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PubMed2000

Autonomic dysfunction in Machado-Joseph disease assessed by iodine123-labeled metaiodobenzylguanidine myocardial scintigraphy.

Iodine123-labeled metaiodobenzylguanidine, a radioiodinated analogue of norepinephrine, is a tracer for evaluating sympathetic function. We used iodine123-labeled metaiodobenzylguanidine myocardial scintigraphy and sympathetic skin response to study autonomic nervous functions in 19 patients with Machado-Joseph disease (MJD) and 20 control subjects. Planar imaging of all the participants was done to evaluate myocardial scintigraphy. The ratio of average counts in the heart to average counts in the mediastinum was calculated for both early and delayed images, the latter of which reflects the cardiac neural uptake of the tracer. Single photon emission computed tomography also was done on 12 patients with MJD to examine regional tracer uptake to the heart. The mean ratio of counts in the heart to counts in the mediastinum in the delayed images was lower for the patients with MJD than for the control subjects (p <0.01). Abnormal sympathetic skin response was present in 6 patients with MJD whose mean ratio of counts in the heart to counts in the mediastinum was lower than that of patients with MJD who had normal sympathetic skin response (p <0.01). A single photon emission computed tomography study showed significantly lower accumulation of the tracer in patients with MJD than in the control subjects in the anterior lateral sectors predominantly innervated by sympathetic nerves but not in the inferior septal sectors reported to be under main innervation by parasympathetic fibers. These results show that MJD is accompanied by cardiac sympathetic dysfunction, as detected by iodine123-labeled metaiodobenzylguanidine myocardial scintigraphy, which appears to be correlated with sudomotor sympathetic dysfunction.

3-Iodobenzylguanidine↗
PubMed1996

Decreased sympatho-adrenal activity in diabetic patients with autonomic dysfunction following mental stress.

The sympathetic nervous system is of major importance in the regulation of numerous physiological functions. While it is clearly established that there is a decreased noradrenergic status in people with autonomic neuropathy, the epinephrine secretion is much more controversial. Basal and mental stress-stimulated plasma catecholamine levels were measured in 42 diabetic patients with and without pathological cardiovascular function tests and in 13 healthy, non-diabetic control subjects. In addition, the excretion of catecholamines was measured in a 24 h urine collection and compared with the stress stimulated plasma levels. During mental stress exposure a diminished epinephrine secretion was found in diabetic patients with autonomic neuropathy compared with diabetic patients without neuropathy and the healthy control group (p < 0.05: respectively). The decreased epinephrine response to mental stress was strongly correlated with a diminished urinary excretion of this "neurotransmitter' (r = 0.46; p < 0.01). Diabetic patients suffering from cardiovascular autonomic neuropathy exhibit a diminished sympatho-adrenal response following mental stress exposure. Both measurement of urinary and mental stress stimulated plasma epinephrine levels following mental stress provide reliable information regarding sympatho-adrenal activity in diabetic patients.

Adrenal Glands↗
PubMed2003

Genetic basis of autonomic dysfunction.

The human genome has become a roadmap for elucidation of the pathophysiology of disease. It is likely that mutations in more than 1000 of the approximately 30,000 human genes will lead to autonomic abnormalities, either directly or indirectly. This review highlights some of these, which exert major effects on catecholamine metabolism and relate specific catecholaminergic phenotypes to neurogenetic disorders. Distinctive catecholamine patterns in several neurogenetic conditions may reflect direct or indirect effects of gene mutations. These neurochemical patterns can provide potentially important clues to the diagnosis, treatment, and pathophysiology of neurogenetic disorders.

Animals↗
PubMed1995

Autonomic dysfunction in patients with achalasia.

It has been previously shown that patients with achalasia may have motor abnormalities of the stomach, small bowel and biliary system. This study investigates whether a disturbance of extraintestinal autonomic function occurs. Autonomic function studies were performed in 15 patients with achalasia and 15 age- and sex-matched healthy controls. Pupillograms were obtained during darkness, light exposure and after pilocarpine administration. Cardiovascular function studies included determinations of heart rate variation during deep breathing and orthostasis. In addition, we determined blood pressure changes in response to sustained handgrip, cold exposure and orthostasis. Neurohormonal function was investigated by measuring serum pancreatic polypeptide (PP) levels prior to and following sham feeding. Pupillary function did not differ in patients as compared with controls. However, 9 of 15 patients (95% CI: 32-84%) and none of the controls showed at least one abnormal autonomic cardiovascular response. A significant difference between the two groups was observed in sympathetic function (P = 0.023). More patients than controls did not respond to sham feeding with a PP increase. It is concluded that some patients with achalasia exhibit an abnormality of the autonomic nervous system that extends beyond the gastrointestinal tract. These abnormalities mainly concern cardiovascular function but may also involve neurohormonal responses.

Adult↗
PubMed2002

Widespread cardiovascular autonomic dysfunction in primary amyloidosis: does spontaneous hyperventilation have a compensatory role against postural hypotension?

