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The automatic nervous system (ANS) is a branch of the peripheral nervous system involved in involuntary neural control of peripheral functions, such as digesting and breathing. The ANS is broken down into two systems: the sympathetic (SNS) and parasympathetic (PNS) nervous systems. The SNS is heavily involved in responses to environmental threats, such as regulating heart and respiration rates. On the other hand, the PNS is heavily involved in facilitating regulation in times of stress (Gibbons, 2019). ANS functioning has been associated with both mental and physical health outcomes across the lifespan (Harker, 2013; Kemp et al., 2014; Liu et al., 2022). In adults, multiple markers of ANS functioning (i.e., electrodermal activity, heart rate variability) have been associated with structural and functional differences in networks that aid emotional responses and peripheral regulation (Banks et al., 2007, 2014; Lane et al., 2009; Xia et al., 2017, p. 201; Zhang et al., 2012). For example, indicators of parasympathetic activity have been associated with blood flow in regions hypothesized to correlate with cardiac autonomic activity (e.g., amygdala, insula, anterior cingulate). (Gianaros et al., 2004). Moreover, markers of sympathetic function (i.e., lower skin conductance levels) have been associated with activation in regulatory nodes of the brain (Zhang et al., 2012). In children, indicators of ANS function have been associated with developmental outcomes, such as emotion dysregulation and mental health disorders (Busso et al., 2014; Calkins, 1997; Pine et al., 1998). Moreover, a study showed that increased heart-rate variability (a marker of PNS regulation) was associated with increased thickness of the orbitofrontal cortex, and these biological markers were associated with decreased depression post-SSRI treatment in children (Koenig et al., 2018). No study to date has explored associations between ANS function and neural correlates of emotional reactivity in early human development. Here, we focus on the salience network (SN), a neural network that detects, coordinates responses to physiological and environmental stressors to promote homeostasis (Lamotte et al., 2021). Indeed, functional activation meta-analyses show that the SN plays a key role in detecting and learning from aversive stimuli, while other neural networks (e.g., default mode) play a greater role in detecting safety cues and inhibiting aversive responses (Fullana et al., 2016, 2018). We propose that markers of ANS function (both within the PNS and the SNS) will be associated with neural recruitment of the SN during emotional reactivity.

Journal of the Autonomic Nervous System 1997: Volume 67 , Issue Index. Digitized from IA1653233-01 . Previous issue: sim_autonomic-neuroscience-basic-clinical_1997-10-13_66_3_0 . Next issue: sim_autonomic-neuroscience-basic-clinical_1997-12-03_67_1-2_0 . Note: This issue has no cover

Journal of the Autonomic Nervous System 1992: Volume 40 , Issue Index. Digitized from IA1652423-04 . Previous issue: sim_autonomic-neuroscience-basic-clinical_1992-07_39_3 . Next issue: sim_autonomic-neuroscience-basic-clinical_1992-08_40_1 .

Journal of the Autonomic Nervous System 1992: Volume 40 , Issue Index. Digitized from IA1653233-03 . Previous issue: sim_autonomic-neuroscience-basic-clinical_1992-07_39_3_0 . Next issue: sim_autonomic-neuroscience-basic-clinical_1992-08_40_1_0 .

Journal of the Autonomic Nervous System 1992: Volume 41 , Issue Index. Digitized from IA1653233-03 . Previous issue: sim_autonomic-neuroscience-basic-clinical_1992-10_40_3_0 . Next issue: sim_autonomic-neuroscience-basic-clinical_1992-11_41_1-2_0 .

Journal of the Autonomic Nervous System 1993: Volume 45 , Issue Index. Digitized from IA1653233-03 . Previous issue: sim_autonomic-neuroscience-basic-clinical_august-september-1993_44_2-3_0 . Next issue: sim_autonomic-neuroscience-basic-clinical_1993-10_45_1_0 .

Journal of the Autonomic Nervous System 1993: Volume 45 , Issue Index. Digitized from IA1653233-03 . Previous issue: sim_autonomic-neuroscience-basic-clinical_august-september-1993_44_2-3_0 . Next issue: sim_autonomic-neuroscience-basic-clinical_1993-10_45_1_0 .

Journal of the Autonomic Nervous System 1996 - 1997: Volume 62 , Issue Index. Digitized from IA1652423-04 . Previous issue: sim_autonomic-neuroscience-basic-clinical_1996-12-14_61_3 . Next issue: sim_autonomic-neuroscience-basic-clinical_1997-01-12_62_1-2 .

Journal of the Autonomic Nervous System 1996: Volume 58 , Issue Index. Digitized from IA1653233-01 . Previous issue: sim_autonomic-neuroscience-basic-clinical_1996-03-07_57_3_0 . Next issue: sim_autonomic-neuroscience-basic-clinical_1996-04-20_58_1-2_0 . Note: This issue has no cover

Journal of the Autonomic Nervous System 1987: Volume 21 , Issue Index. Digitized from IA1652423-04 . Previous issue: sim_autonomic-neuroscience-basic-clinical_1987-10_20_3 . Next issue: sim_autonomic-neuroscience-basic-clinical_1987-11_21_1 .

Journal of the Autonomic Nervous System 1993: Volume 45 , Issue Index. Digitized from IA1652423-04 . Previous issue: sim_autonomic-neuroscience-basic-clinical_august-september-1993_44_2-3 . Next issue: sim_autonomic-neuroscience-basic-clinical_1993-10_45_1 .

Journal of the Autonomic Nervous System 1994: Volume 48 , Issue Index. Digitized from IA1652423-04 . Previous issue: sim_autonomic-neuroscience-basic-clinical_1994-05_47_3 . Next issue: sim_autonomic-neuroscience-basic-clinical_1994-06_48_1 .

