Dysarthria following Stroke

Kristie A. Spencer, Ph.D., CCC-SLP1 and

Katherine A. Brown, M.S., CF-SLP, CBIS1

ABSTRACT

Dysarthria is a common consequence of stroke and can have a

detrimental influence on communication and quality of life. Speech-
language pathologists (SLPs) play an important role in the evaluation

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and rehabilitation of stroke survivors who present with dysarthria. An
understanding of the physiologic reason behind the altered speech
characteristics, such as weakness or incoordination, can facilitate dif-
ferential diagnosis, guide evaluation strategies, and influence treatment
approaches. An initial comprehensive speech evaluation is comprised of
examination of the speech mechanism, screening of speech subsystems,
perceptual assessment, and intelligibility measurement. Management
strategies focus on optimizing communication through compensatory
strategies as well as providing physiologic support. The SLP is also
responsible for educating family and staff regarding strategies that can
facilitate communication.

KEYWORDS: Dysarthria, stroke, evaluation, management,

treatment

Learning Outcomes: As a result of this activity, the reader will be able to (1) identify speech and nonspeech
characteristics associated with each dysarthria type; (2) select five appropriate bedside screening methods to
evaluate the speech mechanism; and (3) implement specific compensatory strategies for speakers with
dysarthria and their significant others.

S peech-language pathologists (SLPs) play a tion, resonance, or prosody due to deviations in

meaningful role in the screening, evaluation, and
management of people who experience dysarthria
from an acute stroke. The dysarthrias are a group
of neurologic motor speech disorders that reflect
abnormalities of respiration, phonation, articula-
strength, speed, range, steadiness, tone, or accu-
racy of the speech mechanism.1 The etiologies of
dysarthria are wide ranging, and encompass con-
ditions that are degenerative, congenital, traum-
atic, inflammatory, and, most germane to this

