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PubMed1985

Autonomic nervous system and epilepsy.

Seizures frequently manifest autonomic dysfunction clinically, and seizure discharges commonly spread into and involve autonomic pathways. These associations are direct and simple in some instances, and the result of multiple indirect and complex relationships in others. Effects of epileptic discharge on the autonomic nervous system are mediated through the cortical, limbic, and hypothalamic systems. Some significant consequences of altered autonomic function include convulsive apnea, abnormal sexual function, and potentially fatal effects on the cardiovascular system.

Adult↗

PubMed2006

Cardiovascular and temperature changes in spinal cord injured rats at rest and during autonomic dysreflexia.

In patients with high spinal cord injuries autonomic dysfunction can be dangerous, leading to medical complications such as postural hypotension, autonomic dysreflexia and temperature disturbance. While animal models have been developed to study autonomic dysreflexia, associated temperature changes have not been documented. Our aim here was to use radiotelemetry and infrared thermography in rodents to record the development of cardiovascular and skin temperature changes following complete T4 transection. In adult male Wistar rats (n=5), responses were assessed prior to spinal cord injury (intact) and for 6 weeks following injury. Statistical analysis by a repeated-measure ANOVA revealed that following spinal cord injury (SCI), rats exhibited decreased mean arterial pressure (MAP, average decrease of 26 mmHg; P<0.035) and elevated heart rate (HR, average increase of 65 bpm, P<0.035) at rest. The basal core body temperature following SCI was also significantly lower than intact levels (-0.9 degrees C; P<0.0035). Associated with this decreased basal core temperature following SCI was an increased skin temperature of the mid-tail and hindpaw (+5.6 and +4.0 degrees C, respectively; P<0.0003) consistent with decreased cutaneous vasoconstrictor tone. Autonomic dysreflexia, in response to a 1 min colorectal distension (25 mmHg), was fully developed by 4 weeks after spinal cord transection, producing increases in MAP greater than 25 mmHg (P<0.0003). In contrast to the tachycardia seen in intact animals in response to colorectal distension, SCI animals exhibited bradycardia (P<0.0023). During episodes of autonomic dysreflexia mid-tail surface temperature decreased (approximately -1.7 degrees C, P<0.012), consistent with cutaneous vasoconstriction. This is the first study to compare cardiovascular dysfunction with temperature changes following spinal cord transection in rats.

Analysis of Variance↗

PubMed2005

Subtle autonomic and respiratory dysfunction in sudden infant death syndrome associated with serotonergic brainstem abnormalities: a case report.

Sudden infant death syndrome (SIDS) is characterized by a sleep-related death in a seemingly healthy infant. Previously, we reported abnormalities in the serotonergic (5-HT) system of the medulla in SIDS cases in 2 independent datasets, including in the Northern Plains American Indians. The medullary 5-HT system is composed of 5-HT neurons in the raphé, extra-raphé, and arcuate nucleus at the ventral surface. This system is thought to modulate respiratory and autonomic function, and thus abnormalities within it could potentially lead to imbalances in sympathetic and parasympathetic tone. We report the case of a full-term American Indian boy who died of SIDS at 2 postnatal weeks, and who had subtle respiratory and autonomic dysfunction measured prospectively on the second postnatal day. Cardiorespiratory assessment of heart rate variability suggested that the ratio of parasympathetic to sympathetic tone was higher than normal in active sleep and lower than normal in quiet sleep in this case. At autopsy, arcuate nucleus hypoplasia and 5-HT receptor-binding abnormalities in the arcuate nucleus and other components of the medullary 5-HT system were found. This case suggests that medullary 5-HT system abnormalities may be able to be identified by such physiological tests before death. Replication of these findings in a large population may lead to the development of predictive cardiorespiratory assessment tools for future screening to identify infants with medullary 5-HT abnormalities and SIDS risk.

Age Factors↗

PubMed2001

Cardiovascular and neurohormonal responses to i. v. l-arginine in two groups with primary autonomic failure.

