Letters to the Editor Did Primitive Man Really Talk Like an Ape?
Using an unprovable hypothesis as part of a theory of stuttering does not help in testing the theory. We already have too many untestable stuttering theories.
Perkins, Kent, and Curlee (1991) argue in their theory of neurolinguistic function in stuttering that our speech developed in part from a primitive nonlinguistic signaling system that was used for essential survival communications. Support for this position was drawn from recent studies of the great apes. However, there are some basic problems with this view of speech development in man. It assumes that what the great apes do now is what primitive humans did long ago. It also suggests that mankind has evolved over the millennia while the great apes have not. We do not have any evidence that such is the case. In fact, none of the authors or those cited in their references have ever heard the speech of a primitive person, or ever will. However, that does not stop them from telling us how such people spoke or what kind of signaling system was used. Stating that, ". . . evolutionary constraints strongly suggest that speech developed in part from a primitive nonlinguistic signaling system .. ." is much too assertive. The paralinguistic code has its own rules and is as elaborate as the linguistic code is. The argument could be made that both systems developed in parallel given the anatomical evidence. Recent research has pretty well established that language functions in humans are strongly associated with an abundance of cortical tissue in the planum temporale of the left hemisphere. This larger cortical area of the left planum temporale is reflected in a longer and more horizontal Sylvian fissure. In fact, Sylvian fissure length may be considered an indirect measure of this region in humans (Yeni-Komshian & Benson, 1976). The anatomical evidence indicates that this longer and more horizontal Sylvian fissure existed in primitive people as well (Galaburda, LeMay, Kemper, & Geschwind, 1978; LeMay, 1976). Since primitive people possessed the same left-right Sylvian fissure relationship as modem people, it is quite reasonable to assume that our ability to use a language symbol system developed in parallel with our nonverbal (nonlinguistic) communications. Speech prosody involves both left and right hemispheres of the brain (Heilman, Bowers, Speedie, & Coslett, 1984; Merewether & Alpert, 1990). These authors suggest that the left hemisphere is responsible for propositional prosody and the right for intentional-emotional prosody. If intentionalemotional prosody skills developed first, and apparently in the right hemisphere, what was the left hemisphere doing during this early period? Admittedly, neither my position nor that of Perkins et al. can be proven. Given the anatomical evidence for primitive humans, I find it as probable that both communication skills developed in parallel since both abilities seem to be functionally and inextricably linked. Besides, an ape is an ape, not a person.
John M. Christensen The University of Tulsa Tulsa, OK References Galaburda, A., LeMay, M., Kemper, T., & Geschwind, N. (1978). Right-left asymmetries in the brain. Science, 199, 852-856 (24 Feb.). Hellman, K., Bowers, D., Speedle, L., & Cosleftt, H. (1984). Comprehension of affective and noneffective prosody. Neurology, 34, 917-921. LeMay, M. (1976). Morphological cerebral asymmetries of modem man, fossil man and nonhuman primate. Annals of the New York Academy of Science, 280, 349-366. Merewether, F., & Alpert, M.(1990). The components and neuroanatomic bases of prosody. Journal of Communicative Disorders, 23, 325-336. Perkins, W., Kent, R., & Curlee, R. (1991). A theory of neuropsycholinguistic function instuttering. Journal of Speech and Hearing Research, 34, 734-752. Yenl-Komshlan, G., & Benson, D. (1976). Anatomical study of cerebral asymmetry inthe temporal lobe of humans, chimpanzees and Rhesus monkeys. Science, 192, 387-389. Received November 7, 1991 Accepted January 14, 1992
Commentary on "A Theory of Neuropsycholinguistic Function in Stuttering" KEY WORDS: stuttering, theories of speech production, speech neurophysiology Perkins, Kent, and Curlee (1991) propose a "neuropsycholinguistic" theory of stuttering that has at its core the hypothesis that stuttering is produced when the neural systems in the brain that generate the prosodic and phonetic components of speech interact with time pressure and become dyssynchronous. Also integral to the theory is the definition of stuttering, a disruption of speech experienced by the speaker as loss of control, proposed earlier by Perkins (1990). Perkins, Kent, and Curlee believe that this theory "saves the phenomena," that is, accounts for the known facts about stuttering, and makes useful empirical predictions to guide future research. I disagree. In the paragraphs that follow I suggest that this theory (a) does not incorporate experimental results relevant to the neural bases of speech production 805
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806 Journal of Speech and Hearing Research
and stuttering, (b) does not "save the phenomena" likely to be significant for the investigation of stuttering, and (c) saves instead a highly speculative model that is not clearly motivated by stutterers' speech error data. First, let us evaluate the extent to which the theory incorporates the known facts about stuttering and the neural bases of speech production. As an introduction to the theory, the reader is provided with discussions of a wide range of background topics. These discussions are remarkably general and often include long sections that apparently reflect the authors' personal beliefs and commentary about the topic at hand, for example, these three paragraphs: With speech, subtlety of expression has increased many-fold. Despite unlimited options for linguistic self-expression, credibility of communication of primitive needs still seems to rely on paralinguistic signals, as reflected insuch aphorisms as "Cutting tones belie soothing words." Thus, a speaker's true feelings and motives seem to be revealed most authentically by the signal system on which a spoken-language system has apparently been superimposed. Whether or not speech content also expresses the same feelings and motives depends on the speakers' communicative intent. If this analysis is accurate, the symbol system has been erected on a social communication signal system. As a result speakers can be in conflict in their management of these two systems. What might be the nature of self-expressive conflict? For an answer, we will turn to the origins and properties of the signal system. One of its ancestral functions, which we must have inherited, was to prevent bloodshed by use of vocal signals of dominance and submission. Once a hierarchy of dominance was established by combat before mating season, dominance and submission signals were used to preserve it. There is no reason to assume that such a successful function would disappear as itevolved inhumans. To the contrary, despite sophisticated human adaptations, males especially still show signs of struggling for dominance, as in activities such as sports, gangs, and contests. Striving for dominance appears to be a pervasive characteristic in humans, particularly inmales, as well as in lower animals (p. 738). We might reasonably assume that the authors do not have first-hand