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At least 19 recordsLinked to original sources

Atrial fibrillation associated with autonomic dysreflexia.

Autonomic dysreflexia is an acute disorder of autonomic homeostasis occurring in persons with spinal cord lesions above the major splanchnic sympathetic outflow. Atrial fibrillation is a serious cardiac arrhythmia characterized by disorganized atrial depolarization and an irregular ventricular response. Previously reported complications of autonomic dysreflexia have included seizures, strokes and cardiac arrhythmias other than atrial fibrillation. We present a 60-yr-old man with C-5 incomplete quadriplegia in whom atrial fibrillation was apparently induced by an episode of autonomic dysreflexia. Mechanisms by which autonomic dysreflexia may cause this arrhythmia include altered cardiac autonomic tone as well as atrial distention. The simultaneous occurrence of autonomic dysreflexia and atrial fibrillation poses special diagnostic problems and treatment risks. Atrial fibrillation incidence increases with age in the general population. With the aging of the spinal cord-injured population, we expect to see more episodes of atrial fibrillation associated with autonomic dysreflexia.

Atrial Fibrillation↗

Catecholamines response of high performance wheelchair athletes at rest and during exercise with autonomic dysreflexia.

Autonomic dysreflexia presents a special situation in high-lesion spinal cord injury, however, intentionally or self-induced autonomic dysreflexia directly before or during competition to increase performance, so called 'boosting', is also being reported. In order to examine the influence of autonomic dysreflexia on plasma catecholamines, cardiocirculatory and metabolic parameters, 6 spinal cord injured wheelchair athletes with high-level lesions underwent wheelchair ergometry without (ST1) and with (ST2) autonomic dysreflexia. At the point of exhaustion significantly higher values for norepinephrine and epinephrine were observed in ST2 than in ST1. During autonomic dysreflexia a significantly higher peak performance (77.5 vs. 72.5 watt), higher peak heart rate (161 vs. 149 x min(-1)), and peak oxygen consumption (1.96 vs. 1.85 l x min(-1)), with comparable peak lactate (7.11 vs. 7.00 mmol x l(-1)) were reached on average. The blood pressure values in ST2 were partially hypertensive and higher than in ST1. In conclusion, autonomic dysreflexia, as a sympathetic spinal reflex, leads to a higher release of catecholamines during exercise. This results in higher peak performance, peak heart rate, peak oxygen consumption, and higher blood pressure values. The peak lactate, as an indicator of the anaerobic lactate metabolism, was unchanged. However, autonomic dysreflexia presents an unpredictable risk, caused predominantly by hypertensive blood pressure values, for high-lesion spinal cord injured persons at rest and more so during exercise; it is seen as a prohibited manipulation by the doping guidelines of the International Paralympic Committee.

Adult↗

Genetic approaches to autonomic dysreflexia.

Autonomic dysreflexia is a potentially life-threatening condition in which episodic hypertension occurs after injuries above the mid-thoracic segments of the spinal cord. Despite the seriousness of this condition, little is known of the molecular mechanisms that lead to its development. The completed sequencing of the mouse genome, its dense genetic map, and the large repository of engineered and spontaneous mouse mutants, make the mouse an ideal model organism in which to study the molecular mechanisms underlying autonomic dysreflexia. We subjected two wild-type strains of mice, 129Sv and C57BL/6, and one spontaneous mouse mutant, Wallerian degeneration slow (Wld s), to spinal cord transection and clip-compression injury. We found that the incidence of autonomic dysreflexia is greatly reduced, compared to spinal cord-transected wild-type mice, in Wld s mice after both injury paradigms and in 129Sv and C57BL/6 that have undergone the clip-compression injury. We also found that the amplitude of the dysreflexic response was greater in cord-compressed 129Sv than in C57BL/6 mice. These results implicate axonal degeneration as an important source of signals that trigger the development of autonomic dysreflexia and are discussed in the context of mouse genetics, interstrain differences and possible molecular mechanisms underlying autonomic dysreflexia after spinal cord injury.

Animals↗

The effect of modified transurethral sphincterotomy on autonomic dysreflexia.

Autonomic dysreflexia continues to be a major problem in spinal cord injury patients. In our report 16 patients with spinal cord lesions above the T6 level and a history of autonomic dysreflexia also had detrusor-sphincter dyssynergia. Of these patients 12 (75 per cent) had evidence of dysreflexia during cystometry. In addition, the dysreflexic response in blood pressure was shown to correlate with the high intravesical and urethral pressures measured during cystometry. Modified transurethral sphincterotomies subsequently were performed on all patients as recommended therapy for detrusor-sphincter dyssynergia. Repeat cystometry revealed significant decreases in intravesical and urethral pressures compared to before sphincterotomy (p less than 0.001) along with an associated significant decrease in blood pressure (p less than 0.01). Other dysreflexic responses also were markedly attenuated. These results suggest an association among detrusor-sphincter dyssynergia, high intravesical and urethral pressures, and autonomic dysreflexia. Our data indicate further that the frequency and magnitude of autonomic dysreflexia can be diminished significantly by modified external sphincterotomy.

Adult↗

Complications of autonomic dysreflexia.

Autonomic dysreflexia can be a life-threatening problem if not promptly recognized and treated. Since the most common cause is bladder distension it is essential that the urologist be familiar with this syndrome. Several patients with serious complications owing to autonomic dysreflexia, including 1 mortality, are presented. The complications of autonomic dysreflexia result from a sudden marked rise in blood pressure, which may be severe enough to rupture single or multiple cerebral blood vessels or lead to a considerable increase in intracranial pressure. The neurophysiology, clinical features and therapeutic measures are discussed.

