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Results for “Autonomic dysfunction”

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At least 1,333 records · Page 74Linked to original sources

PubMed2002

Ambulatory blood pressure monitoring in patients with spinocerebellar degeneration.

OBJECTIVES: The aim of this study was to demonstrate circadian blood pressure trends and to evaluate autonomic function in patients with spinocerebellar degeneration (SCD). MATERIALS AND METHODS: We performed 24-h ambulatory blood pressure monitoring (ABPM) on 10 patients from seven Japanese families with spinocerebellar ataxia type 6 (SCA6), 10 patients with idiopathic cerebellar ataxia (ICA), eight patients with multiple system atrophy (MSA) suffering from cerebellar MSA (MSA-C), and 12 age- and gender-matched normal subjects. We also evaluated autonomic function in these patients. RESULTS: Three SCA6 patients (30%), six ICA patients (60%), eight MSA-C patients (100%) and four normal subjects (33%) were non-dippers. The nocturnal reduction rate of blood pressure in MSA patients was significantly less than those in normal subjects, SCA6 patients and ICA patients. There were no abnormal findings in any patient with SCA6 in autonomic function tests. All dipper patients exhibited normal findings on autonomic function tests. This is the first report of ABPM in patients with SCD. CONCLUSIONS: Blunted reduction of nocturnal blood pressure may be associated with autonomic dysfunction in patients with SCD.

Aged↗

PubMed2002

Extensive Riga-Fede disease of the lip and tongue.

Riga-Fede disease presents in early infancy and is characterized by firm, verrucous plaques arising on the oral mucosal surfaces. These histologically benign lesions occur as a result of repetitive trauma of the oral mucosal surfaces by the teeth. Early recognition of this entity is important, because it may be the presenting sign of an underlying neurologic disorder. We report the case of a 10-month-old boy with extensive Riga-Fede disease involving the lip and tongue that prompted a diagnosis of congenital autonomic dysfunction with universal pain loss.

Autonomic Nervous System Diseases↗

PubMed1985

Cystic fibrosis heterozygotes have normal autonomic innervation of the heart.

Five simple tests of autonomic nerve function based on measurements of cardiovascular responses to various stimuli were used to investigate possible autonomic dysfunction in obligate heterozygotes for cystic fibrosis. There were no significant differences between the heterozygotes and control groups in any of the tests, suggesting that cystic fibrosis heterozygotes have normal autonomic innervation of the heart.

Adult↗

PubMed2005

Post-micturitional hypotension in patients with multiple system atrophy.

BACKGROUND: Patients with multiple system atrophy (MSA) occasionally have episodes of syncope or pre-syncope after micturition. OBJECTIVE: To clarify the mechanism of these episodes by investigating the haemodynamic changes associated with micturition. METHODS: 25 patients with probable MSA and 16 age matched normal controls were studied. Continuous records of blood pressure and heart rate were made during water cystometry, along with the Valsalva manoeuvre, head up tilt testing, measurement of plasma noradrenaline, and calculation of coefficient of variance of RR intervals. RESULTS: Compared with normal controls, MSA patients had a lower baseline blood pressure, smaller blood pressure and heart rate increases during bladder filling, and an abnormal fall in blood pressure for a longer duration after voiding, resulting in significantly lower blood pressure than at baseline (mean systolic blood pressure reduction -15.2 mm Hg), and hypotension compared with control blood pressure (-29.0 mm Hg). The blood pressure fall was greater in patients with micturition syncope/pre-syncope than in those without. It was also greater in patients with abdominal straining resulting from difficulty in voiding. Other cardiovascular indices did not correlate with the fall in blood pressure. CONCLUSIONS: Hypotension after voiding in MSA patients may result from generalised autonomic dysfunction and abnormal abdominal straining, resulting in micturition syncope.

Aged↗

PubMed1987

The significance of impaired pancreatic polypeptide and epinephrine responses to hypoglycemia in patients with insulin-dependent diabetes mellitus.

