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PubMed1998

Neurally mediated hypotension and chronic fatigue syndrome.

A substantial body of clinical evidence now supports an association between various forms of hypotension and both idiopathic chronic fatigue and the chronic fatigue syndrome (CFS). Patients with CFS have a high prevalence of neurally mediated hypotension, and open treatment of this autonomic dysfunction has been associated with improvements in CFS symptoms. Randomized trials are now in progress to evaluate the efficacy of treatments directed at neurally mediated hypotension in those with CFS patients, and the results of these trials should help guide more basic inquiries into the mechanisms of orthostatic intolerance in affected individuals.

Autonomic Nervous System↗

PubMed1987

Effects of combined pancreatic and renal transplantation on diabetic neuropathy: a two-year follow-up study.

To investigate whether diabetic neuropathy can be reversed after pancreatic transplantation 13 diabetic patients were examined by means of conventional electroneurography and tests on autonomic function before and 6, 12, and 24 months after combined renal and pancreatic transplantation. 15 diabetic patients receiving a kidney graft only and 15 non-diabetic kidney graft recipients served as controls. Before transplantation neuropathy was most advanced in the two diabetic groups. Both diabetic groups showed a similar slight but significant improvement of nerve conduction after transplantation. In the non-diabetic group nerve conduction became essentially normal. No group showed improvement in autonomic dysfunction. The improvement in nerve conduction after combined kidney and pancreas transplantation was most probably due to the elimination of uraemia. Furthermore, 2 years of normoglycaemia did not reverse the diabetic neuropathy to an important extent at this late stage of the disease.

Adult↗

PubMed2005

Neuroprotective effects of TEMPOL in central and peripheral nervous system models of Parkinson's disease.

TEMPOL (4-hydroxy-2,2,6,6-tetramethylpiperidine-N-oxyl) is a stable nitroxyl antioxidant. Previous studies have suggested that TEMPOL is protective in acute disorders thought to involve reactive oxygen species (ROS), such as ischemic stroke and cardiac reperfusion injury. Oxidized TEMPOL can be recycled to its redox-active reducing form by co-administration with polynitroxylated albumin, making it a candidate as a pharmacological "reservoir" for reducing potential of use in chronic disorders involving ROS. The present studies examine the efficacy of TEMPOL in cell culture and animal models of the central and peripheral dysfunction associated with Parkinson's disease, a disorder in the pathogenesis of which ROS generated from dopamine have been implicated. Antioxidants have been proposed as both preventive and symptomatic therapy for Parkinson's disease. TEMPOL protects MN9D dopaminergic mesencephalic cells in culture from 6-hydroxydopamine (6-OHDA)-induced apoptosis. Translocation of the p65 component of NF-kappaB to the nucleus accompanies protection by TEMPOL. In vivo, intraperitoneal TEMPOL protects mice from intrastriatal 6-OHDA-induced cell and dopamine metabolite loss in the striatum. TEMPOL also protects mice against the 6-OHDA-induced rotational behavior elicited by intrastriatal administration of d-amphetamine. In addition, TEMPOL protects mice from the ptosis, activity level decrement, and mortality induced by intraperitoneal administration of 6-OHDA, a model of autonomic dysfunction in Parkinson's disease. Adjunctive use of polynitroxylated albumin enhances the in vitro and in vivo effects of TEMPOL.

Active Transport, Cell Nucleus↗

PubMed1997

Personalized surgery for rectal tumours: the patient's opinion counts.

In recent times there have been many important changes in the surgical management of rectal cancer. The general thrust of these changes has been towards a less invasive approach with preservation of intestinal continuity and avoidance of the psychological sequelae of a stoma. It is also becoming increasingly apparent that profound sexual and autonomic dysfunction can be associated with abdominoperineal resection. This paper highlights these issues and the conflict between performing an adequate oncological procedure and reducing the incidence of postoperative psychological morbidity. It outlines the great changes there have been in surgical technique and their relevance to psychological problems after surgery for rectal cancer. The need for auditing psychological morbidity when assessing the outcome of surgical series is emphasised, as is the importance of involving the patient in the medical decision making.

