- Email: [email protected]
Demands and capacities versus demands and performance
DEMANDS AND CAPACITIES VERSUS DEMANDS AND PERFORMANCE RICHARD F. CURLEE University of Arizona, Tucson, Arizona, U.S.A.
This article examines the proposed relabeling of “capacities” as “performance” in the Demands and Capacities Model of stuttering in terms of four issues involving the model’s demands component, theoretical versatility, genetic potential, and current clinical uses. Although the proposed changes should resolve the measurement issues of concern, it is suggested that this change may not be of sufficient value or significance for a Demands and Performance Model to supplant the Demands and Capacities Model. © 2000 Elsevier Science Inc. Key Words: Stuttering; Demands and Capacities Model; Internal variables; Measurement difficulties
The hypothesized mismatch between a child’s speech production “capacities” and the internal and environmental “demands” on speech production has been a central construct of etiological accounts of stuttering (e.g., Andrews et al., 1983) as well as models for treating it (e.g., Riley & Riley, 1979, Starkweather, 1997). It is doubtful that any other construct has had such a pervasive influence on the stuttering literature as have various versions of the Demands and Capacities model (DCM) over the past decade. The model’s popularity during this period likely reflects its inclusion of nearly all factors ever suspected of influencing fluent speech or stuttering. It has also been used as a perspective for discussing the brain-behavior relationships suggested by findings from brain imaging research (e.g., Watson et al., 1994). Despite its widespread popularity and apparent appeal among clinicians and researchers alike, the DCM invites circular reasoning. For example, the model predicts that stuttering will occur whenever demands exceed a child’s capacities, which makes it tempting to conclude that a child’s stuttering is a sign that environmental demands may be too high (Ingham & Cordes, 1997). This limitation can prevent the model’s experimental testing and acceptance as a valid scientific model or theory but may not eliminate its value for clinical work.
Address correspondence to Dr. Richard F. Curlee, Speech and Hearing Sciences Building, University of Arizona, Tucson, AZ 85721, U.S.A.; Phone: (520)621-1961; E-mail: [email protected]
J. FLUENCY DISORD. 25 (2000), 329–336 © 2000 Elsevier Science Inc. All rights reserved. 655 Avenue of the Americas, New York, NY 10010
0094-730X/00/$–see front matter PII S0094-730X(00)00082-6
330
R. F. CURLEE
Siegel’s article in this issue focuses on the DCM that has been described by Starkweather (1997) and his colleagues in several publications (e.g., Starkweather, Gottwald, & Halfond, 1990). Siegel argues that the model’s capacities component(s) is “ephemeral” and lacks “empirical substance,” especially for planning the assessment or treatment of children who stutter, and he suggests recasting it as a Demands and Performance Model (DPM). He believes this change will be more consistent with how the model is used currently in clinical practice and will allow both components (i.e., demands and performance) to be grounded more firmly by observation and empirical measures, as well. The concerns Siegel raises are well founded, and his suggested reconceptualization of “capacities” as “performance” might resolve many of the concerns raised. In my opinion, several other issues should be discussed, which are the focus of this article.
