Strained voice, slow rate of speech,

emotional lability and palilalia (the

Mission
compulsive repetition of utterances in
context of increasing rate and decreasing Increase awareness of
loudness) progressive supranuclear palsy,

PSP
Language and cognitive deficits have been
observed and can limit therapy efforts corticobasal d
egeneration,
and related brain diseases;
Speaker with PSP Strategies:
U
 se compensatory strategies to enhance fund research toward cure and
intelligibility
prevention; educate healthcare
Speech must become a conscious effort
Breathe first, and speak loudly and slowly
professionals; and provide support,
information and hope for affected
Keep sentences short
Repeat entire sentence when necessary vs.
What Every
persons and their families.
isolated word
S
 ay one sentence at a time without SLP
immediate repetition
Establish the context Should Know About
Use gestures
LSVT techniques emphasizing increased
phonatory effort may be of benefit
Progressive Supranuclear
Investigate assistive forms of communication
considering visual, cognitive, and motor Palsy
limitations such as communication board or
SGD Laura Purcell Verdun, M.A., CCC/SLP
Consider personal portable amplifier Sandra McWilliams, M.A., CCC/SLP
Listener Strategies:
Keep comments & questions brief
Stick with familiar topics, and one topic at a
time
Use yes / no question format Executive Plaza III
11350 McCormick Road, Suite 906
Ask for clarification, Did you say...?
Hunt Valley, MD 21031
Provide choices to ease decision making
www.curepsp.org

Phone: 410-785-7004
Toll Free: 800-457-4777
Canada: 866-457-4777
Fax: 410-785-7009

WHAT IS PROGRESSIVE
SUPRANUCLEAR PALSY (PSP)?
O
 riginally described as Steele-Richardson-
Olzewski syndrome (1964)
A rare, aggressive, neurodegenerative disease
which is the most common parkinsonian
disorder after Parkinson disease (PD)
Often misdiagnosed as PD
Presents with early postural instability,
supranuclear gaze palsy (paralysis of voluntary
vertical gaze with preserved reflexive eye
movements), and levadopa-non-responsive
parkinsonism
Onset of symptoms is typically symmetric
P
 athologically classified as a tauopathy
(abnormal accumulation in the brain of the
protein tau)
There are currently 3 described variations
Feeding & Swallowing Symptoms:
of PSP: Richardsons syndrome; PSP-
Parkinsonism (PSP-P); and PSP-Pure akinesia
w/gait freezing (PSP-PAGF)
P
 revalence is 6 per 100,000 people; men >
women
Onset usually in the early 60s but may begin in
the 40s
Life expectancy is 7 years following symptom
onset
Speech Pathology Considerations:
Management of swallowing & speech in PSP
Swallowing Management:
requires changing intervention strategies as
the disease progresses
Changes in swallowing and speech often
occur early in PSP and are typically more
severe and deteriorate more rapidly than in
PD
Index of suspicion for dysphagia in PSP
should be high as it is one of the most
common causes of mortality, with recurrent
respiratory infections and respiratory deaths
more common in PSP than PD
Early swallowing evaluation and frequent
monitoring of swallowing function allow for
problem anticipation and use of supportive
measures
Goal of swallowing therapy is to minimize
complications such as aspiration pneumonia
and malnutrition through early symptomatic
treatment
No efficacious approach to speech therapy
has been documented for this patient
population
Therapy program should be simple and
enhance functional communication as
quickly and efficiently as possible vs. just
speech outcomes alone
SWALLOWING IN PSP
Difficulty looking down at the plate
Mouth stuffing and rapid drinking
Tremor or stiffness interfere with self-feeding
Restricted head & neck posture or
hyperextension
Delayed pharyngeal swallow onset
Poor cough
Occasional difficulty opening the mouth
Person w/PSP may lack awareness of
swallowing difficulties
Clinical swallow evaluation should include
mealtime observations and suggestions to
promote easier and safer swallowing
Query the caregiver about swallowing
symptoms
Family should maintain a journal of
observations to help define and adjust
management strategies
VFSS if conducted, needs to replicate the
home eating environment, and rule out non-
neurogenic contributions
Decompensation and aspiration may not be
observed in a controlled VFSS environment,
thus severity of dysphagia may not be truly
appreciated
Discussions regarding feeding tube options
should take place sooner rather than later,
and repeated frequently
Person w/PSP and family should agree in
advance with MD about what is hoped to be
accomplished with a feeding tube
Treatment Strategies:
Optimize oral hygiene
Supervision at mealtimes
Moist, soft, tender foods; avoid dry,
particulate, textured foods
Keep the plate in the line of vision
Maintain head in a chin-tucked position
Restrict liquid and food bolus volumes
Make sure food is swallowed before taking
more
Put cup and utensils down between bites
and sips
Look for mealtime adaptive devices
including cups, plates and utensils to assist
with self-feeding
Medications with a puree consistency
Ask the neurologist about anti-cholinergic
drugs or botulinum toxin for management of
secretions
COMMUNICATION IN PSP
Motor Speech Symptoms:
Mixed
 dysarthria typically including
hypokinetic and spastic dysarthria, less
commonly ataxic
 Speech is hesitant and halting, with strained
voice and slower speech production
Mission
Slowed rate of speech is a reliable marker Increase awareness of
for acquired apraxia of speech
progressive supranuclear palsy,