experience of all of these events, so we must ask where these ideas originate. Where are the citations to literature in the areas of anthropology, sports psychology, sociology, and so forth, to support these claims? It is also surprising to find that an aphorism is the only support offered for the authors' claim that information communicated by prosodic features takes precedence over information communicated by phonetic/linguistic features. Where are the experimental citations relevant to this issue? If there is not experimental support for these claims, why should the reader be persuaded by the beliefs of the authors concerning gender differences in participatory sports or the precedence of prosodic features? The absence of supporting data on the background topics is paralleled by the absence of citations to experimental work directly related to stuttering. The absence of an experimental context often leads to confusing and contradictory assertions. For example, Perkins, Kent, and Curlee state "Because stutterers, for the most part, speak normally most of the time, we do not assume that a pathologic condition is required to explain stuttering when it occurs" (p. 735). No research is cited to support the assertion that stutterers speak normally most of the time, but, as the authors are
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aware, many recent studies have addressed this issue (e.g., Conture, Colton, & Gleason, 1988; Freeman & Ushijima, 1978; Peters & Boves, 1988; Prosek, Montgomery, & Walden, 1988; Zimmermann, 1980a). Some of these investigations suggest that, even when people who stutter are producing speech that a listener would judge to be fluent, the stuttering person's speech production system shows signs of faulty operation (e.g., Peters & Boves, 1988; Zimmermann, 1980a). Furthermore, the logic here is unclear. The fact that a condition varies in severity over time or is intermittent is not necessarily a sign that there are not continuously present, abnormal, underlying conditions. For example, an individual may continuously test positive for the presence of the virus that produces human laryngeal papilloma, but the lesions associated with this disease may appear intermittently (Abramson, Steinberg, & Winkler, 1987). This analogy should not be interpreted to imply that people who stutter have a virus or a lesion in the brain. What is implied is that it is not known whether people who stutter have continuously present, abnormal, underlying factors that contribute to the disorder. The point is that the issues raised by Perkins et al. in this statement are empirical issues that have not been resolved experimentally. It is not clear why Perkins, Kent, and Curlee do not motivate their theory from experimental data, even when results directly relevant to their arguments are available. Considerable emphasis is given to the role in stuttering of neural systems underlying paralinguistic and emotional components of vocalization. The authors imply that the neural systems underlying primitive vocal signaling systems are precursors to those involved in generating the prosodic features of human speech (e.g., see the three paragraphs quoted above). No mention is made of what these neural systems actually may be, although the neural underpinnings of primate and nonprimate signaling systems have been explored by many researchers (e.g., see the collection of papers in Newman, 1986). A current focus of that literature, in fact, is a debate on whether there is a complete dissociation between neocortical vocal control pathways involved in speech and subcortical centers (such as the periaqueductal gray) that mediate emotional and reflexive vocalizations (e.g., Davis & Zhang, 1991). Likewise, in Perkins, Kent, and Curlee's discussion of an emotional component in stuttering, recent investigations (e.g., Peters & Hulstijn, 1984; Weber & Smith, 1990) of the autonomic correlates of stuttering are not mentioned. The results of these studies do not support the hypothesis that people who stutter, as a group, differ from nonstutterers in emotional reactivity to speaking. Rather, the results suggest that all speakers experience relatively high levels of autonomic arousal associated with speaking. Therefore, if emotional factors play a role in stuttering, it is more likely that people who stutter have an increased vulnerability of speech production processes to heightened autonomic arousal, rather than an increased "dominance conflict" (e.g., Perkins et al., p. 749). A second criterion by which we might evaluate the theory of Perkins, Kent, and Curlee, is one they invoke-that the theory must "save the known phenomena." One might ask:
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Letters
What phenomena does the theory of Perkins et al. save? Certainly, the body of experimental work that is relevant to the neural bases of fluent and disfluent speech production is not saved. In fact, the authors assert that the events in the speech motor system that accompany stuttering are irrelevant to the disorder "because the motor signals to the speech musculature produce movements that generate the acoustic signals of speech disruption, but these acoustic signals have been demonstrated to carry virtually no information about the essence of stuttering, the experience of loss of control (Moore & Perkins, 1990). The cause of this experience must be prior to generation of peripheral motor signals" (p. 740). With this statement the authors effectively throw away a very large number of phenomena associated with stuttering. Furthermore, it is in the motor control realm that we find a phenomenon characteristic of all individuals diagnosed as stuttering: stuttering is characterized by disruptions in speech motor processes. The authors' implication is that one can learn little by studying stutterers' motor behavior because everything that is "interesting" or "causal" happens before the motor output system is activated. There are many problems with such a conclusion. One problem is that it assumes a serially ordered model of language/speech production processes. The model of their Figure 1 (p. 740) is obviously intended by the authors to be very general, but despite its generality, it is misleading. The model does not reflect the potential importance of parallel processing and the existence of a variety of connections between the functional systems arbitrarily placed in separate boxes. For example, the paralinguistic vocalization system operates on the motor system only through "syllable slots" to the "integrator" system. Yet, neurophysiological and anatomical studies have demonstrated output pathways from subcortical "primitive" vocalization systems via brainstem nuclei to the abdominal, laryngeal, pharyngeal, and orofacial motomeuron pools that innervate muscles involved in vocalization (Holstege, 1989; Jurgens & Pratt, 1979). In other words, the experimental data do not support the hypothesis that neural centers for nonspeech vocalization access the motor system only through some (presumably cortical) "slot" and "integrator" systems. In sum, the conclusion that the motor system contains little information relevant to stuttering is ill-founded and arbitrary. It also closes the door on an area that for the last decade has been a promising avenue of research on stuttering (e.g., Peters & Hulstijn, 1987). Having commented on what the theory of Perkins et al. leaves out, let me turn to an assessment of what the theory leaves in: the "neuropsycholinguistic" functions that are the focus of the model. This theory begins with the assertion that the essence of stuttering is a feeling to which only the individual who stutters has access (see Smith, 1990b, for a longer commentary on Perkins' definition of stuttering). From that point, a case is built that the appropriate realm for stuttering research is a speculative model of neurolinguistic function, a model that draws little from neurophysiological concepts of brain function and that appears to be only loosely based on current cognitive-linguistic models of speech production (e.g., Dell, 1988; Levelt, 1989). The theory is an instantiation of what might be referred to as "key factor" models of stuttering. In the past there have been many other
