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At least 595 records · Page 33Linked to original sources
PubMed1997

Autonomic dysfunction and upper digestive functional disorders in untreated adult coeliac disease.

There is recent evidence that upper-gut motor abnormalities may be present in coeliac disease. However, to date, the pathophysiological mechanisms responsible for the above have not been explored. The purpose of the present study was to investigate upper-gut motor activity in coeliac disease and explore the role played by the autonomic nervous system in motility disturbances. Thirty untreated adult coeliac patients were recruited into the study. Oesophageal manometry and cardiovascular autonomic tests were performed in all patients; oesophageal pH-metry was carried out in 20 patients, gastrointestinal manometry in eight and scintigraphic gastric emptying in 13. Oesophageal motor abnormalities were detected in about 50% of patients, pH-metry was abnormal in 30% of them, and up to 75% of coeliac patients displayed gastrointestinal motility alterations. Delayed gastric emptying was documented in about 50% of patients and was correlated with manometric post-prandial hypomotility. Autonomic tests were positive in 45% of patients as a group, and reached pathological score in 19% of them. Autonomic score correlated significantly with the percentage of bi-peaked waves and with the number of fasting intestinal clusters. This study confirms that upper-gut motor abnormalities are frequently present in adult coeliac disease. Extrinsec autonomic neuropathy may play a role, although other pathophysiological mechanisms are likely to occur.

Adolescent↗
PubMed2004

[Use of the B complex multivitamin preparation, Multi-tabs in the treatment of children with autonomic dysfunctions].

The article presents results of the study of vegetative homeostasis in 60 children aged 10-15 with vegetative dysfunctions. The efficacy of treatment with Multi-tabs medication of 30 children with vegetative dysfunctions with has been studied. The Multi-tabs medication treatment showed good results confirmed by positive dynamics of clinical symptoms, ECG, CIG data.

Adolescent↗
PubMed1995

[Relations between autonomic dysfunction and skin sympathetic nerve activity in Guillain-Barré syndrome: a microneurographical assessment].

We investigated the skin sympathetic nerve activity (SSNA) in 4 patients with Guillain-Barré syndrome (CBS) using microneurography. All patients showed transient hypertension, tachycardia and palmoplantar hyperhidrosis in the acute phase of illness, but these symptoms disappeared in the chronic phase. Microelectrode recordings of SSNA performed at the median nerve in the acute phase when hypertension, tachycardia and palmoplantar hyperhidrosis were present and then in the recovery phase. In the acute phase, the level of SSNA was significantly higher than the control levels obtained from 16 healthy subjects, while in the chronic recovery phase the SSNA showed no significant difference from that of the control. The correlation between the SSNA and corresponding changes in the sweat rate and skin blood flow was kept constant both in the acute phase and chronic phase. These findings suggest that the sympathetic nerve dysfunction observed in the acute phase of GBS is partly the consequence of hyperactivity of the skin sympathetic nerve.

Adolescent↗
PubMed1991

Uremic autonomic dysfunction evaluated by pattern recognition analysis.

A pattern recognition analysis of six cardiovascular reflex tests was performed with the aim to increase their diagnostic efficiency. A normal model was defined by SIMCA method using log-transformed values of 85 healthy subjects. The model was tested with data from 60 patients with chronic renal failure. Specificity resulted 94% and sensitivity 96%. 55% of the uremics were recognized affected by autonomic damage. The method allowed a better definition of autonomic function in those patients defined as "borderline" on conventional evaluation of the tests. Pattern recognition analysis of autonomic tests provides a global assessment of all the tests performed. Its use should be encouraged as a diagnostic tool.

Autonomic Nervous System Diseases↗
PubMed1992

Snuffles in infants--infection or autonomic dysfunction.