Abdomen↗

PubMed1986

Decreased myo-inositol content and Na+-K+-ATPase activity in superior cervical ganglion of STZ-diabetic rat and prevention by aldose reductase inhibition.

Decreased sciatic nerve myo-inositol content and Na+-K+-ATPase activity have been associated with slowing of motor nerve conduction in the acutely diabetic rat and have been invoked as possible pathogenic factors in diabetic peripheral neuropathy. Aldose reductase inhibitors prevent these abnormalities in peripheral nerves of the streptozocin (STZ)-diabetic rat. Whether an analogous biochemical abnormality occurs in the autonomic nervous system and plays a role in the development of diabetic autonomic dysfunction is unknown. Therefore we examined the effect of 8 wk of untreated STZ diabetes and administration of 20 mg X kg-1 X day-1 of the aldose reductase inhibitor sorbinil on myo-inositol level and Na+-K+-ATPase activity in rat superior cervical ganglia. Both myo-inositol concentration and Na+-K+-ATPase activity were reduced in ganglia from untreated STZ-diabetic rats, and sorbinil administration prevented these abnormalities. Thus, a sorbinil-responsive metabolic defect involving myotional abnormalities in the somatic and autonomic nervous systems in diabetes.

Aldehyde Reductase↗

PubMed2006

Impaired cardiac autonomic nervous activity predicts sudden cardiac death in patients with operated and unoperated congenital cardiac disease.

OBJECTIVES: Sudden cardiac death is a leading cause of mortality in patients with congenital cardiac disease after surgical correction and is potentially preventable. The identification of patients at risk is therefore of major interest. We sought to assess the prognostic value of impaired cardiac autonomic nervous activity in patients with congenital cardiac disease. METHODS: Forty-three consecutive patients with congenital cardiac disease were included in this prospective study. Parameters of heart rate turbulence and heart rate variability were calculated from Holter electrocardiograms. In addition, serum brain natriuretic peptide levels were measured. A combined end point of sudden cardiac death or nearly missed sudden cardiac death was used. RESULTS: During a mean follow up of 27 +/- 12.7 months, 5 patients died, and another 2 were successfully resuscitated. On univariate analysis, both brain natriuretic peptide levels and parameters of heart rate variability and heart rate turbulence were associated with impaired prognosis. On multivariate analysis, pathologic heart rate turbulence was found to be the strongest independent risk stratifier (hazard ratio, 61.5; P < .001). CONCLUSIONS: Impaired cardiac autonomic nervous activity is associated with an increased risk of sudden cardiac death in congenital cardiac disease. Our results suggest that heart rate turbulence might be superior to established markers of cardiac autonomic dysfunction, such as heart rate variability. The combined use of heart rate turbulence, heart rate variability, and markers of neurohormonal activation, such as brain natriuretic peptide, might further improve the prognostic value.

Adult↗

PubMed2003

[A patient with Guillain-Barré syndrome and recurrent episodes of ST elevation and left ventricular hypokinesis in the anterior wall].

A-65-year old woman who developed total ophthalmoplegia, areflexia in all her limbs and ataxia after upper respiratory tract infection was admitted to our hospital on the second day of illness. On day 3, she developed severe tetraparesis and respiratory failure which required mechanical ventilation, and Guillain-Barré syndrome (GBS) was diagnosed. On day 4, bilateral ptosis, facial diplegia, and neck muscle weakness appeared, and her all limbs were flaccid and immobile. An electrophysiological study suggested axonal damage. Marked blood pressure fluctuation also appeared on day 4. On day 5, an electrocardiogram showed a ST-segment elevation in leads V1 through V4 and the echocardiography showed anterior hypokinesia of the left ventricle. Her serum creatine kinase was normal. Left ventricular dysfunction and ST-segment elevation were normalized within hours, but a transient ST-segment elevation re-occurred on day 6. An electrocardiogram on day 13, showed inverted T waves in diffuse leads, which inversion continued. ST-segment elevation and hypokinesia in this patient were restricted to the left anterior descending branch, therefore, coronary spasm of that branch was considered the possible mechanism. In contrast, inverted T wave was due to either catecholamine cardiotoxicity or diffuse cardiac ischemia. Abnormalities of electrocardiogram were presumably due to cardiovascular autonomic dysfunction of GBS.

