CHAPTER 4
Chapter Overview
Flaccid dysarthria is a motor speech disorder with neuropathology of damage to the
motor units of the cranial or spinal nerves that supply speech muscles (lower motor
neuron involvement); speech problems are caused mostly by muscle weakness and
hypotonia (Singh & Kent, 2000, p. 84). Lower motor neurons are part of the PNS, while
upper motor neurons are part of the CNS. Lower motor neurons are also referred to as
the final common pathway, as they are the last and only “road” that neural impulses from
upper motor neurons can travel to reach muscles. Flaccid dysarthria is caused by
anything that disrupts the flow of neural impulses along the lower motor neurons that
innervate the muscles of respiration, phonation, articulation, prosody, or resonance. The
six pairs of cranial nerves, sometimes referred to as the “cranial nerves of speech
production,” that play a vital role in speech production are the trigeminal, facial,
glossopharyngeal, vagus, accessory, and hypoglossal. These cranial nerves may be
damaged from many different processes, including brainstem stroke, a growing tumor,
viral or bacterial infections, physical trauma, and surgical accidents. Flaccid dysarthria
can result if any of these conditions involve the cranial nerves of speech production. The
specific characteristics of this dysarthria depend on which nerve or combination of
Several conditions that damage lower motor neurons can cause flaccid dysarthria,
including physical trauma, brainstem stroke, myasthenia gravis, Guillain-Barré syndrome,
polio, tumors, muscular dystrophy, and progressive bulbar palsy. It is important to
remember, however, that not all individuals with flaccid dysarthria will demonstrate
deficits in each of these areas, and the severity level within each area will not necessarily
be the same for any two patients. Individual variations in motor speech deficits 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 identified, determine which type of dysarthria it most closely represents.
Flaccid dysarthria is characterized by difficulties with resonance, including
hypernasality, nasal emission, weak pressure consonants, and shortened phrases.
Articulation is characterized by imprecise consonant production. Phonation is
characterized by phonatory incompetence and breathy voice quality. Weakened
respiration may or may not be a component of flaccid dysarthria, causing decreased
Examples of tasks used to detect flaccid dysarthria, include those involving
observation of conversational speech and reading, AMR, prolonged vowels, and
speech stress tests. Treatment depends on which single or combination of cranial
nerves is damaged.
Nonspeech oral strengthening exercises are not supported by research. Because
muscular weakness is such a common characteristic of flaccid dysarthria, many
clinicians assume that strengthening tasks should be an important part of a treatment
plan. However, to date, no definitive research studies have shown that these
exercises make significant contributions to the recovery of speech production. Duffy
(2005) made one of the strongest points against strengthening exercises when he
said, “That strengthening exercise may be unnecessary is supported by the facts that
the tongue and lips use only 10% to 30% of their maximum forces for speech, and the
jaw only 2%, and that up to one third of motor nerve fibers can be lost before
functional impairments are encountered” (p. 477). When treating the speech errors of
individuals with oral weakness, the general rule should be this: if improving speech
production is the goal, treatment activities should concentrate directly on speech
production.
Study Questions and Answers
1. Define flaccid dysarthria in your own words.
2. Flaccid dysarthria can occur after damage to which part of the nervous
system?
3. Why are lower motor neurons also known as the “final common pathway”?
4. What are the six cranial nerves of speech production?
5. Which cranial nerve innervates the intrinsic muscles of the larynx?
6. What role do the spinal nerves play in speech production?
7. How can a brainstem stroke cause flaccid dysarthria?
8. How can it be determined whether the poor breath support demonstrated by a
patient with flaccid dysarthria is the result of weak respiration or poor laryngeal
valving?
