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184 MOTOR SPEECH DISORDERS: DIAGNOSIS AND TREATMENT
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the left hemisphere of the brain. When the right hemisphere
is damaged, this dysarthria often co-occurs with the visual
and cognitive decits associated with injury to that side of
the brain.
n Treatment of unilateral upper motor neuron dysarthria
includes such traditional articulation tasks as intelligibility
drills and phonetic placement.
Study Questions
1. Dene unilateral upper motor neuron dysarthria in your
own words.
2. Why does unilateral damage to the upper motor neurons
result in less severe symptoms as compared with bilateral
damage to these neurons?
3. Unilateral upper motor neuron dysarthria is primarily a
disorder of what?
4. What is the most common cause of unilateral upper motor
neuron dysarthria?
5. Why are traumatic head injuries not a common cause of
unilateral upper motor neuron dysarthria?
6. What is the most common articulation disorder in cases of
unilateral upper motor neuron dysarthria?
7. What did Duffy suggest as the cause of harsh vocal quality
in unilateral upper motor neuron dysarthria?
8. Why are there so few treatment studies for unilateral upper
motor neuron dysarthria?
9. Describe intelligibility drills.
10. What are minimal contrast drills?
Ataxic Dysarthria
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Chapter 7
Definitions of Ataxic Dysarthria
Dysarthria
Neural Pathways to and From the
Cerebellum
The Cerebellum and Speech
Causes of Ataxic Dysarthria
Degenerative Diseases
Stroke
Toxic Conditions
Traumatic Head Injury
Tumors
Other Possible Causes
Speech Characteristics of Ataxic
Dysarthria
Articulation
Prosody
Phonation
Resonance
Respiration
Key Evaluation Tasks for Ataxic
Dysarthria
Treatment of Ataxic Dysarthria
Respiration
Prosody
Rate Control
Stress and Intonation
Articulation
Summary of Ataxic Dysarthria
Study Questions
185
186 MOTOR SPEECH DISORDERS: DIAGNOSIS AND TREATMENT
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Definitions of Ataxic Dysarthria
Damage to the cerebellum is the most common feature in the published denitions of ataxic dysarthria (sometimes called cerebellar
dysarthria). It is mentioned in nearly all instances. This cerebellar damage results in speech errors that are primarily articulatory
and prosodic. These two types of errors often combine to give the
speech of individuals with ataxic dysarthria an unsteady, slurred
quality. All three of the following denitions are good introductions
to ataxic dysarthria.
[A] dysarthria associated with damage to the cerebellar system and
characterized by speech errors relating primarily to timing, giving
equal stress to each syllable; articulation problems are typically characterized by intermittent errors ranging from mild to severe; vocal quality [can be] harsh, with monotonous pitch and volume; prosody may
range from reduced to unnatural stress. (Nicolosi et al., 1983, p. 79)
Ataxic dysarthria is a disorder of sensorimotor control for speech
production that results from damage to the cerebellum or to its input
and output pathways. The dragging and blurred quality of ataxic
dysarthria speech has sometimes been likened to “drunken speech.”
(Cannito & Marquardt, 1997, p. 217)
Acute and chronic, hereditary or acquired cerebellar disorders are
often accompanied by [ataxic dysarthria], especially in patients with
lesions in the left paravermian region [of the cerebellum]. The disorders typically result in slow speech with difculty pronouncing
words and scanning syllables. (Rampello et al., 2016, p. 357)
Neurologic Basis of Ataxic Dysarthria
Up to now, this textbook has discussed dysarthrias that are caused
by damage to motor neurons. Flaccid dysarthria (Chapter 4) is
caused by damage to the lower motor neurons; spastic dysarthria
(Chapter 5) is caused by bilateral damage to the upper motor neurons; and unilateral upper motor neuron dysarthria (Chapter 6)
is caused by unilateral damage to the upper motor neurons. This
chapter examines ataxic dysarthria, which is caused by damage to
the cerebellum or to the neural pathways that connect the cerebellum to other parts of the CNS. Incidentally, the term ataxia means
widespread incoordination and comes from the Greek word for
“lack of order.”
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Although the cerebellum was discussed in Chapter 2, it would
be benecial to review some of the information about it. The cerebellum is located below the occipital lobe and is attached to the
back of the brainstem (Figure 7–1). It is shaped somewhat like a
“small brain” in that it has two hemispheres, a deep ssure between
the hemispheres, and a cortical surface of gray matter that has
many convolutions. The cerebellum is more complex and fully
developed in humans than in any other animal species. This complexity reects a human’s need for very precise muscular control
over certain movements, such as those for speech.
The cerebellum is a very important part of the motor system.
Its primary function is to coordinate the timing and force of muscular contractions so that skilled, voluntary movements appropriate
for an intended task are created. It accomplishes this by processing
sensory information from all over the body and integrating that
information into the execution of a movement. The processing and
integration function of the cerebellum is obvious because there are
about 40 neural bers conveying information into the cerebellum
for every neural ber conveying information out (Brodal, 2010).
Although it is not clearly understood how it performs these functions, the general cellular layout of the cerebellum and its neural
pathways has been documented in detail.
