Pub Date : 2025-12-01DOI: 10.1016/j.autneu.2025.103363
Mika Nishikawa , Toru Kawada , Nana Hiraki , Masafumi Fukumitsu , Kei Sato , Hiroyuki Kinoshita , Shinji Kawahito , Keita Saku
Vericiguat is a soluble guanylate cyclase stimulator that acts via both nitric oxide-dependent and -independent mechanisms. Previously, we found that vericiguat decreases arterial pressure (AP) primarily by reducing systemic vascular resistance without significantly affecting sympathetic nerve activity. In this study, we investigated whether the AP reduction by vericiguat decreases urine excretion. In male Wistar–Kyoto rats (n = 8), the bilateral carotid sinus baroreceptor regions were isolated from the systemic circulation. The relationship between AP and urine excretion was examined during baroreflex-mediated AP changes before and during intravenous vericiguat administration (10 μg·kg−1·min−1). Vericiguat significantly decreased the operating point AP (104.6 ± 4.2 vs. 85.0 ± 4.1 mmHg, P = 0.008), primarily by decreasing the slope of the baroreflex peripheral arc. However, it maintained urine excretion at the operating point AP (55.5 ± 5.9 vs. 59.8 ± 6.9 μL·min−1·kg−1, P = 0.250) by significantly increasing the slope of the relationship between AP and normalized urine flow (0.53 ± 0.09 vs. 0.99 ± 0.14 μL·min−1·kg−1·mmHg−1, P = 0.008). The maintenance of urine excretion during vericiguat administration might be beneficial for patients with fluid retention.
Vericiguat是一种可溶性鸟苷酸环化酶刺激剂，通过一氧化氮依赖性和非依赖性机制起作用。先前，我们发现vericiguat降低动脉压（AP）主要是通过降低全身血管阻力而不显著影响交感神经活动。在这项研究中，我们研究了vericiguat减少AP是否会减少尿液排泄。雄性Wistar-Kyoto大鼠（n = 8）从体循环中分离出双侧颈动脉窦压力感受器区。在静脉给药（10 μg·kg-1·min-1）前和静脉给药期间，通过bar反射介导的AP变化，检测AP与尿排泄的关系。Vericiguat主要通过降低气压反射外周弧线的斜率而显著降低了工作点AP（104.6±4.2 vs 85.0±4.1 mmHg, P = 0.008）。然而，通过显著增加AP与正常尿流之间的斜率（0.53±0.09比0.99±0.14 μL·min-1·kg-1·mmHg-1, P = 0.008），它维持了操作点AP的尿量（55.5±5.9比59.8±6.9 μL·min-1·kg-1, P = 0.250）。在给药期间保持尿液排泄可能对液体潴留患者有益。
{"title":"Acute effects of vericiguat on urine excretion during baroreflex-mediated sympathetic arterial pressure regulation in male rats","authors":"Mika Nishikawa , Toru Kawada , Nana Hiraki , Masafumi Fukumitsu , Kei Sato , Hiroyuki Kinoshita , Shinji Kawahito , Keita Saku","doi":"10.1016/j.autneu.2025.103363","DOIUrl":"10.1016/j.autneu.2025.103363","url":null,"abstract":"<div><div>Vericiguat is a soluble guanylate cyclase stimulator that acts via both nitric oxide-dependent and -independent mechanisms. Previously, we found that vericiguat decreases arterial pressure (AP) primarily by reducing systemic vascular resistance without significantly affecting sympathetic nerve activity. In this study, we investigated whether the AP reduction by vericiguat decreases urine excretion. In male Wistar–Kyoto rats (<em>n</em> = 8), the bilateral carotid sinus baroreceptor regions were isolated from the systemic circulation. The relationship between AP and urine excretion was examined during baroreflex-mediated AP changes before and during intravenous vericiguat administration (10 μg·kg<sup>−1</sup>·min<sup>−1</sup>). Vericiguat significantly decreased the operating point AP (104.6 ± 4.2 vs. 85.0 ± 4.1 mmHg, <em>P</em> = 0.008), primarily by decreasing the slope of the baroreflex peripheral arc. However, it maintained urine excretion at the operating point AP (55.5 ± 5.9 vs. 59.8 ± 6.9 μL·min<sup>−1</sup>·kg<sup>−1</sup>, <em>P</em> = 0.250) by significantly increasing the slope of the relationship between AP and normalized urine flow (0.53 ± 0.09 vs. 0.99 ± 0.14 μL·min<sup>−1</sup>·kg<sup>−1</sup>·mmHg<sup>−1</sup>, <em>P</em> = 0.008). The maintenance of urine excretion during vericiguat administration might be beneficial for patients with fluid retention.</div></div>","PeriodicalId":55410,"journal":{"name":"Autonomic Neuroscience-Basic & Clinical","volume":"262 ","pages":"Article 103363"},"PeriodicalIF":3.3,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145607424","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-11-17DOI: 10.1016/j.autneu.2025.103362
Amro M. Stino , Jodi Nelson , Olivia Gutgsell , Ahmed Eldokla , Jasmine Liu , Cem Akin
We assessed both objective and subjective measures of autonomic severity in patients with formally classified mast cell activation disorder (MCAD), hereditary alpha tryptasemia (HaT), and systemic mastocytosis. In all subjects, autonomic disease severity was objectively mild but subjectively moderate to severe. The presence of MCAD did not yield consistent differences on subjective or objective severity measures, although HaT did associate with lower objective (but not subjective) severity measures. In conclusion, assessment of MCAD and related disorders can be conducted using formal classification criteria, and in those with suspected dysautonomia, the workup should incorporate objective and subjective measures of dysautonomia.