CBD
Initially may have intact written language
YesNo reversal corticobasal d
egeneration,
and related brain diseases;
Speaker with CBD Strategies:
fund research toward cure and
U
 se compensatory strategies to enhance
intelligibility prevention; educate healthcare
Speech must become a conscious effort professionals; and provide support,
Use short phrases and simpler language
information and hope for affected
because of increased errors with increased What Every
rate of speech, number of syllables, and persons and their families.
complexity of language
SLP
Optimize use of written language
Use of gestures may be limited by apraxia
Should Know About
Alert to yes / no confusion
Investigate assistive forms of communication Corticobasal Degeneration
considering cognitive and motor limitations,
such as communication board or SGD

Listener Strategies:
Laura Purcell Verdun, M.A., CCC/SLP
Eliminate distractions to reduce background
noise
Face the speaker with CBD
Keep comments & questions brief
Stick with familiar topics, and one at a time
Use yes / no question format
Ask for clarification, Did you say? Executive Plaza III
11350 McCormick Road, Suite 906
Hunt Valley, MD 21031
www.curepsp.org

Phone: 410-785-7004
Toll Free: 800-457-4777
Canada: 866-457-4777
Fax: 410-785-7009

WHAT IS CORTICOBASAL
DEGENERATION?
O
 riginally described in 1968 by Rebeiz,
Kolodny, and Richardson; with earliest
descriptions by Charcot (1888)
A rare neurodegenerative disease characterized
by apraxia, non-fluent aphasia, frontal
dementia, limb rigidity and dystonia, alien limb
phenomenon, and postural instability
Onset of symptoms is markedly asymmetric
Pathologically classified as a tauopathy
(abnormal accumulation in the brain of the
protein tau)
Diagnosis is difficult because clinical features
often over-lap with Parkinson disease (PD),
progressive supranuclear palsy, Alzheimers,
primary progressive aphasia, and fronto-
temporal dementia
Onset between 60 80 y.o.
Prevalence of 5 7 per 100,00; women > men
Life expectancy is 7-10 years following
symptom onset
Speech Pathology Considerations:
M
 anagement of swallowing & speech
in CBD requires changing intervention
strategies as the disease progresses
C
 hanges in swallowing and speech often
occur early in CBD and are typically more
severe and deteriorate more rapidly than PD
Index of suspicion for dysphagia in CBD
should be high as it is one of the most
common causes of mortality, with recurrent
respiratory infections and respiratory deaths
more common in CBD than PD
Early swallowing evaluation and frequent
monitoring of swallowing function allow for
problem anticipation and use of supportive
measures
G
 oal of swallowing therapy is to minimize
complications such as aspiration pneumonia
and malnutrition through early symptomatic
treatment
No efficacious approach to speech therapy
has been documented for this patient
population
Therapy
 program should be simple and
enhance functional communication as
quickly and efficiently as possible vs. just
speech outcomes alone
SWALLOWING IN CBD
Feeding & Swallowing Symptoms:
Impaired self-feeding
Slow or incomplete chewing
Oral and swallowing apraxia
Slowed swallowing movements
May be aware of swallowing difficulties
Swallowing Management:
C
 linical swallow evaluation should include
mealtime observations and suggestions to
promote easier and safer swallowing
F
 amily should maintain a journal of
observations to help define and adjust
management strategies
VFSS if conducted, needs to replicate the
home eating environment, and rule out non-
neurogenic contributions
Decompensation and aspiration may not be
observed in a controlled VFSS environment,
thus severity of dysphagia may not truly be
appreciated
Discussions regarding feeding tube options
should take place sooner rather than later,
and repeated frequently
Person w/CBD and family should agree in
advance with MD about what is hoped to be
accomplished with a feeding tube
Treatment Strategies:
Optimize oral hygiene
Supervision at mealtimes
Use less-affected side for self-feeding
Maintain head in a chin-tucked position
Avoid highly textured, particulate foods
Blend multiple consistency foods
Proceed with caution with thin liquids
Alternate food and liquid swallows
Medications with a puree consistency
Look for mealtime adaptive devices
including cups, plates, and utensils to assist
with self-feeding
Consider smaller, more frequent meals due
to increased length of time when eating
Ask the neurologist about the role of
anti-cholinergic drugs or botulinum toxin for
management of secretions assist with self-
feeding
COMMUNICATION IN CBD
Motor Speech Symptoms:
C
 haracterized by hypokinetic and spastic
dysarthria, as well as progressive apraxia of
speech and oral apraxia
Progressive non-fluent aphasia
 MSA-A: often ataxic or hypokinetic
dysarthria, but may be mixed with s pastic
Mission
dysarthria
Increase awareness of
MSA-C: ataxic dysarthria is most often
progressive supranuclear palsy,

