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PubMed1990

Impairment of autonomic reflexes in cirrhosis.

Autonomic dysfunction may contribute to the hemodynamic disturbances in cirrhosis. Tests of autonomic function were performed in 20 patients with cirrhosis and 20 healthy subjects. The patients with severe cirrhosis (Child's grade B or C) had significant reductions in the Valsalva ratio, the heart rate variation during both facial immersion in water and deep breathing, the pressor response to forearm isometric exercise, and the heart rate response to dynamic exercise. The cold pressor test and the heart rate response to lying down were unaffected. These results indicate impairment of both sympathetic and parasympathetic reflexes in severe cirrhosis which may contribute to the hemodynamic disturbances of cirrhosis. Further studies are required to define the site of these defects.

Adult↗

PubMed1994

Participation of autonomic nervous system in the pathogenesis of Chagas disease.

Evidences accumulated over the last decade give adequate proof for the existence of circulating antibodies in Chagas disease which binds to beta adrenergic and muscarinic cholinergic receptor of lymphocytes and myocardium. The interaction of the antibodies with lymphocytes and cardiac neurotransmitter receptors behaving as an agonist, triggers in the cells intracellular signal transductions that alter the physiological behaviour of this cells. These events converted the cells in pathologically active cells. Thus, antibodies activating beta adrenergic receptors of T helper (Th) lymphocytes increase cAMP and releases PGE2 by T suppressor/cytotoxic (Ts/c) cell, inducing in this way, immunosuppression by simultaneous inhibition of Th and stimulation of Ts/c cell function. All these antibodies actions were mimetized by parasite's membranes. On the other hand, the interaction of antibodies against heart beta adrenergic and cholinergic receptors trigger physiologic, morphologic, enzymatic and molecular alterations, that leading to cardiac damage. The analysis of the prevalence and distribution of these antibodies shows a strong association with seropositive asymptomatic patients with autonomic dysfunction in comparison with those asymptomatic without alteration of the heart autonomic disorders; pointing to that the presence of these antibodies may partially explain the cardiomyoneuropathy of Chagas disease, in which the sympathetic and parasympathetic systems are affected. The deposit of autoantibodies on the myocardial neurotransmitter receptors, behaving like an agonist, could induced desensitization and/or down regulation of the receptors. This in turn, could led to a progressive blockade of myocardium neurotransmitter receptors, with sympathetic and parasympathetic dennervation, a phenomenon that has been described in the course of Chagas cardioneuropathy.

Animals↗

PubMed1993

Autonomic vagal nerve dysfunction in patients with ulcerative colitis.

Autonomic nerve function was evaluated in 40 patients with total ulcerative colitis and in 25 patients with irritable bowel syndrome by three established non-invasive tests based on the heart reactions to deep breathing (E/I ratio) and tilt (acceleration and brake index). None of the patients were diabetic. Most of the patients with ulcerative colitis were clinically and biochemically inactive; 10 had previously undergone colectomy. The results were compared with a control group consisting of 56 healthy individuals and 33 previously investigated patients with Crohn's disease, 45% of whom demonstrated autonomic neuropathy (AN). Patients with ulcerative colitis had a significantly lower E/I ratio than controls in age-corrected values, indicating vagal nerve dysfunction. Altogether, 35% had signs of AN. In patients with irritable bowel syndrome 36% had evidence of AN, a figure in agreement with observations from other investigators. We conclude that AN is common in patients with ulcerative colitis, regardless of disease activity and previous colectomy. In contrast to a predominantly sympathetic dysfunction in Crohn's disease, AN in ulcerative colitis was vagal.

Adult↗

PubMed1988

Mitral valve prolapse syndrome: neuro-endocrinological aspects.