OBJECTIVE: To investigate the possible causes of abnormal blood pressure control in light chain related (primary, AL) amyloidosis. DESIGN: Cardiovascular, autonomic, and respiratory response to passive tilting were investigated in 51 patients with primary amyloidosis (mean (SEM) age 56 (2) years) and in 20 age matched controls. Spontaneous fluctuations in RR interval, respiration, end tidal carbon dioxide, blood pressure, and skin microcirculation were recorded during supine rest and with tilting. The values were subjected to spectral analysis to assess baroreflex sensitivity and the autonomic modulation of cardiac and vascular responses. SETTING: Tertiary referral centre. RESULTS: Autonomic modulation of the heart and blood pressure was nearly absent in the patients with amyloidosis: thus baroreflex sensitivity and the low frequency (0.1 Hz) fluctuations in all cardiovascular signals were severely reduced (p < 0.01 or more), as were respiratory fluctuations in the RR interval, and no change was observed upon tilting. Despite reduced autonomic modulation, blood pressure remained relatively stable in the amyloid group from supine to tilting. End tidal carbon dioxide was reduced in the amyloid patients (p < 0.001) indicating persistent hyperventilation; the breathing rate correlated inversely with the fall in blood pressure on tilting (p < 0.05). CONCLUSIONS: In primary amyloidosis, pronounced abnormalities in arterial baroreflexes and cardiovascular autonomic modulation to the heart and the vessels may be partly compensated for by hyperventilation at a slow breathing rate.

Amyloidosis↗
PubMed1998

Cardiovascular autonomic dysfunction in parkinsonian patients.

Cardiovascular dysfunction may occur in parkinsonian patients for a variety of reasons. Patients usually are more than 50 years old and on various drugs (both antiparkinsonian and for associated medical disorders), some of which may have cardiovascular effects. Autonomic failure increases with age and also is recognized in parkinsonian patients who have the disorder multiple system atrophy, in which there is substantial cardiovascular dysfunction. Thus, recognition of cardiovascular dysfunction and its causes in parkinsonian patients is of importance in diagnosis (in separating the various parkinsonian diseases), in determining prognosis, and finally in management. This article outlines the major areas of cardiovascular dysfunction, including disorders of blood pressure control, heart rate, and regional circulation, especially to vital organs. Clinical features and evaluation are described, together with abnormalities in different parkinsonian disorders and the principles of management.

Autonomic Nervous System↗
PubMed1993

Autonomic dysfunction in patients with dementia of the Alzheimer type.

Abnormalities of the noradrenergic system have been documented in the central nervous system of patients with dementia of the Alzheimer's type (DAT). To evaluate the autonomic sympathetic system in DAT, we measured lying and standing blood pressure (BP), pulse, and plasma epinephrine (E) and norepinephrine (NE) in 60 DAT patients (mean age +/- SD = 65 +/- 8 years), and 20 normal elderly controls. DAT patients had normal baseline findings (BP, pulse, NE, and E). Upon standing, plasma NE and E significantly increased in both DAT patients and controls, without group differences. However, the systolic BP response to standing was reduced in DAT patients compared with the normal controls (repeated measures ANOVA, p < 0.01). This impaired response of the systolic BP on standing was particularly evident in DAT patients with symptoms of depression. Severely impaired DAT patients did not differ in E, NE, BP, pulse, or in orthostatic changes from mild-to-moderately impaired patients. These results suggest that the sympathetic response to the stress of standing is functionally impaired in DAT. This deficit was especially evident when DAT was accompanied by depression, consistent with prior studies in non-demented depressed patients.

Aged↗
PubMed2001

Autonomic dysfunction and cholelithiasis in patients with cirrhosis.

Gallstones are seen in 33-46% of patients with cirrhosis, and their prevalence is known to increase with the duration and severity of liver disease. We hypothesized that autonomic neuropathy may contribute to the formation of gallstones or gallbladder disease, as in diabetics with autonomic neuropathy, due to impaired gallbladder emptying. The objective of our study was to determine the prevalence of gallstones or gallbladder disease in cirrhotic patients with and without autonomic neuropathy. We determined autonomic function tests, gallstones, and other gallbladder disease in 123 (male 71) with varying severity of liver disease (Child classes: A, 40; B, 45; C, 35). In all, 54 patients had gallstones and an additional 22 patients had other gallbladder disease (cholecystitis, common bile duct stones, or debris). Autonomic neuropathy was seen in 97 patients (one abnormal test in 48 and two or more in 49). The prevalence of gallstones was similar in Child A (57%), Child B (64%), and Child C (63%) cirrhosis. The gallstones or gallbladder disease was not increased in women, blacks, diabetics, or alcoholic cirrhotics. The prevalence of gallbladder disease was increased in patients with autonomic neuropathy (51% vs 35%, P = 0.08); in patients with Child C cirrhosis, gallstones (P = 0.018) and gallbladder disease (P = 0.03) were seen more commonly in patients with autonomic neuropathy. Our findings suggest that autonomic neuropathy may contribute to the formation of gallstones in patients with advanced cirrhosis, perhaps by impairing gallbladder and sphincter of Oddi dysmotility.

Adult↗
PubMed1992

Prevalence of cardiovascular autonomic dysfunction assessed by spectral analysis, vector analysis, and standard tests of heart rate variation and blood pressure responses at various stages of diabetic neuropathy.

