心率变异性对原发性震颤和早期震颤型帕金森病的诊断价值

目的研究心率变异性(HRV)对原发性震颤(ET)和早期震颤型帕金森病(PD)的诊断价值。方法对26例ET患者(ET组)、30例早期震颤型PD患者(早期震颤型PD组)和23例健康对照者(健康对照组)进行24 h ECG检查,比较HRV指标的差异。结果与健康对照组比较,早期震颤型PD组全程NN间期的标准差(SDNN)、相邻NN之差的均方根(RMSSD)、低频功率(LF)和高频功率(HF)显著降低(均P0.01),LF/HF差异无统计学意义(P0.05);ET组RMSSD显著降低(P0.05),SDNN、LF、HF和LF/HF差异无统计学意义(均P0.05)。与早期震颤型PD组比较,ET组SDNN、LF和HF均显著升高(均P0.01),RMSSD、LF/HF差异无统计学意义(均P0.05)。结论震颤型PD患者存在交感和迷走神经的双重损害,早期几乎所有的HRV参数均显著降低。HRV可能有助于区分震颤型PD及ET。     

高血压脑出血患者心率变异性与早期神经功能恶化的相关性

目的观察高血压脑出血(HCH)患者的心率变异性(HRV),记录HCH患者早期神经功能恶化(END)发生情况,并分析心率变异性与END的关系。方法选择河南科技大学第二附属医院2018-01—2019-12收治的72例HCH患者为研究对象,12例发生END,60例未发生END,于治疗前对患者实施动态心电图检查,获取HRV时域指标[24 h每5 s R-R间期平均值标准差(SDNN)、相邻R-R间期差值50 ms的心搏数占比(PNN50)、24 h相邻R-R间期差值的均方根(r-MSSD)];计算HRV频域指标[低频功率(LF)、高频功率(HF)],记录患者治疗后END发生率,分析HRV时域及频域指标与END的关系。结果 72例HCH患者的END发生率为16.67%;END组SDNN、r-MSSD、PNN50、LF、HF均低于非END组,差异有统计学意义(t=3.767、3.516、3.497、3.758、3.423,P0.001、0.001、0.001、0.001、0.001);经Logistic回归分析显示,SDNN、r-MSSD、PNN50、LF、HF低水平是HCH患者发生END的影响因素(OR=1.057、1.317、9.382、1.006、1.017,P=0.002、0.005、0.003、0.002、0.003);绘制ROC曲线显示,SDNN、r-MSSD、PNN50、LF、HF单项检测用于HCH患者END发生风险预测的AUC分别为:0.802、0.854、0.811、0.812、0.815,均0.80,均有一定预测价值。结论 HCH患者END发生率高,HRV与END发生关系密切,可考虑在未来将HRV作为HCH患者END发生的预测指标。     

心理应激对以躯体症状为主的抑郁症患者自主神经影响的研究

目的 应用心率变异性(Heart rate variability,HRV)的短时频域分析,探讨以躯体症状为主的抑郁症患者心理应激与自主神经功能的变化特点.方法 对51例以躯体症状表现为主的抑郁症患者组(躯体症状组)和57例以情绪核心症状为主的抑郁症患者组(情绪障碍组)、42例躯体形式障碍组(躯体形式组)及48例正常对照组分别在静息、应激及放松过程记录LF值、HF值、LF/HF值,应激变化值及放松变化值.结果 (1)躯体症状组LF应激变化值较情绪障碍组、躯体形式组及正常对照组高(P=0.006,0.031,0.000);躯体症状组LF放松变化值较情绪障碍组、躯体形式组及正常对照组低(P=0.040,0.011,0.004).(2)躯体症状组HF应激变化值较情绪障碍组、正常对照组高(P=0.000,0.000);躯体症状组HF放松变化值较躯体形式组、正常对照组低(P=0.014,0.000).(3)躯体症状组LF/HF应激变化值较情绪障碍组、躯体形式组及正常对照组高(P=0.000,0.025,0.000);躯体症状组LF/HF放松变化值较情绪障碍组、躯体形式组及正常对照组低(P=0.018,0.027,0.000).结论 以躯体症状表现为主的抑郁症患者应激后自主神经表现为高反应性,低习惯化和弱恢复性.     