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candidates for the role of "key factor" in stuttering, including auditory processing (Harrington, 1988), cerebral dominance (Orton, 1928), and parental reactions to young children's normal disfluencies (Johnson, 1955). The idea of a key to stuttering is attractive. Stuttering, however, is a complex and heterogeneous disorder, thus the number of phenomena that must be explained are unlikely to yield to a single, "key" factor. In order for a key-factor model to be successful, a myriad of experimental results must lead compellingly to that factor. Do the arguments of Perkins, Kent, and Curlee offer compelling evidence for the primacy of these systems in producing stuttering? The authors invoke the slots-and-fillers model of Shattuck-Hufnagel (1979, 1983, 1987) to develop their dyssynchrony hypothesis. Shattuck-Hufnagel's model was derived from a large corpus of speech error data in which it was found that about 40% of the errors were single-segment errors. The important point is that Shattuck-Hufnagel's model was empirically driven; it was developed to account for patterns of errors observed in a large speech corpus. Where are the error data from stuttering subjects that would motivate application of this model to stuttering? The speech errors made by stutterers that are widely reported in the literature (e.g., Johnson, 1961) would not be predicted by a breakdown in the levels of processing accounted for by the slots-and-fillers model of Shattuck-Hufnagel. The Perkins et al. dyssynchrony hypothesis would predict that stutterers would have the wrong phonemic units inserted into certain slots, so that they would make errors of the type accounted for by Shattuck-Hufnagel (e.g., "theep droat" for "deep throat"). The other prediction of the Perkins et al. theory is that correct phonemic elements would be inserted into the wrong suprasegmental frame, so that a stutterer might say "I hate you" with suprasegmental features appropriate for a different utterance. No error data are offered to support the use of such a model to account for stuttering behavior. Another question that one must raise is why time pressure would have its effect on the hypothetical slots-and-fillers level of speech/language processing. No data are offered to suggest that this level of processing would be particularly vulnerable to time pressure. One must consider that deficits in timing control could occur in many other processes related to speech production. Why wouldn't the execution process be vulnerable to time pressure? In sum, Perkins, Kent, and Curlee do not offer compelling experimental evidence to force our attention to the particular dyssynchrony hypotheses they favor. In conclusion, I would agree with Perkins et al. that we need an integrative theoretical framework for the investigation of stuttering; however it seems highly unlikely that any hypothesis seeking the "essence of" or "key to" stuttering will be successful. As Conture (1990) noted, these are unidimensional solutions to a multidimensional problem. What are the alternatives? Many workers in the area have recently adopted multifactorial models of stuttering (e.g., Conture, 1990; Smith, 1990 a,c; Starkweather, 1987; Van Riper, 1982; Wall & Myers, 1984; Zimmermann, 1980b). In many cases, these have not been detailed models with formal predictions; rather, the writers generally suggest that many different factors, including linguistic, cognitive, motoric, and sociocultural factors play a role in the development and
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maintenance of stuttering (e.g., Van Riper's "esoteric formula"). At this point in time, the types of factors that will probably emerge as significant in stuttering can be named; however, we have much to do before the role of many of the factors is understood well enough to allow the specification of a formal, integrated, multifactorial model of stuttering (Smith 1990a). What a multifactorial conceptual framework provides is a way to organize and integrate the diverse experimental results that seem likely to be important to an explanation of stuttering. My point of view is that, because all individuals diagnosed as stutterers show a breakdown in speech motor control processes, the motor system provides a useful, integrative window for a multifactorial account of stuttering. This theoretical framework was originally developed by Zimmermann (1980a) and has been expanded in a number of later papers (Smith, 1990 a,b,c; Smith & Weber, 1988; Zimmermann, Smith, &8Hanley, 1981). The major advantage of such a model is that it leads to specific, testable hypotheses conceming links between speech motor processes and psychological, linguistic, sociocultural, and other variables relevant to stuttering. For example, it has been found that increased autonomic arousal is associated with the occurrence and severity of disfluency in people who stutter (Weber & Smith, 1990). Our working model now leads us to develop empirical tests of the association between autonomic variables and observable parameters of speech motor breakdown in stuttering. The theory of Perkins, Kent, and Curlee, in contrast, does not lead to testable hypotheses. They write, "Our theory can be demonstrated to be irrelevant by disproving our assumptions or definitions" (p. 750). I would submit that it is not possible to test empirically the hypothesis that stuttering is experienced as a loss of control by the speaker. What does the term "loss of control" mean? Are the authors proposing to develop an experimental test of the sensation of dyssynchrony between hypothetical systems in the brain for prosodic and phonetic processing? The term "loss of control" cannot be defined, thus one is left to seek an experimental test of the "experience" of an undefined phenomenon (Smith, 1990b). In the final analysis, the neuropsycholinguistic theory of Perkins, Kent, and Curlee is built largely on beliefs and speculation about stuttering and speech production, and thus it cannot serve as a secure foundation for research and clinical practice in the area of stuttering. Anne Smith Purdue University West Lafayette, IN Acknowledgment My thanks to Jack Gandour for helpful discussions during the preparation of this commentary and to Edward Conture, Margaret Denny, Ellen Kelly, Laurence Leonard, and Robert Ringel for providing comments on an earlier draft of the manuscript. References Abramson, A. L., Steinberg, B.M., & Wlnkler, B. (1987). Laryngeal papillomatosis: Clinical, histopathologic and molecular studies. Laryngoscope, 97, 678-684.