Based on analysis of 399 symptomatic patients with mitral valve prolapse (MVP) and the reported experience of others, we developed a clinical classification in order to improve nosology, provide better identification and promote insight into the mechanism of symptoms in patients with MVP. The heading of anatomic MVP designates those in whom symptoms or complications were primarily or directly related to valvular dysfunction and the heading of MVP syndrome designates those patients in whom symptoms cannot be explained on the basis of valvular dysfunction alone. Patients with MVP syndrome present with a symptom complex which results from various forms of neuroendocrine or autonomic dysfunction; the most common symptoms include chest pain, palpitations, cardiac arrhythmias, orthostatic phenomena, syncope, presyncope, fatigue, exercise intolerance, dyspnea and neuropsychiatric symptoms (Table 1). Mechanisms underlying the condition have been shown to include increased adrenergic activity, disturbances of catecholamine regulation, hyperresponsiveness to adrenergic stimulation, anomalous beta-adrenergic receptors, dysfunction of the parasympathetic portion of the autonomic nervous system, disturbances in renin-aldosterone regulation, decreased intravascular volume, diminished left ventricular diastolic volume in the upright position as well as abnormal secretion of atrial natriuretic factor (Table 2). In MVP syndrome, alterations of the heart, kidney, the adrenals and the autonomic nervous system coexist and interact, creating a complex "neuro-endocrine cardiovascular process" which may account for many of the symptoms otherwise unexplained on the basis of the valvular abnormality alone.

Arousal↗

PubMed2000

New transthyretin mutation V28M in a Portuguese kindred with amyloid polyneuropathy.

A 62-year-old Portuguese man, with no history of familial amyloid polyneuropathy (FAP), and a 2(1/2)-year history of tingling in the toes and sexual dysfunction was found neurophysiologically to have a sensory-motor axonal polyneuropathy. Autonomic tests showed slight sympathetic and marked parasympathetic involvement. Heart, kidney, and eyes were normal. Single strand conformation polymorphism (SSCP) mutation analysis for the transthyretin (TTR) gene was performed. The SSCP pattern suggested the presence of a mutation in exon 2, but was different from the pattern observed for a control representing the most common TTR mutation associated with FAP, i.e., TTR V30M. DNA sequencing analysis revealed an A-to-G transition in the first base of codon 28 normally encoding a valine, giving rise to a methionine residue. The presence of this extra methionine was confirmed by peptide mapping and mass spectrometry analysis. Biopsy of nerve and skin of the propositus showed amyloid deposits that were immunoreactive for TTR. This is a new variant TTR related to late-onset amyloid neuropathy with autonomic dysfunction. This case confirms that TTR mutation screening should be considered in patients with a clinical disorder consistent with amyloid neuropathy even in the absence of a family history.

Adult↗

PubMed2002

[Diabetic cardiomyopathy: concept, heart function, and pathogenesis].

The diabetic cardiomyopathy is a disease caused by diabetes and is characterised by the presence of diastolic and/or systolic left ventricular dysfunction. Diabetes may produce metabolic alterations, interstitial fibrosis, myocellular hypertrophy, microvascular disease and autonomic dysfunction. It is thought that all of them may cause cardiomyopathy. Other abnormalities that are usually associated with diabetes such as hypertension, coronary artery disease and nephropathy should be excluded before diagnosing diabetic cardiomyopathy. There is no evidence that diabetic cardiomyopathy alone can produce heart failure. However, subclinical ventricular dysfunction has been described in young asymptomatic diabetic patients without other diseases that could affect the cardiac muscle. In these cases we should consider that diabetes is the only cause of the myocardial disease. More studies are needed to know the natural history of diabetic cardiomyopathy.

Adrenergic beta-Antagonists↗

PubMed1994

Manipulation of norepinephrine metabolism with yohimbine in the treatment of autonomic failure.

