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Dysphagia and Related
Disorders: Management
Lecture Three:
Rehabilitation Techniques
Rehabilitative Manoeuvres
• Oral Motor Exercises
• Vocal Adduction Exercises
• Modified Valsalva Swallow or Effortful
Swallow (Logemann, et al.)
• Mendelsohn Manoeuvre (Mendelsohn)
• Tongue Holding Manoeuvre or Masako
Manoeuvre (Fujui, et al.)
• Head Lifting Manoeuvre (Shakir, et al.)
Oral Motor Exercises
• What we know:
• Lazarus (1999): Controlled trial (no OM
exercise, resistance with tongue blade,
exercise with IOPI).
• 31 young healthy subjects…..ie…no tongue
weakness to start with.
• Demonstrated increased lingual pressure
measurements in exercise groups, but
not in control group. No increase in
endurance reported.
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More definitions:
‹ Compensation: Strategies that provide an immediate but
typically transient effect on the efficiency or safety of
swallowing. As a rule, if the strategy is not consistently
executed, swallowing will return to the prior dysfunctional
status. May include but are not necessarily limited to
posturing, adaptations in rate, route or nature of oral
intake.
‹ Rehabilitation: Interventions that when provided over the
course of time and are thought to result in permanent
changes in the substrates underlying deglutition;
ie...changing the physiology of swallowing mechanisms.
May include, but not limited to oral/facial exercises, vocal
adduction exercises, breathing exercises, pharyngeal
strengthening exercises.
Oral Motor Exercises
• What they are:
• Exercises designed to increase strength
and/or control of oral musculature with an
assumed carryover to functional tasks.
• Can address issues of hyperfunction,
hypofunction or dyscoordination
• Range of motion, resistance exercises,
icing, stretching
Oral Motor Exercises
• What we don't know:
• Lots!
• Very little empirical data to support efficacy
despite enormous amounts of clinical belief
• Do rote exercises focusing on completion
of volitional movements carry over to
functional swallowing?
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Oral Motor Exercises
• What we hope to be true:
• Lots!
• Oral motor training programs to improve
oral lingual control of the bolus during
functional swallowing tasks.
Effortful Swallow
• What we know:
• First introduced by Logemann, et al (1990,
1991,1992) as a compensatory technique
• Early research suggested that increased effort in
swallowing will results in immediate increased pressure
on the bolus and thus decreased pharyngeal residual
• Bülow (1999): Effortful swallow results in
decreased hyomandibular distance before the
swallow; but actually reduced laryngeal
excursion/decreased overall hyoid movement
during the swallow in normal.
Effortful Swallow
• Hind, Nicosia, Roecker, Carnes, Robbins
(2001)
– Another study to evaluate effortful swallow with
videofluoro and oral pressure
– Increased oral pressure with effortful swallow
– Increased duration of
• Maximal anterior hyoid excursion
• Laryngeal vestibule closure
• UES opening
– Increased superior hyoid movement
– Trend toward increased oral bolus clearance
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Effortful Swallow
• What it is:
• “Swallow hard”
• Generally thought to be appropriate for the
physiologic abnormality of decreased
pharyngeal stripping, and or pharyngeal
weakness.
• Increased pressure on the bolus is
generated by effortful swallow
Effortful Swallow
• Bülow (2001):
– In Patients with mod to severe pharyngeal phase
dysphagia, effortful swallow results in:
• No change in aspiration/penetration, although depth of
penetrated material higher
• No change in pharyngeal retention
• Does not improve weak pharyngeal contraction
• Bülow (2002): extension of above study
– Same patient group
• No change in peak amplitude or duration of intra-bolus
pharyngeal pressures at the level of UES
• Huckabee, Hiss, Barclay & Jit 2002
– Manoendoscopic evaluation of normal and effortful
swallowing
– PHaryngeal catheter measured upper and middle
pharyngeal pressures and UES pressure during
swallowing
– sEMG measured submental muscle contraction
– RESULTS
• Effortful swallow results in significantly increased
amplitude of all measures.
• But sEMG was not highly correlated with phharyngeal
pressure.
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Effortful Swallow
Huckabee, Hiss, Barclay & Jit 2002
140
• What we don’t know?
120 • Are thre two effortful swallows that
100
accomplish two distinct goals?
80