The presence of excess nasal mucus causing noisy nasal breathing with an obvious mucus discharge (snuffles) is a common problem in infants in the first three months of life. The presence of "snuffles" has traditionally been ascribed, unproven, to an upper respiratory tract infection despite there being no other signs of an acute infection in the majority of infants with "snuffles". To assess the possible role of impaired vasomotor control (autonomic function) in the pathogenesis of snuffles we measured the effect of a change from the supine to the upright position on resting blood pressure in 50 infants with "snuffles" and 50 healthy control infants. The mean age in both groups was 7 weeks post delivery, all infants were attending a well baby clinic for a routine examination, had no signs of an acute infection and none were on any medication (including nasal drops). A fall of greater than 10% of resting blood pressure was taken to indicate postural hypotension. Four of fifty infants in the control group compared to 22 of 50 in the snuffles group demonstrated postural hypotension (Chi square 16.84, p less than 0.001). The results suggest that in some infants "snuffles" may be associated with impaired vasomotor control.

Causality↗
PubMed2004

Variegate porphyria presenting with acute autonomic dysfunction, intussusception and renal infarction.

A 48-year-old man presented with abdominal pain, constipation and irritability one month after starting phenytoin treatment for a generalized seizure. He was hypertensive, tachycardic (BP 174/98, heart rate (HR) 100 bpm supine) and hypovolaemic. Abdominal CT demonstrated transient jejunal intussusception and infarction of the left kidney. Urinary porphobilinogen levels were increased and genetic analysis confirmed the diagnosis of variegate porphyria. Because of ongoing postural hypotension, the patient underwent further autonomic investigations. Levels of blood pressure (MBP), HR and muscle sympathetic activity (MSNA) were increased during the acute attack compared to recovery (131 versus 105 mmHg, 100 versus 60 bpm, 88 versus 26 bursts min(-1)). HR and MSNA did not increase during phase II Valsalva, whereas stroke volume (SV) decays were exaggerated (deltaMBP-56 versus 0-31 mmHg and SV 25% versus 40% baseline). Baroreflex failure causing increased sympathetic activity, decreased sympathetic and parasympathetic rapid responses, loss of splanchnic capacitance and renal salt wasting were the likely mechanisms for postural hypotension. Increased sympathetic activity may also have caused intussusception and focal renal vasoconstriction, both of which may be underdiagnosed causes of abdominal pain in acute porphyria.

Acute Disease↗
PubMed1991

Orthostatic changes of cerebral blood flow velocity in patients with autonomic dysfunction.

Simultaneous registrations of intracranial blood flow velocity parameters achieved by transcranial Doppler sonography and basic cardiovascular parameters were carried out during orthostatic changes in normal controls, diabetic patients and patients with pandysautonomia. Normal subjects had a rapid increase in heart rate at a constant blood pressure and a slight decrease in cerebral blood flow velocities associated with a mild increase of the pulsatility index (PI) after being tilted from a horizontal to a vertical position. Diabetics showed a fixed heart rate reflecting the disturbed autonomic innervation but only minor changes of cerebral blood flow velocity, which is similar to normal cerebrovascular autonomic regulation. Patients with pandysautonomia had a fixed heart rate associated with a decrease of systemic blood pressure but a failure of compensatory cerebral autoregulation to maintain normal flow velocity values after standing up. The results suggest that in diabetics cerebrovascular autonomic regulation is intact in contrast to cardiac autonomic function, while in patients with pandysautonomia both functions are disturbed. Criteria for the interpretation of autonomic regulatory mechanisms involved in cerebrovascular flow measurements are discussed.

Adult↗
PubMed1998

Neurally mediated hypotension and autonomic dysfunction measured by heart rate variability during head-up tilt testing in children with chronic fatigue syndrome.