DEMANDS ISSUES Siegel’s proposed reconceptualization of DCM appears to consider only the environment as sources of demands that affect a child’s speaking performance. Starkweather (1997), however, hypothesizes the demands component of DCM to have two sources, the pressures and demands presented by a child’s environment and those arising from within a child. The environmental sources of primary concern consist mainly of the demands of a child’s communication partners, plus the context and speaking tasks involved. In contrast, the principal internal sources appear to be developmental mismatches between children’s cognitive, linguistic, and affective functions and their speech motor development. Curiously, little attention has been given to the possible effects on a child’s fluency of previous communication experiences and his or her perceptions of the current communication context or setting. Although the earliest sources of such demands may have originated in the environment, it seems highly likely that these sorts internal sources of demands would increase with age and that their effects would soon predominate, especially once a child had begun to stutter. Even more important, findings from a number of studies that have been completed in this area provide little empirical support that environmental demands affect stuttering children’s fluency. A substantial body of literature, largely based on findings from descriptive studies of verbal interactions in parent-child dyads, has been accumulated. In general, this literature indicates that adults, even older children, seem to adapt their communication behaviors to those of young children rather than the reverse; however, the effects of adult’s communication behaviors on young children’s subsequent speech or language development, if any, are yet to be determined (Ratner, 1993). During the past several decades, a number of studies have examined the speech rates, response turn latencies, interruptions, and communication acts of parents conversing with children who do and do not
CAPACITIES VS. PERFORMANCE
331
stutter (e.g., Bernstein Ratner, 1992; Kelly & Conture, 1992; Meyers & Freeman, 1985a,b; Newman & Smit, 1989; Weiss & Zebrowski, 1991, 1992; Wilkenfeld & Curlee, 1997). Even though each of these areas involved communication behaviors that are commonly targeted in treatment and in advising parents of children who stutter (e.g., Starkweather, 1997), findings have been inconsistent, at best, and no reliable effects on fluency or stuttering have been found by the few studies employing experimental designs. In short, the patterns of communication behaviors that have been studied and described in adult-child conversational interactions are not well understood at present, but there appears to be no credible basis for believing that the source of most of the demands that affect a child’s speech fluency is environmental. This leads me to wonder if Siegel’s decision to focus on the environment as the most important source of demands on a child’s fluent speech “performance” and ignore demands that may originate from within the child because of measurement concerns, may diminish rather than strengthen DCM as a tool for guiding the clinical management of children who stutter.
THEORY ISSUES The measurement concerns about DCM’s capacities construct expressed by Siegel echo those of a long list of prominent theorists in the behavioral and social sciences. Indeed, they have avoided, when possible, the conceptual quicksand that may be introduced into theories of human behavior by unobservable, hypothetical constructs or internal variables (MacCorquodale & Meehl, 1948). In contrast, physicists evidence little reluctance or concern in formulating theories about quarks or the weak force, nor did biologists in their early discussions of genes. Theorists in these physical sciences were able, of course, to support the “existence” of such constructs with predictions and findings from empirical research. As Siegel (2000) acknowledged in citing Chomsky’s distinction between competence and performance in his transformational theory of grammar, sound scientific constructs do not have to be accessible to direct observation, but they do need to have sound theoretical or empirical support. It seems possible, therefore, that DCM might provide a useful structure for advancing understanding of stuttering and its treatment if its constructs and their relationships were conceptualized appropriately. Two examples, one clinical and the other etiological, that have attempted to assess the hypothesized diminished capacities of persons who stutter illustrate such efforts. A component model for assessing and treating children who stutter (Riley & Riley, 1979; 1980; 1984) was developed from these authors’ accumulation and analysis of data from a clinical test battery administered to the children seen for treatment of stuttering. Four factors, which were labeled as attending, auditory processing, sentence formulation, and oral motor components, were identified as potential targets for treatment, and findings from a child’s diagnostic evalua-
332
R. F. CURLEE
