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    • It is important to acknowledge a second COMT

    2020-07-31

    It is important to acknowledge a second COMT (COMT2), which is related to COMT1 that regulates dopamine levels in the brain, is widely expressed in inner and outer hair cells of the cochlea. A mutation to a COMT2 shows defects in cochlear function in both mice and humans that are related to hearing loss or deafness phenotype (Du et al., 2008). Hence, it is possible that COMT can also be attributed to a peripheral component that affects hearing and tinnitus. Due to this association, it is possible that COMT could have an impact on tinnitus due to a hearing impairment that is not measurable with a pure tone audiogram (i.e. “hidden hearing loss”) but that might contribute to our findings. Furthermore, research suggests that the COMT Val158Met polymorphism influences the human experience of pain and may underlie interindividual differences in the N-acetyl D-galactosamine australia and responses to pain and other stressful stimuli (Zubieta et al., 2003). Previous research also revealed the existence of an alternative neuronal pathway from the cochlea to the brainstem that is activated by tissue-damaging noise, possibly by type-II cochlear afferents, representing auditory nociception (Flores et al., 2015). As Met carriers are more sensitive to pain, it might be that these subjects respond in a different way to noise induced tinnitus in comparison to Val/Val homozygotes. Progress in finding a treatment for tinnitus has been hampered by the fact that tinnitus represents a highly heterogeneous condition (Schecklmann et al., 2012, 2013). Hence, it was suggested that there might be different subtypes of tinnitus. Our research fits with this idea, showing that there might be different subtypes of tinnitus depending on, for example, the underlying COMT genotype. Further studies should be performed evaluating these results with other functional imaging techniques as well as neuromodulation techniques to confirm this idea of subtyping. It has already been shown, for example, that the effect of tDCS on auditory hallucinations—which can be considered a complex form of tinnitus, analogous to hallucinosis (Vanneste et al., 2013)—depends on the COMT polymorphism (Wiegand et al., 2016). Although the control group and tinnitus group do not significantly differ based on age, gender or hearing loss, a limitation of this study is that the control group is only group-matched, and not individually matched. Furthermore, we only tested hearing acuity in tinnitus patients via standard pure tone audiometry, i.e. limited to 8000 Hz. Recent research has shown that tinnitus can occur in relationship with hearing loss at supra-clinical frequencies (i.e. above 8000 Hz) (Melcher et al., 2013). Future research should also include a high-frequency audiogram as well as audiometric data for healthy subjects. Another limitation is that we did not use a MRI to map the source. In theory, there is no problem in doing EEG source reconstruction, but the way it is computed, is more convoluted and opens up for more potential errors. The major difference is that to construct a lead field for EEG, a volume conductor model that models several compartments in the head—the inner skull, the skull, and the outer skin—is needed. Three layers means more room for errors. However, the areas obtained in this study were already confirmed using structural and functional MRI (Leaver et al., 2011) as well intracranial EEG recordings (electrocorticography, ECoG) (Sedley et al., 2015). In addition, we merged the Val/Met carriers and Met/Met carriers due to a low sample size of Met/Met carriers. Further research in a larger sample could also look at the difference between Val/Met and Met/Met carriers. It is possible that there is a genetic dosage or gradual effect. That is, an effect in the phenotype observed in the heterozygous genotype (Val/Met) that becomes more pronounced in the homozygous (Met/Met).