The impaired epinephrine and glucagon responses to hypoglycemia often found in patients with insulin-dependent diabetes mellitus (IDDM) may be due to autonomic neuropathy. Since the pancreatic polypeptide response to hypoglycemia is mediated by cholinergic mechanisms, we used this response as an indicator of autonomic neuropathy to determine whether deficient epinephrine and glucagon responses in IDDM could be ascribed to an autonomic defect. The relationships between pancreatic polypeptide, epinephrine, and glucagon responses during insulin-induced hypoglycemia were assessed in 18 patients with IDDM who had no overt evidence of autonomic neuropathy, including normal standard cardiovascular reflex tests, and 11 age-matched nondiabetic subjects. All of the diabetic patients had impaired glucagon responses [19 +/- 3 (SEM) vs. 96 +/- 11 pg/ml, peak increment, P less than 0.001]. Ten of the 18 diabetic patients had either impairment of plasma epinephrine or plasma pancreatic polypeptide responses or both to hypoglycemia. Moreover, pancreatic polypeptide responses were significantly correlated with epinephrine responses (r = 0.53, P less than 0.003). There was no association between the plasma glucagon response and the epinephrine (r = 0.02, NS), norepinephrine (r = 0.03, NS), or pancreatic polypeptide (r = 0.35, NS) response. Last, there was no correlation between the plasma hormone responses and the cardiovascular reflex test results. Therefore, the association of impaired plasma pancreatic polypeptide responses with impaired plasma epinephrine responses suggests that the impaired epinephrine responses are due to autonomic neuropathy, whereas the dissociation of plasma glucagon responses with both plasma pancreatic polypeptide and epinephrine responses suggests that the impaired pancreatic alpha-cell response to hypoglycemia is not due to autonomic neuropathy. In addition, the plasma pancreatic polypeptide and epinephrine responses to hypoglycemia appear to be an earlier indicator of underlying autonomic dysfunction than standard cardiovascular reflex tests. Thus, the responses of plasma pancreatic polypeptide and epinephrine to insulin-induced hypoglycemia may be a useful test for the identification of early autonomic neuropathy in IDDM.

Adolescent↗

PubMed1987

Substance P given intrathecally at the spinal T9 level increases arterial pressure and heart rate in the rat.

Administration of 10 micrograms of substance P intrathecally at the spinal T9 level of the unanaesthetized and the anaesthetized rat provoked an increase in arterial pressure and an increase in heart rate. Both cardiovascular responses began within 1-2 min of administration, and the peak of each occurred at 4-10 min. In the anaesthetized rat, which gave rise to the bulk of the responses reported, peak arterial pressure was ca 20 mm Hg greater than pre-administration levels, and peak heart rate was greater by ca 50 beats per min. Similar administration of vehicle failed to alter either parameter. Arterial pressure and heart rate in substance P-treated rats were significantly different from those in vehicle-treated rats up to 15-20 min after administration. Pretreatment with the sympathetic ganglion blocker, hexamethonium (10 mg/kg, i.v.), prevented the responses to intrathecal administration of substance P. Pretreatment with [D-Pro2, D-Phe7, D-Trp9]-substance P, an analogue with antagonist properties in the central nervous system, blocked both responses to substance P but failed to alter similar responses provoked by intrathecal administration of angiotensin II. Pretreatment with vehicle had no effect on responses to substance P or to angiotensin II. The antagonist also had partial agonistic effects. Both arterial pressure and heart rate were transiently increased, but this effect was reversed within 6 min; in the case of heart rate, values returned to the pre-application level but arterial pressure fell to a ca 15 mm Hg below this level. These results demonstrate a pharmacologically specific excitatory effect of substance P on spinal mechanisms controlling sympathetic output to the vessels and the heart; this output can be either via the adrenal medullae or via nerve pathways to the vessels and the heart. Our results also support the possibility that dysfunction of substance P systems at the spinal level may underly some models of hypertension and may be involved in some cases of essential hypertension in man, as well as in autonomic dysfunction associated with some neurological disorders.

Anesthetics↗

PubMed1994

Head-up tilt and hemodynamic changes during orthostatic hypotension in patients with supine hypertension.