Conture, E. G., Colton, R. H., & Gleason, J. R. (1988). Selected temporal aspects of coordination during fluent speech of young stutterers. Journal of Speech and Hearing Research, 31, 640-653. Conture, E. G. (1990). Stuttering (2nd ed.). Englewood Cliffs, NJ: Prentice Hall. Davis, P. J., & Zhang, S. P. (1991). What is the role of the midbrain periaqueductal gray in respiration and vocalization? Midbrain, 14, 57-66. Dell, G. S. (1988). The retrieval of phonological forms in production: Tests of predictions from a connectionist model. Journal of Memory and Language, 27, 124-142. Freeman, F.J., & Ushillma, T. (1978). Laryngeal muscle activity during stuttering. Journal of Speech and Hearing Research, 21, 538-562. Harrlngton, J. (1988). Stuttering, delayed auditory feedback, and linguistic rhythm. Journal of Speech and Hearing Research, 31, 36-17. Holstege, G. (1989). Anatomical study of the final common pathway for vocalization in the cat. The Journal of Comparative Neurology, 284, 242-252. Johnson, W. (1955). A study of the onset and development of stuttering. In W. Johnson & R. R. Leutenegger (Eds.), Stuttering in children and adults. Minneapolis: University of Minnesota Press. Johnson, W. (1961). Measurements of oral reading and speaking rate and disfluency of adult male and female stutterers and nonstutterers. Journal of Speech and Hearing Disorders, Monograph Supplement, 7, 1-20. Jurgens, U., & Pratt, R. (1979). Role of the periaqueductal grey in vocal expression of emotion. Brain Research, 167, 367-378. Levelt, W. J. M. (1989). Speaking: From intention to articulation. Cambridge, MA: The MIT press. Moore, S., & Perkins, W. (1990). Validity and reliability ofjudgments of authentic and simulated stuttering. Journal of Speech and Hearing Disorders, 55, 383-391. Newman, J. D. (Ed.) (1986). The physiological control of mammalian vocalization. New York, NY: Plenum Press. Orton, S. T. (1928). A physiological theory of reading disability and stuttering in children. New England Journal of Medicine, 199, 1045-1052. Perkins, W. (1990). What is stuttering? Journal of Speech and Hearing Disorders, 55, 370-382. Perkins, W. H., Kent, R. D., & Curlee, R. F. (1991). A theory of neuropsycholinguistic function in stuttering. Journal of Speech and Hearing Research, 34, 734-752. Peters, H. F. M., & Boves, L. (1988). Coordination of aerodynamic and phonatory processes in fluent speech utterances of stutterers. Journal of Speech and Hearing Research, 31, 352-361. Peters, H. R. M., & Hulstiln, W. (1984). Stuttering and anxiety: The difference between stutterers and nonstutterers in verbal apprehension and physiologic arousal during the anticipation of speech and non-speech tasks. Journal of Fluency Disorders, 9, 67-84. Peters, H. F. M., & Hulestln, W. (1987). (Eds.). Speech motor dynamics in stuttering. New York: Springer-Verlag. Prosek, R. A., Montgomery, A. A., & Walden, B. E. (1988). Constancy of relative timing for stutterers and nonstutterers. Journal of Speech and Hearing Research, 31, 654-658. Shattuck-Hufnagel, S. (1979). Speech errors as evidence for a serial order mechanism in sentence production. In W. E. Cooper & E. C. T. Walker (Eds.), Sentence processing: Psycholinguistic studies presented to Merrill Garrett. Hillsdale, NJ: Lawrence Erlbaum. Shattuck-Hufnagel, S. (1983). Sublexical units and suprasegmental structure in speech production planning. In P. R. MacNeilage (Ed.), The production of speech. New York: Springer. Shattuck-Hufnagel, S. (1987). The role of word onset consonants in speech production planning: New evidence from speech error pattems. In E. Keller & M. Gopnik (Eds.), Motor and Sensory Processing in Language. Hillsdale, NJ: Lawrence Erlbaum. Smith, A. (1990a). Factors in the etiology of stuttering. American Speech-Language Hearing Association Reports, Research Needs in Stuttering: Roadblocks and Future Directions, 18, 39-47.
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Letters Smith, A. (1990b). Towards a comprehensive theory of stuttering: A commentary. Journal of Speech and Hearing Disorders, 55, 398401. Smith, A. (1990c). An integrative multifactorial approach to stuttering. Paper presented to American Speech-Language-Hearing Association, Seattle. Smith, A., & Weber, C. M. (1988). The need for an integrated perspective on stuttering. American Speech-Language-Hearing Association, 30, 30-32. Starkweather, C.W. (1987). Fluency and stuttering. Englewood Cliffs, NJ: Prentice-Hall. Van Riper, C. (1982). The nature of stuttering (2nd ed.). Englewood Cliffs, NJ: Prentice-Hall. Wall, M., & Myers, F. (1984). Clinical management of childhood stuttering. Baltimore, MD: University Park Press.
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Weber, C. M., & Smith, A. (1990). Autonomic correlates of stuttering and speech assessed in a range of experimental tasks. Journal of Speech and Hearing Research, 33, 690-706. Zlmmermann, G. (1980a). Articulatory dynamics of fluent utterances of stutterers and nonstutterers. Journal of Speech and Hearing Research, 23, 95-107. Zimmermann, G. (1980b). Stuttering: A disorder of movement. Journal of Speech and Hearing Research, 23, 122-136. Zimmermann, G., Smith, A., & Hanley, J. (1981). Stuttering: In need of a unifying conceptual framework. Journal of Speech and Hearing Research, 24, 25-31. Received October 17, 1991 Accepted November 19, 1991
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Using an unprovable hypothesis as part of a theory of stuttering does not help in testing the theory. We already have too many untestable stuttering theories.
