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Updated: Apr 25, 2026

Mapping the After-effects of Theta Burst Stimulation on the Human Auditory Cortex with Functional Imaging
Published on: September 12, 2012
Targeting the parahippocampal area by auditory cortex stimulation in tinnitus
Dirk De Ridder1, Sven Vanneste2
1Brai²n, Sint Augustinus Hospital, Antwerp, Belgium; Department of Surgical Sciences, Section of Neurosurgery, Dunedin School of Medicine, University of Otago, New Zealand.
Background:
The final common pathway in tinnitus generation is considered to be synchronized auditory oscillatory hyperactivity. Intracranial auditory cortex stimulation (iACS) via implanted electrodes has been developed to treat severe cases of intractable tinnitus targeting this final common pathway, in the hope of being a panacea for tinnitus. However, not everybody responds to this treatment.
Objective:
The electrical brain activity and functional connectivity at rest might determine who is going to respond or not to iACS and might shed light on the pathophysiology of auditory phantom sound generation.
Method:
The resting state electrical brain activity of 5 patients who responded and 5 patients who did not respond to auditory cortex implantation are compared using source localized spectral activity (Z-score of log transformed current density) and lagged phase synchronization.
Results:
sLORETA source localization reveals significant differences between responders vs non-responders for beta3 in left posterior parahippocampal, hippocampal and amygdala area extending into left insula. Gamma band differences exist in the posterior parahippocampal areas and BA10. Functional connectivity between the auditory cortex and the hippocampal area is increased for beta2, delta and theta2 in responders, as well as between the parahippocampal area and auditory cortex for beta3.
Conclusion:
The resting state functional connectivity and activity between the auditory cortex and parahippocampus might determine whether a tinnitus patient will respond to a cortical implant. The auditory cortex may only be a functional entrance into a larger parahippocampal based tinnitus network.
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