tion were used to select which component(s) (i.e., capacities) needed training. This approach focused on increasing a child’s capacities rather than decreasing the environment’s demands, as do most current treatments that use the model to plan therapy interventions. A report (Riley & Riley, 1984) of the treatment outcomes of 44 children seen for stuttering using the “component model” indicated that more than 80% evidenced mild or no stuttering at the conclusion of therapy and later follow-up. The next example, the Adaptive Model Theory (AMT) proposed by Neilson, Neilson, and O’Dwyer (1992), illustrates how DCM was used to provide the conceptual structure of an etiological theory of stuttering. AMT applies information processing principles to describe a motor control system, how this system controls movement, and how disorders involving disruptions of movement, such as stuttering, would occur. The anatomical structures and functions proposed by the theory are consistent with current understanding of central nervous system function and findings from neurological and psychobiological research. In brief, the theory (Neilson, Neilson, & O’Dwyer, 1992) proposes that efferent and afferent impulses interact at central and peripheral levels to produce coordinated motor commands under open loop control at one level, which are adjusted intermittently by feedback at another level and then are corrected further at the level of reflexive control to produce speech. Movements of speech production are controlled by the interaction of an anatomically distributed, parallel processing network of neural loops connecting premotor and motor areas of the cortex, supplementary motor area (SMA), basal ganglia, cerebellum, and ascending and descending pathways. It is hypothesized that stuttering results when cortically based distributions of neural resources for the processing loop that connects the basal ganglia, SMA, and premotor area 6 are deficient and compromises the loop’s adaptive control of speech production. AMT describes the neurological structures and functions that produce stuttering, which implies that its hypothetical constructs are not just abstracts of internal functions but have an empirical existence (MacCorquodale & Meehl, 1948), and its specificity in describing these constructs would appear to permit empirical testing of the theory. Neilson and Neilson (1987) tested their hypothesis that deficits in central processing resources is responsible for stuttering by comparing the performance of subjects who do and do not stutter on a series of auditory and visual tracking tasks. They reasoned that the control of motor movements while tracking a continuously changing auditory signal closely parallels the control of movements that transform continuously changing vocal tract configurations into speech and would, therefore, use the same neurological resources responsible for adaptive control of speech production, whereas visual tracking would not. Both groups of subjects performed comparably while tracking a continuously changing visual signal; however, the performance of those who stuttered was significantly poorer when tracking the auditory signal but that of those who did not stutter did not change. The Neilson & Neilson (1987) concluded
CAPACITIES VS. PERFORMANCE
333
that the marked discrepancy in the stuttering group’s performance when tracking the auditory and visual stimuli supported their hypothesis that stuttering results from a deficiency in the neurological resources allocated to perform the sensory-motor control functions necessary for fluent speech production. Neither of these examples has been able to demonstrate a functional relationship between stuttering and the internal variables or capacities that each has measured. However, both obtained empirical measures that differentiate stuttering from nonstuttering speakers that each views as measures of speakers’ capacities hypothesized to affect or cause stuttering. If such group differences continued to be found in carefully controlled, descriptive studies of different subjects on analogous tasks that permitted investigators to rule out alternative explanations, in time these findings could be viewed as convincing support for the hypothesized constructs and relationships that cannot be directly measured or observed. Such findings, for example, have led many investigators to conclude that a genetic predisposition modulates children’s risks of stuttering. If they are correct, DCM might be a useful model in describing how a genetically transmitted predisposition to stutter becomes expressed in phenotypes, which is the next issue to be discussed.
GENETIC ISSUES Identification of the human genome is expected to be completed within the next 2 or 3 years, and efforts to identify the segment(s) of DNA that account for the incidence of stuttering in families are already underway. Assuming that one or more such segments will be found, much additional research will be needed to gain an understanding of how this genetic material affects the formation and development of genotypes and how genotypes and environmental variables interact to produce stuttering phenotypes. Some model or theory, whether formal or informal, correct or incorrect, explicit or implicit, will be required to advance scientific understanding of how the biological mechanisms of stuttering genotype(s) affect speech production behaviors, and it is difficult for me to imagine how an endogenous predisposition comes to be expressed as stuttering unless internal variables are involved, some of which may be hypothesized as capacities or deficits. Thus, more soundly conceptualized versions of DCM could provide valuable insights in formulating models or theories of how this occurs, whether or not the variables hypothesized can be observed or measured reliably. The final issue to be discussed returns to the use of DCM in clinical practice.
