research on speech motor control and its...

J. COMMUN. DISORD. 33 (2000), 391–428© 2000 by Elsevier Science Inc. All rights reserved. 0021-9924/00/$–see front matter655 Avenue of the Americas, New York, NY 10010 PII S0021-9924(00)00023-X

RESEARCH ON SPEECH MOTOR CONTROL AND ITS DISORDERS:A REVIEW AND PROSPECTIVE

RAY D. KENT

Waisman Center, University of Wisconsin-Madison, Madison, Wisconsin

This paper reviews issues in speech motor control and a class of communication disordersknown as

motor speech disorders.

Speech motor control refers to the systems and strategiesthat regulate the production of speech, including the planning and preparation of movements(sometimes called

motor programming

) and the execution of movement plans to result inmuscle contractions and structural displacements. Traditionally, speech motor control is dis-tinguished from phonologic operations, but in some recent phonologic theories, there is adeliberate blurring of the boundaries between phonologic representation and motor functions.Moreover, there is continuing discussion in the literature as to whether a given motor speechdisorder (especially apraxia of speech and stuttering) should be understood at the phonologiclevel, the motoric level, or both of these. The motor speech disorders considered here include:the dysarthrias, apraxia of speech, developmental apraxia of speech, developmental stuttering,acquired (neurogenic and psychogenic) stuttering, and cluttering. © 2000 by Elsevier Sci-

ence Inc.

Educational Objectives:

On the basis of this article, the reader will (1) be acquainted withrecent directions in the study of normal speech motor control; (2) be able to discuss ways toseparate motoric and linguistic factors potentially involved in dysarthria, apraxia of speech,and stuttering; (3) appreciate major current directions for research on speech motor disor-ders; and (4) know the relationship between research and clinical practice pertaining to mo-tor speech disorders.

KEY WORDS:

Dysarthria; Apraxia of speech; Stuttering; Speech motor control; Speechdisorders

INTRODUCTION

Speech motor control refers to the systems and strategies that control the pro-duction of speech. Typically, it is assumed that the input to the system ofspeech motor control is a phonologic representation of language, especially asequence of abstract units such as phonemes. The output of speech motor controlis a series of articulatory movements that convey the intended linguistic message

Address correspondence to Ray D. Kent, Ph.D., Waisman Center, Rm. 435, University of Wiscon-sin-Madison, 1500 Highland Avenue, Madison, WI 53705-2280. Tel: 608-263-7109; Fax: 608-263-0529; E-mail:

,

[email protected]

.

.

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through an acoustic signal that can be interpreted by a listener. Therefore, theprocesses of speech motor control intervene between those of language for-mulation and those of the acoustic signal by which the speaker’s message isusually received. This paper focuses on speech motor control and largely, but notcompletely, excludes related processes in audition and language formulation. Infact, speech motor control ultimately must be understood in relation to the overallprocess of human speech communication, which is summarized diagrammati-cally in Figure 1. The investigation of how we speak draws on the ingenuity ofseveral disciplines, including linguistics, psychology, engineering, physics, anat-omy, biology, speech and hearing science, and computer science. Each of these,and more to be sure, has contributed to knowledge that is reflected in a skeletalform in Figure 1, which is based largely on Cleary and Pisoni (1998), Cutler,Dahan, and Van Donselaar (1997), Kent, Adams, and Turner (1996), Levelt(1989), Levelt, Roelofs and Meyer (1999), Meyer (1997), and Tyler andFrauenfelder (1987). In Figure 1, processes of language formulation and utter-ance production are represented on the left, and processes of speech perceptionand language comprehension are represented on the right. It is assumed thatboth speaker and listener maintain a discourse record, which is a mental log ofprimary points of information exchanged. In much of current theorizing, seg-mental structure and prosodic-affective patterns are processed somewhat inde-pendently, but merge into a unified representation of an utterance.

For all its ordinariness, speech is a remarkable and unique motor accomplish-ment. It is not unusual for speech to be produced at rates of up to six to nine syl-lables (or 20 to 30 phonetic segments) per second, which is faster that any otherdiscrete human motor performance. Furthermore, speech production involvesmore motor fibers than any other human mechanical activity (Fink, 1986). In theface of these complications, speech must generate an acoustic signal that is un-derstood by other listeners both as a linguistic (propositional) message and an af-fective signal. Spoken language is one of the greatest achievements of childhood,for it opens the door to a variety of educational and social experiences. Fortu-nately, speech is a robust faculty that serves most people in the face of variouschallenges to well-being and health. However, it can be impaired by a number ofgenetic and acquired conditions. A major group of these impairments are the mo-tor speech disorders. This paper briefly reviews current research issues in normalspeech motor control and selected motor speech disorders.

NORMAL SPEECH MOTOR CONTROL THROUGHTHE LIFESPAN

The precursor to speech is the birth cry, which is the threshold to vocal com-munication. Infants typically acquire speech readily and naturally, and it ap-pears that babbling anticipates important aspects of spoken language (de Boysson-

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Figure 1. A diagram of the conceptual structures and processes involved in the produc-tion (left side of diagram) and perception (right side of diagram) of spoken language(based on sources listed in text). A variety of linguistic, cognitive, and sensorimotor pro-cesses are involved in spoken language, and the intent of this diagram is to portray someof the major sources of information that cohere in speech communication. The produc-tion of spoken language includes: prelinguistic aspects (intentions, preverbal message),discourse regulation (such as a discourse record mutually maintained by a speaker andlistener), language formulation (lexical selection and syntactic construction), phonologicoperations, phonetic specifications, and the motor control of the speech production sys-tem to generate acoustic patterns. To some degree, the compre-hension of the spokenmessage involves operations inverse to those used in its formulation and production.

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Bardies, 1999; Vihman, 1996). As soon as speech is acquired, children andadults use it with remarkable flexibility. Because speech production reflectsthe maturational status of sensory, motor, and cognitive systems, it is helpful totake a lifespan perspective, beginning with infancy.

Infancy

The developmental period of infancy takes its name from the child’s lack of ar-ticulate speech (

infant

means “incapable of speech”). However, it is clearfrom the last two decades of research that infants make rapid and substantialprogress in both the perception of speech and the production of vocalizationsthat prefigure adult speech. Recent research has applied acoustic and physio-logic methods to the study of infant vocalizations and related oral motor be-haviors such as sucking, chewing, and swallowing (Finan & Barlow, 1998;Green, Moore, Ruark, Rodda, Movee, & van Witzenburg, 1997). Modernphysiologic methods enable the study of important questions in the genesis ofspeech, such as the hoary issue of whether speech emerges from earlier appear-ing movements such as those used in mastication and deglutition. Recent resultsindicate that it does not, which means that in the early developmental period, themotor control for speech is distinct from that for nonspeech oral functions(Moore & Ruark, 1996).