Neural Pathways to and From the Cerebellum
The cerebellum is attached to the brainstem and communicates
with the rest of the CNS through three bundles of neural tracts
called the cerebellar peduncles (Figure 7–2 and Figure 7–3). By
exchanging information through these neural tracts, the cerebellum is able to monitor ongoing movements and communicate with
the cortex concerning planned upcoming movements. Through the
rst of these tracts, the inferior peduncle, the cerebellum receives
sensory information from the entire body about the position of
body parts—including the eyes, the vestibular system of the inner
ear, the joints of the limbs, the skin, tendons, and muscles—before,
during, and after a movement. With this information, the cerebellum is able to recognize what the body is doing during a movement
and whether a motor impulse to the muscles is accomplishing the
intended result. Overall, this access to sensory information allows
the cerebellum to monitor the timing and force of movements while
they are being performed. For example, if a body part encounters
some unexpected resistance during a movement, the cerebellum
detects that resistance immediately through its access to sensory
information from the affected body part. The cerebellum can then
Thalamus
INFERIOR VIEW
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Cerebral
aqueduct
Pons
4th ventricle
Superior cerebellar
peduncle
Primary
fissure
Nodulus of
vermis
LATERAL VIEW
4th ventricle
Vermis
Anterior lobe
Cerebellum
Middle cerebellar
peduncle
Inferior
cerebellar
peduncle
Flocculus
Middle lobe
FIGURE 7–1. A lateral view of the cerebellum showing how it is attached
to the brainstem and an inferior view of the cerebellum.
188
Cerebellar
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peduncles
Superior
Middle
Inferior
Thalamus
Diencephalon
Diencephalon
Mid brain
Mid brain
Pons
Pons
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Medulla
Medulla
FIGURE 7–2. A posterior view of the brainstem and cerebellar peduncles.
In this illustration, the cerebellum has been removed.
send adjusting motor impulses to that body part via the superior peduncle (discussed later) to compensate for the resistance,
thereby keeping the timing and force of the movement appropriate
for the task.
The second pathway, the middle peduncle, is the largest of
the cerebellar peduncles. The neural tracts that travel through the
middle peduncle connect the cortex with the cerebellum. These
tracts are especially important to the motor system, because it is
through them that the cerebellum receives preliminary information from the cortex regarding planned movements. It is thought
190 MOTOR SPEECH DISORDERS: DIAGNOSIS AND TREATMENT
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The superior peduncle
transmits cerebellar
commands to the cortex
and the extrapyramidal
system.
The middle peduncle
transmits planned
movements from the
association cortex to the
cerebellum.
The inferior peduncle
transmits sensory
information from the
entire body to the
cerebellum.
FIGURE 7–3. A schematic diagram of the neural pathways leading into and
out of the cerebellum.
cerebellum
The
that these preliminary motor impulses from the cortex are rough
approximations of intended movements and need to be coordinated by the cerebellum. The cerebellum coordinates these planned
movements by integrating the sensory information it receives from
the body with an individual’s experience of what the appropriate
movement should be. The intended movements are then smoothed
and rened according to the current conditions of the body and
sent back to the cortex via the thalamus. These processed motor
commands are then sent to the motor areas of the cortex, where
they are transmitted to the appropriate muscles.
The third pathway, the superior peduncle, is the cerebellum’s
main output channel to the rest of the CNS, providing several destinations for the neurons coursing through it. One of these destinations is the cerebral cortex. It is through the neural bers in the
superior peduncle that the cerebellum sends its processed motor
impulses to the motor areas of the cortex, thereby completing the
corticocerebellar control circuit. The entire corticocerebellar control circuit, therefore, starts in the cortex and courses down into the
cerebellum through the middle peduncle. The bers of this neural
circuit exit the cerebellum through the superior peduncle and travel
back up to the cortex after passing through the thalamus.
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Along with the neural tracts coursing out of the superior
peduncles to the cortex, additional tracts travel out of the superior
peduncle and connect the cerebellum directly to neurons of the
extrapyramidal tract. By way of these connections to the extrapyramidal system, the cerebellum can stimulate or inhibit the actions
of voluntary muscles. Unlike the neural impulses traveling through
the corticocerebellar control circuit, these cerebellar commands
to the extrapyramidal system do not travel to the cortex before
being sent to the muscles. Instead, these commands take a complex
course through the extrapyramidal system as they make their way to
the appropriate lower motor neurons. Once these cerebellar motor
impulses reach the lower motor neurons, they are then able to coordinate and quickly adjust the movements of the voluntary muscles
according to the changing positions and circumstances of the body.
Incidentally, the neurons that course through these three cerebellar pathways are called cerebellar control circuits, not upper
motor neurons. Although they do transmit motor impulses, these
neurons do not actually synapse with lower motor neurons, which,
by denition is what upper motor neurons do. Most neurons coursing out of the cerebellar peduncles synapse with either true upper
motor neurons (primarily those of the extrapyramidal system) or
interneurons in the brainstem and spinal cord.
