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16 result(s) for "自主神经系统"
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Does the autonomic nervous system contribute to the initiation and progression of prostate cancer
In the July 12 issue of Science maga-zine, researchers from the AlbertEinstein College of Medicine, the Mount Sinai School of Medicine, the Durham VA Medical Centre and Duke University published an elegant study demonstrating that the sym-pathetic nervous system, acting through β2 and β3-adrenoceptors in the prostate, plays an important role in the initiation of prostate can-cer, while the parasympathetic nervous system plays a role in the dissemination of tumour metastases via M1 muscarirdc receptors. These findings are significant because they indicate that receptors associated with the autonomic nervous system may be viable tar-gets for prostate cancer therapy.
重型颅脑创伤术后发作性自主神经功能紊乱:四例报告并文献复习
发作性自主神经功能紊乱是一种临床较为少见的综合征,主要表现为交感神经兴奋、副交感神经兴奋或二者兼有的症状与体征.由于早期临床表现复杂、诊断困难,易误诊为医原性感染、中枢性高热等.本文4例重型颅脑创伤患者均于手术后出现发作性自主神经功能紊乱症状,经溴隐亭、普萘洛尔,以及物理降温和高压氧治疗症状明显改善.
直立后头晕 恶心 呕吐
病历摘要 患者女性,41岁。主诉直立后头晕、恶心、呕吐2周,于2009年11月2日入我院治疗。患者于入院前2周无诱因出现直立后头晕、黑蒙,平卧休息症状可消失,并开始出现恶心、呕吐,呕吐3~4次/d,为胃内容物,伴呃逆,无腹痛、腹泻。8d前在行走过程中突然晕倒,自述意识丧失,约1min后自行清醒,发作时无四肢抽搐、大小便失禁,此后多次出现晕厥,均发生于直立体位时。
第四届中国神经调控大会暨中国医师协会神经调控专业委员会2012’年会征文通知
由中国医师协会神经调控专业委员会主办的"第四届中国神经调控大会暨中国医师协会神经调控专业委员会2012’年会"拟定于2012年9月21-23日在北京世纪金源香山商旅酒店召开。会议以"神经调控在中国的发展"为主题,以世界神经调控技术的发展为背景,邀请国内外著名神经调控专家及学者进行专题讲座,全新展示神经调控技术的临床应用与基础研究的发展。神经调控技术是一项利用植入性或非植入性技术,运用电刺激或药物手段改变中枢神经、外周神经或自主神经系统活性,从而改善患者症状、提高生存质量的生物医学工程技术。
情感障碍的心率变异性研究进展
情感障碍常常伴随自主神经功能紊乱.心率变异性( HRV)分析作为-种无创、定量指标,为了解自主神经系 统功能异常提供了窗口.本文对HRV的分析方法、自主神经系统参与的心脑连接模式、情感障碍的HRV关联研究以及治疗 对其影响作一综述,探讨HRV在临床诊断和治疗中的应用价值.
Trauma-related dissociation and the autonomic nervous system: a systematic literature review of psychophysiological correlates of dissociative experiencing in PTSD patients
Background: Neurophysiological models link dissociation (e.g. feeling detached during or after a traumatic event) to hypoarousal. It is currently assumed that the initial passive reaction to a threat may coincide with a blunted autonomic response, which constitutes the dissociative subtype of post-traumatic stress disorder (PTSD). Objective: Within this systematic review we summarize research which evaluates autonomic nervous system activation (e.g. heart rate, blood pressure) and dissociation in PTSD patients to discern the validity of current neurophysiological models of trauma-related hypoarousal. Method: Of 553 screened articles, 28 studies (N = 1300 subjects) investigating the physiological response to stress provocation or trauma-related interventions were included in the final analysis. Results: No clear trend exists across all measured physiological markers in trauma-related dissociation. Extracted results are inconsistent, in part due to high heterogeneity in experimental methodology. Conclusion: The current review is unable to provide robust evidence that peri- and post-traumatic dissociation are associated with hypoarousal, questioning the validity of distinct psychophysiological profiles in PTSD. There is no consensus on physiological biomarkers of trauma-related dissociation. Peri- and post-traumatic dissociation are physiologically distinct from stress reactions in chronic states. Standardized methodologies may increase the reproducibility and specificity of psychophysiological biomarkers of dissociation.