Journal of the Autonomic Nervous System 1995: Volume 51 , Issue Index. Digitized from IA1653233-01 . Previous issue: sim_autonomic-neuroscience-basic-clinical_1995-01-03_50_3_0 . Next issue: sim_autonomic-neuroscience-basic-clinical_1995-01-20_51_1_0 . Note: This issue has no cover

Journal of the Autonomic Nervous System 1995: Volume 51 , Issue Index. Digitized from IA1653233-01 . Previous issue: sim_autonomic-neuroscience-basic-clinical_1995-01-03_50_3_0 . Next issue: sim_autonomic-neuroscience-basic-clinical_1995-01-20_51_1_0 . Note: This issue has no cover

This article is from Molecular Autism , volume 5 . Abstract Background: Autonomic dysregulation has been recently reported as a feature of autism spectrum disorder (ASD). However, the nature of autonomic atypicalities in ASD remain largely unknown. The goal of this study was to characterize the cardiac autonomic profile of children with ASD across four domains affected in ASD (anxiety, attention, response inhibition, and social cognition), and suggested to be affected by autonomic dysregulation. Methods: We compared measures of autonomic cardiac regulation in typically developing children (n = 34) and those with ASD (n = 40) as the children performed tasks eliciting anxiety, attention, response inhibition, and social cognition. Heart rate was used to quantify overall autonomic arousal, and respiratory sinus arrhythmia (RSA) was used as an index of vagal influences. Associations between atypical autonomic findings and intellectual functioning (Weschler scale), ASD symptomatology (Social Communication Questionnaire score), and co-morbid anxiety (Revised Children’s Anxiety and Depression Scale) were also investigated. Results: The ASD group had marginally elevated basal heart rate, and showed decreased heart rate reactivity to social anxiety and increased RSA reactivity to the social cognition task. In this group, heart rate reactivity to the social anxiety task was positively correlated with IQ and task performance, and negatively correlated with generalized anxiety. RSA reactivity in the social cognition task was positively correlated with IQ. Conclusions: Our data suggest overall autonomic hyperarousal in ASD and selective atypical reactivity to social tasks.

This article is from The Journal of Veterinary Medical Science , volume 76 . Abstract To clarify the origin of efferent nerves containing renal plexus, the retrograde neuronal tracing was utilized with a new exact closed injection system with microcapsules. The microcapsule was positioned in the rat left renal plexus, and the capsule was filled with fluoro-gold. Retrograde labeled cells were observed in the ipsilateral sympathetic trunk, especially T12 and T13, and the ipsilateral suprarenal ganglia (SrG). There were no labeled cells in the parasympathetic nuclei in medulla oblongata and sacral cords. These results indicated that the origins of efferent nerves in the rat renal plexus are almost all sympathetic ganglia, such as sympathetic trunk and SrG, and cells in other ganglia may be secondary or accessory innervations.

Journal of the Autonomic Nervous System 1995: Volume 54 , Issue Index. Digitized from IA1653233-01 . Previous issue: sim_autonomic-neuroscience-basic-clinical_1995-06-25_53_2-3_0 . Next issue: sim_autonomic-neuroscience-basic-clinical_1995-07-14_54_1_0 . Note: This issue has no cover

Journal of the Autonomic Nervous System 1995: Volume 55 , Issue Index. Digitized from IA1652423-04 . Previous issue: sim_autonomic-neuroscience-basic-clinical_1995-09-05_54_3 . Next issue: sim_autonomic-neuroscience-basic-clinical_1995-10-05_55_1-2 .

Journal of the Autonomic Nervous System 1995: Volume 55 , Issue Index. Digitized from IA1653233-01 . Previous issue: sim_autonomic-neuroscience-basic-clinical_1995-09-05_54_3_0 . Next issue: sim_autonomic-neuroscience-basic-clinical_1995-10-05_55_1-2_0 . Note: This issue has no cover

The developmental origins of disease hypothesis posits that early life stress, such as childhood trauma and adversities, can permanently affect health in later life (Gluckman et al., 2005). Consistent with this hypothesis, childhood trauma exposure has been robustly associated with both mental and physical health problems throughout the lifespan (Hogg et al., 2022; Suglia et al., 2015). It has been theorised that neurobiological changes in the body’s stress response systems, including in the autonomic nervous system (ANS), drive these long-term adverse effects of childhood trauma (Agorastos et al., 2018; Beilharz et al., 2020). A key area of growing concern is the robust association between childhood trauma and an increased risk of cardiovascular diseases (CVDs; Jacquet-Smailovic et al., 2022; Suglia et al., 2015), which are among the leading causes of death worldwide (WHO, 2019). However, robust evidence investigating early markers of cardiovascular function is limited. Given that research has consistently found that elevated heart rate (HR) measured in the aftermath of a traumatic event is associated with subsequently reporting more post-traumatic stress symptoms (Morris et al., 2016), and that both childhood trauma and elevated resting HR are associated with increased risk of CVDs (Aune et al., 2017), it is theorised that childhood trauma is associated with a persistently elevated HR. However, research has yielded mixed findings across both adult and youth samples, with trauma linked to both elevated (Beilharz et al., 2020; Pretty et al., 2013) and reduced resting HR (Bailey et al., 2025; Krenichyn et al., 2001) in some studies, and no effects in others (MacMillan et al., 2009; Sigrist et al., 2021). It has been theorised that trauma exposure, particularly cumulative or prolonged traumas, during critical developmental periods could result in chronic hyperactivation or hypoactivation of the stress response system, dependent on trauma timing (e.g., early childhood vs. adolescence; Agorastos et al., 2018) or the type and extent of trauma exposure (Herzog et al., 2018), which could offer some explanation for this mixed pattern of findings. However, there are several key limitations of the existing evidence which may have also contributed to these findings. Firstly, most research has been conducted with relatively small sample sizes and has been conducted primarily in high-income countries. Youth in low- and middle-income countries (LMICs) are especially underrepresented despite the majority of the world’s children living in LMICs (UNICEF, 2005), and these youth being disproportionately more likely to be exposed to traumas than youth in high-income countries (WHO, 2002). More than 75% of children in South Africa were estimated to have been exposed to at least one traumatic event before age 6 years (Tsunga et al., 2023); estimates from high-income country cohorts demonstrate substantially lower rates of trauma exposure even when participants are older (Lewis et al., 2019). Secondly, most studies have used cross-sectional designs. For studies with adults, childhood trauma exposure is therefore reported retrospectively which may introduce significant recall bias. Additionally, cross-sectional studies recruit participants following trauma exposure; therefore the ability to draw causal conclusions regarding trauma-HR associations is limited. Furthermore, because participants have been recruited following trauma exposure, most individuals have been exposed to single-incident traumas, such as road traffic accidents and other accidental injuries. Research has shown that interpersonal childhood traumas, especially those occurring within the family, such as physical, sexual, and domestic violence, are the strongest predictors of psychopathology (Green et al., 2010; McLaughlin et al., 2010). The underrepresentation of these more severe or chronic/repeated traumas in the existing literature may therefore offer some explanation for the mixed findings across studies. Finally, a limitation of all the aforementioned studies is that HR was measured at a single timepoint. HR is not static and decreases naturally with age (Sarganas et al., 2017). Research should therefore utilise repeated measurements of HR to investigate whether childhood trauma exposure is associated with changes in HR development (e.g., slowing of the normal pattern of decline with advancing age). Heart rate variability (HRV), the variation in time intervals between heartbeats, has also been of particular interest in the traumatic stress literature, as it is viewed as a more sensitive measure of ANS function (Appelhans & Luecken, 2006), through indices that capture sympathetic and parasympathetic activity (Nagpal et al., 2013). Lower HRV is thought to reflect impaired functioning/regulation of the ANS, which negatively affects the body’s ability to cope with stressors (Sigrist et al., 2021), and research has shown lower HRV to be associated with an increased risk of cardiovascular events (Hillebrand et al., 2013). Research with adults has shown associations between childhood trauma and reduced resting HRV (Bussone et al., 2023; Jin et al., 2018), though research with youth samples has not observed such effects (MacArthur, 2011; Michels et al., 2013), suggesting that the impact of childhood trauma on HRV may not be evident until later life. Finally, childhood trauma exposures have been associated with blunted ANS reactivity to stressors (Busso et al., 2017; Voellmin et al., 2015). However, again, this evidence is limited by small sample sizes, the use of cross-sectional designs, and an underrepresentation of LMIC samples. To address these limitations of the existing literature, the present study will use data from the Drakenstein Child Health Study (Donald et al., 2018; Stein et al., 2015; Zar et al., 2015), an ongoing prospective birth cohort located in Cape Town, South Africa, to conduct a longitudinal investigation of the impact of childhood trauma on ANS functioning in children living in a LMIC. Research Questions & Aims: 1. Does childhood trauma exposure predict the average levels and rate of change of resting HR during childhood? We aim to estimate change in resting HR between ages 4 and 8 years using growth curve modelling, and to examine trauma exposure up to age 4.5 years as a time-invariant predictor of the resultant growth factors. 2. Is childhood trauma exposure associated with resting HRV during childhood? We aim to use linear regression analyses to examine cross-sectional and longitudinal associations between childhood trauma exposure (assessed at ages 4.5 and 8 years) and indices of resting HRV at age 8. 3. Is childhood trauma exposure associated with altered autonomic reactivity to stress? We aim to use linear regression analyses to examine cross-sectional and longitudinal associations between childhood trauma exposure (assessed at ages 4.5 and 8 years) and HR and HRV reactivity in response to stress at age 8 years (captured via residualized change scores).

