Abstract
This study aimed to explore brain surface-based morphometry cortical thickness changes in patients with idiopathic tinnitus before and after 24 weeks of sound therapy. In this prospective observational study, we recruited 33 tinnitus patients who had undergone 24 weeks of sound therapy and 26 matched healthy controls. For the two groups of subjects, a 3D-BRAVO pulse sequence was acquired both at baseline and at the 24th week. Structural image data preprocessing was performed using the DPABISurf toolbox. The Tinnitus Handicap Inventory (THI) score was assessed to determine the severity of tinnitus before and after treatment. Two-way mixed-model analysis of variance (ANOVA) and Pearson’s correlation analysis were used in the statistical analysis. Student–Newman–Keuls (SNK) tests were used in the post hoc analysis. Significantly lower cortical thickness was found in the left somatosensory and motor cortex (SMC), left posterior cingulate cortex (PCC), and right orbital and polar frontal cortex (OPFC) of the participants in the tinnitus group at baseline than in the participants in the HC group at baseline and after 24 weeks; in the tinnitus group, significantly higher cortical thickness was found after the 24 weeks sound therapy in comparison to the baseline in the left SMC, bilateral superior parietal cortex (SPC), left inferior parietal cortex (IPC), left PCC, and right OPFC. In the HC group, no statistically significant difference in cortical thickness was found after the 24 weeks treatment in comparison to the baseline in the bilateral SMC, bilateral SPC, left IPC, left PCC, or right OPFC. The changes in cortical thickness before and after sound therapy can provide certain reference values for clinical tinnitus treatment. These brain regions could serve as potential targets for neuroimaging.
Highlights
Tinnitus is characterized by the ability to hear sound in the ears or head without any external stimulation (Wegger et al, 2017; Bauer, 2018)
Lower cortical thickness was found in the left somatosensory and motor cortex (SMC), left posterior cingulate cortex (PCC), and right orbital and polar frontal cortex (OPFC) in the tinnitus group at baseline than in the healthy control (HC) group at baseline and after 24 weeks (Figure 2)
Significantly higher cortical thickness was found after the 24 weeks sound therapy in comparison to the baseline in the left SMC, bilateral superior parietal cortex (SPC), left inferior parietal cortex (IPC), left PCC, and right OPFC
Summary
Tinnitus is characterized by the ability to hear sound in the ears or head without any external stimulation (Wegger et al, 2017; Bauer, 2018). In addition to hearing impairments, annoying tinnitus is often associated with sleep disorders, depression, anxiety, and other mental illnesses and severely impairs patients’ quality of life (Reynolds et al, 2004; Langguth et al, 2013; Zeman et al, 2014). These disorders can further exacerbate tinnitus (Bhatt et al, 2017). Previous studies have shown that tinnitus can cause significant changes in brain function and structure, which were closely related to the clinical manifestations of patients (Ryu et al, 2016; Schmidt et al, 2017; Han et al, 2019a)
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