Lateral Medullary

Syndrome (LMS)
and Dysphagia:
Literature
Analysis and
Case Studies
Karen Sheffler, MS, CCC-SLP
Carney Hospital
Steward Healthcare
Karen.Sheffler@steward.org
 Other Terms in the
Literature
Wallenberg Syndrome
Lateral Medullary Infarct (LMI)
Most common form of a Brainstem Stroke

Posterior Circulation Stroke

Vertebrobasilar Stroke
 Goals For Today
Attendees will be able to:

1. Identify the classic signs and

symptoms of LMS during a Clinical
Bedside Swallow
Evaluation, especially how it relates to
voice, swallowing and oral-motor
function.
 Goals For Today
Attendees will be able to:

2. Discuss the aspects of the pharyngeal

dysphagia, in addition to debating the
cause of the cricopharyngeal/UES
dysfunction.
 Goals For Today
Attendees will be able to:
3. Identify methods that prevent
aspiration and aide in the rapid
recovery of swallowing function.
o Specifically, we will discuss head turns,
the Mendelsohn Maneuver, bolus
volume, and the Shaker Exercise.
 Effects of this stroke need not
be devastating when the
Speech-Language Pathologist is
involved immediately
post-onset.
Nucleus ambiguus
motor 9 + 10
Blumenfield, H. (2002). Neuroanatomy Through Clinical Cases.
Sunderland, MA: Sinauer Associates.
 Outline of the
Presentation
Historical LMS Dysphagia
Perspective Research with
Onset & Symptoms Instrumental Exams
Case Example #1 Case Example #2
Prognosis Case Example #3
Challenges in Early Oropharyngeal and
Detection & Esophageal
Differential Dysphagia
Diagnosis UES function and
Examples of ED dysfunction
presentations Treatment Ideas
Historical Perspective
 Wallenberg Syndrome
Initially described by Gaspard
Vieusseux, MD, of Geneva in 1810
Vertigo, unilateral facial numbness, loss
of pain and temperature appreciation in
the opposite limbs, dysphagia and
hoarseness, minor tongue
involvement, hiccups (cured by the
taking of the habit of a morning cigarette)
and a dropped eyelid
(Pearce, 2000, p. 570)
 Wallenberg Syndrome

Vieusseux also noted that a bottle of an

etherized julep felt lukewarm when taken
in the right hand but cold when held in the
left hand.

(Marcet, 1811, p. 221)

 Wallenberg Syndrome
In 1811, Dr Alex Marcet published a highly
detailed case study of Gaspard Vieusseux.
Peculiar sensations and the derangement
of equilibrium arise from a nervous
state, rather than an organic affection
of the brain.

(Marcet, 1811, p. 233)

 Marcet did report the
sudden onset of LMS:
Vomiting, followed by complete loss of
voice (without affecting articulation)
Difficulty swallowing liquids
Weakness of his left side
Insensible right side to being scratched or
pricked
Hiccups by the third day
Adolf Wallenberg
From 1895 to
1922, he provided
case reports and
anatomical evidence
of lesions

(Pearce, 2000)
 Dysphagia to
solids and liquids

Wallenberg described how the patient could

not swallow solids at all.

Liquids went down in minute amounts.

(Robbins & Levine, 1993, p. 43)

Onset and Symptoms of
Wallenberg Syndrome
 J.S. Kim of Korea

J.S. Kim (2003) performed the

first large clinical-MRI
correlation study, which followed
130 patients with pure LMI.
 Kim's Findings on Onset
Sudden onset 75% of the time
Non-sudden onset 25%
Typically starts with:
headache, vertigo, dizziness, and gait
ataxia
Later symptoms:
dysphagia, hoarseness, hiccups, and
sensory signs (Hypalgesia - loss of pain
and thermoanesthesia loss of
temperature sensation)
Sensory Symptoms in 96%
of Patients
Ipsilateral trigeminal and
face, Contralateral limb and body
Contralateral trigeminal/face
Contralateral limb/body
Bilateral trigeminal/face
Contralateral limb/body
Or symptoms only in the face or only
in the limb/body
(J.S. Kim, 2003)
 Signs and Symptoms
Ataxia in 92%. (Limb ataxia 55%)
Dizziness in 92%
Horner's sign in 88% (constricted pupil,
ptosis, decreased sweating in half of the
face)
Dysphagia 65%
Hoarseness 63%
Vertigo 57%
Nystagmus 56%
Nausea and Vomiting 52% (J.S. Kim, 2003)
 Headache in
52% of Patients