MSA
expected, or in combination with spastic
dysarthria corticobasal d
egeneration,
Typically more changes in speech than voice
and related brain diseases;
Cognitive impairment is typically mild
fund research toward cure and
Speaker with CBD Strategies: prevention; educate healthcare
Speech must become a conscious effort
professionals; and provide support,
Emphasis on taking a breath first
information and hope for affected
Reduce
 rate of speech to improve What Every
coordination and accuracy of motor speech persons and their families.
movements
Intelligibility drills with exaggeration of
SLP
articulation movements
Investigate assistive forms of communication
Should Know About
considering motor limitations such as a
communication board or SGD Multi-System Atrophy
Listener Strategies:
Laura Purcell Verdun, M.A., CCC/SLP
Eliminate distractions to reduce background
noise
Face the speaker with MSA
Keep comments & questions brief
Stick with familiar topics, and one topic at a
time
Use yes / no question format
Ask for clarification, Did you say?
Executive Plaza III
Provide choices to ease decision making 11350 McCormick Road, Suite 906
Hunt Valley, MD 21031
www.curepsp.org

Phone: 410-785-7004
Toll Free: 800-457-4777
Canada: 866-457-4777
Fax: 410-785-7009

WHAT IS MULTI-SYSTEM
ATROPHY (MSA)?
F
 irst described in 1962 as Shy-Drager
Syndrome
MSA is now the preferred term to reflect more
than one disease process
A rare neurodegenerative condition
characterized by varying degrees of
parkinsonism, ataxia, and autonomic
dysfunction; occasionally misdiagnosed as
Parkinson disease (PD)
Pathologically classified as a synucleinopathy
(abnormal accumulation in the brain of the
protein alpha synuclein)
There are 3 clinical syndromes under MSA with
varying degrees of parkinsonism
MSA-P (parkinsonian): Striatonigral
degeneration implies parkinsonism (rigidity
and akinesia) with some degree of cerebellar
dysfunction
MSA-A (autonomic): Shy-Drager syndrome
reflects a predominance of autonomic failure
MSA-C (cerebellar): Olivopontocerebellar
atrophy indicates primarily cerebellar defects
with minor degrees of parkinsonism
Prevalence is approximately 3 4 per 100,000
Onset usually after 50 y.o.; men > women
Life expectancy is 7-10 years following
symptom onset
Speech Pathology Considerations:
M
 anagement of swallowing & speech
in MSA requires changing intervention
strategies as the disease progresses
U
 p to 1/3 of individuals with MSA may have
laryngeal stridor possibly caused by vocal
fold abductor paresis or laryngeal dystonia
Early swallowing evaluation and frequent
monitoring of swallowing function allow for
problem anticipation and use of supportive
measures
Mixed dysarthria is common and tends to
emerge earlier in disease course than in
PD, is more severe, and deteriorates more
rapidly
No efficacious approach to speech therapy
has been documented for this patient
population
Therapy
 program should be simple and
enhance functional communication as
quickly and efficiently as possible vs. just
speech outcomes alone
SWALLOWING IN MSA
Feeding & Swallowing Symptoms:
Difficulty sitting upright at mealtimes
Tendency towards bolus holding in oral
cavity, and discoordinated oral bolus
formation and propulsion
Pharyngeal weakness and disruption of the
cricopharyngeal segment
Vocal fold motion impairment may
compromise airway protection later in the
disease progression
May occasionally have tracheotomy
Cough may also be compromised
Swallowing Management:
C
 linical swallow evaluation should include
mealtime observations and suggestions to
promote easier and safer swallowing
Motor Speech Symptoms:
F
 amily should maintain a journal of
observations to help define and adjust
management strategies
VFSS if conducted, needs to replicate the
home eating environment, and rule out non-
neurogenic contributions
Decompensation and aspiration may not be
observed in a controlled VFSS environment,
thus severity of dysphagia may not truly be
appreciated
Discussions regarding feeding tube options
should take place sooner rather than later,
and repeated frequently
Person w/MSA and family should agree in
advance with MD about what is hoped to be
accomplished with a feeding tube
Treatment Strategies:
Optimize oral hygiene
Positioningsupport to sit upright against
the chair back
Maintain head in a chin-tucked position
Alternate food and liquid swallows
Restrict bolus volumes
Moist, soft, tender foods; and blend multiple
consistency items
Look for mealtime adaptive devices
including cups, plates and utensils to assist
with self-feeding
Consider smaller, more frequent meals due
to increased length of time when eating
Ask the neurologist about the role of
anti-cholinergic drugs or botulinum toxin for
management of secretions
COMMUNICATION IN MSA
MSA-P:
 hypokinetic dysarthria is
expected, sometimes mixed with s pastic or
hyperkinetic dysarthria