60 • What is effect of effortful swallow on

40 physiology? Only increased BOT?
20 Increased pharyngeal contraction?
0
-20
• Compensatory -vs- rehabilitative?
effortful
peak semg
sensor 1 normal
sensor 2
UES
rest

Mendelsohn Manoeuvre
• What we really hope to be true? • What is it:
• Long term repetitive execution of this • First identified by Mendelsohn as suggested
technique improves overall underlying as a compensatory technique.
physiology of swallowing. • Swallow---at height of laryngeal excursion
maintain suprahyoid contraction to prolong
• Muscle strengthening of striated the swallow---relax/complete the swallow.
pharyngeal musculature
• Prolonging the swallow prolong UES
opening
• Thought to be effective for addressing
inadequate UES opening, or 2nd weak
hyolaryngeal excursion or pharyngeal
contraction.

Mendelsohn Manoeuvre Mendelsohn Manoevre

• What we know:
• Kahrilas, Logemann, Krugler, Flanagan
• Logemann & Kahrilas (1990) Case report
• 45 year old medullary infarct; studies over 60
(1991)
month period. Mendelsohn improved – Manofluorography evaluation of
swallowing efficiency greater than two-fold mendelsohn in normals
over other techniques. – Increased anterior superior excursion of
• Kahrilas et al. (1991) Manofluorographic the larynx and hyoid
study
– Thereby delayed UES closure
• Mendelsohn results in prolonged UES
opening but not increased diameter of – No comment in this study on bolus flow
the UES. Increases hyolaryngeal superior
displacement but not anterior displacement.