恶劣心境患者述情障碍与自主神经功能的相关研究

目的:探讨恶劣心境患者的人格特质、述情障碍与自主神经功能心理生理反应的相关机制。方法:采用多伦多述情障碍量表中文版(TAS-20-C)及心理健康测查表(PHI)对42例恶劣心境患者组(DD组)、33例重性抑郁症患者组(MD组)及30例健康对照组(NC组)进行述情障碍和心理健康水平和人格特质测定,并分析短时(5min)心率变异性(HRV),评定自主神经功能。结果:DD组TAS-20-C各因子得分及总分显著高于NC组(P<0.01),因子Ⅰ、因子Ⅱ及总分均明显高于MD组(P<0.01或P<0.05);DD组PHI量表躯体化、焦虑、病态人格及疑心因子分明显高于MD组(P<0.01或P<0.05);DD组HRV频谱指标中SDNN、PNN50及HF较MD及NC组均显著下降(P<0.01或P<0.05),LF∕HF较MD及NC组均明显升高(P<0.05);TAS-20-C总分及因子Ⅰ与躯体化、焦虑、病态人格、疑心均相关(︱r︱=0.25～0.38,0.40～0.44,0.47～0.59,0.43～0.42,P<0.01或P<0.05),因子Ⅱ与焦虑及变态人格相关(︱r︱=0.31,0.31,P<0.05);躯体化及焦虑与SDNN、VLF及LF均相关(︱r︱=0.26～0.27,0.39～0.27;︱r︱=0.36～0.28,P<0.05或P<0.01)。结论:恶劣心境患者存在明显的述情障碍,其人格特质可能导致患者焦虑程度更高,伴自主神经功能紊乱。     

失眠症患者睡眠质量与心理健康状况及心率变异性的关系

目的:探讨失眠症患者睡眠质量与心理健康状况及心率变异性(HRV)的关系。方法:对165例失眠症患者进行匹兹堡睡眠质量指数问卷(PSQI)评估,并据此分为高分组85例与低分组80例;采用生理相干与自主平衡训练系统(SPCS)采集HRV,应用症状自评量表(SCL-90)评估患者心理健康状况。结果:高分组SCL-90中焦虑因子及睡眠与饮食因子得分显著高于低分组(P均0.05);两组患者HRV中总功率(TP)、低频功率(LF)、高频功率(HF)、LF/HF比值差异有统计学意义(P均0.05);PSQI总分与HRV中TP、LF、HF呈正相关(r=0.196,0.185,0.223;P0.05或P0.01),与LF/HF呈负相关(r=-0.304,P0.01)。结论:严重失眠的患者易产生焦虑情绪;失眠严重程度与自主神经系统功能失调程度相关。     

复发性抑郁症与长期住院精神分裂症患者的心率变异性差异

目的 比较复发性抑郁症与长期住院精神分裂症患者之间心率变异性（HRV）的差异。 方法 回顾性连续纳入2014 年1 月至2019 年1 月于上海交通大学医学院附属精神卫生中心精神科住 院治疗的多次发作的抑郁症或长期住院精神分裂症患者各120 例,两组患者性别、年龄相匹配。对两 组患者分别开展HRV 检测,使用24 h 动态心电图记录仪和心率变异分析软件进行检测,并对HRV相关 指标R-R间期标准差（ SDNN）、相邻R-R间期差值的均方根（ rMSSD）、相邻R-R间期之间差值＞50 ms的 百分比（PNN50）、低频功率（LF）、高频功率（HF）、LF与HF之间的比值（LF/HF）的结果进行组间比较。采 用Spearman 相关分析分析两组患者住院次数与HRV 各指标的相关性。结果 复发性抑郁症患者组时 阈指标SDNN 高于长期住院精神分裂症组［121.0（95.0,158.0）比111.0（87.0,144.0）ms,t=2.214］,rMSSD、 PNN50 低于长期住院精神分裂症组［22.0（13.0,46.0）比20.0（12.0,28.0）ms,t=3.832;3.0（0,13.0）% 比2.0（0, 7.0）%,t=2.571］,差异均有统计学意义（均P＜ 0.05）;两组频阈指标差异无统计学意义（均P＞ 0.05）。进 一步采用Spearman 相关分析结果显示,复发性抑郁症患者住院次数与rMSSD（r=0.270,P=0.003）、PNN50 （r=0.263,P=0.004）、HF（r=0.246,P=0.015）相关,但精神分裂症患者住院次数与HRV各分析指标无相关（均 P＞ 0.05）。结论 复发性抑郁症患者的自主神经功能失调较长期住院精神分裂症患者严重,复发性抑 郁症患者的住院次数影响患者HRV时阈指标     