Nitric oxide (NO) is synthesised from the amino-acid l-arginine by the enzyme nitric oxide synthetase (NOS) and modulates a wide variety of neural, cardiovascular and hormonal processes. Cardiovascular autonomic dysfunction and impaired neurohormonal secretion characterise patients with primary chronic autonomic failure (AF). To investigate the role of NO, we studied the cardiovascular and neurohormonal effects of intravenous (i. v.) l-arginine (0.5 g/kg) in 20 patients with AF: [10 with multiple system atrophy (MSA) and 10 patients with pure autonomic failure (PAF)] and compared them with age-matched healthy normal subjects. Basal mean arterial pressure (MAP) was higher in MSA and PAF than controls (p < 0.02). Following l-arginine, MAP fell in MSA (mean: -39 +/- 8 mmHg, 95 % CI -21 to -57, p < 0.05) and PAF (-37 +/- 5,95 % CI -26 to -58, p < 0.05) but not in controls. There were no significant changes in HR between the groups. Basal plasma noradrenaline (NA) was similar in controls and MSA, but lower in PAF (p < 0.05). Following l-arginine the percentage rise in plasma NA was similar in controls and MSA, but not in PAF (p < 0.05). Plasma insulin rose similarly in controls and MSA, but was higher in PAF (p < 0.05). Plasma glucose rose to a similar level in all groups. In conclusion, l-arginine, lowered BP in both MSA and PAF. In PAF a contributory factor may be increased insulin release, without a compensatory increase in sympatho-neural activity to counter its potential vasodilator effects. These studies suggest that reducing NO levels, as with NOS inhibitors, may be of benefit in the treatment of postural hypotension and possibly post-prandial hypotension in chronic primary AF.

Adult↗

PubMed2002

Impaired autonomic control of heart interval changes to Valsalva manoeuvre in Chagas' disease without overt manifestation.

BACKGROUND: In the apparent indeterminate form of Chagas' disease, which lacks any overt clinical, electrocardiographic, and radiological manifestations of organ damage, lesions of the intrinsic autonomic innervation of heart are not striking features and evidences for cardiac autonomic dysfunction are elusive and conflicting. OBJECTIVE: To evaluate the cardiac autonomic modulation based on Valsalva manoeuvre-associated heart interval variation in Chagas' disease subjects with apparent indeterminate form. SUBJECTS AND METHODS: We examined 36 outpatient volunteers aged 15-51 years old (median: 36.5), in comparison with 52 healthy control individuals aged 17-49 years old (median: 29) (p<0.001). Each subject sequentially performed in the supine position three to four manoeuvres at an intra-oral pressure of 40 mm Hg during 20 s, under continuous DII lead electrocardiographic registration, and rate- and time-dependent indices of Valsalva manoeuvre-associated R-R interval variation were obtained. The t-test or the Mann-Whitney test was employed to compare the data between the groups. RESULTS: No correlation was found between every index and age for the control group (p=0.39-0.71). The chagasic group presented similar basal to phase IV median increment (relative bradycardia) (23.7% vs. 22.7%; p = 0.63) and smaller basal to phase III median decrement of R-R interval (relative tachycardia) (-31.7% vs. - 35%; p=0.02) in comparison to the control group, respectively. The median Valsalva ratio showed a tendency for reduction in chagasics (1.78 vs. 1.90; p = 0.08). Prolonged median time (14.2 vs. 10.3 s; p < 0.001) and slowed median velocity (5.1%/s vs. 8.9%/s; p < 0.001) of the phases III-IV bradycardia were also observed in chagasic group. The majority (58.3%) of the chagasics presented exclusively at least one depressed, and 8.3% presented at least one enhanced index of rate- and/or time-dependent heart interval responses beyond the 25th or 75th control percentiles, and 27.8% presented at least one depressed and other enhanced index, while 5.6% showed all indices within the control interquartile range. All the indices outside the 25th or 75th control percentiles were noted in 13.9% of chagasics. CONCLUSION: Chagas' disease subjects without overt manifestations presented variable and subtle depression and less frequent enhancement or normality of the rate- and time-dependent tachycardia and bradycardia reflex responses related to Valsalva manoeuvre, which demonstrates distinct patterns of finely disturbed cardiac sinus parasympathetic and sympathetic modulation, probably due to inflammatory or autoimmunological damage of intrinsic innervation and/or to autoantibodies-induced derangement in neurotransmitter receptors.