1
Department of Speech and Hearing Sciences, University of
Washington, Seattle, Washington.
Address for correspondence: Kristie Spencer, Ph.D.,
University of Washington, 1417 NE 42nd Street, Seattle,
WA 98105 (e-mail: kas@uw.edu).
Acute Care Management of Stroke; Guest Editor,
Donna C. Tippett, M.P.H., M.A., CCC-SLP.
Semin Speech Lang 2018;39:15–24. Copyright # 2018 by
Thieme Medical Publishers, Inc., 333 Seventh Avenue,
New York, NY 10001, USA. Tel: +1(212) 584-4662.
DOI: https://doi.org/10.1055/s-0037-1608852.
ISSN 0734-0478.
15
16 SEMINARS IN SPEECH AND LANGUAGE/VOLUME 39, NUMBER 1
article, vascular. Dysarthria affects
41% of the
stroke population,2 and it will be resolved at the
3-month period in fewer than half of stroke
survivors.3 The decreased speech intelligibility
and naturalness associated with dysarthria can
cause challenges with participation in everyday
activities,4 as well as changes in self-identity,
altered relationships, social and emotional disrup-
tions, and feelings of stigmatization.5
Different types of dysarthria have been
identified and are typically associated with spe-
cific types of neurologic deficit or disease.6 Flaccid
dysarthria results from damage to the cranial and/
or spinal nerves. Spastic dysarthria is a conse-
quence of bilateral damage to the upper motor
neurons (corticobulbar/corticospinal tracts).
Both of these dysarthria types can follow a
brainstem stroke. Otherwise, multiple strokes
would be necessary to cause bilateral upper motor
neuron damage and spastic dysarthria. Ataxic
dysarthria results from disruption of the cerebellar
circuit; vascular lesions leading to a dysarthria
would typically involve the superior cerebellar
artery, the posterior-inferior cerebellar artery, or
the anterior-inferior cerebellar artery.1 Hypoki-
netic and hyperkinetic dysarthrias result from
disruption of the basal ganglia circuits. Hypoki-
netic dysarthria is associated most frequently with
the degenerative condition of Parkinson disease,
but can sometimes emerge from vascular etiolo-
gies. Vascular parkinsonism, for example, can
result from diffuse white matter lesions and/or
strategic subcortical infarcts.7,8 It is also uncom-
mon for a hyperkinetic dysarthria to result from a
vascular event. Etiologies for this dysarthria type
are often idiopathic, or from degenerative condi-
tions such as Huntington disease. However,
strokes in the basal ganglia circuit can lead to
movement disorders and hyperkinetic dysarthria,
such as dystonia from putaminal stroke, or chorea
from thalamic stroke.1 Finally, strokes are by far
the most common cause of a unilateral upper
motor neuron (UUMN) dysarthria. Left carotid or
middle cerebral artery occlusions can lead to a
UUMN dysarthria, with likely concomitant
aphasia or apraxia of speech. Right carotid or
middle cerebral artery occlusions can also lead to a
UUMN dysarthria, often with concomitant cog-
nitive-communication impairment, such as
visuospatial neglect or pragmatic deficits. Mixed
dysarthrias, which are a combination of two or
2018
more single dysarthria types (e.g., a mixed spas-
tic-flaccid dysarthria from amyotrophic lateral
sclerosis), are also common and would reflect
features from each relevant dysarthria type.
The importance of identifying and under-
standing the type of dysarthria cannot be over-
stated. Determination of a dysarthria type can (1)
contribute to localization of neurologic disease
within the central or peripheral nervous system,
(2) infer underlying deficits such as weakness or
incoordination, which (3) has important impli-
cations for impairment-based management
approaches.1,9 For example, strengthening exer-
cises would be inappropriate for a person with
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ataxic dysarthria whose dysarthria is driven by
incoordination rather than weakness.
ASSESSMENT
A comprehensive initial speech evaluation is
comprised of (1) history, (2) oral motor/speech
mechanism exam, (3) screening of subsystems
(respiration, phonation, articulation, resonance,
and prosody), (4) perceptual assessment, and (5)
intelligibility evaluation. Most of these procedu-
res overlap with and inform dysphagia assess-
ment as well. Assessment goals vary; in the acute
phase, the emphasis may center on differential
diagnosis, gauging severity, determining the
primary factors contributing to disrupted speech,
and monitoring of clinical symptoms. Dynamic
assessment can also help to determine stimula-
bility for compensatory strategies and possible
impairment-level management approaches.
History
Prior to the evaluation, the SLP reviews the
patient’s medical chart regarding the admission
and makes a note of comorbidities and medica-
tions that may impact speech (and swallowing).10
If available, imaging reports regarding site of
lesion may provide confirmatory evidence for
differential diagnosis. An interview is indispen-
sable and will garner pertinent information such
as the client’s perception and awareness of their
deficit, while providing the clinician an opportu-
nity for observation of speech patterns. Guidance
regarding selective interview questions, in the
acute care stage and beyond, is available in
numerous resources.1,4

