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PubMed1996

Autonomic neuropathy, II: Specific peripheral neuropathies.

Autonomic dysfunction is a common complication of peripheral neuropathies. It is often of little clinical importance, but some conditions may cause profound disturbance of autonomic function. These conditions include acute dysautonomia, diabetes, primary and familial amyloidosis, Guillain-Barré syndrome, porphyria, and some inherited neuropathies. A wide range of neuropathies are associated with lesser degrees of autonomic dysfunction. These include hereditary neuropathies, and neuropathies associated with metabolic disturbances, alcohol abuse, malignancy, medications, infections, and connective tissue disorders.

Amyloidosis↗
PubMed2003

Circadian cardiac autonomic nerve dysfunction in primary hyperparathyroidism improves after parathyroidectomy.

BACKGROUND: Primary hyperparathyroidism has been associated with premature death in cardiovascular diseases, but reversibility and background mechanisms are uncertain. This study investigates autonomic nervous function in hyperparathyroidism because disturbances in this respect have been related to increased cardiovascular morbidity. METHODS: Twenty-one consecutive patients with hyperparathyroidism and 23 matched control subjects without interfering medication underwent electrocardiographic recordings and ambulatory blood pressure (ABP) determination during a 24-hour period. Patients were re-examined at normocalcemia 1 year after parathyroidectomy. Heart rate variability was analyzed in subjects with sinus rhythm and normal atrioventricular conduction; time domain measures were calculated from the RR-intervals, and frequency domain variables were obtained with an autoregressive algorithm, which expressed power distribution (high, low, or very low frequency). RESULTS: Nocturnal increase in low frequency was blunted in cases versus control subjects (103+/-128 m(2) vs 430+/-171 m(2); P=.03). Very low frequency at nighttime correlated inversely with serum parathormone (r=-0.33; P<.05) and increased postoperatively (P=.03). ABP was higher both at daytime and nighttime (P<.05) in patients and remained unchanged after surgery. Systolic ABP correlated with the parathormone (r=0.47; P<.01). CONCLUSION: Results suggest altered circadian autonomic function in hyperparathyroidism that can improve after parathyroidectomy. Despite elevated blood pressure, ABP shows retained diurnal rhythm, which indicates different pathophysiologic mechanisms behind the 2 predictors of cardiovascular death in hyperparathyroidism.

Aged↗
PubMed1995

Striated anal sphincter denervation in patients with progressive supranuclear palsy.

Anal sphincter electromyography may contribute to the differential diagnosis between Parkinson's disease (PD) and other parkinsonisms featuring autonomic dysfunction, such as multiple system atrophy (MSA). Although patients with progressive supranuclear palsy (PSP) do not normally exhibit clinical signs of autonomic dysfunction, a few may be first seen with urinary and fecal incontinence. We performed an electromyographic study of the anal sphincter in 12 patients with clinical criteria of probable or definite PSP, two of them with clinical manifestations of vesical and anal sphincter dysfunction. The results have been compared with those obtained from six patients with PD and six patients with MSA. An abnormal anal sphincter examination was present in five of 12 PSP patients (41.6%). The abnormal motor units of these patients were indistinguishable from those observed in patients with MSA. Patients with MSA had the largest, and patients with PD had the lowest, proportion of abnormal motor units. We conclude that some patients with PSP may have electromyographic signs of denervation in the anal sphincter, which make them indistinguishable by using this test alone from patients with MSA.

Adult↗
PubMed1996

Cisplatin-induced autonomic neuropathy: does it really exist?

