股骨颈骨折合并抑郁老年男性骨密度和骨代谢变化

目的分析老年男性股骨颈骨折合并抑郁患者骨密度和骨代谢生化指标变化，探讨抑郁对骨质疏松骨代谢的影响。 方法选取于北京医院骨科2017年1月至2019年1月住院的老年男性股骨颈骨折患者102例。排除病理性骨折、认知功能障碍等患者。依据老年抑郁量表(GDS)将老年男性股骨颈骨折患者分为抑郁组和对照组。通过测定并比较两组患者的骨密度(BMD)、血清碱性磷酸酶(ALP)、血钙、血磷、25-羟基-维生素D[25(OH)D]、骨钙素(OC)、Ⅰ型原胶原氨基端前肽(P1NP)、血清Ⅰ型胶原羧基末端肽交联β特殊序列(β-CTX)水平，分析抑郁严重程度(GDS评分)与骨密度及骨代谢生化指标的相关性。分类变量的比较采用卡方检验，连续变量的比较采用t检验，两组连续性变量的相关性应用Pearson相关分析。 结果抑郁组患者BMD明显低于对照组(腰椎t ＝5.964、髋部t ＝2.845，P <0.05)。与对照组相比，抑郁组血清25(OH)D水平下降(t ＝3.077，P <0.05)，抑郁组血清OC水平低于对照组(t ＝2.013，P <0.05)，而血清β-CTX水平高于对照组(t ＝2.938，P <0.05)，P1NP水平与对照组差异无统计学意义(t ＝0.684，P >0.05)。抑郁严重程度(GDS评分)与BMD(r＝-0.456，P <0.05)、25(OH)D(r＝-0.546，P <0.05)、OC(r＝-0.215，P <0.05)呈负相关，与P1NP(r＝-0.115，P>0.05)相关性不显著，与β-CTX(r＝0.372，P<0.05)呈正相关。 结论抑郁症患者的骨形成标志物水平降低和骨吸收标志物水平升高，抑郁症是低骨密度和骨折的危险因素。应重视老年抑郁症患者骨代谢指标和25(OH)D的检测，及时进行维生素D的补充和有效的抗骨吸收药物治疗。     

The benefits and costs of changing treatment technique in electroconvulsive therapy due to insufficient improvement of a major depressive episode

BackgroundElectroconvulsive therapy (ECT) technique is often changed after insufficient improvement, yet there has been little research on switching strategies.ObjectiveTo document clinical outcome in ECT nonresponders who were received a second course using high dose, brief pulse, bifrontotemporal (HD BP BL) ECT, and compare relapse rates and cognitive effects relative to patients who received only one ECT course and as a function of the type of ECT first received.MethodsPatients were classified as receiving Weak, Strong, or HD BP BL ECT during three randomized trials at Columbia University. Nonresponders received HD BP BL ECT. In a separate multi-site trial, Optimization of ECT, patients were randomized to right unilateral or BL ECT and nonresponders also received further treatment with HD BP BL ECT.ResultsRemission rates with a second course of HD BP BL ECT were high in ECT nonresponders, approximately 60% and 40% in the Columbia University and Optimization of ECT studies, respectively. Clinical outcome was independent of the type of ECT first received. A second course with HD BP BL ECT resulted in greater retrograde amnesia immediately, two months, and six months following ECT.ConclusionsIn the largest samples of ECT nonresponders studied to date, a second course of ECT had marked antidepressant effects. Since the therapeutic effects were independent of the technique first administered, it is possible that many patients may benefit simply from longer courses of ECT. Randomized trials are needed to determine whether, when, and how to change treatment technique in ECT.     

Brain-derived neurotrophic factor and inflammation in depression: Pathogenic partners in crime?

Major depressive disorder is a debilitating disorder affecting millions of people each year. Brain-derived neurotrophic factor (BDNF) and inflammation are two prominent biologic risk factors in the pathogenesis of depression that have received considerable attention. Many clinical and animal studies have highlighted associations between low levels of BDNF or high levels of inflammatory markers and the development of behavioral symptoms of depression. However, less is known about potential interaction between BDNF and inflammation, particularly within the central nervous system. Emerging evidence suggests that there is bidirectional regulation between these factors with important implications for the development of depressive symptoms and anti-depressant response. Elevated levels of inflammatory mediators have been shown to reduce expression of BDNF, and BDNF may play an important negative regulatory role on inflammation within the brain. Understanding this interaction more fully within the context of neuropsychiatric disease is important for both developing a fuller understanding of biological pathogenesis of depression and for identifying novel therapeutic opportunities. Here we review these two prominent risk factors for depression with a particular focus on pathogenic implications of their interaction.     