Speech evaluation can be confounded when
dysarthria co-occurs with other neurologic com-
munication disorders. This is common, particu-
larly in the acute phase of acquired disorders,4
and SLPs must confirm the presence, and influ-
ence of, concomitant disorders such as aphasia,
cognitive impairment, and apraxia of speech. It is
also important to ascertain the impact of sensory
loss, particularly related to vision and hearing. In
some cases, such as with UUMN dysarthria, the
speech impairment is often overshadowed by
other more pronounced and influential impair-
ments, such as aphasia.
The International Classification for Func-
tioning, Disability, and Health provides a frame-
work for considering the impact of impairment,
activity limitations, and participation restric-
tions. To this end, a bedside evaluation might
include a focus on the impairment (examination
of the oral motor/speech mechanism, screening
of subsystems), activity (perceptual evaluation,
intelligibility testing), and participation (inter-
view, questionnaires, or rating scales).
Examination of the Speech Mechanism
Careful observation of orofacial structures and
movements can help identify the presence,
nature, and degree of motor involvement of
the speech mechanism. As outlined by Duffy,1
clinicians should note abnormalities pertaining
to appearance at rest (size, symmetry) as well as
strength, range of motion, steadiness, speed,
and accuracy of movements. In a standard exam,
the face, lips, jaw, and tongue are observed at
rest, during sustained postures, and during
movement. Sensation of the lips, face, and
tongue can be determined with strategically
placed light touch. The velopharynx should
also be observed at rest and during movement
(e.g., prolonged ah) with evaluation of nasal
emission of air if warranted. Initial determina-
tion of the integrity of the larynx is often based
on voice quality during sustained phonation,
perhaps combined with pitch glides, laryngeal
diadochokinetics,11 or the contrast of a cough
with a glottal coup.1 If indicated, pathologic
reflexes can be tested; the presence of these
reflexes (e.g., jaw jerk, sucking, palmomental) is
most consistent with damage to bilateral upper
motor neurons. See Table 1.
DYSARTHRIA FOLLOWING STROKE/SPENCER, BROWN 17
Speech diadochokinetics can help to in-
form motor control characteristics. These tasks
are also known as alternating motion rates (e.g.,
pa-pa-pa) and sequential motion rates (pa-ta-
ka).1 As this is a maximum performance task, it
is important to first provide a model of fast,
steady, clear production. The clinician should
listen for rate, rhythm, and precision. Norma-
tive values, as reported by Pierce and colleagues,
are summarized in Table 2. Additional resour-
ces for normative data are available.1,12 Specific
profiles are associated with the different dy-
sarthria types. For instance, alternating motion
rate/sequential motion rate performance that is
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markedly slow but regular most often aligns
with spastic dysarthria. Performance that is
arrhythmic from lack of coordination aligns
with ataxic dysarthria, and arrhythmic perfor-
mance from involuntary movements is consis-
tent with hyperkinetic dysarthria.
Results of the speech mechanism evaluation
should help inform the neuromuscular basis of the
dysarthria. In general, weakness following stroke
typically indicates involvement of the lower or
upper motor neurons. Profound weakness, in
particular, reflects lower motor neuron (cranial/
spinal nerve) damage, as the final pathway to the
muscle has been disrupted. Incoordination and
arrhythmic performance following stroke, parti-
cularly in the absence of weakness, is most often
associated with cerebellar lesions. The presence of
involuntary movements is most often associated
with basal ganglia involvement (hyperkinesias).
Finally, movements that are “scaled down,” but
can often be performed adequately in isolation,13
are commonly associated with basal ganglia
disruption (hypokinesias). For instance, a diado-
chokinetic task such as a tongue wag might be
rapid with reduced/underscaled range; in contrast,
isolated testing of tongue range of motion might
be adequate. Slow initiation times would also fit
this profile.
Screening of Subsystems
Following acute stroke, it is expected that
individuals with dysarthria will experience on-
going improvement of their speech. This is
particularly true for the dysarthria that most
often occurs from stroke—UUMN dysarthria.
With this dysarthria, resolution of the speech
18 SEMINARS IN SPEECH AND LANGUAGE/VOLUME 39, NUMBER 1 2018

Table 1 Testing of Normal and Primitive Reflexes

Reflex Method of Testing Normal Response Abnormal Response

Gag Stroke the back of the
reflex tongue, posterior
pharyngeal wall, or faucial
pillars on both sides with a
tongue blade.
Jaw jerk Ask patient to relax with
reflex eyes closed, lips parted,
and jaw about halfway
open. Place tongue blade
Response varies widely,
from no response to a
vigorous gag with gentle
touch of the tongue.
No response (but present in

10% of healthy adults).
Given the wide variability of
responses, only an
asymmetrically elicited gag
is clinically significant for
involvement of the vagus
and/or glossopharyngeal
nerves.
The reflex is a quick jerk of
the jaw toward closing.
An exaggerated or easily
elicited response may be

