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Response to “Stuttering prevention II:” Deja Vu, again
J. FLUENCY DISORD. 17 t 1992). X7-88
COMMENTARY:
HAMRE
I1
RESPONSE TO “STUTTERING PREVENTION II:” DEJA VU, AGAIN
In this second article, I again will leave response to specific hypotheses and studies to other readers. Dr. Hamre criticizes (justifiably) past/ present orientations concerning the origin and development of stuttering. His target continues to be Johnson, Bloodstein, and the Iowa ilk. As before, much of his criticism is directed against the idea that “all” stuttering has a uniform point of origin. 1 think he speaks to an idea whose time has come-some time ago. Rather than leading the charge, I think he is echoing what many authors have been saying and teaching for the past two or three decades. In criticizing the universality of the assumptions he questions, he tends to summate in generalized allisms that are as vulnerable to criticism as the assumptions he criticizes. On a particular point-Dr. Hamre argues that disfluency is not an acceptable baseline or source for dystluency, since “. . . people continue to be quite disfluent throughout their lives . . .” (see p. 74, this issue). In that case, then, “fluency” is not a normal human communication attribute, and stuttering must be regarded as coming out of disfluency. Because we have no functional definition of ‘fluency,” it may be that it is a nonfunctional referent for his purposes. In the end. Dr. Hamre suggests that “. . . it is at least compatible with our science to infer that such first appearance [of stuttering] signifies a lack of CNS integrity” (see p. 75, this issue). This is the kind of generalization Hamre attacks so vigorously in other sections of the two articles. It also puts him right back in the clutches of Iowans Lee Travis, Samuel Orton, and a generation of (dysphemia, pyknolepsy, lateral dominance, etc) Iowa theorists. One also may entertain more recent speculations on neural integrity (Ham, 1991, pp. 35-38). Overall, Dr. Hamre’s articles seem to culminate in the following observations by this writer:
Address correspondence to Dr. Richard E. Ham. Department of CommunicationDisorders. The Florida State University. Tallahassee. FL 32306-2007.
81992 by Elaevier Science Publishing CO.. Inc.
655Avenue
of the America\. New York. NY 10010
a7 0094-730x/9?1$3.50
K.HAM
88
I. Evidence does not support the idea that all stuttering develops from normal disfluency-but neither does it support the contention that no stuttering develops from normal (‘?) disfluency. 2. Parental concern, or over-concern, may or may not be an etiologic agent. However, it could be operative in situations in which predisposition exists (neural integrity ‘?). Also, reduction/dismissal of parents as etiologic agents does not affect the issue of parental significance as precipitating, developing, and/or maintaining elements in stuttering. 3. Saying that stuttering may, or may not, “. . become chronic or more severe over time” is suspect, as Dr. Hamre does not define stuttering. Is he discussing disfluency or dysfluency? His assumption that spontaneously remissed fluency deviations are/were “stuttering” is as debatable as any definition of stuttering we currently argue over. 4. “Prevention” of stuttering cannot be justified, according to the author. In his context, that is true because we do not know what he means by “stuttering.” Basically, it would seem appropriate to continue doing exactly what we have been doing before-but change our rationales for doing them. The bottom line is the question of how Dr. Hamre’s speculations provide a foundation for elimination, revision, and addition within our current frameworks of diagnosis, evaluation, and management of stuttering. As of this writing, I find no changes apparent that do not exist already. I will wait for Dr. Hamre’s third article, Stuttering Pre\>ention III: Applications and Procedures.
REFERENCES Ham, R. E. (1990) Therapy of Stuttering, cence. Englewood Cliffs, NJ: Prentice Manuscript
submitted
and accepted
June
Preschool Hall. 1992.
Through
Adoles-
COMMENTARY:
HAMRE
I1
RESPONSE TO “STUTTERING PREVENTION II:” DEJA VU, AGAIN
In this second article, I again will leave response to specific hypotheses and studies to other readers. Dr. Hamre criticizes (justifiably) past/ present orientations concerning the origin and development of stuttering. His target continues to be Johnson, Bloodstein, and the Iowa ilk. As before, much of his criticism is directed against the idea that “all” stuttering has a uniform point of origin. 1 think he speaks to an idea whose time has come-some time ago. Rather than leading the charge, I think he is echoing what many authors have been saying and teaching for the past two or three decades. In criticizing the universality of the assumptions he questions, he tends to summate in generalized allisms that are as vulnerable to criticism as the assumptions he criticizes. On a particular point-Dr. Hamre argues that disfluency is not an acceptable baseline or source for dystluency, since “. . . people continue to be quite disfluent throughout their lives . . .” (see p. 74, this issue). In that case, then, “fluency” is not a normal human communication attribute, and stuttering must be regarded as coming out of disfluency. Because we have no functional definition of ‘fluency,” it may be that it is a nonfunctional referent for his purposes. In the end. Dr. Hamre suggests that “. . . it is at least compatible with our science to infer that such first appearance [of stuttering] signifies a lack of CNS integrity” (see p. 75, this issue). This is the kind of generalization Hamre attacks so vigorously in other sections of the two articles. It also puts him right back in the clutches of Iowans Lee Travis, Samuel Orton, and a generation of (dysphemia, pyknolepsy, lateral dominance, etc) Iowa theorists. One also may entertain more recent speculations on neural integrity (Ham, 1991, pp. 35-38). Overall, Dr. Hamre’s articles seem to culminate in the following observations by this writer:
Address correspondence to Dr. Richard E. Ham. Department of CommunicationDisorders. The Florida State University. Tallahassee. FL 32306-2007.
81992 by Elaevier Science Publishing CO.. Inc.
655Avenue
of the America\. New York. NY 10010
a7 0094-730x/9?1$3.50
K.HAM
88
I. Evidence does not support the idea that all stuttering develops from normal disfluency-but neither does it support the contention that no stuttering develops from normal (‘?) disfluency. 2. Parental concern, or over-concern, may or may not be an etiologic agent. However, it could be operative in situations in which predisposition exists (neural integrity ‘?). Also, reduction/dismissal of parents as etiologic agents does not affect the issue of parental significance as precipitating, developing, and/or maintaining elements in stuttering. 3. Saying that stuttering may, or may not, “. . become chronic or more severe over time” is suspect, as Dr. Hamre does not define stuttering. Is he discussing disfluency or dysfluency? His assumption that spontaneously remissed fluency deviations are/were “stuttering” is as debatable as any definition of stuttering we currently argue over. 4. “Prevention” of stuttering cannot be justified, according to the author. In his context, that is true because we do not know what he means by “stuttering.” Basically, it would seem appropriate to continue doing exactly what we have been doing before-but change our rationales for doing them. The bottom line is the question of how Dr. Hamre’s speculations provide a foundation for elimination, revision, and addition within our current frameworks of diagnosis, evaluation, and management of stuttering. As of this writing, I find no changes apparent that do not exist already. I will wait for Dr. Hamre’s third article, Stuttering Pre\>ention III: Applications and Procedures.
REFERENCES Ham, R. E. (1990) Therapy of Stuttering, cence. Englewood Cliffs, NJ: Prentice Manuscript
submitted
and accepted
June
Preschool Hall. 1992.
Through
Adoles-