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114 MOTOR SPEECH DISORDERS: DIAGNOSIS AND TREATMENT
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production because they provide the motor innervation for the
muscles of respiration. One of the most important nerves of respiration is the phrenic nerve—a spinal nerve that originates from
the cervical section of the spinal cord and provides the motor
innervation of the diaphragm. The other muscles of inhalation and
exhalation are innervated by the spinal nerves that originate along
the cervical and thoracic portions of the spinal cord.
Damage to the cervical and thoracic spinal nerves can affect
respiration and, thereby, can affect speech. In most instances, however, the damage must be quite widespread before a signicant
impairment of respiration will be evident. An exception to this is
injury to the phrenic nerve, which can paralyze the diaphragm
and result in signicantly weakened inhalation. Individuals with
impaired respiratory abilities might demonstrate decreased speech
loudness as a result of reduced subglottic air pressure. Furthermore,
these individuals could demonstrate shortened speech phrasing
because of the reduced amount of air available for phonation. This
shortened phrasing would almost certainly affect the prosody of
their speech as well. Individuals with impaired respiration also
might attempt to speak in longer phrases than their air supply will
allow, resulting in a breathy or strained vocal quality toward the
end of an utterance (known as “speaking on residual air”).
Causes of Flaccid Dysarthria
Flaccid dysarthria can be caused by anything that disrupts the ow
of motor impulses along the cranial or spinal nerves that innervate
the muscles of speech production. Several conditions that damage
lower motor neurons were briey mentioned earlier in this chapter,
such as brainstem stroke, tumors, and so forth. In the following
paragraphs, the conditions that can cause accid dysarthria are
examined in more detail.
Physical Trauma
Surgical trauma, head injury, and neck injury are common causes of
accid dysarthria. Duffy (2005) indicated that these injuries caused
31% of accid dysarthria cases at the Mayo Clinic during a 23-year
period—the highest percentage of all reported causes of this dysarthria. This high occurrence probably should not be surprising,
given that physical damage leading to accid dysarthria can occur
anywhere along the course of lower motor neurons, from the cell
bodies in the brainstem to the neuromuscular junction.
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Some of the surgical procedures that can lead to inadvertent
damage to the cranial nerves of speech production include carotid
endarterectomy (the removal of plaque deposits in a carotid artery),
cardiac surgery, the removal of head and neck tumors, and dental
surgery. In most of these cases, a cranial nerve is cut accidentally
because of its proximity to the surgical site. Head and neck trauma
resulting from motor vehicle accidents, blows to the head, and falls
also can damage the cranial nerves of speech production. Broken
bones from this type of trauma can compress or cut one of these
cranial nerves. It also is possible that the rotational forces of such
trauma can twist or stretch a nerve enough to cause damage. In any
of these instances, the ability of the cranial nerve to carry motor
impulses will be impaired, resulting in weakness or paralysis in
the muscles innervated by the nerve.
Brainstem Stroke
Flaccid dysarthria can be caused by a stroke, which is more frequently called a cerebrovascular accident (CVA) by medical professionals. A stroke occurs when blood ow to the brain is interrupted
because an artery breaks or is blocked. In either case, brain tissue
is damaged from the lack of blood ow and the disruption of the
neurons’ metabolic processes. As with all other parts of the brain,
the brainstem is rich with arterial blood ow, and when a stroke
occurs in one of the brainstem arteries, the neurons served by that
artery can be destroyed.
A brainstem stroke can affect the cranial nerves directly
because the cell bodies of lower motor neurons (the cranial nerve
nuclei) are located within the brainstem. When the blood supply
to these cell bodies is blocked, many of the neurons will eventually die. This damage will impair the ability of the cranial nerves to
transmit motor impulses to the muscles. The degree of impairment
depends on the number of lower motor neurons that are lost to a
stroke. If only a few neurons are affected, the resulting impairment
of motor innervation might be minimal. If many of a cranial nerve’s
motor neurons are affected, numerous muscles innervated by that
cranial nerve will be weakened or paralyzed.
