SEARCH · PubMed Health

Results for “Autonomic dysfunction”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 739 records · Page 41Linked to original sources

PubMed2026

Impact of Baseline Polyneuropathy Severity on Eplontersen Efficacy in the NEURO-TTRansform Clinical Trial.

BACKGROUND AND AIMS: In the NEURO-TTRansform clinical trial (NCT04136184), eplontersen improved neuropathy impairment and quality of life (QoL) through Week 66 versus the NEURO-TTR historical placebo in patients with hereditary transthyretin amyloidosis with polyneuropathy (ATTRv-PN). This analysis assessed the impact of baseline ATTRv-PN severity on eplontersen response in patients from NEURO-TTRansform. METHODS: This post hoc analysis grouped patients into tertiles by baseline Neuropathy Impairment Score (NIS): T1 (least baseline impairment: 3.5 to < 27.5; n = 67), T2 (27.5 to < 55.0; n = 67), and T3 (55.0 to < 127.8; n = 66). Outcomes assessed were neuropathy impairment (modified NIS+7 [mNIS+7] and NIS, Neuropathy Symptom and Change, Polyneuropathy Disability), QoL (Norfolk QoL-Diabetic Neuropathy), physical functioning (36-Item Short-Form Health Survey Physical Component Summary), nutritional status (modified body mass index), and serum transthyretin levels; these were compared with NEURO-TTR historical placebo. Autonomic dysfunction (Composite Autonomic Symptom Score-31), disability (Rasch-built Overall Disability Scale), and walking speed (10-Meter Walk Test) were also assessed. Final assessments were carried out following 65/66 or 81/85 weeks of treatment. RESULTS: Mean mNIS+7 composite scores were maintained over 85 weeks with eplontersen (changes from baseline of -4.5 [T1], -1.3 [T2], and -2.6 [T3] points). Other disease parameter scores were similarly maintained or improved with eplontersen. Patients receiving placebo experienced disease worsening across outcomes. T1 mean disease scores were typically better than in T2 and T3. INTERPRETATION: Consistent, sustained benefits of eplontersen were observed regardless of baseline ATTRv-PN severity. These findings strengthen the importance of early treatment initiation for patients with ATTRv-PN across the disease spectrum.

Humans↗

PubMedDate not supplied

[The clinical phenomenology of Rett's syndrome].

The work was done to facilitate the clinical diagnosis and understanding of Rett syndrome (RS) by grouping the symptoms and signs in areas of neurological disfunction. This is a retrospective, longitudinal and observational study of 30 young females whose clinical manifestations were grouped using a modified Fitzgerald et al. scale for motor and behavior evaluation of patients with RS. All patients were videotaped at least during one or several appointments during their follow-up for a period of 1 to 10 years. All patients and videotapes were reviewed independently by the three authors. We followed the clinical diagnostic criteria of classic RS, and grouped the symptoms and signs in 12 groups of clinical phenomenology that represented specific areas of central or peripheral nervous system involvement: 1) dementia syndrome (fronto-temporo-parietal and limbic dysfunction); 2) extrapyramidal syndrome (basal ganglia dysfunction); 3) respiratory function disorders (brain stem reticular system disfunction); 4) sleep disorders (reticular system and limbic dysfunction); 5) epilepsy (cortico-subcortical paroxysmal bioelectrical dysfunction); 6) lower motor neuron syndrome (neuropathic dysfunction and/or peripheral neuropathy); 7) body growth retardation; 8) tonic-postural skeletal deformities; 9) deficit of pain sensation (nociceptive deficit); 10) pseudobulbar dysfunction; 11) autonomic dysfunction and 12) others (microcephaly and bruxism). In clinical practice, we recommend the use of this grouping of symptoms and signs because it makes facilities the clinical study, definition of areas of dysfunction and diagnosis of the patient with RS.

Adolescent↗

PubMed1998

A dysautonomia case of Guillain-Barré syndrome with recovery: monitored by Composite Autonomic Scoring Scale.

