnaire (NMS
Quest) for PD patients also includes one question about
swallowing difficulties. However, apart from the fact that
oropharyngeal dysphagia is much more a motor than a non-
motor symptom in a large cohort of PD patients across all
disease stages, the NMS Quest identified only 27 % of
them as potentially having dysphagia [55]. This rate is even
below the pooled prevalence of subjective outcomes in the
above-mentioned meta-analysis, suggesting the dysphagia
rate to be underestimated in PD patients by only using the
NMS Quest [56, 57]. The same fact may apply for the
Unified Parkinson’s Disease Rating Scale (UPDRS). The
presence of PD-related dysphagia is insufficiently evalu-
ated in the UPDRS concerning only one question (part II,
question 7) about this topic [50, 58].
In addition to the results of a questionnaire, clinical
predictors should be taken into account when screening a
PD patient for the presence of dysphagia. The majority of
PD patients in Hoehn and Yahr stages 4 and 5, which is the
advanced stage of PD with the need for help from care-
givers, will have swallowing impairment [11]. Further-
more, a relevant weight loss without other explanation or a
body mass index below 20 is highly indicative of dys-
phagia. Interestingly, 20 % of PD patients are known to
develop malnutrition during the course of their disease [59,
60]. Another predictor of dysphagia and aspiration pneu-
monia is drooling or sialorrhea [24]. Recently, dementia
was also found to independently contribute to the occur-
rence of dysphagia in PD patients [9]. Table 1 summarizes
the clinical predictors of dysphagia in PD [9, 11, 24, 59].
Besides the patients’ unawareness of swallowing prob-
lems, another reason for unrecognized dysphagia in PD
patients may be a lack of attention to swallowing function
during neurological examination. The impossibility to
directly observe the swallowing act by visual examination
may account for this gap. Furthermore, the ‘‘normal’’ water
swallowing test as used in acute stroke patients has been
shown to be non-predictive of severe oropharyngeal dys-
phagia in PD patients [59].
Table 1 Clinical predictors of Parkinson-related dysphagia
Clincial predictors
Hoehn- and Yahr-stadium [3
Relevant loss of weight or body mass index \20 kg/m2
Drooling or sialorhea
Dementia
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I. Suttrup, T. Warnecke: Dysphagia in Parkinson’s Disease
Therefore, the Dutch guideline on speech-language
therapy in Parkinson‘s disease recommends a modified
water test in PD estimating the maximum swallowing
volume or the maximum swallowing speed [61]. The
swallowing speed test is less suitable for PD patients.
Therefore, a measurement of the maximum swallowing
volume that uses a gradual increase of the volume of water
that has to be swallowed should be preferred. PD patients
with a maximum swallowing volume below 20 ml are very
likely to suffer from dysphagia [61–64]. However, when
reviewing the literature about the application of the mod-
ified water test in PD, it becomes evident that this test has
only been evaluated in small and often heterogeneous study
populations and has not been validated against instrumental
tools so far [62–66]. Also studies investigating the optimal
way to perform a detailed clinical swallowing examination
in PD patients, as done by speech and language therapists
(SLTs) in PD patients are lacking [67].
Therefore, in ambiguous cases instrumental tools are
recommended to assess nature and severity of dysphagia
in PD patients [48, 61]. Fiberoptic endoscopic evaluation
of swallowing (FEES) and videofluoroscopic swallowing
study (VFSS) are both considered to be the gold standard
to evaluate oropharyngeal dysphagia [20, 24, 68]. During
a FEES examination, a flexible endoscope is passed
through the nose into the hypopharynx and the pharyngeal
swallowing of different food consistencies and liquids can
be directly viewed from above. The FEES is a
portable tool suitable for clinical bedside examination and
gives a detailed analysis especially about the late oral as
well as the pharyngeal phase of swallowing [69, 70].
Performing VFSS modified barium swallows using several
different food and liquid consistencies are applied to
examine the oral and pharyngeal stages of swallowing
including the upper esophageal sphincter [49, 71]. In
addition, high-resolution manometry (HRM) is a helpful
tool for detection of combined or isolated esophageal
dysphagia in PD patients and might even identify clinical
silent swallowing impairment in earliest stages of PD [35,
72]. A thin tube is passed through the nose into the
stomach to evaluate pressure and timing events in the
pharynx and esophagus during swallowing. The combi-
nation of these three instrumental methods allows a
detailed analysis of disturbance patterns in the oral, pha-
ryngeal, and esophageal phase of swallowing in PD
patients. Table 2 summarizes typical findings that can be
observed in dysphagic PD patients using instrumental
tools [60, 73–76]. Figure 1 shows a tablet getting caught
in the valleculae of a PD patient with motor fluctuations.
