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204 MOTOR SPEECH DISORDERS: DIAGNOSIS AND TREATMENT
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has slash marks or spaces to indicate when pauses are neces­sary while reading aloud. For example, a prepared sentence from a story might look like this: “With a feeling of deep /// yet most singular affection /// I regarded my friend.” At the slash marks, the patient should pause for a brief moment before continuing to read. Such reading materials also can be a useful tool in introducing a patient to the optimal breath group duration tasks that were discussed in the section on respiration decits. They could also be useful for introducing patients to the task of chunking utterances into syntactic units (discussed later).
Stress and Intonation
Stress and intonation exercises for individuals with ataxic dysar­thria should concentrate on developing more natural pitch and loudness variations in connected speech. The following tasks might be appropriate for the initial steps of a treatment plan that addresses the stress and intonation problems of patients with ataxic dysarthria.
n Contrastive stress drills—These tasks are usually designed for
the clinician to ask a question, with the patient answering it by adding stress on key words to convey the intended meaning of the answer (McHenry, 1998). For example, the clinician might ask the following question about a picture of a man playing football: “Is the man playing basketball?” The patient will answer, “No. The man is playing football.” The clinician’s next question might be, “Is the woman playing football?” The patient’s answer to this question would be, “No, the man is playing football.” The length of the questions and the complexity of the pictures for this task can easily be varied according to the abilities of the patient.
n Pitch range exercises—Exercises of this type can be a useful
starting place for work on intonation. Dworkin (1991) recom­mended that these exercises begin with an assessment of the patient’s ability to perceive obvious pitch changes in the clinician’s voice. If the patient is unable to make these distinc­tions, the prognosis is poor for improving the patient’s pitch control. However, if the patient can tell the difference between the pitch changes, the exercises might help. First, have the patient prolong an /a/ at the lowest pitch and then at the highest pitch possible. Once the highs and lows are estab­lished, the patient is asked to sing up and down this pitch
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range by dividing the range into about eight individual notes. In the nal exercises, the patient reads printed sentences that have arrows written above and below key words indicating the normal pitch changes for those words. For example, an upward arrow at the end of a question would indicate that the patient should raise the pitch on the nal word; a downward arrow at the end of a statement would indicate a decrease in pitch.
n Intonation proles—This task uses lines to show intonation
changes in written sentences. Lines immediately below the sentence indicate a at intonation. Lines above words indicate a rise in pitch. Lines below words indicate a drop in pitch. These lines can be added easily to any written sentence, no matter whether it is a statement or a question. For most patients, it is usually best to start with short, simple sentences and then progress to longer sentences. The ultimate goal is to have the patient generalize the pitch changes learned in this structured activity to conversational speech.
n Chunking utterances into syntactic units—Duffy (2020) men-
tioned that some individuals with dysarthria need to learn to divide their utterances according to normal pauses within and between sentences. This is necessary because their dysarthria has limited the number of words they can produce on a single exhalation. To compensate for this limitation, this task teaches the patient to inhale at the points in an utterance at which natural syntactic pauses occur. Examples of these natural pauses include after introductory clauses or phrases (“In the morning, [inhale] I went shopping at the store.”), between clauses or phrases (“She went there, [inhale] but I missed her.”), and between short sentences (“I saw the movie. [inhale] It was pretty good.”). By inserting inhalations at points at which normal pauses occur in an utterance, individuals with ataxic dysarthria are often able to maintain a more natural rhythm in their speech. This rhythm is lost if inhalations are placed haphazardly within an utterance.
Articulation
Although articulation might improve with a slowed rate of speech, individuals with ataxic dysarthria also might need to concentrate directly on improving their productions of phonemes.
n Intelligibility drills—Intelligibility drills (Yorkston et al., 1988)
are tasks in which the patient is given a list of words or
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sentences to read. Then the clinician turns away from the patient so that he or she will only be able to understand the patient’s speech if it is articulated clearly. By not looking at the target word list or at the patient’s mouth, the clinician will depend entirely on the patient’s adequate articulation to understand the target word. If the clinician does not under­stand the target word, the patient needs to determine why the word was unclear and then try saying it again. If this second attempt fails, then the clinician can look at the target word and give the patient specic feedback on why he or she could not understand the utterance (e.g., “I didn’t know it was ‘sleep’ because I couldn’t hear the ‘p.’ Try it again, and let me really hear the ‘p’ this time.”).