OBJECTIVES: This study assessed the mechanism(s) of the decrease in upright blood pressure in patients with supine hypertension by using the tilt test and a hemodynamic approach. BACKGROUND: Orthostatic hypotension in patients with supine hypertension creates a pathophysiologic and therapeutic dilemma. METHODS: We studied 28 consecutive patients with history of orthostatic intolerance amounting to recurrent syncope in 13 of them (15 men, 13 women; mean [SD] age 65 +/- 11 years). They all had supine hypertension (systolic blood pressure > 160 mm Hg) and orthostatic hypotension (found to be a decrease in systolic blood pressure > 30 mm Hg during tilt test). Cardiac output, cardiopulmonary volume and systemic resistance were assessed by radionuclide first-pass technique (technetium-99m red blood cell tagging). Total blood volume was determined by radioiodinated serum albumin, and the ratio of cardiopulmonary to total blood volume was used as an index of venous capacitance. RESULTS: Twenty-one patients had accentuated venous pooling defined as a tilt-induced decrease in cardiopulmonary volume/total blood volume ratio > 15% from baseline or a supine ratio < 14% (normal 16% to 18%), or both. Seven of the 28 patients had autonomic insufficiency; 6 of the 7 also had venous pooling; 1 patient had autonomic insufficiency only. Neither clinical history nor changes during tilt differentiated the subgroups. Plasma catecholamine levels increased during head-up tilt in all subgroups, and differences in their increase were not significant between patients with venous pooling and those with autonomic insufficiency. However, radionuclide hemodynamic variables revealed that patients with venous pooling compensated for the decrease in stroke volume by increasing peripheral resistance, whereas patients with autonomic dysfunction did not. CONCLUSIONS: Orthostatic hypotension in patients with supine hypertension may have multiple etiologies. Hemodynamic assessment with determination of cardiopulmonary volume and systemic vascular resistance differentiated between venous pooling and autonomic insufficiency in these patients; head-up tilt and plasma catecholamine levels did not. These findings may have important therapeutic implications.

Adult↗

PubMed2004

A new model for understanding the role of environmental factors in the origins of chronic illness: a case study of type 1 diabetes mellitus.

There is a need for a new pathophysiological model explaining and linking the role of numerous non-genetic factors believed to contribute to origins of many chronic physical diseases. This article presents a theoretical model for explaining the confusing and often contradictory findings regarding the role of environmental influences in type 1 diabetes, a disease that has been widely studied, for which clear diagnostic criteria exist, and for which development of effective prevention strategies represents significant challenges. The model is formulated from the large database of research regarding increasing understanding of the interaction between environmental factors, physiology, and autonomic regulatory function. Data is integrated from research in the fields of the experience-dependent maturation of the nervous system and the neurophysiology of traumatic stress to demonstrate how disruptions in early bonding and attachment, including adverse events such as traumatic stress, are capable of causing: (1) long-term imbalances in autonomic regulatory function and (2) relative dominance of sympathetic or parasympathetic activity. The proposed model of autonomic dysfunction suggests that ongoing mechanisms promoting high glucose in the context of decreasing insulin production in type 1 diabetes represent a state of relative sympathetic dominance influenced by environmental factors affecting autonomic, immune and endocrine systems during critical period programming. The model further identifies a link between the many seemingly unrelated non-genetic risk factors, and appears capable of explaining contradictions and enigmas in epidemiological and clinical studies regarding non-genetic origins of type 1 diabetes, including the role of stress, variation in age of onset, and duration of the preclinical phase.

Age Distribution↗

PubMed2000

Skin hemodynamics during change from supine to lateral position.

The purpose of this study was to identify the skin hemodynamics during the position change from supine to lateral in patients with neurodegenerative diseases. The participants were 19 patients with neurodegenerative diseases and 12 healthy volunteers. The alteration in the total concentration of oxyhemoglobin and deoxyhemoglobin, indicative of change in blood volume, was measured in the skin of the left flank by using a portable noninvasive tissue oxygen monitor by near-infrared spectroscopy. The positions were changed from the left and right lateral with a return to the supine between each procedure. In healthy volunteers, total hemoglobin concentration (skin blood volume) increased when the position changed from supine to left lateral and decreased when changed from supine to right lateral. The decreased skin blood volume gradually recovered after a change from the supine to the right lateral position in healthy volunteers. However, it did not recover in three sporadic olivopontocerebellar atrophy (OPCA) patients with marked autonomic dysfunction and one Parkinsonian patient with severe orthostatic hypotension. Our study identified that the intracutaneous blood was changing dynamically during the position change from supine to lateral and was regulated by autonomic nerve function.