Adolescent↗

PubMed1993

Central autonomic disorders.

Central autonomic dysfunctions can be due to primary (degenerative) or secondary disorders. Autonomic failure (AF) may be a major manifestation of multiple system atrophy (MSA) and idiopathic Parkinson's disease (IPD). In both MSA and IPD, AF is almost invariably associated with neuronal loss in the intermediolateral cell columns. Dysautonomia in MSA is early, severe, and progressive, including marked orthostatic hypotension and urinary incontinence and is complicated by respiratory disturbances, such as laryngeal stridor and sleep apnea. MSA/AF can be differentiated from primary (or pure) autonomic failure (PAF) without central nervous system involvement. PAF is mainly a disorder of the postganglionic neurons. In contrast to PAF, MSA/AF has preserved basal sympathetic activity, decreased cerebrospinal fluid (CSF) neurotransmitter markers, impaired vasopressin response to hypotension, and impaired adrenocorticotrophic hormone/beta endorphin response to hypoglycemia. AF in IPD is generally less severe than in MSA. Poor response to L-Dopa, abnormal urethral sphincter electromyography, and CSF markers may distinguish MSA from IPD. Secondary autonomic disorders may result from traumatic, vascular, inflammatory, demyelinating, or neoplastic lesions involving corticolimbic, hypothalamic, brainstem, or spinal autonomic network. These disorders can cause AF or autonomic hyperactivity, such as arrhythmia, hypertension, and hyperthermia. However, many disorders may only produce subclinical abnormalities.

Autonomic Nervous System Diseases↗

PubMedDate not supplied

Cardiac dysautonomia in lepromatous leprosy.

Cardiovascular autonomic functions were studied in 32 patients of lepromatous leprosy, including 12 patients of lepra reaction. Fifty age and sex matched healthy subjects served as controls. Variable degree of autonomic dysfunction was observed in the study group. The derangement of autonomic functions in patients of leprosy can be explained on the basis of neurotrophic action of lepra bacilli that infiltrate the sympathetic and the parasympathetic fibres.

Adult↗

PubMed1993

Changes in autonomic nervous function over a 5-year period in non-insulin-dependent diabetic patients.

One hundred and eight non-insulin-dependent diabetic patients who had been tested for autonomic dysfunction in 1984/85 were re-evaluated 5 years later. Autonomic function was assessed by means of four cardiovascular tests (heart rate variation during deep breathing and standing, and blood pressure variation after standing and sustained handgrip). Eighteen subjects were lost to follow-up; in the 90 patients who completed the study, both the deep breathing and the handgrip test significantly worsened (respectively from 13.7 +/- 7.8 to 11.6 +/- 6.3 beats min-1 p < 0.01, and from 16.9 +/- 8.2 to 12.7 +/- 7.1 mmHg, p < 0.001), whereas both the 30:15 ratio and the variation of blood pressure on standing did not change. The impairment of a comprehensive evaluation score (from 2.5 +/- 1.7 to 3.0 +/- 1.5; p < 0.05) also confirmed the gradual deterioration of autonomic function over the study period.

Autonomic Nervous System↗

PubMed1981

The impact of autonomic nervous system dysfunction on breathing during sleep.

Ten patients with autonomic nervous system dysfunction (familial dysautonomia, juvenile diabetes, or Shy-Drager syndrome) were studied to assess the impact of their impairment on breathing during sleep. Several types of breathing dysfunction during sleep were identified independent of the patients' primary complaints. Obstructive sleep apnea syndrome was the most common; central sleep apnea and disturbances of te respiratory oscillator also were seen. Esophageal reflux was found to be the cause of some sleep-related problems. The observed respiratory irregularities were not associated with the usual cardiac response; a "decoupling" of heart rate from the respiratory cycle was noted during sleep in these patients.