To investigate the usefulness of the Composite Autonomic Scoring Scale (CASS) as an indication for autonomic dysfunction with Guillain-Barré syndrome, we quantitated autonomic deficits on follow-up using CASS in a patient with Guillain-Barré syndrome who did not have any autonomic symptoms and had good clinical recovery. Using the CASS we found the patient to have mild autonomic dysfunction but with a period of recovery. The scale showed that adrenergic deficits improved quickly, sudomotor deficits recovered moderately and cardiovagal deficits did not improve. These results suggested that the patient with Guillain-Barré syndrome might have dysautonomia although she did not have any autonomic symptoms. Results also suggest that there might be difference on the degree of improvement among adrenergic, sudomotor and cardiovagal deficits in Guillain-Barré syndrome. The CASS may be a sensitive tool for the detection of autonomic dysfunction in Guillain-Barre syndrome.

Autonomic Nervous System↗

PubMed1993

The effect of phenobarbital on autonomic function and epileptogenic activity induced by the hippocampal injection of penicillin in cats.

This study addressed whether penicillin-induced epileptiform discharges in the right hippocampus produced associated autonomic dysfunction. The study also examined the effect of phenobarbital on the heart rate and blood pressure changes that were induced by the epileptiform discharges. The delay in onset of epileptiform activity at the site of injection ranged from 1 second to 16 minutes, and consisted of interictal discharges or ictal discharges. With the onset of epileptiform activity, blood pressure and heart rate increased significantly from control (P < .05). Electrocardiogram alterations included: P-R interval changes; increased P-wave amplitude; QRS complex changes; T-wave inversion; and ST elevation. Phenobarbital 20 mg/kg intravenously suppressed the epileptogenic activity and depressed the blood pressure and heart rate below control (P < .05). In an additional series of experiments, penicillin G injected into the right hippocampus in five cats produced epileptiform activity and increased the blood pressure and the heart rate significantly from the control (P < .05). Phenobarbital (20 mg/kg, intravenously, and 40 mg/kg, intravenously) also prevented the penicillin-induced epileptiform activity. Phenobarbital (40 mg/kg, intravenously) reversed the effect of penicillin on the blood pressure and heart rate, to levels significantly below that of control (P < .05). Phenobarbital diminished both epileptiform activity and autonomic dysfunction. The autonomic dysfunction related to epileptiform activity induced by focal hippocampal administration of penicillin was similar to that induced by the intravenous administration of pentylenetetrazol.

Animals↗

PubMed1995

Hormonal, renal, and autonomic nerve factors involved in the excretion of sodium and water during dynamic salt and water loading in hypoxaemic chronic obstructive pulmonary disease.

BACKGROUND: Some patients with hypoxaemic chronic obstructive pulmonary disease (COPD) develop sodium and water retention and a subclinical autonomic neuropathy. The possibility that these might be associated has been investigated. METHODS: The ability of 24 patients with COPD to excrete a 6 ml/kg 2.7% intravenous saline or 15 ml/kg oral water load was studied and changes in plasma electrolyte levels, osmolality, plasma aldosterone and vasopressin levels, urinary volume and sodium content, glomerular filtration rate, renal blood flow, and cardiovascular autonomic nerve function were measured. Patients were divided into groups of eight: those in group A (controls) had mild COPD with a Pa02 of > 9 kPa and no oedema, patients in group B were more hypoxaemic but had never been oedematous, whilst those in group C were hypoxaemic and mildly oedematous at the time of the study. RESULTS: Patients in groups B and C excreted less sodium and water during saline loading and a lesser proportion of the water load. Patients in group C had a reduction in renal blood flow and glomerular filtration rate and all had a subclinical autonomic neuropathy, which was also found in three patients in group B. Their plasma aldosterone level was raised but did suppress appropriately on saline loading. Vasopressin levels were abnormally raised for the osmolality in patients in group C and in those with autonomic dysfunction throughout the water load and at 240 minutes after the salt load. Sodium and urine excretion was highly correlated with autonomic dysfunction, aldosterone levels at time zero, and renal blood flow. The 11 patients with autonomic dysfunction were more likely to be oedematous, more hypoxaemic, excreted much less urine and sodium, had lower glomerular filtration rate and renal blood flow, and higher aldosterone and vasopressin levels than the remaining patients. CONCLUSIONS: In patients with COPD the inability to excrete sodium and water is multifactorial. This is the first study to show that autonomic dysfunction is at least associated and might play an important part in the impaired sodium and water homeostasis seen in patients with severe COPD.

Aged↗

PubMed2003

Autonomic nervous system testing may not distinguish multiple system atrophy from Parkinson's disease.

