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194 MOTOR SPEECH DISORDERS: DIAGNOSIS AND TREATMENT
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motor neuron weakness and certain signs of extrapyramidal system
involvement might also be present. Because these other areas of
the motor system can be affected, the dysarthria associated with
Friedreich’s ataxia is often of a mixed type, which is examined in
Chapter 10.
Olivopontocerebellar degeneration is another progressive
cerebellar disorder that tends to run in families. This disorder
results in atrophy of the middle cerebellar peduncle, much of the
cerebellum, and parts of the pons. One of the primary symptoms
of olivopontocerebellar degeneration is cerebellar ataxia. The neuron degeneration associated with this disorder also can involve the
basal ganglia and some of the corticospinal tract. Symptoms of a
parkinsonian nature, such as muscular rigidity and reduced range
of movement, also are often present. As with Friedreich’s ataxia,
the dysarthria associated with olivopontocerebellar degeneration is
usually more mixed in nature rather than a pure ataxic type.
Stroke
As with the other areas of the brain, the cerebellum has a rich arterial blood supply. Several arteries serve the cerebellum, including
the superior cerebellar artery and the anterior inferior cerebellar
artery. Blockage of blood ow through either of these arteries
can cause ataxic dysarthria. Ruptured aneurysms or arteriovenous
malformations in these arteries also have been linked to ataxic
dysarthria. In fact, about 10% of intracerebral hemorrhages primarily affect the cerebellum or the neurons in the cerebellar control
circuits (Heilman et al., 1977). Most cerebellar stokes result in the
sudden onset of a number of “cerebellar signs,” including limb
ataxia, problems with balance, visual decits, and ataxic dysarthria.
Toxic Conditions
Different toxic and metabolic conditions can affect the functioning
of the cerebellum. The toxic conditions that have been associated
with cerebellar dysfunction include lead and mercury poisoning,
long- and short-term consumption of alcohol, and exposure to
chemicals such as acrylamide and cyanide. Most of these conditions
are treatable, and any instances of ataxic dysarthria, if present, will
usually resolve as the toxic levels of these substances decrease.
Toxic levels of phenytoin (Dilantin), an antiseizure drug, also have
been associated with ataxic dysarthria. Unlike many of the other
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toxic conditions, the effects of long-term phenytoin overdosage
might be irreversible.
Other conditions that can result in cerebellar dysfunction
include prolonged vitamin E or B12 deciency, severe cases of
hypothyroidism, and hereditary disorders such as Wilson’s disease.
Each of these can cause ataxic dysarthria, although they are not
common disorders. Incidentally, Wilson’s disease usually results
in mixed dysarthria and is discussed in more detail in Chapter 10.
Traumatic Head Injury
Cerebellar tissue can be distorted and stretched by the force of
head trauma and can be just as susceptible to the dynamics of an
impact as the other parts of the brain. As with most head injuries,
traumatic damage to the cerebellum tends to be diffuse. However,
the cerebellar peduncles are especially vulnerable to the twisting
and rotational forces of such an injury, because the cerebellum is
essentially an appendage that is attached to the brainstem. During a rapid, rotational movement of the head, some of the highest
amounts of axon stretching could be at these points of attachment.
As a result, the axons coursing through the peduncles often are
especially susceptible to damage during a head injury.
Tumors
Tumors can affect cerebellar function in several ways. First, a tumor
could grow in cerebellar tissue, directly destroying cells and compressing the cerebellum if it grows large enough. Second, a tumor
could grow near the cerebellum, for example, on the occipital
lobe, which then compresses cerebellar tissue. Third, a brainstem
tumor could interfere with the functions of the cerebellar control
circuits. The appearance of ataxic dysarthria after the appearance
of a cerebellar tumor depends on the location and size of the tumor.
Duffy (2013) reported that tumors accounted for about 6% of the
cases of ataxic dysarthria at the Mayo Clinic over a 9-year period.
