Clinical Assessment of Motor Speech Disorders in Adults with Concussion

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Michael P. Cannito, Ph.D., CCC-SLP1

ABSTRACT

This article reviews the occurrence of motor speech disorders of dysarthria and apraxia of speech following closed head injury and other traumatic brain injuries in adults as they apply to sport concussion and related trauma. Athletic sideline and speech-language pathology screenings are considered. Procedures for clinical assessment and diagnosis of motor speech disorder, most particularly dysarthria, are discussed with special reference to closed head injury. Included are the evaluation components of cranial nerve and speech mechanism examination, nonspeech musculature examination, perceptual and instrumental assessment procedures, quasi-standardized testing for dysarthria, and the determination of restrictions of participation in everyday life activities. The resultant output of such an evaluation is described in depth. Future directions for clinical research on motor speech disorders following sports concussion are also briefly considered. KEYWORDS: Motor speech disorders, concussion, traumatic brain injury, assessment and diagnosis

Learning Outcomes: As a result of this activity, the reader will be able to (1) discuss the occurrence of motor speech disorders following traumatic brain injury and concussion as they apply to sport-related injury; (2) explain the components of the comprehensive motor speech examination and its resultant output; (3) compare various types of dysarthria and their most characteristic features that may occur following a concussion; and (4) express a clear concise diagnostic statement for a motor speech disorder following concussion.

T

here is currently very little information available regarding the occurrence, assessment, or treatment of motor speech disorders associ-

ated with sport concussion. Motor speech disorders are not among the more common postconcussion sequelae of sport injuries1;

1

Semin Speech Lang 2014;35:221–233. Copyright # 2014 by Thieme Medical Publishers, Inc., 333 Seventh Avenue, New York, NY 10001, USA. Tel: +1(212) 584-4662. DOI: http://dx.doi.org/10.1055/s-0034-1384684. ISSN 0734-0478.

School of Communication Sciences & Disorders, University of Memphis, Memphis, Tennessee. Address for correspondence: Michael P. Cannito, Ph.D., CCC-SLP, School of Communication Sciences & Disorders, University of Memphis, 807 Jefferson Avenue, Memphis, TN 38105 (e-mail: [email protected]). Concussion 101 for SLPs; Guest Editor, Anthony P. Salvatore, Ph.D., CCC-SLP

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however, they do sometimes occur. This is particularly true of more severe concussions, repeated concussions, or the occurrence of intracranial bleeding, as well as brain stem and peripheral nerve damage that may co-occur with sport-related concussion.2–4 Motor speech disorders have significant influence on the quality of life, including speech comprehensibility, social interaction, employability, and self-esteem of affected individuals.5 Therefore, speech-language pathologists (SLPs) should be prepared to evaluate and diagnose these communicative impairments whenever appropriate. Acquired motor speech disorders in adults encompass the occurrence of the various dysarthrias as well as apraxia of speech (AOS). AOS is a disorder affecting the premotor planning and programming of complex multimovement sequences required to actualize an abstract intended utterance as sound. In contrast, the dysarthrias involve the well-modulated execution of neural commands for individual movement components that were specified by the premotor plan/program. AOS is typically associated with damage to the left cerebral hemisphere’s frontal premotor network, including posterior inferior frontal gyrus, inferolateral premotor cortex, and anterior insula, and the white matter interconnections among these regions. It may also be affected by damage to white matter interconnections with somatosensory and auditory cortices with which the frontal network interacts. AOS is extremely uncommon secondary to closed head injury (CHI), and when it does occur, there is probably significant translational trauma to the left anterior regions or an intracranial bleed. Duffy has indicated that 15% of 115 cases of AOS reviewed at the Mayo Clinic exhibited AOS due to traumatic brain injury (TBI)6; however, few cases sustained a CHI. AOS more commonly occurs with open head injury (e.g., missile wound) and most commonly following stroke.6 AOS most often occurs in association with nonfluent aphasia, which also is very infrequent following CHI.7 Given its scarcity as a behavioral sequel to CHI, AOS will not be considered further in this review, except to diagnostically differentiate it from dysarthria. The reader is referred to other useful sources for information regarding assessment and diagnosis of AOS.5,6,8,9

