Hyperactivity Of Autonomic Nervous System Research Articles

Heart Rate Variability and Salivary Biomarkers Differences between Fibromyalgia and Healthy Participants after an Exercise Fatigue Protocol: An Experimental Study.

Previous studies showed that people with Fibromyalgia (FM) suffer from dysautonomia. Dysautonomia consists of persistent autonomic nervous system hyperactivity at rest and hyporeactivity during stressful situations. There is evidence that parameters reflecting the complex interplay between the autonomic nervous system and the cardiovascular system during exercise can provide significant prognostic information. Therefore, this study aimed to investigate the differences between people with FM and healthy controls on heart rate variability (HRV) and salivary parameters (such as flow, protein concentration, enzymatic activities of amylase, catalase and glutathione peroxidase) in two moments: (1) at baseline, and (2) after an exercise fatigue protocol. A total of 37 participants, twenty-one were people with fibromyalgia and sixteen were healthy controls, participated in this cross-sectional study. HRV and salivary samples were collected before and after an exercise fatigue protocol. The fatigue protocol consisted of 20 repetitions of knee extensions and flexions of the dominant leg at 180 °·s−1 (degrees per second). Significant differences were found in the HRV (stress index, LF and HF variables) and salivary biomarkers (with a higher concentration of salivary amylase in people with FM compared to healthy controls). Exercise acute effects on HRV showed that people with FM did not significantly react to exercise. However, significant differences between baseline and post-exercise on HRV significantly induce alteration on the HRV of healthy controls. Catalase significantly increased after exercise in healthy controls whereas salivary flow significantly increased in women with FM after an exercise fatigue protocol. Our study suggests that a higher α-amylase activity and an impaired HRV can be used as possible biomarkers of fibromyalgia, associated with a reduction in salivary flow without changes in HRV and catalase activity after a fatigue exercise protocol. More studies should be carried out in the future to evaluate this hypothesis, in order to find diagnostic biomarkers in fibromyalgia.

Epigenetic Mechanisms in the Neurodevelopmental Theory of Depression.

The genome (genes), epigenome, and environment work together from the earliest stages of human life to produce a phenotype of human health or disease. Epigenetic modifications, including among other things: DNA methylation, modifications of histones and chromatin structure, as well as functions of noncoding RNA, are coresponsible for specific patterns of gene expression. This refers also to mental disorders, including depressive disorders. Early childhood experiences accompanied by severe stressors (considered a risk factor for depression in adult life) are linked with changes in gene expression. They include genes involved in a response to stress (hypothalamic-pituitary-adrenal axis, HPA), associated with autonomic nervous system hyperactivity and with cortical, and subcortical processes of neuroplasticity and neurodegeneration. These are, among others: gene encoding glucocorticoid receptor, FK506 binding protein 5 gene (FKBP5), gene encoding arginine vasopressin and oestrogen receptor alpha, 5-hydroxy-tryptamine transporter gene (SLC6A4), and gene encoding brain-derived neurotrophic factor. How about personality? Can the experiences unique to every human being, the history of his or her development and gene-environment interactions, through epigenetic mechanisms, shape the features of our personality? Can we pass on these features to future generations? Hence, is the risk of depression inherent in our biological nature? Can we change our destiny?

Exploring the effect of various BoNT serotypes in a model of autonomic nervous system hyperactivity from rodents and humans: Paving the way to better targeting therapeutics in autonomic disorders?

Exploring the effect of various BoNT serotypes in a model of autonomic nervous system hyperactivity from rodents and humans: Paving the way to better targeting therapeutics in autonomic disorders?