Certain types of tumors tend to appear frequently in the cerebellum. Metastatic tumors are among the most common. These
tumors are formed when one tumor (the primary tumor) sheds cancerous cells that seed a secondary (metastatic) tumor in another part
of the body. Primary metastatic cerebellar tumors are usually located
in sites such as the skin (melanomas), lungs, kidneys, or breasts.
A slow-growing type of tumor called a low-grade astrocytoma
196 MOTOR SPEECH DISORDERS: DIAGNOSIS AND TREATMENT
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can appear frequently in the cerebellum, especially in children.
More than 50% of these tumors in children are located in the
cerebellum. When it occurs in adults, this type of tumor usually
appears between the ages of 30 and 60. Hemangioblastomas are
benign tumors of proliferated blood vessels found occasionally
in the cerebellum. The symptoms of a hemangioblastoma usually
appear late in childhood, but sometimes they are not evident until
the affected individual is an adult. Progressive cerebellar ataxia
and ataxic dysarthria can be among the symptoms of a cerebellar
hemangioblastoma.
Other Possible Causes
Although the following are not the most common causes of cerebellar dysfunction, ataxic dysarthria also can result from:
n Viral infections that invade the cerebellum.
n Other infections, such as trichinosis, typhus, and syphilis, that
could affect cerebellar functions.
n A bacterial abscess (a localized collection of pus) near the
cerebellum that could compress the surrounding brain tissue.
Such an abscess will probably present symptoms similar to
those of a cerebellar tumor.
Speech Characteristics of Ataxic Dysarthria
In general, individuals with ataxic dysarthria give the impression
that the movements of their speech mechanism are poorly coordinated. As in other cerebellar-based movement problems, patients
with ataxic dysarthria seem to have problems controlling the timing
and force of the many muscular contractions that are needed to
produce clearly articulated speech. It is often reported that individuals with ataxic dysarthria have a drunken quality to their speech.
Patients frequently report that articulation is slurred and prosody is
monotonous. Such symptoms reect the fact that ataxic dysarthria
is primarily a disorder of articulation and prosody (Duffy, 2020).
Some medical professionals use the term scanning speech when
talking about ataxic dysarthria. In that usage, it describes how
individuals with this dysarthria often demonstrate a slow, deliberate production of syllables, with each syllable in a word receiving
equal stress.
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Articulation
Articulation decits are a signicant problem in ataxic dysarthria.
Darley et al. (1969a, 1969b) found that imprecise consonant production was the most prevalent speech error in this type of dysarthria
(Table 7–1). Another common characteristic is distorted vowels. It
is the imperfect articulation of phonemes that gives ataxic dysarthria its characteristic slurred quality. These distortions are caused
by cerebellar damage that disrupts the timing, force, range, and
direction of movements needed to maintain normal articulation.
Such decits in the performance of complex movements requiring
more than one body part are sometimes called decomposition of
movement.
The articulation errors in ataxic dysarthria, however, might not
always be consistent. Some individuals with ataxic dysarthria also
might demonstrate irregular articulatory breakdowns, meaning
that their imprecise consonant and vowel productions can vary
from utterance to utterance. These intermittent breakdowns will
usually occur most frequently in sentences that contain several multisyllabic words, but the errors might not appear on every production of such a sentence. The breakdowns often give the appearance
that the syllables are being compressed during the production of a
word. Incidentally, hyperkinetic dysarthria (Chapter 9) is the only
TABLE 7–1
Rank Speech Production Errors
1 Imprecise consonants
2 Excess and equal stress
3 Irregular articulatory breakdown
4 Distorted vowels
5 Harsh voice quality
6 Prolonged phonemes
7 Prolonged intervals
8 Monopitch
9 Monoloudness
10 Slow rate
Source: From “Clusters of Diagnostic Patterns of Dysarthria,” by F. L. Darley, A. E. Aronson, and
J. R. Brown, 1969, Journal of Speech and Hearing Research, 12, p. 256. Copyright 1969 by
American Speech-Language-Hearing Association. Reprinted with permission.