BACKGROUND: Formal laboratory testing of autonomic function is reported to distinguish between patients with Parkinson's disease and those with multiple system atrophy (MSA), but such studies segregate patients according to clinical criteria that select those with autonomic dysfunction for the MSA category. OBJECTIVE: To characterise the profiles of autonomic disturbances in patients in whom the diagnosis of Parkinson's disease or MSA used criteria other than autonomic dysfunction. METHODS: 47 patients with parkinsonism and autonomic symptoms who had undergone autonomic laboratory testing were identified and their case records reviewed for non-autonomic features. They were classified clinically into three diagnostic groups: Parkinson's disease (19), MSA (14), and uncertain (14). The performance of the patients with Parkinson's disease was compared with that of the MSA patients on five autonomic tests: RR variation on deep breathing, heart rate changes with the Valsalva manoeuvre, tilt table testing, the sudomotor axon reflex test, and thermoregulatory sweat testing. RESULTS: None of the tests distinguished one group from the other with any statistical significance, alone or in combination. Parkinson's disease and MSA patients showed similar patterns of autonomic dysfunction on formal testing of cardiac sympathetic and parasympathetic, vasomotor, and central and peripheral sudomotor functions. CONCLUSIONS: This study supports the clinical observation that Parkinson's disease is often indistinguishable from MSA when it involves the autonomic nervous system. The clinical combination of parkinsonism and dysautonomia is as likely to be caused by Parkinson's disease as by MSA. Current clinical criteria for Parkinson's disease and MSA that direct patients with dysautonomia into the MSA group may be inappropriate.

Aged↗

PubMed1997

Do high proinsulin and C-peptide levels play a role in autonomic nervous dysfunction?: Power spectral analysis in patients with non-insulin-dependent diabetes and nondiabetic subjects.

BACKGROUND: Immunoreactive insulin has been shown to predict the development of parasympathetic autonomic neuropathy. It is possible that constituents of immunoreactive insulin could explain this association. In this cross-sectional study, the relationship of specific insulin, C-peptide, and proinsulin with autonomic nervous dysfunction was evaluated in 57 NIDDM patients and 108 control subjects. METHODS AND RESULTS: The frequency-domain analysis of heart rate variability was determined by using spectral analysis from stationary regions of registrations while the subjects breathed spontaneously in a supine position. Total power was divided into three frequency bands: low (0 to 0.07 Hz), medium (MFP, 0.07 to 0.15 Hz), and high (HFP, 0.15 Hz to 0.50 multiplied by the frequency equal to the mean RR interval). In NIDDM patients, total power, the three frequency bands (P<.001 for each), and the MFP/HFP ratio (P=.016), which expresses sympathovagal balance, were reduced compared with control subjects. Fasting proinsulin (r(s)=-.324, P=.014 for diabetics and r(s)=-.286, P=.003 for control subjects), C-peptide (r(s)=-.492, P<.001 for diabetics and r(s)=-.304, P=.001 for control subjects), and total immunoreactive insulin (r(s)=-.291, P=.028 for diabetics and r(s)=-.228, P=.017 for control subjects) were inversely related to MFP/HFP. For proinsulin and C-peptide the results did not change after controlling for the effects of age, body mass index, and fasting glucose. CONCLUSIONS: Both proinsulin and C-peptide levels were significantly associated with the sympathovagal balance of autonomic nervous function in NIDDM patients and control subjects, but this study cannot determine whether these compounds are directly involved in autonomic nervous dysfunction.

Aged↗

PubMed1998

Autonomic functions in restrictive cardiomyopathy and constrictive pericarditis: a comparison.

