Neurology -- Correspondence for Foundas et al., 57 (2) 207-215

Correspondence published:

Reply to Dr Perkins: David B Rosenfield (25 September 2001)

Anomalous anatomy of speech–language areas in adults with persistent developmental stuttering: William H Perkins (25 September 2001)

Reply to Dr Perkins 25 September 2001

David B Rosenfield
Baylor College of Medicine Houston TX
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Re: Reply to Dr Perkins

davidr{at}bcm.tmc.edu David B Rosenfield

Briefly, Dr. Perkins’ contends that the cerebrum, especially Broca’s and Wernicke’s Areas, is cognitively and linguistically too slow to process high-speed speech sounds. He mistakenly presumes that cerebral processing for speech is purely sequential and, if he is willing to accept the importance of subcortical and cerebellar mechanisms in the control of phonation/articulation, overlooks their important cortical connections. [3, 4, 5]
Miller’s thesis of the Magic Number Seven involves paradigms of memory, not solely the mode of thinking.[2] Believing that “syllable and cognitive thinking rates turn out to be roughly the same…” would mean that we think no faster than we talk, which has absolutely no basis in neuropsychology. [3, 4, 5]
We do not select the sounds within our sentences from the larynx or other non-brain structures, any more than our gall bladder tells us what food to buy or our kidney chooses our beverage. Whether the selection and control of our sound output resides in our cortical or subcortical networks, negating cerebral influence leaves what alternative? [3, 4, 5]
Simply put, when speaking, the message-to-be-communicated develops in stages and the output of one stage provides input to the other; planning and programming of speech in chunk-sized units precedes their actual production, making it likely that low-speed cognitive/linguistic equipment can indeed produce high-speed speech sounds There is evidence (within the brain) for a rhetorical/semantic/syntactic system, which controls lexico- syntactic structures, as well as a phonological/phonetic system, which generates articulatory shapes. Both systems, whose functions temporally overlap, can access the mental lexicon. The former system can also access relevant memories and the latter access the mental syllabary. [4, 6]
Further, recent data focus on left inferior frontal cortex and right motor/pre-motor cortex as relevant in merging linguistic and affective prosody in speech-motor output, a system possibly disrupted in stutterers. [7]
Scientific inquiry focuses on testable hypotheses with alternative models. Seemingly, Dr. Perkins does not dispute Foundas’ et al data. [1] Therefore, what is the significance of their findings? True, the cortical aberrations they elegantly describe may not be causal to stuttering—they could result from stuttering behaviors or be phenomena. Regardless, the authors do not infer direct causality but, rather, contend that anomalous anatomy is a risk factor for the development of stuttering.
The lack of a genuine nosology for stuttering has obfuscated our attempts to find the etiology for this malady.. Unfortunately, the area of speech pathology includes many ailments in which the symptom, sign, and disease process are interchangeable and isomorphic (i.e., one has the symptom of stuttering, the sign of stuttering, and is diagnosed as a stutterer). Imagine were that the standard approach to back pain or coma!
Foundas’ et al data provides a possible nosology for stuttering. [1] Such information can sequester different stutterers based upon shared/different anomalous cortical structures, recognizing inputs and ouputs to subcortical systems, and point the way for future novel genetic, imaging, clinical, and therapeutic approaches.
References:
1. Foundas Al, Bollich AM, Corey DM, Hurley M, Heilmann KM. Anomalous anatomy of speech-language areas in adults with persistent of developmental stuttering. Neurology 2001;57:207-215.
2. Miller G. The psychology of communication. New York, NY: Basic Books, 1967.
3. Kandel ER, Schwartz JH, Jessell TM. Principles of Neural Science. New York: McGraw Hill, 2000:1169-1187.
4. Indefrey P, Levelt WJM. The neural correlates of language production. In: Gazzaniga MS, ed, The new cognitive neurosciences. Cambridge, Mass: MIT Press, 2000; 1169-1187.
5. Mesulam MM. Principles of behavioral and cognitive neurology. New York: Oxford, 2000.
6. Levelt WJM. Speaking: From intention to articulation. Cambridge, Mass: MIT Press, 1989.
7. Salmelin R, Schnitzler F, Schmitz F, Freund HJ. Single word reading in developmental stutters and fluent speakers. Brain 2000;123:1184-1202.