It also is very possible for a single brainstem stroke to damage more than one cranial nerve. If the stroke is large enough to
damage the cells in more than one cranial nerve nucleus, it will
affect more than one cranial nerve. In fact, the damaging stroke
does not have to be all that massive before it will affect more than
one cranial nerve. Many cranial nerve nuclei are in close proximity
in the brainstem. For example, the cranial nerve nuclei of the glossopharyngeal, vagus, and accessory nerves are quite close to each
116 MOTOR SPEECH DISORDERS: DIAGNOSIS AND TREATMENT
Blocking Auto-Antibodies (Myasthenia gravis)
Muscle activation Muscle activation inhibited
Auto-antibody to AChR
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other in the brainstem. A single brainstem stroke in that area could
affect the lower motor neurons in all three of those cranial nerves.
Myasthenia Gravis
Myasthenia gravis is a rare disease that affects the neuromuscular
junction—the point where lower motor neurons synapse with muscle tissue. The primary symptom of this condition is the rapid fatigue
of muscle contractions, with recovery occurring after a period of
rest. Myasthenia gravis is caused by antibodies that block and, to a
lesser extent, damage the parts of muscle tissue (the acetylcholine
receptors) that receive the neurotransmitter acetylcholine from the
lower motor neurons (Figure 4–9). The reception of acetylcholine
at the muscle is what triggers a muscular contraction. When too
many of these receptors are blocked, the muscle is not able to
use enough acetylcholine for a full contraction. Consequently, the
muscle cannot maintain the strength of its contractions over time,
and the result is rapid fatigue and weakness. With rest, the muscle
can make more efcient use of the acetylcholine, and stronger
contractions will occur once again, but only for a short time.
There are several ways in which myasthenia gravis may progress
in affected individuals. In about 51% of patients, the initial complaint
is about eye muscle weakness that causes double vision or drooping of the upper eyelid. About 16% of patients have oral-pharyngeal
weakness as the rst symptom, which can cause accid dysarthria
Nerve
AChR
FIGURE 4–9. In myasthenia gravis, immune system antibodies impede the
transmission of acetylcholine from lower motor neurons by blocking neurotransmitter receptors in muscle tissue.
Nerve
Acetycholine
Muscle cell
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or dysphagia. In some patients the condition eventually spreads to
the limbs and trunk, causing a generalized myasthenia gravis.
Specic drugs can aid in the diagnosis of this disorder. An
injection of Tensilon or similar anticholinesterase medications can
almost immediately improve muscle contractions by prolonging the
presence of acetylcholine in the neuromuscular junction, thereby
providing more time for the neurotransmitter to be absorbed by
the muscle. A patient with suspected myasthenia gravis will show
rapidly improved muscle strength while the drug is present in the
neuromuscular junction.
Effective medical treatments for myasthenia gravis are available. For example, immunosuppressant drugs are often used to
inhibit the antibodies, which can minimize the blockage of acetylcholine receptors. Plasmapheresis can produce short-term benets
during acute attacks by ltering the antibodies from the blood.
Some patients can benet from the surgical removal of the thymus
gland, which contains the lymphocytes that produce the antibodies
(Dresser et al., 2021; Lazaridis & Tzartos, 2020).
Speech-language pathologists typically do not treat the speech
decits caused by myasthenia gravis, but they can be helpful in
referring suspected cases to medical doctors for appropriate care.
In a motor speech examination, myasthenia gravis is tested by having the patient count from 1 to 100 or read a long paragraph. If
the disease is affecting the speech muscles, the patient will show
a gradual onset of accid dysarthria during the prolonged speaking task, demonstrating hypernasality, decreased loudness, breathy
voice quality, and imprecise articulation.