BACKGROUND: This study was undertaken to analyze autonomic functions in restrictive cardiomyopathies. Restrictive cardiomyopathies have clinical and hemodynamic similarity with chronic constrictive pericarditis. Autonomic dysfunction has been described in the latter. METHODS AND RESULTS: Autonomic function analysis has not been reported in restrictive cardiomyopathy. Six consecutive patients with restrictive cardiomyopathy were included in this study (5 men, 1 woman, mean age 35+/-5.4 years). The tests performed were designed to test the sympathetic efferent pathway, that is, by cold hand immersion and loud noise tests, parasympathetic efferent pathway by Valsalva ratio and expiration/inspiration ratio and the baroreceptor function by testing their sensitivity slope. The results were compared with 20 patients with chronic constrictive pericarditis and with 10 healthy age- and sex-matched control subjects previously studied. The rise of systolic blood pressure after cold hand immersion and sudden loud noise was not significantly different compared with control subjects. The expiration/inspiration ratio was 1.1+/-0.01 compared with 1.57+/-0.1 in the control group (p < 0.01). The Valsalva ratio was significantly lower (1.1+/-0.04) compared with control subjects (1.83+/-0.1, p < 0.01). The baroreceptor sensitivity was not reduced compared with that in control subjects. In comparison to constrictive pericarditis, sympathetic efferent pathway is preserved in restrictive cardiomyopathy (p < 0.0001). The parasympathetic efferent pathway is borderline abnormal in restrictive cardiomyopathy but not significantly as compared with constrictive pericarditis (p=not significant). The baroreceptor sensitivity slope is normal in patients with restrictive cardiomyopathy as compared with significant depression seen in constrictive pericarditis (p < 0.05). Autonomic functions are better preserved in patients with restrictive cardiomyopathies compared with chronic constrictive pericarditis. CONCLUSIONS: Autonomic dysfunction is localized to parasympathetic efferent pathway. This is in comparison to constrictive pericarditis, in which severe autonomic dysfunction is a universal feature and includes all segments of autonomic nervous system.

Adolescent↗

PubMed2006

The relationship of heart rate variability with severity and prognosis of cirrhosis.

Many studies have demonstrated that cirrhosis is frequently associated with autonomic dysfunction. The aim of this study was to test autonomic dysfunction in cirrhotic patients by analyzing heart rate variability (HRV), to determine whether or not the degree of autonomic dysfunction is correlated with the severity of disease, and, also, to compare the changes of HRV between survivor and nonsurvivor groups after 2-year follow-up periods. HRV was analyzed using 24-hr ECG recording in 30 cirrhotic patients and 28 normal controls. The changes in HRV parameters including mean normal-to-normal (N-N) interbeat intervals (mean NN), standard deviation of all N-N intervals (SDNN), standard deviation of the average of N-N intervals for each 5-min period over 24 hr (SDANN), root mean square succesive differences (r-MSSD; msec), and percentage of adjacent N-N intervals that are >50 msec apart (pNN50), all as time domain parameters, were evaluated. The cirrhotic patients were also evaluated according to Child-Pugh classification scores as markers of the disease severity. The time-domain measures of HRV in cirrhotic patients were significantly reduced compared with those in the control group (for all parameters; P < 0.001). The severity of disease was associated with reduced HRV measures (for all parameters; P < 0.001). After the 2-year follow-up periods, HRV measurements in cirrhotic patients were significantly much lower in nonsurvivors than in survivors (P < 0.001 for all). We conclude that increasing severity of cirrhosis is associated with a reduction in HRV. This finding may be an indicator of poor prognosis and mortality for cirrhosis.

Analysis of Variance↗

PubMed2006

[The autonomic pupillary dysfunction in type II diabetes mellitus].

OBJECTIVE: To evaluate the pupillary disorder associated with autonomic neuropathy of type II diabetes mellitus by investigating pupil diameters under mesopic, photopic and pharmacologically dilated conditions. METHODS: Forty of type II diabetic patients were divided into two groups based on the results of fundus fluorescein angiography, one group was the subclinic diabetic retinopathy and another was the NPDR (nonproliferative diabetic retinopathy), 20 age-matched healthy subjects were selected as control. High-resolution images of the pupil in 60 subjects were taken using an infrared-sensitive camera under mesopic, photopic and pharmacologically dilated conditions, respectively. From the images, the pupil diameters, constriction ratio and dilatation ratio were analyzed using Photoshop, Acdsee, and Imagetools software. RESULTS: The mean pupil diameter of tested subjects in mesopic control, subclinic and the NPDR were (6.02 +/- 0.48), (5.87 +/- 0.99), (4.95 +/- 1.12)mm, respectively. The mean photopic pupil diameter in three groups were (3.40 +/- 0.33), (3.37 +/- 0.31), (3.25 +/- 0.47) mm, respectively, where the mean pharmacologically dilated pupil diameter in three groups were (7.37 +/- 0.59), (6.91 +/- 1.00), (5.49 +/- 1.24) mm, respectively. The mean constriction ratio of these three groups were (43 +/- 7)%, (41 +/- 10)%, (32 +/- 14)%, respectively. The mean dilatation ratio of these three groups were (23 +/- 8)%, (19 +/- 13)%, (11 +/- 5)%, respectively. There were statistically significant differences among three groups in dark adapted pupil diameter, dilated pupil diameter, constriction ratio and dilatation ratio (P < 0.05). CONCLUSIONS: Autonomic pupillary dysfunction occurs early in type II diabetic patients. Pupillary diameters under mesopic and pharmacologically dilated conditions, and other pupil changes such as constriction ratio and dilatation ratio can be the reliable sign to evaluate autonomic neuropathy of type II diabetes mellitus.