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Dysarthria occurs more frequently than AOS following CHI. Survey estimates of dysarthria occurrence following TBI range from 23% in outpatient clinics to 65% in acute care settings.10 Other prevalence data suggest overall occurrence of dysarthria in about one third of TBI survivors.11 The dysarthrias are a heterogenous collection of motor speech disorders resulting from diverse motor system damage ranging over a broad expanse of neural tissue: This includes the upper motor neurons of the primary motor cortex and their descending corticobulbar and corticospinal tracts, the lower motor neuron pools giving rise to the motor components of cranial and spinal nerves involved in speech, and subcortical motor structures such as the basal ganglia and cerebellum with their white matter interconnections. The various dysarthrias have in common that they are generalized motor disturbances that affect the musculature for speech. For example, if the tongue exhibits paralysis or incoordination, it does so for both speech and nonspeech movements, including feeding and swallowing (unlike AOS, which is a speech-specific phenomenon). The dysarthrias may encompass all speech production processes including articulation, resonation, phonation, and respiration, or they may affect any single process or any combination of these processes.12 The specific type of dysarthria exhibited will depend upon the neuromotor structures and pathways involved. Given the current paucity of information available on motor speech disorders associated with sport concussion, clinical guidance for assessment and diagnosis must be gleaned from the existing literature on TBI and neurologic impairment more generally. For example, Theodoros et al reported characteristics of 43 cases with dysarthria following severe TBI13; however, sport-related injuries accounted for only six of the cases (14%), excluding motor cycle accidents, which may or may not have been sport-related. These included football injury, waterskiing accident, cycling accident, and other unspecified sport injury. It should be noted that this is based on an Australian sample, and it might be smaller than found in an American one, due to the prevalence of American football in the U.S. culture.

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ASSESSMENT AND DIAGNOSIS OF MOTOR SPEECH DISORDERS Screening Screenings in the field are necessarily limited. Athletic trainers may be instructed to listen to the player’s speech for slurred pronunciation or abnormal voice quality or the absence of speech following an impact. Some field screenings recommend including a check of cranial and spinal nerve functions.14 Sideline information is important because if such findings are present, they probably suggest a more severe level of deficit that may affect decisions regarding return to play. If such findings are absent but develop later, they may indicate the occurrence of an intracranial hemorrhage.15 Screening within the clinic should be administered by a certified SLP and include brief functional assessments of cranial nerves (CNs) V, VII, IX, X, XI, and XII, which are important to the production of speech (see Table 1). An audiometric pure tone hearing screening should also be administered (CN VIII). The SLP then listens carefully to the patient’s speech production in conversation and reading to determine whether intelligibility, rate, and naturalness are at all impaired. If there are indications of cranial motor nerve involvement that may affect speech production or perceived difficulties with speech intelligibility, rate, or naturalness, then a comprehensive motor speech evaluation (CMSE) should be completed.

Input to the CMSE The CMSE asks a series of 10 pertinent diagnostic questions (see Table 2). The components of the CMSE include a case history, indepth speech mechanism examination, formal perceptual speech assessment, standardized dysarthria testing, examination of nonspeech motor behaviors, and assessment of restrictions of participation in everyday activities. The potential need for specialized instrumental evaluation techniques should also be determined. The CMSE outputs a diagnostic report summarizing the procedures and the findings of the evaluation and culminating in a diagnostic statement, prognosis, and specific clinical recommendations.

The case history should include a patient interview to explore any difficulties, symptoms, and functional limitations the patient may be experiencing with respect to speech, language, or communication. Especially significant is the concussion history: Repeated concussion or second impact syndrome and even multiple subclinical concussions may lead to more severe deficits associated with chronic traumatic encephalopathy, which may result in motor speech disorders.16,17 Initial and current overall severity of CHI as determined by the Rancho Los Amigos Scale or similar instruments and the time postinjury are also important,18 as more severe deficits that have subsequently resolved are more likely to be associated with motor speech disorders. It may be some months or years postinjury before such a patient sufficiently recovers to be a viable candidate for direct work on speech production. Initial medical records should be reviewed to check for evidence of intracranial bleeding, hematoma, cerebral or brain stem contusions, or co-occurring peripheral nerve damage, all of which both increase the likelihood of occurrence and provide an explanatory context for a motor speech disorder that the patient exhibits. Preexisting conditions related to communication should be noted as these may contribute to a postconcussive speaking problem even if they had been successfully managed prior to the injury. These include stuttering, articulation disorder, cleft palate, respiratory illness, hearing loss, visual impairment, or learning disabilities. Results of prior and current cognitive assessments should be noted as these commonly occur with CHI and may affect current testing as well as treatment planning decisions. The clinician must be mindful of pervasive cognitive impairments that are known to occur in this population, affecting processing speed, attention, working memory, long-term memory, executive functions, and learning.19–21 It is critical that the component structures of each subsystem for speaking (i.e., respiration, phonation, resonance, articulation, and prosody) be carefully evaluated for dysfunction in the areas of muscular strength and tonus, coordination, speed, accuracy, and steadiness.12 Detailed instructions for speech motor examination are available in other sources.5,6 Structures should

