In major depressive disorder (MDD), event-related potentials that are involved in auditory cortex function (i.e. N100 and P300) often have greater latencies and decreased amplitudes. The auditory mismatch negativity (MMN) is thought to be produced by generators in the auditory cortex, as well as the frontal lobes. Reports on differences in MMN in those with MDD have been varied. It was hypothesized that the wide range of results in the literature may be due to the use of different deviant types in eliciting the MMN. To attempt and explain these inconsistencies, the current study employed a multifeature MMN paradigm with 5 deviant tone types in community-dwelling participants with a diagnosis of MDD. We found those with MDD had higher MMN amplitudes following tones that deviated in intensity and location, but no difference in MMNs elicted by the other deivants (relative to unaffected controls). Location MMN deviants were negatively correlated with depression severity scores (i.e. larger MMN with greater severity). We also found longer MMN latencies following the pitch deviant. These results suggest the early auditory change detection process is altered in MDD, but only following certain types of auditory stimuli. Potential explanations for these findings, including high levels of anxiety and the influence of tryptophan are explored. Equally, the current report highlights the importance of using various deviant types when examining the MMN in clinical populations.
Individuals with schizophrenia use twice as much caffeine on average when compared to healthy controls. Knowing the high rates of consumption, and the potential negative effects of such, it is important we understand the cortical mechanisms that underlie caffeine use, and the consequences of caffeine use on neural circuits in this population. Using a randomized, placebo controlled, double-blind, repeated measures design, the current study examines caffeine's effects on resting electroencephalography (EEG) power in those who have been recently diagnosed with schizophrenia (SZ) compared to regular-using healthy controls (HC). Correlations between average caffeine consumption, withdrawal symptoms, drug related symptoms and clinical psychosis symptoms were measured and significant correlations with neurophysiological data were examined. Results showed caffeine had no effect on alpha asymmetry in the SZ group, although caffeine produced a more global effect on the reduction of alpha2 power in the SZ group. Further, those with more positive symptoms were found to have a greater reduction in alpha2 power following caffeine administration. Caffeine also reduced beta power during eyes closed and eyes open resting in HC, but only during eyes closed resting conditions in the SZ group. These findings provide a descriptive profile of the resting EEG state following caffeine administration in individuals with schizophrenia. The findings ultimately suggest caffeine does not affect alpha or beta power as readily in this population and a higher dose may be needed to achieve the desired effects, which may elucidate motivational factors for high caffeine use.
Cannabis has been shown to cause structural and functional neurocognitive changes in heavy users. Cannabis use initiation aligns with brain development trajectories; therefore, it is imperative that the potential neurological implications of cannabis use are understood. Males and females reach neurodevelopmental milestones at different rates making it necessary to consider biological sex in all cannabis and brain-based research. Through use of a systamatic review in accordance with PRISMA guidelines, we aimed to understand the interaction between biological sex and cannabis use on brain-based markers. In total, 18 articles containing a sex-based analysis of cannabis users were identified. While the majority of studies ( n = 11) reported no sex by cannabis use interactions on brain-based markers, those that reported findings ( n = 8) suggest females may be more susceptible to cannabis’ neurotoxic effects. Unfortunately, a large portion of the literature was excluded due to no sex-based analysis. In addition, studies that reported no sex differences often contained a reduced number of females which may result in some studies being underpowered for sex-based analyses, making it difficult to draw firm conclusions. Suggestions to improve cannabis and sex-based reseach are proposed.
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