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OBJECTIVE: To quantify the variation, triggers and impact on quality of life of symptom flares in women with chronic pelvic pain (CPP). DESIGN: Cross-sectional questionnaire within the Translational Research in Pelvic Pain clinical cohort study. SETTING: Women with CPP, with subgroups of women with endometriosis (EAP), interstitial cystitis/bladder pain syndrome (BPS), comorbid endometriosis and interstitial cystitis/bladder pain syndrome (EABP), and those with pelvic pain without endometriosis or interstitial cystitis/bladder pain syndrome (PP). POPULATION OR SAMPLE: A total of 100 participants. METHODS: Descriptive and comparative analysis from flares questionnaire. MAIN OUTCOME MEASURES: The prevalence, characteristics and triggers of short, medium and long symptom flares in CPP. RESULTS: We received 100 responses of 104 questionnaires sent. Seventy-six per cent of women with CPP have ever experienced symptom flares of at least one length (short, medium and/or long). Flares are associated with painful and non-painful symptoms. There is large variation for the frequency, duration, symptoms and triggers for flares. Over 60% of participants reported flares as stopping them from doing things they would usually do, >80% reported thinking about symptoms of flares and >80% reported flares being bothersome. CONCLUSIONS: Flares are prevalent and clinically very important in CPP. More research is needed to elucidate the mechanisms and characteristics underlying flares. Clinical practice should include an enquiry into flares with the aim of finding strategies to lessen their burden.
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Background/objectives: Impulsive aggressive behaviour, although not a core symptom, is often part of the clinical presentation of attention-deficit/hyperactivity disorder (ADHD). Recently, impulsive aggression has been attributed to emotion dysregulation, which is currently conceptualised as a transdiagnostic factor and seems to contribute to the co-occurrence of other problems in ADHD. Thus, this study investigated the presence of impulsive aggressive behaviour and explored whether emotion dysregulation mediates the relationship between inhibitory control difficulties and aggressive behaviour in children with ADHD. Because ADHD may act as a risk factor for the development of other conditions, such as internalising problems, we aimed to understand whether depressive symptoms contribute to this relationship. Methods: Seventy-two children were recruited from a hospital and the community, 38 of whom had ADHD and 34 were typically developing (TD). Parents completed the Child Behaviour Checklist, the Behaviour Rating Inventory of Executive Function, and the Emotion Regulation Checklist. Simple mediation and serial mediation models were performed to test our hypotheses. Results: Aggressive behaviour was significantly higher in ADHD children compared to TD children. Emotion dysregulation fully mediated the relationship between inhibitory control difficulties and aggressive behaviour in ADHD children. Adding depressive symptoms to the model increased the explained variance in aggressive behaviour. Conclusion: The main result of our study supports the role of emotion dysregulation and depressive symptoms in mediating the relationship between inhibitory control difficulties and impulsive aggressive behaviour in children with ADHD. This highlights that aggressive behaviour is, in part, a result of the inability of the child to appropriately regulate their emotions. Future interventions may be tailored to improve emotion regulation skills to address aggressive behaviour.
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Gut microorganisms have been shown to significantly impact on central function and studies that have associated brain disorders with specific bacterial genera have advocated an anomalous gut microbiome as the pathophysiological basis of several psychiatric and neurological conditions. Thus, our knowledge of brain-to-gut-to microbiome communication in this bidirectional axis seems to have been overlooked. This review examines the known mechanisms of the microbiome-to-gut-to-brain axis, highlighting how brain-to-gut-to-microbiome signaling may be key to understanding the cause of disrupted gut microbial communities. We show that brain disorders can alter the function of the brain-to-gut-to-microbiome axis, which will in turn contribute to disease progression, while the microbiome-to gut-to brain direction presents as a more versatile therapeutic axis, since current psychotropic/neurosurgical interventions may have unwanted side effects that further cause disruption to the gut microbiome. A consideration of the brain-to-gut-to-microbiome axis is imperative to better understand how the microbiome-gut-brain axis overall is involved in brain illnesses, and how it may be utilized as a preventive and therapeutic tool.