Guillain-Barré Syndrome
Guillain-Barré syndrome results in the progressive inammatory
loss of the myelin sheath around axons (Figure 4–10). The exact
cause of this disorder is undetermined, but it frequently occurs
after certain infections or immunization. The demyelination usually
occurs in the PNS and tends to affect motor neurons more than
sensory neurons. The progression can be quite rapid, often developing over a period of days or a few weeks. The peak of severity
is often reached in about 2 weeks. This is in striking contrast to
some of the better known progressive neurologic disorders, such
as Parkinson’s disease, which typically progress over a period of
months or years.
total paralysis of the entire body. Symptoms of weakness and numbness in the limbs are common early in this disorder, especially in the
In severe cases, Guillain-Barré syndrome can result in a near
118 MOTOR SPEECH DISORDERS: DIAGNOSIS AND TREATMENT
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Normal Peripheral
Nerve
Exposed fiber
Peripheral Nerve
affected by
Guillain-Barre
Damaged myelin
FIGURE 4–10. Guillain-Barré syndrome is an immune system disorder that
causes damage to the myelin sheath around axons, primarily in the peripheral
nervous system.
legs. Other early symptoms include accid dysarthria and dysphagia
once the demyelination affects the cranial nerves. The recovery rate
from Guillain-Barré syndrome is usually high, but 3% to 10% of
affected individuals die during the acute stages of the disorder, often
from either respiratory failure, blood pressure instability, or heart
arrhythmia (Leonhard et al., 2019). Typical recovery occurs over a
period of weeks or months. However, persons with the most severe
cases might not fully recover and will always have some permanent
weakness. For example, Shahrizaila et al. (2021) reported that 20%
of Guillain-Barré patients have difculty walking without assistance
1 year after onset. Speech-language pathologists can be involved
with these patients during several stages of the disorder’s progression. By monitoring changes in swallowing and speech intelligibility
during the initial onset of symptoms, speech-language pathologists
can make recommendations for oral feeding and for augmentative and alternative communication in those cases where speech
becomes unintelligible. Speech-language pathologists might also be
involved in the later recovery phase as swallowing improves and
oral feeding gradually becomes possible again.
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Polio
Polio is an infectious viral disease that attacks the cell bodies of
lower motor neurons. Although vaccines have reduced the incidence of this disease greatly, unvaccinated individuals can become
infected after close contact with a recently vaccinated child (Wiederholt, 2000). Polio most frequently affects the cervical and thoracic spinal nerves, often resulting in isolated respiratory weakness.
When respiratory weakness occurs, the motor speech symptoms
can include labored inhalation during speech, shortened speech
phrases, speaking on residual air, and decreased loudness. Unfortunately, a polio infection is not always restricted to the spinal nerves.
It also can affect the cranial nerves. In about 10% to 15% of polio
cases, the virus can damage the lower motor neurons in the trigeminal, facial, glossopharyngeal, and vagus nerves (Duffy, 2020),
resulting in weakness in the muscles innervated by those nerves.
Other Causes of Flaccid Dysarthria
Many additional disorders can cause accid dysarthria; this is a
summary of just a few of them. A tumor growing in or near the
brainstem can compromise a cranial nerve’s ability to transmit its
neural impulses to muscles. Tumors occurring along the course of
a cranial nerve’s pathway, such as in the neck or in any orofacial
structure, also can affect the nerve’s functioning. Muscular dystro-
phy is a disease that causes a progressive degeneration of muscle
tissue. It can result in weakness in many muscles served by the
cranial nerves, such as the tongue, face, and pharynx. Progressive
bulbar palsy is a disorder that can affect both upper and lower
motor neurons, although it often is present only in the lower motor
neurons. When the lower motor neurons are affected, progressive
bulbar palsy can cause accid dysarthria. When it is present in both
sets of motor neurons, it can result in a mixed dysarthria, usually
of the accid-spastic type (see Chapter 10).
Speech Characteristics of Flaccid Dysarthria
This section examines the typical speech characteristics of accid
dysarthria. The effects of accid dysarthria on resonance, articulation, phonation, respiration, and prosody are discussed. It is important to remember, however, that not all individuals with accid
120 MOTOR SPEECH DISORDERS: DIAGNOSIS AND TREATMENT
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dysarthria will demonstrate decits in each of these areas, although
some will. Furthermore, the severity level within each area will not
necessarily be the same for any two patients. Individual variations
in motor speech decits are common for all the dysarthrias, even
when the affected individuals share the same type of dysarthria.