CLINICAL ISSUES In an earlier section I expressed concern that Siegel’s focus on environmental variables as the source of demands that result in stuttering may have uninten-
334
R. F. CURLEE
tionally weakened DCM’s value as a clinical tool. As he noted, most of the literature describing how DCM can be applied clinically appears to focus on environmental demands, and I suspect this is the focus of most clinicians, especially in counseling or advising parents. I must confess that is true in my own interactions with parents in the clinic, even though I do not believe the model is valid. Most of the parents I see ask why their child has begun to stutter at some time during their case history interview, and a few may even express concern that the child’s stuttering may be related to something they have or haven’t done. In such situations, I usually relate my own version of DCM. For example, after telling them that the cause of stuttering is not known, I may add that I know of no evidence indicating that anything they may have done or not done would cause their child to stutter. Then, I often continue by saying that many clinicians believe that whenever the demands of a situation tax a child’s speech or language skills, he is likely to be disfluent. If they ask if there is anything they can do, which many do, I typically preface the usual suggestions with “Many clinicians ask parents to... .” It is my impression that few parents are satisfied or feel comfortable with the truth, that the cause of stuttering is unknown. Most seem to feel more at ease if they are given some way of thinking about why their child may stutter some times but not others and if things they can do that may help their child’s fluency are suggested. The DCM is an easily understood, plausible, and satisfying explanation for parents in my experience. Perhaps I should be concerned that this explanation of stuttering and the suggestions for helping have little empirical support. Indeed, I might be if I were not more concerned at such times in trying to reduce any concerns or guilt and some of the “mystery” of stuttering for parents and to suggest things to do that may help them feel that they are helping the child.
CONCLUDING COMMENTS As was noted earlier, I believe that Siegel’s concerns are well founded and hope that his article will encourage more critical consideration and use of DCM as a scientific explanation of stuttering. However, it is a superficially plausible conceptual model whose current popularity belies the weakness of its empirical support, and it is not clear to me that relabeling “capacities” as “performance” will resolve the integrity of the model or enhance its use as a clinical tool. The absence of empirical support for environmental demands having reliable or measurable effects on children’s fluency and stuttering undermines the credibility of DPM as a valid model or clinical tool, even if it does resolve the measurement issues of Siegel’s concern. Lastly, I am uncertain that the model’s general conceptual structure of comparing or contrasting communicative demands with a person’s communicative capacities has to invite circular reasoning or cannot be conceptualized soundly. Only time will tell if DPM will be accepted as a new and improved model of stuttering or
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viewed as a repackaged current model with differently labeled features. The long lives and continuing use of theories of stuttering that have little if any credible empirical support indicate that such theories and models can survive and continue to be used, without scientific support, until a more plausible or useful theory or model is available to replace them. The outcome of DCM versus DPM is too close to call.
REFERENCES Andrews, G., Craig, A., Feyer, A., Hoddinott, S., Howie, P., & Neilson, M. (1983). Stuttering: A review of research findings and theories circa 1982. Journal of Speech and Hearing Disorders 48, 226–246. Bernstein Ratner, N. (1992). Measurable outcomes of instructions to modify normal parent-child verbal interactions: Implications for indirect stuttering therapy. Journal of Speech and Hearing Research 35, 1256–1257. Ingham, R., & Cordes, A. (1997). Self-measurement and evaluating stuttering treatment efficacy. In R.F. Curlee & G.M. Siegel (Eds.), Nature and treatment of stuttering: New Directions (2nd ed.) (pp. 413–437). Boston: Allyn & Bacon. Kelly, E., & Conture, E. (1992). Speaking rates, response time latencies, and interrupting behaviors of young stutterers, nonstutterers, and their mothers. Journal of Speech and Hearing Research 35, 14–20. MacCorquodale, K., & Meehl, P. (1948). On a distinction between hypothetical constructs and intervening variables. Psychological Review 55, 95–107. Meyers, S., & Freeman, F. (1985a). Mother and child speech rates as a variable in stuttering and disfluency. Journal of Speech and Hearing Research 28, 436–444. Meyers, S., & Freeman, F. (1985b). Interruptions as a variable in stuttering and disfluency. Journal of Speech and Hearing Research 28, 428–435. Neilson, M., & Neilson, P. (1987). Speech motor control and stuttering: A computational model of adaptive sensory-motor processing. Speech Communication 6, 325–333. Neilson, M., Neilson, P., O’Dwyer, N. (1992). Adaptive model theory: Application to disorders of motor control. In J.J. Summers (Ed.), Approaches to the study of motor control. New York: Elsevier Science. Newman, L., & Smit, A. (1989). Some effects of variations in response time latency on speech rate, interruptions, and fluency in children’s speech. Journal of Speech and Hearing Research 32, 635–644. Ratner, N.B. (1993). Parents, children, and stuttering. Seminars in Speech and Language 14, 238–250.