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on patient’s chin and tap
with finger.
Sucking Briskly stroke upper lip with
reflex a tongue blade, from lateral
to medial position. Conduct
on both sides while patient
has eyes closed.
Snout Lightly tap your finger on
reflex the patient’s philtrum while
their eyes are closed.
Palmomental While patient’s eyes are
reflex closed, vigorously stroke a
tongue blade across the
palm of the hand.
No response (but present in
3% of healthy, young
adults37).
No response (but present in
17þ% of healthy adults).
No response (but present in
37þ% of healthy adults).
indicative of bilateral UMN
disease.
Pursing/pouting of the lips
can be indicative of UMN
disease. The rooting reflex
(e.g., turning mouth toward
tactile stimulus) is an
exaggerated form of the
reflex.
Puckering; protrusion and
elevation of lower lip.
Slight elevation of muscles
in the ipsilateral chin can be
indicative of UMN
involvement.

UMN, upper motor neuron.


Drawn from Duffy.1

Table 2 Normative Values for Diadochokinetic Rate (Syllables per Second) by Task, Age, and
Gender38
Males Females
Group Mean Standard Range Mean Standard Range
Deviation Deviation
65–74 y
/pa/ 6.9 0.81 5.3–7.8 6.3 0.69 5.2–7.5
/ta/ 6.8 0.43 5.7–7.3 5.9 1.00 4.0–7.7
/ka/ 6.3 0.75 5.0–8.1 5.6 1.03 3.3–7.3
/pataka/ 6.1 1.41 3.0–8.0 5.9 1.09 3.7–7.8
74–86 y
/pa/ 6.7 0.74 5.4–8.1 5.9 1.02 4.1–7.6
/ta/ 6.4 1.08 3.6–8.2 5.9 0.87 3.9–7.2
/ka/ 5.8 1.17 3.5–7.2 5.2 1.06 3.2–6.9
/pataka/ 5.4 1.67 2.5–9.0 5.7 0.69 4.3–6.9

symptoms in the weeks following the stroke is
quite common. Regardless, attention to the
subsystems of speech ensures that the SLP is
providing physiologic support where needed.
Screening of respiratory-phonatory function
includes observation of abnormalities that sug-
gest decreased respiratory drive (e.g., shallow
breathing, decreased loudness, short breath
groups) or respiratory incoordination (e.g., irre-
gular breathing rate, uncontrolled loudness,
breaths at syntactically inappropriate junctures).
A water glass manometer is a quick way to
determine respiratory drive for speech, which is
reflected by ability to generate and sustain 5 cm
H2O of pressure for 5 seconds.14 Phonatory
abnormalities are typically determined via audi-
tory-perceptual assessment, described later, alt-
hough acoustic measures are sometimes obtained
to compliment this subjective assessment. Scree-
ning of velopharyngeal function could include
auditory-perceptual assessment of hypernasal (or
hyponasal) resonance, and observation of a
change with occlusion of the nares to intelligibi-
lity, pressure consonants, speaking effort, and
syllables per breath group.4 Additionally, a test of
nasal emission of air can be conducted by holding
a small mirror under the speaker’s nostril while
they produce sentences loaded with pressure
consonants. Screening of articulation and pro-
sody is infused in the speech examination and
perceptual assessment described later.
Perceptual Evaluation
Auditory-perceptual evaluation is the gold
standard for the description, quantification,
and differential diagnosis of the dysarthrias.9,15
Although the variability among raters can be
sizeable,15 it can decrease with perceptual trai-
ning.1 Elicitation tasks involving connected
speech are most useful, such as conversation,
narration, and reading. “The Caterpillar” pas-
sage is a contemporary reading option designed
specifically to facilitate examination of motor
speech disorders.16 This passage contains all
English phonemes, and incorporates prosodic
contrasts, words of increasing length and com-
plexity, and other useful features into the text.
Rating forms can be a helpful tool to guide
the evaluation of the speech characteristics asso-
ciated with the dysarthrias.1,4,15 Comprehensive
DYSARTHRIA FOLLOWING STROKE/SPENCER, BROWN 19
rating forms typically involve determination of
the presence/severity of abnormalities across the
subsystems of speech: respiration, phonation,
articulation, resonance, and prosody. Clinicians
listen for the presence of characteristics such as a
harsh voice, hypernasality, equalized stress
patterns, and slow rate. It is the constellation
of these perceptual features, coupled perhaps
with other diagnostic signs, that leads to the
dysarthria diagnosis. For example, the observa-
tion of the distinguishing characteristics of
breathiness and severe hypernasality, along
with the less distinguishing characteristics of
monopitch, monoloudness, and imprecise arti-
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culation, would argue fairly convincingly for a
diagnosis of flaccid dysarthria. This speech diag-
nosis would be supported by the presence of
atrophy, fasciculations, or diminished reflexes,
and would localize damage to the cranial nerves,
particularly the vagus nerve. In contrast, the
presence of the distinguishing perceptual features
of slow rate and a strained-strangled voice
quality, along with the less distinguishing charac-
teristics of monopitch, monoloudness, and
imprecise articulation, would argue for a diagno-
sis of spastic dysarthria. This speech diagnosis
would be further supported by the presence of
pathologic reflexes and emotional lability, and
would localize damage to the upper motor
neurons, bilaterally. Please see Table 3 for a
summary of characteristics per dysarthria type.
Intelligibility and Speaking Rate
As discussed by Yorkston and colleagues,4 the
clinical measurement of speech intelligibility and
speaking rate is critical because it provides a
useful, objective index of the severity of the
dysarthria and change with treatment (or spon-
taneous recovery). As reduced intelligibility and
speaking rate are nearly universal consequences
of dysarthria, it is imperative for SLPs to have
the tools available to adequately assess these
characteristics. One well-established option is
the Speech Intelligibility Test,17 which provides
an objective measure of sentence intelligibility
and speaking rate. The speaker is recorded while
reading sentences from 5 words to 15 words in
length; an unfamiliar listener is later asked to
transcribe the sentences. Although more time-
consuming than simply estimating intelligibility,