n Phonetic placement—This procedure treats articulation errors
by instructing patients on the correct position of the articula­tors before they attempt to produce a target sound. Phonetic placement can be valuable in that it educates patients on how certain speech sounds are produced. Many individuals with dysarthria realize they are producing speech sounds incorrectly, but they have little understanding of why their productions are in error. For example, phonetic placement can help speakers with ataxic dysarthria understand why their production of a /d/ actually sounds closer to a /z/ or their /p/ sounds closer to a /b/ and so forth.
n Exaggerating consonants—Also known as overarticulation,
exaggerating consonants is a treatment procedure that teaches the patient to fully articulate all consonant phonemes. Darley et al. (1975) suggested that most patients need to concentrate especially on medial and nal consonants because these are the sounds most likely to be poorly articulated in connected speech. The improvements in intelligibility can be dramatic when individuals with ataxic dysarthria fully articulate the medial and nal consonants in words.
Park et al. (2016) used exaggerating consonants as the basis of an intensive treatment program for dysarthria. Their patients had a variety of different types of dysarthria, caused by either traumatic head injury or stroke. The study used a small group repeated measures design to determine the effects of overarticulation (in combination with slower and slightly louder speech) on dysarthric patients’ single-word and sentence intelligibility. There were 16 treatment sessions (1-hr sessions, four times a week, for 4 weeks). The patients were rst oriented to the treatment tasks so that they knew
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what was expected. The treatment sessions started with 10 min of prepractice where patients reviewed a random selection of the tasks that were to be used later in the session. The following 10 min required the patients to repeat 10 functional phrases ve times each (e.g., “What are we doing tomorrow?”). The next 10 min had the patients repeating 10 service requests ve times each (e.g., “Where is the _____?”). During the nal 30 min, the patients read aloud, described pictures, and engaged in conversation. Feedback during most of the sessions consisted of whether the patients’ utterances were clear or unclear. Homework also was a part of the treatment procedure. The results showed that naive listeners noted improved conversational intelligibility in all patients compared to pretreatment samples. Many of the other outcome measures also were positive.
n Minimal contrast drills—These tasks have the patient con-
centrate on producing pairs of words that vary by only one phoneme. The distinction between the words can be in the voicing (park–bark), manner of production (pine–mine), or place of production (sea–she) of consonants. The distinc­tion also can be between vowels (man–men) but working on consonants does more to enhance intelligibility in most patients. These word pairs can be used alone, in phrases, or in sentences, depending on the needs of the specic patient.
Summary of Ataxic Dysarthria
n Ataxic dysarthria can be caused by any process that results in
n Usually, articulation and prosody are affected most signi-
n The speech characteristics of ataxic dysarthria include
n Treatment for ataxic dysarthria often concentrates on control-
damage to the cerebellum or the cerebellar control circuits. Degenerative disease and stroke are common causes of ataxic dysarthria.
cantly in cases of ataxic dysarthria.
imprecise consonant production and irregular articulatory breakdowns.
ling respiration for speech, increasing articulatory accuracy, and developing optimal rate and intonation in connected speech.
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Study Questions
1. Dene ataxic dysarthria in your own words.
2. What is the primary function of the cerebellum?
3. Describe the neural pathways leading to and from the
cerebellum.
4. What are the two ways that the cerebellum probably inu-
ences speech production?
5. What is autosomal dominant cerebellar ataxia of late onset?
6. Describe the three ways in which a tumor can affect cere-
bellar function.
7. Which two components of speech production are usually
affected most in cases of ataxic dysarthria?
8. What is decomposition of movement?
9. Is hypernasality a signicant problem in most cases of ataxic
dysarthria?
10. Describe an exercise that can help individuals with ataxic
dysarthria more accurately control their airow during speech production.
Chapter 8
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Hypokinetic Dysarthria
Definitions of Hypokinetic
Dysarthria
Neurologic Basis of Hypokinetic
Dysarthria
Characteristics of Parkinsonism
Causes of Parkinsonism
Causes of Hypokinetic Dysarthria
Idiopathic Parkinson’s Disease
Neuroleptic-Induced Parkinsonism
Postencephalitic Parkinsonism
Traumatic Head Injury
Toxic Metal Poisoning
Stroke
Speech Characteristics of
Hypokinetic Dysarthria
Prosody
Articulation
Phonation
Respiration
Resonance
Key Evaluation Tasks for
Hypokinetic Dysarthria
Treatment of Hypokinetic
Dysarthria
Pharmacologic Treatments for
Parkinsonism
Surgical Treatments for
Parkinsonism
Stem-Cell Implantation
Behavioral Treatments for
Parkinsonism
Articulation
Phonation
Respiration
Prosody
Summary of Hypokinetic
Dysarthria
Study Questions
209
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Definitions of Hypokinetic Dysarthria
Most denitions of hypokinetic dysarthria mention that individuals with this disorder have reduced vocal loudness, a harsh or breathy vocal quality, and abnormal speaking rates. Although these are not all of the characteristics of hypokinetic dysarthria, they are among the most common ones. It is interesting to note that many indi­viduals with this dysarthria have slow speaking rates, but in some there can be an abnormally increased rate of speech. The following two denitions encompass many of the most important aspects of hypokinetic dysarthria.