Autonomic Pathways↗

PubMed2026

Downbeat nystagmus without ataxia as an early manifestation of spinocerebellar ataxia, autosomal recessive type 10 (SCAR10): a case report.

The differential diagnosis of dizziness is broad and can include both vestibular and autonomic pathology. Vestibular dizziness is typically described as a sensation of movement (e.g. the world is spinning) while dizziness related to autonomic dysfunction is typically described as symptoms of orthostatic intolerance (e.g. postural lightheadedness). It is important to differentiate the type of dizziness to guide proper diagnostic and therapeutic workup. We describe the case of a young patient evaluated in the autonomic clinic for dizziness, ultimately found to have a rare cerebellar neurodegenerative disorder. A 23-year-old female with a past medical history of migraine without aura presented in autonomic clinic with a four-month history of slow, progressive onset of vestibular dizziness. Neurological exam was notable for downbeat nystagmus, but no appendicular or truncal ataxia was appreciated. Subsequent vestibular evaluation was consistent with central vestibular dysfunction. Magnetic resonance imaging (MRI) of the brain with and without contrast was notable for severe cerebellar atrophy. The patient subsequently underwent genetic testing which demonstrated a pathogenic and likely pathogenic variant in the Anoctamin 10 (ANO10) gene, which is seen in Autosomal Recessive Spinocerebellar Ataxia, Autosomal Recessive Type 10 (SCAR10). To our knowledge, this case represents the first reported instance of SCAR10 presenting with the sole neurologic exam finding of downbeat nystagmus without cerebellar ataxia. Additionally, the finding of severe cerebellar atrophy seen on MRI, without gait or limb ataxia on exam is an interesting clinicoradiological dissociation. This case suggests that nystagmus may represent an early disease marker, even in the absence of clinical ataxia in patients with SCAR10.

Humans↗

PubMed1998

Bladder involvement in systemic sclerosis: urodynamic and histological evaluation in 23 patients.

Lower tract involvement of systemic sclerosis is an uncommon manifestation. In this study we have evaluated the functional and morphologic vesical changes in 23 female patients with systemic sclerosis to investigate if bladder dysfunction was correlated with an extended skin sclerosis and/or a more serious organ involvement. Urodynamic alterations were observed in only 3 cases. Urinary symptoms and urodynamic features were correlated neither with severity of vesical fibrosis nor with visceral involvement. Autonomic dysfunction was detected in 13 patients.

Adult↗

PubMed1990

Gastroparesis after a presumed viral illness: clinical and laboratory features and natural history.

Gastroparesis after a viral infection has rarely been reported. In this article, we describe the clinical features and long-term outcome of 7 patients who had gastroparesis after a presumed viral illness and who were identified in a retrospective review of 103 consecutive cases of gastroparesis seen at our institution from 1977 through 1988. The three male and four female patients with gastroparesis after a suspected viral illness were young (mean age, 26.9 years) and healthy before the onset of the illness, which manifested as low-grade fever, fatigue, and myalgia with or without diarrhea. A mean of 4.5 days after spontaneous resolution of the viral illness, persistent nausea, vomiting, and epigastric pain developed in these patients. In all seven patients, delayed emptying of the gastric contents was substantiated. Autonomic neuropathy was found in all three patients who underwent autonomic function tests. During a mean follow-up of 32.3 months, five of the seven patients had complete resolution of gastroparetic symptoms, and the other two had considerable improvement of their condition. We conclude that postviral gastroparesis is uncommon, is frequently associated with autonomic dysfunction, and is associated with an apparently excellent prognosis.

Acute Disease↗

PubMed1990

Ocular autonomic nerve function in Lambert-Eaton myasthenic syndrome.