It has been postulated that alpha 2-adrenergic receptors play a modulatory role in the regulation of blood pressure. Activation of alpha 2-receptors located in the central nervous system results in inhibition of sympathetic tone and decrease of blood pressure. This indeed may be the mechanism of action of central sympatholytic antihypertensives such as alpha-methyldopa. Presynaptic alpha 2-receptors also are found in adrenergic nerve terminals. These receptors act as a negative feedback mechanism by inhibiting the release of norepinephrine. The relevance of alpha 2-adrenergic receptors for blood pressure regulation can be explored with yohimbine, a selective antagonist of these receptors. Yohimbine increases blood pressure in resting normal volunteers. This effect is associated with an increase in both sympathetic nerve activity, reflecting an increase in central sympathetic outflow, and in norepinephrine spillover, reflecting potentiation of the release of norepinephrine from adrenergic nerve terminals. These actions, therefore, underscore the importance of alpha 2-adrenergic receptors for blood pressure regulation even under resting conditions. Patients with autonomic failure, even those with severe sympathetic deprivation, are hypersensitive to the pressor effects of yohimbine. This increased responsiveness can be explained by sensitization of adrenergic receptors, analogous to denervation supersensitivity, and by the lack of autonomic reflexes that would normally buffer any increase in blood pressure. Preliminary studies suggest that the effectiveness of yohimbine in autonomic failure can be enhanced with monoamine oxidase inhibitors. Used in combination, yohimbine increases norepinephrine release, whereas monoamine oxidase inhibitors inhibit its degradation. Therefore, yohimbine is not only a useful tool in the study of blood pressure regulation, but may offer a therapeutic option in autonomic dysfunction.

Autonomic Nervous System Diseases↗

PubMed2006

An update on autonomic neuropathy affecting the gastrointestinal tract.

Gastrointestinal symptoms and disordered gut motility occur frequently in the diabetic population and are generally regarded as manifestations of gastrointestinal "autonomic dysfunction," although the relationships between both symptoms and dysmotility with abnormal cardiovascular autonomic function are weak. It is now recognized that the blood glucose concentration is both a determinant of and determined by gastrointestinal function. An improved definition of the underlying pathophysiology should facilitate the development of therapies that are targeted more effectively.

Animals↗

PubMed2000

Autonomic dysreflexia increases plasma adrenaline level in the chronic spinal cord-injured rat.

Autonomic dysreflexia (AD) occurs in up to 80% of quadriplegics and high paraplegics and is characterized by exaggerated sympathetic reflexes which induced paroxysmal hypertension. The aim of this study was to determine if plasma catecholamine levels increased during autonomic dysreflexia in the chronic spinal cord-injured (SCI) rats with special care to adrenaline. Catecholamine samples were collected before, during and 1 h after AD induced hypertension with colorectal distension. Results showed that plasma noradrenaline and adrenaline levels increased respectively 1.5-fold and 5-fold during AD in the chronic SCI rats. This suggests substantial roles for these two hormones in mediating the cardiovascular changes during AD. Knowledge of catecholamine levels during AD may thus aid in determining pathophysiology and potential pharmacologic treatments of this autonomic dysfunction.

Animals↗

PubMed2002

Management of dysautonomia in fibromyalgia.

The realization of dysautonomia in FM has opened the possibility for new and different therapeutic interventions. Much more research is needed to better define the role of ANS in the pathogenesis of FM. If this research supports current hypotheses, therapeutic trials with disciplines and substances intended to correct autonomic dysfunction will be indicated.

Autonomic Nervous System Diseases↗

PubMed2003

Sleep disordered breathing may not be an independent risk factor for diabetes, but diabetes may contribute to the occurrence of periodic breathing in sleep.