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MOTOR SPEECH DISORDERS IN ADULTS WITH CONCUSSION/CANNITO

Vagus

Glossopharyngeal

IX

gia, stridor, altered laryngeal reflexes, dysphonia, dysprosody, dysarthria; Ipsilateral or bilateral paresis/paralysis of soft palate and larynx, hypernasality, nasal

valving; controls esophagus, cardiac, gastrointestinal tract, lungs; taste and general sensation for larynx, hypopharynx

nucleus; nucleus solitarius

tongue VF paralysis (RLN)—dyspha-

eral posterior portion of

tion; loss of general & taste sensation of pharynx ipsilat-

muscles; decreased saliva-

flex, dysphagia; partial paresis of the pharyngeal

Phonation; cough; velar

secretions; taste; somesthesia

nucleus; nucleus solitarius

torted taste perception Loss/reduction of gag re-

decreased salivation; dis-

of nasolabial fold, hyperacusis; Bell’s palsy, dysarthria;

droop on affected side; loss

Paralysis of ipsilateral facial muscles; drooling, labial

sation; trigeminal neuralgia

Nucleus ambiguous; dorsal motor

Swallowing; regulates

Facial expression; regulates secretions; taste

Nucleus ambiguous; inferior salivatory

Facial motor nucleus; superior salivatory; nucleus; nucleus solitarius

viates toward affected side

anterior oral cavity

on opening; numbness (ipsilateral); loss of tactile sen-

al muscles of mastication, atrophy, dysarthria; jaw de-

and; mastication; somatosensory for face, head,

Paresis/paralysis of ipsilater-

Jaw movement; speech

Pathology

Trigeminal motor nucleus; primary senso-

Function

ry nucleus; spinal trigeminal nucleus; mesencephalic nucleus

Nuclei

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Motor sensory

Motor sensory

Motor sensory

Motor sensory

Type

SEMINARS IN SPEECH AND LANGUAGE/VOLUME 35, NUMBER 3

X

Facial

Trigeminal

V

VII

Cranial Nerve

Summary of Cranial Nerves Involved in Speech Production

NNo.

Table 1

224 2014

Hypoglossal

XII

Hypoglossal nucleus

Spinal accessory nucleus

Nuclei

Tongue movement

be raised; restricted head

ment; stability

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protrusion

dysarthria, no tongue

upon protrusion; bilateral lesion: severe dysphagia &

tongue deviates to affected

tongue is paralyzed (fasciculations, atrophy), dysarthria;

Ipsilateral lesion: half of

movement; weakness of muscles supplied by nerve

for larynx and hypopharynx Dropped shoulders cannot

and general somesthesia

lum/uvula deviates to unaffected side, loss of taste

lesions may be fatal), ve-

fects autonomic functions & visceral reflexes (bilateral

emission, regurgitation; af-

Pathology

Head & shoulder move-

Function

Not directly involved in speech; however, head control is important to maintaining a stable postural background for speaking.



Motor

Spinal accessory

XI

Motor

Type

Cranial Nerve

NNo.

Table 1 (Continued)

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Table 2

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Ten Pertinent Diagnostic Questions

Specific Diagnostic Questions

Clinical Commentary

1. Does a clinical communication problem

From patient description, presenting symptoms, initial

exist?

screening; not every referral will exhibit a communication disorder, although there may be other issue (e.g., mild cognitive impairment, impulsivity, etc.)