Adolescent↗

PubMed2005

The smoking gun: many conditions associated with tobacco exposure may be attributable to paradoxical compensatory autonomic responses to nicotine.

Tobacco exposure is implicated in many illnesses such as cardiovascular disease and cancer, but the mechanisms underlying these associations are poorly understood. The mechanisms by which tobacco induces pro-sympathetic and pro-inflammatory changes also remain elusive. Some studies have attributed these changes to the direct effects of nicotine, but such findings run counter to the pro-vagal, anti-inflammatory nature of the nicotinic pathway. We hypothesize that the illnesses associated with smoking may be partly attributable to autonomic dysfunction, sympathetic bias, and T helper (Th)2 inflammation induced by a paradoxical compensatory response to intermittent nicotinic exposure. The confusion of interpreting the adrenergia and inflammation associated with nicotine as a primary response instead of a secondary compensation may be explained by the unusually rapid absorption, action, and serum elimination of nicotine. Given the fast action and clearance of nicotine, even heavy smokers spend large portions of the day and the entire night in nicotine withdrawal, at which time rebound sympathetic bias may manifest as a result of desensitization of nicotinic receptors. This may help reconcile why the features observed in smokers such as tachycardia, hypertension, inflammation, insomnia, and anxiety, which are perhaps mistakenly attributed to the direct action of nicotine, are identical to those seen during acute nicotine withdrawal after smoking cessation. On the other hand, delayed responses to cessation of smoking such as weight gain and increased heart rate variability are compatible with reduced sympathovagal ratio and resensitization of nicotinic receptors. Sympathetic bias and the associated Th2 inflammation underlie many systemic diseases. Tobacco-related cancers may be partly attributable to immunomodulatory properties of chronic nicotine exposure by dampening Th1 immunity and enabling tumoral evasion of immune surveillance. Other conditions associated with tobacco exposure may also operate through similar autonomic and immune dysfunctions. Therapeutic implications are discussed.

Anxiety↗

PubMed1997

Creutzfeldt-Jakob disease associated with autonomic nervous system dysfunction in the early stage.

A 54-year-old man presented with tremor and unusual behavior. He was admitted two months later because of dementia and myoclonus. Periodic synchronous discharges were observed on the electroencephalogram. Based on these findings, we diagnosed the case as Creutzfeldt-Jakob disease. About two weeks after admission, decubitus, bowel dysfunction and hypohidrosis occurred. We observed various autonomic nervous system dysfunctions such as abnormal pupillary response to autonomic drugs, reduced coefficient of variation of R-R interval, and abnormal diurnal blood pressure variation.

Atrophy↗

PubMed2002

Effects of a startle on heart rate in patients with multiple system atrophy.

The patient cooperation usually required for neurophysiological assessment of autonomic cardioregulatory function is difficult to obtain from patients with bradykinesia. A particularly interesting condition occurs in multiple system atrophy (MSA), which features both bradykinesia and autonomic dysfunction. Another characteristic of patients with MSA is their normal motor reaction to a startling stimulus. We used startle as a stimulus for testing autonomic cardioregulatory function in patients with MSA, thus avoiding the need for patient cooperation. In 10 healthy volunteers and 8 MSA patients, we recorded the electrocardiographic QRS complex with surface electrodes attached over the chest and delivered an acoustic startle stimulus after 8 seconds of baseline recording. We calculated the ratio between the pre-stimulus and the post-stimulus heart beat intervals (R-R ratio) by dividing the mean prestimulus R-R interval by the shortest R-R interval obtained within 10 seconds poststimulus. Healthy volunteers had a significant shortening of the R-R interval. The peak of the effect occurred after 2 to 5 seconds, with a mean R-R ratio of 1.14 (S.D. = 0.09). In contrast, R-R shortening was markedly reduced in patients, even though they had a normal motor response. The mean R-R ratio in patients was 1.03 (S.D. = 0.03), significantly lower than in healthy volunteers (P < 0.01). Our results demonstrate an abnormally reduced modulation of the heart beat frequency in patients with MSA, compatible with a dysfunction on pathways responsible for autonomic regulation. The method described here may be useful in the assessment of cardioregulatory function in poorly cooperative patients with normal startle responses.