{"title":"Autonomic function testing and symptom severity in patients with suspected mast cell activation disorders","authors":"Amro M. Stino , Jodi Nelson , Olivia Gutgsell , Ahmed Eldokla , Jasmine Liu , Cem Akin","doi":"10.1016/j.autneu.2025.103362","DOIUrl":"10.1016/j.autneu.2025.103362","url":null,"abstract":"<div><div>We assessed both objective and subjective measures of autonomic severity in patients with formally classified mast cell activation disorder (MCAD), hereditary alpha tryptasemia (HaT), and systemic mastocytosis. In all subjects, autonomic disease severity was objectively mild but subjectively moderate to severe. The presence of MCAD did not yield consistent differences on subjective or objective severity measures, although HaT did associate with lower objective (but not subjective) severity measures. In conclusion, assessment of MCAD and related disorders can be conducted using formal classification criteria, and in those with suspected dysautonomia, the workup should incorporate objective and subjective measures of dysautonomia.</div></div>","PeriodicalId":55410,"journal":{"name":"Autonomic Neuroscience-Basic & Clinical","volume":"262 ","pages":"Article 103362"},"PeriodicalIF":3.3,"publicationDate":"2025-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145566481","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-10-23DOI: 10.1016/j.autneu.2025.103360
Yihan Yang , Ruifang Pu , Diaofeng Zhang , Jie Wu , Wei Deng , Guocan Shen , Jiao Gao , Bo Feng , Liming Cheng , Jiangang Li
Background
Post-traumatic stress disorder (PTSD) is a prevalent psychiatric condition linked to diminished health-related quality of life, physical difficulties, and significant socioeconomic expenses. The stellate ganglion block (SGB) approach is increasingly utilized in patients with PTSD. Due to its efficacy and the variety of treatment alternatives, there is an urgent necessity for consistent and high-quality evidence about the usefulness of this intervention. This study aimed to investigate the effectiveness of SGB in treating PTSD and its related symptoms.
Methods
A systematic search of the PubMed, EMBASE, Web of Science, Cochrane Library, Wan Fang, VIP, and China Knowledge Network databases was performed till November 2024. Risks of bias were analyzed, and the methodological quality of the available literature was assessed. Data extraction and meta-analysis of the studies were conducted to determine the validity of SGB.
Results
Following the evaluation of 394 records, two randomized controlled trials and one case-control trial were incorporated into this meta-analysis. The methodological rigor of the included randomized controlled trials was elevated. In comparison to the control group, the pooled mean difference (MD) in the post-traumatic stress scale (CAPS) scores was diminished by −6.24 (95 % CI [−10.71, −1.78], P = 0.006) in the random-effects model, indicating that SGB treatment alleviated the symptoms of patients with PTSD.
Conclusion
The SGB treatment demonstrates efficacy in alleviating symptoms in people with PTSD. Nonetheless, the limited quantity of randomized controlled trials included necessitates a more extensive collection of high-quality randomized controlled trials to substantiate this result further.
背景：创伤后应激障碍（PTSD）是一种普遍的精神疾病，与健康相关的生活质量下降、身体困难和显著的社会经济支出有关。星状神经节阻滞（SGB）方法越来越多地用于PTSD患者。由于其疗效和治疗方案的多样性，迫切需要一致和高质量的证据来证明这种干预措施的有效性。本研究旨在探讨SGB治疗PTSD及其相关症状的有效性。方法：系统检索PubMed、EMBASE、Web of Science、Cochrane Library、万方、VIP、中国知识网等数据库，检索时间截止到2024年11月。对偏倚风险进行分析，并对现有文献的方法学质量进行评估。对研究进行数据提取和meta分析，以确定SGB的效度。结果：在对394份记录进行评估后，本meta分析纳入了2项随机对照试验和1项病例对照试验。纳入的随机对照试验的方法学严谨性得到了提高。与对照组相比，随机效应模型中创伤后应激量表（CAPS）评分的汇总平均差值（MD）降低了-6.24 (95% CI [-10.71, -1.78], P = 0.006)，表明SGB治疗减轻了PTSD患者的症状。结论：SGB治疗能有效缓解PTSD患者的症状。然而，由于纳入的随机对照试验数量有限，因此需要更广泛的高质量随机对照试验来进一步证实这一结果。
{"title":"Stellate ganglion blockade for the treatment of post-traumatic stress disorder: A systematic review and meta-analysis","authors":"Yihan Yang , Ruifang Pu , Diaofeng Zhang , Jie Wu , Wei Deng , Guocan Shen , Jiao Gao , Bo Feng , Liming Cheng , Jiangang Li","doi":"10.1016/j.autneu.2025.103360","DOIUrl":"10.1016/j.autneu.2025.103360","url":null,"abstract":"<div><h3>Background</h3><div>Post-traumatic stress disorder (PTSD) is a prevalent psychiatric condition linked to diminished health-related quality of life, physical difficulties, and significant socioeconomic expenses. The stellate ganglion block (SGB) approach is increasingly utilized in patients with PTSD. Due to its efficacy and the variety of treatment alternatives, there is an urgent necessity for consistent and high-quality evidence about the usefulness of this intervention. This study aimed to investigate the effectiveness of SGB in treating PTSD and its related symptoms.</div></div><div><h3>Methods</h3><div>A systematic search of the PubMed, EMBASE, Web of Science, Cochrane Library, Wan Fang, VIP, and China Knowledge Network databases was performed till November 2024. Risks of bias were analyzed, and the methodological quality of the available literature was assessed. Data extraction and meta-analysis of the studies were conducted to determine the validity of SGB.