2. What is the underlying nature of the

From case history and medical records; note onset and

problem? 3. What is the specific type and subtype?

course, etiology, complicating factors From evaluation findings determine a differential diagnosis; type: apraxia of speech versus dysarthria versus aphasia, etc.; subtype: spastic versus flaccid versus ataxic, etc. (in the case of dysarthria)

4. What are the most salient character-

Even within a specific subtype (e.g., flaccid) there will

istics of this individual’s speech disorder?

be individual differences among patients, usually cast as perceptual descriptors (e.g., hypernasality) by order of prominence

5. How severe is the problem?

Determine primarily from ratings of intelligibility and naturalness; objective impairment may differ from subjective impairment as perceived by the patient

6. What specific structural components and speech processes are involved?

Behavioral examination of the speech mechanism and listening to patient’s speech; may vary across individuals even of the same subtype and severity

7. Are there any nonspeech concomitant physical symptoms that may affect com-

Includes sensory impairments, loss of facial expression, limb impairments restricting gestures, or limiting AAC

munication or rehabilitation?

options, etc.

8. How has the speech disorder restricted participation in everyday activities?

May vary depending on premorbid participation levels, present communication needs, and patient outcome expectations

9. What is the prognosis?

Clinical judgment of expected improvement based on prognostic factors and clinical experience, both with and without recommended treatment

10. What course of action is recommended?

Supplemental testing, medical referral, behavioral or nonbehavioral treatment, counseling, none

Abbreviation: AAC, augmentative and alternative communication.

be evaluated at rest, during nonspeech movements, and during speech or speech like tasks (e.g., sustained vowels). Co-occurring nonspeech motor abnormalities external to the speaking mechanism also should be examined (e.g., eye tracking, head and limb control) both to support the diagnosis (e.g., ataxia) and to identify dysfunction that may limit access to augmentative or alternative communication (AAC) approaches during treatment. For dysarthria, a formal perceptual speech assessment is usually accomplished using the Mayo Clinic Scales.6 A standard reading sample and sustained vowel productions are obtained. The clinician then rates 42 specifically defined

perceptual attributes using a 5-point ordinal scale (0 ¼ no impairment, 4 ¼ severe deviation) to characterize a patient’s pitch, loudness, voice quality, resonance, intraoral pressure, respiration, prosody, and articulation. In the hands of an experienced dysarthria clinician, this approach can be both reliable and valid.6 Based on resultant perceptual features, the dysarthria is then classified into one of six types indicative of the locus of nervous system involvement and its effect on muscle function, including flaccid, spastic, ataxic, hypokinetic, hyperkinetic, and specific mixed dysarthrias (e.g., spastic-ataxic). Each type exhibits a characteristic perceptual profile (see Table 3). Based on the oral reading

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Stroke (brain stem), bulbar palsy, myasthenia gravis;

Flaccid (bulbar)

ments, variable muscle tone, intermittent hypertonia, muscle spasms

Quick or slow involuntary move-

spasmodic dysphonia, TBI

Extrapyramidal system

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audible inspiration

downs, harsh or strained-strangled voice quality,

cess loudness variations, prolonged phonemes, distorted vowels, irregular articulatory break-

intervals, variable rate, inappropriate silences, ex-

precise consonants Intermittently imprecise consonants, prolonged

prolonged silences, excessive rate variation, im-

pects of movement

Hypophonia, breathiness, short rushes of speech, accelerated rate, monopitch, monoloudness, reduced loudness, reduced stress, harsh voice,

Slow movement; limited ROM;

imprecise consonants, harsh voice, monopitch, monoloudness, excess loudness variations

articulatory breakdowns, excess & equal stress,

immobility, rigidity; paucity of movement; loss of automatic as-

nia; tardive dyskinesia,

Huntington’s chorea, dysto-

induced, multi-infarct dementia, TBI

Extrapyramidal system

dysrhythmia; dysmetria

Parkinson’s disease, drug

movement; hypotonia;

nopitch, & monoloudness Slow rate, prolonged speech segments, irregular

fects, TBI

Cerebellar system

nasality (inconsistent), imprecise consonants, mo-

movement inaccurate movement; slow

phrases Strained strangled voice quality, slow rate, hyper-

itch, monoloudness, imprecise consonants, short

Consistent breathiness, reduced loudness, hypernasality, nasal emission, inhalation stridor, monop-

Characteristic Speech Attributes

limited ROM; slowness of

Spastic paralysis; weakness;

fasciculations

Flaccid paralysis; weakness; hypotonia; muscle atrophy;

Neuromuscular Conditions

Friedrich’s ataxia, toxic ef-

stroke, tumor, ataxic CP,

eral if permanent)

Upper motor neuron (bilat-

Lower motor neurons

Location

Abbreviations: CP, cerebral palsy; CVA, cardiovascular accident; ROM, range of motion; TBI, traumatic brain injury.  Mixed dysarthrias involve combinations of the primary types as a result of widespread or multifocal neurologic damage.