Table 3 Dysarthria Types and Associated Characteristics
Site of disruption
% with vascular etiology
Possible
concomitant signs
Typical neuromuscular
findings for speech
mechanism tasks
Most distinguishing
speech characteristics
Diagnostic hints

Distribution of cases from Mayo Clinic 1999 to 2008.1
20
Flaccid Spastic Ataxic Hypokinetic Hyperkinetic Unilateral Upper
Motor Neuron
Cranial and/or spinal Upper motor neurons Cerebellar circuit Basal ganglia circuit Basal ganglia circuit Upper motor neurons
nerves bilaterally unilaterally
9% 17% 11% 4% 1% 92%
Fasciculations, atrophy, Pathologic reflexes, Ataxic gait, intention Resting tremor, Involuntary limb/trunk Hemiparesis, aphasia/
hypotonia, diminished emotional lability, tremor, nystagmus postural abnormalities movements apraxia, or cognitive-
reflexes, flaccid spasticity in limbs communication
paralysis impairment
Weakness, reduced Weakness, reduced Irregular rhythm, slow Fast rate, decreased Irregular rhythm, can be Mild weakness
range of motion, range of motion, slow; rate; intact range of range when repetitive slow
possibly slow; rhythm rhythm intact motion and strength movement; rhythm
intact intact
SEMINARS IN SPEECH AND LANGUAGE/VOLUME 39, NUMBER 1
Hypernasality, Strained-strangled voice Excess and equal Monopitch, monoloud- Depends on type of Imprecise articulation
breathiness, nasal quality, slow rate stress, distorted ness, reduced stress, involuntary movement may be only
emission, audible vowels, loudness fast rate of speech; (dyskinesia); irregular abnormality
2018
inspiration, short variations, trouble ability to increase prosody, voice, and
phrases coordinating speaking loudness on command articulation
and breathing
Stroke must occur in Would only result from Look for uncoordinated Stroke not a common Stroke not a common Will typically have
brainstem; facial multiple cortical/subcor- performance during cause, but can have cause, but possible unilateral lower facial
paralysis would affect tical strokes or nonspeech diadochoki- vascular parkinsonism (e.g., hemichorea, weakness and, often,
upper and lower face brainstem stroke netics (e.g., rapid, palatal myoclonus) unilateral tongue
continuous pucker- weakness
smile)
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it is more valid and reliable. General estimates of
intelligibility are known to be overestimated,
particularly in the moderate range of severity.4
Additional options for measuring intelligibility,
such as rating scales or published tests, are
summarized elsewhere.1,15
Questionnaires/Rating Scales
Numerous rating scales are available that allow
the person with dysarthria, or their caregiver,
to voice their opinion about the impact of
dysarthria on their daily life and well-being.
These scales, such as the Dysarthria Impact
Profile,18 Living with Dysarthria,19 and the
Communication Participation Item Bank,20
are perhaps most useful upon discharge,
once the person is back in the community
and experiencing the chronic consequences of
dysarthria. These insights offer the opportu-
nity to gain valuable information relevant to
ensuring patient-centered therapy. One gene-
ral rating scale for motor speech, the Func-
tional Communication Measure,21 developed
by the American Speech-Language-Hearing
Association, can serve as a severity rating of
functional speech over time.
TREATMENT
The evidence base for management of post-
stroke dysarthria is weak, particularly in the
acute phase of recovery. This is not surprising
given the often-rapid evolution, and sometimes
resolution, of speech impairment.
In the acute phase, severity and functional
limitations are perhaps the strongest factors
driving treatment decisions. Personal motiva-
tion, prognosis, and involvement of commu-
nication partners are also considerations for
management. Due to the typically brief nature
