Neural Substrates of Tinnitus in an Auditory Brainstem Implant Patient: A Preliminary Molecular Imaging Study Using H215O-PET Including a 5-Year Follow-Up of Auditory Performance and Tinnitus Perception

Annick Gilles 1,2,3 Jae-Jin Song 4 Anouk Hofkens 1 Griet Mertens 2 Cordula Matthies 5 Steven Deleye 6 Steven Staelens 6 Sarah Ceyssens 6 Sigrid Stroobants 6 Paul Van de Heyning 1,2
1Department of Otorhinolaryngology - Head and Neck Surgery, Antwerp University Hospital, Edegem, Belgium
2Department of Translational Neurosciences, Antwerp University, Antwerp, Belgium
3Department of Human and Social Welfare, University College Ghent, Ghent, Belgium
4Department of Otorhinolaryngology - Head and Neck Surgery, Seoul National University Bundang Hospital, Seongnam, South Korea
5Department of Neurosurgery, University Hospital Würzburg, Würzburg, Germany
6Molecular Imaging Centre, University Antwerp, Antwerp, Belgium

Introduction: It is currently unknown whether stimulation through ABI renders tinnitus reduction in patients with incapacitating tinnitus. The current case study reports on the subjective tinnitus perception during a five-year follow-up period. In addition, a first H215O PET imaging study in an ABI patient is carried out revealing underlying neural substrates of tinnitus.

Methods: A 56-year old male single-sided deaf ABI patient with incapacitating tinnitus was assessed in this study. Audiological follow-up is carried out during a five-year follow-up period. In order to investigate the neural substrates of tinnitus in this subject H215O PET tomography scans were acquired in 3 different conditions with various effects of the ABI on tinnitus reduction: ABI OFF, ABI ON and ABI ON + noise stimulation.

Results: Subjectively the patient reported a significant tinnitus reduction after implantation which remained stable over time during the five-year period. Comparing the ABI OFF and ABI ON condition significant increase of rCBF was observed in brain areas involved in the salience network showing immediate suppression of tinnitus only by electrical stimulation in the absence of auditory stimuli. The NOISE condition showed relatively decreased rCBF in the insula (as well as in the orbitofrontal cortex) as compared with the ABI OFF condition. Abnormally activated areas comprising the salience network may have been significantly suppressed by the NOISE condition both by acoustic and electrical stimulations of the auditory pathway.

Conclusion: The reduction of tinnitus in the current ABI subject may be attributable to partial peripheral reafferentation-induced deactivation of the PHC-based tinnitus generator as well as the salience network.









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