Aged↗

PubMed2001

Ambulatory norepinephrine treatment of severe autonomic orthostatic hypotension.

OBJECTIVES: This study was designed to establish a patient-controlled, ambulatory norepinephrine treatment of refractory orthostatic hypotension due to primary autonomic failure. BACKGROUND: Autonomic dysfunction leads to disabling postural hypotension. Particularly in primary autonomic dysfunction, repeated syncope and immobilization can be the result. Medical treatment of orthostatic hypotension often fails in advanced cases. METHODS: Ambulatory, patient-controlled norepinephrine therapy was initiated in six patients with orthostatic hypotension due to primary autonomic failure that had been refractory to conventional treatment. Before this therapy, three patients were bedridden; one was immobilized in a wheelchair. All had recurrent syncope and tolerated upright tilt-table testing for less than 15 min despite extensive medical treatment. For ambulatory treatment, a port-a-cath system was implanted and, using a CADD ambulatory infusion pump, norepinephrine was infused in individually adjusted dosages. RESULTS: Norepinephrine infusion therapy enabled all patients to sit, stay and walk around for more than 45 min. One patient died after a five-year treatment period, another after nine months because of nonhemorrhagic brain stem infarctions, both in the absence of norepinephrine treatment. The remaining four patients are still mobile after a period of 19, 10, 9 and 7 months, respectively. None of them has suffered complications due to arterial hypo- or hypertension, and there has been no infection of the infusion system. CONCLUSIONS: In these selected patients with refractory orthostatic hypotension due to primary autonomic dysfunction, ambulatory norepinephrine infusion therapy has proved to be a promising new therapeutic option. Further long-term studies including more patients are necessary to assess additional indications, reliability and safety of this new method.

Aged↗

PubMed2001

Autonomic function in chronic liver disease assessed by Heart Rate Variability Study.

BACKGROUND: Chronic liver disease is associated with cardiovascular changes, including hyperdynamic circulation with increased blood volume and cardiac output, and with reduced peripheral vascular resistance. Autonomic dysfunction is a common finding in these patients, being involved in the pathogenesis of the hyperdynamic condition. The aim of our study was to evaluate autonomic function in cirrhotic patients by using the 24 hour Heart Rate Variability study. We also sought to relate the degree of autonomic dysfunction with the severity of the liver disease. MATERIAL AND METHODS: We studied 22 cirrhotic patients, 50% of whom were male, mean age 44.14 +/- 11.32 years. The etiology was alcohol related in 12 (54.6%), virus hepatitis in 6 (27.2%), autoimmune related in two (9.1%) and other in the remaining two (9.1%). In terms of severity liver disease 6 patients were in Child-Pugh's class A (27.3%), 9 in Child-Pugh's class B (40.9%) and 7 in Child-Pugh's class C (31.8%). Thirteen patients (59%) had ascites. Both patients and 20 age-sex matched healthy volunteers underwent 24 hour ECG Holter study with assessment of Heart Rate Variability (time and frequency domains). RESULTS: The cirrhotic patients showed severe decrease in Heart Rate Variability when compared to healthy volunteers: SDNN (84.14 +/- 35.78 ms vs 148.9 +/- 33.97 ms; p < 0.0001), pNN50 (3.54 +/- 4.61 vs 11.17 +/- 9.88; p = 0.004). The spectral analysis revealed markedly decrease of average total power, with reduction of all components (VLF, LF, HF), in the absence of significant difference in LF/HF ratio (2.52 +/- 1.40 vs 2.98 +/- 1.57; p = NS). Ascites had relationship with more pronounced autonomic impairment: SDNN (70.31 +/- 30.32 ms vs 104.11 +/- 34.97 ms; p = 0.03). On the other hand, alcohol related etiology did not influence Heart Rate Variability parameters. Moreover, we found significant positive correlations between SDNN (dependent variable) and Prothrombin activity (r = 0.64; p = 0.001), as well as with Serum Albumin (r = 0.40; p = 0.05), but not with Total Bilirubin (r = -0.14; p = 0.51). Prothrombin activity was the only independent predictor of autonomic dysfunction. CONCLUSION: Chronic liver disease is accompanied by a significant Heart Rate Variability decrease. Alcohol related etiology does not indicate further autonomic dysfunction. The greater the hepatopathy severity, the greater the Heart Rate Variability impairment. Hepatocellular dysfunction indicators have more accuracy to demonstrate autonomic disturbances than cholestasis indicators.