Ipsilateral occipital region was the most

common
Frontal headache was second most
common
Less Common Symptoms
Skew deviation
Diplopia
Dysarthria
Facial Paresis
Gaze deviation
Loss of vibration sense (12%)
 Older Studies
Many were performed with smaller numbers
of participants and with concomitant features
of previous CVAs, TIAs, or cerebellar
involvement.
Similar results in the following:
Sacco et al. (1993) 33 patients
Kim, J.S., Lee, J.H., Suh, D.C. & Lee,
M.C. (1994) 33 patients
Kim, J.S.. Lee, J.H. & Choi, C.G. (1998)
34 patients
 Martino et al. (2001)
65 year old man evaluated 12 weeks post
with a R rostral dorsal LMI:
Ipsilateral facial paresis, ipsilateral palatal
paresis
Crossed sensory signs
R-sided Ataxia, incoordination, R Horner's
Hoarseness, profound dysphagia
Martino, Terrault, Ezerzer, Mikulis, & Diamant (2001)
 Signs Common with LMS Structures Affected

Ipsilateral loss of pain and thermal Spinothalamic tract and descending

sense over half of face nucleus and tract of cranial nerve V

Ipsilateral Ataxia, falling to side of lesion Inferior cerebellar peduncle,

spinocerebellar tract

Ipsilateral Horners syndrome Descending sympathetic tract

Dysphagia, dysarthria, ipsilateral Efferent fibers of cranial nerves IX and X,

paralysis of palate and vocal cord, and nucleus ambiguus (NA)
diminished ipsilateral gag reflex

Contralateral impaired pain and thermal Spinothalamic tract and nucleus of cranial
sense over half of limbs and trunk nerve V carrying pain and temperature
sense to the opposite side of the body

Vertigo/dizziness Vestibular nuclei, vestibulo-cerebellar

pathway in the inferior cerebellar peduncle
(J.S. Kim, 2000)

Nausea/vomiting, nystagmus, diplopia Vestibular nuclei (J.S. Kim, 2000)

 Note on Chart:
Adapted from Dysphagia in a Patient with
Lateral Medullary Syndrome: Insight into
the Central Control of Swallowing, by R.
Martino, N. Terrault, F. Ezerzer, D. Mikulis,
and N. Diamant, 2001, Gastroenterology
121, p. 421. Copyright 2001 by the
American Gastroenterological Association.
Last two rows are additions made to the
original chart in the publication.
When we are familiar with the
classic signs of Wallenberg
Syndrome, we can assist the
medical team with differential
diagnosis.
 CASE EXAMPLE #1
SLP ~ critical member in critical care
Vascular Supply
Rostral versus Caudal
 Cerebellar Infarct with LMI
47 y/o Female
MRI report initially only
noted several acute
infarcts in L cerebellum &
cerebellar flocculus.

However, Neurologist
and SLP noted diplopia,
horizontal nystagmus in
extreme right gaze, and
dysphagia to solids.
 Beginning of
Hospital Course
ONSET: Sudden
dizziness, Nausea/Vomiting, Left side
weak & numb.
Bedside Swallow Evaluation:
o Pushed down solids with sips of liquids.
o Needed moist ground.
o Was using large bites and effortful swallows.
 Finding the Lateral
Medullary Lesion

SLP reviewed MRI with radiologist due to

suspicion of a LMI. There was a small
infarct in the caudal medulla.
Research shows that small superficial
infarcts in the LOWER or CAUDAL
medulla have less dysphagia.
Patient had MRA the Next
Day Due to Small LMI
MRA Brain Findings:
No flow in L Vertebral Artery which is likely
occluded. Otherwise symmetric branching in
intracranial circulation. Circle of Willis is
patent.
MRA Neck Findings:
Left VA is small in caliber (string sign). V3 &
V4 segments are not visualized indicating
slow flow or thrombosis. Suggestive of VA
dissection.
No VA No PICA
on Left on Left
MRA
VA
Dissection or
Thrombosis
on Left Side
MRA Neck: String Sign in VA
Distal thrombosis or slow flow
 Started Heparin Drip
Dysphagia to solids resolved by next day.
o Upgraded to regular solids.
o Denied any difficulty with bolus clearing on one
swallow. No need to wash down with liquids. MBSS
cancelled per ICU team.
Minimal dizziness, no diplopia, no
nystagmus, no further nausea.
Heparin drip increased blood flow in VA or
increased collateral blood flow to medulla
 Vascular Supply
Lateral medullary arteries arise from the
VA and the PICA
73% of patients with LMI had vertebral
artery disease (Sacco et al., 1993)
29% of the patients with LMI had VA
dissection (Kameda et al., 2004)
 J.S. Kim's Research on
VA vs PICA
Kim's large study in 2003 found:
VA disease was present in 67% of patients
PICA disease in 10%
Short-segment VA disease (<2cm) was
most associated with the classic diagonal
band-shaped lesions confined to the
lateral medulla.
 Negative MRA Results
MRA frequently fails to provide reliable and
precise information on the PICA
(J.S. Kim, 2000; J.S. Kim, 2003; J.S. Kim et al., 1998).
Normal MRA findings may mean that the
exact pathogenesis is unknown
(J.S. Kim, 2000).
Normal angiograms frequently had a cardiac
source of embolism or an occlusion that then
re-canalized at the time of the angiography
(J.S. Kim et al., 1998).
 Notes on Rostral vs
Caudal LMI