Perkins, Kent, and Curlee (1991) argue in their theory of neurolinguistic function in stuttering that our speech developed in part from a primitive nonlinguistic signaling system that was used for essential survival communications. Support for this position was drawn from recent studies of the great apes. However, there are some basic problems with this view of speech development in man. It assumes that what the great apes do now is what primitive humans did long ago. It also suggests that mankind has evolved over the millennia while the great apes have not. We do not have any evidence that such is the case. In fact, none of the authors or those cited in their references have ever heard the speech of a primitive person, or ever will. However, that does not stop them from telling us how such people spoke or what kind of signaling system was used. Stating that, ". . . evolutionary constraints strongly suggest that speech developed in part from a primitive nonlinguistic signaling system .. ." is much too assertive. The paralinguistic code has its own rules and is as elaborate as the linguistic code is. The argument could be made that both systems developed in parallel given the anatomical evidence. Recent research has pretty well established that language functions in humans are strongly associated with an abundance of cortical tissue in the planum temporale of the left hemisphere. This larger cortical area of the left planum temporale is reflected in a longer and more horizontal Sylvian fissure. In fact, Sylvian fissure length may be considered an indirect measure of this region in humans (Yeni-Komshian & Benson, 1976). The anatomical evidence indicates that this longer and more horizontal Sylvian fissure existed in primitive people as well (Galaburda, LeMay, Kemper, & Geschwind, 1978; LeMay, 1976). Since primitive people possessed the same left-right Sylvian fissure relationship as modem people, it is quite reasonable to assume that our ability to use a language symbol system developed in parallel with our nonverbal (nonlinguistic) communications. Speech prosody involves both left and right hemispheres of the brain (Heilman, Bowers, Speedie, & Coslett, 1984; Merewether & Alpert, 1990). These authors suggest that the left hemisphere is responsible for propositional prosody and the right for intentional-emotional prosody. If intentionalemotional prosody skills developed first, and apparently in the right hemisphere, what was the left hemisphere doing during this early period? Admittedly, neither my position nor that of Perkins et al. can be proven. Given the anatomical evidence for primitive humans, I find it as probable that both communication skills developed in parallel since both abilities seem to be functionally and inextricably linked. Besides, an ape is an ape, not a person.
John M. Christensen The University of Tulsa Tulsa, OK References Galaburda, A., LeMay, M., Kemper, T., & Geschwind, N. (1978). Right-left asymmetries in the brain. Science, 199, 852-856 (24 Feb.). Hellman, K., Bowers, D., Speedle, L., & Cosleftt, H. (1984). Comprehension of affective and noneffective prosody. Neurology, 34, 917-921. LeMay, M. (1976). Morphological cerebral asymmetries of modem man, fossil man and nonhuman primate. Annals of the New York Academy of Science, 280, 349-366. Merewether, F., & Alpert, M.(1990). The components and neuroanatomic bases of prosody. Journal of Communicative Disorders, 23, 325-336. Perkins, W., Kent, R., & Curlee, R. (1991). A theory of neuropsycholinguistic function instuttering. Journal of Speech and Hearing Research, 34, 734-752. Yenl-Komshlan, G., & Benson, D. (1976). Anatomical study of cerebral asymmetry inthe temporal lobe of humans, chimpanzees and Rhesus monkeys. Science, 192, 387-389. Received November 7, 1991 Accepted January 14, 1992
Commentary on "A Theory of Neuropsycholinguistic Function in Stuttering" KEY WORDS: stuttering, theories of speech production, speech neurophysiology Perkins, Kent, and Curlee (1991) propose a "neuropsycholinguistic" theory of stuttering that has at its core the hypothesis that stuttering is produced when the neural systems in the brain that generate the prosodic and phonetic components of speech interact with time pressure and become dyssynchronous. Also integral to the theory is the definition of stuttering, a disruption of speech experienced by the speaker as loss of control, proposed earlier by Perkins (1990). Perkins, Kent, and Curlee believe that this theory "saves the phenomena," that is, accounts for the known facts about stuttering, and makes useful empirical predictions to guide future research. I disagree. In the paragraphs that follow I suggest that this theory (a) does not incorporate experimental results relevant to the neural bases of speech production 805
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806 Journal of Speech and Hearing Research
and stuttering, (b) does not "save the phenomena" likely to be significant for the investigation of stuttering, and (c) saves instead a highly speculative model that is not clearly motivated by stutterers' speech error data. First, let us evaluate the extent to which the theory incorporates the known facts about stuttering and the neural bases of speech production. As an introduction to the theory, the reader is provided with discussions of a wide range of background topics. These discussions are remarkably general and often include long sections that apparently reflect the authors' personal beliefs and commentary about the topic at hand, for example, these three paragraphs: With speech, subtlety of expression has increased many-fold. Despite unlimited options for linguistic self-expression, credibility of communication of primitive needs still seems to rely on paralinguistic signals, as reflected insuch aphorisms as "Cutting tones belie soothing words." Thus, a speaker's true feelings and motives seem to be revealed most authentically by the signal system on which a spoken-language system has apparently been superimposed. Whether or not speech content also expresses the same feelings and motives depends on the speakers' communicative intent. If this analysis is accurate, the symbol system has been erected on a social communication signal system. As a result speakers can be in conflict in their management of these two systems. What might be the nature of self-expressive conflict? For an answer, we will turn to the origins and properties of the signal system. One of its ancestral functions, which we must have inherited, was to prevent bloodshed by use of vocal signals of dominance and submission. Once a hierarchy of dominance was established by combat before mating season, dominance and submission signals were used to preserve it. There is no reason to assume that such a successful function would disappear as itevolved inhumans. To the contrary, despite sophisticated human adaptations, males especially still show signs of struggling for dominance, as in activities such as sports, gangs, and contests. Striving for dominance appears to be a pervasive characteristic in humans, particularly inmales, as well as in lower animals (p. 738). We might reasonably assume that the authors do not have first-hand experience of all of these events, so we must ask where these ideas originate. Where are the citations to literature in the areas of anthropology, sports