Autonomic innervation to the eye and ocular adnexae was assessed in seven patients with Lambert-Eaton Myasthenic Syndrome and 50 age-matched control subjects. Pupil responses to light were abnormal in 69% of LEMS patients, compared with 18% of the control group. Reflex tear production--a screening test for parasympathetic innervation to the lacrimal gland--was below the accepted normal limit in 69% of LEMS patients. Parasympathetic and sympathetic denervation hypersensitivity of the iris musculature were individually present in 57% of LEMS patients, compared with 6% of control subjects. The association between autonomic dysfunction and Lambert-Eaton Myasthenic Syndrome is discussed.

Adult↗

PubMed1994

Effect of autonomic nervous system dysfunction on the circadian pattern of myocardial ischemia in diabetes mellitus.

OBJECTIVES: The aim of this study was to determine the prevalence and characteristics of ambulatory myocardial ischemia in patients with diabetes mellitus and to delineate the relation between the presence and severity of autonomic nervous system dysfunction and the incidence and time of onset of myocardial ischemia. BACKGROUND: Conflicting data exist with regard to the circadian pattern of myocardial infarction and other cardiovascular events, such as ambulatory ischemia, in diabetes. METHODS: We performed ambulatory electrocardiographic monitoring in 60 patients with diabetes and coronary artery disease. Autonomic nervous system testing was performed in a subgroup of 25 patients with myocardial ischemia after discontinuation of all antianginal medications. RESULTS: Thirty-eight of 60 patients had evidence of ambulatory ischemia; 91% of all ischemic episodes were asymptomatic. The 25 patients with ambulatory ischemia who underwent autonomic nervous system testing had a peak incidence of ischemia between 6 AM and noon (46 of 133 ischemic episodes, p < 0.007), compared with the other three 6-h periods. Fifteen of the 25 patients had no or mild autonomic nervous system dysfunction and demonstrated a similar peak incidence of ischemia between 6 AM and noon (p = 0.0009). However, the 10 patients with moderate to severe autonomic nervous system dysfunction did not experience a morning peak of ischemia, and the number of ischemic episodes was distributed evenly throughout the day (p = 0.4). CONCLUSIONS: Silent ischemia is highly prevalent among patients with diabetes and coronary artery disease. Time of onset of ischemia in diabetic patients follows a circadian distribution, with a peak incidence in the morning hours. However, patients with significant autonomic nervous system dysfunction did not demonstrate such a peak, suggesting that alterations in sympathovagal balance may have an effect on the circadian pattern of cardiovascular events.

Aged↗

PubMed2005

Human immunodeficiency virus (HIV) related heart disease: a review.

Recent advances in the knowledge of human immunodeficiency virus (HIV) replication and transmission as well as the emergence of effective antiretroviral therapies are leading to longer survival times for HIV-infected individuals. As a result, organ related manifestations of late stage HIV infection, including HIV-related heart diseases have emerged. It is now clear that cardiac involvement in HIV seropositive patients is relatively common and is associated with increased morbidity and mortality. Cardiac involvement in HIV infection is multifactorial. The epidemiology has changed dramatically since the introduction of highly active antiretroviral therapy (HAART), but studies carried out before the introduction of HAART remain relevant because of limited access to this treatment in many areas of the world. A variety of cardiac lesions have been reported in HIV infection and AIDS, including pericardial disease with effusion and tamponade, nonspecific or infectious myocarditis, dilated cardiomyopathy with global left ventricular dysfunction, endocardial valvular disease due to marantic or infective endocarditis, arrhythmias, pulmonary hypertension and neoplastic invasion. In the post HAART-era, coronary artery disease and dyslipidaemia, drug related cardiotoxicity and cardiac autonomic dysfunction are becoming increasingly prevalent. In this review, we highlight the importance of cardiac complications in HIV disease and discuss measures that can be taken to improve survival.

HIV Infections↗

PubMed2000

Flurothyl-induced seizures in rats activate Fos in brainstem catecholaminergic neurons.