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This article is from BMC Psychiatry , volume 12 . Abstract Background: Antipsychotic drugs are considered a trigger factor for autonomic dysregulation, which has been shown to predict potentially fatal arrhythmias in schizophrenia. However, the dose-dependent effect of antipsychotic drugs and other psychotropic drugs on autonomic nervous system (ANS) activity remain unclear. The purpose of this study was to investigate the dose-dependent effect of antipsychotic drugs and other clinical factors on ANS activity in an adequate sample size of patients with schizophrenia. Methods: A total of 211 Japanese patients with schizophrenia and 44 healthy subjects participated in this study. ANS activity was assessed by means of heart rate variability (HRV) power spectral analysis. Antipsychotic drug treatment and various clinical factors were investigated for each participant. The patient group was categorized into three subgroups according to daily dose of antipsychotic drug, and HRV was compared between groups. Results: The results showed significantly decreased low-frequency and high-frequency components of HRV in the patient group compared to the control group. The high-dose group showed a significantly lower HRV than the medium-dose group and an even lower HRV than the low-dose group. In addition, a significant association between HRV and antipsychotic drug dose was identified by multiple regression analysis. HRV was not associated with age, sex, body mass index, duration of illness, or daily dose of other psychotropic drugs. Conclusion: These results suggest that antipsychotic drugs exert a significant dose-dependent effect on the extent of decline in ANS activity, and that optimal antipsychotic medication is required to avoid possible cardiovascular adverse events in patients with schizophrenia.

This article is from BMC Psychiatry , volume 12 . Abstract Background: Antipsychotic drugs are considered a trigger factor for autonomic dysregulation, which has been shown to predict potentially fatal arrhythmias in schizophrenia. However, the dose-dependent effect of antipsychotic drugs and other psychotropic drugs on autonomic nervous system (ANS) activity remain unclear. The purpose of this study was to investigate the dose-dependent effect of antipsychotic drugs and other clinical factors on ANS activity in an adequate sample size of patients with schizophrenia. Methods: A total of 211 Japanese patients with schizophrenia and 44 healthy subjects participated in this study. ANS activity was assessed by means of heart rate variability (HRV) power spectral analysis. Antipsychotic drug treatment and various clinical factors were investigated for each participant. The patient group was categorized into three subgroups according to daily dose of antipsychotic drug, and HRV was compared between groups. Results: The results showed significantly decreased low-frequency and high-frequency components of HRV in the patient group compared to the control group. The high-dose group showed a significantly lower HRV than the medium-dose group and an even lower HRV than the low-dose group. In addition, a significant association between HRV and antipsychotic drug dose was identified by multiple regression analysis. HRV was not associated with age, sex, body mass index, duration of illness, or daily dose of other psychotropic drugs. Conclusion: These results suggest that antipsychotic drugs exert a significant dose-dependent effect on the extent of decline in ANS activity, and that optimal antipsychotic medication is required to avoid possible cardiovascular adverse events in patients with schizophrenia.

Journal of the Autonomic Nervous System 1996: Volume 61 , Issue Index. Digitized from IA1652423-04 . Previous issue: sim_autonomic-neuroscience-basic-clinical_1996-09-12_60_3 . Next issue: sim_autonomic-neuroscience-basic-clinical_1996-10-07_61_1 .

Journal of the Autonomic Nervous System 1998: Volume 68 , Issue Index. Digitized from IA1653233-01 . Previous issue: sim_autonomic-neuroscience-basic-clinical_1997-12-11_67_3_0 . Next issue: sim_autonomic-neuroscience-basic-clinical_1998-01-19_68_1-2_0 . Note: This issue has no cover

Journal of the Autonomic Nervous System 1998: Volume 70 , Issue Index. Digitized from IA1652423-04 . Previous issue: sim_autonomic-neuroscience-basic-clinical_1998-04-30_69_2-3 . Next issue: sim_autonomic-neuroscience-basic-clinical_1998-05-28_70_1-2 .