Because of these variations, it is important to look for clusters of
symptoms when trying to diagnose a particular type of dysarthria.
Once a cluster of symptoms has been identied, determine which
type of dysarthria it most closely represents. This holds true for the
diagnosis of any motor speech disorder, not just accid dysarthria.
Resonance
In their landmark study of dysarthria, Darley et al. (1969a, 1969b)
examined the abnormal speech characteristics of 30 subjects with
accid dysarthria. Table 4–1 ranks these subjects’ nine most prominent speech errors. Hypernasality was the most noticeable error.
It was present in the speech of 25 of the 30 subjects. Hypernasality
is certainly an important diagnostic marker for accid dysarthria.
Although it is not unique to accid dysarthria, it tends to be more
noticeable in this type of dysarthria as compared with the other
dysarthrias. Other resonance-related problems in accid dysarthria
include nasal emission due to incomplete velopharyngeal closure,
weak pressure consonants caused by decreased intraoral air pres-
TABLE 4–1
Note: 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. 251. Copyright 1969 by
American Speech-Language-Hearing Association. Reprinted with permission.
Most Common Speech Production Errors in 30 Individuals
With Flaccid Dysarthria
Rank Speech Production Errors
1 Hypernasality
2 Imprecise consonants
3 Breathiness (continuous)
4 Monopitch
5 Nasal emission
6 Audible inspiration
7 Harsh voice quality
8 Short phrases
9 Monoloudness
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sure, and shortened phrases, which are the result of wasted air that
escapes through the nasal cavity during speech. All of these resonance decits primarily reect bilateral damage to the pharyngeal
branch of the vagus nerve because it innervates most of the muscles of the velum. Watch the PluralPlus Flaccid Dysarthria Case 1
video for an example of signicant hypernasality in a patient with
accid dysarthria following a head injury.
Articulation
Imprecise consonant production was the second most prominent
abnormal speech characteristic of accid dysarthria reported by
Darley et al. (1969a, 1969b). There can be a large range of severity
for misarticulated phonemes in individuals with accid dysarthria,
from only a mild distortion to complete unintelligibility. Damage
to the facial and hypoglossal nerves is usually cited as a reason for
these problems with the production of consonant phonemes (Duffy,
2020). Bilateral damage to the facial nerve can have a signicant
effect on the production of bilabial and labiodental phonemes, as
well as of consonants and vowels requiring lip rounding. Bilateral
damage to the hypoglossal nerve will likely result in misarticulations of phonemes requiring the elevation of the tongue, especially
the tongue tip. For example, a damaged hypoglossal nerve can
affect the production of the linguadental and linguapalatal phonemes, such as /j/ and /l/. In severe cases of bilateral hypoglossal
nerve damage, the production of the linguavelar phonemes also
will be impaired. Watch the PluralPlus Flaccid Dysarthria Case 2
video for an example of imprecise consonants in connected speech
secondary to a brainstem stroke.
Damage to the trigeminal nerve also can affect articulation. As
mentioned previously, bilateral damage to this nerve can result in
difculty elevating the jaw sufciently to bring the articulators into
contact with each other. Without proper jaw elevation, it might be
impossible for an affected individual to accurately produce any of
the consonants and most of the vowels. Such an individual might
need to elevate the jaw by hand or use a device known as a “jaw
sling” before intelligible speech is possible.
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Phonation
Another common abnormal speech characteristic of accid dysarthria is phonatory incompetence (Darley et al., 1969a, 1969b).