</div></div><div><h3>Results</h3><div>Following the evaluation of 394 records, two randomized controlled trials and one case-control trial were incorporated into this meta-analysis. The methodological rigor of the included randomized controlled trials was elevated. In comparison to the control group, the pooled mean difference (MD) in the post-traumatic stress scale (CAPS) scores was diminished by −6.24 (95 % CI [−10.71, −1.78], <em>P</em> = 0.006) in the random-effects model, indicating that SGB treatment alleviated the symptoms of patients with PTSD.</div></div><div><h3>Conclusion</h3><div>The SGB treatment demonstrates efficacy in alleviating symptoms in people with PTSD. Nonetheless, the limited quantity of randomized controlled trials included necessitates a more extensive collection of high-quality randomized controlled trials to substantiate this result further.</div></div>","PeriodicalId":55410,"journal":{"name":"Autonomic Neuroscience-Basic & Clinical","volume":"262 ","pages":"Article 103360"},"PeriodicalIF":3.3,"publicationDate":"2025-10-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145395283","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-10-20DOI: 10.1016/j.autneu.2025.103361
Bruno Rojas-Roel , Julia Devanne , Olivier Després , Thierry Pebayle , André Dufour , Ségolène Lithfous
This study aimed to investigate the role of cutaneous vasodilation in heat pain tolerance during aging. We hypothesized that reduced vasodilation in response to heat would lead to a less efficient heat dissipation, and thus be associated with diminished heat pain tolerance. Due to their efferent role in vasomotor function, we hypothesized that C-fiber functionality would be associated to the efficacy of cutaneous vasodilation. Twenty younger and forty older subjects participated in a 15-min heat pain tolerance test, during which pain ratings were continuously measured, along with skin temperature. Participants could terminate the test at any time if the pain became unbearable. A local thermal hyperemia protocol was conducted to assess cutaneous vasodilation using laser Doppler flowmetry. Warm detection and heat pain thresholds were measured to evaluate small fiber functionality. Older subjects were divided into two groups according to their pain tolerance duration. The older MAX group (n = 22; i.e., 55 %) completed the tolerance test, while the older LOW group did not. Older MAX had preserved cutaneous vasodilation compared to young subjects, whereas older LOW had reduced heat-induced vasodilation. In addition, the skin temperature of older LOW subjects reached a higher level during the pain tolerance test, which was associated to higher pain ratings compared to the two other groups. Older LOW also had higher warm detection threshold, pointing to diminished C-fiber functionality. Reduced cutaneous vasodilation, possibly linked to impaired C-fiber functionality in aging, affects heat pain tolerance due to less efficient heat dissipation.
{"title":"Age-related decrease in heat pain tolerance is associated with a simultaneous decline in C-fiber functionality and local cutaneous vasodilation","authors":"Bruno Rojas-Roel , Julia Devanne , Olivier Després , Thierry Pebayle , André Dufour , Ségolène Lithfous","doi":"10.1016/j.autneu.2025.103361","DOIUrl":"10.1016/j.autneu.2025.103361","url":null,"abstract":"<div><div>This study aimed to investigate the role of cutaneous vasodilation in heat pain tolerance during aging. We hypothesized that reduced vasodilation in response to heat would lead to a less efficient heat dissipation, and thus be associated with diminished heat pain tolerance. Due to their efferent role in vasomotor function, we hypothesized that C-fiber functionality would be associated to the efficacy of cutaneous vasodilation. Twenty younger and forty older subjects participated in a 15-min heat pain tolerance test, during which pain ratings were continuously measured, along with skin temperature. Participants could terminate the test at any time if the pain became unbearable. A local thermal hyperemia protocol was conducted to assess cutaneous vasodilation using laser Doppler flowmetry. Warm detection and heat pain thresholds were measured to evaluate small fiber functionality. Older subjects were divided into two groups according to their pain tolerance duration. The older MAX group (n = 22; i.e., 55 %) completed the tolerance test, while the older LOW group did not. Older MAX had preserved cutaneous vasodilation compared to young subjects, whereas older LOW had reduced heat-induced vasodilation. In addition, the skin temperature of older LOW subjects reached a higher level during the pain tolerance test, which was associated to higher pain ratings compared to the two other groups. Older LOW also had higher warm detection threshold, pointing to diminished C-fiber functionality. Reduced cutaneous vasodilation, possibly linked to impaired C-fiber functionality in aging, affects heat pain tolerance due to less efficient heat dissipation.</div></div>","PeriodicalId":55410,"journal":{"name":"Autonomic Neuroscience-Basic & Clinical","volume":"262 ","pages":"Article 103361"},"PeriodicalIF":3.3,"publicationDate":"2025-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145356829","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-10-20DOI: 10.1016/j.autneu.2025.103359
Roberto Braz Pontes, Paulo Ricardo Lopes, Débora S.A. Colombari, Patrícia M. De Paula, Eduardo Colombari, Carina A.F. Andrade, Laurival A. De Luca Jr, José V. Menani