Hyperkinetic

Hypokinetic

Ataxic

cephalitis, spastic CP, TBI

TBI Spastic (pseudobulbar) Stroke (CVA), tumor, en-

peripheral nerve damage,

Example Etiologies

Primary Dysarthria Types Reported following Traumatic Brain Injury

Type

Table 3

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sample, speech is rated for overall intelligibility, an estimate of how well the patient would be understood by an unfamiliar listener, and for naturalness, which, although primarily a prosodic construct, may also be influenced by other speech processes (e.g., voice quality, articulation). From these two ratings, the clinician arrives at a judgment of overall severity of dysarthria. Although there remains no straightforward formula by which this may be accomplished, intelligibility may weigh more heavily in identification of greater severity levels, whereas milder severity levels may involve relatively preserved intelligibility but impaired naturalness. In their 43-patient sample, Theodoros et al observed the occurrence of spastic, hypokinetic, flaccid, ataxic, and various mixed dysarthrias secondary to TBI, with severity ranging from mild to moderate to severe.13 They observed the 10 most frequent deviant speech characteristics occurring in TBI (ordered from most to least frequent) to be hypernasality, reduced rate, imprecise consonants, reduced pitch variation, decreased breath support for speech, abnormal stress patterning, reduced phrase length, impaired overall intelligibility, prolonged intervals, reduced loudness variation. Findings were generally similar to those of a 20-patient sample that was restricted to CHI.22 Although these authors did not observe hyperkinetic dysarthria in their TBI sample, the occurrence of seven cases of spasmodic dysphonia (laryngeal dystonia) secondary to TBI have been reported.23 Spasmodic dysphonia is a focal or single process, hyperkinetic dysarthria that affects phonation, prosody, speaking rate, and intelligibility.24 Additional useful tasks for evaluating motor speech involve repetitive syllable sequences, known as alternating motion rates (AMRs) and sequential motion rates (SMRs), as well as production of sustained vowels and imitation of simple and complex words. AMRs require repeated production of a specific syllable (e.g., /puh/) as rapidly as possible. SMRs required rapid repetition of a syllable sequence (e.g., /puhtuh/ or /puhtuhkuh/). A patient with dysarthria only will give the impression of equal difficulty (e.g., slowness, distortion) for AMRs and SMRs, differentiating it from AOS where-

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in greater difficulty is exhibited for SMRs. These measures can readily be quantified as syllables per second using a digital timer and recorder. Acoustic and kinematic studies have demonstrated impaired AMRs secondary to CHI in comparison to control speakers.25–27 Sustained vowel production and imitation of monosyllabic and polysyllabic words also help to differentiate dysarthria from AOS. Patients with AOS have little difficulty with vowel prolongation, whereas speakers with dysarthria will often exhibit problems with phonation, resonance, or articulation (i.e., difficulty maintaining a specific vowel target over time) during these productions. Speakers with AOS will have greater difficulty producing polysyllabic than monosyllabic words, (e.g., in sequences such as “please, pleasing, pleasingly”). In contrast, the speaker with dysarthria will typically exhibit similar difficulties across these productions. The underlying diagnostic principle is that because AOS is a motor planning and programming disorder, it is exacerbated by increasing articulatory length and complexity demands. In addition, AOS tend to exhibit inconsistent articulation errors of distortion, substitution, omission, and addition along with inconsistently correct productions, whereas dysarthria tends to result in more consistent distortion errors, although other types of articulation errors may occasionally occur. Impairments of prosody are common in dysarthria and have been documented following CHI, including intonation,28 emphatic stress,29 and pausing.30 Prosody is a major contributor to the percept of speech naturalness; however, prosodic variables also normally provide a listener with meaningful cues to phrase segmentation and word identification and thus are important to intelligibility in connected speech. Consequently, the clinician should routinely evaluate these elements using a connected speech sample. Other prosodic markers such as lexical stress and juncture (i.e., interword transitions) should also be examined. Speaking rate abnormalities have also been documented following TBI, including both reduced and increased rates in comparison to control speakers.27,31 Two quasi-standardized and widely used diagnostic tests that are commercially available