To establish a test battery for the detection and characterization of cardiovascular autonomic neuropathy (CADN) and to evaluate its prevalence, a number of autonomic function tests based on spectral analysis, vector analysis, and standard tests of heart rate variation and blood pressure responses were performed in 261 diabetic patients aged 11-76 years with various stages of peripheral neuropathy. The percentages of abnormal results in the individual tests based on heart rate variation were 6-31% in 115 patients without peripheral neuropathy, 16-45% in 61 patients with subclinical neuropathy, 22-59% in 73 patients with symptomatic peripheral neuropathy, and 67-100% in 12 patients with the latter in conjunction with autonomic symptoms (p < 0.05). The most frequently abnormal indices, each representing a different physiological basis, were the coefficient of variation, low-frequency and mid-frequency power spectrum at rest, mean circular resultant, postural change in systolic blood pressure, and, in particular, the max/min 30:15 ratio and Valsalva ratio. CADN, defined as the presence of > or = 3 abnormalities among these seven parameters was detected in none of 120 control subjects, 13.0% of the patients without peripheral neuropathy, 34.4% of those with subclinical neuropathy, 49.3% of those with symptomatic peripheral neuropathy, and in 100% of the subjects with the latter and concomitant autonomic symptoms (p < 0.05). The overall prevalence of CADN in 103 patients completing all parameters was 46.6%. The corresponding rate of CADN defined as > or = 2 abnormalities among the five tests included in an optimized version of the battery proposed by Ewing and Clarke was 38.8%.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1989

[Autonomic dysfunctions in acute intermittent porphyria].

A young woman with acute intermittent porphyria is described. She was admitted in a prolonged attack and had developed a flaccid quadriplegia. During the course she showed various manifestations of the autonomic nervous system, including pupils, gastrointestinal tract, cardiovascular system and others. On admission her pupils were equally mydriatic, and reacted to light sluggishly. Dilation of the pupils was seen when cocaine was instilled, but not when adrenalin. It was suggested that the parasympathetic control of pupils was disturbed. She complained repeatedly abdominal pain, nausea, vomiting, and constipation. However, diarrhea was rarely found. Radiological examinations revealed that her bowel movements were markedly impaired. Sinus tachycardia and elevation of blood pressure were frequently observed with attacks, and they correlated with the clinical course. With tachycardia the coefficient variance of R-R interval was markedly decreased, and large dose of atropine failed to accelerate the heart rate. These indicate that the vagal function was markedly impaired with attacks. The effects of isoproterenol and of propranolol on the heart rate were normal. Phenylephrine and phentolamine changed the blood pressure normally. From these it was concluded that the sympathetic nervous function was not so impaired at the time examined. However, with the elevation of blood pressure plasma and urinary noradrenaline were markedly increased. Other autonomic and related manifestations observed during the course included disorders of sweating, loss of sphincter control, fever of unknown cause and amenorrhea.

Acute Disease↗
PubMed1987

Autonomic dysfunction in severe tetanus: magnesium sulfate as an adjunct to deep sedation.

We studied the use of continuous iv magnesium (Mg) infusion to control the sympathetic crises in a patient with severe tetanus characterized by pronounced autonomic nervous system instability. Our results suggested that Mg is a useful adjunct to the CNS depressants traditionally used. This therapy controlled the sympathetic crises and also suppressed the release of catecholamines, although Mg infusions alone appeared to be inadequate therapy.

Adult↗
PubMed1993

[A new ocular sign of autonomic dysfunction].

The author discovered a new sign of vegetative dysregulation, asymmetry of ocular glisten. This symptom can exist separately or combine with other ocular vegetative symptoms. Its mechanism lies in increased or decreased reflection of the eye surface tissues as a result of more or less intensive tonicity of the smooth muscular fibers of the retrobulbar fat or due to changes in the intraocular pressure. The symptom may be used in practice for diagnosis of vegetative dysfunction, primarily vegetative regulatory asymmetry, of pathological alterations in vegetative structures, for topical diagnosis.

Autonomic Nervous System↗
PubMed1987

Correlation of autonomic dysfunction to CSF concentrations of noradrenaline and 3-methoxy-4-hydroxyphenylglycol in Parkinson's disease.

In order to study the role of the neurotransmitter noradrenaline (NA) and its main brain metabolite 3-methoxy-4-hydroxyphenylglycol (MHPG) in autonomic failure in Parkinson's disease (PD), an analysis of the relation of cerebrospinal fluid (CSF) NA and MHPG levels and a rating of autonomic nervous system (ANS) impairment was carried out. The mean baseline NA level in CSF of PD patients was 220.0 +/- 110.0 pg/ml, and the mean baseline MHPG level 9.9 +/- 3.9 ng/ml. These levels did not differ from those of age-matched controls. Within the group of patients with PD neither the duration of the disease nor its medication influenced the results. No correlation could be found in patients with PD between the CSF NA levels and the severity of autonomic failure, but a clear correlation was found between the CSF MHPG concentrations and the severity of autonomic failure.

Aged↗