Rostrally located lesions: dysphagia, facial

paresis, and dysarthria more often
(J.S. Kim, 2003)

Increased dysphagia in rostral lesions

(Kameda et al., 2004)
 Notes on Rostral vs
Caudal LMI
J.S. Kim et al. (1994) noted that all
patients in the rostral group had more
hoarseness, dysphagia & needed
nasogastric tube insertion for feeding.
Rostral lesions: tend to be thicker/deeper
Caudal lesions: tend to be superficial
Only 2/21 caudal-lesion patients had transient
dysphagia.
Prognosis
Prognosis for LMI Patients
Only 1 patient in 130 died during the
hospitalization. Overall excellent
prognosis. (Kim, J.S., 2003)
Progress was rather slow, although
steady (Aydogdu, et al., 2001, p. 2084)
Dysphagia initially severe, but improves
rapidly in 1-2 months. Due to early
treatment, none of the patients in the
treatment program developed pneumonia.
(Kim, H., et al., 2000)
 Challenges in Early
Detection and Differential
Diagnosis
 Finding the Lesion

The CT is unable to detect brainstem

infarcts due to bony artifacts that obscure
the anatomic details

(Sacco et al., 1993; J.S. Kim et al., 1994)

 Younger Mean
Age of Onset
Researchers have recorded mean ages
from 57 to 60 years old, with as young as
24 years old in one study and 37 years
old in another.
More common in men than women.

(Sacco et al., 1993; Aydogdu et al., 2001;

Kameda et al., 2004; J.S. Kim, 2003)
 Presentations to ED
The patient may be misdiagnosed with:
Gastrointestinal infection due to the
nausea/vomiting
Respiratory infection due to the
hoarseness and cough from dysphagia
Drug overdose or alcohol intoxication from
bizarre behavior and ataxia
 Mimics Other Disorders
J.S. Kim (2000): 3 patients with LMI with
isolated vertigo and ataxia
Could mimic labyrinthine disorders

H. Lee & Sohn (2002): patient had only

horizontal nystagmus on R gaze & axial
lateropulsion (compelling sensation of
being pulled toward the side of the lesion)
 Examples of ED
Presentations and
Clarification of Symptoms
 36 y/o Vietnamese Male
HTN, smoker, Schizophrenia
Presentation to ED
Sudden onset of altered mental
status, bizarre behavior, unsteady
gait, change in speech & voice, inability to
eat/drink.
Mumbled, and garbled speech per notes.
Blurred vision, dizziness, nausea/vomiting
History of Schizophrenia. Pt stated: I took
too many of the wrong pills.
Given charcoal absorbital liquid (a liquid
slurry) and went into respiratory distress
Intubated/ventilated until day 2.
 36 y/o Vietnamese Male
HTN, smoker, Schizophrenia
Clarification of Symptoms
Ataxia, leaning right
Weak right side on transfer per nurse
Dysarthria per interpreter
No facial asymmetry
Doctor noted nystagmus
Decreased gag bilaterally
Hoarseness started one week PTA, sustained
ah = 2 seconds
Lingual deviation to right with moderate
weakness
 56 y/o Vietnamese Male
HTN, diabetes, smoker
Presentation to ED
Nausea, vomited twice in the ED, 5x total
Headache all day
Left facial droop
Dizziness, unsteady gait
Scratchy throat per ED notes, cough
Initial ED diagnosis: dizziness and upper
respiratory infection
 56 y/o Vietnamese Male
HTN, diabetes, smoker
Clarification of Symptoms on day two
Progressive headache that started 4 wks prior
Diplopia started night of admission
Numbness, decreased sensation on right
upper and lower extremities
Horners syndrome (L eyelid), nystagmus
Absent gag bilaterally
Dysphagia, choked on soup on Day 1
Hoarse, ah < 2 seconds
Lingual deviation to right
 We are DETECTIVES!
Use interpreters
Gather background info and interview
patient and family
Perform thorough bedside exams that
address: oral-motor status, voice, speech,
language, cognition, and swallowing
Add more sensory testing
specifically cold sensation
Literature shows Dysphagia
Occurs with LMI at 53-65%