Autonomic changes accompany seizures in both animals and humans. While ictal autonomic dysfunction can be life-threatening, the participating neural networks involved are poorly understood. In this study we examined the activation of Fos following generalized seizures in brainstem structures known to mediate autonomic function. Adult female rats were sacrificed 2 h after flurothyl-induced seizures. Double-immunostaining for c-Fos and dopamine-beta-hydroxylase (DBH), and c-Fos and phenylethanol-N-methyl-transferase (PNMT) were performed in brainstem slices. Numbers of DBH-labeled neurons expressing Fos-like immunoreactivity (FLI) (DBH/Fos) and PNMT labeled neurons expressing FLI (PNMT/Fos) were counted in the noradrenergic (A1, A2, A5, A7) and adrenergic (C1, C2) cell groups localized in pons and medulla oblongata. Among the experimental animals, the highest degree of co-localization of DBH/Fos neurons was observed in the locus coeruleus (A6; 87.7%), and in the A1(72.8%) cell group located in the caudal ventrolateral medulla (VLM). No co-localization of DBH/Fos neurons was observed in control animals. The highest degree of co-localization of PNMT/Fos neurons was observed in the C1 adrenergic cell group (84.2%) located in the rostral VLM. Control animals showed very few (5.5%) PNMT/Fos co-localized neurons in the C1 adrenergic cell group. Our results indicate that flurothyl-induced generalized seizures in rats activate catecholaminergic neurons in the pons and medulla oblongata. Further studies are necessary to determine whether activation of brainstem catecholaminergic neurons contribute to the autonomic manifestations that frequently accompany epileptic seizures.

Animals↗

PubMed2004

Passive transfer of autoimmune autonomic neuropathy to mice.

Autoimmune autonomic neuropathy (AAN) is an acquired, often severe, form of dysautonomia. Many patients with AAN have serum antibodies specific for the neuronal ganglionic nicotinic acetylcholine receptor (AChR). Rabbits immunized with a fusion protein corresponding to the N-terminal extracellular domain of the ganglionic AChR alpha3 subunit produce ganglionic AChR antibodies and develop signs of experimental AAN (EAAN) that recapitulate the cardinal autonomic features of AAN in man. We now demonstrate that EAAN is an antibody-mediated disorder by documenting sympathetic, parasympathetic, and enteric autonomic dysfunction in mice injected with rabbit IgG containing ganglionic AChR antibodies. Recipient mice develop transient gastrointestinal dysmotility, urinary retention, dilated pupils, reduced heart rate variability, and impaired catecholamine response to stress. The autonomic signs are associated with a reversible failure of nicotinic cholinergic synaptic transmission in superior mesenteric ganglia. Mice injected with IgG from two patients with AAN (of three tested) demonstrated a milder phenotype with evidence of urinary retention and gastrointestinal dysmotility. The demonstration that ganglionic AChR-specific IgG causes impaired autonomic synaptic transmission and autonomic failure in mice implicates an antibody-mediated pathogenesis for AAN. The antibody effect is potentially reversible, justifying early use of immunomodulatory therapy directed at lowering IgG levels and abrogating IgG production in patients with AAN.

Animals↗

PubMedDate not supplied

Dimensions of sexual dysfunction in Parkinson disease.

OBJECTIVE: The authors sought to better understand the factors related to sexual dysfunction in Parkinson disease (PD). METHODS: Twenty-one PD patients and their partners received the Derogatis Interview for Sexual Functioning-Self Report (DISF-SR). Additional measures assessed disease severity, autonomic dysfunction, mood, and social circumstance. RESULTS: Data from 17 male patients demonstrated profound impairment in the dimensions of sexual arousal, behavior, orgasm, and drive, with most patients scoring below the 1st percentile on these Derogatis Interview subscales. All four dimensions showed significant intercorrelations. In contrast, 53% of patients scored above the 50th percentile in sexual fantasy. Sexual fantasy subscale scores were positively correlated with duration of PD. CONCLUSIONS: The usefulness of the DISF-SR in this PD population was limited by extremely low scores and strong correlations among the subscales. The increase in sexual fantasy with greater PD duration suggests that patients with advancing disease remain interested in sex and that sexual dysfunction in PD is clinically relevant in this group.

Adult↗