Anomalous anatomy of speech–language areas in adults with persistent developmental stuttering 25 September 2001

William H Perkins
University of California Los Angeles, CA
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Re: Anomalous anatomy of speech–language areas in adults with persistent developmental stuttering

w.h.perkins{at}us.net William H Perkins

I read with interest the recently published paper by Foundas et al., which is the latest in a line of neurologic reports that confuse cause and effect of stuttering (stammering). [1] The observations associated with this clinical problem of chronic involuntary blockage are not disputed. That these observations can be interpreted as a cause of blockage is neurologically impossible.
Because unintended blockage of speech is an aberration of normal speech processing, which is a manifestation of synchronization of phonation (for speech power) with articulation (that shapes phonatory power into the sounds of speech), the essence of fluent speech is timing of speech sound phonatory/articulatory synchronization.
Any cause of blockage has to account for why it can be involuntary (otherwise it would never become chronic), and more to the point, how high -speed speech sounds can be produced with low-speed, cognitive/linguistic equipment.
Synchronization speed is revealed by the syllable rate (no sound can be produced outside the context of a syllable) multiplied by the number of sounds per syllable. Syllable and cognitive thinking rates turn out to be roughly the same, which is fortunate, otherwise we would be unable to speak at the same rates we think. George Miller, decades ago, demonstrated the cognitive rate to be 7+/-2 per second. [2]
Inadvertently in 1964, I discovered this is also the syllable rate when I found that voluntary fluency prevented stammering when each sound is under voluntary control. Unfortunately for treatment, each sound had to be a syllable unto itself, which resulted in a speech rate so slow that it, droned. [3]
Natural speech consists of syllables with up to six or more sounds per syllable. Thus, sounds in the word “sounds” are synchronized at about 25 to 45 per second (7 plus or minus 2 syllables per second times 5 syllable. Thus, sounds in the word “sounds” are synchronized at about 25 to 45 per second (7 plus or minus 2 syllables per second times 5 articulatory adjustments per five sound syllable).
In 1965, Stromsta defined stammering as a static involuntary articulatory posture that blocks fluent overlapping coarticulatory transitions. [4] This definition was confirmed by being the basis of predictions of recovery for 63 two-to-four-year-olds suspected of early stammering. The outcomes that were verified ten years later, every child who showed the defining signs of stammering had become chronic, the others spoke normally.
The reason the Tulane study cannot have causal implications for stammering is because the enlarged linguistic areas of Broca and Wernicke are intimately related to the slow cognitive function rates Miller described, and are readily available to voluntary control that disqualifies them as a cause of involuntary blockage. Wernicke’s area is for speech perception and Broca’s area for speech planning. Aside from the fact that neither can operate at rates even close to speech synchronization rates, Wernicke’s area is far too slow to have any role in the timing of high-speed speech. Broach’s area, although it provides the specifications for speech-sound production, it likewise too slow to have any role in the timing of high-speed phonatory/articulatory synchronization. It is when timing is awry that stammering occurs. Thus, the investigators postulate “that anomalous cerebral dominance, reflected by anomalous cortical anatomy in various regions, may put an individual at increased risk for the development of stuttering” (stammering) reports a consequence of chronic stammering, not a cause. It should be noted that Lee Edward Travis, the primary author of the cerebral dominance theory, tested and rejected it in the mid 1930’s as a cause of stammering. [5]
Complex as this letter may seem, it merely scratches the surface of normal speech production, let alone stammering and its causes. The Tulane study and others like them that attempt, by implication, to suggest an underlying cerebral disorder as a basis of stammering is contradicted by how the neural mechanism of speech is organized. The cerebrum has nothing to do with high-speed speech timing.
References
1) Foundas AL, Bollich AM, Corey DM, Hurley M, Heilmann KM. Anomalous anatomy of speech-language areas in adults with persistent of developmental stuttering. Neurology 2001;57:207-215.
2) Miller G. The psychology of communication. New York City NY: Basic Books, 1967.
3) Perkins WH. Neural mechanisms of stammering. Reno NV: Athens Press, in press.
4) Stromsta C. Elements of stuttering. Oshtermo, MI: Atsmorts Publishing, 1986.
5) Travis L. Personal communication, 1962.
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