David B.Rosenfield, Director, Speech and Language Center, Neurological institute, Methodist Hospital; Professor, Weill Medical College of Cornell Universitydrosenfield@tmhs.org
Submitted September 07, 2012
The article by Lu et al. [1] and accompanying editorial by Dr. Kell [2] document successful therapy treatment for people who stutter by examining normalized brain imaging connectivity between the speech network and the supplementary motor area and also decreased resting-state functional connectivity with the midline cerebellum.
The authors and Dr. Kell note brain activity at rest (not speaking) and provide a window into what might transpire in brain activity during a task-dependent state (speaking, fluently or otherwise). The obfuscating factor is that if stuttering is a response to an underlying abnormality and not the abnormality itself, then the meaning of the data becomes suspect. For example we have long queried whether stuttering is the speaker's response to an instability in an altered speech-motor-auditory feedback loop. [3,4] Documented improvement of stuttering behavior/output may be a valid finding, but only in so far as this improvement is a response to the underlying deficit causing stuttering (e.g., stuttering is a response to that deficit) and not directly reflect any improvement in the deficit.
The "core" of the stuttered response remains and may have nothing to do with the changes in imaging at rest, during speech, or following therapy.
1. Lu C, Chen C, Peng D, et al. Neural anomaly and reorganization in
speakers who stutter: a short-term intervention study. Neurology 2012; 79:625-632.
2. Kell, CA, Resting-state MRI: A peek through the keyhole on therapy for
stuttering. Neurology 2012; 614-615.
3. Nudelman HB, Hoyt B, Herbrich KE, and Rosenfield DB. A neuroscience
model of stuttering. J Fluency Disord 1989; 14:399-427.
4. Rosenfield DB. Stuttering and Dysfluency. In: Stemmer B,
Whitaker HA, editors. Handbook of the Neuroscience of Language, London,
England: Academic Press; 2008: 309-318.
For disclosures, contact the editorial office at journal@neurology.org.
The article by Lu et al. [1] and accompanying editorial by Dr. Kell [2] document successful therapy treatment for people who stutter by examining normalized brain imaging connectivity between the speech network and the supplementary motor area and also decreased resting-state functional connectivity with the midline cerebellum.
The authors and Dr. Kell note brain activity at rest (not speaking) and provide a window into what might transpire in brain activity during a task-dependent state (speaking, fluently or otherwise). The obfuscating factor is that if stuttering is a response to an underlying abnormality and not the abnormality itself, then the meaning of the data becomes suspect. For example we have long queried whether stuttering is the speaker's response to an instability in an altered speech-motor-auditory feedback loop. [3,4] Documented improvement of stuttering behavior/output may be a valid finding, but only in so far as this improvement is a response to the underlying deficit causing stuttering (e.g., stuttering is a response to that deficit) and not directly reflect any improvement in the deficit. The "core" of the stuttered response remains and may have nothing to do with the changes in imaging at rest, during speech, or following therapy.
1. Lu C, Chen C, Peng D, et al. Neural anomaly and reorganization in speakers who stutter: a short-term intervention study. Neurology 2012; 79:625-632. 2. Kell, CA, Resting-state MRI: A peek through the keyhole on therapy for stuttering. Neurology 2012; 614-615. 3. Nudelman HB, Hoyt B, Herbrich KE, and Rosenfield DB. A neuroscience model of stuttering. J Fluency Disord 1989; 14:399-427.
4. Rosenfield DB. Stuttering and Dysfluency. In: Stemmer B, Whitaker HA, editors. Handbook of the Neuroscience of Language, London, England: Academic Press; 2008: 309-318.
For disclosures, contact the editorial office at journal@neurology.org.