[On the treatment of autonomic dysfunction].
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Autonomic Nervous System↗
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[The treatment of autonomic dysfunction].
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Autonomic Nervous System↗
[Genuine posttraumatic autonomic dysfunction].
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Autonomic Nervous System↗
The mechanisms of the ocular autonomic dysfunction during the intracarotid amytal suppression test.
We report the eye findings during selective injections of amytal to the internal carotid artery and to trunk and branches of the middle cerebral artery in three patients. This report comes a propos of our previous observation that fairly dense visual obscuration (probably secondary retinal suppression by the amytal), pupillary dilatation (mydriasis) and impairment of visual accommodation (cycloplegia) are not uncommon during the intracarotid amytal suppression test (AST). Selective injections in these three cases offered additional-insight into the mechanisms of the autonomic dysfunction observed in the eye ipsilateral to injection of amytal (EII). Injection of amytal into the trunk and branches of the middle cerebral artery, above the origin of the ophthalmic artery, did not produce ocular autonomic changes in any of the three patients. Injection of amytal in the internal carotid, below the origin of the ophthalmic artery, resulted in pupillary dilatation in the EII in two of the three patients. Based on the anatomy of the vasculature and autonomic innervation of the eye, we postulate that the pupillary dilatation and deficit of visual accommodation observed after intracarotid amytal injection are secondary to parasympathetic suppression in the ciliary ganglion. Amytal reaches the ciliary ganglion via the posterior ciliary arteries, branches of the ophthalmic artery. In summary, injection of amytal in the internal carotid artery below the origin of the ophthalmic artery, but not above it, can impair visual acuity and in some cases, entirel suppress the vision in the EII secondary to retinal suppression. Dilatation of the pupil due to parasympathetic dysfunction is also common and is likely secondary to suppression of the ciliary ganglion in the orbit.
Amobarbital↗
Antidiuretic hormone response to volume depletion in diabetic patients with cardiac autonomic dysfunction.
Thirty-three insulin-dependent diabetic patients were separated into two groups from the results of three different tests for cardiac vagal neuropathy: heart rate response to deep breathing, Valsalva manoeuvre and heart rate response to postural change. Seventeen patients were considered as without ('intact' patients) and 16 as with ('denervated' patients) cardiac autonomic dysfunction. One patient with a transplanted heart was also studied. Plasma antidiuretic hormone (ADH), plasma aldosterone and plasma renin activity (PRA) were measured immediately before and 60 min after intravenous administration of frusemide and passage from lying to standing. The kinetics of hormonal responses were analysed more precisely (five blood collections) in six patients of each group who were studied again. Heart rate and blood pressure were recorded before each blood collection. Volume depletion estimated from the rise in plasma protein (+ 11.9 and + 12.2% in 'denervated' and 'intact' patients respectively) and heart rate response (+ 1.06 and + 14.7%) were similar in both groups. Mean blood pressure was unchanged in the 'intact' patients whereas it fell in the 'denervated' patients (-13.5%). PRA (+ 161.5 and + 231.2% in 'denervated' and 'intact' patients respectively) and plasma aldosterone (+ 318.2 and 279%) increased in both groups whereas plasma ADH was stimulated only in 'intact' patients (+ 55.3%).(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Autonomic dysfunction in experimental autoimmune neuritis: heart rate.
Autonomic nervous system (ANS) dysfunction occurs in more than half of Guillain--Barré syndrome (GBS) patients and is an important cause of death in the disease. In this study we examined heart rate (HR) changes in an animal model of GBS, experimental autoimmune neuritis (EAN), induced by immunization with myelin extracted from bovine spinal roots. The animals developed progressive motor weakness accompanied by significant weight loss and hypothermia. HR was measured in 33 EAN rats at rest (rHR) and followings stressful stimulation (sHR). Average pre-immunization rHR was 341+/-28 beats per minute (b.p.m.) and sHR was 486+/-21 bpm. Although the mean rHR in rats with EAN was not significantly different compared to that at baseline, there was a significant increase of variation of rHR with six rats demonstrating bradycardia (<280 b.p.m.) and 10 tachycardia (>400 b.p.m.) (P<0.01, F-test). sHR in EAN rats was significantly lower (P<0.01), suggesting sympathetic system impairment. These findings may serve as a basis for testing treatments of ANS dysfunction in EAN.
Animals↗
Immune response, nitric oxide, autonomic dysfunction and stroke: a puzzling linkage on Trypanosoma cruzi infection.