Adult↗

PubMed1999

Brainstem dysfunction in chiari malformation presenting as profound hypoglycemia: presentation of four cases, review of the literature, and conjecture as to mechanism.

OBJECTIVE: We report four patients whose cases resulted in our observation that profound hypoglycemia resulting from intermittent hyperinsulinism plays a significant role in patients with brainstem dysfunction from Chiari I or II malformations who have intermittent autonomic dysfunction ("blue spells"). METHODS: The records of four children with severe brainstem dysfunction associated with hindbrain herniation (Chiari I or II malformation) were reviewed retrospectively. Each patient had severe lower cranial nerve dysfunction that required tracheotomy and feeding tube placement. After we found that profound hypoglycemia had occurred during a spell of autonomic dysfunction in one patient, the charts of the other three patients were reviewed for evidence of hypoglycemia. Now, whenever one of them has evidence of autonomic dysfunction, prospective studies of glucose and insulin levels are performed. Three of the patients had Chiari II malformation in association with myelomeningocele, and one patient had a Chiari I malformation resulting from Pfeiffer's syndrome. RESULTS: Hypoglycemia occurred in these patients episodically, and usually when their shunts were functioning. The hypoglycemia was associated with hyperinsulinemia in each patient. The brainstem structures of these children (presumably the dorsal motor nuclei of the vagus) were extremely sensitive to changes in local or regional intracranial pressure. These changes were triggered by intermittent shunt failure, agitation from pain, abdominal distention from constipation, and retention of CO2. In patients with Chiari malformations, even mild increases in intracranial pressure lead to brainstem dysfunction. One possible explanation is that pressure on the deformed Xth cranial nerve nuclei may lead to insulin release and life-threatening hypoglycemia. Continuous-drip feeds are necessary to prevent this complication. CONCLUSION: Patients with severe intermittent brainstem dysfunction after decompression of Chiari I or Chiari II malformations should have laboratory studies of glucose levels performed at the time of the episodes to rule out hypoglycemia.

Adolescent↗

PubMed2004

Many diseases may reflect dysfunctions of autonomic balance attributable to evolutionary displacement.

We hypothesize that many ailments are attributable to dysfunctions of autonomic balance. The autonomic system is a primitive, highly-adaptive response system that allows differential allocation of biologic effort under varying conditions. The autonomic system, however, can execute a response that is inappropriate for the system stressor due to evolutionary displacement. Evolutionary displacement is a situation in which a trait that evolved as an adaptive response to certain conditions now faces a new set of conditions. Modern human evolution since the Pleistocene era is characterized by substantial evolutionary displacement, brought on in large part by the accelerating ability of humans to change their own environment. In the setting of evolutionary displacement, previously adaptive systems such as the autonomic system can be rendered unhelpful or even counterproductive. Emergence of chronic conditions, maladaptation of the trauma response, and extension of human lifespan are examples of evolutionary displacements that can induce inappropriate sympathetic bias in hosts. We postulate that many diseases are manifestations of this general phenomenon. Implications for existing and future therapeutic strategies are discussed.

Biological Evolution↗

PubMed1990

Autonomic function and human immunodeficiency virus infection.