The neurotoxic side-effects of cisplatin affect predominantly the large, myelinated fibres of peripheral nerves, leading to a sensory neuropathy. Several reports of cisplatin-associated autonomic neuropathy have been published. Autonomic dysfunction however, is caused by a neuropathy of small unmyelinated nerve fibres. By using the absolute pupil diameter as a parameter of autonomic nervous system function, we studied autonomic neuropathy in the eye of cisplatin-intoxicated rats. In addition, we examined autonomic cardiovascular function by measuring the change in heart rate (HR) and mean arterial blood pressure (MAP) in response to intravenous phenylephrine (PHE) and tyramine (TYR). No significant differences in mean pupil diameter developed in cisplatin-intoxicated rats (n = 12) in the course of 9 weeks (total cumulative dose cisplatin 18 mg/kg) compared with normal controls (n = 9) MANOVA, F1,19 = 0.88, P < 0.36). The PHE- and TYR-induced changes in MAP and HR were virtually the same in cisplatin-intoxicated rats when compared with normal controls. We conclude that cisplatin probably does not cause autonomic dysfunction, at least not in rats, in doses commonly used and which are known to cause a peripheral sensory neuropathy.

Analysis of Variance↗
PubMed2001

Limits of clinical tests to screen autonomic function in diabetes type 1.

OBJECTIVES: A precocious detection of cardiac autonomic dysfunction is of major clinical interest that could lead to a more intensive supervision of diabetic patients. However, classical clinical exploration of cardiac autonomic function is not easy to undertake in a reproducible way. Thus, respective interests of autonomic nervous parameters provided by both clinical tests and computerized analysis of resting blood pressure were checked in type 1 diabetic patients without orthostatic hypotension and microalbuminuria. MATERIAL AND METHODS: Thirteen diabetic subjects matched for age and gender to thirteen healthy subjects volunteered to participate to the study. From clinical tests (standing up, deep breathing, Valsalva maneuver, handgrip test), autonomic function was scored according to Ewing's methodology. Analysis of resting beat to beat blood pressure provided autonomic indices of the cardiac function (spectral analysis or Z analysis). RESULTS: 5 of the 13 diabetic patients exhibited a pathological score (more than one pathological response) suggesting the presence of cardiovascular autonomic dysfunction. The most discriminative test was the deep breathing test. However, spectral indices of BP recordings and baro-reflex sensitivity (BRS) of these 5 subjects were similar to those of healthy subjects and of remaining diabetic subjects. CONCLUSION: Alteration in Ewing's score given by clinical tests may not reflect an alteration of cardiac autonomic function in asymptomatic type 1 diabetic patients, because spectral indices of sympathetic and parasympathetic (including BRS) function were within normal range. Our results strongly suggest to confront results provided by both methodologies before concluding to an autonomic cardiac impairment in asymptomatic diabetic patients.

Adult↗
PubMed1994

[A study on the pathogenesis of hyporeninemia in diabetics].

Hyporeninemic hypoaldosteronism has mainly been described in patients with diabetes mellitus. In order to elucidate the mechanisms of hyporeninemia in diabetic patients, the author studied the response of active renin concentration (ARC) and inactive renin concentration (IRC) to the administration of captopril or sodium depletion in patients with diabetes mellitus and glomerulonephritis and in normal subjects. The diabetic patients were separated into four groups: Group 0, diabetic patients without neuropathy or nephropathy; Group I, those with neuropathy without nephropathy; Group II, those without neuropathy with nephropathy; Group III, those with neuropathy and nephropathy. Diabetic patients with some complications had slightly lower plasma active renin levels than those without complications. The mean increase in plasma active renin after captopril (delta ARC) and sodium depletion was lower in group I than in group 0, and there was no difference between group II and group 0. There was no correlation between delta ARC and creatinine clearance (Ccr) in diabetes mellitus. Plasma prorenin was higher in group I than in group 0, and there was no difference between group II and group 0. No significant change of prorenin after captopril was observed in all groups, but the mean increase in plasma inactive renin after sodium depletion was slightly higher in groups I and III than in groups 0 and II. ARC/IRC was significantly lower in group I than in group 0, and there was no difference between group II and group 0. There was no correlation between ARC/IRC and Ccr in diabetes mellitus, but significant correlation between ARC/IRC and postural change in systolic blood pressure. In three diabetic patients with hyporeninemic hypoaldosteronism, the postural fall in systolic blood pressure was significant, and ARC/IRC was significantly low, but IRC was not high. These results suggest that autonomic dysfunction is a major factor in an impairment of the processing of prorenin to active renin in diabetic patients, and severe autonomic dysfunction may impair the biosynthesis of prorenin in patients with hyporeninemic hypoaldosteronism.