Previous works suggest that hydrogen peroxide (H2O2), a reactive oxygen species, attenuates brain angiotensin II-mediated hypertension in rats. Moreover, the subcutaneous (s.c.) administration of 3-amino-1,2,4-triazole (ATZ), a catalase inhibitor that increases H2O2 availability, reduces hypertension and sympathetic activity simultaneously with an increase in angiotensinergic activity in spontaneously hypertensive rats (SHRs). It is not clear how much the increase in angiotensinergic activity affects the sympatho-inhibition and the antihypertensive effect of ATZ, and if this is specific for SHRs. The present study evaluated the effects of s.c. ATZ and losartan (angiotensin II AT1 antagonist), alone or combined for 7 days, on mean arterial pressure (MAP) in nitric oxide synthase-inhibited hypertensive rats (L-NAME model). In addition, angiotensinergic and sympathetic activities were also investigated using acute intravenous losartan and hexamethonium (ganglionic blocker) in the same rats. The treatment with ATZ + losartan s.c. reduced MAP slightly below to normotensive levels in L-NAME hypertensive rats (88 ± 8, vs. L-NAME + saline: 162 ± 7 mmHg), whereas s.c. losartan alone partially reduced MAP (133 ± 7 mmHg). The hypotensive responses produced by hexamethonium were reduced in rats treated with ATZ + losartan s.c. (−44 ± 12, vs. L-NAME + saline: −71 ± 6 mmHg), suggesting that the treatment with ATZ + losartan s.c. significantly reduced sympathetic activation in L-NAME-treated rats. These findings suggest that the combination of ATZ and losartan efficiently blocks sympathetic and angiotensinergic activation in L-NAME hypertensive rats, abolishing hypertension. Further research is necessary on the mechanisms of H2O2 and ATZ antihypertensive action.
{"title":"Antihypertensive effects of the treatment with ATZ and losartan in L-NAME hypertensive rats","authors":"Roberto Braz Pontes, Paulo Ricardo Lopes, Débora S.A. Colombari, Patrícia M. De Paula, Eduardo Colombari, Carina A.F. Andrade, Laurival A. De Luca Jr, José V. Menani","doi":"10.1016/j.autneu.2025.103359","DOIUrl":"10.1016/j.autneu.2025.103359","url":null,"abstract":"<div><div>Previous works suggest that hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>), a reactive oxygen species, attenuates brain angiotensin II-mediated hypertension in rats. Moreover, the subcutaneous (s.c.) administration of 3-amino-1,2,4-triazole (ATZ), a catalase inhibitor that increases H<sub>2</sub>O<sub>2</sub> availability, reduces hypertension and sympathetic activity simultaneously with an increase in angiotensinergic activity in spontaneously hypertensive rats (SHRs). It is not clear how much the increase in angiotensinergic activity affects the sympatho-inhibition and the antihypertensive effect of ATZ, and if this is specific for SHRs. The present study evaluated the effects of s.c. ATZ and losartan (angiotensin II AT1 antagonist), alone or combined for 7 days, on mean arterial pressure (MAP) in nitric oxide synthase-inhibited hypertensive rats (L-NAME model). In addition, angiotensinergic and sympathetic activities were also investigated using acute intravenous losartan and hexamethonium (ganglionic blocker) in the same rats. The treatment with ATZ + losartan s.c. reduced MAP slightly below to normotensive levels in L-NAME hypertensive rats (88 ± 8, vs. L-NAME + saline: 162 ± 7 mmHg), whereas s.c. losartan alone partially reduced MAP (133 ± 7 mmHg). The hypotensive responses produced by hexamethonium were reduced in rats treated with ATZ + losartan s.c. (−44 ± 12, vs. L-NAME + saline: −71 ± 6 mmHg), suggesting that the treatment with ATZ + losartan s.c. significantly reduced sympathetic activation in L-NAME-treated rats. These findings suggest that the combination of ATZ and losartan efficiently blocks sympathetic and angiotensinergic activation in L-NAME hypertensive rats, abolishing hypertension. Further research is necessary on the mechanisms of H<sub>2</sub>O<sub>2</sub> and ATZ antihypertensive action.</div></div>","PeriodicalId":55410,"journal":{"name":"Autonomic Neuroscience-Basic & Clinical","volume":"262 ","pages":"Article 103359"},"PeriodicalIF":3.3,"publicationDate":"2025-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145363495","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-10-17DOI: 10.1016/j.autneu.2025.103357
Zoe H. Adams , Lydia L. Simpson , Emma C. Hart , Rachel N. Lord
Polycystic ovary syndrome (PCOS) is the most common endocrinopathy affecting premenopausal females. Alongside the endocrine, reproductive and psychological consequences of the condition, PCOS has now been linked to increased risk of cardiovascular and metabolic disease e.g., insulin resistance. The mechanisms behind this excess risk are not fully understood and multiple characteristics of PCOS (e.g., hyperandrogenism, obesity and vascular dysfunction) likely contribute to individual risk. Autonomic dysfunction may also drive cardiovascular risk in PCOS, via its effects on both blood pressure control and the modulation of sex hormone release at the ovaries. Whilst current studies are limited by moderate sample sizes and one-off measurements, evidence broadly suggests that sympathetic activity may be increased, and vagal control of heart rate may be reduced in PCOS. In this review, we examine the potential mechanisms by which autonomic dysfunction may occur in PCOS. Finally, we discuss how PCOS may interact with ageing and ethnicity to modulate cardiovascular risk secondary to autonomic dysfunction.