However, much of the literature has

poorly classified dysphagia
Rarely using videoflouroscopy
Definitions of dysphagia are unclear

Kwon, Lae and J.S. Kim (2005)

LMS Dysphagia Research
with Instrumental Exams
 Kwon, Lae and J.S. Kim
(2005)
Studied 46 patients total; 37 with LMI &
9 with MMI (Medial Medullary Infarction)
Importance of instrumental exam due to silent
aspiration. Used Videoflouroscopy.
MMI: problems in the timing of the
hyolaryngeal elevation
LMI: problems in the excursion of the
hyolaryngeal elevation
Direct involvement of the Nucleus
Ambiguus (NA)
 Martino et al. (2001)
MBSS at 3, 9, 14, 27 months post LMI:
3 MONTHS: Normal A-P propulsion, but
absent pharyngeal swallow

9 MONTHS: Anterior and vertical elevation

of larynx only slightly reduced, but
epiglottic deflection absent. No contraction
of middle and inferior pharyngeal
constrictors. UES failed to open. Boluses
pooled in hypopharynx. Penetration.
 Martino et al. (2001)
14 MONTHS: Implemented a volitional
elevation of the larynx to clear bolus through
UES. Piecemeal swallows effective with
liquids and soft solids.

27 MONTHS: More consistent epiglottic

deflection for airway protection. More
efficient pharyngeal phase, but still impaired.
Still needed volitional laryngeal elevation.
 Vigderman et al. (1998)
Studied 57 year old:
L rostral dorsolateral medullary infarct with
aphagia, using MBSS and Manometry.
Small unilateral lesion can cause a
severe bilateral pharyngeal paresis and
aphagia
 Vigderman et al. (1998)
DAY 11: Weak pharyngeal contractions (peak
11.6 mm Hg, Normal is 40-250 mm Hg)
2 MONTHS: Pharyngeal contraction was
improved, but occurring before UES
relaxation. Poorly coordinated swallowing
pattern. Able to take only thick liquids.
20 MONTHS: mild pooling on MBSS.
Manometry still showed the peak pharyngeal
contraction occurring before the full UES
relaxation. PEG removed. Patient on a
regular diet.
 Kim, H., Chung, C.S.,
Lee, K.H. & Robbins, J. (2000)
Studied 23 LMI patients
44% had full aspiration, additional 3
patients penetrated.
(Told to hold the bolus)
No aspiration was noted in patients with
lower level medullary lesions (inferior-
dorsal lesion), as the dorsal region of the
lower medulla does not contain the NA
Combined lower and middle lesions were
all aspirators
 Aydogdu et al. (2001)
Studied 20 patients with LMS
9 of the 20 patients needed non-oral
feeding
95% had some dysphagia. Only 1 out of the
20 exhibited no clinical s/sx of dysphagia.
EMG testing: laryngeal sensors detected
o the onset and duration of the swallow response,
o the upward laryngeal movement,
o variations in the swallow response time, and
o pathological use of piecemeal swallows
 Aydogdu et al. (2001)