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for dysarthria assessment are the Assessment of Intelligibility of Dysarthric Speech32 (AIDS) and the Frenchay Dysarthria Assessment, Second Edition33 (FDA-2). The AIDS is a tool for quantifying intelligibility in isolated words and sentences. It also provides a measure of speaking rate and an estimate of communication efficiency in terms of intelligible words per minute. Its subtests include a single-word task and a sentence intelligibility test (SIT). For single words, the patient is audio-recorded reading or imitating 50 words, each of which is randomly selected by the clinician from its own pool of 12 phonetically similar words. A judge, other than the clinician, then listens to the words using one of two response formats, orthographic transcription or multiple choice. The clinician then calculates a percent singleword intelligibility score. The SIT requires the clinician to select 20 sentences from a single pool of 100 different sentences of varying lengths. Two sentences are selected from each length ranging from 5 to 15 words. The patient is then recorded reading or imitating the sentences. The judge then transcribes the sentences and a percentage of words understood is calculated by the clinician. Rate of speech in words per minute is also calculated by dividing the number of target words (n ¼ 220) by the cumulative durations of the sentences that were produced. Rate of intelligible speech is similarly calculated. A communication efficiency ratio is obtained by dividing the rate of intelligible speech by 190 or the mean speaking rate for normal speakers who are highly intelligible. Normative data for the AIDS was limited to mean intelligible words per minute for 20 normal speakers (10 males, 10 females). Intrajudge reliability (Pearson r) for the single-word task was 0.90 for the multiple-choice formal and 0.87 for the transcription format. Interjudge reliability (Pearson r) for the SIT was 0.96 for percent intelligibility and 0.99 for intelligible words per minute. Theodoros et al employed the AIDS to document a mean single-word intelligibility of 60.03% (standard deviation [S.D.] ¼ 19.63%), a mean sentence intelligibility of 79.89% (S.D. ¼ 23.32%), and a mean speaking rate of 127.31 words per minute (S.D. ¼ 45.68).13 The mean intelligible words per minute was

106.32 (S.D. ¼ 56.24), and the mean communication efficiency ratio mean was 0.55 (S.D. ¼ 0.29). All of these values were markedly reduced in CHI in comparison with control speakers. The FDA-2 uses an 5- point equal-appearing interval scale by which the clinician rates the patient’s performance on multiple tasks involving 7 sections, each with several subparameters: reflexes (3 parameters), respiration (2 parameters), lips (5 parameters), palate (3 parameters), larynx (4 parameters), tongue (6 parameters), and intelligibility (3 parameters). Specific instructions for rating each parameter are provided. The manual indicates that the test was normed on 157 normal healthy adults ranging in age from 15 to 97 years. However, no normal means, S.D.s, percentiles, or other normative values are provided in the test manual. Interjudge reliability (Pearson r), obtained using videotapes from 113 subjects with dysarthria, was reported to range from 0.70 to 0.92 for various pairs of judges. Interjudge reliability obtained from audio recordings (for audible subtests only) from six listeners ranged from 0.72 to 0.92. Reliability data are not broken out by section (e.g., intelligibility) nor subsection (e. g., sentence intelligibility) but appear rather to have been based on an overall score of some type that remains unspecified in the test manual. Profiles with means and standard deviations for five subtypes of dysarthria (i.e., spastic, ataxic, flaccid, hypokinetic, and mixed) are provided in the manual, as well as an evaluation of validity utilizing discriminant function analysis to classify patients into their respective groups, which was accomplished with over 90% accuracy. Within the framework of the World Health Organization’s International Classification of Functioning, Disability and Health (ICF), many of the dysarthria assessment variables measured or rated by SLPs are considered measures of impairment of functional integrity (e.g., alternating motion rate, perceived hypernasality). In contrast, intelligibility, naturalness, and speaking rate are considered measures of activity limitation, specifically the activity of spoken communication.11 Within the ICF framework, however, it is also important to determine participation restrictions, or a disorder’s influence on an individual’s degree of