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Mendelsohn Manoevre
• Miller and Watkins (1997)
– Real Time Ultrasound study of lateral
pharyngeal wall movement during
mendelsohn
– Increased duration of lateral pharyngeal
wall movement compared to normal
swallow during mendelsohn
Masako Manoeuvre
• What it is:
• First identified by Fujui (199 )
• Tongue holding manoeuvre….Swallow
with tongue stabilized anteriorly
between teeth.
• Designed specifically to address
inadequate BOT to PPW approximation
Masako Manoeuvre
• What we don't know:
• What effect on other aspects of swallowing?
Recall Bülow study
• What we really hope with all our hearts to
be true:
• Repetitive execution of manoeuvre ultimately
results in greater activation of the
posterior pharyngeal wall thus
improving pharyngeal swallowing
function
• Neuromuscular re-ed training programs
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Mendelsohn Manoeuvre
•What we don't know:
•What effect on other aspects of swallowing?
Recall Bülow study
•What effect on bolus flow?
•With or without a bolus?
•What we really hope with all our hearts to be
true:
•Repetitive ‘stretching’ of UES ultimately
results in more function UES opening
•Neuromuscular re-ed training programs
Masako Manoeuvre
• What we know:
• Fujiu et al (1995). Radiographic documentation
of patients with BOT resection to have greater
PPW anterior movement.
• Fujiu et al (1996).Radiographic evaluation
• 10 non-resected individuals. Technique results in
significantly increased anterior bulging of the
posterior pharyngeal wall. Recruits greater activation
of the pharyngeal constrictors as a compensation.
• Increased aspiration risk with a bolus….
not a compensatory technique (except….)
Head-lifting Manoeuvre
• What it is:
• First identified by Shaker (1997)
• Lying in bed, raise head from level
repetitively, raise and hold.
• Not a direct swallowing task
• Intended for use in patients with
inadequate opening of the UES.
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Head-lifting Manoeuvre
• What we know:
• Shaker et al (1997). Manofluorographic analysis
• Two groups elders: sham exercise, head lift
exercise performed for 6 months.
• No change in group with sham; Those with head
lift exercise demonstrated increased laryngeal
excursion, increased width and duration
of UES opening, decreased intra-bolus
pressure.
• Nicely done cross over design
Head-lifting Manoeuvre, cont...
• Shaker et al (1999):
• 17 dysphagic patients;
videofluoroscopic assess.
• Two groups (sham & Shaker
exercise) then crossover
• Aspiration resolved in 15/17 patients
with Shaker ex.
• Follow up 4-12 mos later…no decline.
Emerging modalities
• Neuromuscular electrical stimulation
– Defined as "the external control of
innervated, but paretic or paralytic,
muscles by electrical stimulation of the
corresponding intact peripheral nerves"
(Baker, et al., 1993).
– Achieved through the carefully regulated
administration of pulsed electrical current
at predetermined frequencies and
amplitudes to nerves, myoneural junctions
or muscles (Ragnarrson, 1994).
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Head-lifting Manoeuvre, cont...
• Jurell (1996): EMG study
• EMG evidence of fatigue in submental muscles
suggestnig increased work with manoeuvre
• Alfonzo,et al. (1998): EMG study
• Increased amplitude in supra- and infra-hyoid
muscles with this technique.
Head-lifting Manoeuvre, cont...
• What we don't know:
• How does this work? Other effects on
swallowing? Spontaneous recovery
effects? Head rotation as an option?
• What we really hope with all our hearts
to be true:
Effects of NMES
• Alternations range from changes in permeability of the
cell membrane at the cellular level, to systemic changes
such as analgesia secondary to neurotransmitter
release, circulatory changes secondary to vasoactive
polypeptide release, and kidney and cardiac changes
secondary to modulation of internal organ activity
• The therapeutic benefit is a consequence of tissue level
changes which are manifested in part by skeletal muscle
contraction and subsequent effects on strength, reaction
time and stamina (Alon, 1991).
• Very simply stated, the current administered during
electrical stimulation changes the ionic composition of
the neural or muscular cell membrane and if of adequate
intensity, triggers transmission of a motor unit action
potential with a subsequent motor response.
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• The conduction of an action potential and the
chemical synaptic transmission created by
artificial electrical stimulation involves the
same processes of neurosecretion and
chemoreception as a naturally occurring
excitation.
• However, the externally stimulated
contraction differs from physiologic muscle
activity in the ordering of muscle fiber
recruitment, the synchronicity of individual
motor units and the intensity of stimuli
required to produce these changes.
Indications
• The US FDA documents present indications for
electrical stimulation to include the therapeutic goals
of muscle re-education, prevention of disuse atrophy,
and maintenance of range of motion
• The literature in physical medicine and rehabilitation
reports numerous applications of electrical
stimulation, including increasing muscle strength and
range of motion, correcting contractures from
spasticity, increasing sensory awareness and
volitional muscle control and decreasing antagonistic
spasticity (Kasman, 1994).
• May also be specific contraindications
• Freed et al. (2002)
for use around head and neck
"Severe spasm of the laryngeal and
pharyngeal muscles may occur when
the electrodes are positioned over the
neck or mouth. The contractions may be
strong enough to close the airway or
cause difficulty in breathing" (FDA,
1985).
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The complexity of stimulation
• Therapeutic application of this stimulation is not
a simple process and requires knowledge of
neural transmission, electrophysiology, biologic
impedance and muscle physiology.
• The effectiveness of the treatment is dependent
on precisely chosen stimulation parameters for a
selected therapeutic goal. These parameters are
critical for treatment effectiveness but also to
ensure patient safety.
– Type of current applied
– Pulse amplitude
– Duration
– Repetition rate
– Duty cycle
