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Perturbation of the left inferior frontal gyrus triggers adaptive plasticity in the right homologous area during speech production

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Citation

Hartwigsen, G., Saur, D., Price, C. J., Ulmer, S., Baumgaertner, A., & Siebner, H. R. (2013). Perturbation of the left inferior frontal gyrus triggers adaptive plasticity in the right homologous area during speech production. Proceedings of the National Academy of Sciences of the United States of America, 110(41), 16402-16407. doi:10.1073/pnas.1310190110.


Cite as: http://hdl.handle.net/11858/00-001M-0000-0028-AB0B-9
Abstract
The role of the right hemisphere in aphasia recovery after left hemisphere damage remains unclear. Increased activation of the right hemisphere has been observed after left hemisphere damage. This may simply reflect a release from transcallosal inhibition that does not contribute to language functions. Alternatively, the right hemisphere may actively contribute to language functions by supporting disrupted processing in the left hemisphere via interhemispheric connections. To test this hypothesis, we applied off-line continuous theta burst stimulation (cTBS) over the left inferior frontal gyrus (IFG) in healthy volunteers, then used functional MRI to investigate acute changes in effective connectivity between the left and right hemispheres during repetition of auditory and visual words and pseudowords. In separate sessions, we applied cTBS over the left anterior IFG (aIFG) or posterior IFG (pIFG) to test the anatomic specificity of the effects of cTBS on speech processing. Compared with cTBS over the aIFG, cTBS over the pIFG suppressed activity in the left pIFG and increased activity in the right pIFG during pseudoword vs. word repetition in both modalities. This effect was associated with a stronger facilitatory drive from the right pIFG to the left pIFG during pseudoword repetition. Critically, response became faster as the influence of the right pIFG on left pIFG increased, indicating that homologous areas in the right hemisphere actively contribute to language function after a focal left hemisphere lesion. Our findings lend further support to the notion that increased activation of homologous right hemisphere areas supports aphasia recovery after left hemisphere damage.