Journal of the Autonomic Nervous System 1998: Volume 70 , Issue Index. Digitized from IA1652423-04 . Previous issue: sim_autonomic-neuroscience-basic-clinical_1998-04-30_69_2-3 . Next issue: sim_autonomic-neuroscience-basic-clinical_1998-05-28_70_1-2 .

Journal of the Autonomic Nervous System 1995: Volume 52 , Issue Index. Digitized from IA1652423-04 . Previous issue: sim_autonomic-neuroscience-basic-clinical_1995-03-02_51_3 . Next issue: sim_autonomic-neuroscience-basic-clinical_1995-03-18_52_1 .

This article is from Yonsei Medical Journal , volume 52 . Abstract Purpose: The objective of this study is to evaluate the effects of heat and massage application on autonomic nervous system. Materials and Methods: One hundred thirty-nine subjects volunteered and completed this study. Heat and massage was daily applied for 40 minutes, 5 days a week for 2 weeks. Primary-dependent measures included heart rate variability, sympathetic skin response, and serum cortisol and norepinephrine levels. Results: Serum cortisol levels were significantly decreased at 2 weeks compared to baseline (p=0.003). Plasma norepinephrine levels at 4 weeks were significantly decreased compared to baseline (p=0.010). Heart rate, using the power spectra, increased significantly after 2 weeks compared to baseline. Of autonomic nerve conduction measures, latency was significantly increased at 2 and 4 weeks compared to baseline (p=0.023, 0.012), and amplitude was significantly decreased at 4 weeks compared to baseline (p=0.008). There were no serious adverse events such as burns or other major complications. Conclusion: The results of this study suggest that heat and massage applications provide relaxation to the autonomic nervous system without serious adverse events.

This scoping review examines the complex relationships between mental health, cognitive functioning, and the autonomic nervous system (ANS). Mental health disorders and cognition are increasingly recognized as interrelated, often influenced by the regulation of the autonomic nervous system (ANS). The exact mechanisms connecting these domains remain unclear. This scoping review aims to map the existing evidence and identify patterns.

Book Source: Digital Library of India Item 2015.550091 dc.contributor.author: White, James C. dc.date.accessioned: 2015-10-14T21:31:09Z dc.date.available: 2015-10-14T21:31:09Z dc.date.copyright: 1952 dc.date.digitalpublicationdate: 2011/03 dc.date.citation: 1952 dc.identifier.barcode: 04990010030918 dc.identifier.origpath: /data8/upload/0228/200 dc.identifier.copyno: 1 dc.identifier.uri: http://www.new.dli.ernet.in/handle/2015/550091 dc.description.scannerno: Banasthali University dc.description.scanningcentre: C-DAK, Kolkata dc.description.main: 1 dc.description.tagged: 0 dc.description.totalpages: 648 dc.format.mimetype: application/pdf dc.language.iso: Sanskrit dc.publisher.digitalrepublisher: Digital Library of India dc.publisher: London, Henry Kimpton dc.rights: Copyright permitted dc.source.library: Dr. Robert Heiling Library, S.m.s.medical College, Jaipur dc.subject.classification: Medical dc.title: The Autonomic Nervous System(third Edition) dc.type: Print - Paper dc.type: Book

This is a low quality sub par track of mierda shit crap garbage and trite bollocks used to counter psychotronic, Lilly Wave, Scalar Wave, DIA, DOD, Mossad, GCHQ, DHS, Telepathic mind control done on everyday citizens on a global scale...

Audio to accompany slides uploaded to Slideshare

Book Source: Digital Library of India Item 2015.552691 dc.contributor.author: White, James C. dc.date.accessioned: 2015-10-14T22:17:27Z dc.date.available: 2015-10-14T22:17:27Z dc.date.copyright: 1941 dc.date.digitalpublicationdate: 2011/03 dc.date.citation: 1941 dc.identifier.barcode: 99999990041829 dc.identifier.origpath: /data8/upload/0239/112 dc.identifier.copyno: 1 dc.identifier.uri: http://www.new.dli.ernet.in/handle/2015/552691 dc.description.scannerno: Banasthali University dc.description.scanningcentre: Banasthali University dc.description.main: 1 dc.description.tagged: 0 dc.description.totalpages: 524 dc.format.mimetype: application/pdf dc.language.iso: Sanskrit dc.publisher.digitalrepublisher: Digital Library of India dc.publisher: London, Henry Kimpton dc.rights: Copyright permitted dc.source.library: Dr. Robert Heiling Library, S.m.s.medical College, Jaipur dc.subject.classification: Medical dc.title: The Autonomic Nervous System(second Edition) dc.type: Print - Paper dc.type: Book

Book Source: Digital Library of India Item 2015.552692 dc.contributor.author: White, James C. dc.date.accessioned: 2015-10-14T22:17:29Z dc.date.available: 2015-10-14T22:17:29Z dc.date.copyright: 1952 dc.date.digitalpublicationdate: 2011/03 dc.date.citation: 1952 dc.identifier.barcode: 99999990041830 dc.identifier.origpath: /data8/upload/0239/113 dc.identifier.copyno: 1 dc.identifier.uri: http://www.new.dli.ernet.in/handle/2015/552692 dc.description.scannerno: Banasthali University dc.description.scanningcentre: Banasthali University dc.description.main: 1 dc.description.tagged: 0 dc.description.totalpages: 648 dc.format.mimetype: application/pdf dc.language.iso: Sanskrit dc.publisher.digitalrepublisher: Digital Library of India dc.publisher: London, Henry Kimpton dc.rights: Copyright permitted dc.source.library: Dr. Robert Heiling Library, S.m.s.medical College, Jaipur dc.subject.classification: Medical dc.title: The Autonomic Nervous System(third Edition) dc.type: Print - Paper dc.type: Book

