The dysarthrias are a group of neurological disorders that reflect disturbances in the strength, speed, range, tone, steadiness, timing, or accuracy of movements necessary for prosodically normal, efficient and intelligible speech. They result from central or peripheral nervous system conditions that adversely affect respiratory, pho-natory, resonatory, or articulatory speech movements. They are often accompanied by nonspeech impairments (e.g., dysphagia, hemiplegia), but sometimes they are the only manifestation of neurological disease. Their course can be transient, improving, exacerbating-remitting, progressive, or stationary.
Endogenous or exogenous events as well as genetic influences can cause dysarthrias. Their neurological bases can be present congenitally or they can emerge acutely, subacutely, or insidiously at any time of life. They are associated with many neurological conditions, but vascular, traumatic, and degenerative diseases are their most common cause in most clinical settings; neo-plastic, toxic-metabolic, infectious, and inflammatory causes are also possible.
Although incidence and prevalence are not precisely known, dysarthria often is present in a number of frequently occurring neurological diseases, and it probably represents a significant proportion of all acquired neurological communication disorders. For example, approximately one-third of people with traumatic brain injury may be dysarthric, with nearly double that prevalence during the acute phase (Sarno, Buonaguro, and Levita, 1986; Yorkston et al., 1999). Dysarthria probably occurs in 50%-90% of people with Parkinson's disease, with increased prevalence as the disease progresses (Logemann et al., 1978; Mlcoch, 1992), and it can be among the most disabling symptoms of the disease in some cases (Dewey, 2000). Dysarthria emerges very frequently during the course of amyotrophic lateral sclerosis (ALS) and may be among the presenting symptoms and signs in over 20% (Rose, 1977; Gubbay et al., 1985). It occurs in 25% of patients with lacunar stroke (Arboix and Marti-Vilata, 1990). In a large tertiary care center, dysarthria was the primary communication disorder in 46% of individuals with any acquired neurological disease seen for speech-language pathology evaluation over a 4-year period (Duffy, 1995).
The clinical diagnosis is based primarily on auditory perceptual judgments of speech during conversation, sentence repetition, and reading, as well as performance on tasks such as vowel prolongation and alternating motion rates (AMRs; for example, repetition of "puh," ''tuh,'' and ''kuh'' as rapidly and steadily as possible). Vowel prolongation permits judgments about respiratory support for speech as well as the quality, pitch, and duration of voice. AMRs permit judgments about the rate and rhythm of repetitive movements and are quite useful in distinguishing among certain dysarthria types (e.g., they are typically slow but regular in spastic dys-arthria, but irregular in ataxic dysarthria). Visual and physical examination of the speech mechanism at rest and during nonspeech responses (e.g., observations of asymmetry, weakness, atrophy, fasciculations, adventitious movements, pathological oral reflexes) and information from instrumental measures (e.g., acoustic, endoscopic, videofluorographic) often provide confirmatory diagnostic evidence.
Dysarthria severity can be indexed in several ways, but quantitative measures usually focus on intelligibility and speaking rate. The most commonly used intelligibility measures are the Computerized Assessment of Intelligibility in Dysarthric Speakers (Yorkston, Beukelman, and Traynor, 1984) and the Sentence Intelligibility Test (Yorkston, Beukelman, and Tice, 1996), but other measures are available for clinical and research purposes (Enderby, 1983; Kent et al., 1989).
A wide variety of acoustic, physiological, and anatomical imaging methods are available for assessment. Some are easily used clinically, whereas others are primarily research tools. Studies using them have often
Dysarthrias: Characteristics and Classification
yielded results consistent with predictions about patho-physiology from auditory-perceptual classification, but discrepancies that have been found make it clear that correspondence between perceptual attributes and physiology cannot be assumed (Duffy and Kent, 2001). Methods that show promise or that already have refined what we understand about the anatomical and physiological underpinnings of the dysarthrias include acoustic, kinematic, and aerodynamic methods, elec-tromyography, electroencephalography, radiography, tomography, computed tomography, magnetic resonance imaging, functional magnetic resonance imaging, positron emission tomography, single-photon emission tomography, and magnetoencephalography (McNeil, 1997; Kent et al., 2001).
The dysarthrias can be classified by time of onset, course, site of lesion, and etiology, but the most widely used classification system in use today is based on the auditory-perceptual method developed by Darley, Aronson, and Brown (1969a, 1969b, 1975). Often referred to as the Mayo Clinic system, the method identifies dysarthria types, with each type representing a perceptually distinguishable grouping of speech characteristics that presumably reflect underlying pathophysi-ology and locus of lesion. The following summarizes the major types, their primary distinguishing perceptual attributes, and their presumed underlying localization and distinguishing neurophysiological deficit.