85% of the 20 patients had hoarseness

100% had vocal cord paresis

Weak cough 80% of the time

 Dysphagia Limit
Duplication of swallowing or piecemeal
swallowing with <20 ml of water in ALL
patients with LMS
40% of LMS patients could handle only
1ml of water on one swallow
Dysphagia Limit was consistently lower for
the LMS patients (in contrast with the
th
patients with hemispheric CVA or 9 and
10th cranial nerve palsy).
Extremely Delayed Pharyngeal
Swallow Response
Severity of the dysphagia was greater in
LMI, when compared to patients with
unilateral CVA and 9th/10th cranial nerve
palsy
Greater variation in duration of laryngeal
movements
Although a medullary lesion is
unilateral, its effect on swallowing is
bilateral
Laryngopharyngeal paresis
Unilateral LMI produces bilateral
pharyngeal and laryngeal
dysfunction per
electrophysiological
evidence, making the dysphagia
severe.
(Aydogdu et al., 2001)
 Acute disconnection
syndrome
Between the 2 halves of swallowing centers.
Between the NTS and NA
Between the medullary pre-motor neurons
(located in NTS, NA, surrounding reticular
formation) and the synaptic connections with
peripheral afferents through cranial nerves.
Between the medulla and cortical
swallowing-associated areas.
Aydogdu et al. (2001)
 Acute disconnection
syndrome
Disconnection and disruption results in:
o Central Pattern Generator (CPG) for
swallowing to NOT perform it's sequential
muscle activity
o Severely incoordinated muscle activity
o Prolonged pharyngeal phase
o Even caused bilateral dysfunction of the
submental muscles (laryngeal elevators)
 Central Pattern
Generators (CPG)
Swallowing is a patterned sequence of
motor activity that results from the
bilateral input from the swallowing centers
in the rostral dorsolateral medulla.
Swallowing centers: nucleus of the
solitary tract (NTS), nucleus ambiguus
(NA), and the reticular formation.

Vigderman et al.(1998); Aydogdu et al.(2001)

 Martino et al. (2001)
on the CPG
Serial network of linked neurons within the
nucleus of the solitary tract (NTS) and
neighboring reticular formation (p. 423)
Sequential excitation rostrally to caudally
along the deglutition pathway. Activates
the cranial nerve motor neurons (NA and the
vagal dorsal motor nucleus), which in turn
innervate the muscles of swallowing.
Dysphagia in LMS: lesion in the area that
connects the CPG (which is more dorsal and
medial in the brainstem) to the NA (which is
deeper and more lateral in the brainstem).
 Robbins et al. (2008)
on the CPG
Neural networks that are flexibly organized
and multifunctional.
This flexible organization coordinates the
swallowing activity, rather than containing
all the neural circuitry to initiate a
pharyngeal swallow response.
CASE STUDY #2
Pure LMI
 66 y/o Caucasian Male
HTN, COPD, ETOH
Presentation to ED
Fatigue, Ataxia, R-Sided weakness x3 days
Slurred speech
Nausea/vomiting x5 days
Symptoms started one week prior to
admission, but progressed
Head CT Negative
Initial ED diagnosis: recurrent
hyponatremia, daily ETOH
 66 y/o Caucasian Male
HTN, COPD, ETOH
Clarification of Symptoms per SLP
Hoarseness, unable to sustain phonation
Not managing secretions, wet voice
Mild ipsilateral palatal weakness, absent
gag
Overt s/sx aspiration with thin and nectar
thick by cup
Ipsilateral loss of thermal sense on R face
and contralateral loss of thermal sense on
L UE/LE
MRI Findings: R dorsal-
lateral medullary infarct
MRA: Non-visualization of
R VA R PICA

consistent with occlusion

MRA of Brain
Maximum Image
Projection (MIP).
Absent Right
Vertebral Artery
 MBSS 8 Days Post-onset
Moderate Dysphagia
Pharyngeal swallow delay with spillage to
pyriforms with thin and nectar thick
Decreased pharyngeal peristalsis: mod-
severe residue after swallow. Residue
bilateral, but R > L
Moderately decreased laryngeal elevation
with minimal anterior hyolaryngeal excursion
UES Dysfunction
Silent penetration with thin and nectar thick
1 bolus: Paste/Puree -
st