Background/Aims Hannah Campbell PhD, Dimitri Fiani MD, Marco Solmi MD, Jess Gerard Fiedorowicz MD, Chadi Calarge MD Psychiatric conditions such as depression have been associated with increased morbidity and mortality due to co-morbid medical illness including cardiovascular disease. This may be in part due to changes in cardiac autonomic regulation found in patients with psychiatric illness. However, evidence has suggested that this change in autonomic regulation, may be in part secondary to the effects of antidepressant treatment. However, while the effect of serotonin norepinephrine reuptake inhibitors (SNRIs) and tricyclic antidepressants (TCAs) on the autonomic nervous system has been established, data regarding the effects of selective serotonin reuptake inhibitors (SSRIs) on autonomic nervous system activity has been more varied in the literature. Therefore, we aim to conduct a systematic review and meta-analysis to examine the available evidence regarding the effect of SSRIs relative to other classes of antidepressants and controls on autonomic nervous system activity. We also aim to examine the contribution of gender, psychiatric diagnosis, presence of medical illness, age, and treatment duration on the heterogeneity between studies. Review question Is there an association between different classes of antidepressants, including SSRIs, and autonomic nervous system activity, across different clinical populations, and compared with non-clinical populations? Searches PubMed, Scopus Search Terms to be used: ("antidepressant" or “antidepressants” or “psychotropic” or "citalopram" or "escitalopram" or "fluoxetine" or "fluvoxamine" or "paroxetine" or "sertraline" or “SSRI” or “selective serotonin reuptake inhibitor" or “serotonin and norepinephrine reuptake inhibitor” or “tricyclic antidepressant” or “tetracyclic antidepressant” or “dopamine reuptake blocker” or “monoamine oxidase inhibitor” or “SNRI” or “venlafaxine” or “duloxetine” or “levomilnacipran” or “desvenlafaxine” or “TCA” or “amitriptyline” or “amoxapine” or “clomipramine” or “desipramine” or “doxepin” or “imipramine” or “nortriptyline” or “protriptyline” or “trimipramine” or “maprotiline” or “bupropion” or “vilazodone” or “nefazodone” or “trazodone” or “vortioxetine” or “MAOI” or “isocarboxazid” or “phenelzine” or “selegiline” or “tranylcypromine” or “noradrenergic antagonist” or “mirtazapine”) AND ("heart rate variability" or "HRV" or “RR variability” or “heart period variability” or “pre-ejection period” or “impedance cardiography” or “skin conductance” or “sympathetic nerve activity” or “cardiac autonomic”) Inclusion Criteria Study Design Randomized controlled trials, cohort studies, cross-sectional studies Participants/population Any population receiving a treatment with antidepressants Intervention(s), exposure(s) antidepressants Comparator(s)/control Clinical psychiatric or medical population without antidepressant treatment, or non-clinical population, or antidepressant status within the same population (pre-post) Main outcome(s) HRV, Skin conductance latency, pre-ejection period/impedance cardiography, sympathetic nerve activity (microneurography), skin conductance response/latency Data extraction Two reviewers will search literature and determine if studies meet inclusion/exclusion criteria (H.C., D.F.). If discrepancies, a third collaborator (M.S.) will be asked to resolve. The following data will be extracted: study design, population, medication type(s), doses, duration of treatment, stress conditions, psychiatric diagnosis, anxiety and or depression/mania scale, overall population demographics, outcome data including all reported parameters of heart rate variability, descriptive results of secondary-outcome measures, effect sizes. Risk of bias (quality) assessment Cohort studies will be evaluated using the Newcastle Ottawa scale. Controlled intervention studies are to be evaluated using the NIH-NHLBI quality assessment tools. Two evaluators will work independently to assess quality (H.C., D.F.). Strategy for data synthesis/statistical analysis When at least two studies with the same design and PICO combination will report on autonomic activity we will pool them in a random-effect meta-analysis and calculate pooled Cohen’s d with standardized effect sizes with Comprehensive Meta-Analysis (CMA). If unable to perform meta-analysis on similar outcome measurements, we will report results descriptively. Controlled trials vs cohort studies vs pre-post studies will be analyzed and reported separately. Heterogeneity will be assessed using standard I2 calculations. Additional sensitivity analyses include subgrouping by medication, psychiatric diagnosis, medical diagnosis, age, gender, treatment duration, stress vs. non-stressed measurement. Contact details for further information, Hannah Campbell [email protected] Organizational affiliation of the review Baylor College of Medicine Type and method of review Meta-analysis, Systematic review Anticipated or actual start date October 16, 2021 Anticipated completion date January 2021 Funding sources/sponsors None Conflicts of interest None known Language English Country United States of America Stage of review Review Ongoing Date of registration in OSF October 15, 2021

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Play is a method in which children can better explore their immediate environment and navigate the world. This is especially pertinent for children enduring trauma or difficult circumstances. When children are highly aroused and enter into pressurized environments, this can take a toll on their mental, social-emotional well-being, as well as impairing their achievement in cognitive tasks. Play can serve as a coping method for children enduring stressors, and can improve cognitive capacity, especially for children at a young, impressionable age demographic. This project seeks to answer the research questions: 1) to what extent can play aid children's cognitive capacity?, 2) can play decrease children's arousal after a pressure situation? 3) how is cognitive capacity in children impacted by aroused states of being? The data collected seeks to provide empirical evidence for how play should be prioritized in supporting children enduring ACEs for their social-emotional well-being, physiological arousal, and cognitive skill development. Children in the North Carolina community, aged 5-11, will be randomly assigned to one of three experimental conditions. During the brief session, the children will be wearing a FirstBeat HR monitor and electrodes tracking their autonomic nervous system arousal, engaging in experimental tasks, and completing a No-go/Go working memory cognitive task three times (baseline, after the primary task, and after the secondary task depending on their condition). Data will be analyzed with acknowledgement of demographic exploratory variables and will be specifically evaluating the influence of play on arousal and cognitive performance. This is an IRB approved study that will be conducted at Marble's Kids Museum in Raleigh, North Carolina, with data collection December 2023-February 2024.

Autonomic Nervous System Table: Laminated Card by Babette Rothschild / W. W. Norton & Company

This article is from Nutrition & Metabolism , volume 9 . Abstract Protein restriction during lactation has been used as a rat model of metabolic programming to study the impact of perinatal malnutrition on adult metabolism. In contrast to protein restriction during fetal life, protein restriction during lactation did not appear to cause either obesity or the hallmarks of metabolic syndrome, such as hyperinsulinemia, when individuals reached adulthood. However, protein restriction provokes body underweight and hypoinsulinemia. This review is focused on the regulation of insulin secretion and the influence of the autonomic nervous system (ANS) in adult rats that were protein-malnourished during lactation. The data available on the topic suggest that the perinatal phase of lactation, when insulted by protein deficit, imprints the adult metabolism and thereby alters the glycemic control. Although hypoinsulinemia programs adult rats to maintain normoglycemia, pancreatic β-cells are less sensitive to secretion stimuli, such as glucose and cholinergic agents. These pancreatic dysfunctions may be attributed to an imbalance of ANS activity recorded in adult rats that experienced maternal protein restriction.