An additional promise of this research is the possibility of using prespeechvocalizations to identify infants at risk for communication disorders or devel-opmental disabilities. The vocalizations of interest include both cries (Moller& Schonweiler, 1999) and babble (Oller, Eilers, Neal, & Schwartz, 1999).Some particular points of progress in recent research include: evidence thatthe onset of canonical babbling marks a period in which infants use auditoryawareness to control motor activities (Ejiri, 1998); physiologic studies of thecoordination of lip and jaw movements in infants (Green, Moore, Higash-ikawa, & Steeve, 2000); description of patterns of breathing associated withdifferent vocalization types (Boliek, Hixon, Watson, & Morgan, 1996, 1997);development of computer programs for automatic analysis of cry or babble(Fell, Macauslan, Ferrier, & Chenausky, 1999; Moller & Schonweiler, 1999);incorporation of babbling and auditory feedback in computer models of speechdevelopment in children (Bailly, 1997; Callan, Kent, Guenther, & Vorperian,2000); and reports that babbling is sensitive to early-onset otitis media (Pet-inou, Schwartz, Mody, & Gravel, 1999; Rvachew, Slawinski, Williams, &Green, 1999), cerebral palsy (Levin, 1999), and maternal smoking (Obel,Henriksen, Hedegaard, Secher, & Ostergaard, 1998). The general value ofbabbling in the prediction of communication disorders in children has beendescribed by Oller et al. (1999), among others.

Taken together, these studies demonstrate the value of babbling in under-


standing communicative development and the possibility of early identifica-tion based on babbling patterns. Babbling, one of the infant’s earliest venturesinto speech motor control, reflects the child’s neurologic integrity as well asspecific sensory and motor functions. The apparent early divergence betweenspeech and nonspeech motor activities indicates that separate neural controlsystems are established in infancy. Further evidence of this separation is re-viewed later in this paper. The continuity of babbling and other early vocaliza-tions with phonetic patterns in early speech development points to the use ofearly vocalizations as a tool to identify infants at risk for communication dis-orders. This possibility speaks to an important health issue, given that “speechdelays are the most common developmental concern seen by the general pedi-atrician, yet they often are not well understood or diagnosed expediently”(Johnson & Blasco, 1997, p. 224).

Childhood and Adolescence

The traditional studies of speech development were based on perceptual pho-netic methods in which one or more examiners transcribed the speech of childparticipants (Vihman, 1996). Although these data were important in chartingthe developmental progress toward a mature phonetic system, the studies hadlimitations that may have affected the validity and reliability of the observa-tions. Several advances have been made toward quantitative assessment ofspeech, including: structural magnetic resonance imaging (MRI) studies of thedevelopmental anatomy of the vocal tract (Fitch & Giedd, 1999; Vorperian,Kent, Gentry, & Yandell, 1999), structural MRI studies of human brain devel-opment related to speech (Paus, Zijdenbos, Worsley, Collins, Blumenthal,Giedd, Rapoport, & Evans, 1999), acoustic profiles of speech developmentspanning childhood and adolescence (Lee, Potamianos & Narayanan, 1999),and improved indices of the maturation of speech movements in the articula-tory and respiratory systems (Goffman & Smith, 1999; Smith & Goffman,1998; Solomon & Charron, 1998).

Whereas traditional studies of speech development relied heavily on per-ceptual descriptions, much of the contemporary research uses quantitativemethods that offer greater objectivity and sensitivity. In addition, the stage isbeing set for promising investigations into the coordination between differentaspects of development and the potential for defining predictive measures thatoperate across behavioral domains. One example is the relationship betweenperformance on a task of nonword repetition and language abilities in typi-cally developing children (Baddeley, Gathercole, & Papagno, 1998). It alsohas been shown in several studies that children with language impairment per-form more poorly than their typically developing peers on the task of nonwordrepetition (Bishop, North, & Donlan, 1996; Dollaghan & Campbell, 1998;

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Sahlen, Wagner, Nettelbladt, & Radeborg, 1998; Stark, & Blackwell, 1997).To be sure, nonword repetition represents the combined influence of severalspeech and language processes, including auditory memory and phonologicprocessing. But it also entails preparation and execution of a speech move-ment sequence—which is to say, speech motor control.

Young to Late Adulthood

Much of adulthood pertains primarily to the maintenance and deployment ofwell established processes of speech motor control. Speech is vital to a widerange of vocations, and it is the means to various social and recreational plea-sures. It is expected that speech will increasingly become a major form of hu-man–machine interaction, and as it does so, productivity gains will surely follow.That is, the machines of the future will increase, rather than reduce, the need forspeech as the means of communication for commercial and noncommercial pur-suits. Machines will become more and more humanized, and a major dimensionof humanization will be the sharing of speech between human and machine (Syr-dal, Bennett, & Greenspan, 1995). Speech also will meet the need for miniatur-ization, because it will require only a small microphone for user input. Further-more, speech can be used even as the arms and hands are devoted to other tasks.

With advancing age, speech changes in its precision, fluency, voice qual-ity, and communicative effectiveness (Linville, 1996; Weismer & Liss, 1991;Wohlert & Smith, 1998). These changes may be similar to the more remark-able changes in speech that accompany a variety of diseases that occur mostfrequently in older adults. At the least, the age-related changes in speech man-date the use of age-appropriate normative data in the assessment of speechdisorders in older adults. Although robust, speech is also intricate. The cogni-tive, sensory, and motor demands of speech production can be compromisedby apparently normal aging processes and by a variety of diseases that becomemore common with advancing age.

Recent physiologic studies have provided much new information on non-speech oromotor behaviors such as swallowing (Chi-Fishman, Stone, & Mc-Call, 1998; Rademaker, Pauloski, Colangelo, & Logemann, 1998). These datashould help considerably in determining the extent of similarity or dissimilar-ity between the regulation of speech and nonspeech movements and they alsocontribute to an understanding of the effects of aging on general motor func-tions of the oral and perioral musculature.

Finally, neuroimaging methods have opened the door to many exciting dis-coveries about neural activity associated with speech and language. Lauter(1995) reviewed these methods and described their potential for fundamentaladvances in identifying the neural structures and circuits involved in the per-ception and production of spoken language.


NORMAL SPEECH MOTOR CONTROL: PROMISING LINES OF RESEARCH

Speech Motor Control Models

Speech has been modeled at various levels (e.g., information, neural, motor,acoustic) and with various methods (e.g., stage models, computational net-works; Kent, Adams, & Turner, 1996). Each of these contributes to an overallunderstanding of speech as human behavior. Although a review of these ef-forts cannot be attempted within this brief paper, it is important to note at leasta few recent advances that have the potential for understanding both normaland disordered speech motor control.

As is discussed later, one of the challenges in understanding speech motordisorders generally is to distinguish impairments of phonology from impair-ments of motor control per se. Possibly, impairments at both levels coexist insome disorders, and it is therefore important to determine the severity and na-ture of the two types of impairment. Phonologic theory can be relevant to clin-ical assessment and treatment and also to the theoretical understanding of thenature of a disorder. In some important respects, several contemporary phono-logic theories emphasize the phonetic or articulatory bases of phonologic rep-resentations. Indeed, gestural (articulatory) phonology goes so far as to pro-pose that abstract specifications of movements are phonologic primitives, thatis, movements themselves are the means of phonologic representation (Brow-man & Goldstein, 1986, 1992). This proposal can have profound implicationsfor understanding motor plans or programs in speech production. Another ex-ample of changing views in speech production research is a move away fromthe traditional segment-concatenation approach in which speech is thought tobe controlled primarily with respect to concatenations of phonemic or pho-netic segments. An alternative approach emphasizes a syllable organization,as implemented in the converter/distributor model (Fujimura, 1992, 1994).

