Language and Speech Disorders: Motor Speech Disorders: Dysarthria and Apraxia of Speech

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Chapter 12B Language and Speech Disorders

Motor Speech Disorders: Dysarthria and Apraxia of Speech


Dysarthrias involve the abnormal articulation of sounds or phonemes. The pathogenic mechanism in dysarthria is abnormal neuromuscular activation of the speech muscles, affecting the speed, strength, timing, range, or accuracy of movements involving speech (Duffy, 1995). The most consistent finding in dysarthria is the distortion of consonant sounds. Speech disorders can be mechanical, as in patients with physical disorders of the pharynx and larynx, but dysarthrias are neurogenic, related to dysfunction of the central nervous system, nerves, neuromuscular junction, or muscle, with a contribution of sensory deficits in some cases. Dysarthria can affect not only articulation but also phonation, breathing, and prosody (emotional tone) of speech. Total loss of ability to articulate is called anarthria.

Like the aphasias, dysarthrias can be analyzed in terms of the brain lesion sites associated with specific patterns of speech impairment. Analysis of dysarthria at the bedside is useful for the localization of neurological lesions and the diagnosis of neurological disorders. An experienced examiner should be able to recognize the major types of dysarthria, rather than referring to “dysarthria” as a single disorder.

The examination of speech at the bedside should include having the patient repeat syllables, words, and sentences. Repeating consonant sounds (such as /p/, /p/, /p/) or shifting consonant sounds (/p/, /t/, /k/) can help identify which consonants consistently cause trouble. Repetition of polysyllabic words such as “impossibility” or “catastrophe” 4 or 5 times can elicit both the consistent errors of dysarthria and the inconsistent errors of apraxia of speech (see later discussion).

The Mayo Clinic classification of dysarthria (Duffy, 1995), widely used in the United States, includes six categories: (1) flaccid, (2) spastic and “unilateral upper motor neuron,” (3) ataxic, (4) hypokinetic, (5) hyperkinetic, and (6) mixed dysarthria. These types of dysarthria are summarized in Table 12B.1.

Flaccid dysarthria is associated with disorders involving lower motor neuron weakness of the bulbar muscles, such as polymyositis, myasthenia gravis, and bulbar poliomyelitis. The speech pattern is breathy and nasal, with indistinctly pronounced consonants. In the case of myasthenia gravis, the patient may begin reading a paragraph with normal enunciation, but by the end of the paragraph the articulation is soft, breathy, and frequently interrupted by labored respirations.

Spastic dysarthria occurs in patients with bilateral lesions of the motor cortex or corticobulbar tracts, such as bilateral strokes. The speech is harsh or “strain-strangle” in vocal quality, with reduced rate, low pitch, and consonant errors. Patients often have associated features of pseudobulbar palsy, including dysphagia, exaggerated jaw jerk and gag reflexes, and easy laughter and crying (synonyms: emotional incontinence, pseudobulbar affect, or pathological laughter and crying). Another variant is the opercular syndrome, described later in this chapter.

A milder variant of spastic dysarthria, unilateral upper motor neuron (UUMN) dysarthria, is associated with unilateral upper motor neuron lesions, such as strokes (Duffy, 1995). This type of dysarthria has similar features to spastic dysarthria, but UUMN dysarthria is less severe. Unilateral upper motor neuron dysarthria is one of the most common types of dysarthria, since it occurs in patients with unilateral strokes. In a study by Urban and colleagues (2006), left hemisphere strokes were more likely than right hemisphere strokes to be associated with dysarthria.

Ataxic dysarthria, associated with cerebellar disorders, is characterized by one of two patterns: irregular breakdowns of speech with explosions of syllables interrupted by pauses, or a slow cadence of speech with excessively equal stress on every syllable. The second pattern of ataxic dysarthria is referred to as scanning speech. A patient with ataxic dysarthria, attempting to repeat the phoneme /p/ as rapidly as possible, for example, produces either an irregular rhythm, resembling popcorn popping, or a very slow rhythm. Causes of ataxic dysarthria include cerebellar strokes, tumors, multiple sclerosis, and cerebellar and spinocerebellar degenerations. A recent report localized ataxic dysarthria to the upper cerebellar loci of the quadrangularis and simplex lobules by magnetic resonance imaging (MRI) (Ogawa et al., 2010).

Hypokinetic dysarthria, the typical speech pattern in Parkinson disease (PD), is notable for decreased and monotonous loudness and pitch, rapid rate, and occasional consonant errors. In a study of brain activation by positron emission tomography (PET) methodology, Liotti and colleagues (2003) described premotor and supplementary motor area activation in patients with PD and untreated hypokinetic dysarthria, but not in normal subjects. After completion of a voice treatment protocol, these premotor and motor activations diminished, whereas right-sided basal ganglia activations increased.

Hyperkinetic dysarthria, a pattern in some ways the opposite of hypokinetic dysarthria, is characterized by marked variation in rate, loudness, and timing, with distortion of vowels, harsh voice quality, and occasional sudden stoppages of speech. This speech pattern is seen in hyperkinetic movement disorders such as Huntington disease (HD) and dystonia musculorum deformans.

The final category, mixed dysarthria, involves combinations of the other five types. One common mixed dysarthria is a spastic-flaccid dysarthria, seen in amyotrophic lateral sclerosis (ALS). The ALS patient has the harsh, strain-strangle voice quality of spastic dysarthria, combined with the breathy and hypernasal quality of flaccid dysarthria. Multiple sclerosis may feature a spastic-flaccid-ataxic or spastic-ataxic mixed dysarthria, in which slow rate or irregular breakdowns are added to the other characteristics seen in spastic and flaccid dysarthria. Wilson disease can involve hypokinetic, spastic, and ataxic features.

The management of dysarthria includes speech therapy techniques to strengthen muscles, train more precise articulations, slow the rate of speech to increase intelligibility, or teach the patient to stress specific phonemes. Devices such as pacing boards to slow articulation, palatal lifts to reduce hypernasality, amplifiers to increase voice volume, communication boards for subjects to point to pictures, and augmentative communication devices and computer techniques can be used when the patient is unable to communicate in speech. Visual cues may help dysarthric speakers become more intelligible (Hustad and Garcia, 2005). Surgical procedures such as a pharyngeal flap to reduce hypernasality or vocal fold Teflon injection or transposition surgery to increase loudness may help the patient speak more intelligibly. Treatment of PD can improve dysarthria in terms of both speech therapy and pharmacological treatments (DeLetter et al., 2005; Pinto et al., 2004; Trail et al., 2005

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