Symptômes du bas appareil urinaire secondaire à une hyperplasie bénigne de prostate et dysfonction érectile : une revue systématique de la littérature

To provide a systematic review of epidemiological data regarding the association between erectile dysfunction (ED) and lower urinary tract symptoms (LUTS) in men. A research has been conducted on the Medline database using the keywords: ("erectile dysfunction" or "sexual dysfunction") and ("benign prostatic hyperplasia" or "lower urinary tract symptoms"). The eligibility of studies was defined using the PICOS method in accordance with the PRISMA statement. Cross-sectional studies and prospective cohorts assessing the association between LUTS and ED in the primary care setting or in general practice (i.e. exclusion of patients seen in outpatient urology or andrology) were included. Among 898reports assessed, seven studies were included in this systematic review (whole cohort: 1,196,393men). There were five cross-sectional studies and two prospective cohorts. The whole seven studies reported an association between LUTS and ED (range of odds-ratio: 1.52-4.03). Four common pathogenic mechanisms were found in the literature, all of them being somewhat related with metabolic syndrome and cardiovascular risk factors: reduced nitric oxide (NO) pathway signalling, increased RhoA-Rho kinase signalling, autonomic nervous system hyperactivity and pelvic atherosclerosis. The main limitations of this review were: a possible publication bias, the relatively low number of included studies and the lack of assessment of potential confounders such as factors related to sexual partner. The close epidemiological and pathogenic links between LUTS and ED have given rise to a new nosological entity: the erectile urogenital dysfunction, which should be assessed globally with special considerations to frequently associated comorbidities such as metabolic syndrome and cardiovascular risk factors.

Low baseline salivary alpha-amylase in drug-naïve patients with short-illness-duration first episode major depressive disorder

BackgroundAltered monoamine neurotransmission accompanied by hypothalamic–pituitary–adrenal axis dysfunction and autonomic nervous system hyperactivity have been associated with major depressive disorder (MDD). Salivary α-amylase (sAA) is indicative of autonomic activation and reflects central noradrenergic activity. Scarce studies on sAA in MDD produce confounded results and no data is available regarding baseline sAA activity. MethodsThe basal, non-stimulated sAA activity was studied in this cross-sectional case-control study on 20 non-late-life adult, short-illness-duration first-episode, treatment-naïve MDD patients and in 20 age- and sex-matched healthy controls. Depressed patients showed a basal score in the Hamilton Rating Scale for Depression (HAMD-17) higher than 20. ResultsThe sAA was significantly lower in depressed individuals as compared to controls (p=0.011). In post hoc analysis significantly lower sAA was present in melancholic MDD (p=0.016) as related to controls whereas no difference was seen between non-melancholic MDD patients and controls. The sAA activity was not significantly correlated neither with duration nor the severity of depressive symptoms as measured by the total HAMD-17 score. LimitationsThe current study is limited by its cross-sectional design, small sample size, and factors related to saliva sampling methodology. ConclusionLow baseline sAA levels were found in MDD in basal, non-stimulated conditions. The study provides no support for elevated sAA in drug-naïve patients with short-illness-duration first episode MDD. The results support the evidence for decreased central noradrenergic transmission in MDD when sAA activity is considered indicative of central noradrenergic function.

The relationship between lower urinary tract symptoms associated with benign prostatic hyperplasia and erectile dysfunction: the role of autonomic hyperactivity.

To investigate whether autonomic nervous system (ANS) hyperactivity may be a potential cause for the relationship between lower urinary tract symptoms (LUTS) and erectile dysfunction (ED). Twenty-four patients were recruited for this study. Complete physical examinations, urine analysis, uroflowmetry, and postvoid residual urine volume (PVRU) analysis were performed. The potential impact of some factors such as hyperglycemia, obesity, and hyperlipidemia were analyzed. These values were correlated with the various symptom scores. We performed an electromyographic and an electrocardiographic evaluation. The alterations after treatment with 2 different alpha-blockers were also analyzed. The electromyographic and electrocardiographic assessments revealed a minimal increase in ANS activity and it did not change significantly after treatment (P > 0.05). After treatment, maximum flow rate increased and PVRU decreased significantly (P < 0.001 and P < 0.001, respectively); total and free testosterone levels increased significantly (P = 0.0068 and P = 0.0071, respectively). There was a statistically significant difference between the 2 treatment groups regarding the outcomes of the Danish Prostate Symptom Score questionnaire (P = 0.047). This current study suggested that the effect of ANS hyperactivity is not the fundamental factor underlying the relationship between LUTS and ED.