{"title":"Autonomic dysfunction in polycystic ovary syndrome","authors":"Zoe H. Adams , Lydia L. Simpson , Emma C. Hart , Rachel N. Lord","doi":"10.1016/j.autneu.2025.103357","DOIUrl":"10.1016/j.autneu.2025.103357","url":null,"abstract":"<div><div>Polycystic ovary syndrome (PCOS) is the most common endocrinopathy affecting premenopausal females. Alongside the endocrine, reproductive and psychological consequences of the condition, PCOS has now been linked to increased risk of cardiovascular and metabolic disease e.g., insulin resistance. The mechanisms behind this excess risk are not fully understood and multiple characteristics of PCOS (e.g., hyperandrogenism, obesity and vascular dysfunction) likely contribute to individual risk. Autonomic dysfunction may also drive cardiovascular risk in PCOS, via its effects on both blood pressure control and the modulation of sex hormone release at the ovaries. Whilst current studies are limited by moderate sample sizes and one-off measurements, evidence broadly suggests that sympathetic activity may be increased, and vagal control of heart rate may be reduced in PCOS. In this review, we examine the potential mechanisms by which autonomic dysfunction may occur in PCOS. Finally, we discuss how PCOS may interact with ageing and ethnicity to modulate cardiovascular risk secondary to autonomic dysfunction.</div></div>","PeriodicalId":55410,"journal":{"name":"Autonomic Neuroscience-Basic & Clinical","volume":"262 ","pages":"Article 103357"},"PeriodicalIF":3.3,"publicationDate":"2025-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145350160","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-10-16DOI: 10.1016/j.autneu.2025.103352
Ying Zhou, Guangqiang Chen, Guangzhi Shi
Background
Paroxysmal sympathetic hyperactivity (PSH) is a rare complication of brain tumor, mostly occurred after craniotomy for brain tumor resection. The purpose of this study is to characterize the pathogenesis and clinical features of PSH in brain tumor.
Methods
All PSH cases with brain tumor at a single center over a 4-year period were retrospectively identified based on medical records. A systematic literature review of the PSH cases with brain tumor was also conducted. PubMed and Web of Science databases were searched.
Results
We identified nine patients at our center and 14 patients in the literature with brain tumor and PSH. There were 10 adult patients and 13 pediatric patients with a median age of 13 years. Most tumors (96 %) were located in deep brain regions. The brainstem and adjacent structures were the most common tumor locations, accounting for 70 %. Glioma (39 %) was the most common pathology type. The onset of PSH occurred after tumor resection or biopsy in 18 patients, during tumor resection in two patients, and during conservative treatment in three patients. The most common PSH symptoms in brain tumor were hypertension (100 %) and tachycardia (96 %).
Conclusions
PSH is not only an underlying complication of brain tumor resection, but also a rare clinical manifestation of brain tumor. We speculate that damage to the midbrain or pons, especially close to the midline of the tegmentum, might be one of the lesion patterns underlying PSH.