OBJECTIVE(S): (a) To determine if self-reported diabetes mellitus is independently associated with sleep-disordered breathing (SDB); (b) to determine if diabetes mellitus is specifically associated with central sleep apnea including periodic breathing (Cheyne-Stokes breathing pattern) during sleep. STUDY POPULATION: The study population reflected participants in the on-going Sleep Heart Health Study (SHHS). Analyses were conducted utilizing data obtained from 4872 SHHS participants without prevalent cardiovascular disease (CVD) and 1002 participants with self-reported CVD, defined as hospitalization for non-fatal coronary heart disease, congestive heart failure, myocardial infarction, coronary artery bypass graft, and stroke. METHODS: SHHS methodologies have been previously reported and include performance of overnight, in-home polysomnography (PSG), which recorded variables reflecting sleep architecture and breathing, permitting identification of obstructive and central apneas, hypopneas, periodic breathing and oxyhemoglobin saturation (SpO(2)). Anthropomorphic metrics as well as systemic blood pressure measurements were obtained at the time of PSG. Other health data were available from questionnaires and the data sets of the parent cohorts from whom SHHS participants were recruited. The investigators assessed and compared breathing parameters, sleep architecture and CVD variables in diabetic and non-diabetic participants. The relationships between diabetes and the various study parameters, independent of potential confounders, were examined by multivariable modeling. Linear regression modeling was employed to examine the relationship between continuously distributed variables such as respiratory disturbance index log (RDI). The relationships between diabetes and dichotomous outcome variables such as central apnea index (CAI), obstructive apnea index (OAI), periodic breathing and the percentage of time spent at various levels below SpO(2) 90% were examined by the logistic regression model. Age, gender, race, BMI and neck circumference were forced into all multivariable analyses since these factors are associated with both diabetes mellitus and SDB. RESULTS: The investigators reported that the prevalence of CVD risk factors including increased BMI, waist circumference, neck circumference, triglycerides, reduced HDL cholesterol and hypertension was greater in diabetic than non-diabetic participants. Native Americans represented a disproportionately high percentage of the diabetic population. Unadjusted data obtained from participants without prevalent CVD indicated that the mean RDI was higher in the diabetic participants. Moreover, there was a greater percentage of diabetic participants in the higher RDI categories (e.g. 23.8% of the 470 diabetics and 15.6% of the 4402 non-diabetics had RDI>15, P<0.001). Similarly, the unadjusted data indicated that a significantly greater proportion of the diabetic participants spent >5% and >10% of sleep time below SpO(2) 90%, compared with the non-diabetic participants. The unadjusted data from participants without prevalent CVD indicated that the diabetic and non-diabetic participants did not differ with regard to distribution by category of OAI severity (e.g. > or =2 events/h, > or =3 events/h, or > or =4 events/h). On the other hand, although the prevalence of central apneas was low, a significantly greater proportion of diabetic participants were in the CAI categories (> or =2 events/h and > or =3 events/h) than non-diabetic subjects. There was no difference between diabetic and non-diabetic individuals with regard to CAI prevalence in the > or =4 events/h category. Of note, a greater percentage of diabetic patients exhibited periodic breathing (3.8% vs. 1.8%, diabetic and non-diabetic participants, respectively, P=0.002). Repeating the above analyses with inclusion of the participants with prevalent CVD did not change these relationships, and in fact, the differences between diabetic and non-diabetic participants with respect to central events and periodic breathing became more evident (the data forre evident (the data for this were not provided in the paper). Linear regression analyses demonstrated that BMI, age and male gender were independently related to increased RDI among participants without prevalent CVD. Furthermore, after adjusting for age, gender, race, BMI and neck circumference, there was no difference in geometric mean RDI between the diabetic and non-diabetic participants. The adjusted odds of having RDI> or =15 and the adjusted odds for spending> or =5% or > or =10% of sleep time with SpO(2) <90% did not differ between the diabetic and non-diabetic individuals. The investigators also examined sleep architecture in the study cohort. There were no differences between the diabetic and non-diabetic groups with regard to the adjusted proportion of time spent in non-REM sleep stages, although the mean percent time spent in REM sleep was 1.1% less in the diabetic individuals. The findings were the same with or without inclusion of participants with known CVD. Even after adjustment for potential confounders, in a sample without or with prevalent CVD, diabetic participants had increased adjusted odds for periodic breathing odds ratio (1.8, 95% confidence interval (CI) with a range of 1.02--3.15 in diabetic participants without prevalent CVD vs. 1.74, 95% CI with a range of 1.16--2.62 in diabetic participants with prevalent CVD). There was a suggestion of increased odds for CAI in diabetic subjects when analyzing populations with and without prevalent CVD. CONCLUSION: The authors concluded that diabetes mellitus is associated with sleep apnea but that this association is largely explained by risk factors in common for both disorders, most notably obesity. After adjusting for confounding factors there was no difference between diabetic and non-diabetic participants with regard to obstructive events. However, even after adjusting for potential confounders, there was a greater prevalence of periodic breathing in diabetic subjects. Although not reaching statistical significance, there was a suggestion of an increased prevalence of central events in the diabetic population, particularly when the sample included participants with known CVD. The investigators believed it unlikely that the findings were attributable to underlying congestive heart failure in as much as the diabetic subjects without prevalent CVD exhibited increased prevalence of periodic breathing and possibly increased central events. The authors proposed that diabetes mellitus might be a cause of SDB, mediated through autonomic neuropathy that may alter ventilatory control mechanisms. In this context, the authors commented that autonomic neuropathy may cause perturbations in ventilatory control by altering chemoreceptor gain or altering cardiovascular function (although the authors discounted underlying congestive heart failure as an explanation for the higher prevalence of periodic breathing in diabetic participants). To reinforce their conclusions, the authors cited the literature indicating increased prevalence of sleep apnea in diabetic patients with autonomic dysfunction, as well as the association between Shy--Drager syndrome, in which autonomic insufficiency is a constitutive element, and central sleep apnea.