Molecular and Genetic Basis of Stress

A person’s reaction to trauma depends on the traumatic situation itself, personality characteristics of the person exposed to trauma, and posttraumatic social environment. Stressor must be extreme event that is extremely dangerous or fatal nature, and which is outside normal human experience [ 1 ]. Studies investigating psychological consequences of military and civil trauma confirmed the correlation between the nature and intensity of trauma, previous traumatic experience, and psychological consequences. Stress causes the autonomic nervous system hyperactivity. If the stress is extreme or constant symptoms of hyperactivity, increased heart rate, increased respiration, sweating, muscle tension, insomnia and increased anxiety are becoming significant for the prolonging the symptoms of PTSD. Our cells are well adapted to exposure to a mild stress for a short time. In contrast there are potentially serious consequences of exposure to the prolonged stress[ 2 ]. Various damages arising from the war in Bosnia (1992 - 1995) are almost undetectable, and the consequences for the mental health of the population of Bosnia and Herzegovina are long and painful. It is estimated that in Bosnia and Herzegovina there are 1.75 million people who have some stress-related mental disorders, of which 1 million in the Federation. PTSD may be represented by mutations that must be carried by many genes. There may even be epigenetic reasons for the disorder that have nothing to do with heritable mutations per se. Epigenetic means related to functional changes in the genome that can be regulated by external environmental events that do not involve alterations in the genetic code. One epigenetic mechanism is called “methylation,” a molecular process that affects the activity of a large percentage of genes. Epigenetic investigations say that methylation may be involved in the development of stress regulation in early life[ 3 ]. A number of longitudinal studies have looked at independent variables spanning the entire course of the illness. A 10-year follow-up study in Holocaust survivors clearly demonstrated decline in stress hormone levels for those patients in whom PTSD developed or in whom PTSD was chronic. No such decline was shown for those survivors who did not present with PTSD. Indeed, they showed a relative increase in hormone levels [ 4 ]. Hippocampal volume has also been studied (using the same types of experiments as the twin studies described previously). Hippocampal volume can be quite variable. It can change as a result of environmental exposure, duration of certain illnesses, and even the age of the subject. As noted, shrunken hippocampal volume has been shown in PTSD patients, but most of these are younger cohorts. When one examines PTSD in older cohorts, the differences in volume evaporate, and no linkage with disease is observed [ 5 ]. Microarray analysis is a powerful way to look at global gene expression profiles in tissues which can identify relevant molecular processes. On that way we have enough tools on hand to find the genes responsible for the disorder. Studying such genes can lead to creating effective treatments, including designing medications that are not only specific to the disorder but also specific to an individual’s experience with the disorder.

The increase in sympathetic nerve density in the atrium facilitates atrial fibrillation in patients with rheumatic heart disease

BackgroundAtrial fibrillation (Af) is frequently observed in patients with rheumatic heart disease (RHD). The hyperactivity of autonomic nervous system is known to contribute to the occurrence of Af in RHD patients. This study investigated the association between the autonomic density and the risk of Af in RHD patients. MethodsSeventy-five patients were enrolled: (1) RHD patients with Af (N=25, Group 1); (2) RHD patients without Af (N=25, Group 2); (3) congenital heart disease patients without Af (N=25, Group 3). The baseline characteristics and the blood concentrations of renin, C-reaction protein and angiotensin II were collected from all patients. The tissues were obtained from the right atrial appendage during the open-heart surgery and then stained using immunohistochemical methods with autonomic antibodies. ResultsThe sympathetic nerve density was significantly higher in RHD patients with Af than RHD patients without Af and congenital heart disease patients, both endocardially and epicardially. The parasympathetic nerve density did not show significant difference among the three groups. The left atrial diameter was larger in RHD patients with Af than the other two groups. The blood concentrations of renin and angiotensin II were higher in RHD patients with Af than the other two groups. The erythrocyte sedimentation rate and blood concentrations of C-reaction protein did not show significant change among the three groups. ConclusionThis study provided direct evidence of the increase in sympathetic nerve density in atrium in patients with RHD. This phenomenon may be associated with the development of Af in RHD patients.

Does gastroesophageal reflux contribute to development of acquired nasolacrimal duct obstruction?