Inquiries into the control of speech production encounter an immediatequestion: What is (are) the primary variable(s) controlled by the nervous sys-tem? An answer to this question is central to theories of speech motor controland also can be highly important in assessing and treating disorders of speechmotor control. Several regulated variables have been proposed, includingacoustic targets, aerodynamic values, positions of individual structures, over-all vocal tract configuration, and rates of muscle contraction. It is possible thatmore than one variable ultimately is needed to understand the neural controlof speech, and perhaps the robustness of speech derives in part from aspeaker’s flexibility in choosing among these variables. In the case of velo-pharyngeal inadequacy in craniofacial disorders, a theory has been advancedto explain the regulation of speech in terms of the air pressure head (Warren,1986; Warren, Dalston, & Dalston, 1990; Warren, Dalston, Morr, Hairfield, &Smith, 1989). This theory has a definite unifying value for a number of clini-

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cal observations, including the speaker’s selection of compensatory articula-tions. Whereas Warren and associates emphasized the role of active reflexivecompensatory responses in maintaining air pressure for speech, Moon,Folkins, Smith, and Luschei (1993) explained air pressure regulation in termsof intrinsic physiologic properties of the respiratory system. Although theseideas on air pressure regulation were introduced especially with regard to cleftpalate, they could be applied more widely, for example, to the motor speechdisorders.

Another way of stating the controlled variable problem is to ask what kindof target reference frame is used by the neural system to govern speech articu-lation. Currently, two primary alternatives are considered. One type of refer-ence frame is a gestural target based on the degree of constriction at variouslocations in the vocal tract (Saltzman & Munhall, 1989). The other is an audi-tory or acoustic target that is used to derive the articulatory movement (Guen-ther, 1995; Guenther, Hampson, & Johnson, 1998; Perkell, Matthies, Lane,Guenther, Wilhelms-Tricarico, Wozniak, & Guiod, 1997). Internal modelshave been particularly important in recent speech production theories, andthey may hold value in understanding the motor speech disorders.

An important area of progress is the development of biomechanical modelsof the speech production system (Lucero & Munhall, 1999; Sanguineti, La-boissiere, & Ostry, 1998). As these models become increasingly sophisticatedand accurate, they will offer insights not only into normal speech productionbut also into various speech disorders.

Animal Models

There are no universally accepted animal models for spoken language, be-cause no other species exhibits vocal behaviors that embrace the complexityand power of human speech. However, it is possible to use animal models forlanguage-like behaviors in other methods (such as signing) or for certain com-ponents of speech production, such as phonation or vocal learning. Birds havebeen of particular interest because many species of birds learn the conspecificsong through auditory exposure and a period of extended practice (Doupe &Kuhl, 1999; Hauser, 1996). Moreover, like human speech, “birdsong requirescomplex learned motor skills involving the coordination of respiratory, vocalorgan and craniomandibular muscle groups” (Suthers, Goller, & Pytte, 1999,p. 927). Progress also has been made in understanding the acoustics of theavian vocal tract (Fletcher & Tarnopolsky, 1999). Certainly the biology andphysics of birdsong differ in some respects from human speech, but there isnonetheless a potential benefit from studies of song learning and from re-search on the neural substrates of birdsong perception and production. It mayeven be possible that certain disorders of human communication have paral-lels in birdsong (e.g., deafness and stuttering, the latter being discussed later in


this paper). Although human vocalizations may differ in number and com-plexity from those of other species, some issues can be addressed in compara-tive studies, one example being the neural control of the muscle system coor-dination required for vocalization. Studies of vocalization in cats led to theproposal that the periaqueductal gray matter is an essential brain site for mam-malian voice production (Davis, Zhang, Winkworth, & Bandler, 1996).

DISORDERS OF SPEECH MOTOR CONTROL

The disorders considered here are those that have been defined or studied interms of speech motor control dysfunction, beginning with dysarthria andapraxia of speech (often termed

the motor speech disorders

; Duffy, 1995) andconcluding with stuttering and cluttering, which are disorders of fluency.Classification of this broad range of disorders as motor speech disorders doesnot meet with universal approval. The fluency disorders, in particular, are notalways classified in this way, although they have been studied extensivelywith methods and models from speech motor control. However, there is prece-dent for the classification used here (Caruso & Strand, 1999), and further-more, the purpose of this paper is not to insist on a classification so much as itis to explore what a particular classification means in the contemporary under-standing of a speech disorder.

Dysarthria

Dysarthrias are speech disorders that result from neurologic impairments as-sociated with weakness, slowness, or incoordination of the musculature usedto produce speech. These speech disorders occur with considerable frequencyin individuals with Parkinson disease, stroke, cerebellar disease, amyotrophiclateral sclerosis, multiple sclerosis, cerebral palsy, and traumatic brain injury(Duffy, 1995; McNeil, 1997). Dysarthrias can be (a) congenital or acquired;(b) static, improving, or worsening in their course; (c) the consequence ofpathologic conditions in multiple areas of the central or peripheral nervoussystem; and (d) associated with various causes (Duffy, 1994). The modernclassification of the dysarthrias rests largely on two articles published threedecades ago (Darley, Aronson, & Brown, 1969a, 1969b). These articles de-scribed the perceptual dimensions for the rating of dysarthria and identifiedseven types of dysarthria (Table 1) associated with distinctive clusters of devi-ant perceptual dimensions (Table 2). The authors also commented on the neu-ropathologies underlying each type of dysarthria, thereby contributing to aclinicoanatomic description. Remarkably, the seminal papers by Darley et al.have never been thoroughly replicated with an independent sample of individ-uals with dysarthria and an independent panel of judges (Kent, Kent, Duffy, &Weismer, 1998). The hegemony of the Darley et al. articles is testimony to the

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seminal nature of their work and, unfortunately, to the limited scope of inves-tigation during the last 30 years. But there is evidence of increased nationaland international scientific effort. This renewal is aided by several improve-ments in laboratory methods including acoustics, electromyography, move-ment transduction, electropalatography, and neuroimaging.

Generally, the dysarthrias have global, rather than focal, effects on thespeech production systems of respiration, phonation, and articulation and reso-nance (Auzou, Ozsancak, Jan, Leonardon, Menard, Gaillard, Eustache, & Han-nequin, 1998; Kent et al., 1998). Accordingly, they often affect multiple dimen-sions of spoken language (voice quality, intelligibility, prosody, and affect), andthey present with challenges in clinical and scientific description. Significant

Table 1.

