Psychological therapies for chronic widespread pain and fibromyalgia syndrome

Psychological factors such as adverse childhood experiences, traumatic life events, interpersonal conflicts and psychological distress play an important role in the predisposition, onset and severity of chronic widespread pain (CWP) and fibromyalgia syndrome (FMS). Therefore, psychological therapies might have the potential to reduce disability as well as symptom and economic burden in patients with CWP and FMS. Recent interdisciplinary guidelines have suggested different strengths of recommendation for psychological therapies for FMS. The aims of this narrative review are to summarise:• Mechanisms of actions.• Evidence on efficacy, tolerability and safety.• Knowledge gaps and needs for future researchof psychological therapies for CWP and FMS for non-mental health professionals.     

Clinical Review: Breast Development in Trans Women Receiving Cross-Sex Hormones

IntroductionIn trans women (male-to-female transsexual persons), cross-sex hormone therapy is administered to induce feminization. Breast development is an important part of feminization for most trans women.AimThe aim of this study is to assess the effect of cross-sex hormone therapy on breast development in adult trans women. Additionally, we aimed to investigate the benefit or harm of administration of progestogens on breast development.MethodsA review of the literature in Embase, Medline, The Cochrane Library, PsycINFO databases, PubMed, and Web of Knowledge until January 2014.Main Outcome MeasuresEffects of cross-sex hormone therapy and progestogens on breast development in trans women.ResultsOnly few studies with low quality of evidence addressed these topics. The available evidence suggests that breast development is insufficient for the majority of trans women and that type and dosage of hormonal therapy seem not to have an important role on final breast size.ConclusionsOur knowledge concerning the natural history and effects of different cross-sex hormone therapies on breast development in trans women is extremely sparse and based on low quality of evidence. Current evidence does not provide evidence that progestogens enhance breast development in trans women. Neither do they prove the absence of such an effect. This prevents us from drawing any firm conclusion at this moment and demonstrates the need for further research to clarify these important clinical questions.Wierckx K, Gooren L, and T'Sjoen G. Clinical review: Breast development in trans women receiving cross-sex hormones. J Sex Med 2014;11:1240–1247.     