抑郁症患者的皮质醇、甲状腺功能及心率变异性特征对照研究

目的研究抑郁症患者的皮质醇、甲状腺功能及心率变异性特点,探讨其与躯体症状、失眠及性别因素的关系。方法检测60例抑郁症患者和60名正常对照的血清皮质醇(Cortisol,COR)、三碘甲状腺原氨酸(triiodothyronine,T3)、四碘甲状腺原氨酸(tetraiodothyronine,T4)、促甲状腺素(Thyroid stimulating hormone,TSH)水平,当日进行心率变异性检查,进行两组的比较,并按照躯体症状、失眠及不同性别进行分组比较。结果患者组的R-R间期平均标准差(standard deviation of average RR intervals,SDNN)、低频功率(low frequen-cy band,LF)、高频功率(high frequency band,HF)分别为[(34.21±14.31),186.64(846.67,113.87),125.00(839.22,48.50],对照组依次为[(43.86±12.61),375.92(2542.70,233.08),247.51(1547.36,142.33)],前者显著低于后者(均P<0.01)。与对照组相比,患者组COR水平增高[(15.35=6.45)vs.(11.81±6.32),P<0.01],TSH、T3及T4水平无显著差异(P>0.05)。伴躯体症状患者组COR水平显著高于对照组及不伴躯体症状组(P<0.01),SDNN、LF及HF指数均显著低于后两组(P<0.01)。伴失眠的患者组血清COR水平显著高于对照组及不伴失眠组(均P<0.01),SDNN、LF及HF指数均显著低于后两组(均P<0.05)。男性患者组SDNN、LF、HF指数均显著低于正常男性组(均P<0.05);女性患者组血清COR水平显著高于正常女性组(P<0.01),SDNN、LF指数均显著低于正常女性组(均P<0.05)。结论抑郁症HPT轴无紊乱,仅HPA轴及自主神经功能出现紊乱,且HPA轴激素水平及心率变异性与躯体症状、失眠及性别因素有关。     

HRV改变对植物神经功能紊乱的诊断价值分析

目的 研究基于HRV改变的时、频域分析对植物神经功能紊乱的诊断价值.方法 从近年来我院心血管内科住院病人中,筛选出植物神经功能紊乱确诊病例38例,另选健康人38例作为研究对象,将所选材料的DCG数据经统计学处理,提取出HRV的时、频域指标进行对比.结果 时域指标SDNN的24 h观察取值,患病者高于健康者,夜间取值基本持平;频域指标LF和HF的功率谱密度(PSD)值两项,患病者分别高于和低于健康者;LF/HF比值为患病者高.结论 依据时域指标SDNN与频域指标LF确定交感神经兴奋性增强;由频域LF和HF两项指标确定迷走神经兴奋性减弱,从而确诊植物神经功能紊乱;由LF/HF比值的大小,判断自主神经失衡的程度,为冠心病的早期诊断和积极防治提供理论参考.     

肌电生物反馈对高血压前期患者心率变异性的影响

目的 研究肌电生物反馈对高血压前期患者血压及心率变异性(HRV)的影响.方法 观察分析12例进行生物反馈放松训练的高血压前期患者与12例对照者血压值及HRV的时域指标与频域指标.结果 与对照组相比,生物反馈组的收缩压下降趋势显著(P＜0.05),且至少可以维持6个月,心率下降趋势较显著(P＜0.05),SDNN和HF有明显升高的趋势(P＜0.05),LF和LF/HF明显降低(P＜0.05).结论 肌电生物反馈可以使高血压前期患者的血压降低至理想范围,其机制可能主要与HF升高、副交感神经的兴奋性增高有关.     

伴有抑郁的老年冠心病患者自主神经功能的改变

目的:探讨伴有抑郁老年冠心病患者自主神经功能的改变。方法:根据汉密尔顿抑郁量表(HAMD)、Zung氏抑郁自评量表(SDS)、以及冠状动脉造影结果,将163例住院患者及健康体检者分为冠心病伴抑郁组(48例)、冠心病组(65例)、正常对照组(50例);并行24 h动态心电图检查,分析心率变异各项指标及其与抑郁程度的相关性。结果:与正常对照组相比,冠心病伴抑郁组与单纯冠心病组,时域指标均下降,频域指标中低频功率(LF)、LF/高频功率(HF)值上升。冠心病伴抑郁组的抑郁严重度与24 h正常RR间期标准差(SDNN)呈负相关,与LF/HF之间呈正相关(r=-0.967,r=0.971,P均0.05)。结论:伴有抑郁症状老年冠心病患者自主神经功能改变更明显,并与抑郁程度相关。     