Trypanosoma cruzi (T. cruzi) is a tissue parasite causing American trypanosomiasis or Chagas' disease (ChD) affecting, mostly, the cardiovascular and gastrointestinal systems. We have recently found that people infected by T. cruzi are also more prone to developing ischemic strokes than the general population, even without heart complications; the pathomechanism of it is not yet well understood. However, after infection occurs, immune response induces endothelial dysfunction due to an endothelial nitric oxide synthase (eNOS) inhibition and increased activity of inducible nitric oxide synthase (iNOS). These factors are active in inducing vasoconstriction and cerebral microvascular spasms, leading to ischemic stroke. In addition, patients with ChD, regardless of cardiopathy, also have autonomic dysfunction, all of which may enhance the risk of developing ischemic stroke. Moreover, the possibility that these neuroimmunomodulatory pathways are disturbed in patients with other types of stroke seems possible, and is worthy of investigation.
Animals↗
Occult respiratory and autonomic dysfunction in craniovertebral anomalies and upper cervical spinal disease.
Sudden unexplained death may be seen with treatment of craniovertebral anomalies and surgery of the upper cervical spine. Death is due to sleep-induced apnea, premonitored by periods of confusion, lethargy, and asthenia. There may be associated hypotension, bradycardia, hyponatremia, hypothermia, inappropriate antidiuretic hormone secretion, and difficulty in micturition. The potential for respiratory failure may be predicted if a CO2 response test demonstrates an attenuated or abnormal response. Apnea during sleep may be reversed by arousal or may require ventilatory support for a period of time. The condition is self-limiting, but remains the major life-threatening complication. Both apnea and autonomic dysfunction are treatable and curable with appropriate diagnosis and management.
Asthenia↗
Intrathecal baclofen alleviates autonomic dysfunction in severe brain injury.
Sympathetic storm phenomena are well known therapeutic problems in patients with severe brain injury. We have treated four patients with intrathecal baclofen (ITB) who suffered from severe hypertension, tachycardia and other sympathetic storm phenomena after different primary events. In all patients conventional therapy with sedatives and antiadrenergic medication had been taken to the upper limits before initiating ITB. Autonomic dysfunction immediately improved in three of four patients. In all patients ITB, via lumbar or ventricular route, proved safe and without complications. The anatomical and pharmacological basis of the GABA-B agonist action on such sympathetic storm phenomena are not yet fully understood. However, the positive results observed in three out of four patients are promising and require further investigation. ITB is a new therapeutic approach to control otherwise unresponsive sympathetic storm phenomena in severe brain injury.
Adult↗
Is undetected autonomic dysfunction responsible for sudden death in Type 1 diabetes mellitus? The 'dead in bed' syndrome revisited.
AIMS: Sudden nocturnal death in young persons with Type 1 diabetes mellitus has been recently described, and is known as the 'dead in bed' syndrome. Its aetiology is unknown, and we have therefore explored the details of all papers recording the syndrome, to formulate a hypothesis of causation. METHODS: Literature review of 'dead in bed' reports as well as of nocturnal hypoglycaemia, and autonomic dysfunction in relation to baroreceptor-cardiac reflex sensitivity. RESULTS: Clinical reports of 'dead in bed' cases strongly suggest that nocturnal hypoglycaemia is a likely precipitant, but that the death is sudden and probably arrhythmic. Ventricular dysrhythmias may occur in the context of early autonomic neuropathy, with relative sympathetic overactivity, in young Type 1 diabetic persons. CONCLUSION: We conclude that the 'dead in bed' syndrome probably occurs in Type 1 diabetic persons with early autonomic neuropathy, resulting in relative sympathetic overactivity. In such persons, risks of ventricular dysrhythmias will be compounded by nocturnal hypoglycaemia, which may be associated with an increase in the electrocardiographic Q-T interval, and Q-T dispersion. This could lead to the observed sudden death in undisturbed beds. Further research in this area is urgently needed, in particular into the possible protective use of drugs that modulate the autonomic nervous system.
Autonomic Nervous System Diseases↗
Diabetic ketoacidosis associated with Guillain-Barré syndrome with autonomic dysfunction.
A 37-year-old woman was admitted in a comatose state, after exhibiting fever and diarrhea. Diabetic ketoacidosis was diagnosed due to an increased blood glucose level (672 mg/dl), metabolic acidosis, and positive urinary ketone bodies. On the fifth hospital day, despite recovery from the critical state of ketoacidosis, the patient suffered from dysphagia, hypesthesia and motor weakness, followed by respiratory failure. Cerebrospinal fluid analysis was suggestive of Guillain-Barre syndrome (GBS). Autonomic dysfunction was manifested as tachycardia and mild hypertension in the acute stage. Marked orthostatic hypotension persisted long after paresis was improved, indicating an atypical clinical course of GBS.
Adult↗
Prostacyclin biosynthesis and platelet function in autonomic dysfunction.