of the patient’s acute stay and likely inability
to tolerate more intensive treatment, manage-
ment strategies should focus on education, as
well as communication-oriented and physio-
logic supports.
Education
An integral role of the SLP is to provide
education to family, significant others, and
DYSARTHRIA FOLLOWING STROKE/SPENCER, BROWN 21
staff. Education can include basic information
about the dysarthria, prognosis for improve-
ment, and the expected course of treatment. In
the context of reduced intelligibility, the SLP
educates all key communication partners regar-
ding strategies for supporting communication,
as outlined next.
Strategies for Speakers and
Communication Partners
A pivotal aspect of an SLP’s initial management
plan is to provide a means to communicate and
to enhance communication between the speaker
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with dysarthria and his or her communication
partners. These strategies should be used by
family members, significant others, and medical
center staff to promote effective and meaningful
interactions. The aim of these interventions is
to maximize communication opportunities and
participation for the person with stroke, and
also to foster optimal involvement in the reha-
bilitation and recovery process.10 The following
strategies can be considered:
STRATEGIES FOR THE SPEAKER WITH
DYSARTHRIA4,10
 Use pen and paper (using the nondominant
hand if necessary).
 Use an alphabet board (can point to the first
letter of each word or spell out a whole
word).22,23
 Amplify voice.24
 Employ the clear speech strategy.25
 Use electronic communication devices.26
 Try ionic gestures.27
 Introduce topics first; avoid abrupt topic
shifts.22,23
 Establish and maintain a partner’s attention
before initiating communication.
 Preserve grammar in messages (versus in-
tentionally speaking telegraphically).
 Use turn maintenance signals.
 Discuss important topics when energy level
at highest.
 Select conducive communication environ-
ments; reduce noise/distractions in the
environment.
 Engage in one-to-one interactions when
possible.
22 SEMINARS IN SPEECH AND LANGUAGE/VOLUME 39, NUMBER 1
STRATEGIES FOR FAMILIES, SIGNIFICANT
OTHERS, AND STAFF MEMBERS4,10
 Do not pretend that you understand; seek
clarification if you have not understood.
 Pay attention to the speaker.
 Avoid communication over long distances.
 Maintain topic identity; piece together clues.
 Allow adequate processing/speaking time.
 Check that you have understood the mes-
sage by paraphrasing or repeating.
 Have your hearing checked.
 Talk one-to-one where possible.
 Choose a conducive environment; reduce
noise/distractions in the environment.
 Encourage the speaker with dysarthria to use
any communication device/strategy develo-
ped for them.
 Develop a communication diary that stays
with the person with dysarthria.
Finding mutually agreeable rules and signals to
use during communication helps the speaker
maintain a level of independence. The SLP
should facilitate a discussion about the best
ways to avoid, and manage, a communication
breakdown. For instance, does the patient want
a spouse to communicate on their behalf with a
care provider? To shadow or parrot their speech
to ensure understanding? Proactive discussions
about the communication plan can mitigate
potential frustration and embarrassment.
Impairment-Level Management
Although focus on impairment-level deficits in an
acute care setting is likely limited, it is important
to provide physiologic support for speech if
indicated. For the respiratory-phonatory system,
this might include postural adjustments, practice
using appropriate speech breathing pattern, or
effort closure techniques.4,28 For severe velopha-
ryngeal impairment, initial physiologic support
may be provided by a nasal obturator,29 or situa-