The Most Common Speech Production Errors in
30 Individuals With Ataxic Dysarthria
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other dysarthria in which irregular articulatory breakdowns could
be present, although Duffy and Folger (1986) did nd it in a few
of their subjects with unilateral upper motor neuron dysarthria. In
general, the articulation errors in most of the other dysarthrias tend
to be quite consistent during speech (Darley et al., 1975). Watch
the PluralPlus Ataxia Dysarthria Case 1 and 2 videos for examples
www
of the articulation and prosody difculties in this disorder.
Prosody
Prosodic errors also are prominent in ataxic dysarthria. At least six
prosodic decits can be present in the speech of individuals with
this type of dysarthria:
n Equal and excess stress
n Prolonged phonemes
n Prolonged intervals between phonemes
n Monopitch
n Monoloudness
n Slow rate
Darley et al. (1969a, 1969b) ranked each of these within the top 10
most deviant speech characteristics of their subjects with cerebellar lesions.
Equal and excess stress is the tendency of many speakers
with ataxic dysarthria to put equal stress on syllables or words that
would normally have varied stress patterns. Some speakers with
ataxic dysarthria tend to put excessive stress on syllables or words
that are not normally stressed to that degree. This stress pattern
can be a distinguishing characteristic of ataxic dysarthria. When listening to an individual speaking in this manner, the syllable stress
on such words as record (the noun) and record (the verb) might
appear to be quite similar, with the listener needing to infer the
correct word from the context. This stress pattern gives the impression that each syllable or word is produced separately, without one
part of a word or sentence being inuenced by the others.
The next two prosodic errors, prolonged phonemes and prolonged intervals between phonemes, are related. One of the hallmarks of cerebellar damage is slow movement on both single and
repetitive motion tasks. This slowness includes the movements of
the speech musculature, resulting in a slowed production of phonemes and a lengthening of the intervals between phonemes. Net-
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sell and Kent (1976) indicated that these prolongations are probably
caused by decreased muscle tone (hypotonia). They suggested that
this hypotonia results in a general slowness in the contractions of
the speech muscles, resulting in an overall prolongation of speech
production. These prolongations of phonemes and intervals contribute to a slow rate of speech, which is another prosodic defect
that is very common in ataxic dysarthria.
Darley et al. (1969a, 1969b) noted monopitch in 20 and monoloudness in 18 of their 30 subjects with cerebellar damage. They
suggested that these two prosodic errors also are caused by hypotonia of the speech muscles. It is logical to assume that the equalizing
of stress also contributes to the perception of these two characteristics in individuals with ataxic dysarthria.
Phonation
Few phonatory decits are usually noted in ataxia dysarthria. Darley et al. (1969a, 1969b) found that harsh vocal quality is certainly
the most prominent phonatory decit that could be evident in this
dysarthria. They identied this phonatory problem in 21 of their
30 subjects. These researchers suggested that this condition is caused
by decreased muscle tone in the laryngeal and respiratory structures, which prevents the full contraction of these muscle groups.
Another possible phonatory problem in ataxic dysarthria is
voice tremor. Cerebellar damage might cause tremors that affect vari
ous body parts, and when the laryngeal or respiratory muscles are
involved, the result can be a distinguishable voice tremor. Although
not common, it has been observed in some individuals with this
dysarthria (Ackermann & Ziegler, 1991; Darley et al., 1969a, 1969b).
-
Resonance
Hypernasality is seldom a serious problem in ataxic dysarthria.
Darley et al. (1969a, 1969b) did not rank it as one of the signicant
speech errors in their study of subjects with cerebellar lesions,
although 10 of their 30 subjects demonstrated some instances of it.