Contraindications
• Since electrical stimulators introduce active
current into biologic tissue, and at much
higher intensity levels than endogenous
current, there are contraindications related to
patient safety.
• NMES is contraindicated in patients with:
– demand type pacemakers
– superficial metal implants or orthotics
– skin breakdown
– Cancer
– history of cardiac or seizure disorder
– impaired peripheral nerve conduction systems
– pregnancy.
So what do we know about NMES
applications to swallowing?
– Methods:
• Stroke patients with swallowing disorder were
alternatelyassigned to one of the two treatment groups
(Thermal Simulation or NMES).
• NMES was administeredwith a modified hand-held
battery-powered electrical stimulator connected to a
pair of electrodes positioned on the neck.
• Daily treatments of TS or ES lasted 1hour.
• Swallow function before and after the treatment
regimen was scored from 0(aspirates own saliva) to 6
(normal swallow) based on substances the
patientscould swallow during a modified barium
swallow.
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– RESULTS:
• Both treatment groups showed improvement in
swallow score, but the final swallow scores
were higher in the ES group (p >0.0001).
• In addition, 98% of ES patients showed some
improvement, whereas 27% of TS patients
remained at initial swallow score and 11% got
worse.
• These results are based on similar numbers of
treatments (average of 5.5 for ES and 6.0
forTS, p = 0.36).
– ?? NMES paired with dilitation of UES
Basic Research
• Power et al (2002)
– Evaluated 15 healthy subjects
– 10 minutes of electrical stim applied to anterior faucial
pillars at two frequencies (0.2 and 5 Hz), 75% max
tolerated intensity.
– TCMS used immediately after and 30, 60 minutes
after stimulation.
– Results:
• At 5 Hz, faciaul pillar stimulation induced inhibition of
swallowing motor cortex, whereas at 0.2 Hz stimulation there
was excitation.
• On VFSS eval, 5 Hz lengthened pharyngeal delay time,
whereas 0.2 Hz produced no change.
• Maximal response seen 30 min after stim
– Results: frequency
• Stimulation at 1 or 5 Hz increased excitability,
wtihout altering latency as determined by
greater response amplitude of TMS potentials
• Stimulation at 10, 20 and 40 Hz actually
decreased excitability of neural transmission.
Presented an inhibitory effect on neural
conduction.
• Overall 5 Hz stimulation had greatest effect
with maximum effect at 30 and 60 minutes after
stimulation.
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Alon, in a chapter on neuromuscular electrical
stimulation, comments:
“The present disarray, and the natural tendency
to accept nonscientific, subjective and
commercially motivated claims….may
threaten the substantive potential that
electrical stimulation can offer as an objective
clinical modality” (1991).
• Fraser et al (2002)
– Methods:
• 8 healthy subjects received NMES at different
frequencies, intensities and duration through
bipolar pharyngeal electrode inserted trans-
orally or nasally.
• E stim provided for 10 min at frequencies of 1,
5 10, 20 & 40 Hz. Intensity set at 75% of max
tolerated.
• EMG responses evoked in the pharynx by TMS
were tested before stimulation, immediately
after, 30 and 60 minutes afterwards.
– Results: Intensity
• Higher the intensity of tolerated stimulation, the
larger the effect on corticobulbar excitability.
• Increasing effect over time….with larger
response at 60 minutes compared with
immediately after stimulation.
– Results: Duration
• Stimulation for 5 or 20 minutes facilitated motor
evoked potentials less than stimulation for 10
minutes.
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• Fraser, cont…
– Three subjects underwent detailed
bihemispheric topographic mapping before
and after stim.
• Increase in the size of pharyngeal area of
response occurred in all subjects, with the
effect largest in the pharyngeal dominant
hemisphere.
• Confirmed by fMRI studies
Basic Research
• Burnett et al. (2002)
– Goal: to develop intramuscular stimulation
device to imporve hyolaryngeal elevation
– Methods:
• Evaluated kinematic and pressure effectives of
stimulating select extrinsic laryngeal muscles in
normals using manofluoroscopy
• Hooked wire electrodes in mylohyhoid,
geniohyoid and thyrohyoid regions bilaterally
• Stimulation in 1 sec trains of 0.2 ms pulses at
30 hz. Amplitude to max effect without pain
Current approach to rehab
• State of the art in swallowing rehab typically views
recovery of muscle function through a very narrow
lens…muscle weakness.
• However, neuromuscular deficits can be classified
into three categories of physiologic impairment:
– Flaccidity or hypofunction
– Spasticity or hyperfunction
– Muscle dyscoordination or apraxia
(wow…fascinating issue in terms of dysphagia!)
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• Fraser, cont….
– 16 dysphagic patients
• 10 randomised to estim group; 6 to no tx.
• Stim group: 10 min stim at 5 Hz.
• All had videofluro before and 1 hour after stim
– Pharyngeal stimulation resultsed in reduction in pharyngeal
transit time, swallowing response time and aspiration score,
compared to pre-stim values.
– No treatment group had no change in swallowing
– Highly signirficant correlation within patients between total
change in excitability after stim and the change in
aspiration.
– Establishes causal relationship between increased cortical
exccitability and improvement in swallowing function across
individuals.
– Results:
• Equivalent degrees of laryngeal elevation were
achieved by stimulation fo all muscle pairs
• Hyoid elevation was greatest with bilateral MH
or ipsilateral MH + GH stimulation.
• Anterior hyoid movementn during bilateral GH
stimulation was greater than that seen in
normal swallowing
• Ipsilateral combined stimulation of GH and MH
or TH produced marked anterior hyoid
movement
• Increassed anterior hyoid movement resulted in
decreased UES pressure
Flaccidity or hypotonicity
• Characteristic of patients with cranial nerve
lesions or isolated pyramidal tract lesions
from cortical stroke
– Typically presents unilaterally
– Weakness is the cardinal feature
• Typical approach to rehab
– Strengthening exercises
– Effortful swallows, mendelsohns, masakos, OM
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Spasticity or hypertonicity Spasticity, cont...