Adult↗
PubMed1993

Detection of autonomic nervous dysfunction by SL manoeuvre.

We have evaluated the immediate heart rate response to standing and lying and in 100 Diabetic subjects aged 43 +/- 10 years who underwent five other cardiovascular autonomic tests. Using a specially devised scoring system the patients were divided into three groups: a) 58 subjects without autonomic neuropathy, b) 15 borderliners, c) 27 with autonomic neuropathy. The results were compared with 50, sex and age matched controls. We studied SL1 = ratio between R-R mean before lying and R-R maximum between the 20th to 25th beat and R-R minimum over the first 5 beats after lying. In controls SL1 was 1.35 +/- 0.18 and SL2 was 1.52 +/- 0.23. In diabetic subjects without autonomic neuropathy SL1 was 1.20 +/- 0.86 (p < 0.01), SL2 1.50 +/- 0.02 (p < 0.001). In the group with autonomic neuropathy SL1 was 1.04 +/- 0.02 (p < 0.001) and SL2 was 1.20 +/- 0.09 (p < 0.001). We propose that the lowest normal and highest abnormal limits of SL1 are 1.12 and 1.08 respectively and that normal and highest abnormal limits of SL2 are 1.23 and 1.18 respectively. We suggest the use of SL1 as a pure parasympathetic test and SL2 as a mixed but predominantly sympathetic test in the diagnosis of autonomic neuropathy.

Adolescent↗
PubMed1984

Multiple system atrophy. Clinical aspects, pathophysiology, and treatment.

Progressive autonomic failure is a clinical syndrome of autonomic dysfunction that may occur in isolation as in idiopathic orthostatic hypotension (IOH) or in association with a central neurologic disorder, multiple system atrophy (MSA). MSA and IOH can be distinguished on the basis of biochemical and pharmacologic tests. Plasma norepinephrine levels are low in IOH and normal in MSA; neither group increases the plasma norepinephrine level adequately in response to postural change. Both MSA and IOH manifest an exaggerated pressor response to administered norepinephrine. However, only patients with IOH have true adrenergic receptor supersensitivity. The autonomic dysfunction in IOH primarily involves the peripheral autonomic neurons whereas the defect in MSA is the failure to activate appropriately an intact distal sympathetic nervous system. Neuropathologic studies reveal a multisystem degeneration in MSA; the few postmortem examinations of the central nervous system in IOH reveal lesions confined to the intermediolateral columns of the spinal cord. Orthostatic hypotension may be treated with a number of medications although supine hypertension limits the usefulness of these drugs. Further development and testing of a sympathetic neural prosthesis may help to resolve this therapeutic dilemma. Only the parkinsonian features in MSA respond to treatment with anticholinergic drugs.

Arrhythmia, Sinus↗
PubMed1993

Cardiovascular and sweating dysfunction in patients with Holmes-Adie syndrome.

A cross-sectional study is reported in which 53 patients with Holmes-Adie syndrome have been subjected to a battery of tests of autonomic nervous function referable to the cardiovascular system, to two objective tests of sweating function, and to subjective assessment of sweating by application of quinizarin powder followed by body heating. The majority of patients were consecutive referrals; none was selected because of clinical indications of autonomic dysfunction. Eighty three per cent of these patients had at least one, 57% at least two, and 40% at least three objective test abnormalities, as defined by values lying outside 95 percentiles of healthy subjects who were matched for age and subjected to the same tests. In the context of multiple testing, the probability of finding outside values was such that a minimum of 3 was required to define abnormality. On this basis 40% of patients were found to have significant evidence of autonomic dysfunction. The most frequent abnormalities were impaired digital vasoconstriction to cold (23%), a reduced heart rate response to the Valsalva manoeuvre (17%), and excessive variability in sweating between test sites (in one of the tests, 43%) which is consistent with patchy loss. Abnormal quinizarin test appearances were seen in 10 patients and in a further five patients the appearances were thought to be suggestive of abnormality. Though assessment of the results of this test are subjective, the observations are consistent with the findings obtained from the objective tests which were applied. Cardiovascular and sweating abnormality did not concur significantly and only the former was found to increase progressively with known duration of the pupillotonia. It is concluded that Holmes-Adie syndrome is commonly accompanied by progressive mild but widespread autonomic involvement but rarely is this symptomatic. If symptoms suggestive of autonomic neuropathy are found in a patient with tonic pupils, a careful search for some other generalised disorder is recommended.