Clinicoanatomic Relationships for Major Types of Dysarthria. Shownfor Each Type of Dysarthria (Determined by Auditory Perception) is the PrimaryLesion Site

Dysarthria type Primary lesion site

Flaccid Lower motor neuron (one or more cranial nerves)Spastic Upper motor neuron (pyramidal tract)Spastic-flaccid Both upper and lower motor neuronsAtaxic Cerebellum or its outflow pathwaysHypokinetic Basal ganglia, especially substantial nigraHyperkinetic Basal ganglia, especially putamen, caudate, or both

Table 2.

Major Clusters of Deviant Perceptual Dimensions for Dysarthria, as Reported by Darley, Aronson, and Brown (1969a, 1969b)

Type ofDysarthria Clusters of Deviant Dimensions

Ataxicdysarthria

Articulatory inaccuracy, prosodic excess, phonatory-prosodic insufficiency

Spasticdysarthria

Prosodic excess, prosodic insufficiency, articulatory-resonatory incompetence

Flacciddysarthria

Phonatory incompetence, resonatory incompetence, phonatory-prosodic insufficiency

Spastic-flacciddysarthria

Prosodic excess, prosodic insufficiency, articulatory-resonatory incompetence, phonatory stenosis, phonatory incompetence, resonatory incompetence

Hypokineticdysarthria

Prosodic insufficiency, phonatory incompetence

Hyperkineticdysarthria(Chorea)

Articulatory inaccuracy, prosodic excess, prosodic insufficiency, articulatory-resonatory incompetence, phonatory stenosis

Hyperkineticdysarthria(Dystonia)

Articulatory inaccuracy, prosodic excess, prosodic insufficiency, phonatory stenosis


progress has been made in the description of the dysarthrias through acousticanalyses (Kent, Weismer, Kent, Vorperian, & Duffy, 1999; Weismer, 1997) andphysiologic methods (Barlow, 1999; McNeil, 1997) as well as continued per-ceptual descriptions. In addition, now on the research horizon are contributionsfrom neuroimaging techniques, especially positron emission tomography (PET)and magnetoencephalography, and perhaps eventually functional magnetic res-onance imaging (fMRI) as soon as the problem of movement artifacts in the he-modynamic response is resolved. In addition, recent studies have applied trans-cranial magnetic stimulation, electrical stimulation, or both (Chen, Wu, & Chu,1999; Ghezzi & Baldini, 1998; Trompetto, Caponnetto, Buccolieri, Marchese,& Abbruzzese, 1998; Urban, Vogt, & Hopf, 1998). It is expected that the use ofneuroimaging methods and stimulation methods such as transcranial magneticstimulation, combined with quantitative analyses of speech, will lead to rapidadvances in the understanding of the dysarthrias. However, it should be notedthat transcranial magnetic stimulation results are subject to some questions ofinterpretation (Epstein, 1998; Epstein, Meador, Loring, Wright, Weissman,Sheppard, Lah, Puhalovich, Gaitan, & Davey, 1999).

Assessment and classification of dysarthria.

Dysarthria typically is as-sessed perceptually (especially by auditory pattern) and classified either withrespect to the neurologic diagnosis (e.g., Parkinson disease) or a perceptualclassification system (Edwards, 1984; Gerratt, Till, Rosenbek, Wertz, & Boy-sen, 1991; McNeil, 1997; Simmons & Mayo, 1997; Strand & Yorkston,1994). Frequently used perceptual classifications are those of Darley et al.(1969a, 1969b) or Enderby (1983, 1986). One of the limitations of perceptualassessment is that it can be difficult even for highly trained auditors to differ-entiate the multiple dimensions of dysarthric impairment. It is not uncommonfor an individual with dysarthria to have concurrent disorders of respiration,phonation, articulation, and resonance. Consequently, perceptual methods of-ten are supplemented with acoustic analyses, imaging techniques, aerody-namic recordings, or movement transduction. These supplemental tools notonly help to ascertain the function of individual components of speech pro-duction, but they also can be used to detect or infer pathophysiologic featuressuch as weakness, rigidity, slowness, or dyscoordination. Ideally, these meth-ods would be used in a thorough replication and extension of the original stud-ies by Darley et al. (1969a, 1969b). Certainly, the stage is set for an expandedprogram of research that incorporates acoustic and physiologic measures.

Research has shown both age- and sex-related variations in dysarthria. Oneof the few extensive reviews of childhood dysarthria concluded that “definitesimilarities to adult dysarthria were not evident [and that] acquired childhooddysarthria requires its own classification” (Van Mourik, Catsman-Berrevoets,Paquier, Yousef-Bak, & van Dongen, 1997, p. 299). Additional support forthis conclusion appeared in a study of children with cerebellar or brainstem tu-mors (Van Mourik, Catsman-Berrevoets, Yousef-Bak, Paquier, & van Don-

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gen, 1998). Strong similarities were not seen between the children’s dysarthricfeatures and those that have been reported for adults. The recent literature at-tests to an increasing awareness of the need for developmentally appropriateassessments and treatments, together with a theory of disorder that incorpo-rates various types of developmental information (Caruso & Strand, 1999;Paul & Marans, 1999).

Sex-dependent features of dysarthria only recently have been identified(Hertrich, Spieker, & Ackermann, 1998; Kent, Kent, Rosenbek, Weismer,Martin, Sufit, & Brooks, 1992). In some respects, sex-related differences arenot surprising given the sexual dimorphism of the speech production systemand sex-related differences in the effects of aging on speech and voice. Sexdifferences may emerge more powerfully in communication disorders than inother aspects of impaired function, such as control of the limbs and fingers.The further description and classification of the dysarthrias may well entailconsiderations related to both age and sex of the speaker.

Treatment of dysarthria.

Many treatments have been used for individu-als with dysarthria. The selection of treatment varies with type and severity ofthe dysarthria, and with the general cognitive, affective, and sensorimotor sta-tus of the individual patient. Treatment outcomes have not been studied exten-sively, but Yorkston’s (1996) review indicated that several interventions havebeneficial effects. However, she also noted that a given treatment is not uni-formly effective for all types of dysarthria. Therefore, “Guidelines are neededthat specify which treatments are most effective for the various dysarthrias”(Yorkston, 1996, p. S53). One particular behavioral intervention designed es-pecially for individuals with Parkinson disease, the Lee Silverman VoiceTreatment (Ramig, Bonitati, Lemke, & Horii, 1994; Ramig, 1998), probablyhas been more systematically investigated than any other. The series of stud-ies on this treatment may well serve as a model for other treatments for othertypes of dysarthria.

Many dysarthrias result from chronic conditions that cannot be treated suc-cessfully with surgery or medications. Accordingly, there is a strong need forbehavioral interventions with demonstrated effectiveness. For many individu-als with dysarthria, a combination of behavioral and drug or prosthetic treat-ments should be beneficial, but there is very little systematic research on thisissue. Perhaps future work will demonstrate the value of “supportive drugtherapy” such as the use of piracetam in conjunction with language therapy inpoststroke aphasia (Huber, 1999; Poeck, 1998). However, at least with respectto some current drug and surgical treatments for Parkinson disease, it is doesnot appear that speech derives the same benefit as nonspeech motor control.For example, recent studies of levodopa treatment, pallidotomy, and pallidalstimulation have shown positive effects on finger movements, handwriting, oroverall performance on the Unified Parkinson’s Disease Rating Scale but neu-tral or even negative effects on speech (Gentil, Tournier, Perrin, & Pollak,


1998; Poluha, Teulings, & Brookshire, 1998; Schrag, Samuel, Caputo, Scar-avilli, Troyer, Marsden, Thomas, Lees, Brooks, & Quinn, 1999; Scott, Gre-gory, Hines, Carroll, Hyman, Papanasstasiou, Leather, Rowe, Silburn, &Aziz, 1998; Solomon, McKee, Larson, Nawrocki, Tuite, Eriksen, Low, &Maxwell, 2000).