We measured urinary excretion of the principal metabolite of prostacyclin, PGI-M (2,3-dinor-6-keto-PGF1 alpha) in two patients with Shy-Drager syndrome and three with idiopathic orthostatic hypotension. All patients had a rise in blood pressure (30 +/- 6 mm Hg) after ingestion of 50 mg indomethacin. Urinary excretion of PGI-M was normal and fell 57 +/- 11% after administration of indomethacin. In two subjects, there was no evidence of any circulating inhibitor of platelet aggregation when hypotension was induced by upright posture or ingestion of a meal. Despite the efficacy of indomethacin, these patients with autonomic dysfunction did not show increased production of the vasodilator prostanoid prostacyclin.
6-Ketoprostaglandin F1 alpha↗
Severe autonomic dysfunction in an 11-year-old girl with generalised tetanus.
Tetanus can occur even after minor injuries, and proper immunisation status must be ascertained and documented in every surgical patient. Failure to do so can have dramatic consequences. An 11-year-old non-immunised girl was admitted to the intensive care unit with severe generalised tetanus 8 days following an open fracture of the right forearm. Although she was under deep sedation and received high doses of opiates while being paralysed and mechanically ventilated, she developed pronounced cardiovascular instability with tachycardia and periods of rapid changes between arterial hyper- and hypotension secondary to severe autonomic dysfunction. Her cardiovascular status only began to stabilise after 14 days under concomitant treatment with clonidine, magnesium sulphate and labetalol.
Autonomic Nervous System Diseases↗
Autonomic dysfunction, peripheral neuropathy, and depression.
A 15-year-old boy with diarrhea, dizziness, dysesthesias, and depression is described. On admission, his blood pressure was 110/84 reclining but less than 40 systolic while standing. Vibratory sensation and nerve conduction velocities were decreased in his lower extremities. CSF protein concentration was normal but sural nerve biopsy demonstrated generalized demyelination. Extensive toxicologic and metabolic screening proved unremarkable. Norepinephrine concentrations in plasma and urine, and CSF concentration of 3-methoxy-4-hydroxy phenylglycol (MHPG) were markedly reduced. The patient demonstrates a combination of autonomic dysfunction, peripheral neuropathy, and affective disorder. This collection of clinical and neurochemical findings represents a previously unreported entity involving a defect of both central and peripheral noradrenergic systems.
Adolescent↗
Secondary amyloidosis with severe autonomic dysfunctions.
A 46-year-old male underwent hemodialysis because of progressed glomerulo-nephritis. Since he suffered from severe diarrhea during the course of the illness, both gastric and colon biopsies were performed. Significant amyloid deposition was recognized in the submucosal layer of these specimen. This amyloid was positive for anti-AA-protein antibody staining and soluble in KMnO4 solution, indicating secondary induced amyloid. Despite of absence of orthostatic hypotension, examinations revealed extreme reduction in tears and salivary secretion, anhidrosis, a decrease in the coefficiency of variation of the cardiographic R-R interval, and a decrease in the accumulation of [123I]meta-iodobenzylguanidine (MIBG) in the heart, suggesting that severe glandular and visceral autonomic dysfunctions had occurred in the patient.
3-Iodobenzylguanidine↗
Hyperreactivity to nitrovasodilators in forearm vasculature is related to autonomic dysfunction in insulin-dependent diabetes mellitus.
BACKGROUND: The link between diabetes and vascular disease is poorly understood. Data regarding endothelial function in vivo in patients with insulin-dependent diabetes mellitus (IDDM) have been inconsistent with in vitro studies demonstrating hyperglycemia-induced impairments in endothelium-dependent vasodilation. METHODS AND RESULTS: We determined whether alterations in neural control of the vascular tone might contribute to blood flow responses to intrabrachial infusions of acetylcholine (ACh), sodium nitroprusside (SNP), and L-N-monomethyl-arginine (L-NMMA) in 22 men with IDDM (12 with normoalbuminuria. HbA1c = 8.6 +/- 0.3%; 10 with macroalbuminuria, HbA1c = 8.6 +/- 0.3%) and 11 matched normal men. Autonomic function was assessed from reflex vasoconstriction to cold, the blood pressure response to standing and hand grip, and heart rate variation, including spectral analysis, during controlled breathing, and the Valsalva maneuver. IDDM with macroalbuminuria exhibited hyperresponsiveness to both ACh and SNP compared with the patients with normoalbuminuria or normal subjects. Reflex sympathetic vasoconstriction to cold was severely impaired in the IDDM patients with macroalbuminuria (-19 +/- 6%) compared with normoalbuminuric patients (-39 +/- 5%, P < .05) and normal subjects (-54 +/- 7%, P < .001). The macroalbuminuric patients also had evidence of autonomic dysfunction during controlled and deep breathing tests and during the Valsalva maneuver. Within the group of IDDM patients, neither the urinary albumin excretion rate nor other parameters such as HbA1c or serum cholesterol correlated with forearm blood flow during the vasoactive drug infusions. There were, however, significant inverse correlations between several measures of both sympathetic and parasympathetic autonomic functions and vascular hyperresponsiveness to SNP and ACh. For example, the Valsalva ratio was inversely correlated with the increase in blood flow in response to infusion of 3 (r = -.74, P < .001) and 10 (r = -.73, P < .001) micrograms/min SNP and 7.5 (r = -.73, P < .001) and 15 (r = -.75, P < .001) micrograms/min ACh. CONCLUSIONS: These data are consistent with idea that altered neurotransmission is an important determinant of vascular reactivity of diabetic blood vessels to nitrovasodilators in vivo.