Background/Aims Hannah Campbell PhD, Marco Solmi MD, Dimitri Fiani MD, Jess Gerard Fiedorowicz MD, Chadi Calarge MD Psychiatric conditions such as depression has been associated with increased morbidity and mortality due to co-morbid medical illness including cardiovascular disease. This may be in part due to changes in cardiac autonomic regulation found in patients with psychiatric illness. However, evidence has suggested that this change in autonomic regulation, as often measured by changes in heart rate variability (HRV), may be in part secondary to the effects of antidepressant treatment. However, while the effect of serotonin norepinephrine reuptake inhibitors and tricyclic antidepressants on the autonomic nervous system has been established, data regarding the effects of selective serotonin reuptake inhibitors (SSRIs) on autonomic nervous system activity has been more varied in the literature. Therefore, we aim to conduct a systematic review and meta-analysis to examine the available evidence regarding the effect of SSRIs on autonomic nervous system activity as measured through HRV. We also aim to examine the contribution of gender, psychiatric diagnosis, presence of cardiovascular disease, age, and treatment duration on the heterogeneity between studies. Review question Is there an association between SSRIs and HRV, across different clinical populations, and compared with non-clinical population? Searches PubMed, Scopus, Google scholar Search Terms to be used: (“selective serotonin reuptake inhibitors” or “antidepressants” or “citalopram” or “escitalopram” or “fluoxetine” or “fluvoxamine” or “paroxetine” or “sertraline” or SSRI) AND (“autonomic” or “heart rate variability” or “HRV”) Inclusion Criteria Study Design Randomized controlled trials, cohort studies, cross-sectional studies Participants/population Any population receiving a treatment with SSRIs Intervention(s), exposure(s) SSRIs Comparator(s)/control Clinical psychiatric or medical population without SSRI, or non-clinical population, or SSRI status within the same population (pre-post) Main outcome(s) HRV, without any restrictions in measure Data extraction Two reviewers will search literature and determine if studies meet inclusion/exclusion criteria (H.C., D.F.). If discrepancies, a third collaborator (M.S.) will be asked to resolve. The following data will be extracted: study design, population, medication type(s), doses, duration of treatment, stress conditions, psychiatric diagnosis, anxiety and or depression scale, overall population demographics, outcome data including all reported parameters of heart rate variability, descriptive results of secondary-outcome measures, effect sizes. Risk of bias (quality) assessment Cohort studies will be evaluated using the Newcastle Ottawa scale. Controlled intervention studies are to be evaluated using the NIH-NHLBI quality assessment tools. Two evaluators will work independently to assess quality (H.C., D.F.). Strategy for data synthesis/statistical analysis When at least two studies with the same design and PICO combination will report on HRV we will pool them in a random-effect meta-analysis and calculate pooled Cohen’s d with Comprehensive Meta-Analysis (CMA). If unable to perform meta-analysis on similar outcome measurements, we will report results descriptively. Controlled trials vs cohort studies vs pre-post studies will be analyzed and reported separately. Heterogeneity will be assessed using standard I2 calculations. Additional sensitivity analyses include subgrouping by medication, psychiatric diagnosis, medical diagnosis, age, gender, treatment duration, stress vs. non-stressed measurement. Contact details for further information, Hannah Campbell [email protected] Organizational affiliation of the review Baylor College of Medicine Type and method of review Meta-analysis, Systematic review Anticipated or actual start date September 28 2021 Anticipated completion date December 2021 Funding sources/sponsors None Conflicts of interest None known Language English Country United States of America Stage of review Review Ongoing Date of registration in OSF September 28, 2021

Objective: This study investigated if differences in autonomic nervous system activity exist in patients with chronic neck pain as compared to controls measured by using a fully automated pupillometry system. Methods: 100 chronic neck pain subjects and 50 controls participated in this quasi-experimental study design evaluating the effect of chronic pain on the autonomic nervous system using a fully automated method of pupillometry. The Chisquare test for categorical data was used to establish homogeneity of baseline characteristics. The Mann-Whitney U test determined the difference in pupil diameter between the chronic neck pain group and the healthy control group. The Spearman’s rho test was used to relate the pupil diameter to the Neck Disability Index (NDI) scores, subject’s age, and the duration of chronic neck pain. Results: This study demonstrated that the chronic neck pain group had a statistically significant smaller pupil diameter than the healthy control group (p=0.022). This study showed that there was no relationship between the NDI scores and the pupil diameter change. However, there was a weak to moderate correlation between age and pupil size (p<0.001), indicating that there is a significant negative relationship and that the pupil diameter decreases with age. There was a weak but non-significant correlation between the pupil diameter and the duration of chronic neck pain (p>0.05). Discussion: The results of this study demonstrate that subjects with chronic neck pain exhibited a smaller pupil diameter than healthy controls. This is a direct indication of an altered autonomic balance.