tional occlusion of the nares, to allow buildup of
intraoral air pressure. Slowing rate of speech may
be the most powerful, modifiable variable for
improving intelligibility.30 Although individuals
with dysarthria often speak more slowly than their
healthy peers, their speech rates may still be
excessively fast given the physiologic limitations
2018
imposed on their speech mechanisms.25 Strate-
gies conducive to the acute care setting might be
alphabet boards, pacing boards, and finger
tapping.4
Though controversial, strength training
using nonspeech oromotor exercises is a common
treatment poststroke.31 As a whole, this approach
is not recommended for the vast majority of
people with dysarthria. The preponderance of
evidence suggests that improvements in speech
production are best achieved through practice of
speech, versus nonspeech, tasks,32–36 though
further research is warranted.35 The principle of
specificity suggests that the effects of strength
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training are highly specific to the trained beha-
vior. Thus, clinicians should match the exercise as
closely as possible to the desired movement
outcome. By employing strength training in the
context of speech, the principle of specificity is
met and the exercises are therefore expected to
result in greater functional gains.33 Additionally,
nonspeech oromotor exercises can be contraindi-
cated for several clinical populations, including
people who already have high muscle tone (e.g.,
those with spasticity or rigidity).33 Judicious use
of this treatment method may be appropriate in
select circumstances, such as for those with non-
progressive tongue weakness from cranial nerve
XII damage, but only with adherence to the
theoretical foundations of neuromuscular treat-
ments, such as specificity of training, progression
(i.e., the systematic increasing of resistance, con-
traction velocity, and/or duration), and overload
(i.e., taxing a muscle beyond its typical workload
in terms of force or time requirements).31,33
CONCLUSIONS AND FUTURE
DIRECTIONS
The role of the SLP in acute phase dysarthria
includes clinical examination, differential diag-
nosis, implementing communicative supports,
management of physiologic constraints, and
intervention recommendations.
Assessment and management requires
knowledge of the systems that are impaired
and how they interact. It is crucial that SLPs
understand and identify the types of dysarthria to
help elucidate the active disease process, docu-
ment and monitor progression (including spon-
taneous recovery), and guide recommendations.

Presence of confirmatory features must be consi-
dered along with speech mechanism exam fin-
dings to establish relevant diagnostic possibilities.
Perceptual methods are of particular importance
in differential diagnosis and quantification of
dysarthria.
In the poststroke acute phase, the clinician’s
role extends beyond identification and quantifi-
cation of dysarthria to intervention for partici-
pation restrictions. Maximizing communicative
participation supports recovery and enhances an
individual’s involvement in the rehabilitation
process. Utilizing speaker and communication
partner strategies, as well as providing physio-
logic support, can enhance comprehensibility of
dysarthric speech and mitigate communication
breakdowns.
There is still much to learn about dysarthria
following stroke, specifically surrounding best
practices for evaluation, including sensitive mea-
sures for monitoring change, and management.
Efforts to determine efficacious management
strategies, and the candidacy criteria for patient
selection, are warranted.
REFERENCES
1. Duffy JR. Motor Speech Disorders: Substrates,
Differential Diagnosis, and Management. 3rd ed.
St. Louis, MO: Elsevier Mosby; 2013
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