Approach to the Patient with Dysarthria

Sarah S. Kramer

Michael J. Schneck

José Biller

Normal speech production involves the integration and coordination of five primary physiological subsystems: respiration, phonation, articulation, resonance, and prosody. Impairment of any of these elements may lead to dysarthria or slurring of speech. Dysarthria may occur secondary to lesions along the neuroaxis that produce motor dysfunction of any of these five speech systems. Lesions can be unilateral or bilateral and localize to the cerebral cortex, subcortical structures, brainstem, cerebellum, basal ganglia, cranial nerves, upper cervical nerves, or even the neuromuscular junction or musculature.

I. DEFINITION

Dysarthria is defined as “difficult, poorly articled speech resulting from interference in the control and execution over the muscles of speech usually caused by damage to a central or peripheral motor nerve.” Dysarthria is a group of speech disorders characterized by muscle control disturbance leading to impaired articulation of sounds. The words are slurred, but the language content is normal. Dysarthria should be differentiated from mutism, dysphonia, aphasia, and apraxia of speech.

II. CLINICAL PICTURE

A normal speech pattern is achieved through the smooth coordination of respiration, phonation, articulation, resonance, and prosody. Adequate breath support and forced exhalation gives way to changes in vocal fold length, position, and vibratory pattern. As exhalation occurs, changes in the size and shape of the oral cavity in conjunction with the articulators produce phonemes for speech production. At the same time, changes in prosody attach meanings to phonemes with alterations in pitch, intonation, stress, and rate. Together, these speech mechanisms allow us to effectively participate in daily conversation. The semiology of dysarthria may include: slurred speech, slow or rapid speech, whispering speech, abnormal intonation, and changes in quality such as nasal or hoarse sounding speech, breathy sounding speech. Associated clinical findings include limited or abnormal movements of the tongue, jaw or lips, drooling, and difficulty chewing or swallowing.

III. TYPES OF DYSARTHRIA

Differentiating among the dysarthrias is not simple as there is much overlap in the semiology of the various types of dysarthia, although certain speech characteristics are often associated with specific types of dysarthria. The flaccid, spastic, mixed, ataxic, hypokinetic, and hyperkinetic dysarthria are best characterized and described below (see also Table 19.1):

A. Flaccid dysarthria, as seen in bulbar palsy, is characterized by excessive hypernasality. Articulation of consonants and/or vowels is imprecise with slow and labored speech rate. It is typically caused by damage to cranial nerves V (motor division), VII, X, and XII that supply muscles of articulation and mastication. Muscle weakness, hypotonia, and/or atrophy may be observed. One common cause of flaccid dysarthria is idiopathic seventh nerve (Bell’s) palsy. Often these patients complain of changes in speech, drooling, and oral dysphagia. The face may appear asymmetrical during range of motion tasks even if normal at rest.

B. Spastic dysarthria, as seen in pseudobulbar palsy, results from damage to the upper motor neuron (UMN) pathways in the frontal cortex, subcortical regions, or brainstem. Speech is shallow and labored with imprecise articulation. Pitch is low with a strained vocal quality, and hypernasality can be considerable. Dysphagia may be documented as well. In addition to spastic dysarthria, the patient with pseudobulbar palsy may often exhibit emotional lability that may exhibit spontaneous outbursts of laughter or crying known as “pseudobulbar affect.” Spastic dysarthria may also result from ischemic insults. Isolated or “pure” dysarthria results mainly from lacunar infarcts involving the internal capsule or corona radiata. Isolated dysarthria and facial paresis are considered a variant of the dysarthria-clumsy hand lacunar syndrome. Occasionally, an isolated lacune will interrupt the corticolingual fibers from the motor cortex, causing dysarthria but without hemiparesis. Other common causes of spastic dysarthria include traumatic brain injury, spastic cerebral palsy, multiple sclerosis (MS), and amyotrophic lateral sclerosis (ALS).

