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Updated: Apr 25, 2026
Cochlear Implant Surgery and Electrically-evoked Auditory Brainstem Response Recordings in C57BL/6 Mice
Published on: January 9, 2019
Neural substrates of conversion deafness in a cochlear implant patient: a molecular imaging study using H₂¹⁵O-PET
Jae-Jin Song1, Griet Mertens, Steven Deleye
1*Department of Otorhinolaryngology-Head and Neck Surgery, Seoul National University Bundang Hospital, Seongnam, Korea; †Department of Otorhinolaryngology and Head and Neck Surgery, University Hospital Antwerp, Edegem, Belgium; ‡Molecular Imaging Center, University of Antwerp, Edegem, Belgium; §School of Behavioral and Brain Sciences, The University of Texas at Dallas, Dallas, Texas, U.S.A.; ∥Department of Translational Neuroscience, Faculty of Medicine, University of Antwerp, Edegem, Belgium; ¶Department of Surgical Sciences, Section of Neurosurgery, Dunedin School of Medicine, University of Otago, Dunedin, New Zealand; #BRAI2N, Sint Augustinus Hospital, Antwerp, Belgium; and **Department of Neuropsychiatry, Seoul National University Bundang Hospital, Seongnam, Korea.
Objective:
Conversion deafness is characterized by sudden hearing loss without any identifiable cause. In the current study, we investigated presumed conversion deafness in a cochlear implant user using H₂¹⁵O-positron emission tomography (PET) scan with speech and noise stimuli in conjunction with audiologic tests such as impedance test and auditory response telemetry. Also, by performing a follow-up PET scan after recovery and comparing prerecovery and postrecovery scans, we attempted to find possible neural substrates of conversion deafness.
Patient:
A 51-year-old man with conversion deafness after 4 years of successful cochlear implant use.
Intervention:
Supportive psychotherapy.
Main Outcome Measures:
Prerecovery and postrecovery H₂¹⁵O-PET scans
Results:
The prerecovery H₂¹⁵O-PET scan revealed auditory cortex activation by sound stimuli, which verified normal stimulation of the central auditory pathway. Notably, compared with the prerecovery state, the postrecovery state showed relative activation in the right auditory cortex both under the speech and noise stimulus conditions. Moreover, the bilateral prefrontal and parietal areas were activated more in the postrecovery state than in the prerecovery state. In other words, relative deactivation of the prefronto-parieto-temporal network, a network responsible for conscious sensory perception, or relative dysfunction of top-down and bottom-up attention shifting mediated by the ventral and the dorsal parietal cortices, may have resulted in conversion deafness in the patient.
Conclusion:
Relative deactivation of the prefronto-parieto-temporal network or dysfunction in the ventral and the dorsal parietal cortices may be related to the development of conversion deafness.
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