Acquired Apraxia of Speech (Verbal Apraxia)

Like dysarthria, apraxia of speech can appear developmentally as a childhooddisorder or it can appear as an acquired disorder in adults. Both the develop-mental and acquired forms have engendered a literature that defies easy sum-mary. One major obstacle is the lack of agreement on how (and even if)apraxia of speech should be recognized as a clinical entity. It is also uncertainif the developmental form of the disorder parallels the acquired form in itssymptomatologic features and cause. The two forms are distinguished in thisreview, which begins with the acquired form in adults.

Assessment and classification of apraxia of speech.

Acquired apraxia ofspeech in adults is generally thought to result from focal brain (especially ce-rebral) damage that impairs especially the processes of planning or program-ming speech movements in the face of essentially normal strength, speed, andcoordination of the speech musculature (especially for nonspeech tasks butalso for some speech tasks; Duffy, 1995). With some risk of oversimplifica-tion, it may be said that apraxia of speech impairs the programming of speechmovements, whereas the dysarthrias affect the execution of movements. Thatis, it often is assumed that in apraxia of speech, the movement plan is dis-turbed but the muscular system itself may be essentially intact. In dysarthria,the movement plan is intact, but the muscular systems of speech productioncannot realize the movement plan. Early perceptual descriptions of apraxia ofspeech remarked on the large number of substitution errors, the impression ofa slow and groping articulatory pattern, and pronounced difficulty with longor phonetically complex sequences. The disorder has been described variouslyas phonologic, motoric, or cognitive, and perhaps all three will be subsumedin an eventual understanding. Contemporary articles reflect the continuing ef-fort to define the nature and cause of apraxia of speech (Code, 1998; Dogil &Mayer, 1998; Rogers & Storkel, 1999; Whiteside & Varley, 1998; Varley,Whiteside, & Luff, 1999).

Several recent studies indicate that the lesion responsible for apraxia ofspeech may be quite discrete. Dronkers (1996) reported that patients withstrokes and “articulatory planning” deficits (apraxia of speech) had lesionsthat included a region of the left precentral gyrus of the insula. Patients with-out lesions in this structure did not have deficits in articulatory planning. Aconfirmatory case report described apraxia of speech occurring after an acute

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infarct limited to the precentral gyrus of the left insula (Nagao, Takeda, Ko-mori, Isozaki, & Hirai, 1999). A role of the insula in speech planning also issupported by studies of normal subjects using the functional imaging methodsof magnetoencephalography (Kuriki, Mori, & Hirata, 1999) and PET (Wise,Greene, Buchel, & Scott, 1999).

Assessment and classification of developmental apraxia of speech.

De-velopmental apraxia of speech was first described by Yoss and Darley (1974),who apparently observed similar symptomatologic features between a speechdisorder in children and a speech disorder in adults that had been previouslydescribed. Whether the symptomatologic features are, in fact, similar remainsin question. A major difference between the two forms is that the develop-mental form may affect the phonologic or motoric processes, or both, bywhich spoken language is learned, whereas the acquired form is an impair-ment of previously acquired processes.

A central issue in research on developmental apraxia of speech is whetherthis disorder can be reliably distinguished from more general speech impair-ments in children (Davis, Jakielski, & Marquardt, 1998; Hall, Jordan, &Robin, 1993; McCabe, Rosenthal, & McLeod, 1998; Ozanne, 1995). Recentarticles on developmental apraxia of speech have identified characteristics ofthe disorder that could be used as diagnostic markers. The characteristics varysomewhat across studies, and they include limitations in maximum perfor-mance tasks (Murdoch, Attard, Ozanne, & Stokes, 1995; Thoonen, Maassen,Gabreels, & Schreuder, 1999; Thoonen, Maassen, Gabreels, Schreuder, & deSwart, 1997); distinctive patterns of segmental errors (Groenen, Maassen,Crul, & Thoonen, 1996; Forrest & Morrisette, 1999); perception or productionof rhyme (Marion, Sussman, & Marquardt, 1993); or developmentally inap-propriate patterns of stress (Shriberg, Aram, & Kwiatkowski, 1997a, 1997b,1997c; Skinder, Strand, & Mignerey, 1999). Given (a) the typically smallnumber of participants recruited in these studies, (b) differences in resultsacross studies, and (c) the possibility of nonhomogeneity in the clinical popu-lation, it is premature to assert a single diagnostic marker. Progress would befacilitated by data collection at multiple centers using a well-defined protocolof clinical examination. Suggestions for diagnostic criteria have been pro-posed, and these would be helpful in assuring a common diagnostic system(Hodge, 1994; Hodge & Hancock, 1994).

Developmental apraxia of speech presumably is one form of a more gen-eral developmental apraxia, although this assumption should not be accepteduncritically. Even the more general form of the disorder, which has been rec-ognized for almost 100 years, is by no means straightforward in its definitionand description (Dewey, 1995). One simplification that may apply to non-speech apraxia is that the developmental and acquired forms appear to be sim-ilar (Poole, Gallagher, Janosky, & Qualls, 1997). It is not at all clear that asimilar statement can be made for apraxia of speech.


Neuroimaging has rarely been used to study developmental apraxia ofspeech, but PET and MRI results were reported for members of a large, three-generation pedigree (the KE family), half of whom had a pronounced apraxiaof speech presenting especially as difficulties in sequential articulation andorofacial praxis (Vargha-Khadem, Watkins, Price, Ashburner, Alcock, Con-nelly, Frackowiak, Friston, Pembrey, Mishkin, Gadian, & Passingham, 1998).Abnormalities were detected in both cortical and subcortical motor-related ar-eas of the frontal lobe. Magnetic resonance imaging revealed that the caudatenucleus was abnormally small bilaterally. A linkage study of the family local-ized the abnormal gene to a 5.6-centiMorgan interval in the chromosomalband 7q31 (Fisher, Vargha-Khadem, Watkins, Monaco, & Pembrey, 1998).These results are particularly interesting in that they are among the first toshow a specific genetic mutation or deletion that is associated with develop-mental apraxia of speech and with specific neural abnormalities. (A similar ef-fort has been described for a family with autosomal dominant rolandic epi-lepsy and speech dyspraxia [Scheffer, Jones, Pozzebon, Howell, Saling, &Berkovic, 1995].) If future studies confirm involvement of the caudate nu-cleus in developmental apraxia, it may be significant that the volume of boththe caudate and lenticular nuclei declines with maturation in males but not fe-males (Giedd, Snell, Lange, Rajapakse, Casey, Kozuch, Vaituzis, Vauss,Hamburger, Kaysen, & Rapoport, 1996). Possibly, sex-related differences inbrain maturation account at least in part for the preponderance of males inpopulations with developmental apraxia of speech (and stuttering as well).