Primary acquired nasolacrimal duct obstruction results from inflammation of unknown cause that eventually leads to fibrosis and occlusion. The nasolacrimal duct is within the medial wall of maxillary sinus and open into the nasal cavity. It may be affected by gasteroesophageal reflux disease (GERD) by the possible direct noxious effect of the refluxate on the nasal mucosal cavity surrounding of the nasolacrimal duct opening at the inferior meatous and ascending of inflammation to the mucosa of the duct may leads to chronic inflammation and fibrosis. In addition to, the GERD may induce autonomic nervous system hyperactivity resulting in hyperemia of venous plexus surrounding nasolacrimal duct leading to secondary mucosal edema of nasolacrimal duct and dacryostenosis.

Primary Hyperhidrosis and Anxiety: a Prospective Preoperative Survey of 158 Patients

To determine the location of hyperhidrosis, the accompanying signs and symptoms, and patient anxiety assessed on 2 scales and standardized psychometric instruments. A prospective study of patients with hyperhidrosis was carried out between September 1, 2001 and June 30, 2003 with a self-administered preoperative questionnaire. The variables studied included the location of hyperhidrosis, the accompanying signs and symptoms, and the self-reported degree of anxiety and perception of its effect on daily life assessed by the State-Trait Anxiety Inventory (STAI) and a questionnaire designed in our department. Palmar hyperhidrosis was reported by 93.6% of patients, plantar by 70.2%, axillary by 66.4%, facial by 12.1%, groin by 8.2%, chest by 5%, and abdominal by 2%. While more than 50% of the patients reported facial blushing and palpitations as accompanying signs and symptoms, approximately 30% experienced epigastric pain, trembling, and headaches. Over half of the patients reported that their anxiety was incapacitating, and a mere 1.2% experienced none at all. STAI scores were similar to those of the general population whereas scores on our department's questionnaire reflected those of the self-reported anxiety ratings. Primary hyperhidrosis is a disorder in which excessive sweating occurs mainly, but not exclusively, on the palms. The condition is accompanied by signs and symptoms typical of autonomic nervous system hyperactivity and by a degree of anxiety that has an incapacitating effect on normal life, although that anxiety is not detected by the STAI questionnaire alone.

Psychological aspects of ″environmental illness,” ″multiple chemical sensitivity,” and building-related illness

Psychological aspects of ″environmental illness,” ″multiple chemical sensitivity,” and building-related illness

Psychological aspects of “environmental illness,” “multiple chemical sensitivity,” and building-related illness

Psychological aspects of “environmental illness,” “multiple chemical sensitivity,” and building-related illness

A SUPPLEMENT OF PATHOLOGICAL PHYLOLICAL PHYSIOLOGY ON THE SO-CALLED LABYRINTHINE DEAFNESS

In order to study the origin of labyrinthine deafness, 70 patients with labyrinthine deafness were examined for their auditory function and autonomic nerve function. The results obtained were as follows :The causes of labyrinthine deafness were classified, Those due to hereditary factors were 5, Meniere's disease 5, middle ear disease 4, Presbycusis 4, Occupational deafness 3, syphilis 3, Typhus 2, Epidemic cerebrospinal meningitis 1, Pregnancy 1 and Unknown cause 39.The function of antonomic nervous system were examined by using adrergic and cholinergic drug and classified as follows: Unbalance of antonomic nervous system 1, Hyperactivity of autonomic nervous system 11, Sympathicotonia 10, Unbalance of parasympathetic nervous system 7, Vagotonia 22, Hypoactivity of autonomic nervous system 7, Normal 12.The condition of vagotonia was often found in patients with hearing impairment by unknown etiology, especially in late stage of the disease. Generally, at the begining of hearing impairment and Meniere's disease, the patients have a tendency of sympathicotonia.In patients with hypoactivity of vestibular function which was diagnosed by rotatory nystagmus test, condition of vagotonia, vagotonic unbalance and hypoactivity of autonomic nervous system was noticed, Vestibular dysfunction was not always marked in labyrinthine deafness. Hearing impairment was severe in degree in cases with vestibular dysfunction. In conclusion, sympathicotonic condition seems to manifest itself in early stage of labyrinthine deafness, while it shifts vagotonic condition in later stage.