Traumatic stress and the circadian system: neurobiology, timing and treatment of posttraumatic chronodisruption
Background: Humans have an evolutionary need for a well-preserved internal 'clock', adjusted to the 24-hour rotation period of our planet. This intrinsic circadian timing system enables the temporal organization of numerous physiologic processes, from gene expression to behaviour. The human circadian system is tightly and bidirectionally interconnected to the human stress system, as both systems regulate each other's activity along the anticipated diurnal challenges. The understanding of the temporal relationship between stressors and stress responses is critical in the molecular pathophysiology of stress-and trauma-related diseases, such as posttraumatic stress disorder (PTSD). Objectives/Methods: In this narrative review, we present the functional components of the stress and circadian system and their multilevel interactions and discuss how traumatic stress can affect the harmonious interplay between the two systems. Results: Circadian dysregulation after trauma exposure (posttraumatic chronodisruption) may represent a core feature of trauma-related disorders mediating enduring neurobiological correlates of traumatic stress through a loss of the temporal order at different organizational levels. Posttraumatic chronodisruption may, thus, affect fundamental properties of neuroendocrine, immune and autonomic systems, leading to a breakdown of biobehavioral adaptive mechanisms with increased stress sensitivity and vulnerability. Given that many traumatic events occur in the late evening or night hours, we also describe how the time of day of trauma exposure can differentially affect the stress system and, finally, discuss potential chronotherapeutic interventions. Conclusion: Understanding the stress-related mechanisms susceptible to chronodisruption and their role in PTSD could deliver new insights into stress pathophysiology, provide better psychochronobiological treatment alternatives and enhance preventive strategies in stress-exposed populations. * The human circadian and stress system are both essential for biobehavioural regulation with numerous reciprocal interaction. * Posttraumatic chronodisruption (i.e., circadian dysregulation after trauma) represents a core feature of PTSD, mediating neurobiological correlates of trauma through multilevel temporal order loss.
Community and domestic violence are associated with DNA methylation GrimAge acceleration and heart rate variability in adolescents
Background: Cumulative exposure to violence can change the regulation of epigenetic and physiological markers. Although violence has been associated with accelerated cellular aging, little is known about associations with cardiac autonomic activity. Objective: The current study aimed to investigate the relationship of exposure to community and domestic violence (CDV) with vagal activity and epigenetic aging acceleration. Methods: A total of 86 adolescents (57% female) were evaluated and interviewed at two time-points in São Gonçalo (2014-2019), a Brazilian city with high levels of violence. Exposure to CDV was assessed in both time-points. GrimAge acceleration was calculated from saliva DNA methylation using Infinium HumanMethylation450K (Illumina) collected in the first assessment. Heart rate variability (HRV) was collected during two stress tasks at the second assessment. Results: The exposure to violence witnessed or directly experienced at home and in the community increased significantly (t = 4.87, p < .01) across two-time points, and males had reported higher violence exposure (t = 2.06, p = .043). Violence at 1st assessment was significantly associated with GrimAge acceleration (B = .039, p value = .043). Violence at both assessments were associated with HRV measured during the narration of the worst trauma (traumaHRV) (B = .009, p value = .039, and B = .007, p value = .024, 1st and 2nd assessment respectively). GrimAge acceleration was significantly associated with traumaHRV (B = .043, p value = .049), and HRV measured during a 3D roller coaster video (B = .061, p value = .024). Conclusions: We found relevant evidence that experiencing violence during adolescence is associated with epigenetic aging and stress-related vagal activity. Understanding these factors during this period could contribute to the development of early interventions for health promotion. HIGHLIGHTS Higher exposure to Community and domestic violence is associated with increased GrimAge acceleration. Higher GrimAge acceleration is associated with increased stress-related vagal activity. Exposure to community and domestic violence increased significantly over time.
The enemy in the mirror: self-perception-induced stress results in dissociation of psychological and physiological responses in patients with dissociative disorder
Background: Patients suffering from dissociative disorders (DD) are characterized by an avoidance of aversive stimuli. Clinical experience has shown that DD patients typically avoid the confrontation with their own faces in a mirror (CFM). Objective: To investigate potential CFM-associated self-reported and psychophysiological stress reactions of DD patients, which most likely inform on the still unknown pathophysiology of dysfunctional self-perception in DD. Method: Eighteen DD patients and 18 healthy controls (HCs) underwent CFM. They were assessed for CFM-induced subjective self-reported stress, acute dissociative symptoms and sympathetic and parasympathetic drive using impedance cardiography. Results: DD patients experienced more subjective stress and acute dissociation than HCs upon CFM. Their psychological stress response did not activate the sympathetic and parasympathetic nervous system. Conclusions: In DD patients, CFM constitutes serious self-reported stress and is associated with a blunted autonomic reactivity. Therapeutic approaches promoting self-perception and self-compassion, in particular by using CFM, might serve as goal-oriented diagnostic and therapeutic tools in DD.
Propofol and arrhythmias: two sides of the coin
The hypnotic agent propofol is effective for the induction and maintenance of anesthesia. However, recent studies have shown that propofol administration is related to arrhythmias. Propofol displays both pro- and anti-arrhythmic effects in a concentration-dependent manner. Data indicate that propofol can convert supraventricular tachycardia and ventricular tachycardia and may inhibit the conduction system of the heart. The mechanism of the cardiac effects remains poorly defined and may involve ion channels, the autonomic nervous system and cardiac gap junctions. Specifically, sodium, calcium and potassium currents in cardiac cells are suppressed by clinically relevant concentrations of propofol. Propofol shortens the action potential duration (APD) but lessens the ischemia-induced decrease in the APD. Furthermore, propofol suppresses both sympathetic and parasympathetic tone and preserves gap junctions during ischemia. All of these effects cumulatively contribute to the antiarrhythmic and proarrhythmic properties of propofol.