A pilot investigation of an intensive theta burst stimulation protocol for patients with treatment resistant depression

IntroductionAccelerated or intensive forms of repetitive transcranial magnetic stimulation (rTMS) are increasingly being explored for their potential to produce more efficient and rapid treatment benefits in major depressive disorder (MDD). However, accelerated or intensive protocols using standard forms of rTMS are still quite time-consuming to apply. Theta burst stimulation (TBS) is a novel form of magnetic stimulation with the potential to produce similar anti-depressant effects but in a much abbreviated period of time. The aim of this study was to investigate the comparative efficacy of an intensive TBS protocol compared to standard rTMS treatment.Methods74 outpatients (36 female, mean age 44.36 ± 12.1 years) with MDD received either intensive TBS (3 intermittent TBS treatments per day for 3 days in week 1, 3 treatments a day for 2 days in week 2, and 3 treatments in 1 day in week 3 and in week 4, or standard rTMS (5 daily sessions per week for 4 weeks). Patients were assessed weekly throughout the treatment course, and at 4 weeks after treatment end.ResultsThere were no significant differences in the degree of reduction in depressive symptoms, the rate of reduction in depressive symptoms, remission or response rates (response rates = 27.8% for intensive group, 26.3% for the standard group, p > 0.05 for all analyses) between the intensive TBS and standard rTMS treatment groups. However, the overall response and remission rates were limited in both groups. There was no difference in rates of side effects, no serious adverse events and no alterations in cognitive performance.ConclusionIntensively applied TBS appears to have similar efficacy to standard rTMS when these were applied as delivered in this study but does not produce more rapid clinical benefits. The overall response rates in both groups in this study were limited, most likely by the total doses provided in both study arms.Clinical trials registrationAustralian New Zealand Clinical Trials Registry: ACTRN12616000443493.     

Pain Catastrophizing,Fear of Pain,and Depression and Their Association with Female Sexual Pain

IntroductionPainful sexual intercourse or dyspareunia is a common complaint among women, affecting 12–21% of premenopausal women. Recent studies have begun to focus on the role of fear avoidance and pain catastrophizing (PC) in genital pain and have consistently highlighted the importance of psych-affective factors in sexual pain.AimTo establish the importance of PC, fear of pain, and depression for the development and maintenance of female sexual pain.MethodsThis longitudinal study was conducted in the United Kingdom to assess sexual pain at 2 different time points, in 2009 and 2013, in a convenience sample of N = 979 British women.Main Outcome MeasureWell-validated questionnaires including the Pain Catastrophizing Scale, the Pain Anxiety Symptom Scale, and the Female Sexual Function Index (recent and lifelong version) were applied.ResultsMultilevel modeling showed a strong increase of short-lived sexual pain over the 4 years (π₀₁ = –0.33; P < .001). According to the moderation analyses, only depression influenced the change in short-lived pain over the 4 years (π₁₁ = 0.46; P = .016). Similarly, only depression turned out to be independently associated with sexual pain when entered into the multiple regression model, as women reporting higher depression levels also reported more sexual pain (P < 0.05).Clinical ImplicationsClinicians should be aware that the mechanisms influencing short-lived sexual pain and changes in sexual pain seem to be different from the more enduring psychological factors that lead to the development and maintenance of “chronic” sexual pain.Strengths & LimitationsA very generic and unidimensional definition of sexual pain was used without information on pain frequency or intensity, and no information on the possible underlying (medical or psychological or both) causes was available. However, as far as we know this represents the first study to use repeated measures to assess how pain changes over a 4-year period and to explore the role of potential psychoaffective risk factors.ConclusionAmong the variables studied, symptoms of depression seemed to be the only independent predictor of lifelong sexual pain, overriding potential influences of pain catastrophizing or fear of pain.Burri A, Hilpert P, Williams F. Pain Catastrophizing, Fear of Pain, and Depression and Their Association with Female Sexual Pain. J Sex Med 2020;17:279–288.     

Comprendre les troubles du sommeil de patients adultes atteints d’une maladie de Crohn pris en charge en ambulatoire