psychology, sociology, and so forth, to support these claims? It is also surprising to find that an aphorism is the only support offered for the authors' claim that information communicated by prosodic features takes precedence over information communicated by phonetic/linguistic features. Where are the experimental citations relevant to this issue? If there is not experimental support for these claims, why should the reader be persuaded by the beliefs of the authors concerning gender differences in participatory sports or the precedence of prosodic features? The absence of supporting data on the background topics is paralleled by the absence of citations to experimental work directly related to stuttering. The absence of an experimental context often leads to confusing and contradictory assertions. For example, Perkins, Kent, and Curlee state "Because stutterers, for the most part, speak normally most of the time, we do not assume that a pathologic condition is required to explain stuttering when it occurs" (p. 735). No research is cited to support the assertion that stutterers speak normally most of the time, but, as the authors are
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aware, many recent studies have addressed this issue (e.g., Conture, Colton, & Gleason, 1988; Freeman & Ushijima, 1978; Peters & Boves, 1988; Prosek, Montgomery, & Walden, 1988; Zimmermann, 1980a). Some of these investigations suggest that, even when people who stutter are producing speech that a listener would judge to be fluent, the stuttering person's speech production system shows signs of faulty operation (e.g., Peters & Boves, 1988; Zimmermann, 1980a). Furthermore, the logic here is unclear. The fact that a condition varies in severity over time or is intermittent is not necessarily a sign that there are not continuously present, abnormal, underlying conditions. For example, an individual may continuously test positive for the presence of the virus that produces human laryngeal papilloma, but the lesions associated with this disease may appear intermittently (Abramson, Steinberg, & Winkler, 1987). This analogy should not be interpreted to imply that people who stutter have a virus or a lesion in the brain. What is implied is that it is not known whether people who stutter have continuously present, abnormal, underlying factors that contribute to the disorder. The point is that the issues raised by Perkins et al. in this statement are empirical issues that have not been resolved experimentally. It is not clear why Perkins, Kent, and Curlee do not motivate their theory from experimental data, even when results directly relevant to their arguments are available. Considerable emphasis is given to the role in stuttering of neural systems underlying paralinguistic and emotional components of vocalization. The authors imply that the neural systems underlying primitive vocal signaling systems are precursors to those involved in generating the prosodic features of human speech (e.g., see the three paragraphs quoted above). No mention is made of what these neural systems actually may be, although the neural underpinnings of primate and nonprimate signaling systems have been explored by many researchers (e.g., see the collection of papers in Newman, 1986). A current focus of that literature, in fact, is a debate on whether there is a complete dissociation between neocortical vocal control pathways involved in speech and subcortical centers (such as the periaqueductal gray) that mediate emotional and reflexive vocalizations (e.g., Davis & Zhang, 1991). Likewise, in Perkins, Kent, and Curlee's discussion of an emotional component in stuttering, recent investigations (e.g., Peters & Hulstijn, 1984; Weber & Smith, 1990) of the autonomic correlates of stuttering are not mentioned. The results of these studies do not support the hypothesis that people who stutter, as a group, differ from nonstutterers in emotional reactivity to speaking. Rather, the results suggest that all speakers experience relatively high levels of autonomic arousal associated with speaking. Therefore, if emotional factors play a role in stuttering, it is more likely that people who stutter have an increased vulnerability of speech production processes to heightened autonomic arousal, rather than an increased "dominance conflict" (e.g., Perkins et al., p. 749). A second criterion by which we might evaluate the theory of Perkins, Kent, and Curlee, is one they invoke-that the theory must "save the known phenomena." One might ask:
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Letters
What phenomena does the theory of Perkins et al. save? Certainly, the body of experimental work that is relevant to the neural bases of fluent and disfluent speech production is not saved. In fact, the authors assert that the events in the speech motor system that accompany stuttering are irrelevant to the disorder "because the motor signals to the speech musculature produce movements that generate the acoustic signals of speech disruption, but these acoustic signals have been demonstrated to carry virtually no information about the essence of stuttering, the experience of loss of control (Moore & Perkins, 1990). The cause of this experience must be prior to generation of peripheral motor signals" (p. 740). With this statement the authors effectively throw away a very large number of phenomena associated with stuttering. Furthermore, it is in the motor control realm that we find a phenomenon characteristic of all individuals diagnosed as stuttering: stuttering is characterized by disruptions in speech motor processes. The authors' implication is that one can learn little by studying stutterers' motor behavior because everything that is "interesting" or "causal" happens before the motor output system is activated. There are many problems with such a conclusion. One problem is that it assumes a serially ordered model of language/speech production processes. The model of their Figure 1 (p. 740) is obviously intended by the authors to be very general, but despite its generality, it is misleading. The model does not reflect the potential importance of parallel processing and the existence of a variety of connections between the functional systems arbitrarily placed in separate boxes. For example, the paralinguistic vocalization system operates on the motor system only through "syllable slots" to the "integrator" system. Yet, neurophysiological and anatomical studies have demonstrated output pathways from subcortical "primitive" vocalization systems via brainstem nuclei to the abdominal, laryngeal, pharyngeal, and orofacial motomeuron pools that innervate muscles involved in vocalization (Holstege, 1989; Jurgens & Pratt, 1979). In other words, the experimental data do not support the hypothesis that neural centers for nonspeech vocalization access the motor system only through some (presumably cortical) "slot" and "integrator" systems. In sum, the conclusion that the motor system contains little information relevant to stuttering is ill-founded and arbitrary. It also closes the door on an area that for the last decade has been a promising avenue of research on stuttering (e.g., Peters & Hulstijn, 1987). Having commented on what the theory of Perkins et al. leaves out, let me turn to an assessment of what the theory leaves in: the "neuropsycholinguistic" functions that are the focus of the model. This theory begins with the assertion that the essence of stuttering is a feeling to which only the individual who stutters has access (see Smith, 1990b, for a longer commentary on Perkins' definition of stuttering). From that point, a case is built that the appropriate realm for stuttering research is a speculative model of neurolinguistic function, a model that draws little from neurophysiological concepts of brain function and that appears to be only loosely based on current cognitive-linguistic models of speech production (e.g., Dell, 1988; Levelt, 1989). The theory is an instantiation of what might be referred to as "key factor" models of stuttering. In the past there have been many other