The role of early adversity and recent life stress in depression severity in an outpatient sample

Pre-, peri-, and postnatal stress have frequently been reported to be associated with negative health outcomes during adult life. However, it is unclear, if these factors independently predict mental health in adulthood. We estimated potential associations between reports of pre-, peri-, and postnatal stress and depression severity in outpatients (N = 473) diagnosed with depression, anxiety or somatoform disorders by their family physician. We retrospectively assessed pre-, peri-, and postnatal stress and measured depression severity as well as recent life stress using questionnaires. First, we estimated if depression severity was predicted by pre-, peri- and/or postnatal stress using multiple regression models. Second, we compared pre- and postnatal stress levels between patient subgroups of different degrees of depression severity, performing multilevel linear modeling. Third, we analyzed if an association between postnatal stress and current depression severity was mediated by recent life stress.We found no associations of pre-, or perinatal stress with depression severity (all p > 0.05). Higher postnatal stress was associated with higher depression severity (p < 0.001). Patients with moderately severe and severe depression reported higher levels of postnatal stress as compared to patients with none to minimal, or mild depression (all p < 0.05). Mediation analysis revealed a significant indirect effect via recent life stress of the association between postnatal stress and depression severity (p < 0.001).In patients diagnosed for depression, anxiety, and/or somatoform disorders, postnatal but neither pre- nor perinatal stress predicted depression severity in adult life. This association was mediated by recent life stress.     

Chronic and acute stress and the prediction of major depression in women

Background: This study explored the relatively neglected role of chronic stress in major depression, examining the independent contributions of co‐occurring chronic and acute stress to depression, whether chronic stress predicts acute life events, and whether the two types of stress interact such that greater chronic stress confers greater sensitivity—or resistance—to the depressive effects of acute stressors. Methods: From a sample of 816 community women, those who had a major depression onset in the past 9 months and those without major depressive episodes (MDE) onset and with no history of current or recent dysthymic disorder were compared on interview‐based measures of antecedent acute and chronic stress. Chronic stress interviews rated objective stress in multiple everyday role domains, and acute stress was evaluated with contextual threat interviews. Results: MDE onset was significantly associated with both chronic and acute stress; chronic stress was also associated with the occurrence of acute events, and there was a trend suggesting that increased acute stress is more strongly associated with depression in those with high versus low chronic stress. Conclusions: Results suggest the importance of including assessment of chronic stress in fully understanding the extent and mechanisms of stress–depression relationships. Depression and Anxiety, 2009. Published 2009 Wiley‐Liss, Inc.     

Early life stress modulates oxytocin effects on limbic system during acute psychosocial stress

Early life stress (ELS) is associated with altered stress responsivity, structural and functional brain changes and an increased risk for the development of psychopathological conditions in later life. Due to its behavioral and physiological effects, the neuropeptide oxytocin (OXT) is a useful tool to investigate stress responsivity, even though the neurobiological underpinnings of its effects are still unknown. Here we investigate the effects of OXT on cortisol stress response and neural activity during psychosocial stress. Using functional magnetic resonance imaging in healthy subjects with and without a history of ELS, we found attenuated hormonal reactivity and significantly reduced limbic deactivation after OXT administration in subjects without a history of ELS. Subjects who experienced ELS showed both blunted stress reactivity and limbic deactivation during stress. Furthermore, in these subjects OXT had opposite effects with increased hormonal reactivity and increased limbic deactivation. Our results might implicate that reduced limbic deactivation and hypothalamic–pituitary–adrenal axis responsivity during psychosocial stress are markers for biological resilience after ELS. Effects of OXT in subjects with a history of maltreatment could therefore be considered detrimental and suggest careful consideration of OXT administration in such individuals.     

Repeated,non-habituating stress suppresses inflammatory plasma extravasation by a novel,sympathoadrenal dependent mechanism

The mechanism by which chronic stress affects the course of inflammatory diseases is still not well understood. We have evaluated the effect of two types of nonhabituating stress on a major component of the inflammatory response, synovial plasma extravasation, induced by perfusion of the potent inflammatory mediator, bradykinin and evaluated the underlying neuroendocrine mechanism in the rat. Chronic intermittent noise or ether stress induced profound inhibition of bradykinin-induced plasma extravasation, which is associated with increased adjuvant-arthritis severity. This inhibition, however, took 24 h to fully develop after the last exposure to stress and persisted for at least 48 h. The inhibition could be reversed by an additional exposure to the stressor, just prior to measuring the inflammatory response, suggesting that the delay is due to stress-induced release of a factor that acutely masks the inhibition of the inflammatory response. This novel, unexpected feature of the effect of nonhabituating stress on inflammation may help explain variability in effects of stress in patients with inflammatory disease. The effect of nonhabituating stress on inflammation was dependent on the sympathoadrenal axis with no detectable contribution by the hypothalamic-pituitary-adrenal axis.     