Retention of pills in the hypopharynx for long periods of
time may account for erratic absorption of levodopa with
delayed or unpredictable clinical response to oral medi-
cations [48].
I. Suttrup, T. Warnecke: Dysphagia in Parkinson’s Disease
Table 2 Patterns of Parkinson-related dysphagia in different phases
of swallowing: oral phase, pharyngeal phase, and esophageal phase
Phase of Frequent findings
swallowing
Oral Repetitive pump movements of the tongue
Oral residue
Premature spillage
Piecemeal deglutition
Pharyngeal Residue in valleculae [[[ pyriform sinuses
Aspiration in 50 % of dysphagic PD patients
Somatosensory deficits
Reduced rate of spontaneous swallows (48/h vs.
71/h)
Esophageal Hypomotility
Spasms
Multiple contractions
Fig. 1 Endoscopic detection of a tablet residue in the pharynx of a
PD patient after the swallow. The tablet is later on dissolved in the
valleculae. In this case, pharyngeal dysphagia accounts for motor
fluctuations because dopaminergic medication is not reliably trans-
ported into the small intestine where it is usually resorbed
Recently, it was demonstrated that, similar to gait per-
formance, swallowing function of PD patients may be
altered when a dual task paradigm is performed. In the dual
task condition, the PD patients had to swallow thin liquid
while completing a digits forward task under VFSS [77].
Therefore, duals task situations should be integrated into
standard instrumental swallowing evaluations of PD
patients.
Treatment
In general, swallowing therapy as performed by SLTs is
considered to be the main component in the treatment of
PD-related dysphagia. However, when reviewing the
published data on this approach it has to be concluded that
high-quality studies according to the criteria of evidence-
based medicine are quite rare. Furthermore, the results of
the available studies cannot be compared with one another
because of heterogeneous study populations and therapy
methods as well as different outcome measures [78, 79]. As
no general recommendations can be derived from the lit-
erature, the most effective measures have to be imple-
mented individually for each PD patient [48]. In a first step,
the specific nature of dysphagia should be examined.
Second, the effectiveness of different treatment options has
to be tested before starting a permanent treatment. For
example, residues in the valleculae may be treated using
the effortful swallow maneuver, whereas premature spil-
lage will be reduced by improving oral bolus control.
Nevertheless, there is first evidence from two high-
quality studies that expiratory muscle strength training
(EMST) and video-assisted swallowing therapy (VAST)
may be effective non-pharmacological dysphagia treat-
ments in PD patients. A randomized, blinded, sham-con-
trolled trial with sixty participants providing Class I
evidence shows that the penetration aspiration scale (PAS)
measured by VFSS improves in dysphagic PD patients
after performing a 4-week-training of the expiratory mus-
cles using a specific device (EMST150, Aspire Products;
5 days per week, 25 breathes per day) [80]. The EMST
group also demonstrated improvement of hyolaryngeal
function during swallowing. However, the clinical effect of
the intervention as measured in this study seems to be
rather small (Mean values of PAS: pre EMST:
2.64 ± 1.87; post EMST: 2.07 ± 1.28). A follow-up study
after a 3-month detraining period showed a slight
improvement of the maximal expiratory pressure without
any significant effect on swallowing safety [81]. Further
randomized controlled studies on this promising approach
are necessary to better understand its possible role in the
treatment of PD-related dysphagia. For example, changes
in diet, swallowing-related quality of life or pneumonia
rates would be outcome parameters with high relevance for
clinicians.
Another recently published randomized controlled trial
showed that FEES may be successfully used in the treat-
ment of PD-related dysphagia for biofeedback purposes.
Forty two PD patients with dysphagia randomly completed
either video-assisted swallowing therapy (VAST) or con-
ventional swallowing treatment. As part of all VAST ses-
sions, PD patients were also exposed to FEES videos of the
swallowing process in general as well as of their own
swallowing process. A significantly greater reduction in
food residues in the pharynx as measured by FEES was
observed in the VAST group compared to the control
group. Additionally, the VAST group demonstrated sig-
nificant improvement in swallowing-related quality of life
123

[82]. However, in this study only PD patients with mild and
moderate forms of dysphagia had been enclosed. Hence, a
general statement for all stages of PD cannot be made.
Although clinical experience may suggest an improve-
ment of PD-related dysphagia by the Lee Silverman Voice
Treatment (LSVT -LOUD), only one study including
eight PD patients without any control group has been
published so far. In this study, VFSS demonstrated
improvement of oral tongue and tongue base function
during the oral and pharyngeal phases of swallowing after
LSVT -LOUD [83]. However, larger randomized con-
trolled trials about the effectiveness of LSVT -LOUD in
dysphagic PD patients should be performed to confirm the
results of this pilot study.