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candidates for the role of "key factor" in stuttering, including auditory processing (Harrington, 1988), cerebral dominance (Orton, 1928), and parental reactions to young children's normal disfluencies (Johnson, 1955). The idea of a key to stuttering is attractive. Stuttering, however, is a complex and heterogeneous disorder, thus the number of phenomena that must be explained are unlikely to yield to a single, "key" factor. In order for a key-factor model to be successful, a myriad of experimental results must lead compellingly to that factor. Do the arguments of Perkins, Kent, and Curlee offer compelling evidence for the primacy of these systems in producing stuttering? The authors invoke the slots-and-fillers model of Shattuck-Hufnagel (1979, 1983, 1987) to develop their dyssynchrony hypothesis. Shattuck-Hufnagel's model was derived from a large corpus of speech error data in which it was found that about 40% of the errors were single-segment errors. The important point is that Shattuck-Hufnagel's model was empirically driven; it was developed to account for patterns of errors observed in a large speech corpus. Where are the error data from stuttering subjects that would motivate application of this model to stuttering? The speech errors made by stutterers that are widely reported in the literature (e.g., Johnson, 1961) would not be predicted by a breakdown in the levels of processing accounted for by the slots-and-fillers model of Shattuck-Hufnagel. The Perkins et al. dyssynchrony hypothesis would predict that stutterers would have the wrong phonemic units inserted into certain slots, so that they would make errors of the type accounted for by Shattuck-Hufnagel (e.g., "theep droat" for "deep throat"). The other prediction of the Perkins et al. theory is that correct phonemic elements would be inserted into the wrong suprasegmental frame, so that a stutterer might say "I hate you" with suprasegmental features appropriate for a different utterance. No error data are offered to support the use of such a model to account for stuttering behavior. Another question that one must raise is why time pressure would have its effect on the hypothetical slots-and-fillers level of speech/language processing. No data are offered to suggest that this level of processing would be particularly vulnerable to time pressure. One must consider that deficits in timing control could occur in many other processes related to speech production. Why wouldn't the execution process be vulnerable to time pressure? In sum, Perkins, Kent, and Curlee do not offer compelling experimental evidence to force our attention to the particular dyssynchrony hypotheses they favor. In conclusion, I would agree with Perkins et al. that we need an integrative theoretical framework for the investigation of stuttering; however it seems highly unlikely that any hypothesis seeking the "essence of" or "key to" stuttering will be successful. As Conture (1990) noted, these are unidimensional solutions to a multidimensional problem. What are the alternatives? Many workers in the area have recently adopted multifactorial models of stuttering (e.g., Conture, 1990; Smith, 1990 a,c; Starkweather, 1987; Van Riper, 1982; Wall & Myers, 1984; Zimmermann, 1980b). In many cases, these have not been detailed models with formal predictions; rather, the writers generally suggest that many different factors, including linguistic, cognitive, motoric, and sociocultural factors play a role in the development and
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maintenance of stuttering (e.g., Van Riper's "esoteric formula"). At this point in time, the types of factors that will probably emerge as significant in stuttering can be named; however, we have much to do before the role of many of the factors is understood well enough to allow the specification of a formal, integrated, multifactorial model of stuttering (Smith 1990a). What a multifactorial conceptual framework provides is a way to organize and integrate the diverse experimental results that seem likely to be important to an explanation of stuttering. My point of view is that, because all individuals diagnosed as stutterers show a breakdown in speech motor control processes, the motor system provides a useful, integrative window for a multifactorial account of stuttering. This theoretical framework was originally developed by Zimmermann (1980a) and has been expanded in a number of later papers (Smith, 1990 a,b,c; Smith & Weber, 1988; Zimmermann, Smith, &8Hanley, 1981). The major advantage of such a model is that it leads to specific, testable hypotheses conceming links between speech motor processes and psychological, linguistic, sociocultural, and other variables relevant to stuttering. For example, it has been found that increased autonomic arousal is associated with the occurrence and severity of disfluency in people who stutter (Weber & Smith, 1990). Our working model now leads us to develop empirical tests of the association between autonomic variables and observable parameters of speech motor breakdown in stuttering. The theory of Perkins, Kent, and Curlee, in contrast, does not lead to testable hypotheses. They write, "Our theory can be demonstrated to be irrelevant by disproving our assumptions or definitions" (p. 750). I would submit that it is not possible to test empirically the hypothesis that stuttering is experienced as a loss of control by the speaker. What does the term "loss of control" mean? Are the authors proposing to develop an experimental test of the sensation of dyssynchrony between hypothetical systems in the brain for prosodic and phonetic processing? The term "loss of control" cannot be defined, thus one is left to seek an experimental test of the "experience" of an undefined phenomenon (Smith, 1990b). In the final analysis, the neuropsycholinguistic theory of Perkins, Kent, and Curlee is built largely on beliefs and speculation about stuttering and speech production, and thus it cannot serve as a secure foundation for research and clinical practice in the area of stuttering. Anne Smith Purdue University West Lafayette, IN Acknowledgment My thanks to Jack Gandour for helpful discussions during the preparation of this commentary and to Edward Conture, Margaret Denny, Ellen Kelly, Laurence Leonard, and Robert Ringel for providing comments on an earlier draft of the manuscript. References Abramson, A. L., Steinberg, B.M., & Wlnkler, B. (1987). Laryngeal papillomatosis: Clinical, histopathologic and molecular studies. Laryngoscope, 97, 678-684.