Adie Syndrome↗
PubMed1998

Nine-year follow-up study of heart rate variability in patients with Duchenne-type progressive muscular dystrophy.

OBJECTIVES: The purpose of this study was to investigate the progression of autonomic dysfunction in patients with Duchenne-type progressive muscular dystrophy (DMD) over time by using heart rate variability. BACKGROUND: Although previous studies suggest the presence of autonomic dysfunction in patients with DMD, the precise cause is not known. On the other hand, it is well known that analysis of heart rate variability provides a useful, noninvasive means of quantifying autonomic activity. High frequency power is determined predominantly by the parasympathetic nervous system, whereas low frequency power is determined by both the parasympathetic and sympathetic nervous systems. METHODS AND RESULTS: Frequency and time domain analyses of heart rate variability during ambulatory electrocardiographic monitoring were performed in 17 patients with DMD over a 9-year period. At the time of entry, the mean patient age was 11 years and the mean Swinyard-Deaver stage was 4. In the first year, high frequency power was significantly lower and the ratio of low frequency to high frequency was significantly higher in patients with DMD than in the normal control subjects. These differences become significantly greater as the disease progressed. At the time of entry, low and high frequency powers increased at night in both groups. However, over time, high and low frequency powers at night tended to decrease. All of the time domain parameters were significantly lower in the patients with DMD at all time points compared with the normal control subjects. CONCLUSIONS: We concluded that DMD patients have either a decrease in parasympathetic activity, an increase in sympathetic activity, or both as their disease progresses.

Adolescent↗
PubMed1999

Multiple system atrophy: clinical presentation and diagnosis.

Multiple system atrophy (MSA) describes a relatively uncommon, debilitating disorder that is frequently misdiagnosed as Parkinson's disease. Patients with MSA show various combinations of parkinsonism, cerebellar ataxia, pyramidal signs and progressive autonomic failure, especially cardiovascular and urologic autonomic dysfunction. Few treatment options exist. Although some patients initially respond well to dopaminergic treatment for their parkinsonian symptoms, striatal degeneration occurs, and levodopa often becomes ineffective. Thus, physicians may provide only symptomatic treatment and support for patients with MSA. In this paper, we present a case study of a 68-year-old woman who came to the Vanderbilt Movement Disorders Clinic with severe autonomic dysfunction and parkinsonism, previously diagnosed as Parkinson's disease. Following autonomic function tests as well as clinical evaluation, she was diagnosed with MSA and began treatment for orthostatic hypotension and micturition dysfunction.

Aged↗
PubMed1998

[Sympathetic nervous system and pain--some open questions].

BACKGROUND: Neuropathic pain syndromes may be treated by intervention at the sympathetic nervous system. The pain in these syndromes is therefore called sympathetically maintained pain (SMP). Typical disorders with a SMP component are complex regional pain syndromes (reflex sympathetic dystrophy and causalgia), traumatic neuralgias and herpes zoster. RESULTS: Open questions are how the efferent sympathetic nervous system is capable of influencing pain sensation and which mechanisms underly the autonomic dysregulation often observed in these syndromes.(1) Somatic afferents that project through the sympathetic trunk do not exist. Therefore, a pure sympathetic block does not block afferent information arising from the affected extremity. What alternatives are possible? Under pathophysiological conditions a functional interaction of efferent sympathetic fibers and afferent nociceptive fibers could be demonstrated in patients and animal studies. The intensity of this coupling varies considerably between individual patients and is not necessary for the diagnosis of the disorder. (2) Sympathetically maintained pain and signs of autonomic dysfunction are independent clinical and pathophysiological phenomena without any causal relation. However, it is possible to treat both the SMP and the autonomic dysfunction with sympathetic blocks.