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Riley, G., & Riley, J. (1979). A component model for diagnosing and treating children who stutter. Journal of Fluency Disorders 4, 279–293. Riley, G., & Riley, J. (1980). Motoric and linguistic variables among children who stutter: A factor analysis. Journal of Speech and Hearing Disorders 45, 504–514. Riley, G., & Riley, J. (1984). A component model for treating stuttering in children. In M. Peins (Ed.), Contemporary approaches in stuttering therapy. Boston: Little Brown. Siegel, G. M. (2000). “Demands and capacities” or “demands and performance.” Journal of Fluency Disorders 25. Starkweather, C.W. (1997). Therapy for younger children. In R.F. Curlee and G.M. Siegel (Eds.), Nature and treatment of stuttering, (2nd ed.) (pp. 257– 279). Boston: Allyn and Bacon. Starkweather, C.W., Gottwald, S.R., & Halfond, M.H. (1990). Stuttering prevention: A clinical method. Englewood Cliffs, NJ: Prentice-Hall. Watson, B., Freeman F.J., Devous, M.D., Chapman, S.B., Finitzo, T., & Pool, K.D. (1994). Linguistic performance and regional cerebral blood flow in persons who stutter. Journal of Speech and Hearing Research 37, 1221– 1228. Weiss, A., & Zebrowski, P. (1991). Patterns of assertiveness and responsiveness in parental interactions with stuttering and fluent children. Journal of Fluency Disorders 16, 125–141. Weiss, A., & Zebrowski, P. (1992). Disfluencies in the conversations of children who stutter: Some answers about questions. Journal of Speech and Hearing Research 35, 1230–1238. Wilkenfeld, J., & Curlee, R. (1997). The relative effects of adult questions and comments on children’s stuttering. American Journal of Speech-Language Pathology 6, 79–89.
This article examines the proposed relabeling of “capacities” as “performance” in the Demands and Capacities Model of stuttering in terms of four issues involving the model’s demands component, theoretical versatility, genetic potential, and current clinical uses. Although the proposed changes should resolve the measurement issues of concern, it is suggested that this change may not be of sufficient value or significance for a Demands and Performance Model to supplant the Demands and Capacities Model. © 2000 Elsevier Science Inc. Key Words: Stuttering; Demands and Capacities Model; Internal variables; Measurement difficulties
The hypothesized mismatch between a child’s speech production “capacities” and the internal and environmental “demands” on speech production has been a central construct of etiological accounts of stuttering (e.g., Andrews et al., 1983) as well as models for treating it (e.g., Riley & Riley, 1979, Starkweather, 1997). It is doubtful that any other construct has had such a pervasive influence on the stuttering literature as have various versions of the Demands and Capacities model (DCM) over the past decade. The model’s popularity during this period likely reflects its inclusion of nearly all factors ever suspected of influencing fluent speech or stuttering. It has also been used as a perspective for discussing the brain-behavior relationships suggested by findings from brain imaging research (e.g., Watson et al., 1994). Despite its widespread popularity and apparent appeal among clinicians and researchers alike, the DCM invites circular reasoning. For example, the model predicts that stuttering will occur whenever demands exceed a child’s capacities, which makes it tempting to conclude that a child’s stuttering is a sign that environmental demands may be too high (Ingham & Cordes, 1997). This limitation can prevent the model’s experimental testing and acceptance as a valid scientific model or theory but may not eliminate its value for clinical work.