[Hypokinetic dysarthria (HD)] is manifested in all dimensions of human speech and voice production, specically in the areas of articulation, phonation, prosody, speech uency, and faciokinesis. HD is characterized by rigidity and bradykinesia, together with reduced muscular control of the larynx, articulatory organs, and other physiological support mechanisms of human speech produc­tion. Since self-monitoring of speech is abnormal in [Parkinson’s disease (PD)], HD has a serious impact on the quality of life of PD patients. (Chen et al., 2020, p. 712)
[Hypokinetic dysarthria is] a distinctive perceptual motor speech
disorder associated with basal ganglia control circuit pathology. . . .
This may appear in all of the respiratory, phonatory, resonatory, articulatory and prosody levels of speech, but its characteristics are most evident in voice, articulation and prosody. This specic speech disorder is characterized by reduced loudness, imprecise consonants, vowel centralization, and rate changes accompanied by involuntary facial movements. [Its] deleterious effects on patient’s communication and social participation may lead to social isolation, reducing the quality of life. (Muñoz-Vigueras et al., 2021, p. 640)
Neurologic Basis of Hypokinetic Dysarthria
In several ways, hypokinetic dysarthria is unique. It is the only dysarthria in which increased rate of speech can be one of the symptoms. It also is the only dysarthria in which the vast majority of cases share the same causative factor (parkinsonism). Because it accounts for so much of the hypokinetic dysarthria seen in clini­cal caseloads, parkinsonism is considered the de facto cause of this dysarthria throughout most of this chapter. Keep in mind, however, that parkinsonism is not the only cause of hypokinetic dysarthria.
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A few other disorders can lead to this dysarthria, and they are dis­cussed in the section on causes in this chapter.
Hypokinetic dysarthria occurs when the symptoms of parkin­sonism affect the muscles of speech production. The parkinsonian symptoms that have the greatest effect on speech are muscle rigid­ity, reduced range of motion, and slowed movement. In nearly every instance, these symptoms are caused by dysfunction in the basal ganglia or by damage to the basal ganglia’s neural connec­tions to other parts of the CNS. The term hypokinetic might be misleading to readers encountering it for the rst time. Initially, it might be confused with hypotonia, which is decreased muscle tone. A beginning clinician might consequently assume that an individual with parkinsonism will have weak and oppy muscles. This assumption would be quite wrong, however. Literally, hypoki­netic means “less motion,” not decreased muscle tone. In fact, indi­viduals with parkinsonism usually demonstrate increased muscle tone. When applied to individuals with parkinsonism, “hypoki­netic” describes their decreased range and frequency of movement. For example, individuals with parkinsonism usually demonstrate a shufing, “baby step” type of walking known as festinating gait, and their ability to express emotion through their facial expres­sions will be greatly diminished, a phenomenon known as masked facies. In addition, they might blink their eyes infrequently and have difculty starting or stopping movements. The reasons for these behaviors are discussed in the following sections.
Characteristics of Parkinsonism
Parkinsonism has a distinctive collection of symptoms. One of the most prevalent symptoms is resting tremor, present in about 80% of patients. Parkinsonian tremors are seen most commonly in the ngers and hands, but they also can involve the limbs and face. These tremors have a frequency of about four to six oscillations per second. They are called resting tremors because they are most noticeable while the body is not moving. Interestingly, the tremors might become less pronounced or disappear completely when the body is completely relaxed or when an affected body part is being moved voluntarily. During moments of agitation or nervousness, however, the tremors tend to become signicantly worse.
which causes slow and reduced range of movement. The shufing walk and the lack of facial expression mentioned previously are good examples of bradykinesia. Limb, trunk, and neck movements also are frequently affected by bradykinesia. Typically, the move­ments of affected body parts are slow, labored, and very limited
A very common symptom of parkinsonism is bradykinesia,
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in their range. In addition to the difculties of walking and facial expression, bradykinesia also can affect speech, nger movements, writing, and many other voluntary movements. It is important to note, however, that the slowness and reduced range of movement of bradykinesia is not the result of muscle weakness. Individu­als with parkinsonism usually demonstrate nearly normal muscle strength. As with all the symptoms of parkinsonism, bradykinesia is caused by dysfunction in the basal ganglia.