The Cerebellum and Speech
Without doubt, the cerebellum plays an important role in coordinating the many intricate muscular contractions needed to produce
intelligible speech. However, the precise nature of the cerebellum’s
inuence on speech is unclear. There are probably at least two
ways in which the cerebellum inuences speech movements. One
of these is through the corticocerebellar control circuit discussed
previously. The planned motor impulses of a planned speech act
are sent from the cortex to the cerebellum. The cerebellum coordinates and renes these preliminary speech movements according
to (a) sensory information about the positions and conditions of the
articulators, and (b) prior practice with regard to what the skilled
target movement should be. These coordinated motor impulses
are then sent to the thalamus for additional renement and then
forwarded to the motor cortex. From there, the motor impulses
are transmitted to the appropriate muscles for speech production.
Another way in which the cerebellum might inuence speech
movements is through its connections to the extrapyramidal system.
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As described in the preceding section of this chapter, the cerebellum can make rapid adjustments in the timing and force of
movements to compensate for unexpected changes in the circumstances of a movement. For example, if someone is attempting to
talk with food in his or her mouth, the cerebellum will detect that
tongue movements are being slowed by the presence of the food.
To maintain intelligible articulation of speech sounds, the cerebellum will adjust the ring of the appropriate motor neurons to the
tongue so that intelligible articulation can be maintained despite
this resistance to tongue movement during speech. Because of this
remarkable dual ability to coordinate and modify both planned and
ongoing speech movements, the cerebellum is a key player in the
motor speech system. However, because it is so important, damage
to the cerebellum or to its control circuits can signicantly harm
an individual’s ability to produce normal speech.
Causes of Ataxic Dysarthria
Damage to different parts of the cerebellum or its control circuits
can result in a variety of movement disorders. In general, individuals with cerebellar damage have problems coordinating their
voluntary movements. It seems as if they have trouble controlling
the timing and force of their movements, especially at the beginning and ending of an action. For example, their movements might
be wavering and jerky when reaching to pick up an object. This
unsteadiness indicates that the range and direction of movements
also can be affected by cerebellar damage. Altogether, these movement decits of timing, force, range, and direction are known as
cerebellar ataxia.
Impairment of equilibrium during walking can be one of the
more obvious symptoms of cerebellar damage. In these cases, individuals walk with a wide-based, staggering gait, frequently giving
the impression that they are just about to fall. Cerebellar damage
also can cause decits in voluntary eye movements, intention tremors, hypotonia of the muscles, and problems with motor learning.
Because so much about the operation of the cerebellum is
unknown, neuroscientists are unclear about how different types
of cerebellar damage affect speech production. Darley et al. (1975)
stated that ataxic dysarthria often occurs when there is generalized or bilateral damage to the cerebellum. They also reported that
speech coordination might be especially dependent on a part of the
cerebellum at the midpoint between the cerebellar hemispheres,
called the vermis (see Figure 7–1). Some research has suggested
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that focal lesions also can cause ataxic dysarthria. Duffy (2020)
cited several studies suggesting that ataxic dysarthria can be caused
by focal damage to the superior peduncle, the lateral portions of
the cerebellar hemispheres, or areas near the vermis.
Degenerative Diseases
A number of degenerative disorders result in progressive cerebellar dysfunction and are frequent causes of ataxic dysarthria.
Autosomal dominant cerebellar ataxia of late onset is a hereditary disease that usually begins in middle age. Ataxic dysarthria is
only one of many features that could be present in this disorder.
Progressive cerebellar ataxia, retinal degeneration, muscle rigidity,
sensorineural deafness, balance decits, dementia, and a number
of other neurologic features also might be evident. The presence
of these symptoms can vary signicantly among individuals with
this disease, even among affected members of the same family. It
is a terminal disease, with death usually occurring within several
years of the rst appearance of symptoms.
Idiopathic sporadic late-onset cerebellar ataxia is similar
to autosomal dominant cerebellar ataxia of late onset, except that
it usually does not include as many neurologic symptoms. It often
results only in progressive cerebellar ataxia, ataxic dysarthria, and
balance decits. This disorder also tends to begin in middle age,
but its survival rate is about 20 years from onset. As its name suggests (“idiopathic” means spontaneous occurrence of a pathologic
condition with an unknown or obscure origin), the cause of idiopathic sporadic late-onset cerebellar ataxia is unclear, but it might
be the combined result of unrecognized genetic and environmental
factors (Lieto et al., 2019).
Friedreich’s ataxia is a progressive hereditary disease that can
affect the spinal cord as well as the cerebellum and is accordingly
classed as a spinocerebellar disease. Although often described as
a common cause of cerebellar ataxia, it is actually a rare disorder
with a prevalence of only 2 per 100,000 population. The symptoms
of Friedreich’s ataxia, which usually become evident when individuals are 10 to 15 years of age, include cerebellar ataxia affecting gait and manual dexterity, dysarthria, and visual disorders (Tai
et al., 2018). The less common symptoms include dementia and
sensorineural deafness. Few people with this disorder survive past
their 40s, with death often occurring after coma or heart failure.
The dysarthria associated with Friedreich’s ataxia is not necessarily purely ataxic in nature because this disorder does not usually
affect only the cerebellum and its control circuit. Evidence of lower
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