Address correspondence to Dr. Richard F. Curlee, Speech and Hearing Sciences Building, University of Arizona, Tucson, AZ 85721, U.S.A.; Phone: (520)621-1961; E-mail: [email protected]
J. FLUENCY DISORD. 25 (2000), 329–336 © 2000 Elsevier Science Inc. All rights reserved. 655 Avenue of the Americas, New York, NY 10010
0094-730X/00/$–see front matter PII S0094-730X(00)00082-6
330
R. F. CURLEE
Siegel’s article in this issue focuses on the DCM that has been described by Starkweather (1997) and his colleagues in several publications (e.g., Starkweather, Gottwald, & Halfond, 1990). Siegel argues that the model’s capacities component(s) is “ephemeral” and lacks “empirical substance,” especially for planning the assessment or treatment of children who stutter, and he suggests recasting it as a Demands and Performance Model (DPM). He believes this change will be more consistent with how the model is used currently in clinical practice and will allow both components (i.e., demands and performance) to be grounded more firmly by observation and empirical measures, as well. The concerns Siegel raises are well founded, and his suggested reconceptualization of “capacities” as “performance” might resolve many of the concerns raised. In my opinion, several other issues should be discussed, which are the focus of this article.
DEMANDS ISSUES Siegel’s proposed reconceptualization of DCM appears to consider only the environment as sources of demands that affect a child’s speaking performance. Starkweather (1997), however, hypothesizes the demands component of DCM to have two sources, the pressures and demands presented by a child’s environment and those arising from within a child. The environmental sources of primary concern consist mainly of the demands of a child’s communication partners, plus the context and speaking tasks involved. In contrast, the principal internal sources appear to be developmental mismatches between children’s cognitive, linguistic, and affective functions and their speech motor development. Curiously, little attention has been given to the possible effects on a child’s fluency of previous communication experiences and his or her perceptions of the current communication context or setting. Although the earliest sources of such demands may have originated in the environment, it seems highly likely that these sorts internal sources of demands would increase with age and that their effects would soon predominate, especially once a child had begun to stutter. Even more important, findings from a number of studies that have been completed in this area provide little empirical support that environmental demands affect stuttering children’s fluency. A substantial body of literature, largely based on findings from descriptive studies of verbal interactions in parent-child dyads, has been accumulated. In general, this literature indicates that adults, even older children, seem to adapt their communication behaviors to those of young children rather than the reverse; however, the effects of adult’s communication behaviors on young children’s subsequent speech or language development, if any, are yet to be determined (Ratner, 1993). During the past several decades, a number of studies have examined the speech rates, response turn latencies, interruptions, and communication acts of parents conversing with children who do and do not
CAPACITIES VS. PERFORMANCE
331
stutter (e.g., Bernstein Ratner, 1992; Kelly & Conture, 1992; Meyers & Freeman, 1985a,b; Newman & Smit, 1989; Weiss & Zebrowski, 1991, 1992; Wilkenfeld & Curlee, 1997). Even though each of these areas involved communication behaviors that are commonly targeted in treatment and in advising parents of children who stutter (e.g., Starkweather, 1997), findings have been inconsistent, at best, and no reliable effects on fluency or stuttering have been found by the few studies employing experimental designs. In short, the patterns of communication behaviors that have been studied and described in adult-child conversational interactions are not well understood at present, but there appears to be no credible basis for believing that the source of most of the demands that affect a child’s speech fluency is environmental. This leads me to wonder if Siegel’s decision to focus on the environment as the most important source of demands on a child’s fluent speech “performance” and ignore demands that may originate from within the child because of measurement concerns, may diminish rather than strengthen DCM as a tool for guiding the clinical management of children who stutter.
