Abstract
The purpose of this paper is to explain and illustrate the process of differential diagnosis of the dysarthrias using an ELMS analysis. Using a simple acronym, the clinician compiles and integrates the available information pertaining to the patient’s Etiology, Lesion site, Motor signs, and Speech deficits to arrive at an accurate diagnosis of the type of dysarthria (or, at least rule out other types). The “hallmark” speech characteristics of each type of dysarthria will be briefly described. In addition, the neuromuscular basis of each type of dysarthria will be presented, along with descriptions of various etiologies, sites of lesion, and non-speech motor signs. Lastly, the use of this model in the process of differential diagnosis will be illustrated via case analyses.
Introduction
Why are there so many types of dysarthria, and are they really that different from one another? What is the difference between an upper motor neuron and a lower motor neuron, and does it really matter clinically? How can I tell if my patient’s muscles are spastic or flaccid just by listening to their speech? If hypokinetic dysarthria and hyperkinetic dysarthria are both caused by damage to the basal ganglia, then why are the speech deficits so different? Why do all types of dysarthria have so many of the same speech characteristics? Why do I need to know the site of lesion in order to diagnose my patient? Can I figure it out just by listening to their speech?
These and many other legitimate questions are often asked by clinicians and graduate students when attempting to differentially diagnosis a patient with dysarthria. The term "dysarthria" actually refers to a group of speech disorders involving any or all of the basic speech production processes (i.e., respiration, phonation, resonance, articulation, and prosody) and resulting from disturbances in muscular control secondary to neurological damage (e.g., degenerative diseases, cerebral vascular accidents, traumatic brain injury, etc.) (Darley, Aronson & Brown, 1975). Dysarthria is typically, though not necessarily, characterized by some degree of weakness, slowness, incoordination, or alteration of muscle tone of the speech apparatus (Freed, 2012; Duffy, 2013).
The dysarthrias are generally sub-divided into six “pure” dysarthrias (flaccid, spastic, unilateral upper motor neuron, ataxic, hypokinetic, and hyperkinetic), as well as numerous “mixed” dysarthrias (i.e., combinations of one or more pure dysarthrias) (Freed, 2012; Duffy, 2013). Each sub-type is characterized by a constellation (or “cluster”) of speech deficits, as well a corresponding neuromuscular basis. For example, spastic dysarthria results from bilateral upper motor neuron damage, which leads to spasticity of the affected muscles (i.e., hyperactive or unregulated reflexive contractions). As a result, these patients usually display speech characteristics that reflect spasticity of the affected muscles, such as harsh or strained-strangled voice, articulatory imprecision, slow speech rate, hypernasality, monopitch and monoloudness. Although patients with other types of dysarthria may also exhibit many of these same deficits, it is usually due to a different neuromuscular pathology (e.g., flaccidity). Clinically, this is a critically important distinction, as a spastic patient would typically be treated quite differently than a flaccid patient, despite several common speech characteristics. For example, strength training might be appropriate for some patients with flaccidity of the affected muscles, but would usually be contraindicated for a patient with spastic muscles. Thus, an accurate diagnosis is crucial for effective and safe management of the patient. Simply memorizing lists of associated speech characteristics is insufficient for successful differential diagnosis of the dysarthrias (Blanchet, 2013).