Aged↗

PubMed1991

Mitral valve prolapse.

Mitral Valve Prolapse (MVP) is a common cardiac disorder in our community. It is estimated that 4% to 15% of the general population have the anatomical defect of prolapsed mitral valve leaflets during ventricular systole. Patients with MVP that suffer from chest pain, dyspnea, fatigue, dizziness, syncope, palpitations, cardiac arrhythmias, anxiety, and panic attacks are diagnosed as having Mitral Valve Prolapse Syndrome. There is much controversy in the medical literature as to the causes of MVPS symptomatology. Some scientists believe that autonomic dysfunction, adrenergic, and vagal responsiveness are factors which appropriately explain the symptoms of MVPS. Pharmacological therapy, depending on the severity of the symptoms, is one option for treatment. Education on the etiology of their symptoms, instruction on lifestyle modifications, and reassurance from their physician are appropriate methods for the management of MVPS patients.

Autonomic Nervous System↗

PubMed1984

[Orthostatic hypotension].

The practicing physician commonly encounters patients with hypotensive disturbances of orthostatic blood pressure regulation. These include the functional orthostatic syndrome as well as the true forms of orthostatic hypotension due to hypovolemia, certain cardiac, pulmonary or endocrine diseases, or (particularly in the elderly) autonomic dysfunction of varying etiology. The possible pathogenetic mechanisms are also many and varied, while various drugs may play a causative or contributory role. Careful evaluation and treatment with general measures and, if indicated, pharmacologic agents may (even in the presence of severe neurogenic orthostatic hypotension) often lead to marked improvement in blood pressure and in quality of life.

Autonomic Nervous System Diseases↗

PubMed2006

Decreased heart rate variability may predict the progression of carotid atherosclerosis in type 2 diabetes.

Heart rate variability (HRV), a measure of autonomic function, can predict survival outcomes. Cardiovascular disease is a known complication of diabetes, and we aimed to determine if autonomic dysfunction was associated with carotid artery atherosclerotic plaques in type 2 diabetic patients. We assessed frequency domain HRV from power spectral analysis of 24 h Holter ECG recordings, expiration/inspiration (E/I) ratio during deep breathing, acceleration index (AI) of R-R interval in response to head-up tilt, and the degree of carotid artery atherosclerosis in 61 type-2 diabetic patients (39 males, 45-69 years). Studies were carried out 5-6 years after diagnosis (baseline) and repeated 8 years after diagnosis (follow-up). At baseline, patients diagnosed with autonomic neuropathy, with abnormal E/I ratio and abnormal AI measurements, had decreased low frequency (LF) HRV. Baseline E/I ratio correlated with day (r = 0.34; P < 0.001) and night-time (r = 0.44; P < 0.001) LF power. Night-time HRV did not differ in patient with and without autonomic neuropathy. Reduced common carotid artery diameter and atherosclerotic intima-media thickness (IMT) both correlated with HRV at baseline. At follow-up, all HRV variables decreased significantly. Furthermore, patients with lower LF power at baseline, had a larger increase in the thickness of the carotid bulb intima-media at follow-up. Our results show that LF HRV power is associated with the extent and progression of carotid atherosclerosis in type 2 diabetes. A low LF HRV may predict the progression of atherosclerosis in these patients.

Aged↗

PubMed2005

Secondhand smoke as an acute threat for the cardiovascular system: a change in paradigm.