• Typically characterized by increased tone that is • Typical approach to rehab
variable within an individual muscle and across
muscles. – Relaxation
– movement is imprecise and difficult to initiate. – Inhibition of spasticity
– Rigidity is characterized by consistent muscle tension across
muscles, which inhibits range of motion. – Emergence of voluntary activity upon the
• Caused typically by lesions to the UMN or backdrop of relaxation
extrapyramidal system and involves disordered – Mendelsohns & head lift for UES
input from basal ganglia, cerebellum, impairment?
red nucleus & other structures

Dyscoordination/apraxia Limitation in our approach to

• Considered to result from damage to rehabilitation
supplemental motor area, premotor areas,
inferior parietal lobe • Theoretical understanding of why they work
– Disorder of voluntary movement; inability to execute at a biomechanical level.
purposeful movement
• Parkinsonism with extraneous movement • But no understanding of how rehabilitative
(tremor?) efforts influence neuronal recovery.
• Typical approach to rehab • Brute force vs neuronal reorganization
– Patterning of the motor response
– Maximizing external cues • Peripheral vs central processes

Effects of Neural Injury

• We don’t understand the extent or mechanisms of cortical
control of swallowing.
• Preliminary data suggest that it is significant in
establishing a “preparatory set” for swallowing, maximizing
neural control
• Thus, enhancing cognitive awareness of oral intake will
likely improve efficiency in swallowing
• What do we know about neural recovery mechanisms
…..nuttin!
• If we understood more about how patients get better,
ie…what happens in the brain, we may be much more
effective in developing rehab techniques that focus directly
on those recovery mechanisms.
• Current practice focuses on addressing physiology and
biomechanics. But it is relatively hit and miss. Greater
information yields more precision in rehab development.
• Centrally, symptoms of insult caused by
– Cell death resulting from the event
– Secondary physiologic shutdown of associated neurons
• “Diaschisis: functional standstill or abolition of electrical
excitability transmitted to neuronal areas that are related to
damaged part of system
• Peripherally, when an axon is cut, the two ends
close, swell and retract from each other.
– Axons and myelin sheath degenerate, macrophages
absorb and destroy the debris
– Glial cells proliferate and form a scar around the trauma
– Degeneration proceeds in both directions
– As it approaches the cell body, cell death occurs.
.

