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IntroductionObstructive sleep apnoea (OSA) is more prevalent in men. Several studies suggested that higher testosterone levels were associated with a greater risk of OSA. We aimed to determine whether testosterone administration in transgender men would accentuate symptoms of OSA.MethodsThe study involved 94 adult people undergoing a female-to-male transition with testosterone administration. The participants answered the Berlin Questionnaire (BQ) and a separate question on snoring before starting testosterone treatment and after at least 1 year of being on testosterone treatment.ResultsA higher proportion of participants at the follow-up answered positively to the first category of BQ devoted to snoring. A lower proportion of participants at follow-up answered positively to the second category of BQ devoted to tiredness. The percentage of subjects with a high risk of sleep apnoea, according to BQ, and of those who answered the question on snoring positively did not change significantly.ConclusionAn increased number of transgender men who reported snoring in BQ after testosterone administration indicate a higher risk of OSA development.

Background: Parkinson's disease (PD), even though generally perceived as a dominantly motor disorder, is associated with a wide range of non-motor symptoms, including mixed anxiety-depressive disorder (MADD). Objectives: The aim of the presented study was to determine whether deep brain stimulation (DBS) of the subthalamic nucleus (STN) brings the functional characteristics of non-motor networks closer to the condition detected in healthy population and whether pre-DBS presence of MADD in PD patients was associated with different reaction to this therapeutic modality. Methods: Resting-state fMRI signature elicited by STN DBS activation and deactivation in 81 PD patients was compared against healthy controls, with the focus on measures of efficiency of information processing and localised subnetwork differences. Results: While all the MRI metrics showed statistically significant differences between PD patients in DBS OFF condition and healthy controls, none were detected in such a comparison against DBS ON condition. Furthermore, in the post-DBS evaluation, PD patients with MADD in the pre-DBS stage showed no differences in depression scales compared to pre-DBS psychiatrically intact PD patients, but still exhibited lower DBS-related connectivity in a subnetwork encompassing anterior and posterior cingulate, dorsolateral prefrontal and medial temporal cortices. Conclusions: STN DBS improved all the metrics of interest towards the healthy state, normalising the resting-state MRI signature of PD. Furthermore, pre-DBS presence of MADD, even though clinically silent at post-DBS MRI acquisition, was associated with lower DBS effect in areas highly relevant for depression. This finding points to a possibly latent nature of post-DBS MADD, calling for caution in further follow-up of these patients.