Recent investigations suggest a role for neurally mediated hypotension (NMH) in the symptomatology of chronic fatigue syndrome (CFS) in adults. Our previous observations in children with NMH and syncope (S) unrelated to CFS indicate that the modulation of sympathetic and parasympathetic tone measured by indices of heart rate variability (HRV) is abnormal in children who faint during head-up tilt (HUT). In order to determine the effects of autonomic tone on HUT in children with CFS we performed measurements of HRV during HUT in 16 patients aged 11-19 with CFS. Data were compared to 26 patients evaluated for syncope and with 13 normal control subjects. After 30 minutes supine, patients were tilted to 80 degrees for 40 minutes or until syncope occurred. Time domain indices included RR interval, SDNN, RMSSD, and pNN50. An autoregressive model was used to calculate power spectra. LFP (.04-.15 Hz), HFP (.15-.40Hz), and TP (.01-.40Hz). Data were obtained supine (baseline) and after HUT. Thirteen CFS patients fainted (CFS+, 5/13 pure vasodepressor syncope) and three patients did not (CFS-). Sixteen syncope patients fainted (S+, all mixed vasodepressor-cardioinhibitory) and 10 did not (S-). Four control patients fainted (Control+, all mixed vasodepressor-cardioinhibitory) and nine did not (Control-). Baseline indices of HRV were not different between Control+ and S+, and between Control- and S-, but were depressed in S+ compared to S-. HRV indices were strikingly decreased in CFS patients compared to all other groups. With tilt, SDNN, RMSSD, and pNN50 and spectral indices decreased in all groups, remaining much depressed in CFS compared to S or control subjects. With HUT, sympathovagal indices (LFP/HFP, nLFP, and nHFP) were relatively unchanged in CFS, which contrasts with the increase in nLFP with HUT in all other groups. With syncope RMSSD, SDNN, LFP, TP, and HFP increased in S+ (and Control+), suggesting enhanced vagal heart rate regulation. These increases were not observed in CFS+ patients. CFS is associated with NMH during HUT in children. All indices of HRV are markedly depressed in CFS patients, even when compared with already low HRV in S+ or Control+ patients. Sympathovagal balance does not shift toward enhanced sympathetic modulation of heart rate with HUT and there is blunting in the overall HRV response with syncope during HUT. Taken together these data may indicate autonomic impairment in patients with CFS.

Adolescent↗
PubMed1985

Diabetic autonomic dysfunction, blood pressure, and sleep.

We measured serially the blood pressure of 7 normal controls and 11 Type I insulin-dependent and 6 Type II non-insulin-dependent diabetic patients during sleep. All subjects underwent 2 or 3 nights of monitoring during which blood pressure was measured with an arteriosonde, a Doppler-type system with a cuff that automatically inflates every 15 minutes. All 7 normal controls, 3 of 11 Type I, and all 6 Type II diabetic patients had normal results from bedside tests of autonomic function. The Type I patients had abnormal systolic blood pressure measurements throughout the night. Unlike normal controls and Type II diabetics, their blood pressure did not rise progressively in the early morning hours. During rapid eye movement (REM) sleep, their blood pressure measurements were significantly higher and lower than values measured during non-REM sleep, in sharp contrast to those in the other two groups, whose REM sleep-related blood pressure values were slightly above the preceding non-REM sleep measurements.

Adult↗
PubMed1999

Multiorgan autonomic dysfunction in mice lacking the beta2 and the beta4 subunits of neuronal nicotinic acetylcholine receptors.