We compared autonomic function in 26 patients infected by the human immunodeficiency virus (HIV) (18 AIDS and 8 ARC) to 22 controls. A significant decline in autonomic function was present across groups. Autonomic dysfunction correlated strongly with signs of HIV-associated nervous system disease. We observed significant differences across groups in tests of heart rate variation (expiratory-inspiratory ratio, maximum minus minimum heart rate difference, and mean square successive difference), the mean arterial blood pressure fall to tilting, and the blood pressure response to isometric exercise. A trend of declining autonomic function from controls to AIDS was present in the 30:15 ratio, the Valsalva ration, the systolic blood pressure fall to standing and tilt, and the cold pressor test. We did not observe any correlation between autonomic dysfunction and individual neurologic signs, prior therapeutic agents, and concurrent HIV-associated inflammatory or neoplastic processes. This study provides support for the presence of autonomic dysfunction in association with HIV infection. Autonomic dysfunction occurs more frequently and with greater severity in patients with AIDS; however, it may be present in the early stages of HIV infection and appears to progress during the illness.

AIDS-Related Complex↗

PubMed2005

Reduced cardiac parasympathetic activity in children with autism.

Many of the clinical symptoms of autism suggest autonomic dysfunction. The aim of this study was to measure baseline cardiovascular autonomic function in children with autism using the NeuroScope, a device that can measure this brainstem function in real-time. Resting cardiac vagal tone (CVT), cardiac sensitivity to baroreflex (CSB), mean arterial blood pressure (MAP), diastolic blood pressure (DBP), systolic blood pressure (SBP) and heart rate (HR) were recorded in three different groups of children. The symptomatic group (n = 15) consisted of those with autism who exhibited symptoms or signs of autonomic dysfunction. The asymptomatic group (n = 13) consisted of children with autism but without symptoms or signs of autonomic dysfunction and the healthy children were in the control group (n = 17) [corrected]. The CVT and CSB were significantly lower in association with a significant elevation in HR, MAP and DBP in all children with autism compared with the healthy controls. Further more, the levels of CVT and CSB were lower in the symptomatic than in the asymptomatic group. The levels of CVT and CSB were not related to age in all the three groups. These results suggest that there is low baseline cardiac parasympathetic activity with evidence of elevated sympathetic tone in children with autism whether or not they have symptoms or signs of autonomic abnormalities.

Animals↗

PubMed2002

A longitudinal cardiovascular autonomic function study in mild Guillain-Barré syndrome.

To identify subclinical autonomic dysfunction in mild Guillain-Barré syndrome (GBS), a set of autonomic function tests was serially performed for up to 6 months in 5 GBS patients with mild disability at the nadir. Parasympathetic autonomic function tests consisted of Valsalva ratio and R-R interval variation during rest and deep breathing. Sympathetic autonomic function was evaluated by blood pressure responses to sustained handgrip, hand immersion in ice water, and active standing. The results showed that abnormal parasympathetic and sympathetic function was frequently encountered in all 5 patients during the acute stage of the illness. Autonomic dysfunction occurred both in axonal and demyelinating types of GBS. There was a trend of improvement in most autonomic function tests after 3 months, comparable to the recovery of motor function. In conclusion, subclinical autonomic dysfunction was present in mild GBS. It was temporary and would resolve spontaneously.

Adolescent↗

PubMed2006

Guillain-Barré syndrome as a cause of reversible cardiomyopathy.

Although autonomic dysfunction is a common manifestation of Guillain-Barré syndrome, cardiovascular involvement in this setting has rarely been reported in the literature. We describe a case of reversible left ventricular systolic dysfunction in a 60-year-old man with Guillain-Barré syndrome. Our patient had no history or signs of cardiac dysfunction on initial presentation. During the clinical manifestation of his autonomic dysfunction, he developed electrocardiographic changes accompanied by mildly elevated cardiac enzymes and severe left ventricular systolic dysfunction and segmental wall motion abnormality, which coincided with elevated urinary catecholamine and vanilmandelic acid levels. These abnormalities, and his symptoms, resolved rapidly once the acute episode was over. We believe the reversible left ventricular dysfunction was due to the toxic effect of increased catecholamines and to the transiently damaged sympathetic nerve endings in the myocardium, presumably a consequence of Guillain-Barré syndrome. We recommend that echocardiography be performed in patients with clinical signs of autonomic dysfunction, especially if they are associated with abnormal electrocardiographic findings, cardiac enzyme elevation, or hemodynamic instability, so that appropriate medical therapy can be instituted in a timely manner.

Guillain-Barre Syndrome↗