THEORY ISSUES The measurement concerns about DCM’s capacities construct expressed by Siegel echo those of a long list of prominent theorists in the behavioral and social sciences. Indeed, they have avoided, when possible, the conceptual quicksand that may be introduced into theories of human behavior by unobservable, hypothetical constructs or internal variables (MacCorquodale & Meehl, 1948). In contrast, physicists evidence little reluctance or concern in formulating theories about quarks or the weak force, nor did biologists in their early discussions of genes. Theorists in these physical sciences were able, of course, to support the “existence” of such constructs with predictions and findings from empirical research. As Siegel (2000) acknowledged in citing Chomsky’s distinction between competence and performance in his transformational theory of grammar, sound scientific constructs do not have to be accessible to direct observation, but they do need to have sound theoretical or empirical support. It seems possible, therefore, that DCM might provide a useful structure for advancing understanding of stuttering and its treatment if its constructs and their relationships were conceptualized appropriately. Two examples, one clinical and the other etiological, that have attempted to assess the hypothesized diminished capacities of persons who stutter illustrate such efforts. A component model for assessing and treating children who stutter (Riley & Riley, 1979; 1980; 1984) was developed from these authors’ accumulation and analysis of data from a clinical test battery administered to the children seen for treatment of stuttering. Four factors, which were labeled as attending, auditory processing, sentence formulation, and oral motor components, were identified as potential targets for treatment, and findings from a child’s diagnostic evalua-
332
R. F. CURLEE
tion were used to select which component(s) (i.e., capacities) needed training. This approach focused on increasing a child’s capacities rather than decreasing the environment’s demands, as do most current treatments that use the model to plan therapy interventions. A report (Riley & Riley, 1984) of the treatment outcomes of 44 children seen for stuttering using the “component model” indicated that more than 80% evidenced mild or no stuttering at the conclusion of therapy and later follow-up. The next example, the Adaptive Model Theory (AMT) proposed by Neilson, Neilson, and O’Dwyer (1992), illustrates how DCM was used to provide the conceptual structure of an etiological theory of stuttering. AMT applies information processing principles to describe a motor control system, how this system controls movement, and how disorders involving disruptions of movement, such as stuttering, would occur. The anatomical structures and functions proposed by the theory are consistent with current understanding of central nervous system function and findings from neurological and psychobiological research. In brief, the theory (Neilson, Neilson, & O’Dwyer, 1992) proposes that efferent and afferent impulses interact at central and peripheral levels to produce coordinated motor commands under open loop control at one level, which are adjusted intermittently by feedback at another level and then are corrected further at the level of reflexive control to produce speech. Movements of speech production are controlled by the interaction of an anatomically distributed, parallel processing network of neural loops connecting premotor and motor areas of the cortex, supplementary motor area (SMA), basal ganglia, cerebellum, and ascending and descending pathways. It is hypothesized that stuttering results when cortically based distributions of neural resources for the processing loop that connects the basal ganglia, SMA, and premotor area 6 are deficient and compromises the loop’s adaptive control of speech production. AMT describes the neurological structures and functions that produce stuttering, which implies that its hypothetical constructs are not just abstracts of internal functions but have an empirical existence (MacCorquodale & Meehl, 1948), and its specificity in describing these constructs would appear to permit empirical testing of the theory. Neilson and Neilson (1987) tested their hypothesis that deficits in central processing resources is responsible for stuttering by comparing the performance of subjects who do and do not stutter on a series of auditory and visual tracking tasks. They reasoned that the control of motor movements while tracking a continuously changing auditory signal closely parallels the control of movements that transform continuously changing vocal tract configurations into speech and would, therefore, use the same neurological resources responsible for adaptive control of speech production, whereas visual tracking would not. Both groups of subjects performed comparably while tracking a continuously changing visual signal; however, the performance of those who stuttered was significantly poorer when tracking the auditory signal but that of those who did not stutter did not change. The Neilson & Neilson (1987) concluded
CAPACITIES VS. PERFORMANCE
333
that the marked discrepancy in the stuttering group’s performance when tracking the auditory and visual stimuli supported their hypothesis that stuttering results from a deficiency in the neurological resources allocated to perform the sensory-motor control functions necessary for fluent speech production. Neither of these examples has been able to demonstrate a functional relationship between stuttering and the internal variables or capacities that each has measured. However, both obtained empirical measures that differentiate stuttering from nonstuttering speakers that each views as measures of speakers’ capacities hypothesized to affect or cause stuttering. If such group differences continued to be found in carefully controlled, descriptive studies of different subjects on analogous tasks that permitted investigators to rule out alternative explanations, in time these findings could be viewed as convincing support for the hypothesized constructs and relationships that cannot be directly measured or observed. Such findings, for example, have led many investigators to conclude that a genetic predisposition modulates children’s risks of stuttering. If they are correct, DCM might be a useful model in describing how a genetically transmitted predisposition to stutter becomes expressed in phenotypes, which is the next issue to be discussed.