with no strategies cued

Larger bolus of puree
with strategies:
Thin liquid by cup with head
turn and tuck to right
 Meat vs. Cracker
Effortful Swallow Mendelsohn Added
Ground Meat Cracker
 Bread -
with strategies
 MBSS Recommendations
Honey thick liquid by cup: safer to use the
larger bolus sizes for more effective UES
distention.
Dysphagia Ground with caution (refused
puree). No breads. Trained
Mendelsohn, Effortful-piston-like swallow.
Double swallows. Alternate liquids and solids
with honey thick. Cough/Reswallow.
Medication: embedded in applesauce with
liquid washes.
Acute Rehab. Shaker Exercises.
Repeat MBSS per SLP within 2 weeks.
CASE STUDY #3
 56 y/o Vietnamese Male
HTN, diabetes, smoker
Presentation to ED
Nausea, vomited twice in the ED (Total 5x)
Headache all day
Left facial droop
Dizziness, unsteady gait
Scratchy throat per ED notes, cough
Initial ED diagnosis: dizziness and upper
respiratory infection
 56 y/o Vietnamese Male
HTN, diabetes, smoker
Clarification of Symptoms
Progressive headache that started 4 wks
prior
Diplopia started night of admission
Numbness, decreased sensation on right
upper and lower extremities
Horners syndrome (L eyelid), nystagmus
Absent gag bilaterally
Dysphagia, choked on soup on Day 1
Hoarse, ah < 2 seconds
Lingual deviation to right
 MRI Images:
DWI Image ADC map
MRI Description
Small area of
restricted diffusion
within the left dorsal
mid/lower medulla,
with corresponding
T2 hyperintensity in
the region (left: T2
picture)
MRI showed a combined lower
and middle lesion, and he had
significant aspiration issues on
his MBSS.
According to the study by H.
Kim et al. (2000), patients with
this type of large LMI were all
aspirators.
 Day 2 Clinical Bedside
Swallowing Evaluation
Appeared to initially tolerate puree. Then
overt s/sx of aspiration with prolonged
distress with honey thick by spoon, and
delayed sensation of residue.
Expectoration of all puree and honey trials
bedside after 10 min, showing that it must
have pooled in pharynx.
NPO that weekend
 Day 6 MBSS
Moderate oropharyngeal dysphagia
Delayed pharyngeal swallow
UES dysfunction, decreased UES
opening, proximal esophageal stasis
Aspiration with thin and nectar
Tolerated puree and honey thick liquid with
head turn and tuck to L (weaker side).
Effortful swallow. Double swallow to clear
residue above UES.
 MBSS at 3 months
post-stroke
Minimal oropharyngeal dysphagia.
Mildly delayed pharyngeal swallow, mildly
reduced laryngeal elevation.
Penetration above the VC with thin liquids,
but ejected. No aspiration, even with large
sips.
Improved anterior excursion of larynx and
no residue above the UES with solids.
Minimal residue in the proximal
esophagus.
 Puree

Good anterior hyolaryngeal excursion. Good UES opening.

 Solid bolus

Piecemeal swallow, but good UES opening and distention.

Thin liquid

No penetration
 Oropharyngeal
Dysphagia, or
Oropharyngeal PLUS
Esophageal Dysphagia?
 Debate: Is this just a
pharyngeal dysphagia, or a
combination of pharyngeal
and esophageal?
What is causing the UES
dysfunction?
 The Debate
OPINION A: OPINION B:
Reduced laryngeal
Weakness and
elevation and mechanical issues
anterior excursion are present, PLUS
Pharyngeal
Cricopharyngeal
weakness and
decreased bolus muscle is actually
pressure spastic,
All deficits reduce Dysfunction in

mechanical UES striated portion of

opening proximal esophagus
 Opinion A:
Decreased laryngeal elevation and
bolus pressure
Logemann (1998): CP muscle is not actually
spastic. Decreased laryngeal movement & lack
of bolus pressure does not allow for adequate
UES opening or distention.
Jacob et al. (1989): UES opening seems to be
an active mechanical event dependent on
muscular traction to the anterior sphincter wall
rather than simply a consequence of
cricopharyngeal relaxation
 Logemann et. al. (1989)
Studied head rotation in 9 normal and 5 LMS
Abnormal swallows with LMS characterized:
1. Barium residue unilaterally due to pharyngeal
weakness
2. Decreased laryngeal elevation during swallow
3. Barium residue in pyriform on weaker side
Logemann discussed Passive (CP relaxation)
and Active opening forces (superior and anterior
excursion of the larynx to mechanically open the
sphincter segment)
 Logemann's conclusion (1989)
Although head turning was shown to diminish
UES pressure in healthy subjects, and this could
be of therapeutic importance in in the subset of
patients with defective UES relaxation or
diminished compliance of the sphincter as a
pathophysiologic process, the improvement
observed in our (LMS) patients seems to have
been more dependent on maximizing the
impact of opening forces brought to bear on
the sphincter.
(p. 771)
 Recall the Vigderman
et al.'s (1998) Case Study
Patient unable to initiate swallow.
Pharyngeal manometry showed low resting
pressures and weak pharyngeal contractions.
Severe bilateral pharyngeal paresis.
UES relaxation was normal per manometry.
But the UES resting pressures were reduced.
However, they found incoordinated swallowing:
Pharyngeal contractions occurring BEFORE
UES relaxation (similar to Aydogdu).
 Opinion B:

Opinion A is true, AND the cricopharyngeal

muscle and striated portion of esophagus

are spastic.
 Martino et al. (2001)
Motility Studies at 8 months post LMI found:
1. Absent pharyngeal contraction 1 cm
above the UES,
2. No effective relaxation of the
cricopharyngeal muscle,
3. No swallow activity at the level of the
UES,
4. No definite contractile activity in the
proximal 6 cm of the upper esophagus
(striated region).
 Martino et al. (2001)
Basal UES pressure = 44 mm Hg
(significant resting tone)
However, the patient did have a discrete
proximal pharyngeal contraction at 2.5 cm
above the UES, as well as normal
contractile activity lower in the esophagus
at 8-15 cm (smooth muscle).
LES pressure was WNL at 36 mm Hg.
10 Grain Barium Pill
 Robbins & Levine (1993)
62 y/o female with a left LMI secondary to
a left VA occlusion
Bolus flow remained absent due to a
hypertonic cricopharyngeal muscle
Mendelsohn and lingual piston-thrust-
swallow could override the UES high
pressure zone to an extent, but it was still
in the presence of impaired
cricopharyngeal relaxation
 Robbins & Levine (1993)
Manometry: UES sphincter pressure was
distinctly abnormal at 130-160 mmHg with
incomplete relaxation
Needed a Cricopharyngeal Myotomy:
approach from the left side of the neck as the
left true vocal fold was found to be paralyzed
 Robbins & Levine (1993)
Repeat MBSS after Myotomy:
Increased duration & range of motion of the UES
opening
90% of the small liquid bolus to pass into the UES
However, when the patient was coached to
perform a head turn to the left, use the piston
swallow, and perform the Mendelsohn maneuver,
she swallowed the bolus without any post-swallow
residue in the pharynx.
 Robbins & Levine (1993)
Hypopharyngeal suction pump (HSP) needs
cricopharyngeal relaxation as a prerequisite.
Then the hyolaryngeal anterior and superior
excursion can provide the traction to
mechanically open the UES, resulting in a
negative pressure or suction that pulls the
bolus into the esophagus
(Robbins & Levine, 1993)
 Robbins & Levine (1993)