Conture, E. G., Colton, R. H., & Gleason, J. R. (1988). Selected temporal aspects of coordination during fluent speech of young stutterers. Journal of Speech and Hearing Research, 31, 640-653. Conture, E. G. (1990). Stuttering (2nd ed.). Englewood Cliffs, NJ: Prentice Hall. Davis, P. J., & Zhang, S. P. (1991). What is the role of the midbrain periaqueductal gray in respiration and vocalization? Midbrain, 14, 57-66. Dell, G. S. (1988). The retrieval of phonological forms in production: Tests of predictions from a connectionist model. Journal of Memory and Language, 27, 124-142. Freeman, F.J., & Ushillma, T. (1978). Laryngeal muscle activity during stuttering. Journal of Speech and Hearing Research, 21, 538-562. Harrlngton, J. (1988). Stuttering, delayed auditory feedback, and linguistic rhythm. Journal of Speech and Hearing Research, 31, 36-17. Holstege, G. (1989). Anatomical study of the final common pathway for vocalization in the cat. The Journal of Comparative Neurology, 284, 242-252. Johnson, W. (1955). A study of the onset and development of stuttering. In W. Johnson & R. R. Leutenegger (Eds.), Stuttering in children and adults. Minneapolis: University of Minnesota Press. Johnson, W. (1961). Measurements of oral reading and speaking rate and disfluency of adult male and female stutterers and nonstutterers. Journal of Speech and Hearing Disorders, Monograph Supplement, 7, 1-20. Jurgens, U., & Pratt, R. (1979). Role of the periaqueductal grey in vocal expression of emotion. Brain Research, 167, 367-378. Levelt, W. J. M. (1989). Speaking: From intention to articulation. Cambridge, MA: The MIT press. Moore, S., & Perkins, W. (1990). Validity and reliability ofjudgments of authentic and simulated stuttering. Journal of Speech and Hearing Disorders, 55, 383-391. Newman, J. D. (Ed.) (1986). The physiological control of mammalian vocalization. New York, NY: Plenum Press. Orton, S. T. (1928). A physiological theory of reading disability and stuttering in children. New England Journal of Medicine, 199, 1045-1052. Perkins, W. (1990). What is stuttering? Journal of Speech and Hearing Disorders, 55, 370-382. Perkins, W. H., Kent, R. D., & Curlee, R. F. (1991). A theory of neuropsycholinguistic function in stuttering. Journal of Speech and Hearing Research, 34, 734-752. Peters, H. F. M., & Boves, L. (1988). Coordination of aerodynamic and phonatory processes in fluent speech utterances of stutterers. Journal of Speech and Hearing Research, 31, 352-361. Peters, H. R. M., & Hulstiln, W. (1984). Stuttering and anxiety: The difference between stutterers and nonstutterers in verbal apprehension and physiologic arousal during the anticipation of speech and non-speech tasks. Journal of Fluency Disorders, 9, 67-84. Peters, H. F. M., & Hulestln, W. (1987). (Eds.). Speech motor dynamics in stuttering. New York: Springer-Verlag. Prosek, R. A., Montgomery, A. A., & Walden, B. E. (1988). Constancy of relative timing for stutterers and nonstutterers. Journal of Speech and Hearing Research, 31, 654-658. Shattuck-Hufnagel, S. (1979). Speech errors as evidence for a serial order mechanism in sentence production. In W. E. Cooper & E. C. T. Walker (Eds.), Sentence processing: Psycholinguistic studies presented to Merrill Garrett. Hillsdale, NJ: Lawrence Erlbaum. Shattuck-Hufnagel, S. (1983). Sublexical units and suprasegmental structure in speech production planning. In P. R. MacNeilage (Ed.), The production of speech. New York: Springer. Shattuck-Hufnagel, S. (1987). The role of word onset consonants in speech production planning: New evidence from speech error pattems. In E. Keller & M. Gopnik (Eds.), Motor and Sensory Processing in Language. Hillsdale, NJ: Lawrence Erlbaum. Smith, A. (1990a). Factors in the etiology of stuttering. American Speech-Language Hearing Association Reports, Research Needs in Stuttering: Roadblocks and Future Directions, 18, 39-47.
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Letters Smith, A. (1990b). Towards a comprehensive theory of stuttering: A commentary. Journal of Speech and Hearing Disorders, 55, 398401. Smith, A. (1990c). An integrative multifactorial approach to stuttering. Paper presented to American Speech-Language-Hearing Association, Seattle. Smith, A., & Weber, C. M. (1988). The need for an integrated perspective on stuttering. American Speech-Language-Hearing Association, 30, 30-32. Starkweather, C.W. (1987). Fluency and stuttering. Englewood Cliffs, NJ: Prentice-Hall. Van Riper, C. (1982). The nature of stuttering (2nd ed.). Englewood Cliffs, NJ: Prentice-Hall. Wall, M., & Myers, F. (1984). Clinical management of childhood stuttering. Baltimore, MD: University Park Press.
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Weber, C. M., & Smith, A. (1990). Autonomic correlates of stuttering and speech assessed in a range of experimental tasks. Journal of Speech and Hearing Research, 33, 690-706. Zlmmermann, G. (1980a). Articulatory dynamics of fluent utterances of stutterers and nonstutterers. Journal of Speech and Hearing Research, 23, 95-107. Zimmermann, G. (1980b). Stuttering: A disorder of movement. Journal of Speech and Hearing Research, 23, 122-136. Zimmermann, G., Smith, A., & Hanley, J. (1981). Stuttering: In need of a unifying conceptual framework. Journal of Speech and Hearing Research, 24, 25-31. Received October 17, 1991 Accepted November 19, 1991
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