GENETIC ISSUES Identification of the human genome is expected to be completed within the next 2 or 3 years, and efforts to identify the segment(s) of DNA that account for the incidence of stuttering in families are already underway. Assuming that one or more such segments will be found, much additional research will be needed to gain an understanding of how this genetic material affects the formation and development of genotypes and how genotypes and environmental variables interact to produce stuttering phenotypes. Some model or theory, whether formal or informal, correct or incorrect, explicit or implicit, will be required to advance scientific understanding of how the biological mechanisms of stuttering genotype(s) affect speech production behaviors, and it is difficult for me to imagine how an endogenous predisposition comes to be expressed as stuttering unless internal variables are involved, some of which may be hypothesized as capacities or deficits. Thus, more soundly conceptualized versions of DCM could provide valuable insights in formulating models or theories of how this occurs, whether or not the variables hypothesized can be observed or measured reliably. The final issue to be discussed returns to the use of DCM in clinical practice.
CLINICAL ISSUES In an earlier section I expressed concern that Siegel’s focus on environmental variables as the source of demands that result in stuttering may have uninten-
334
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tionally weakened DCM’s value as a clinical tool. As he noted, most of the literature describing how DCM can be applied clinically appears to focus on environmental demands, and I suspect this is the focus of most clinicians, especially in counseling or advising parents. I must confess that is true in my own interactions with parents in the clinic, even though I do not believe the model is valid. Most of the parents I see ask why their child has begun to stutter at some time during their case history interview, and a few may even express concern that the child’s stuttering may be related to something they have or haven’t done. In such situations, I usually relate my own version of DCM. For example, after telling them that the cause of stuttering is not known, I may add that I know of no evidence indicating that anything they may have done or not done would cause their child to stutter. Then, I often continue by saying that many clinicians believe that whenever the demands of a situation tax a child’s speech or language skills, he is likely to be disfluent. If they ask if there is anything they can do, which many do, I typically preface the usual suggestions with “Many clinicians ask parents to... .” It is my impression that few parents are satisfied or feel comfortable with the truth, that the cause of stuttering is unknown. Most seem to feel more at ease if they are given some way of thinking about why their child may stutter some times but not others and if things they can do that may help their child’s fluency are suggested. The DCM is an easily understood, plausible, and satisfying explanation for parents in my experience. Perhaps I should be concerned that this explanation of stuttering and the suggestions for helping have little empirical support. Indeed, I might be if I were not more concerned at such times in trying to reduce any concerns or guilt and some of the “mystery” of stuttering for parents and to suggest things to do that may help them feel that they are helping the child.
CONCLUDING COMMENTS As was noted earlier, I believe that Siegel’s concerns are well founded and hope that his article will encourage more critical consideration and use of DCM as a scientific explanation of stuttering. However, it is a superficially plausible conceptual model whose current popularity belies the weakness of its empirical support, and it is not clear to me that relabeling “capacities” as “performance” will resolve the integrity of the model or enhance its use as a clinical tool. The absence of empirical support for environmental demands having reliable or measurable effects on children’s fluency and stuttering undermines the credibility of DPM as a valid model or clinical tool, even if it does resolve the measurement issues of Siegel’s concern. Lastly, I am uncertain that the model’s general conceptual structure of comparing or contrasting communicative demands with a person’s communicative capacities has to invite circular reasoning or cannot be conceptualized soundly. Only time will tell if DPM will be accepted as a new and improved model of stuttering or
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viewed as a repackaged current model with differently labeled features. The long lives and continuing use of theories of stuttering that have little if any credible empirical support indicate that such theories and models can survive and continue to be used, without scientific support, until a more plausible or useful theory or model is available to replace them. The outcome of DCM versus DPM is too close to call.
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