Transcripts for the beta2 and the beta4 nicotinic acetylcholine receptor (nAChR) subunits are found throughout the CNS and the peripheral nervous system. These two beta subunits can form heteromultimeric channels with any of the alpha2, alpha3, alpha4, or alpha5 subunits in heterologous expression systems. Nonetheless, the subunit composition of native nAChRs and the role of different nAChR subtypes in vivo remain unclear. We prepared null mutations for the beta2 and the beta4 genes and bred beta2-/-beta4-/- mice by mating mice of identical beta2-/-beta4+/- or beta2+/-beta4-/- genotype. The beta2-/- and the beta4-/- single-mutant mice grow to adulthood with no visible phenotypic abnormalities. The beta2-/-beta4-/- double mutants survive to birth but have impaired growth and increased perinatal mortality. They also present enlarged bladders with dribbling urination and develop urinary infection and bladder stones. The ocular pupils are widely dilated and do not constrict in response to light. Histological studies revealed no significant abnormalities of brain or peripheral tissues except for hyperplasia in the bladder mucosa of beta4-/- and beta2-/-beta4-/- mutants. Bladder strips from beta2-/-beta4-/- mice did not respond to nicotine but contracted when stimulated with a muscarinic agonist or electric field stimulation. Bladder strips from beta4 mutants did not respond to nicotine despite the absence of major bladder dysfunction in vivo. Acetylcholine-activated whole-cell currents were absent in superior cervical ganglion neurons from beta2-/-beta4-/- mice and reduced in neurons from beta4-/- mice. Although there is apparent redundancy and a superficially normal phenotype in beta2-/- and beta4-/- mice, physiological studies indicate major deficits in the beta4-/- mice. Our previous description of a similar phenotype in alpha3-/- mice and the current data suggest that the alpha3 and the beta4 subunits are major components in autonomic nAChRs. The phenotype of the beta2-/-beta4-/- and alpha3-/- mice resembles the autosomal recessive megacystis-microcolon-hypoperistalsis syndrome in humans.

Animals↗
PubMed2006

Fatalities after taking ibogaine in addiction treatment could be related to sudden cardiac death caused by autonomic dysfunction.

Ibogaine is the most important alkaloid of the Central African Iboga-shrub. It is the central drug in Gabonian initiation ceremonies in which it is used to cause a near-death experience. In Western countries it is used in private clinics to treat addiction. However, in the United States and most European countries it is classified as an illegal drug because at least eight persons have died after having taken Ibogaine. These fatalities occurred in most cases several days after ingestion or following the intake of very small doses. There is no conclusive explanation at the present time for these deaths. We hypothesize, that these deaths may be a result of cardiac arrhythmias, caused by a dysregulation of the autonomic nervous system. Ibogaine affects the autonomic nervous system by influencing several neurotransmitter-systems and the fastigial nucleus. The cerebellar nucleus responds to small doses with a stimulation of the sympathetic system, leading to a fight or flight reaction. High doses, however, lead to a vagal dominance: a "feigned death". The risk of cardiac arrhythmias is increased in situations of sympathetic stimulation or coincidence of a high parasympathetic tonus and a left-sided sympathetic stimulation. This could occur under influence of small doses of ibogaine and also at times of exhaustion with a high vagal tonus, when sudden fear reactions could cause a critical left-sided sympathetic stimulation. Gabonian healers prevent these risks by isolating their patients from normal life and by inducing a trance-state with right-hemispheric and vagal dominance for several days.

Autonomic Nervous System↗
PubMedDate not supplied

Pulmonary edema induced by fluid administration in acquired immune deficiency syndrome patients with cardiac autonomic dysfunction.

Two patients with the acquired immune deficiency syndrome developed acute pulmonary edema following intravenous fluid administration. Both recovered with diuretic therapy. In neither case was there evidence of persistent severe left ventricular dysfunction, nor was there evidence (either clinically or by thallium study) of flow limiting coronary lesions or of cardiac uptake of iodine-123 meta-iodobenzylguanidine, pointing to ventricular sympathetic neuropathy. It is hypothesized that destruction of the cardiac sympathetics contributed importantly to the development of pulmonary edema following the intravenous fluid load.

3-Iodobenzylguanidine↗
PubMed2003

Simultaneous measurement of instantaneous heart rate and chest wall plethysmography in short-term, metronome guided heart rate variability studies: suitability for assessment of autonomic dysfunction.