Journal Article↗

PubMed1990

Cardiovascular reflexes in workers exposed to hand-arm vibration.

In the present study autonomic function was observed by measuring cardiovascular reflexes. The quiet breathing test, the deep breathing test and the Valsalva manoeuvre were used. The aim was to study the effects of long-term exposure to hand-arm vibration on the cardiovascular reflexes. The study group included 47 workers (lumberjacks and railroad workers) who were exposed to hand-arm vibration. 36% of the subjects had vibration induced white finger (VWF). Comparisons were also made with 5 primary Raynaud's cases. The changes of the R-R interval in the quiet and deep breathing tests had a significant negative correlation with the ages of the subjects. In all the results there was no evidence that hand-arm vibration could cause autonomic dysfunction in general, but there were signs that it could reduce the autonomic function among workers who are susceptibility to developing white finger reactions. Also, it is possible that the primary Raynaud's cases had reduced cardiovascular reflex responses.

Adult↗

PubMed2001

[Finapres, efficient technique in the assessment of orthostatic hypotension, autonomic neuropathy, and vaso-vagal syncope].

Finapres is a device able to continuously and non invasively measure arterial blood pressure by photoplethysmography in the finger. It can be used in various dynamic tests which involve cardiocirculatory adjustments, as a passive posture test ("tilt test") or an active orthostatic test (from squatting to standing position in the so-called squatting test). It represents a valuable help in the diagnosis of orthostatic hypotension (of endogenous or iatrogenic origin), of autonomic neuropathy (secondary to diabetes mellitus or to a neurological disease) or of vasovagal syncope. All these conditions are characterized by a defect of arterial and venous vasoconstriction and by an insufficient reflex tachycardia because of autonomic dysfunction.

Autonomic Nervous System Diseases↗

PubMed2006

Approach to a case of autonomic peripheral neuropathy.

Autonomic neuropathy is the term used to describe autonomic disturbances resulting from diseases of the peripheral autonomic nervous system. This is a group of disorders in which the small, lightly myelinated and unmyelinated autonomic nerve fibers are selectively targeted. Most often, autonomic neuropathies occur in conjunction with a somatic neuropathy (i.e. with motor weakness and/or sensory loss), but they can occur in isolation. Causes of autonomic neuropathies are immune-mediated, paraneoplastic, infectious, toxic and drug-induced, hereditary, nutritional and idiopathic. Amongst all, diabetes mellitus is the most common cause. Autonomic features, which involve the cardiovascular, gastrointestinal, urogenital, sudomotor, and pupillomotor systems, occur in varying combination in these disorders. Orthostatic hypotension is often the first recognized and most disabling symptom. Noninvasive, well-validated clinical tests of autonomic functions along with a host of laboratory tests are of immense value to diagnose the presence and to demonstrate the distribution of autonomic failure. Treatment aims to treat specific cause of the autonomic neuropathy (if possible) and to control symptoms of autonomic dysfunction. Present review attempts to outline clinical approach to a case of autonomic peripheral neuropathy.

Arrhythmias, Cardiac↗

PubMed1991

[Spinal cord injury and secondary autonomic function disorders].

Autonomic dysfunction is frequently reported after high level spinal cord injury. These disorders usually occur in the first days and resolve spontaneously within 3 to 6 weeks. Usual clinical aspects are hemodynamic abnormalities and often bradycardia which can lead to death. These dysfunctions rarely reappear during neurological status recovery. In this case report, usual autonomic disorders were noted after a T5 level spinal injury with partial motor lesions. However during motor recovery periods, arrhythmias occurred, including ventricular extrasystoles and bursts of ventricular tachycardia. Physiopathological mechanisms are discussed and regulation changes of sympathetic and parasympathetic autonomic nervous system are evoked.