Patients with epilepsy have a higher risk of chronic conditions, including psychiatric comorbidities, lower quality of life, status epilepticus, and worse cognitive function (4–6). Apart from the increased morbidity, Patients who have epilepsy have a higher risk of unnatural premature death compared to the general population (7,8). The leading cause of death in patients with DRE, especially in young adults, with an approximate incidence of 1-6 per 1000 persons per year, is attributed to sudden unexpected death in epilepsy (SUDEP). The mechanisms for SUDEP are still unclear and are presumed to be multifactorial. The three main hypotheses are: respiratory dysfunction, cardiac arrhythmias, and alterations in cerebral blood flow autoregulation (9,14–16). Contributing pathophysiological events implicate broad autonomic dysfunction (17,18). Other factors that could play a role in SUDEP include: comorbidities such as sleep apnea, obesity and cardiovascular conditions, antiseizure medications (carbamazepine), and genetic predisposition (19). Seizures frequently have autonomic manifestations especially when they originate from limbic structures (21,22). The amygdala, anterior and mid cingulate, orbitofrontal cortex, insula, thalamus, hypothalamus, periaqueductal grey matter, parabrachial nucleus, medial prefrontal cortex, hippocampus and medullary regions are part of a central autonomic network (CAN) that regulate responses via the sympathetic and parasympathetic systems (23–27). The cornerstone for preventing SUDEP is achieving seizure freedom, particularly freedom of bilateral tonic clonic seizures. Epilepsy surgery offers the greatest chance of seizure freedom for up to 70% of appropriately selected patients (28,29). When the information obtained during the phase I (non-invasive) evaluation does not allow to proceed directly to surgery, a phase II (invasive) evaluation with intracranial electrodes (SEEG: Stereo electroencephalography, SDG: Subdural grid) is required (29,30). Cortical stimulation is a procedure used as part of the phase II evaluation for epilepsy surgery. It is a non-physiological method based on electrical stimuli that would inhibit or excite specific brain functions (31). The principal objectives of this study are to disclose the eloquent cortex that are areas of the brain associated with critical functions (such as language) and to aid in localizing the epileptogenic network involved in seizure generation (31–34). Cortical stimulation has been used in studies to analyze different physiological responses after stimulating specific structures in the brain in patients with epilepsy. A “breathing modulating network” has being described involving limbic and para-limbic structures (35). Central apnea and oxygen desaturation has been provoked when seizures originate from, or spread to, the amygdala (24). Other studies have shown enhancement of respiration after stimulating the amygdala, anterior cingulate gyrus, anterior insula, temporal pole, and thalamus (36). The subcallosal neocortex has been implicated in lowering the blood pressure during stimulation (37). The dysfunction of these brain structures during or in between seizures has been suggested to be associated with the physiopathology of SUDEP. When resective surgery is not an option, non-curative palliative procedures can also be performed to reduce the seizure burden and improve quality of life of patients and caregivers. In our center, patients with epilepsy are evaluated in the epilepsy monitoring unit (EMU) to assess the burden of their epilepsy and/or to see if they could be candidates for epilepsy surgery. In this scenario we can asses how the autonomic system behaves at baseline, during and/or after seizures. Additionally, for the patients with SEEG we can explore the relationship between stimulating a specific structure within the brain and the autonomic response while the patient undergoes the cortical stimulation study, in addition the normal recording epochs. The study design is a prospective study of patients admitted to our epilepsy monitoring unit (EMU) as part of the standard-of-care to try to control their seizures. We will collect information in regard to their epilepsy. Additionally, a research team member will assess physiological parameters at baseline, during and/or after seizures. Patients who are implanted with depth electrodes, may also choose to participate in the portion of the study where the physiological parameters be assessed during the cortical stimulation, in addition to the other times proposed for the patients admitted for Phase I, including the ones who underwent to previous intervention. All the patients will complete two questionnaires, one related the sleep apnea (Epworth Scale) and one to evaluate autonomic complaints (COMPASS-31). With this project we wish to expand the knowledge of the autonomic system in patients with epilepsy and its potential implications for SUDEP.

Patients with epilepsy have a higher risk of chronic conditions, including psychiatric comorbidities, lower quality of life, status epilepticus, and worse cognitive function (4–6). Apart from the increased morbidity, Patients who have epilepsy have a higher risk of unnatural premature death compared to the general population (7,8). The leading cause of death in patients with DRE, especially in young adults, with an approximate incidence of 1-6 per 1000 persons per year, is attributed to sudden unexpected death in epilepsy (SUDEP). The mechanisms for SUDEP are still unclear and are presumed to be multifactorial. The three main hypotheses are: respiratory dysfunction, cardiac arrhythmias, and alterations in cerebral blood flow autoregulation (9,14–16). Contributing pathophysiological events implicate broad autonomic dysfunction (17,18). Other factors that could play a role in SUDEP include: comorbidities such as sleep apnea, obesity and cardiovascular conditions, antiseizure medications (carbamazepine), and genetic predisposition (19). Seizures frequently have autonomic manifestations especially when they originate from limbic structures (21,22). The amygdala, anterior and mid cingulate, orbitofrontal cortex, insula, thalamus, hypothalamus, periaqueductal grey matter, parabrachial nucleus, medial prefrontal cortex, hippocampus and medullary regions are part of a central autonomic network (CAN) that regulate responses via the sympathetic and parasympathetic systems (23–27). The cornerstone for preventing SUDEP is achieving seizure freedom, particularly freedom of bilateral tonic clonic seizures. Epilepsy surgery offers the greatest chance of seizure freedom for up to 70% of appropriately selected patients (28,29). When the information obtained during the phase I (non-invasive) evaluation does not allow to proceed directly to surgery, a phase II (invasive) evaluation with intracranial electrodes (SEEG: Stereo electroencephalography, SDG: Subdural grid) is required (29,30). Cortical stimulation is a procedure used as part of the phase II evaluation for epilepsy surgery. It is a non-physiological method based on electrical stimuli that would inhibit or excite specific brain functions (31). The principal objectives of this study are to disclose the eloquent cortex that are areas of the brain associated with critical functions (such as language) and to aid in localizing the epileptogenic network involved in seizure generation (31–34). Cortical stimulation has been used in studies to analyze different physiological responses after stimulating specific structures in the brain in patients with epilepsy. A “breathing modulating network” has being described involving limbic and para-limbic structures (35). Central apnea and oxygen desaturation has been provoked when seizures originate from, or spread to, the amygdala (24). Other studies have shown enhancement of respiration after stimulating the amygdala, anterior cingulate gyrus, anterior insula, temporal pole, and thalamus (36). The subcallosal neocortex has been implicated in lowering the blood pressure during stimulation (37). The dysfunction of these brain structures during or in between seizures has been suggested to be associated with the physiopathology of SUDEP. When resective surgery is not an option, non-curative palliative procedures can also be performed to reduce the seizure burden and improve quality of life of patients and caregivers. In our center, patients with epilepsy are evaluated in the epilepsy monitoring unit (EMU) to assess the burden of their epilepsy and/or to see if they could be candidates for epilepsy surgery. In this scenario we can asses how the autonomic system behaves at baseline, during and/or after seizures. Additionally, for the patients with SEEG we can explore the relationship between stimulating a specific structure within the brain and the autonomic response while the patient undergoes the cortical stimulation study, in addition the normal recording epochs. The study design is a prospective study of patients admitted to our epilepsy monitoring unit (EMU) as part of the standard-of-care to try to control their seizures. We will collect information in regard to their epilepsy. Additionally, a research team member will assess physiological parameters at baseline, during and/or after seizures. Patients who are implanted with depth electrodes, may also choose to participate in the portion of the study where the physiological parameters be assessed during the cortical stimulation, in addition to the other times proposed for the patients admitted for Phase I, including the ones who underwent to previous intervention. All the patients will complete two questionnaires, one related the sleep apnea (Epworth Scale) and one to evaluate autonomic complaints (COMPASS-31). With this project we wish to expand the knowledge of the autonomic system in patients with epilepsy and its potential implications for SUDEP.