These researchers, nevertheless, concluded that it is not a prominent characteristic of this dysarthria. Duffy (2020) also reported
that abnormal resonance is infrequent, but he noted that intermittent hyponasality could be evident in some individuals, probably
because of timing errors between the muscles of the velum and the
other muscles of articulation.
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Respiration
Cerebellar damage can cause uncoordinated movements in the
respiratory muscles, which can contribute to the speech decits
heard in ataxic dysarthria. Although few studies have examined
the respiration of individuals with ataxic dysarthria, several have
shown that respiration during speech can contain exaggerated or
paradoxical movements (Luchsinger & Arnold, 1965; Murdoch et al.,
1991). Paradoxical movements occur when different muscle groups
work against each other rather than in coordination. Such abnormal
respiratory movements can affect speech production. Exaggerated
movements of the respiratory muscles can lead to excessive loudness variations during many speech tasks, including conversation.
Paradoxical movements of the intercostal muscles and the diaphragm can reduce the vital capacity of the lungs and thereby
limit the amount of subglottic air available for speech. Insufcient
subglottic air pressure during conversational speech often leads the
affected individual to speak on residual air. This, in turn, can lead
to an increased rate of speech, decreased loudness, and a harsh
vocal quality. Ultimately, these abnormal respiratory movements can
affect the prosody of individuals with ataxic dysarthria. Incidentally,
Darley et al. (1969a, 1969b) did not notice any rapid involuntary
inhalations or exhalations of air in their subjects with ataxic dysarthria. Such involuntary respiratory movements are observed much
more frequently in cases of hyperkinetic dysarthria (Chapter 9).
Key Evaluation Tasks for Ataxic Dysarthria
1. Speech alternate motion rates can be one of the most valu-
2. Reading, conversational speech, and repeating sentences
able evaluation tasks when ataxic dysarthria is suspected.
The overall rate will probably be slower than normal. In
addition, many individuals with this dysarthria will be
unable to maintain a steady rhythm as they repeat the target
sounds. In the most severe cases, they might speed up
abruptly and then, just as unexpectedly, slow down during
this speech production task. Their difculty in maintaining a
regular rhythm highlights how cerebellar damage can affect
the timing of movements by different muscle groups.
containing numerous multisyllabic words also are important
evaluation tasks (Duffy, 2020). The complexity of these
longer speech activities will reveal any inaccurate speech
movements. As such, they can be especially effective at
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evoking the irregular articulatory breakdowns that often
appear in ataxic dysarthria. Remember that these breakdowns tend to occur more frequently on multisyllabic
words than on words of shorter length. Furthermore, these
three tasks should reveal any prosodic errors that might be
present in connected speech.
Treatment of Ataxic Dysarthria
As stated previously, ataxic dysarthria is the result of damage to
the cerebellum or the cerebellar control circuit. This damage often
affects the speed, force, and timing of movements by the articulators, which results in movements that are typically described
as “uncoordinated.” In a majority of instances, the most evident
speech errors in this dysarthria are those related to articulation
and prosody.
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Respiration
Most patients with ataxic dysarthria do not need to work on strengthening their respiration abilities. Rather, they usually should concentrate on controlling their airow more accurately during speech.
The uncoordinated movements of their respiratory muscles can
leave them speaking on residual air, which affects prosody and
phonation. There are numerous tasks that could be useful in helping these patients gain better breath control during speech.
n Slow and controlled exhalation—In this simple task, the
patient is asked to inhale fully and then exhale in a slow,
steady stream. Using a stopwatch, the clinician times the
length of the exhalation. The goal is to increase the length
and steadiness of the airow over several sessions. Dworkin
(1991) described an advanced variation on this task in which
the patient is asked to inhale fully, begin a slow exhalation
for 3 s, stop the exhalation by holding the breath for about
1 s, then continue with the exhalation. The difculty of
this task can be increased until the patient is holding and
releasing the air three times on a single breath.
n Speak immediately on exhalation—Because of poor coordina-
tion of the respiratory and laryngeal muscles, many patients
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with ataxic dysarthria waste a signicant amount of their
subglottic air by beginning their phonations a second or two
after they have started to exhale. The task of speaking immediately on exhalation concentrates on making sure patients
initiate phonation the moment they begin an exhalation.