Flaccid dysarthria is due to weakness in muscles supplied by cranial or spinal nerves that innervate respiratory, laryngeal, velopharyngeal, or articulatory structures. Its specific characteristics depend on which nerves are involved. Trigeminal, facial, or hypoglossal nerve lesions are associated with imprecise articulation of phonemes that rely on jaw, face, or lingual movement. Vagus nerve lesions can lead to hypernasality or weak pressure consonant production when the pharyngeal branch is affected or to breathiness, hoarseness, dip-lophonia, stridor, or short phrases when the laryngeal branches are involved. When spinal respiratory nerves are affected, reduced loudness, short phrases, and alterations in breath patterning for speech may be evident. In general, unilateral lesions and lesions of a single nerve produce relatively mild deficits, whereas bilateral lesions or multiple nerve involvement can have devastating effects on speech.
Spastic dysarthria is usually associated with bilateral lesions of upper motor neuron pathways that innervate relevant cranial and spinal nerves. Its distinguishing characteristics are attributed to spasticity, and they often include a strained-harsh voice quality, slow rate, slow but regular speech AMRs, and restricted pitch and loudness variability. All components of speech production are usually affected.
Ataxic dysarthria is associated with lesions of the cerebellum or cerebellar control circuits. Its distinguishing characteristics are attributed primarily to incoordination, and they are perceived most readily in articulation and prosody. Characteristics often include irregular articulatory breakdowns, irregular speech
AMRs, inappropriate variations in pitch, loudness, and duration, and sometimes excess and equal stress across syllables.
Hypokinetic dysarthria is associated with basal ganglia control circuit pathology, and its features seem mostly related to rigidity and reduced range of motion. Parkinson's disease is the prototypic disorder associated with hypokinetic dysarthria, but other conditions can also cause it. Its distinguishing characteristics include reduced loudness, breathy-tight dysphonia, monopitch and monoloudness, and imprecise and sometimes rapid, accelerating, or "blurred" articulation and AMRs. Dys-fluency and palilalia also may be apparent.
Hyperkinetic dysarthria is also associated with basal ganglia control circuit pathology. Unlike hypokinetic dysarthria, its distinguishing characteristics are a product of involuntary movements that interfere with intended speech movements. Its manifestations vary across several causal movement disorders, which can range from relatively regular and slow (tremor, palatophar-yolaryngeal myoclonus), to irregular but relatively sustained (dystonia), to relatively rapid and predictable or unpredictable (chorea, action myoclonus, tics). These movements may be a nearly constant presence, but sometimes they are worse during speech or activated only during speech. They may affect any one or all levels of speech production, and their effects on speech can be highly variable. Distinguishing characteristics usually reflect regular or unpredictable variability in phrasing, voice, articulation, or prosody.
Unilateral upper motor neuron dysarthria has an anatomical rather than pathophysiological label because it has received little systematic study. It most commonly results from stroke affecting upper motor neuron pathways. Because the damage is unilateral, severity usually is rarely worse than mild to moderate. Its characteristics often overlap with varying combinations of those associated with flaccid, spastic, or ataxic dysarthria (Duffy and Folger, 1996; Hartman and Abbs, 1992).
Mixed dysarthrias reflect combinations of two or more of the single dysarthria types. They occur more frequently than any single dysarthria type in many clinical settings. Some diseases are associated only with a specific mix; for example, flaccid-spastic dysarthria is the only mix expected in ALS. Other diseases, because the locus of lesions they cause is less predictable (e.g., multiple sclerosis, traumatic brain injury), may be associated with virtually any mix. The presence of mixed dysarthria is very uncommon or incompatible with some diseases (e.g., myasthenia gravis is associated only with flaccid dysarthria), so sometimes the presence of a mixed dys-arthria can make a particular disease an unlikely cause or raise the possibility that more than a single disease is present.
Because of their potential to inform our understanding of the neural control of speech, and because their prevalence in frequently occurring neurological diseases is high and their functional effects are significant, dys-arthrias draw considerable attention from clinicians and researchers. The directions of clinical and more basic research are broad, but many current efforts are aimed at the following: refining the differential diagnosis and indices of severity; delineating acoustic and physiological correlates of dysarthria types and intelligibility; more precisely establishing the relationships among perceptual dysarthria types, neural structures and circuitry, and acoustic and pathophysiological correlates; and developing more effective treatments for the underlying impairments and functional limitations imposed by them. Advances are likely to come from several disciplines (e.g., speech-language pathology, speech science, neurology) working in concert to integrate clinical, anatomical, and physiological observations into a coherent understanding of the clinical disorders and their underpinnings.
See also dysarthrias: management.
—Joseph R. Duffy References
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