The effect of dopaminergic medication and particularly
levodopa on swallowing function and its role in dysphagia
treatment is controversially discussed [84–86]. Although
some pilot studies did not reveal clear results, a marked
improvement of dysphagia in some PD patients after oral
L-Dopa-intake, subcutaneous apomorphine application, or
transdermal rotigotine delivery has been observed while
others do not respond [24, 69, 87–89]. One relevant argu-
ment in favor of a positive effect of L-Dopa on dysphagia
is the improvement of mortality rate in PD patients com-
pared to the pre-L-Dopa era. This improved mortality rate
may in part result from improvements in swallowing
function because aspiration pneumonia is the leading cause
of death in PD [84].
Mild or undetected PD dysphagia may often ameliorate
unnoticed by implementation of dopaminergic treatment
during the first years after disease onset [90]. In more
advanced PD, older studies mainly using VFSS found that
33–50 % of patients showed an improved swallowing
function in the on-state (after L-Dopa or apomorphine
application) compared to the off-state condition [74].
Furthermore, non-dyskinetic PD patients receiving a lower
cumulative daily dose of levodopa demonstrated less
oropharyngeal swallowing efficiency during VFSS com-
pared to dyskinetic PD patients with greater levodopa dose
[68].
Overall, it can be concluded that in the clinical routine
swallowing function in PD patients should always be
evaluated in both, off-state, and on-state condition [24, 60].
In case of fluctuating dysphagia with deterioration in the
off-state, an optimizing of dopaminergic medication is
recommended [24, 87]. For an endoscopic evaluation of
swallowing function in off- and on-state condition of PD
patients, the standardized ‘‘FEES-Levodopa-Test’’ protocol
may be useful [24].
Studies assessing the effect of deep brain stimulation
(DBS) on swallowing, i.e., subthalamicus nucleus (STN)
stimulation or globus pallidus internus (GPi) stimulation,
were not able to identify clinically significant improvement
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I. Suttrup, T. Warnecke: Dysphagia in Parkinson’s Disease
or decline in swallowing dysfunction with DBS [25].
Lengerer and colleagues examined 18 PD patients preop-
eratively and postoperatively with deep brain stimulation-
on and deep brain stimulation-off at the STN using vide-
ofluoroscopy. Their data suggested that deep brain stimu-
lation of the STN modulates the pharyngeal phase of
swallowing without relevant clinical impact [91]. Sundst-
edt et al. evaluated eight patients with bilateral caudal zona
Incerta DBS by performing FEES without clinically sig-
nificant decline or improvement to swallowing function
[92]. The same results were shown in two studies by
evaluating 11 patients with uni- or bilateral STN DBS [93]
and 14 patients with bilateral STN DBS [94]. In spite of
subjectively reported improvement of swallowing function
by most patients, no clinical relevant change in deglutition
had been found using FEES [93] or VFS [94].
Although these studies did not reveal clinical relevant
findings, they indicate mild subclinical modulation to
swallowing function as reviewed by Troche et al. [25].
While there are no experimental studies directly comparing
both approaches, available data suggest STN stimulation to
cause more subclinical impairment on swallowing function
than GPi stimulation [25, 95, 96]. Interestingly, a recently
published study was able to demonstrate that compared to
the routine 130 Hz, the 60 Hz stimulation significantly
improved swallowing function in patients with PD treated
by bilateral STN DBS, which persisted over the 6-week
study period [97]. Therefore, low frequency STN stimu-
lation may be beneficial in PD patients with DBS and
dysphagia.
Furthermore, STN stimulation in PD patients might even
affect esophageal motility. In a cross-over study, 16 PD
patients with a 6-month history of STN stimulation were
evaluated in the on- and off-state by esophageal high-res-
olution manometry presenting increased esophageal body
contractions and enhanced LES opening in the on-state.
These findings suggest an involvement of the nigrostriatal-
striatonigral loop in the control of esophageal motility [98].
The clinical relevance of these findings has to be revealed
in future studies.
Future Directions
In conclusion, there are at least three areas of dysphagia in
PD in which an urgent need of basic as well as clinical
research is required. First, further prospective studies for a
better understanding of the natural course of dysphagia in
PD and its underlying pathophysiology are needed. Second,
valid and standardized screening methods and clinical
assessment tools for an early detection of all aspects of
dysphagia in PD should be developed. Finally, randomized
controlled multicenter trials with clinical relevant outcome
I. Suttrup, T. Warnecke: Dysphagia in Parkinson’s Disease
measures such as quality of life or pneumonia rate should
be initiated to evaluate and compare the effectiveness of
different treatment approaches of dysphagia in PD. In
addition, animal models might be used for preclinical
testing of promising pharmacological and non-pharmaco-
logical treatment strategies.
Compliance with Ethical Standards
Conflict of interest The authors declare that there are no conflicts
of interest.
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Inga Suttrup MD
Tobias Warnecke MD
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