Swigert (2010) suggested that the patient place a hand on the
abdomen and begin a simple /m/ phonation the moment the
hand starts to move inward on the exhalation. The clinician
can place his or her hand on the patient’s hand to know when
to cue the patient to begin the phonation, if necessary.
n Stop phonation early—Because individuals with ataxic dysar-
thria often have shallow respiration, they might try to speak
for a longer period than their limited subglottic air supply
allows. This results in speaking on residual air and frequently
leads to harsh vocal quality, decreased loudness, and increased
rate of speech. Consequently, it is often necessary for the
patient to learn to end an utterance before running low on air.
This can often be initially accomplished by having the clinician provide verbal and visual cues that tell the patient when
to stop phonating and take another breath. Over time, as the
patient becomes more independent at stopping phonation
before speaking on residual air, the clinician’s cues can be
withdrawn.
n Optimal breath group—This task is somewhat similar to the
stopping phonation early procedure. The optimal breath
group task teaches the patient how many syllables or words
can be said clearly on one full inhalation (Linebaugh, 1983).
Once a baseline has been established, the patient can work
on increasing the length of the breath group, perhaps through
deeper inhalations, more controlled exhalations, or beginning
phonations immediately on exhalation. The optimal breath
group task is similar to cued reading materials and chunking
utterances into syntactic units activities, which are described
later.
Prosody
The prosodic problems experienced by individuals with ataxic dysarthria usually involve rate, stress, and intonation. By slowing their
rate, these individuals often can improve their intelligibility. By
incorporating more typical stress and intonation into their utterances, their speech could exhibit a more natural quality.
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Rate Control
Although a slow or irregular rate of speech is characteristic of
ataxic dysarthria, many individuals with this disorder still attempt
to speak at a rate that is too rapid for their speech production
capabilities. By speaking too rapidly, they do not give their articulators sufcient time to reach target positions, nor do they give a
listener enough time to assimilate the spoken message. The amount
of slowing needed to improve intelligibility does not always have
to be signicant. Often minimal decreases in rate can result in
noticeably more understandable speech. The following rate control
tasks are some of the procedures that might successfully slow the
speaking rate of individuals with ataxic dysarthria. These tasks
are highly structured and are probably most appropriate for the
initial treatment steps in which increasing a patient’s awareness of
a slower, more intelligible rate is the primary goal.
n Reciting syllables to a metronome—Dworkin (1991) suggested
using a metronome to set the pace of syllable production. In
this task, the metronome is set to the appropriate rate, and
the patient is asked to recite or read familiar passages such as
the Pledge of Allegiance, a well-known poem, or something
similar. The patient should produce one syllable for every
beat of the metronome. Although the resulting speech will
sound automated, this is acceptable because the goal in this
task is to build the patient’s awareness of a more appropriate
speech rate. With enough practice, the slower pace set by the
metronome could become habituated into the patient’s conversational speech.
n Finger or hand tapping—Finger or hand tapping can be substi-
tuted for a metronome to set the pace of appropriate syllable
production. Initially, the clinician sets the pace by tapping with
a nger or hand, with the patient following the tempo while
reading a familiar passage. Once the pace is established, the
patient can try to do the tapping. Be aware, however, that the
typically uncoordinated movements of such a patient might
make it very difcult for him or her to maintain a regular pace
when trying to tap independently.
n Cued reading material—Various rate cueing techniques can
be used with written sentences or paragraphs. One type of
cueing is to have the clinician point to a word or syllable at
the desired rate and ask the patient to read the material at that
pace. Another type of cueing is to have reading material that
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