ObjectivesResearch has shown that sleep disturbances can negatively influence the progression of chronic inflammatory diseases, including chronic inflammatory bowel disease (IBD). More specifically, poor sleep quality is strongly related to the clinical activity of the disease. Nevertheless, some patients suffer from sleep disorders even when the disease is clinically inactive. Psychological factors, such as depression and anxiety, are also known to contribute to poor sleep quality. Depression and anxiety are common in chronic diseases. In addition, while the link between depression or anxiety and sleep disorders is well-known, the link between sleep disorders and inflammation has only been studied recently. Sleep studies in IBD patients have generally excluded patients with clinically diagnosed depression or anxiety in order to neutralize their effects on the relationship between inflammation and sleep disorders. Nevertheless, there is no consensus on the relationship between depression and anxiety and the clinical activity of the disease. When a patient with chronic inflammatory bowel disease (Crohn's disease here) complains of fatigue or poor sleep, the subjective aspects of these complaints therefore lead the clinician to consider them simply as: a characteristic of IBD, exhaustion related to the chronicity of the disease, unsatisfactory sleep quality, a manifestation of a depressive mood, or a consequence of an anxious state. When a patient reports a subjective complaint of poor sleep or fatigue in a complex, multi-determined clinical situation, it can thus be difficult to identify its most likely cause and to establish the best possible therapeutic intervention.Patients, materials and methodsThe aim of this work was to determine which element (disease activity, inflammation, depression, anxiety) is most closely related to sleep disorders in patients with Crohn's disease (CD) referred for outpatient psychological assessment. Ninety-seven patients with CD participated in this study. Their mean age was 34.70 (± 10.85) years. They were asked about their sleep (IQSP, ISI, ESD) and mood (HADS). They also provided details of clinical disease activity (Harvey–Bradshaw Index) and inflammation (CRP). In order to determine the nature and extent of the relationship between the variables, Spearman correlation coefficients were calculated, supplemented by multiple regression analyses to determine the variables that could explain the sleep disorders.ResultsThe results show that sleep quality (IQSP) was significantly predicted by the Harvey–Bradshaw score (β = 0.21; β standardized = 0.24; t = 2.6; P = 0.01) and depression (β = 0.45; β standardized = 0.41; t = 4.55; P < 0.001). The Harvey–Bradshaw score (β = 26; β standardized = 2; t = 2.27; P = 0.026) and depression score (β = 75; β standardized = 47; t = 5.34; P < 0.001) were related to the insomnia score (ISI). Finally, daytime sleepiness (DSA) was predicted by the depression score (β = 42; β standardized = 432; t = 3.17; P = 0.002) and by the CRP (β = − 0.05; β standardized = − 0.21; t = − 2.13; P = 0.036). The results show that the severity of clinical activity of the disease was associated with poor sleep quality and insomnia. However, there was a stronger association between the intensity of depression and sleep disturbances than between these variables and clinical disease activity. It therefore seems important that sleep disorders and their management should be considered first from the perspective of depression. However, it is important that CD is not assumed to be the sole cause of depression: other factors (dispositional or situational) should also be taken into consideration. Nevertheless, while our results show a weaker link between inflammation and sleep disorders than other studies, they confirm the link between sleep disorders and disease activity.ConclusionsIn order to predict the likelihood and nature of relapses, it seems important that future research should take into account not only disease activity and inflammation, but also disorders of arousal and nocturnal awakenings experienced by the patient.     

The effect of short or long sleep duration on quality of life and depression: an internet-based survey in Japan

BackgroundTo date, no previous studies have evaluated the relationship between sleep duration and quality of life (QOL) or depression in the general population after controlling for daytime sleepiness and sleep disturbances.MethodsA web-based cross-sectional survey was conducted with 8698 subjects aged 20–69 years. We examined the relationships between weekday sleep duration and daytime sleepiness, sleep disturbance, QOL and depression, using the Epworth Sleepiness Scale, Pittsburgh Sleep Quality Index (without the item for sleep duration), 8-item Short Form and Center for Epidemiological Studies Depression Scale (CES-D).ResultsDaytime sleepiness tended to increase in proportion to shorter weekday sleep durations. Sleep disturbances, physical and mental QOL, and CES-D scores were worse in both the shorter and longer sleep groups compared with the group with 7–8 h of sleep. Hierarchical logistic regression analyses revealed that short sleep duration but not long sleep duration was significantly associated with reduction of both physical and mental QOL, even after controlling for the presence of daytime sleepiness and sleep disturbance. Both short and long sleep duration were independently and significantly correlated with depression after controlling for daytime sleepiness; however, there was no statistically significant association after adjusting for the effects of sleep disturbance.ConclusionsThe results suggested adverse effects of short sleep but not long sleep on both physical and mental QOL. In addition, the negative impact of specific types of sleep disturbance on depression may be greater than the impact of shortening of sleep duration.     

Multimodal multi-center analysis of electroconvulsive therapy effects in depression: Brainwide gray matter increase without functional changes

BackgroundElectroconvulsive therapy (ECT) is an effective treatment for severe depression and induces gray matter (GM) increases in the brain. Small-scale studies suggest that ECT also leads to changes in brain functioning, but findings are inconsistent. In this study, we investigated the influence of ECT on changes in both brain structure and function and their relation to clinical improvement using multicenter neuroimaging data from the Global ECT-MRI Research Collaboration (GEMRIC).MethodsWe analyzed T1-weighted structural magnetic resonance imaging (MRI) and functional resting-state MRI data of 88 individuals (49 male) with depressive episodes before and within one week after ECT. We performed voxel-based morphometry on the structural data and calculated fractional amplitudes of low-frequency fluctuations, regional homogeneity, degree centrality, functional connectomics, and hippocampus connectivity for the functional data in both unimodal and multimodal analyses. Longitudinal effects in the ECT group were compared to repeated measures of healthy controls (n = 27).ResultsWide-spread increases in GM volume were found in patients following ECT. In contrast, no changes in any of the functional measures were observed, and there were no significant differences in structural or functional changes between ECT responders and non-responders. Multimodal analysis revealed that volume increases in the striatum, supplementary motor area and fusiform gyrus were associated with local changes in brain function.ConclusionThese results confirm wide-spread increases in GM volume, but suggest that this is not accompanied by functional changes or associated with clinical response. Instead, focal changes in brain function appear related to individual differences in brain volume increases.