Crosstalk between endoplasmic reticulum stress and oxidative stress in schizophrenia: The dawn of new therapeutic approaches

Disruption of oxidant/anti-oxidant ratio as well as endoplasmic reticulum (ER) stress are thought to be involved in the pathophysiology of schizophrenia. These stresses can lead to impairments in brain functions progressively leading to neuronal inflammation followed by neuronal cell death. Moreover, the cellular stresses are interlinked leading us to the conclusion that protein misfolding, oxidative stress and apoptosis are intricately intertwined events requiring further research into their mechanistic and physiological pathways. These pathways can be targeted by using different therapeutic interventions like anti-oxidants, sigma-1 receptor agonists and gene therapy to treat the neurodegenerative course of schizophrenia. We have also put empahsis on use of synthetic and natural ER stress inhibitors like 4-phenylbutyrate or salubrinal for the treatment of this disorder. This would provide an opportunity to create new therapeutic benchmarks in the field of neuropsychiatric disorders like schizophrenia, dissociative identity disorder and obsessive compulsive disorder.     

Acetyl-L-Carnitine Effect on Pituitary and Plasma β-Endorphin Responsiveness to Different Chronic Intermittent Stressors

The aims of the present study were: 1) to compare the effect of two different chronic intermittent stressors i.e. cold-swimming versus ether, on the pituitary opioidergic system; 2) to evaluate the response of pituitary and plasma β-endorphin (βS-EP) to an acute stress in chronically stressed rats; and 3) to evaluate the effect of acetyl-l-carnitine treatment (10 mg/day/rat per os at night) on pituitary and plasma β-EP changes induced by two different types of chronic stress. The stressors were applied twice a day for 10 days. Rats were killed either before, during or after the last swimming or ether stress session. β-EP was measured by radioimmunoassay in anterior pituitary and in neurointermediate lobe extracts and in plasma. The following observations were made; 1) Chronic intermittent cold-swimming stress increased anterior pituitary contents and plasma β-EP levels; 2) both chronic intermittent cold-swimming stress and ether stress caused an increase of neurointermediate lobe β-EP contents; 3) as in control animals, rats exposed to chronic intermittent swimming stress reduced pituitary β-EP contents and raised plasma β-EP levels in response to the last acute swimming stress; 4) in contrast to control animals, rats exposed to chronic intermittent ether stress did not show any significant response of the pituitary-plasma opioidergic system to the last acute ether session; 5) the acetyl-l-carnitine treatment counteracted the changes evoked by chronic intermittent cold-swimming stress on the pituitary and plasma β-EP levels. The present data show that chronic intermittent ether stress impairs the capacity to respond to the acute stress and that acetyl-l-carnitine may modulate the changes of β-EP levels following chronic cold-swimming stress exposure.     

Stress and ageing interactions: a paradox in the context of shared etiological and physiopathological processes

Gerontology has made considerable progress in the understanding of the mechanisms underlying the ageing process and age-related neurodegenerative disorders. However, ways to improve quality of life in the elderly remain to be elucidated. It is now clear that stress and the ageing process share a number of underlying mechanisms bound in a very close, if not indissociable, relationship. The ageing process is regulated by the factors underlying the ability to adjust to stress, whilst stress has an influence on the life span and the quality of ageing. In addition, the ability to cope with stress in adulthood predicts life expectancy and quality of life at senescence. The ageing process and stress also share several common mechanisms, particularly in relation to the energy factor. Stress consumes energy and ageing may be considered as a cost of the energy expended to deal with the stressors to which the body is exposed throughout its lifetime. This suggests that the ageing process is associated with and/or a consequence of a long-lasting activation of the major stress responsive systems. However, despite common features, the interaction between stress and the ageing process gives rise to some paradoxes. Stress can either diminish or exacerbate the ageing process just as the ageing process can worsen or counter the effects of stress. There has been little attempt to understand how ageing and stress might interact to promote "successful" or pathological ageing. A key factor in this respect is the individual's ability to adapt to stress. Viewed from this angle, the quality of life of aged subjects may be improved through therapy designed to improve the tolerance to stress.