La EMT-r (rTMS) sobre la corteza temporal, bloquea la producción del habla ; sobre la corteza DLPF , impide la memoria de tarea , y , sobre la corteza occipital induce defectos visuales (fosfenos ) . Estos fenómenos disruptivos temporarios se utilizan en neurología con fines diagnósticos y de investigación.

 

Speech Apraxia During Low Rate Transcranial Magnetic Stimulation (TMS) to Dorsolateral Frontal Cortex

Shalini Narayana , Nitin Tandon , Roger Ingham , Jan Ingham , Michael Martinez , Jack L. Lancaster , Steven Dodd , Jinhu Xiong , Peter T. Fox

Research Imaging Center, University of Texas Health Science Center at San Antonio
Division of Neurosurgery, University of Texas Health Science Center at San Antonio
Department of Speech and Hearing Sciences, Univeristy of California at Santa Barbara

Abstract

Introduction
A major drawback of high stimulus rates used in surgical procedures (50-60Hz) and high rate TMS (15-30Hz) to localize language areas is the absence of differentiation of function. Further, there is no consensus on the location of speech arrest, rate, and the mechanism of action of high rate TMS (Table 1)(1-5). We report the identification and localization of a frontal area in the language dominant hemisphere which causes speech apraxia in normals using low rate TMS.

Methods
Six normals were fitted with a cap marked with the 10-20 electrode system (6). Under video monitoring, rTMS was delivered over left and right frontal regions at 4 Hz in 5 second trains. While subjects read aloud, the TMS coil was moved anteriorly and laterally from C3/C4, until speech was disrupted. The position of TMS coil on the scalp producing speech disruption was marked with lipid capsules which were identifiable on MRI. A 3D aMRI, and fMRI while subjects performed a silent verb generation task were acquired.

Results
4 Hz rTMS over left D3 and D5 areas (6) produced reproducible speech apraxia in all volunteers, the hallmark of which was cessation of fluent reading and utterance of repetitive and meaningless syllables. All subjects could not get past the word they were reading at the start of rTMS. Silent reading and comprehension were preserved. Review of video recording confirmed that contractions of facial muscles and tongue were not causing this apraxia. rTMS of the homologous location in the right hemisphere produced a milder apraxia in one subject. fMRI of verb generation task confirmed the left hemisphere language dominance in all subjects. An additional activation (-32, 40, 24) corresponding to BA 9/8 was identified. In 3 subjects, this cortical area was directly beneath the fiducial where TMS was applied (Figure 1). In others, the cortical area beneath the fiducial (-47, 4, 44) was identified to be lateral premotor cortex (BA6).

Conclusion
The location of speech apraxia area reported here is in agreement with published speech arrest reports (2,4,5). Activation of lateral premotor cortex in articulatory planning has been demonstrated in a PET study (7). Our data supports this, and indicates that the mechanism of action of rTMS is by interference with articulatory processing in the dominant hemisphere, and not by interrupting short term memory or by direct motor interference. However, unlike other reports, we have demonstrated that low rate TMS can produce speech disruption. With its ability to locate language areas and identify their function, low rate TMS of language areas may bridge the gap between high rate TMS and surgical procedures, which identify only location of language areas, and lesion data which are more indicative of the function of individual regions.

References
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