背景：阵发性交感神经亢进（PSH）是一种罕见的脑肿瘤并发症，多发生在脑肿瘤切除术开颅手术后。本研究旨在探讨脑肿瘤PSH的发病机制及临床特点。方法：回顾性分析4年内同一中心所有PSH合并脑肿瘤的病例。对PSH合并脑肿瘤的病例也进行了系统的文献回顾。检索了PubMed和Web of Science数据库。结果：我们在本中心发现了9例患者，文献中发现了14例脑肿瘤和PSH患者。成人患者10例，小儿患者13例，中位年龄13岁。大多数肿瘤（96%）位于脑深部。脑干及邻近结构是最常见的肿瘤部位，占70%。胶质瘤（39%）是最常见的病理类型。18例患者在肿瘤切除或活检后发病，2例患者在肿瘤切除期间发病，3例患者在保守治疗期间发病。脑肿瘤患者最常见的PSH症状是高血压（100%）和心动过速（96%）。结论：PSH不仅是脑肿瘤切除术的潜在并发症，而且是脑肿瘤罕见的临床表现。我们推测，中脑或脑桥的损伤，特别是靠近被盖中线的损伤，可能是PSH的病变模式之一。
{"title":"Clinical features of paroxysmal sympathetic hyperactivity in brain tumor: a retrospective case series study and literature review","authors":"Ying Zhou, Guangqiang Chen, Guangzhi Shi","doi":"10.1016/j.autneu.2025.103352","DOIUrl":"10.1016/j.autneu.2025.103352","url":null,"abstract":"<div><h3>Background</h3><div>Paroxysmal sympathetic hyperactivity (PSH) is a rare complication of brain tumor, mostly occurred after craniotomy for brain tumor resection. The purpose of this study is to characterize the pathogenesis and clinical features of PSH in brain tumor.</div></div><div><h3>Methods</h3><div>All PSH cases with brain tumor at a single center over a 4-year period were retrospectively identified based on medical records. A systematic literature review of the PSH cases with brain tumor was also conducted. PubMed and Web of Science databases were searched.</div></div><div><h3>Results</h3><div>We identified nine patients at our center and 14 patients in the literature with brain tumor and PSH. There were 10 adult patients and 13 pediatric patients with a median age of 13 years. Most tumors (96 %) were located in deep brain regions. The brainstem and adjacent structures were the most common tumor locations, accounting for 70 %. Glioma (39 %) was the most common pathology type. The onset of PSH occurred after tumor resection or biopsy in 18 patients, during tumor resection in two patients, and during conservative treatment in three patients. The most common PSH symptoms in brain tumor were hypertension (100 %) and tachycardia (96 %).</div></div><div><h3>Conclusions</h3><div>PSH is not only an underlying complication of brain tumor resection, but also a rare clinical manifestation of brain tumor. We speculate that damage to the midbrain or pons, especially close to the midline of the tegmentum, might be one of the lesion patterns underlying PSH.</div></div>","PeriodicalId":55410,"journal":{"name":"Autonomic Neuroscience-Basic & Clinical","volume":"262 ","pages":"Article 103352"},"PeriodicalIF":3.3,"publicationDate":"2025-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145423527","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Hypermobility Spectrum Disorders (HSD) and hypermobile Ehlers-Danlos syndrome (h-EDS) are multisystemic connective tissue disorders involving joint hypermobility and numerous other manifestations. Autonomic dysfunction, chronic pain, and chronic fatigue are known comorbidities of HSD and h-EDS that can affect patient quality of life (QoL), but there are limited data on the severity of autonomic symptoms, prevalence of comorbid conditions and QoL in patients with HSD/h-EDS.
Methods
We utilized the Composite Autonomic Symptom Scale (COMPASS-31) to assess autonomic symptom severity, Short-Form 36 (SF-36) to assess QoL, and the Beck Depression Inventory Second Edition (BDI-II) in a cohort of women with physician-diagnosed HSD or h-EDS, who completed these questionnaires anonymously.
Results
84 women (mean age of 37.1 ± 8.4 years) completed the study. 58.3 % reported having physician-diagnosed postural orthostatic tachycardia syndrome (POTS), 32.1 % had mast cell activation syndrome (MCAS), 54.8 % had migraine, 26.2 % had myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and 98.8 % reported experiencing chronic pain. Importantly, 25 % of patients reported having all three diagnoses: HSD/h-EDS, POTS and MCAS. Mean COMPASS-31 score was 54.45 (range 18.79–80.93), indicating severe autonomic dysfunction, which was significantly higher than in patients with multiple sclerosis, diabetic neuropathy, scleroderma, and psoriatic arthritis as shown in prior studies. Mean SF-36 score was 32.38 (SD = 22.91) indicating poor QoL, which was worse than in patients with POTS, multiple sclerosis, rheumatoid arthritis, and lupus as determined by prior studies.
Conclusions
This study demonstrates that women with HSD/h-EDS experience severe autonomic dysfunction, chronic pain, chronic comorbid conditions and reduced QoL. More than half of participants in this cohort had POTS and migraine, with one in four having a clinical triad of HSD/h-EDS, POTS and MCAS.