Acetylcholine↗
Non-dipping is a potent predictor of cardiovascular mortality and is associated with autonomic dysfunction in haemodialysis patients.
BACKGROUND: Lack of nocturnal blood pressure (BP) fall (non-dipping) is common among haemodialysis (HD) patients, but much less is known regarding its association with cardiovascular (CV) disease morbidity and mortality. METHODS: Eighty HD patients initially underwent 24 h ambulatory BP monitoring (ABPM), and then they were defined as either 'dippers' (n=24, nocturnal BP fall > or = 10%) or 'non-dippers' (n=56, fall <10%). Coronary angiography was performed in the patients who had signs and/or symptoms of coronary artery disease (CAD). Twenty-four hour ambulatory ECG was recorded in 20 dippers and 20 non-dipper HD patients, and in 20 normal subjects. All patients were followed for up to 5.8 years (33.0+/-19.1 months). The outcome events studied were the hospitalisations due to CV diseases and CV death. RESULTS: Compared with dippers, non-dippers initially had a higher incidence of coronary artery stenosis (P<0.05) along with left ventricular asynergy (both Ps<0.01). The circadian rhythm of autonomic function was impaired in non-dippers. The incidences of CV events and CV deaths were 3.5 and 9 times higher in non-dippers than in dippers. The cumulative CV event-free survival and CV survival rates were lower in non-dippers than in dippers (P=0.02 and P=0.005, respectively). Based on Cox analysis, non-dipping was associated positively with CV events and CV mortality [hazard ratio (HR) 2.46, 95% CI 1.02-5.92, P=0.038 and HR 9.62, 95% CI 1.23-75.42, P=0.031, respectively]. Meanwhile, nocturnal systolic BP fall, diurnal systolic BP and diurnal pulse pressure were negatively associated with CV event/death. The clinic BP was not associated with CV event/death. CONCLUSIONS: The non-dipping phenomenon is closely related to a high incidence of CV diseases, a poor long-term survival and profound autonomic dysfunction. ABPM is useful in predicting long-term CV prognosis in HD patients.
Aged↗
Cardiovascular parameters: sensitivity to detect autonomic dysfunction and influence of age and sex in normal subjects.
In 137 healthy volunteers between 18 and 85 years of age, blood pressure (BP) and heart rate (HR) were measured continuously with the Finapres device during active change of posture (ACP), i.e. standing upright, passive tilt (PT, i.e. head-up tilt), Valsalva manoeuvre (VM), deep breathing (DB), isometric muscle exercise (IME) and a mental arithmetic task (MA). Mean HR activation was attenuated with increasing age in all manoeuvres, but was unrelated to sex. In non-orthostatic challenge procedures like MA and IME mean BP increases were independent of age and sex, despite lower increases in HR in the elderly. This points to a preserved sympathetic efferent activity. Following a forced fall in BP during ACP, PT and VM, the initial responses and maintenance values of BP showed a significant age-related decrease. This finding was strongly related to lower BP values in males compared with females, which became more pronounced with increasing age. Further studies to investigate age-related changes in the activation of the various components of the cardiovascular regulation need to consider the mode of activation of the autonomic nervous system and sex as factors of influence. Normal ranges, and also some new points in time not previously measurable, were calculated for all standard autonomic tests based on the continuous measurement of BP and HR. The minimum length of time necessary to assess the cardiovascular responses during ACP and PT was found to be 60 s. The upper time limits for reaching maximum activation during IME and MA were 3.5 min and 1 min, respectively. Age had a relevant influence on the lower limits of normal of all HR parameters and of some BP measurements during PT, ACP and VM. Sex was found to have no relevant impact on normal ranges. Over 65 years of age the normal values for HR activation during VM and DB hardly exceeded baseline values. The possibility of increasing the sensitivity of detection of autonomic dysfunction by measuring BP continuously must be approached with caution, as sufficient sensitivity was only reached at the lower limits of normal during late phase II of the VM. The initial increase of HR after ACP and the BP values after 60 s standing time proved to be the parameters with the best sensitivity for detecting an affection of the regulation of HR and BP over the whole range of age.
Adolescent↗