Instantaneous heart rate and chest wall motion were measured using a 3-lead ECG and an air pressure chest wall plethysmography system. Chest wall plethysmography traces were found to accurately represent the breathing pattern as measured by spirometry (average correlation coefficient 0.944); though no attempt was made to calibrate plethysmography voltage output to tidal volume. Simultaneous measurements of heart rate and chest wall motion were made for short periods under metronome guided breathing at 6 breaths per minute. The average peak to trough heart rate change per breath cycle (AVEMAX) and maximum correlation between heart rate and breathing cycle (HRBRCORR) were measured. Studies of 44 normal volunteers indicated clear inverse correlation of heart rate variability parameters with age (AVEMAX R = -0.502, P < 0.001) but no significant change in HRBRCORR with age (R = -0.115). Comparison of normal volunteers with diabetics with no history of symptoms associated with autonomic failure indicated significant lower heart rate variability in diabetics (P = 0.005 for AVEMAX) and significantly worse correlation between heart rate and breathing (P < 0.001 for HRBRCORR). Simultaneous measurement of heart rate and breathing offers the possibility of more sensitive diagnosis of autonomic failure in a simple bedside test and gives further insight into the nature of cardio-ventilatory coupling.

Adult↗
PubMed2001

Association of autonomic dysfunction and clozapine. Heart rate variability and risk for sudden death in patients with schizophrenia on long-term psychotropic medication.

BACKGROUND: Antipsychotic medications cause a wide range of adverse effects and have been associated with sudden death in psychiatric patients. AIMS: To supply power spectral analysis of heart rate variability as a tool to examine the arrythmogenic effects of neuroleptics. METHOD: Heart rate analysis was carried out in patients with schizophrenia on standard doses of neuroleptic monotherapy -- 21 were on clozapine, 18 on haloperidol and 17 on olanzapine -- and in 53 healthy subjects. RESULTS: Patients with schizophrenia on clozapine had significantly higher heart rate, lower heart rate variability and lower high-frequency and higher low-frequency components compared with patients on haloperidol or olanzapine and matched control subjects. Prolonged QTc intervals were more common in patients than controls. CONCLUSIONS: Patients treated with neuroleptic medications, especially clozapine, showed autonomic dysregulation and cardiac repolarisation changes. Physicians should be aware of this adverse reaction.

Adult↗
PubMed2005

Relationship between autonomic dysfunction, insulin resistance and hypertension, in diabetes.

Sympathovagal imbalance and insulin resistance are the common underlying disorders linking hypertension and diabetes. The role of hyperinsulinemia, however, on sympathovagal balance and blood pressure has never been clearly dissected from that of hyperglycemia. Nevertheless, the study of animal models of hypertension showed that hypertension does not invariably result in the onset of insulin resistance. This suggests that insulin resistance precedes the onset of hypertension and (possibly) contributes to its pathogenesis, mainly through sympathetic activation. To examine this hypothesis, recent studies investigated the relationship between insulin sensitivity and sympathetic activity in subjects with insulin resistance but free of overt hyperglycemia and obesity, i.e., insulin-resistant offspring of type 2 diabetic patients, demonstrating a prevalence of sympathetic over vagal activity. Therefore insulin resistance and sympathovagal imbalance come before hypertension, but a clear causative role cannot be demonstrated since other mechanisms, including an inappropriate lifestyle, must be taken into account to determine clinical hypertension. Finally, several experiments in human healthy volunteers suggest that the modulation of autonomic regulation at the forearm level can regulate insulin sensitivity, tempting us to speculate that it is the primary autonomic imbalance, through vasoconstriction, that results in both insulin resistance and hypertension. In conclusion, the close relationship between autonomic imbalance, insulin resistance and hypertension is unquestionable; although logical hypothesis can be constructed, which of the three is the earliest event is still not understood, and further research is required.

Autonomic Nervous System Diseases↗
PubMed1988

Moyamoya disease in an infant with autonomic dysfunction: angiographic and MRI findings.

An infant with persistent Harlequinism went on to develop a hemiparesis secondary to Moyamoya disease at 2 1/2 months of age. The sympathetic nervous system is proposed to be an etiologic factor in the pathophysiology of Moyamoya disease as well as Harlequinism. This is one of the youngest patients reported in the English literature with Moyamoya disease and the only report of the coexistence of Moyamoya disease and atypical Harlequinism. Magnetic resonance imaging led to the diagnosis, which was confirmed by cerebral angiography.

Arterial Occlusive Diseases↗