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  • Although the control group and tinnitus group do not

    2019-10-17

    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 Spautin-1 (Val/Met) that becomes more pronounced in the homozygous (Met/Met). In conclusion, our results show that the interaction between the level of hearing loss and the COMT Val158Met polymorphism can increase the susceptibility to the clinical manifestation of tinnitus. We demonstrated that the PHC becomes involved in tinnitus in patients with hearing loss that are Met carriers. The PHC sends more tinnitus related information to the pgACC and AUD that is related with increased loudness perception, but at the same time the pgACC, which normally functions as a gatekeeper, is not cancelling this auditory information, leading to increased tinnitus loudness.
    Conflicts of interest
    Significance statement Permanently affecting one in seven adults, chronic tinnitus lacks both widely effective treatments and adequate understanding of its brain mechanisms. This is largely due to the fact that tinnitus represents a highly heterogeneous condition. Consistent with this idea, our research shows that tinnitus indeed has different subtypes related to the underlying neurogenetic architecture of hearing loss induced tinnitus. We establish, in a human study tightly controlled for hearing loss, that the amount of hearing loss and the COMT Val158Met polymorphism can increase the susceptibility to the clinical manifestation of tinnitus that goes together with not cancelling auditory information, leading to increased tinnitus loudness.
    Introduction With an estimate between 128 million and 238 million users, cannabis is the most widely used illicit substance in the world (United Nations Office on Drugs and Crime, 2017). It produces a broad range of acute, dose-dependent psychotropic effects, such as ‘feeling high’, relaxation and euphoria, which are regarded as the main reasons why people use cannabis (Green et al., 2004, Mané et al., 2015). In addition, cannabis has been shown to acutely induce increased heart rate, perceptual alterations and psychotic symptoms (Ashton, 2001, Hall and Degenhardt, 2009, Sherif et al., 2016), and to impair cognitive functions such as learning and memory (Bossong et al., 2014a, Broyd et al., 2016). Finally, epidemiological studies indicate that the use of cannabis increases the risk for developing schizophrenia (Marconi et al., 2016, Moore et al., 2007, Vaucher et al., 2017). These effects are primarily produced through action of ∆9-tetrahydrocannabinol (THC), the main psychoactive ingredient of cannabis, on the cannabinoid 1 (CB1) receptor (Huestis et al., 2001; Ledent, 1999).