The evidence that active smoking is a risk factor for cardiovascular disease (CVD) and the leading cause of preventable death is overwhelming. However, numerous epidemiological findings indicate that even passive exposure to cigarette smoke may exert detrimental effects on vascular homoeostasis. Recent experimental data provide a deeper insight into the pathophysiological mechanisms linking secondhand smoke (SHS) to CVD. Importantly, most of these effects appear to be characterized by a rapid onset. For example, the relatively low doses of toxins inhaled by passive smoking are sufficient to elicit acute endothelial dysfunction, and these effects may be related, at least in part, to the inactivation of nitric oxide. Moreover, passive smoking may directly impair the viability of endothelial cells and reduce the number and functional activity of circulating endothelial progenitor cells. In addition, platelets of non-smokers appear to be susceptible to pro-aggregatory changes with every passive smoke exposure. Overall, SHS induces oxidative stress and promotes vascular inflammation. Apart from vasoconstriction and thrombus formation, however, the myocardial oxygen balance is further impaired by SHS-induced adrenergic stimulation and autonomic dysfunction. These data strongly suggest that passive smoking is capable of precipitating acute manifestations of CVD (atherothrombosis) and may also have a negative impact on the outcome of patients who suffer acute coronary syndromes.

Cardiovascular Diseases↗

PubMed2004

The comparison of QT dispersion and 24 hour ambulatory blood pressure monitoring amongst diabetic patients with and without microalbuminuria.

Diabetes mellitus is an important coronary artery disease risk factor. The presence of microalbuminuria, which indicates renal involvement in diabetic patients, is associated with an increased cardiovascular risk. There are suggestions that diabetic patients with microalbuminuria have more adverse risk profile such as higher ambulatory blood pressure and total cholesterol levels to account for the increased cardiovascular morbidity and mortality. QT dispersion is increasingly being recognized as a prognostic factor for coronary artery disease and sudden death. Some studies have suggested that QT dispersion is an important predictor of mortality in Type II diabetic patients. Our cross sectional study was to compare the QT dispersion and 24 hour ambulatory blood pressure monitoring between diabetic patients with microalbuminuria and those without microalbuminuria. Diabetic patients with overt coronary artery disease were excluded from the study. A total of 108 patients were recruited of which 57 patients had microalbuminuria and 51 were without microalbuminuria. The mean value of QT dispersion was significantly higher in patients with microalbuminuria than in patients without microalbuminuria (58.9 +/- 27.9 ms vs. 47.1 +/- 25.0 ms, p < 0.05). The mean 24 hour systolic and diastolic blood pressures were significantly higher in patients with microalbuminuria than in patients without microalbuminuria (129.5 +/- 12.3 mm Hg vs 122.3 +/- 10.2 mm Hg, p < 0.05 and 78.4 +/- 6.9 mm Hg vs 75.3 +/- 6.8 mm Hg, p < 0.05, respectively). Our study suggests that QT dispersion prolongation, related perhaps to some autonomic dysfunction, is an early manifestation of cardiovascular aberration in diabetic patients with microalbuminuria. The higher blood pressure levels recorded during a 24-hour period min diabetics with microalbuminuria could also possibly account for the worse cardiovascular outcome in this group of patients.

Adolescent↗

PubMed2004

Differential effects of various treatment combinations on cardiovascular dysfunction in patients with Parkinson's disease.

OBJECTIVES: Patients with Parkinson's disease (PD) frequently suffer from cardiovascular dysfunction, which may be enhanced to various extents by different antiparkinsonian drugs. MATERIALS AND METHODS: We analysed electrocardiogram (ECG) abnormalities, cardiovascular reflexes (CVR) and orthostatic hypotension (OH) in 148 patients with idiopathic PD assigned to five different combination therapies of levodopa (LD) plus either bromocriptine (BRO), ropinirole (ROP), selegiline (SEL), anticholinergic (ACH) or amantadine (AMA) or to LD monotherapy before and after a 1-week washout of the add-on drug. Patients were matched for age and disease severity (Hoehn and Yahr stage 2-3). Rater-blinded cardiovascular testing was performed at baseline, and following a 1-week washout period of the add-on drugs. RESULTS: We found that the incidence of cardiovascular dysfunction was generally higher in patients receiving a combination therapy compared with patients on LD monotherapy. ECG abnormalities were found in 40-52% of patients in combination therapy, but in only 20% of the patients receiving LD monotherapy. After discontinuation of BRO and SEL, there were significant improvements in ECG, OH and CVR. After washout of ACH and AMA, a significant improvement was found only in the CVR score. AMA and ROP were the add-on drugs with the least adverse cardiovascular effects. CONCLUSION: We conclude that pre-existing cardiovascular autonomic dysfunction should be investigated and taken into account when deciding which combination therapy to choose in the treatment of parkinsonian patients.