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What do we know about
neural recovery
• Recovery of synaptic effectiveness
• Synaptic hypereffectiveness
• Denervation supersensitivity
• Recruitment of silent synapses
• Collateral sprouting
• Vicarious function
• Denervation supersensitivity:
– A mechanism similar to that above, denervation
supersensitivity holds that residual neurons near
the site of injury will increase the number of
receptor sites for neurotransmitter released by
residual incoming axons.
• Recruitment of silent synapses:
– Normally quiescent neurons, typically not
needed for function, become activated in
response to injury.
Stimulation Studies
• Hamdy, Aziz, Rothwell, Power, Singh,
Nicholson, Tallis & Thompson, 1998
– 22 stroke patients underwent cortical brain
mapping at one week, one month and three
months post onset using the transcranial magnetic
stimulation protocol.
– Of those patients who were initially dysphagic but
recovered swallowing function by three months,
there was a statistically significant increase in the
area of pharyngeal representation at both the 1-
and 3-months studies as compared to
representation at onset.
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Mechanisms of neural
recovery
• Recovery of synaptic effectiveness:
– Neural injury results in edema from retained fluid in the
brain. Very simply put, after the swelling resolves,
injured neurons can recover some degree of function.
– Resolution of diaschisis
• Synaptic hypereffectiveness:
– This theory holds that post injury, residual neurons
near the site of injury will increase the amount of
neurotransmitter released into the post synaptic
threshold, to increase the likelihood of synaptic
connections to other residual neurons.
• Collateral sprouting:
– Injury produces a change in the dendritic
aborization of remaining neurons and collateral
sprouting of spared axons to supply innervation to
targeted denervated neurons.
• Vicarious function or Redundancy:
– This simply means that there may be more than
one region of the brain for a single function which
initiates greater activity following injury.
• Hamdy et al., cont…
– However, dysphagic patients who did not recover
and those patients who were not dysphagic at
onset did not demonstrate this change in
pharyngeal representation.
– This study demonstrates that swallowing recovery
is related to increased cortical excitability of the
unimpaired hemisphere, or a shifting of cortical
representation for swallowing, and is the first
documentation of cortical plasticity as an identified
contributor to swallowing recovery.
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Hamdy et al.
• Further work by Hamdy in an extended series
of studies suggests that overall pharyngeal
representation in the undamaged hemisphere
increased remarkably as a function of
recovery, whereas no change in
representation was seen in those that did not
recover or those without dysphagia.
• Additionally, no changes were seen in the
damaged hemsiphere of any group
• Thus suggests that recovery of swallowing is
A=not dysphagic; b=dysphagic and recovered;
purely issue of hemispheric cortical shifting,
c=dysphagic and not recovered rather than intra-hemispheric reorganisation

Keefe, 1995
But these are all considered to be
• Changes in synaptic functions of the nervous
mechanisms of spontaneous system.
recovery (within minutes, – Keefe describes the theories of long term and associative
potentiation in which stimulation of a neural input pathway
hours,days or weeks after insult). produces a sustained increase in neural transmission at a
given synapse (synaptic hypereffectiveness and
What about latent recovery denervation supersensitivity).
– This further potentiate the synaptic response of
mechanisms; rehabilitative temporally related, but convergent, neural input. Keefe
recovery mechanisms? speculates that optimising the temporal relationship
between stimulus presentation of impaired and
nonimpaired modalities may facilitate this neural
mechanism.

Keefe, cont.. The last bit of Keefe

• Structural changes in the nervous system
(collateral sprouting).
– dendritic branching of non-injured axons occurs not
only in the regions immediately adjacent to the injury,
but in areas remote to the injury as well, such as the
contralateral cortex, providing evidence for both injury
related and experientially related changes.
– degree and pattern of dendritic branching has shown
to be clearly related, both positively and negatively, to
behavioural influences.
• Changes in neural networks, or cortical
reorganization (vicarious function).
– three additional features that may influence cortical
reorganization as a result of intervention:
• intensive repetition of tasks may be required to facilitate this shift,
• cortical shifting may return to pre-treatment status if tasks are
discontinued, suggesting the need for rigorous carryover,
• cortical shifting appears only to be effected for the modality which
is directly trained, thus implying the need for focused attention to
the treatment task.

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What is the role of rehabilitation in

swallowing?
Many more questions than answers.

• Hamdy documents spontaneous recovery

• Can we facilitate neural change (neural reorganisation)
– Are we re-organising and restructuring the neurophysiological
basis of swallowing?
• Can we facilitate peripheral change? (muscle changes)
• Central vs peripheral process
– The quandry of oral motor exercises, Head Lift exercise
• Can we make these changes happen?
• How do we make these changes happen?
• How much required to make changes?

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