{"title":"Autonomic symptom burden, comorbidities and quality of life in women with Hypermobility Spectrum Disorders and hypermobile Ehlers-Danlos syndrome","authors":"Meagan L. Collins Hutchinson , Emily Liang , Emily Fuster , Svetlana Blitshteyn","doi":"10.1016/j.autneu.2025.103356","DOIUrl":"10.1016/j.autneu.2025.103356","url":null,"abstract":"<div><h3>Background</h3><div>Hypermobility Spectrum Disorders (HSD) and hypermobile Ehlers-Danlos syndrome (h-EDS) are multisystemic connective tissue disorders involving joint hypermobility and numerous other manifestations. Autonomic dysfunction, chronic pain, and chronic fatigue are known comorbidities of HSD and h-EDS that can affect patient quality of life (QoL), but there are limited data on the severity of autonomic symptoms, prevalence of comorbid conditions and QoL in patients with HSD/h-EDS.</div></div><div><h3>Methods</h3><div>We utilized the Composite Autonomic Symptom Scale (COMPASS-31) to assess autonomic symptom severity, Short-Form 36 (SF-36) to assess QoL, and the Beck Depression Inventory Second Edition (BDI-II) in a cohort of women with physician-diagnosed HSD or h-EDS, who completed these questionnaires anonymously.</div></div><div><h3>Results</h3><div>84 women (mean age of 37.1 ± 8.4 years) completed the study. 58.3 % reported having physician-diagnosed postural orthostatic tachycardia syndrome (POTS), 32.1 % had mast cell activation syndrome (MCAS), 54.8 % had migraine, 26.2 % had myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and 98.8 % reported experiencing chronic pain. Importantly, 25 % of patients reported having all three diagnoses: HSD/h-EDS, POTS and MCAS. Mean COMPASS-31 score was 54.45 (range 18.79–80.93), indicating severe autonomic dysfunction, which was significantly higher than in patients with multiple sclerosis, diabetic neuropathy, scleroderma, and psoriatic arthritis as shown in prior studies. Mean SF-36 score was 32.38 (SD = 22.91) indicating poor QoL, which was worse than in patients with POTS, multiple sclerosis, rheumatoid arthritis, and lupus as determined by prior studies.</div></div><div><h3>Conclusions</h3><div>This study demonstrates that women with HSD/h-EDS experience severe autonomic dysfunction, chronic pain, chronic comorbid conditions and reduced QoL. More than half of participants in this cohort had POTS and migraine, with one in four having a clinical triad of HSD/h-EDS, POTS and MCAS.</div></div>","PeriodicalId":55410,"journal":{"name":"Autonomic Neuroscience-Basic & Clinical","volume":"262 ","pages":"Article 103356"},"PeriodicalIF":3.3,"publicationDate":"2025-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145350233","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and the prolonged sequelae after COVID-19 (>3 months; Long COVID) have similar symptomology, are both associated with autonomic dysfunction, and a growing proportion of Long COVID patients are developing ME/CFS. We aimed to determine an autonomic phenotype of patients with ME/CFS vs Long COVID. We hypothesized that the groups would differ from controls yet be similar to one another. We recruited sedentary controls (n = 10), mild/moderate ME/CFS patients (n = 12), and Long COVID patients (n = 9) to undergo 1) breathing 5 % CO2, 2) breathing 10 % O2, and 3) 5-minutes of 70° head-up tilt. Respiratory, hemodynamic, and cerebrovascular variables were measured throughout the 3 trials. Resting vascular function and cognitive-motor-integration were also assessed. ME/CFS and Long COVID were similar to the healthy controls and each other with regard to resting vascular function and the hemodynamic responses to hypoxia, hypercapnia, and head-up tilt (p > 0.05). However, in ME/CFS we observed a greater reduction of cerebrovascular resistance (p = 0.041) and impaired autoregulation (p = 0.042) during hypercapnia alongside impaired cognitive-motor integration (p < 0.02), and in Long COVID we observed reduced peripheral and end-tidal oxygen (p < 0.04) and less vagal withdrawal during tilt (p = 0.028). Our findings suggest unique phenotypes when comparing ME/CFS and Long COVID whereby we have shown that Long COVID patients experience hypoxia while upright contributing to less vagal withdrawal, and ME/CFS patients experience impaired cerebrovascular control during hypercapnia potentially leading to reduced cognitive-motor integration. These differences could stem from disease severity/duration or some unique aspect of the COVID-19 virus.
{"title":"Autonomic phenotyping, brain blood flow control, and cognitive-motor-integration in Long COVID and myalgic encephalomyelitis/chronic fatigue syndrome: A pilot study","authors":"Smriti Badhwar , Tania J. Pereira , Kathleen Kerr , Riina Bray , Farah Tabassum , Lauren Sergio , Heather Edgell","doi":"10.1016/j.autneu.2025.103358","DOIUrl":"10.1016/j.autneu.2025.103358","url":null,"abstract":"<div><div>Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and the prolonged sequelae after COVID-19 (>3 months; Long COVID) have similar symptomology, are both associated with autonomic dysfunction, and a growing proportion of Long COVID patients are developing ME/CFS. We aimed to determine an autonomic phenotype of patients with ME/CFS vs Long COVID. We hypothesized that the groups would differ from controls yet be similar to one another. We recruited sedentary controls (<em>n</em> = 10), mild/moderate ME/CFS patients (<em>n</em> = 12), and Long COVID patients (<em>n</em> = 9) to undergo 1) breathing 5 % CO<sub>2</sub>, 2) breathing 10 % O<sub>2</sub>, and 3) 5-minutes of 70° head-up tilt. Respiratory, hemodynamic, and cerebrovascular variables were measured throughout the 3 trials. Resting vascular function and cognitive-motor-integration were also assessed. ME/CFS and Long COVID were similar to the healthy controls and each other with regard