Aged↗

PubMed1997

Selective autonomic and sensory deficits in slow transit constipation.

Chronic idiopathic constipation is likely to be a heterogeneous condition. Our previous studies on the stimulated sweating response suggested that autonomic dysfunction may be a cause in a subset of patients. Our aims were to test selectively the neural and sweat gland components of the sweat response and to test unmyelinated sensory fibres so as to determine whether a small fibre neuropathy is present. Twelve female patients with proven slow transit constipation and nineteen age-matched healthy volunteers took part in the study. The sensory tests included thermal thresholds and axon reflex vasodilatation in response to intradermal capsaicin, measured with a laser Doppler. Direct and axon reflex sweating was induced with intradermal methacholine and nicotine, respectively, and measured with an evaporimeter. Non-parametric tests were used for statistical comparison with a group of seven control subjects. Results are expressed as medians and range. All four patients who reported constipation from childhood had a selective deficit of unmyelinated afferent fibre function in the feet, with markedly elevated thresholds to warm sensation (controls 5.2; 4.3-10.6, patients 13.8; 11.8-16.1 delta T (degree C), P < 0.02) and heat pain (controls 10.6; 8.2-14.7, patients 18.1; 13.9-22.6 delta T (degree C), P < 0.05) and a reduced response to capsaicin (controls 47.0; 24-117, patients 13.5; 12-30 delta Flux (V), P < 0.005). In contrast, patients with adult onset constipation (n = 7) had a selective neural sweating deficit (controls 49.8; 32.0-61.8; patients 27.7; 7.3-44.3 g/m2 h, P < 0.05), indicating dysfunction of post-ganglionic sympathetic cholinergic fibres. Patients from both groups were shown to have normally functioning sweat glands in direct response to methacholine. Our findings suggest that patients with severe chronic idiopathic constipation may have selective small fibre neuropathies, of which constipation is a manifestation.

Adult↗

PubMed2001

A placebo-controlled study examining the effect of allopurinol on heart rate variability and dysrhythmia counts in chronic heart failure.

AIMS: Allopurinol improves endothelial function in chronic heart failure by reducing oxidative stress. We wished to explore if such an effect would attenuate autonomic dysfunction in CHF in line with many other effective therapies in CHF. METHODS: We performed a prospective, randomized, double-blind cross-over study in 16 patients with NYHA Class II-IV chronic heart failure (mean age 67 +/- 10 years, 13 male, comparing allopurinol (2 months) at a daily dose of 300 mg (if creatinine < 150 micromol l-1) or 100 mg (if creatinine > 150 micromol l-1) with matched placebo. Mean heart rate and dysrhythmia counts were recorded from 24 h Holter tapes at monthly intervals for 6 months. We assessed autonomic function using standard time domain heart rate variability parameters (HRV): SDNN, SDANN, SDNN index, rMSSD and TI. RESULTS: Allopurinol had no significant effect on heart rate variability compared with placebo; the results are expressed as a difference in means +/- s.d. with 95% confidence interval (CI) between allopurinol and placebo: SDNN mean = 6.5 +/- 4.8 ms, P = 0.18 and 95% CI (-3.7, 17); TI mean = -2.1 +/- 1.4, P = 0.16 and 95% CI (-5.2, 0.8); SDANN mean = -2.8 +/- 7 ms, P = 0.68 and 95% CI (-18, 12); SDNNi mean = 2 +/- 6.6, P = 0.7 and 95% CI (-12, 16); RMSSD mean = -0.9 +/- 2, P = 0.68 and 95% CI (-5.6, 3.7). For mean heart rate the corresponding results were 0.9 +/- 1.4, P = 0.5 and 95% CI (-2, 3.8). Log 24 h ventricular ectopic counts (VEC) were 0.032 +/- 0.37, P = 0.7 and 95% CI (-0.1, 0.2). Patient compliance with study medication was good since allopurinol showed its expected effect of reducing plasma uric acid (P < 0.001). CONCLUSIONS: Allopurinol at doses, which are known to reduce oxidative stress appear to have no significant effect on resting autonomic tone, as indicated by time domain heart rate variability or on dysrhythmia count in stable heart failure patients.