English Abstract↗
PubMed2005

Autonomic cardiovascular regulation in subjects with acute mountain sickness.

The aims of this study were 1) to evaluate whether subjects suffering from acute mountain sickness (AMS) during exposure to high altitude have signs of autonomic dysfunction and 2) to verify whether autonomic variables at low altitude may identify subjects who are prone to develop AMS. Forty-one mountaineers were studied at 4,559-m altitude. AMS was diagnosed using the Lake Louise score, and autonomic cardiovascular function was explored using spectral analysis of R-R interval and blood pressure (BP) variability on 10-min resting recordings. Seventeen subjects (41%) had AMS. Subjects with AMS were older than those without AMS (P < 0.01). At high altitude, the low-frequency (LF) component of systolic BP variability (LF(SBP)) was higher (P = 0.02) and the LF component of R-R variability in normalized units (LF(RR)NU) was lower (P = 0.001) in subjects with AMS. After 3 mo, 21 subjects (43% with AMS) repeated the evaluation at low altitude at rest and in response to a hypoxic gas mixture. LF(RR)NU was similar in the two groups at baseline and during hypoxia at low altitude but increased only in subjects without AMS at high altitude (P < 0.001) and did not change between low and high altitude in subjects with AMS. Conversely, LF(SBP) increased significantly during short-term hypoxia only in subjects with AMS, who also had higher resting BP (P < 0.05) than those without AMS. Autonomic cardiovascular dysfunction accompanies AMS. Marked LF(SBP) response to short-term hypoxia identifies AMS-prone subjects, supporting the potential role of an exaggerated individual chemoreflex vasoconstrictive response to hypoxia in the genesis of AMS.

Acute Disease↗
PubMed2006

Homocysteine levels are associated with the results of 123I-metaiodobenzylguanidine myocardial scintigraphy in type 2 diabetic patients.

PURPOSE: Elevated total plasma homocysteine (tHcy) levels and cardiovascular autonomic dysfunction are associated with a high mortality in type 2 diabetic patients. We tested the hypothesis that hyperhomocysteinemia is associated with insulin resistance and cardiovascular autonomic dysfunction in type 2 diabetic patients not receiving insulin treatment. METHODS: The study group consisted of 17 type 2 diabetic patients with high tHcy levels (>15 mmol/l, age 58+/-5 years, high tHcy group). The control group consisted of 23 age-matched type 2 diabetic patients with normal tHcy levels (<or=15 mmol/l, age 58+/-9 years, normal tHcy group). Cardiovascular autonomic function was assessed by baroreflex sensitivity, heart rate variability, plasma norepinephrine concentrations, and cardiac (123)I-metaiodobenzylguanidine (MIBG) scintigraphy. RESULTS: Early and delayed (123)I-MIBG myocardial uptake values were lower (p<0.005 and p<0.01, respectively) and the percent washout rate of (123)I-MIBG was higher (p<0.001) in the high tHcy group than in the normal tHcy group. The fasting plasma insulin concentrations (p<0.0001) and the homeostasis model assessment (HOMA) index values (p<0.0001) were higher in the high tHcy group than in the normal tHcy group. Multiple regression analysis revealed that the level of tHcy was independently predicted by the HOMA index values and the myocardial uptake of (123)I-MIBG at the delayed phase. CONCLUSION: Our results demonstrate that high levels of tHcy are associated with depressed cardiovascular autonomic function and insulin resistance in patients with type 2 diabetes mellitus.

3-Iodobenzylguanidine↗