to resting vascular function and the hemodynamic responses to hypoxia, hypercapnia, and head-up tilt (<em>p</em> > 0.05). However, in ME/CFS we observed a greater reduction of cerebrovascular resistance (<em>p</em> = 0.041) and impaired autoregulation (<em>p</em> = 0.042) during hypercapnia alongside impaired cognitive-motor integration (<em>p</em> < 0.02), and in Long COVID we observed reduced peripheral and end-tidal oxygen (<em>p</em> < 0.04) and less vagal withdrawal during tilt (<em>p</em> = 0.028). Our findings suggest unique phenotypes when comparing ME/CFS and Long COVID whereby we have shown that Long COVID patients experience hypoxia while upright contributing to less vagal withdrawal, and ME/CFS patients experience impaired cerebrovascular control during hypercapnia potentially leading to reduced cognitive-motor integration. These differences could stem from disease severity/duration or some unique aspect of the COVID-19 virus.</div></div>","PeriodicalId":55410,"journal":{"name":"Autonomic Neuroscience-Basic & Clinical","volume":"262 ","pages":"Article 103358"},"PeriodicalIF":3.3,"publicationDate":"2025-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145363496","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-10-14DOI: 10.1016/j.autneu.2025.103355
Eduardo Costa Alexandre , Alline Araujo Curiel , Jessica Mariana Dias , Fabio H. da Silva , Edson Antunes , Mariana G. de Oliveira
Epidemiological studies identify age as the primary unmodifiable risk factor for male lower urinary tract symptoms (LUTS). While research has focused on the bladder and prostate, the urethra remains understudied. This study investigates aging-induced changes in rat urethral structure and function and their impact on voiding. Male Wistar rats, young (3.5 months) and middle-aged (10 months), were used. Cystometry assessed voiding in vivo, and isolated urethras were used in vitro. Middle-aged rats showed irregular micturition with increased basal pressure, bladder capacity, compliance, and non-voiding contractions, suggesting elevated outlet resistance. Histology showed no significant differences. Contractions to electrical-field stimulation and the α1-adrenoceptor agonist phenylephrine were enhanced, along with a twofold increase in α1A-adrenoceptor mRNA. Conversely, relaxation to nitric oxide (NO) donors sodium nitroprusside (SNP) and glyceryl trinitrate (GTN) was reduced, while responses to the cGMP analog 8Br-cGMP and the soluble guanylate cyclase (sGC) stimulator BAY 41-2272 were unchanged. Lower NO levels, despite increased endothelial NO synthase (eNOS) mRNA, were observed in middle-aged urethras, with no changes in neuronal NOS (nNOS) or sGC subunit β1. Phosphodiesterase type 5 (PDE5) mRNA was elevated, correlating with reduced basal and SNP-stimulated cGMP. Oxidative stress was evident, with increased superoxide and reduced expression of antioxidant enzymes superoxide dismutase (SOD), glutathione peroxidase (GPX), and catalase (CAT). NADPH oxidase 2 (NOX2) and xanthine dehydrogenase (XDH) mRNA were upregulated, while hypoxia-inducible factor 1-alpha (HIF1α) remained unchanged. In summary, middle-aged rats show urethral hypercontractility, impaired relaxation, and oxidative stress, without tissue remodeling or ischemia.
{"title":"Aging impairs urethral function in male rats: Increased outlet resistance and oxidative stress","authors":"Eduardo Costa Alexandre , Alline Araujo Curiel , Jessica Mariana Dias , Fabio H. da Silva , Edson Antunes , Mariana G. de Oliveira","doi":"10.1016/j.autneu.2025.103355","DOIUrl":"10.1016/j.autneu.2025.103355","url":null,"abstract":"<div><div>Epidemiological studies identify age as the primary unmodifiable risk factor for male lower urinary tract symptoms (LUTS). While research has focused on the bladder and prostate, the urethra remains understudied. This study investigates aging-induced changes in rat urethral structure and function and their impact on voiding. Male Wistar rats, young (3.5 months) and middle-aged (10 months), were used. Cystometry assessed voiding in vivo, and isolated urethras were used in vitro. Middle-aged rats showed irregular micturition with increased basal pressure, bladder capacity, compliance, and non-voiding contractions, suggesting elevated outlet resistance. Histology showed no significant differences. Contractions to electrical-field stimulation and the α1-adrenoceptor agonist phenylephrine were enhanced, along with a twofold increase in α1A-adrenoceptor mRNA. Conversely, relaxation to nitric oxide (NO) donors sodium nitroprusside (SNP) and glyceryl trinitrate (GTN) was reduced, while responses to the cGMP analog 8Br-cGMP and the soluble guanylate cyclase (sGC) stimulator BAY 41-2272 were unchanged. Lower NO levels, despite increased endothelial NO synthase (eNOS) mRNA, were observed in middle-aged urethras, with no changes in neuronal NOS (nNOS) or sGC subunit β1. Phosphodiesterase type 5 (PDE5) mRNA was elevated, correlating with reduced basal and SNP-stimulated cGMP. Oxidative stress was evident, with increased superoxide and reduced expression of antioxidant enzymes superoxide dismutase (SOD), glutathione peroxidase (GPX), and catalase (CAT). NADPH oxidase 2 (NOX2) and xanthine dehydrogenase (XDH) mRNA were upregulated, while hypoxia-inducible factor 1-alpha (HIF1α) remained unchanged. In summary, middle-aged rats show urethral hypercontractility, impaired relaxation, and oxidative stress, without tissue remodeling or ischemia.</div></div>","PeriodicalId":55410,"journal":{"name":"Autonomic Neuroscience-Basic & Clinical","volume":"262 ","pages":"Article 103355"},"PeriodicalIF":3.3,"publicationDate":"2025-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145314191","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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