This term refers to the incomplete adduction of the vocal folds
during phonation. It is caused by damage to the recurrent branch
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of the vagus nerve, which provides motor innervation to almost
all of the intrinsic muscles of the larynx. Injury to this cranial
nerve can leave the vocal-fold adductor and abductor muscles weak
or paralyzed. If the adductor muscles are primarily affected, the
vocal folds will not meet with enough strength to produce a clear
phonation. The result will be phonation that has a breathy voice
quality, which can almost sound like a whisper in severe cases.
If the abductor muscles are primarily affected, the vocal folds will
not be able to fully abduct during inhalation. When abduction is
incomplete, there can be an audible inhalatory stridor.
As with hypernasality, phonatory incompetence is an especially valuable conrmatory sign for the diagnosis of accid dysarthria. It can be quite prominent in cases of accid dysarthria, to
a degree that is not found in the other dysarthrias (Duffy, 2020).
Moreover, the combined presence of hypernasality and phonatory
incompetence is the strongest conrmatory sign that accid dysarthria is the correct diagnosis.
Respiration
Weakened respiration might or might not be a component of accid
dysarthria. If the cervical and thoracic spinal nerves responsible for
innervating the diaphragm and the intercostal muscles are damaged, the result can be decreased inhalation or impaired control of
exhalation during speech. In either instance, the affected individuals will not have adequate amounts of subglottic air pressure for
speech. Without enough subglottic air, the speech of individuals
with accid dysarthria could demonstrate reduced loudness and
shortened phrase length. Their speech might have a strained vocal
quality if they speak on residual air to prolong the length of their
phrases. Reduced loudness, shortened phrase length, and strained
vocal quality will affect prosody. In addition, Darley et al. (1975)
mentioned that individuals with weakened respiration also might
demonstrate monoloudness and monopitch.
A Problem of Respiration or Phonation?
Many individuals with accid dysarthria inhale frequently while
speaking, which can adversely affect the prosody of their speech.
Although frequent inhalations are usually easy to identify, it is
sometimes difcult to determine whether the problem is one of air
wastage because of poor laryngeal valving or reduced vital capac-
ity because of weakened respiration. In either case, the affected
individual will probably demonstrate reduced loudness, shortened
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phrase length, and strained vocal quality in conversational speech.
But how is a clinician to determine whether the problem is one of
respiration or phonation? Duffy (2020) described a simple procedure
to help determine which is the most likely cause of this problem.
1. Ask the individual to produce a good cough; listen to how
sharp it sounds. A breathy, feeble cough might indicate
weakness in the vocal-fold adductor muscles, inadequate
respiration, or perhaps both.
2. Then ask the individual to produce a hard glottal stop; again
listen to how sharp it sounds. Producing a hard glottal stop
requires rm closure of the vocal folds but little respiratory
effort. Consequently, the individual who produces a breathy
cough and a sharp glottal stop might be demonstrating poor
respiration. In turn, a breathy cough and a weak glottal stop
might indicate that the cause of the air supply problem is
either weak laryngeal closure or a combination of weak
laryngeal and respiratory functioning.
Prosody
Individuals with accid dysarthria might demonstrate speech that
has monopitch and monoloudness. Darley et al. (1969a, 1969b)
noted both of these prosodic errors in their subjects with accid
dysarthria. It is likely that these qualities are primarily the result of
weakened laryngeal muscles that are unable to make the many ne
vocal-fold adjustments needed for normal pitch and loudness variations. For example, if the cricothyroid muscle is weakened by damage to the superior laryngeal branch of the vagus nerve, it might not
be able to tense and stretch the vocal folds sufciently to produce
normal changes in pitch and loudness. Incidentally, monopitch and
monoloudness are not unique to accid dysarthria; they can appear
in a number of other dysarthrias, such as spastic and ataxic dysarthria. Consequently, the presence of monopitch and monoloudness
are not denite diagnostic markers for accid dysarthria, unlike the
co-occurrence of hypernasality and phonatory insufciency.
Key Evaluation Tasks for Flaccid Dysarthria
The following assessment tasks in Appendix 3–1 might be particularly useful in detecting key characteristics of accid dysarthria
(Hegde & Freed, 2022):
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