C. Mixed dysarthria is caused by simultaneous damage to two or more primary motor components of the nervous system, such as combined UMN and lower motor neuron (LMN) lesions. This form of dysarthria is common in patients with MS, ALS, or severe traumatic brain injury. The patients may speak with very slowly and with great effort. Articulation is markedly impaired with considerable hypernasality. Pitch continues to be low with a strained or strangled vocal quality. Prosody is completely disrupted with intonation errors and inappropriately shortened phrases/sentences. Bulbar involvement in ALS often presents in this fashion with dysarthria, hypophonia, drooling of saliva, and progressive swallowing difficulties (Fig. 19.1).

D. Ataxic dysarthria is usually associated with cerebellar disorders. Patients present with decreased motor coordination for accurate articulation with abnormal speech rhythm and syllable repetition. Likewise, patients are unable to accurately complete dysdiadochokinetic tasks with variations in pitch and loudness. Prosody impairment is characterized by prolonged intervals between syllables or words with excess stress on certain syllables and words. Ataxic dysarthria is caused by damage to the cerebellum or cerebellar connections to other parts of the brain. Isolated cerebellar dysarthria has also been reported with small infarcts in the left paravermian zone of the ventral cerebellum (lobulus simplex and semilunaris superior).

E. Hypokinetic dysarthria, most typically seen in parkinsonism, is associated with hypophonia or reduced vocal loudness, in addition to monotonous speech with a slow and flat rhythm. Initiation of speech is difficult, resulting in inappropriate silences intermixed, however, with short rushes of speech. The rate is variable with wide fluctuations in pitch.

F. Hyperkinetic dysarthria also occurs secondary to damage to the basal ganglionic pathways and is typified Huntington’s disease. Damage to this system causes involuntary movements
such as tremors, dyskinesias, athetosis, and dystonia. Vocal quality may be described as harsh, strained, or strangled and is often associated with spasmodic dysphonia.

TABLE 19.1 Mayo Clinic Classification of Dysarthria

Dysarthria Type	Neurologic Condition	Location of Lesion	Most Distinctive Speech Deviation
Flaccid	Bulbar palsy	LMN	Marked hypernasality, often with nasal air emission; continuous breathiness; audible inspiration
Spastic	Pseudobulbar palsy	UMN	Very imprecise articulation; slow rate; low pitch; harsh strained or strangled voice
Ataxic	Cerebellar ataxia	Cerebellum	Excess stress and monostress; phoneme and interval prolongation; dysrhythmia of speech and syllable repetition; slow rate; some excess loudness variation
Hypokinetic	Parkinsonism	Extrapyramidal system	Monopitch, monoloudness, reduced overall loudness; variable rate; short rushes of speech; some inappropriate silences
Hyperkinetic 1. Quick	Chorea	Extrapyramidal system	Highly variable pattern of imprecise articulation; episodes of hypernasality; sudden variations in loudness
	Myoclonus		Rhythmic hypernasality; rhythmic phonatory interruption
	Tourette syndrome		Sudden tic-like grunts, barks, coprolalia
2. Slow	Athetosis	Extrapyramidal system	No distinct deviation
	Dyskinesias	Extrapyramidal system	No distinct deviation
	Dystonia	Extrapyramidal system	Prolongations of phonemes, intervals, unsteady rate, loudness
3. Tremors	Organic voice tremor	Extrapyramidal system	Rhythmic alterations in pitch, loudness, voice stoppages
Mixed	ALS	Multiple motor systems	Grossly defective articulation; extremely slow, laborious rate; marked hypernasality; severe harshness, strained or strangled voice; nearly complete disruption of prosody
	Wilson’s disease		Reduced stress; monopitch; monoloudness; similar to hypokinetic dysarthria except no short rushes of speech
	MS		Impaired control of loudness; harshness
Adapted from Johns DF, ed. Clinical Management of Neurogenic Communicative Disorders. 2nd ed. Boston, MA: Little Brown, 1985, with permission.