Dysarthria and Apraxia of Speech

Dysarthrias

Dysarthrias involve the abnormal articulation of sounds or phonemes, or more precisely, abnormal neuromuscular activation of the speech muscles, affecting the speed, strength, timing, range, or accuracy of movements involving speech ( ). The most consistent finding in dysarthria is the distortion of consonant sounds. Dysarthria is neurogenic, related to dysfunction of the central nervous system, nerves, neuromuscular junction, or muscle, with a contribution of sensory deficits in some cases. Speech abnormalities secondary to local, structural problems of the palate, tongue, or larynx do not qualify as dysarthrias. Dysarthria can affect not only articulation but also phonation, breathing, or 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 specific 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 repeating syllables, words, and sentences. Repeating consonant sounds (such as /p/, /p/, /p/) or shifting consonant sounds (/p/, /t/, /k/) can help to identify which consonants consistently cause trouble.

The Mayo Clinic classification of dysarthria ( ), 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 14.1 .

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 the features of “pseudobulbar palsy,” including dysphagia, exaggerated jaw jerk and gag reflexes, and easy laughter and crying (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” dysarthria, is associated with unilateral upper motor neuron lesions ( ). This type of dysarthria has features similar to those of spastic dysarthria, only in a less severe form. Unilateral upper motor neuron dysarthria is one of the commonest types of dysarthria, occurring in patients with unilateral strokes. Strokes, depending on their location, can also cause mixed patterns of dysarthria (see later). There is considerable evidence for the efficacy of speech therapy for poststroke dysarthria ( ).

Ataxic dysarthria or “scanning speech,” 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, 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 degenerations.

Hypokinetic dysarthria, the typical speech pattern in Parkinson disease, 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 ( ), premotor and supplementary motor area activations were seen in untreated patients with Parkinson disease and hypokinetic dysarthria but not in normal subjects. Following a voice treatment protocol, these premotor and motor activations diminished, whereas right-sided basal ganglia activations increased. Hypokinetic dysarthria responds both to behavioral therapies and to pharmacological treatment of Parkinson disease, although the efficacy of speech therapy in Parkinson disease has not been proved ( ).

Hyperkinetic dysarthria, a pattern in some ways opposite to 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 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. A recent publication found that tongue movements were particularly affected by multiple sclerosis ( ). Wilson disease can involve hypokinetic, spastic, and ataxic features.

The management of dysarthria includes speech therapy techniques for strengthening muscles, training more precise articulations, slowing the rate of speech to increase intelligibility, or teaching 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. 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 to speak more intelligibly. In Parkinson disease, most patients have elements of dysarthria and dysphonia, and treatment can include speech therapy, drug treatment, deep brain stimulation, and even surgical options ( ;). Deep brain stimulation may improve motor speech, although with variations depending on location and frequency of stimulation ( ).