慢性硬膜下血肿并发行为异常的影响因素分析

目的研究慢性硬膜下血肿并发行为异常的影响因素。方法回顾性连续纳入2009年1月至2019年10月四川省德阳市人民医院收治的慢性硬膜下血肿207例,将所有患者依据是否并发行为异常分为行为异常组及非行为异常组。收集患者一般人口学资料如性别、年龄及病史(如外伤史、吸烟史、饮酒史、脑血管病史、高血压病史、糖尿病史、血脂异常病史、凝血异常史),记录患者入院时格拉斯哥昏迷量表(GCS)评分,收集入院时CT及脑CT灌注等影像学资料,包括血肿量、血肿部位、血肿密度、CT中线移位、镰下疝、脑灌注缺损等资料。由专业的心身医学科医师进行精神检查,并进行汉密尔顿抑郁量表(HAMD)、修订韦氏成人记忆量表(WMS-RC)及力量表(WAIS-RC)测试。以HAMD评分>7分为抑郁状态,记忆商及总智商<79分作为记忆障碍和智能障碍的判断标准。采用Logistic回归分析影响慢性硬膜下血肿并发行为异常的独立危险因素。结果慢性硬膜下血肿患者并发行为异常的发生率为73.43%(152/207)。单因素分析结果显示,两组慢性硬膜下血肿患者在性别、年龄、凝血异常史方面差异无统计学意义(均P>0.05);两组患者在外伤史(χ^2=8.763)、吸烟史≥10年(χ^2=11.491)、饮酒史≥10年(χ^2=14.365)、脑血管病史(χ^2=11.492)、高血压病史≥10年(χ^2=13.057)、糖尿病史≥10年(χ^2=9.534)、血脂异常病史(χ^2=13.274)、病程≥3个月(χ^2=7.731)、血肿量≥30 ml(χ^2=12.763)、额颞部血肿(χ^2=21.458)、混杂密度血肿(χ^2=8.736)、CT中线移位≥5 mm(χ^2=14.572)、镰下疝(χ^2=10.396)、GCS<8分(χ^2=7.216)、额颞叶脑灌注缺损(χ^2=6.781)方面比较,差异均有统计学意义(均P<0.05)。Logistic回归分析结果显示,外伤史(OR=2.164,95%CI:1.083~2.934)、吸烟史≥10年(OR=2.346,95%CI:1.191~2.835)、饮酒史≥10年(OR=2.941,95%CI:1.284~3.157)、脑血管病史(OR=3.178,95%CI:1.893~4.597)、高血压病史≥10年(OR=2.783,95%CI:1.231~2.957)、糖尿病史≥10年(OR=2.841,95%CI:1.309~3.637)、有血脂异常病史(OR=3.237,95%CI:1.794~5.124)、病程≥3个月(OR=3.957,95%CI:1.997~5.463)、血肿量≥30 ml(OR=4.875,95%CI:1.982~5.875)、额颞部血肿(OR=4.763,95%CI:1.898~5.968)、混杂密度血肿(OR=4.537,95%CI:1.795~5.362)、CT中线移位≥5 mm(OR=4.876,95%CI:1.897~5.985)、并发镰下疝(OR=4.495,95%CI:1.754~5.247)、GCS<8分(OR=4.875,95%CI:1.897~5.876)、额颞叶脑灌注缺损(OR=4.237,95%CI:1.651~4.896)是影响慢性硬膜下血肿患者并发行为异常的独立危险因素。结论慢性硬膜下血肿并发行为异常受外伤史、吸烟史、饮酒史、脑血管病史、高血压病史、糖尿病史、高血脂病史、病程、血肿量、血肿部位、血肿密度、CT中线移位、镰下疝、GCS、脑灌注等因素影响,有针对性给予干预可能有效降低慢性硬膜下血肿发生行为异常的发生率。     

Patient quality of life after vestibular schwannoma removal: possibilities and limits to measuring different domains of patients' wellbeing

European Archives of Oto-Rhino-Laryngology - Since the 1980s, health-related quality of life (HRQOL) has been recognized in the assessment of medical treatment. To determine the health-related...     

Dietary N-3 PUFA deficiency affects sleep-wake activity in basal condition and in response to an inflammatory challenge in mice

Essential polyunsaturated fatty acids (PUFA) from the n-3 and n-6 series constitute the building blocks of brain cell membranes where they regulate most aspects of cell physiology. They are either biosynthesized from their dietary precursors or can be directly sourced from the diet. An overall increase in the dietary n-6/n-3 PUFA ratio, as observed in the Western diet, leads to reduced n-3 PUFAs in tissues that include the brain. Some clinical studies have shown a positive correlation between dietary n-3 PUFA intake and sleep quantity, yet evidence is still sparse. We here used a preclinical model of dietary n-3 PUFA deficiency to assess the precise relationship between dietary PUFA intake and sleep/wake activity. Using electroencephalography (EEG)/electromyography (EMG) recordings on n-3 PUFA deficient or sufficient mice, we showed that dietary PUFA deficiency affects the architecture of sleep-wake activity and the oscillatory activity of cortical neurons during sleep. In a second part of the study, and since PUFAs are a potent modulator of inflammation, we assessed the effect of dietary n-3 PUFA deficiency on the sleep response to an inflammatory stimulus known to modulate sleep/wake activity. We injected mice with the endotoxin lipopolysaccharide (LPS) and quantified the sleep response across the following 12 h. Our results revealed that n-3 PUFA deficiency affects the sleep response in basal condition and after a peripheral immune challenge. More studies are now required aimed at deciphering the molecular mechanisms underlying the intimate relationship between n-3 PUFAs and sleep/wake activity.