Patients with epilepsy have a higher risk of chronic conditions, including psychiatric comorbidities, lower quality of life, status epilepticus, and worse cognitive function (4–6). Apart from the increased morbidity, Patients who have epilepsy have a higher risk of unnatural premature death compared to the general population (7,8). The leading cause of death in patients with DRE, especially in young adults, with an approximate incidence of 1-6 per 1000 persons per year, is attributed to sudden unexpected death in epilepsy (SUDEP). The mechanisms for SUDEP are still unclear and are presumed to be multifactorial. The three main hypotheses are: respiratory dysfunction, cardiac arrhythmias, and alterations in cerebral blood flow autoregulation (9,14–16). Contributing pathophysiological events implicate broad autonomic dysfunction (17,18). Other factors that could play a role in SUDEP include: comorbidities such as sleep apnea, obesity and cardiovascular conditions, antiseizure medications (carbamazepine), and genetic predisposition (19). Seizures frequently have autonomic manifestations especially when they originate from limbic structures (21,22). The amygdala, anterior and mid cingulate, orbitofrontal cortex, insula, thalamus, hypothalamus, periaqueductal grey matter, parabrachial nucleus, medial prefrontal cortex, hippocampus and medullary regions are part of a central autonomic network (CAN) that regulate responses via the sympathetic and parasympathetic systems (23–27). The cornerstone for preventing SUDEP is achieving seizure freedom, particularly freedom of bilateral tonic clonic seizures. Epilepsy surgery offers the greatest chance of seizure freedom for up to 70% of appropriately selected patients (28,29). When the information obtained during the phase I (non-invasive) evaluation does not allow to proceed directly to surgery, a phase II (invasive) evaluation with intracranial electrodes (SEEG: Stereo electroencephalography, SDG: Subdural grid) is required (29,30). Cortical stimulation is a procedure used as part of the phase II evaluation for epilepsy surgery. It is a non-physiological method based on electrical stimuli that would inhibit or excite specific brain functions (31). The principal objectives of this study are to disclose the eloquent cortex that are areas of the brain associated with critical functions (such as language) and to aid in localizing the epileptogenic network involved in seizure generation (31–34). Cortical stimulation has been used in studies to analyze different physiological responses after stimulating specific structures in the brain in patients with epilepsy. A “breathing modulating network” has being described involving limbic and para-limbic structures (35). Central apnea and oxygen desaturation has been provoked when seizures originate from, or spread to, the amygdala (24). Other studies have shown enhancement of respiration after stimulating the amygdala, anterior cingulate gyrus, anterior insula, temporal pole, and thalamus (36). The subcallosal neocortex has been implicated in lowering the blood pressure during stimulation (37). The dysfunction of these brain structures during or in between seizures has been suggested to be associated with the physiopathology of SUDEP. When resective surgery is not an option, non-curative palliative procedures can also be performed to reduce the seizure burden and improve quality of life of patients and caregivers. In our center, patients with epilepsy are evaluated in the epilepsy monitoring unit (EMU) to assess the burden of their epilepsy and/or to see if they could be candidates for epilepsy surgery. In this scenario we can asses how the autonomic system behaves at baseline, during and/or after seizures. Additionally, for the patients with SEEG we can explore the relationship between stimulating a specific structure within the brain and the autonomic response while the patient undergoes the cortical stimulation study, in addition the normal recording epochs. The study design is a prospective study of patients admitted to our epilepsy monitoring unit (EMU) as part of the standard-of-care to try to control their seizures. We will collect information in regard to their epilepsy. Additionally, a research team member will assess physiological parameters at baseline, during and/or after seizures. Patients who are implanted with depth electrodes, may also choose to participate in the portion of the study where the physiological parameters be assessed during the cortical stimulation, in addition to the other times proposed for the patients admitted for Phase I, including the ones who underwent to previous intervention. All the patients will complete two questionnaires, one related the sleep apnea (Epworth Scale) and one to evaluate autonomic complaints (COMPASS-31). With this project we wish to expand the knowledge of the autonomic system in patients with epilepsy and its potential implications for SUDEP.

The study design is a prospective study of patients admitted to our epilepsy monitoring unit (EMU) as part of the standard-of-care to try to control their seizures. We will collect information in regard to their epilepsy. Additionally, a research team member will assess physiological parameters at baseline, during and/or after seizures. Patients who are implanted with depth electrodes, may also choose to participate in the portion of the study where the physiological parameters be assessed during the cortical stimulation, in addition to the other times proposed for the patients admitted for Phase I, including the ones who underwent to previous intervention. All the patients will complete two questionnaires, one related the sleep apnea (Epworth Scale) and one to evaluate autonomic complaints (COMPASS-31).

A scoping review on the relationship between the immune system and autonomic nervous system in individuals with major depressive disorder.

This is the protocol for a systematic review of the literature on the effects of mild traumatic brain injury (mTBI) on autonomic nervous system functioning as measured by various physiological biomarkers in a pediatric population.

We analyze the relationship between anxiety and autonomic nervous system response

Headache is a very common symptom, with approximately 70% of the population suffering from headaches within a year (Deutsche Migräne- und Kopfschmerzgesellschaft e.V. o. J.) and 10 to 15% of the population suffering from migraine (Deutsche Migräne- und Kopfschmerz-Gesellschaft e.V. o.J.). To date, the pathophysiology of migraine has not been conclusively clarified. A link between migraine and the autonomic nervous system (ANS) is evident in that not only do many migraine patients suffer from symptoms of autonomic dysfunction (nausea/vomiting, facial flushing, pallor, palpitations, lightheadedness, pupillary dilation, syncope; Miglis 2018), but also many patients with primary autonomic dysfunction (e.g., postural tachycardia syndrome (Khurana & Eisenberg 2011), chronic fatigue syndrome, fibromyalgia, or collagenosis disorders such as Ehlers-Danlos syndrome; Miglis 2018) suffer from migraine. Treatment of migraine according to current guidelines (Deutsche Gesellschaft für Neurologie 2012) is primarily based on drug therapy; non-drug interventions such as aerobic exercise, relaxation techniques, and behavioral therapy methods can be used concomitantly to reduce attack frequency. To date, few studies have been conducted on physiotherapy treatment of migraine (Luedtke et al. 2020; Lemmens et al. 2019). Treatment of the upper thoracic spine did not play a role in these studies. However, this could be important because migraine patients* can express a variety of autonomic symptoms (Miglis 2018) and mobilization of the upper thoracic spine can influence the autonomic nervous system (Picchiottino et al. 2019). Thus, a relationship of treatment of the upper thoracic spine and reduction of migraine-associated symptoms could be suspected.