Acoustic Stimulation↗

PubMed1980

AV node dysfunction in the mitral valve prolapse syndrome.

The mitral valve prolapse syndrome is associated with a variety of atrial and ventricular arrhythmias. A portion of these patients manifest bradyarrhythmias, which in turn, may be the cause of lightheadedness and syncope. Thie study details the clinical and electrophysiologic characteristics of seven patients with symptomatic mitral valve prolapse and AV node dysfunction. The electrophysiology study demonstrated either a prolonged AH interval or abnormal response to atrial pacing in six of seven patients. A significant proportion of these patients had abnormalities of sinus node function and distal His-Purkinje conduction in addition to AV node dysfunction. AV node dysfunction in symptomatic patients with mitral valve prolapse may be secondary to autonomic dysfunction of diffuse conduction system disease.

Adolescent↗

PubMed2005

REM sleep behaviour disorder.

REM sleep behaviour disorder (RBD) is a parasomnia characterised by nocturnal complex motor activity associated with dream mentation. RBD, which affects mainly older men, may be idiopathic or associated with other neurological disorders. A strong association between RBD and alpha-synucleinopathies has been recently observed, with the parasomnia often heralding the clinical onset of the neurodegenerative disease. The idiopathic form accounts for up to 60% of the cases reported in the three largest series of RBD patients. Follow-up studies in small samples revealed that a proportion of RBD patients will eventually develop Parkinson's disease and/or a dementia of Lewy bodies type in the years following the RBD diagnosis. Recently, neurophysiological and neuropsychological studies in idiopathic RBD have found evidence of central nervous system dysfunction. An impairment of cortical activity, specific neuropsychological deficits, signs of autonomic dysfunction and olfactory impairment have been observed in these patients, challenging the concept of idiopathic RBD. The detection of early markers of neurodegenerative disorders in idiopathic RBD, and the evaluation of their value by the combined application in prospective studies may be crucial for developing early intervention strategies.

Aggression↗

PubMed1996

Antiadrenergic and muscarinic receptor antibodies in Chagas' cardiomyopathy.

Evidence accumulated over the last decade gives adequate proof for the existence of circulating antibodies in Chagas' disease which bind to beta adrenergic and muscarinic cholinergic receptors of myocardium. The interaction of antibodies with cardiac neurotransmitter receptors behaving as an agonist, triggers intracellular signal transductions in the cells that alter the physiological behaviour of the heart. These events convert the normal to pathologically active cells. The interaction of antibodies against heart beta adrenergic and cholinergic receptors triggers physiologic, morphologic, enzymatic and molecular alterations, 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. The presence of these antibodies may thus 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, induced desensitization and/or down regulation of the receptors. This in turn, could lead 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.

Chagas Cardiomyopathy↗

PubMed2004

Human sympathetic activation by alpha2-adrenergic blockade with yohimbine: Bimodal, epistatic influence of cytochrome P450-mediated drug metabolism.

BACKGROUND: alpha2-Adrenergic blockade responses suggest adrenergic dysfunction in hypertension. alpha2-Blockade is also used to treat autonomic dysfunction. However, pharmacokinetic determinants of yohimbine disposition are not understood. METHODS: We evaluated alpha2-blockade with intravenous yohimbine in 172 individuals. Specific cytochrome P450 (CYP) isoform-mediated metabolism was investigated. Results were evaluated by ANOVA and by maximum likelihood analysis for bimodality of response distributions. RESULTS: Yohimbine metabolism to 11-hydroxy-yohimbine displayed greater than 1000-fold variability, with 17 individuals showing no metabolism. Nonmetabolizers differed from others in ethnicity but not in age, sex, body habitus, blood pressure, heart rate, or family history of hypertension. Bimodality of metabolism was suggested by frequency histogram, as well as maximum likelihood and cluster analysis. Among ethnic groups, subjects of European ancestry had the highest frequency of nonmetabolism. In vitro oxidation suggested that the major route of metabolism (lowest Michaelis-Menten constant and greatest intrinsic clearance) was likely via CYP2D6 to 11-hydroxy-yohimbine. In vivo genotypes at both CYP2D6 and CYP3A4 were necessary to predict metabolism (overall F = 3.03, P =.005); an interaction of alleles at these 2 loci (interaction F = 3.05, P =.033) suggested an epistatic effect on drug metabolism in vivo. Nonmetabolizers had greater activation of sympathetic nervous system activity. Yohimbine increased blood pressure, an effect mediated hemodynamically by elevation of cardiac output rather than systemic vascular resistance. Blood pressure and cardiac output responses did not differ by metabolizer group. CONCLUSIONS: We conclude that heterogeneous, bimodally distributed yohimbine metabolism depends on common genetic variation in both CYP2D6 and CYP3A4 and contributes to differences in sympathetic neuronal response to alpha2-blockade. These results have implications for both diagnostic and therapeutic uses of this alpha2-antagonist.