Muscular rigidity is the result of increased muscle tone. The muscles of individuals with this condition are always in a greater than normal state of contraction, both at rest and during move­ment. Rigidity most typically affects the neck, trunk, and limbs. The effects of rigidity can usually be observed easily. For instance, constant resistance is present when an affected body part is pulled to an extended position. This is sometimes described as “lead pipe resistance,” because it feels to the person who is doing the pull­ing that a piece of soft metal is being bent. In some joints, how­ever, there might be a subtle, rhythmic alteration in the rigidity as a body part is being moved. This intermittent change in rigidity is described as “cogwheel resistance” because of its step-by-step, ratchet-like motion. Although rigidity and bradykinesia are sepa­rate symptoms of parkinsonism, rigidity can exacerbate the slowed and restricted movements of bradykinesia.
It should be noted that there are differences between rigidity and spasticity, although they are both the result of increased muscle tone. One of the clearest distinctions between them is how they react to passive movement. In spasticity, increasing resistance to the passive movement is followed by an abrupt relaxation of the muscle being tested. The increase in resistance is especially evident when the passive movement is rapid. In contrast, rigidity demon­strates a more or less constant resistance to the passive movement, no matter how quickly the examiner moves the affected body part (Wiederholt, 2000).
Akinesia is a delay in the initiation of movements and is yet another common characteristic of parkinsonism. Examples of aki­nesia can be seen in many of the movements of individuals with parkinsonism. For instance, when an individual with parkinsonism is asked to verbally answer a question, there might be a notice­able pause before any words are spoken. This delayed initiation of speech could last only a few seconds, but sometimes it is much longer. Although it is rare, someone with severe akinesia might become stuck in a certain posture and be completely unable to move. Strangely, when an individual is stuck in one of these fro­zen positions, a brief touch from another person is sometimes all that is needed to initiate or continue a movement. In addition to this difculty in initiating movements, many individuals with
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parkinsonism can have trouble stopping a movement once it is started. For instance, while reaching for a glass of water, they might knock it over because they were unable to stop reaching once the movement was initiated. Not surprisingly, it is often reported that individuals with akinesia are reluctant to actively move about their home or other surroundings because they are afraid of being injured when they do so.
Disturbances of postural reexes also are seen in individuals with parkinsonism. Such disturbances are especially evident when these individuals are doing relatively automatic tasks. For example, they might have difculty maintaining their balance while walking. In addition, the normal walking arm swing will be absent; their arms will hang stify at their sides. If pushed lightly while standing, they are likely to fall because they cannot quickly shift their center of balance. They might be unable to rise from a chair because they do not naturally shift their trunk forward as they attempt to stand. Normally, the basal ganglia help regulate these postural reexes through neural connections with the extrapyramidal system. How­ever, when the basal ganglia are not functioning properly, these postural problems of balance and movement can become obvious. These impaired reexes contribute greatly to the 62% to 68% of people with Parkinson’s disease who have falls and related injuries.
Although tremor, bradykinesia, rigidity, akinesia, and disturbed postural reexes are the primary symptoms of parkinsonism, there are numerous other symptoms that could appear in individuals with this disorder, including depression, swallowing difculties, dementia, and hypokinetic dysarthria. These additional symptoms do not appear in all individuals with parkinsonism; nevertheless, they can be common features of this disorder.
Causes of Parkinsonism
As already mentioned, parkinsonism is caused by dysfunction in the basal ganglia, which are a collection of subcortical, gray mat­ter structures that play an important role in controlling movement (Figure 8–1). The individual members of the basal ganglia are the caudate nucleus, the globus pallidus, and the putamen (Andreatta, 2023; Seikel et al., 2020). Because the caudate nucleus and the putamen are made of many of the same type of neurons and are functionally related, they are known together as the striatum. The basal ganglia are located deep in the brain and are quite complex in their interconnections with each other and with other parts of the CNS. One of the most important neural pathways of the basal ganglia is the looped control circuit that connects it to the cerebral cortex (Figure 8–2). The rst part of this control circuit is composed