Treatment of apraxia of speech and developmental apraxia of speech.

Because rather similar treatments have been recommend for both the acquiredand developmental forms of this disorder, the two forms are considered to-gether. A range of treatments for the acquired form are described by McNeil,Robin, and Schmidt (1997). Generally, these treatments focus on articulatoryplacement, temporal sequencing, or integral (cross-method) stimulation com-bined with progressive task difficulty. Efficacy data for most of these ap-proaches are rare or nonexistent, although some treatment outcomes havebeen described (Wambaugh, Kalinyakfliszar, West, & Doyle, 1998). Treat-ments for developmental apraxia of speech have been described by Pann-backer (1988), Square (1994, 1999), and Strand and Skinder (1999). Amongthe treatments are integral stimulation, tactile-kinesthetic facilitation, rhyth-mic and melodic facilitation, and gestural cuing. Data on treatment outcome,effectiveness, and efficacy are limited.

Fluency Disorders

The fluency disorders include developmental stuttering, cluttering, and ac-quired stuttering in the older child or adult. Terminology and diagnostic crite-ria are not uniform, but recent efforts to clarify and systematize the terminol-

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ogy and defining characteristics have been made (“Terminology pertaining tofluency and cluency disorder,” 1999; Perkins, 1994). The developmental andacquired forms are distinguished here because they are associated with some-what different symptomatologic features and perhaps causes. The present dis-cussion emphasizes developmental stuttering (which typically appears in earlychildhood) and acquired neurogenic or psychogenic stuttering (which occursespecially in adults). Only passing reference is made to cluttering, which isnot well represented in the scientific literature and is open to much debateconcerning its nosologic status.

Assessment and classification of developmental stuttering.

The follow-ing quotation from a recent article in the

American Family Physician

is a goodpoint of departure for a discussion of developmental stuttering:

The etiology of stuttering is controversial. The prevailing theories point to mea-surable neurophysical dysfunctions that disrupt the precise timing required to pro-duce speech. Stuttering is a common disorder that usually resolves by adulthood.Almost 80 percent of children who stutter recover fluency by the age of 16 years.Mild stuttering is self-limited but more severe stuttering requires speech therapy,which is the mainstay of treatment. Delayed auditory feedback and computer-assisted training are currently used to help slow down speech and control otherspeech mechanisms. Pharmacologic therapy is seldom used although haloperidolhas been somewhat effective. (Lawrence & Barclay, 1998, p. 2175)

The cause of developmental stuttering is in fact unclear, but a major line ofresearch over at least three decades has investigated the possibility of a motorcontrol disorder as at least one component (Ingham, 1998; Peters, 2000;Postma, Kolk, & Povel, 1990). Evidence for a motor control involvement inthe cause of stuttering is reviewed here, but it should be noted that this in-volvement is controversial, and some authors have questioned if research todate has securely established that stuttering should be viewed as a disorder ofspeech motor control (Ingham, 1998).

Part of the theoretic uncertainty hinges on the degree to which stuttering isa motoric disorder or a linguistic disorder. In particular, three major hypothe-ses have been advanced regarding motoric and linguistic factors in stuttering(Peters, 2000; Peters & Starkweather, 1990). The first hypothesis is that atleast two subgroups should be recognized among stutterers, one subgroupwith a predominant motoric deficit and another with a predominant linguisticdeficit. Confirmation of this hypothesis requires epidemiologic studies of asuitably large number of subjects with well-defined criteria to distinguish thehypothesized motoric and linguistic subtypes. A variant of this first hypothe-sis is that a developmental imbalance between motoric and linguistic factorsaccounts for stuttering. That is, as the child acquires language, the skills forlanguage and speech motor control may not be commensurate. The second hy-pothesis is that language formulation and the motor processes of speech are


mutually interfering, and it is this interference that explains stuttering. Ac-cording to this view, both motoric and linguistic abnormalities should be evi-dent. The third hypothesis is that speech fluency is affected by various lan-guage processes, including aspects of language competence (such as lexiconsize and number of syntactic forms) and language performance (for example,word finding and sentence construction). In this view, various linguistic stres-sors may lead to dysfluencies, and the identification of these stressors is aprime objective in research on stuttering. In addition to these hypotheses, italso should be acknowledged that the movement abnormalities observed in in-dividuals who stutter may not be core motor disturbances, but rather compen-sations used in an attempt to produce fluent speech (Jancke, Bauer, Kaiser, &Kalveram, 1997; Van Lieshout, Hulstijn, & Peters, 1996a, 1996b).

Evaluation of these hypotheses requires the investigation of both motoricand linguistic factors in stuttered speech, along with paradigms such as con-current attention-demanding tasks (Bosshardt, 1999), detailed analysis of lan-guage associated with dysfluencies (Howell, Au-Yeung, & Sackin, 1999; Logan& LaSalle, 1999; Ratner, 1997a, 1997b; Yaruss, 1999), and further assessmentsof nonspeech motor skill (Ward, 1997; Zelaznik, Smith, Franz, & Ho, 1997).

Recent advances in stuttering research include applications of neuroimagingand the use of acoustic and physiologic measurements of motor coordination. Inaddition, studies have been carried out to examine the genetics, epidemiologic,comorbid, predispositional, and neurologic correlates of stuttering. These arecomplex topics that can be mentioned only briefly and selectively here.

Neuroimaging results point to atypical patterns of activation in the brains ofstutterers compared with nonstuttering control participants. However, differencesin methods and results across studies make it difficult to draw a unified conclu-sion at this time. A PET study of three individuals who stutter indicated increased6-FDOPA uptake in ventral limbic cortical and subcortical regions, which wasinterpreted as evidence for an overactivity in the presynaptic dopamine system inbrain structures that control speech (Wu, Maguire, Riley, Lee, Keator, Tang, Fal-lon, & Najafi, 1997). Another PET study showed increased activity in anteriorforebrain regions but reduced activation in postrolandic regions concerned withperception and sensory decoding (Braun, Varga, Stager, Schulz, Selbie, Maisog,Carson, & Ludlow, 1997). Neuromagnetic responses to monaural tones also dis-tinguished individuals who stutter from those who do not, and it was suggestedthat a nonoptimal processing of auditory input may contribute to dysfluencies(Salmelin, Schnitzler, Schmitz, Jancke, Witte, & Freund, 1998). In a PET func-tional activation study by Fox and associates (Fox, Ingham, Ingham, Hirsch,Downs, Martin, Jerabek, Glass, & Lancaster, 1996), individuals who stutter haddistinguishing and significant activations in the supplementary motor area, supe-rior lateral premotor cortex, and primary motor cortex with right dominance.Those who stutter also showed a prominent cerebellar activation and, interest-ingly, nonactivation or deactivation of auditory areas of superior temporal cortex.

