Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_4390_Библиотеки_им_академика_М_И_Перельмана
.pdf
204 MOTOR SPEECH DISORDERS: DIAGNOSIS AND TREATMENT
https://t.me/medicina_free
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 decits. 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

7. ATAXIC DYSARTHRIA 205
https://t.me/medicina_free
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 proles—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

206 MOTOR SPEECH DISORDERS: DIAGNOSIS AND TREATMENT
https://t.me/medicina_free
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 specic 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

7. ATAXIC DYSARTHRIA 207
https://t.me/medicina_free
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 specic 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.

208 MOTOR SPEECH DISORDERS: DIAGNOSIS AND TREATMENT
https://t.me/medicina_free
Study Questions
1. Dene 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 inu-
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 signicant problem in most cases of ataxic
dysarthria?
10. Describe an exercise that can help individuals with ataxic
dysarthria more accurately control their airow during
speech production.

Chapter 8
https://t.me/medicina_free
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

210 MOTOR SPEECH DISORDERS: DIAGNOSIS AND TREATMENT
https://t.me/medicina_free
Definitions of Hypokinetic Dysarthria
Most denitions 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 denitions encompass many of the most important aspects of
hypokinetic dysarthria.
[Hypokinetic dysarthria (HD)] is manifested in all dimensions of
human speech and voice production, specically 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 specic
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.

8. HYPOKINETIC DYSARTHRIA 211
https://t.me/medicina_free
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 shufing, “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 difculty 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 signicantly worse.
which causes slow and reduced range of movement. The shufing
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,

212 MOTOR SPEECH DISORDERS: DIAGNOSIS AND TREATMENT
https://t.me/medicina_free
in their range. In addition to the difculties 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 difculty in initiating movements, many individuals with

8. HYPOKINETIC DYSARTHRIA 213
https://t.me/medicina_free
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 reexes 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 difculty maintaining their balance while walking.
In addition, the normal walking arm swing will be absent; their
arms will hang stify 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 reexes
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 reexes 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 reexes are the primary symptoms of parkinsonism, there
are numerous other symptoms that could appear in individuals
with this disorder, including depression, swallowing difculties,
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
Соседние файлы в папке Библиотека им академика М.И. Перельмана