Adult↗

PubMed1995

Postural hypotension enhanced by exercise in patients with chronic autonomic failure.

The effect of supine exercise on blood pressure (BP), measured while recumbent and after head-up postural change, was investigated in three groups with marked postural hypotension due to chronic autonomic failure: 15 with associated neurological impairment (Shy-Drager syndrome, SDS, multiple system atrophy); 15 with pure autonomic failure (PAF) and two with a deficiency of the enzyme dopamine beta hydroxylase (DBH deficiency). Fifteen normal subjects were controls. In controls, exercise increased supine BP, and there was no postural fall before or after exercise. In SDS and PAF, however, exercise produced a substantial fall in BP, which was greater in PAF. In both groups, BP fell to a lower level on standing after than before exercise. In DBH deficiency, there was little change in BP with exercise, but BP fell to a lower level on standing after exercise. In all three groups with autonomic failure, there were more symptoms of postural hypotension on standing after exercise. The influence of exercise on both supine and postural BP, therefore, should be considered in the clinical and laboratory assessment of autonomic dysfunction.

Aged↗

PubMed1992

Natural history of autonomic neuropathy in chronic liver disease.

To determine the natural history of autonomic neuropathy in chronic liver disease we used standard cardiovascular autonomic tests to evaluate prospectively 60 patients (33 male, 27 female) with initially well-preserved hepatic function. On initial testing, 27 patients (45%; median [range] age 56 [32-67] years) had vagal neuropathy. Autonomic dysfunction was equally common in patients with alcohol-related and nonalcoholic-related liver disease. The cumulative 4-year mortality rate in patients with vagal neuropathy was 30% compared with 6% in those with normal autonomic function. Multiple logistic regression analysis showed that presence of vagal neuropathy and severity of hepatic damage were independent predictors of mortality. Serial testing showed that whereas disease progression occurred in some patients, in others mild abnormalities in autonomic function were reversible. Vagal dysfunction is common in well-compensated chronic liver disease and its presence identifies a subgroup of patients with a substantially worse outlook.

Adult↗

PubMed2004

Impaired chemoreflex sensitivity in adult patients with multiple organ dysfunction syndrome--the potential role of disease severity.

OBJECTIVE: The cardiac chemoreflex sensitivity is a powerful predictor of autonomic dysfunction in chronic heart failure and after myocardial infarction. The objective of the present study was to characterize cardiac chemoreflex sensitivity in patients with multiple organ dysfunction syndrome (MODS). We also aimed to elucidate the effect of the severity of MODS on the assessment of cardiac chemoreflex sensitivity. DESIGN: Prospective cohort study. SETTING: Twelve-bed medical intensive care unit in a university center. PATIENTS: Forty consecutively admitted patients with MODS during a 7-month period. Patients with MODS were identified by an APACHE II score of 20 or more. Sepsis was defined as a Sepsis Score, according to Elebute and Stoner, of 12 or more. INTERVENTIONS: The cardiac chemoreflex sensitivity was assessed using the regression of heart interval (ms) versus arterial oxygen pressure (mmHg). MEASUREMENTS AND RESULTS: First, we established a new method to assess cardiac chemoreflex sensitivity and applied it to healthy controls and patients. Second, we found that cardiac chemoreflex sensitivity correlated with the severity of MODS as calculated by the APACHE II score ( r(2)=0.34, p=0.001). This relation was best fitted by a model including minimum heart rate and standard bicarbonate in 24 h ( r(2)=0.5, p<0.001) and Glasgow Coma Scale ( r(2)=0.5, p=0.005). Age, however, did not significantly contribute ( r(2)=0.001, p=0.8). CONCLUSIONS: The calculation of cardiac chemoreflex sensitivity enabled us to quantify an important component of the cardiorespiratory interactions in patients with MODS. Severity of illness was a more pronounced determinant of impaired cardiac chemoreflex sensitivity than age. The quantification of the cardiorespiratory interactions by measuring the cardiac chemoreflex sensitivity has potential to identify a subgroup of patients with worse prognosis.

APACHE↗