Adrenergic alpha-2 Receptor Antagonists↗

PubMed1996

Central and peripheral haemodynamic responses to high carbohydrate and high fat meals in human cardiac transplant recipients.

1. Patients with autonomic dysfunction and elderly people with an age-related decline in autonomic function can suffer from a fall in blood pressure after eating. While the cardiovascular changes after eating and the effect of meal composition on these changes are well established, the underlying mechanisms are less clear. 2. This study assessed the cardiac, circulatory and humoral responses to ingestion of isoenergetic (2.5 MJ) high carbohydrate and high fat meals in nine orthotopic cardiac transplant recipients, who before transplantation had significant circulatory, metabolic and autonomic abnormalities and after transplantation had complete or partial extrinsic cardiac denervation, and compared them to the responses seen in nine healthy age-matched control subjects. 3. All variables were measured non-invasively. Cardiac transplant recipients, despite cardiac denervation, showed a normal heart rate response to high carbohydrate and high fat meals (maximal increase at 30 min postprandially + 7.8 +/- 1.1 and + 63 +/- 1.4 beats/min respectively), a normal cardiac output response to the high carbohydrate meal (maximal increase at 30 min + 1.16 +/- 0.25 l/min), but a significantly attenuated cardiac output response to the high fat meal. Cardiac transplant recipients had attenuated superior mesenteric artery blood flow responses after both meals (P < 0.05) and an attenuated calf vascular resistance response after the high fat meal (P < 0.01). Throughout the study after both meals, cardiac transplant recipients maintained blood pressure. 4. This study demonstrates that cardiac transplant recipients, despite partial or complete cardiac denervation, have a normal chronotropic response to food and a normal cardiac output response to a high carbohydrate meal. The attenuated cardiac output response to a high fat meal did not compromise blood pressure, due at least in part to decreased splanchnic vasodilatation.

Adult↗

PubMed1999

Impaired ascendant central pathways conduction in impotent diabetic subjects.

OBJECTIVES: Diabetic impotence is generally due to peripheral neuropathy, but a central pathway impairment has also been suggested. We evaluated somatosensory transmission in a group of impotent diabetic men to assess the role of central nervous system (CNS) involvement. MATERIALS AND METHODS: Somatosensory evoked potentials (SEPs) of pudendal (pdn) and posterior tibial (ptn) nerves were recorded in 74 patients. Type and duration of diabetes, severity of sexual dysfunction, medium term metabolic control, occurrence of microangiopathic chronic complications and autonomic neuropathy were evaluated. RESULTS: Our data show an impairment of central conduction times in pdn (25.7%) and ptn (39.2%) greater than peripheral nervous impairment (pdn 12.2%, ptn 8.1%), in impotent diabetic patients without any further major complication. Central nervous conduction delay resulted to be correlated with poor glycemic control. Significant evident autonomic dysfunction was found only in a minority of cases. CONCLUSION: Our data might suggest that altered conduction along CNS and somatic peripheral neuropathy might develop independently. We confirm the hypothesis of a "central diabetic neuropathy" and suggest that central sensory pathways involvement, not related to peripheral impairment, could play a role in the pathogenesis of erectile dysfunction in diabetic patients.

Adult↗