Aged↗

PubMed1991

Immunohistochemical quantification of substance P in spinal dorsal horns of patients with multiple system atrophy.

Using a computer-assisted image analyser, an immunohistochemical quantification method of substance P-like immunoreactivity (SPLI) in laminae I + II of spinal dorsal horn was established and applied to 13 patients with multiple system atrophy (MSA) with no disturbance of pain sensation, including olivo-ponto-cerebellar atrophy and striatonigral degeneration, and 13 neurologically normal controls. To investigate whether alteration of SPLI is related to an autonomic disorder, myelinated fibre counts of the fourth thoracic ventral roots were performed. Eleven of 13 MSA patients showed a significant decrease in small and large myelinated fibres, and were diagnosed with definite Shy-Drager syndrome (SDS), with the exception of two who had no apparent history of autonomic dysfunction. SPLIs in laminae I + II in 10 of these 11 patients, when adjusted for age, were significantly decreased at both levels of the fourth thoracic and third lumbar spinal segments. The results suggest the disorder of SP-containing synapses of primary afferent neurons and/or those of interneurons in SDS.

Adult↗

PubMed1992

[Connection between microalbuminuria and subclinical cardiovascular autonomic neuropathy in diabetic children].

Cardiovascular tests were investigated in 16 microalbuminuric, in 20 normoalbuminuric diabetic children and a control group of 20 healthy children. Comparing to the control group, in both of two diabetic groups a similar increase in resting heart rate (74.5 +/- 2.5/min vs. 87.8 +/- 3.5/min, p less than 0.01, and 83.6 +/- 3.2/min, p less than 0.05) and a decrease in hyperventilatory arrhythmia (32.3 +/- 1.2/min vs. 20.1 +/- 0.8/min, p less than 0.01, and 17.2 +/- 0.8/min, p less than 0.01) was observed. In the diabetic group with microalbuminuria in comparison with both the control group and the normoalbuminuric group there was a lower standing/lying heart rate ratio (1.02 +/- 0.03 vs. 1.30 +/- 0.05, p less than 0.01, and 1.22 +/- 0.05, p less than 0.05), a pronounced orthostatic decrease in blood pressure (15.1 +/- 0.3 mmHg vs. 2.0 +/- 0.1 mmHg, p less than 0.001, and 5.0 +/- 0.2 mmHg, p less than 0.01) and a diminished increase in blood pressure during sustained handgrip (6.3 +/- 0.2 mmHg vs. 14.0 +/- 0.3 mmHg, p less than 0.01, and 12.2 +/- 0.3 mmHg, p less than 0.05). The occurrence of cases with distinct autonomic dysfunction (3 or more abnormal cardiovascular tests) proved to be more frequent in the group with microalbuminuria than in the diabetic group with normal albumin excretion (6/16 vs. 1/20, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Albuminuria↗

PubMed1984

Neuroleptic malignant syndrome complicated by disseminated intravascular coagulation.

The neuroleptic malignant syndrome (NMS), clinically manifested by hyperpyrexia, mental status changes, muscular rigidity, and autonomic dysfunction, is an idiosyncratic reaction to major neuroleptic pharmacologic agents. The reported causes of morbidity and mortality include respiratory insufficiency, cardiovascular collapse, arrhythmias, and renal failure. Coagulopathy does not seem to be a prominent component of the syndrome. We observed a case of NMS in which disseminated intravascular coagulation was a prominent feature.

Adult↗