Thalamic-Induced Stuttering (Surgical Observations) Repetitive dysfluencies of speech were elicited by mechanical perturbation of the thalamus in a patient, preparatory to therapeutic lesion placement for chronic pain Perturbation consisted of a 2 mm advancement of a 1 mm diameter electrode in the posteroventromedial thalamus. A thalamogram revealed electropathologic discharges at the site of perturbation. ... Research Note
Research Note  |   August 01, 1991
Thalamic-Induced Stuttering (Surgical Observations)
 
Author Affiliations & Notes
  • Orlando J. Andy
    Department of Neurosurgery University of Mississippi Medical Center
  • Subhash C. Bhatnagar
    Department of Speech Pathology and Audiology Marquette University and Department of Neurosurgery University of Mississippi Medical Center
  • Requests for reprints should be sent to Subhash C. Bhatnagar, Department of Speech Pathology and Audiology, Marquette University, Milwaukee, WI 53233.
Article Information
Speech / Research Notes
Research Note   |   August 01, 1991
Thalamic-Induced Stuttering (Surgical Observations)
Journal of Speech, Language, and Hearing Research, August 1991, Vol. 34, 796-800. doi:10.1044/jshr.3404.796
History: Received May 15, 1990 , Accepted October 16, 1990
 
Journal of Speech, Language, and Hearing Research, August 1991, Vol. 34, 796-800. doi:10.1044/jshr.3404.796
History: Received May 15, 1990; Accepted October 16, 1990

Repetitive dysfluencies of speech were elicited by mechanical perturbation of the thalamus in a patient, preparatory to therapeutic lesion placement for chronic pain Perturbation consisted of a 2 mm advancement of a 1 mm diameter electrode in the posteroventromedial thalamus. A thalamogram revealed electropathologic discharges at the site of perturbation. These findings are of special interest anatomically because in other patients, electrical stimulation at the same site was found to alleviate stuttering (Andy, 1987; Andy, 1989; Andy & Jurko, 1985; Bhatnagar & Andy, 1989). It is suggested that dysfluencies in this patient may have resulted from an electrophysiologic disturbance of the mesothalamic component of a speech-regulating corticomesothalamic feedback circuit.

Acknowledgment
We thank Franklin H. Silverman for his comments on an early version of this paper and Ann Marie Dybas for her assistance in the preparation of the manuscript. A part of this research was presented at the American Speech-Language Hearing Association Annual Convention in Cincinnati, November 1983. This research, in its present form, was read at the Annual Meeting of the Pavlovian Society of North America in Philadelphia, September 1990
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