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Interpretation of the neuroimaging data is not straightforward. A skeptic mayconclude that the studies simply show that behavioral disturbances are associatedwith abnormal patterns of neural activation, much as different neural activationsmay be seen for limping versus normal walking. For that matter, fundamentalquestions remain to be answered, such as whether additivity of activation pat-terns can be assumed (Sidtis, Strother, Anderson, & Rottenberg, 1999). How-ever, neuroimaging studies eventually may point to inherent differences in brainorganization as well as showing how differential neural activations are associatedwith fluency versus dysfluency. There is also potential for a synthesis of evi-dence from studies of brain activation, stuttering-related brain lesions, and corti-cal stimulation that either induces or prevents stuttering. Recently, for example,Muroi, Hirayama, Tanno, Shimizu, Watanabe, and Yamamoto (1999) reportedon an individual who stopped stuttering after bilateral thalamic infarction. Theypointed out that the infarction affected two thalamic nuclei that have been impli-cated in stuttering in previous activation, lesion, and stimulation studies. It wasconcluded that both developmental and acquired stuttering are associated withdisturbed function of one or both of two reciprocal thalamocortical circuits, onebetween supplementary motor area and the thalamic centromedian nucleus, andthe other between the dorsomedial nucleus of thalamus and the lateral prefrontalarea. It is noteworthy that a dopaminergic association with stuttering has beenproposed (Anderson, Hughes, Rothi, Crucian, & Heilman, 1999; Canter, 1971)and that the thalamus has been implicated as a central generator for parkinsoniantremor, with involvement of peripheral inputs as either part of an unstable reflexloop or as a modulator of the central oscillator (Hua, Reich, Zirh, Perry, Dough-erty, & Lenz, 1998). Still another neural correlate was reported for an individualwho had Tourette syndrome with comorbid obsessive-compulsive disorder, at-tention-deficit hyperactivity disorder, stuttering, and gait disturbance (Demirkol,Erdem, Inan, Yigit, & Guney, 1999). Magnetic resonance imaging scans re-vealed bilateral and symmetrical globus pallidus lesions with a specific “tiger’seye” appearance.

The identification of specific structures or pathways involved in the causeof stuttering is problematic because of the lack of agreement among publishedstudies. However, the foregoing discussion chronicles recent progress thatmay herald a new understanding of neurologic abnormalities associated withdevelopmental stuttering. At least three general interpretations may be drawnfrom the available data. First, stuttering can result from a variety of neurologicdisturbances and is not necessarily related to damage to any one structure orneural pathway. Second, stuttering is particularly associated with anomalies inhemispheric asymmetry. Third, stuttering reflects damage to the extrapyrami-dal motor pathway, especially the basal nuclei, thalamus, or thalamocorticalconnections.

Several writers have reported on both progress and potential in epidemio-logic and genetic studies of stuttering (Felsenfeld, 1996, 1997; Kidd, 1980;


Yairi, 1999). Several intriguing results have been reported, but consensus hasnot been reached on some critical issues. Felsenfeld (1997) suggested that thecourse of research should consider: (a) the development of a standard assess-ment battery that can be used to diagnose stuttering through the lifespan; (b)examination of the relationship between family history status and epidemio-logic variables (e.g., stuttering severity and probability of spontaneous remis-sion); (c) exploration of extrinsic (environmental) factors that may precipitateor maintain the disorder; and (d) increase the pool of high-density pedigreesavailable for genetic modeling and linkage analyses.

It has long been known that children who stutter are more likely than non-stuttering control children to have other speech and language disorders. Cer-tainly, it can be argued whether the comorbidity reflects a general susceptibil-ity to communication disorder, or if the associated problems are secondary tothe stuttering (e.g., the stuttering interferes with speech and language develop-ment, so children who stutter are disadvantaged). Recent work has helped todemonstrate associations between stuttering and a variety of other conditions,including Tourette syndrome features (Abwender, Trinidad, Jones, Como,Hymes, & Kurlan, 1998), specific language impairment with phonologic in-volvement (Hall, 1999), phonologic delay (for children whose stuttering ispersistent; Yairi & Ambrose, 1999), and hyperfunction of auditory self-moni-toring (Ratner, 1997a). Perhaps none of these accompanying features points toa definite causal link, but all of them together could possibly define a neuro-behavioral composite.

It also may be critical to take a lifespan perspective to create a coherentview of stuttering and its correlates. For example, the apparent hyperfunctionof auditory self-monitoring observed in children’s stuttering (Ratner, 1997a,1997b) stands in contrast to the reduced or atypical activation of auditory cor-tex seen in adults who stutter (Braun et al., 1997; Fox et al., 1996; Salmelin etal., 1998). It is known that adults who do not stutter tend to show an inhibitionof auditory cortex during self-produced speech (Numminen, Salmelin, &Hari, 1999), but it is not clear when and how this inhibitory effect emerges.One interpretation of the data on persons who stutter is that children who ex-perience stuttering initially have a highly activated auditory cortex duringstuttering but gradually learn to inhibit activity strongly in this cortex, espe-cially during episodes of dysfluency. It also should be noted that neuroana-tomic studies suggest that there is a protracted structural maturation of the fi-ber pathways associated with auditory and motor speech functions (Paus,Zijdenbos, Worsley, Collins, Blumenthal, Giedd, Rapoport, & Evans, 1999),which means that early sensorimotor experience with speech could shape theneural pathways. Structural maturation of the brain is accomplished duringchildhood, as speech and language are acquired.

The value of a lifespan perspective is shown by other recent work as well.It appears that the loci of dysfluencies change with language maturation. A

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change in stuttering locus from function words to content words was reportedby Howell, Au-Yeung, and Sackin (1999). In a latent trait study of the devel-opment of persistent stuttering, it was concluded that stuttering progressedthrough four general stages that reflected an increasing integration and stabili-zation (Kalinowski, Kalinowski, Stuart, & Rastatter, 1998).

Is it possible that stuttering-like behaviors occur in animals? Leonardo andKonishi (1999) reported that perturbations of auditory feedback in adult zebrafinches caused a decrystalization (disintegration of mature song) that includeda “stuttering” effect. This demonstration of a stuttering-like phenomenon inbirds joins studies of deafening in birds as routes to the use of animal modelsfor certain kinds of communication disorders in humans. As a highly specula-tive example, consider the following. It has been proposed that developmentalstuttering is related to transmission of a single major genetic locus (Ambrose,Yairi, & Cox, 1993). It has also been reported that motor-driven gene expres-sion occurs in songbirds (Jarvis & Nottebohm, 1997). Perhaps a motor-drivengene expression is involved in the explanation of stuttering in humans.

Treatment of developmental stuttering.

Because most of the literatureon treatment of stuttering pertains to the developmental form, discussion oftreatment is limited here to developmental stuttering. Given that most childrenwho stutter will recover, what distinguishes the child who will recover fromthe child who will not? An answer to this question could determine the use ofclinical intervention. It has been suggested that resistant and recovered stutter-ing have a common genetic cause, with persistence being related partly to ad-ditional genetic factors (Ambrose, Cox, & Yairi, 1997). It is not only childrenwho recover from stuttering, but some adults as well (Finn, 1996, 1998). Thedistinction between resistant and recovered stuttering is important both to effi-cient clinical intervention but also to an understanding of stuttering itself.