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MOTOR SPEECH DISORDERS IN ADULTS WITH CONCUSSION/CANNITO

SEMINARS IN SPEECH AND LANGUAGE/VOLUME 35, NUMBER 3

involvement in life situations. Few measures of this type have as yet been developed for motor speech disorders; however, the Communicative Effectiveness Survey is a useful self-report inventory examining how well a speaker communicates in various social situations and should be used in conjunction with an inventory of the speaker’s communicative needs.5 Instrumental evaluation procedures are becoming more widely used in everyday clinical practice by SLPs. These are not routine components of the CMSE, but should be regarded as specialized supplemental tests that may be recommended if needed to further characterize a patient’s motor speech disorder. Two such techniques are endoscopy and acoustic analysis, both of which may provide valuable information to supplement the conventional behavioral CMSE. Nasolaryngeal fiberoptic videoendoscopy is a physiological technique that enables the visualization and recording of the velopharyngeal and laryngeal valves at rest and during various voice and speech production activities. Combined with stroboscopy, it also may be used to determine the integrity of vocal fold vibration. The KayPENTAX Motor Speech Profile system (KayPENTAX, Montvale, NJ) is a protocol-driven software tool that quantifies acoustic aspects of various tasks for assessment of voice, articulation, and prosody for patients with dysarthria.34 It includes normative data, and the analysis procedures are largely automated. A variety of other instrumental procedures are available for aerodynamic,35 electromyographic,36 and kinematic37 assessments of speech motor functions, but these are less widely available in everyday clinical practice, remaining primarily research tools. Using such instruments, electroglottographic evidence of dysphonia, accelerometric evidence of hypernasality, and kinematic evidence of articulatory dysfunction have been documented patients with CHI.38,39

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and the resultant findings. In addition, the output should culminate in a diagnostic statement, prognostic statement, and specific recommendations. The diagnostic statement indicates the severity, disorder type, the subtype (e.g., if appropriate), individual characteristics, and the etiology. Following the diagnostic statement, there should also be indications of the speech subsystems specifically affected in the individual, the impact of the speech disorder on the patients’ participation in everyday activities, and any concomitant nonspeech abnormalities that affect communication or limit access to AAC approaches for subsequent treatment (see Table 4). A prognostic statement is desirable; however, there is limited information upon which to base predictions of speech recovery following TBI. Prognostic indicators for overall recovery from TBI include initial severity of injury, as indicated by such factors as duration of coma, duration of posttraumatic amnesia, as well as cognitive and behavioral characteristics. Additional patient-related variables such as age, history of substance abuse, as well as premorbid intelligence, socioeconomic status, personality, or emotional disorders may Table 4 Example of a Diagnostic Statement (Output from the Comprehensive Motor Speech Examination) Mrs. X has a severe spastic dysarthria secondary to closed head injury due to a soccer accident. Her condition is characterized by imprecise consonants, distorted vowels, strained-strangled voice, and a slow rate of speech. & Severity ¼ severe & Type ¼ dysarthria & Subtype ¼ spastic & Etiology ¼ closed head injury & Most salient characteristics ¼ imprecise consonants, distorted vowels, strained strangled voice and slow rate of speech In addition, there should be specific statements regarding: (1) the speech subsystems affected (i.e., respiration, phonation, resonation, articulation, proso-

Output of the CMSE Output of the CMSE typically takes the form of a diagnostic report that includes the case history and clinical description of the patient and the presenting problems, as well as a summary of assessment procedures employed

dy), (2) nonspeech findings that may affect communication or limit access to AAC approaches, (3) the affect of the disorder on participation in everyday activities, and (4) a recommended course of action. Abbreviation: augmentative and alternative communication.

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MOTOR SPEECH DISORDERS IN ADULTS WITH CONCUSSION/CANNITO

CONCLUSION Although sport-related concussion does not usually result in motor speech disorders, there is ample indication that they can occur, particularly for more severe levels of injury. When a motor speech disorder does occur, a CMSE is warranted to provide a diagnosis, prognosis, and appropriate recommendations. Clearly, there is a critical need for further research focusing specifically on the occurrence of dysarthria in individuals with sport-related concussion. Of particular interest is the milder range of overall impairment, following an initial impact, wherein there may be mild, subclinical, or subjective difficulties with retrieval and execution of the pronunciation of low-frequency,

phonetically complex words. Such patients also may have difficulty with speaking in difficult and distracting situations, such as giving a presentation in a noisy environment or under conditions of fatigue. To date these intriguing possibilities remain to be explored. ACKNOWLEDGMENT

The author gratefully acknowledges Mrs. Ghada G. Alharbi, M.S., a doctoral student in Communication Sciences and Disorders at the University of Memphis, for technical assistance with the preparation of the manuscript.

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Clinical assessment of motor speech disorders in adults with concussion.

This article reviews the occurrence of motor speech disorders of dysarthria and apraxia of speech following closed head injury and other traumatic bra...
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