If the dysphagia of LMS was caused by the

oropharyngeal deficits alone, then the
extensive therapy with maneuvers and
strategies should have been sufficient to
pass the bolus through the UES.
 More Research Needed
Pharyngeal constrictor muscle paresis:
damage of the nucleus ambiguus and
vagus nerve, controlling the striated
muscles of the palate, the base of
tongue, the pharynx, and the larynx
(H. Kim, 2000)
However, most studies do not discuss the
striated muscles of the cervical esophagus
as did the two studies above.
Treatment Ideas
 Larger Bolus Volume
Larger boluses found to increase
Pharyngeal wall movement
Duration of hyolaryngeal excursion
Superior UES movement
A-P dimension/width of UES opening
Magnitude and duration of intrabolus
pressure
Velocity through UES
Duration of UES opening
(Jacob et al., 1989)
 Larger Bolus Volume
Stroke patients had decreased pharyngeal
delay, increased duration of laryngeal closure,
longer CP opening. Lazarus et al.(1993)
Prolonged UES opening seen in 8 normals
Kahrilas & Logemann (1992)
Decreased pharyngeal delay time in
neurologically impaired groups with increased
bolus volume and viscosity. Bisch et al. (1994)
Increased median intrabolus pressure during
UES relaxation (using HRM) Ghosh, et al. (2006)
Increase in UES opening duration (HRM) Hoffman
et al. (2010)
Head Turn to Weaker Side
Neck CT evidence of closure above the level
of the pyriform sinus to the level of the hyoid
(in a LMS patient). (Tsukamoto, 2000)
Head turn more effective than chin tuck
strategy for LMS:
*Chin tuck and thickening liquids were
more effective in patients with Medial
Medullary Infarction, in contrast to
treatment for increased range of
hyolaryngeal movement and pharyngeal
peristalsis for LMS. (Kwon et al., 2005)
 Mendelsohn Maneuver
in Normals
Longer durations of pharyngeal contraction &
longer bolus transit time. (Boden et al., 2006)
Only the submental group
(suprahyoid/laryngeal elevators =
digastrics, mylohyoid, geniohyoid)
demonstrated a difference with Mendelsohn
per EMG findings. (Ding et al., 2002)
Mendelsohn increases duration of UES
opening, but Shaker exercise increases
magnitude or diameter of UES opening.
(Shaker et al., 2002)
 Shaker Exercise
Increased A-P diameter of UES opening
Increased max anterior laryngeal excursion
No change in:
o hyoid bone anterior/superior excursion,
o superior laryngeal elevation, or
o lateral laryngeal excursion. (Shaker et al., 2002)
Most effective in patients with aspiration after
the swallow (Mepani et al., 2009; Shaker et al., 2002;
Logemann et al., 2009)
 Shaker Exercise
Mepani et al. (2009): small numbers
6 patients completed traditional therapy
5 completed Shaker protocol
Contraction of the UES opening muscles is
amenable to direct rehabilitation. (p. 30)
Increased anterior-superior hyoid excursion,
allowing for increased A-P UES opening.
Thyrohyoid muscle shortening +
strengthening the suprahyoid muscles. The
effect of shortening and contraction of the
thyrohyoid had not been studied prior.
 Transcranial magnetic
stimulation (TMS)
11 LMI and 11 Brainstem acute stroke patients
(pontomedullary dysfunction)
Randomly selected to receive active vs sham
Active rTMS: 10 trains of 3 Hz stimulation, each
lasting 10 seconds. Repeated every minute for 10
minutes. 5 consecutive days.
Positioned over oesophageal cortical area of
both hemispheres. Intensity of 130% of the
resting motor threshold (RMT), to spread as much
as 2-3 cm from the coil.
(Khedr & Abo-Elfetoh, 2009)
 Transcranial magnetic
stimulation (TMS)
No instrumental pre or post testing
Patients scored with swallowing
questionnaire and bedside examination
Given a degree of dysphagia (DD) rating:
o DD-I: no clinical signs or symptoms
o DD-II: Very mild dysphagia without patient complaint
of symptoms
o DD-III: Patient complaint of dysphagia and clinical
signs, but still taking PO intake.
o DD-IV: Obvious signs and symptoms of
dysphagia, including aspiration, and severe enough
for non-oral feeding.
 Transcranial magnetic
stimulation (TMS)
Tested prior to, after the 5th session, and then
at one and two months post treatment.
Five daily sessions of rTMS produced a more
substantial improvement in dysphagia rating
versus the sham TMS group.
Beneficial effects lasted up to two months.
Researchers speculated: could rTMS have
sped up the natural spontaneous recovery?
However, a LMS patient can improve in the
matter of days without intervention.
 Further Discussion
Cases
Treatment ideas
Research ideas
 Public Health Reminder
Posterior circulation strokes present
differently. Look for
dizziness, nausea, vomiting. May have low
NHI stroke score.
LMS patients need early identification
within the emergency department to avoid
any oral intake prior to a formal swallowing
evaluation.
This can prevent aspiration, intubation and
life-threatening aspiration pneumonia.
 Special Thanks
Alissa Saunders, MD Radiologist
John Mahoney, MD Neurologist
Jeanne Goodman Software Specialist
Thank you for your
attention and
participation!
 UES Relaxation vs
Opening
Need to separate the Passive relaxation
from the Active opening.
Need manometry to test relaxation.
We perceive opening on our MBSS.
These are two different stages of UES
functioning.
Need further discussion of the UES before
discussing treatment strategies.
(supplemental info on UES)
 UES Opening
Sum effect of the relaxation of the
cricopharyngeal (CP) muscle, its
pliability, and the distraction forces imparted
on the sphincter.

(Shaker et al., 1997, p. G1518)

Normal UES function per
Jacob et al. (1989)
1. Relaxation: cessation of tonic activity of
striated muscles. During laryngeal elevation.
0.1 seconds before opening.
2. Opening: Anterior and superior laryngeal
excursion. Infrahyoid compartment
shortening 0.2 seconds before the opening.
Suprahyoid (also called submental) and
thyrohyoid contraction. Hyoid traction on the
anterior wall of the sphincter, as CP muscle
is attached to the lateral aspect of cricoid
cartilage. Intraluminal negative pressure
creates a suction. (Hypopharyngeal Suction
Pump)
Normal UES function per
Jacob et al. (1989)
3. Distention: modulated by intrabolus
pressures due to posterior tongue thrust,
pharyngeal wall contraction, initiation of
pharyngeal peristalsis. Max distention
occurred within 0.13 seconds of opening.
4. Collapse
5. Contraction: closure occurs when the tail
of the bolus transverses the sphincter
 Background on UES -
Crucial to plan treatment
CP Myotomy for chronic impairments in
relaxation. But we can affect OPENING and
DISTENTION
Jacob et al. (1989) suggested that 3 variables
can be manipulated in the sequence:
1. Diameter,
2. Duration, and
3. Velocity of the head of the bolus
Dantas et al. (1990) found increased bolus
volume increases anterior hyolaryngeal
excursion, pharyngeal expansion, and UES
opening and distention.
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