A variety of treatment approaches have been developed for stuttering, andprogress also has been made in defining criteria for studies of treatment out-comes and efficacy (Cordes, 1998; Ingham & Riley, 1998). Conture (1996),who reviewed published data on treatment outcomes, concluded that “[th]eaverage number of people estimated to stutter who benefit from treatment (7of 10) undoubtedly varies with age (younger clients appear to improve some-what more quickly and more easily than older clients), severity, type, and/orlength of stuttering (longer history of stuttering appears to increase the dura-tion of treatment and decrease likelihood of a complete recovery)” (p. S24). Amore recent study demonstrated that the benefits of treatment for children andadolescents are evident for several years after intervention (Hancock, Craig,McCready, McCaul, Costello, Campbell, & Gilmore, 1998).

Assessment and classification of acquired stuttering.

Acquired stutter-ing is associated with various conditions, but especially brain lesions, pharma-cologic effects, and psychogenesis. Studies in the first two of these areas donot point to discrete or focal causes of neurogenic stuttering. In a study of four


individuals with stuttering occurring after stroke at presentation, Grant, Bi-ousse, Cook, and Newman (1999) concluded that both the clinical presenta-tion and lesion sites were variable across the four individuals. Other lesionsites have included either bilateral diffuse lesions or a unilateral lesion (Heuer,Sataloff, Mandel, & Travers, 1996), a hemispheric lesion in addition to a cal-losal lesion (Tsumoto, Nishioka, Nakikita, Hayashi, & Maeshima, 1999), andstriatocapsular infarction (Kono, Hirano, Ueda, & Nakajima, 1998). As notedearlier, thalamocortical pathways have been proposed as primary lesion sitesin both developmental and acquired stuttering, and these should receive atten-tion in future studies. With respect to drug-induced stuttering, Brady’s (1998)review did not identify a single neurotransmitter system as causative, butrather suggested that stuttering results from multiple, interacting neurotrans-mitter systems. Psychogenic stuttering is distinguished from neurogenic stut-tering primarily in response to treatment, with the former showing a relativelyrapid and favorable response to behavioral therapy and associated manage-ment strategies (Baumgartner & Duffy, 1997). Possibly, dysfluent speech is abehavioral consequence of a variety of neural disturbances, and there may notbe a common neuropathologic characteristic across the various reports of ac-quired stuttering.

Assessment and classification of cluttering.

Cluttering is recognized bysome authorities as another dysfluency disorder, distinct from stuttering. Theliterature on cluttering is quite small and, even for its limited quantity, ad-dresses uncertainties of diagnosis and cause similar to those already consid-ered for stuttering. A special issue of the

Journal of Fluency Disorders

(1996,Volume 21, Numbers 3–4) is devoted to cluttering. One of the contributions isa bibliography for papers published since 1964 (Myers, 1996). Clutteringwould benefit from the same general research directions summarized for stut-tering and apraxia of speech.

CONCLUSIONS

Research progress has been made on several fronts, and it is clear that the var-ious areas of research have the potential for a powerful convergence on adeeper understanding of how speech is controlled and how the desired regula-tion is affected by disorders such as dysarthria, apraxia of speech, and fluencydisorders. General conclusions regarding the research literature on these dis-orders are as follows:

1. There are continuing uncertainties with regard to cause and assessment.2. There is a limited research effort on treatment outcomes and efficacy, with

a nearly total absence of randomized clinical trials.3. Quantitative instrumental methods (acoustic and physiologic techniques)

are being increasingly applied in the study of these disorders, and these

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methods complement the perceptual descriptions that have formed much ofthe clinical literature.

4. Neuroimaging methods are beginning to be used to detect neuropatholo-gies, but the numbers of participants in such studies are quite small and theresults are not always consistent across studies.

5. Particularly for dysarthria and apraxia of speech, the literature reflects alimitation in the amount and variety of data. Developmental stuttering isassociated with an immense literature, but fundamental questions remainabout this disorder.

6. Each of these disorders will very likely be illuminated by research methodsand technologies now at hand. A particularly promising direction is formultidisciplinary and multitechnology studies. For example, several writ-ers have endorsed a program of research for stuttering that embraces epide-miology, genetics, neurology, speech pathology, and speech science. Thesame combination of specialties are needed for research on dysarthria andapraxia of speech.

7. For all of these disorders, both a developmental form and an acquired(adult) form have been recognized. However, despite some general similar-ities in symptomatologic factors, it is not clear that the developmental andadult forms reflect the same mechanisms of impairment. It may be unwiseto impose clinical nosology for adults unto children. Disorders that affectspeech motor learning in children may be fundamentally different from thedisorders that disrupt previously acquired speech motor skills in adults.

8. Finally, research on both normal and disordered speech confronts the ques-tion of how linguistic and motoric aspects can be distinguished in the plan-ning and execution of speech movements. Important advances could wellturn on the resolution of this question, which is a contemporary issue inboth theory and empirical research.

This work was supported in part by the National Institute on Deafness and Other CommunicativeDisorders (grant no. 5 R01 DC 00319). The author is indebted to many colleagues who graciouslyshared reprints and suggestions for the development of this paper. The author thanks in particularAnn Cordes, Joseph Duffy, Jordan Green, Roger Ingham, David Kuehn, John Rosenbek, AnnSmith, and Ehud Yairi, as well as Nancy Solomon and an anonymous reviewer for their construc-

tive comments.

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CONTINUING EDUCATION

Research on Speech Motor Control and Its Disorders: A Review and Prospective

1. Compared with other motor skills in humans, speech:a. Is relatively slow in the rate of movements performedb. Is produced at rates faster that any other discrete human motor perfor-

mancec. Involves more motor fibers than any other human mechanical activityd. Both b and c

2. Recent research reviewed in this article indicates that the motor behavior inbabbling and other infant vocalizations:a. Derives directly from other oral behaviors such as chewing and swal-

lowingb. Has little or no value in identifying children with health problems or

with potential communication problemsc. Is continuous with some aspects of later speech developmentd. Is completely unaffected by the child’s hearing status

3. Dysarthrias are defined as speech disorders that:a. Involve disturbances in the motor programs that specify movement se-

quencesb. Are characterized primarily by excessive or exaggerated movements in

the production of speechc. Result from neurologic impairments associated with weakness, slow-

ness, or incoordination of the musculature used to produce speechd. Result exclusively from damage to the peripheral nervous system (the

cranial and spinal nerves)4. Children who stutter are:

a. More likely than children who do not stutter to have other speech andlanguage disorders

b. Very unlikely to overcome the speech disorder without therapyc. Less likely than adults who stutter to improve with therapyd. Both b and c

5. Which of the following structures has been shown by recent neuroimagingstudies to be associated with articulatory planning and the disorder ofapraxia of speech in adults?a. Cerebellumb. Insulac. Putamend. All of the above

research on speech motor control and its...

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