Adolescent↗

Ovarian cyst and autonomic dysreflexia.

Autonomic dysreflexia may present itself as a medical emergency in quadriplegics and paraplegics above the T6 level. Common causes are bladder/bowel dysfunction and pressure ulcers. A case study is presented in which an ovarian cyst was the cause of autonomic dysreflexia. Excision of the ovarian cyst stopped recurrence of paroxysmal hypertension and completely alleviated signs and symptoms of autonomic dysreflexia.

Adult↗

Rehabilitation medicine: 1. Autonomic dysreflexia.

Autonomic dysreflexia is an acute syndrome of excessive, uncontrolled sympathetic output that can occur in patients who have had an injury to the spinal cord (generally at or above the sixth thoracic neurologic level). It is caused by spinal reflex mechanisms that remain intact despite the patient's injury, leading to hypertension. This review describes the clinical features of autonomic dysreflexia, its common causes (most frequently stimulation of the lower urinary tract) and a recommended approach to treatment. The condition can nearly always be managed successfully, but prompt recognition is essential--without treatment there may be dire consequences, including death.

Adult↗

Pathophysiology involved in autonomic dysreflexia.

Autonomic dysreflexia has potentially life-threatening consequences in quadriplegics and high paraplegics. Seizures, subarachnoid hemorrhage, and fatal stroke may result. This article explains the pathophysiology of autonomic dysreflexia. Appropriate nursing interventions to prevent serious complications are described.

Autonomic Nervous System Diseases↗

Management of autonomic dysreflexia.

Autonomic dysreflexia is a syndrome that affects those with a spinal cord lesion above the mid-thoracic level. The symptoms of the syndrome, its causes, how to recognise it, and how to alleviate it are described. The author explains how patients can be educated to recognise the symptoms of the condition, and take action to alleviate them.

Algorithms↗

Seizures and cortical blindness after meglumine (hypaque) administration: a variant of autonomic dysreflexia.

Autonomic dysreflexia (AD) is a syndrome that consists of facial flushing, excessive sweating, nasal congestion, throbbing headache and paroxysmal hypertension which may occur in response to bladder distension in patients with spinal cord lesions above the T6 level. We report the case of a C2 quadriplegic patient who developed clinical features of AD along with cortical blindness and seizures after administration of meglumine (Hypaque) for diagnostic cystogram.

Adult↗

Autonomic dysreflexia.

Autonomic dysreflexia (AD) may complicate spinal cord injured (SCI) subjects with a lesion level above the sixth thoracic level. There are several ways to remove triggering factors and, furthermore, new trigger mechanisms may be added by the introduction of new treatments. New data about the pathogenic mechanisms have been suggested in recent years as well as signs of metabolic effects associated with the reaction. This review of the syndrome includes clinical aspects of the AD reaction; the known pathogenic mechanisms, the incidence and prevalence and triggering factors. AD is associated with some cases of severe morbidity, including cerebral haemorrhage, seizures and pulmonary oedema. Symptomatic as well as specific treatments are discussed. Finally, some further questions are raised by the necessity of a proper definition of the syndrome, the revealing of the underlying pathophysiology, and new investigations concerning incidence and prevalence.

Autonomic Nervous System Diseases↗

Surgical aspects of autonomic dysreflexia.

Autonomic dysreflexia (AD) is a characteristic syndrome that occurs in spinal cord injury (SCI) patients with lesions above the sympathetic outflow at T6 and rarely in those with lesions below T10. Symptoms are initiated by noxious stimuli below the level of injury which result in massive sympathetic discharges from the isolated cord. These produce what may be called a sympathetic storm manifest by severe life threatening hypertension. Anesthesiologists and surgeons dealing with SCI patients must know how to recognize this syndrome, how to prevent its occurrence and how to manage it aggressively. Choice of anesthesia is frequently difficult and, in particular, it may be difficult to decide which type of anesthesia is best for patients susceptible to the syndrome. Therefore, we have conducted a retrospective study of SCI patients in the Department of Veterans Affairs Medical Center, Long Beach, California, where the Spinal Cord Injury Service is one of the largest in the country.

Adult↗

Long-term follow-up of sphincterotomy in the treatment of autonomic dysreflexia.

Autonomic dysreflexia (AD) is a syndrome affecting a majority of patients with high spinal cord lesions. An association between AD and detrusor-sphincter dyssynergia (DSD) is often seen. Between 1980 and 1988 we performed 51 transurethral sphincterotomies in 38 patients. Twelve of these patients underwent procedures primarily for the prevention of AD related to bladder distension. This study presents their long-term follow-up. One patient was lost to follow-up secondary to unrelated death; the remaining 11 patients were followed on average 117.5 months (94-154) after the initial operative procedure. Repeat sphincterotomy was required in 9 of 11 patients (82%). Six (66%) of these were performed within 24 months. One patient (11%) required delayed sphincterotomy greater than 100 months from the initial procedure. Overall, sphincterotomy was successful in controlling symptoms of AD in 10 of 11 (91%) patients. No major complications were recorded. Sphincterotomy is a safe and effective treatment for AD associated with DSD, however long-term urologic follow-up and management are necessary.

Adult↗

Autonomic dysreflexia revisited.

Autonomic dysreflexia (AD) is a clinical phenomenon that affects patients with spinal cord injury (SCI) above the major sympathetic outflow tract. The lesion is most often at or above the T-6 level. Any noxious stimuli below this level initiate reflex sympathetic activity resulting in life threatening hypertension uncontrollable by the feedback parasympathetic activity. The episodes of hypertension generally persist until the offending stimulus is removed. Absence of higher control over reflex sympathetic activity due to transection of the cord is an anatomical explanation of the phenomenon. Current evidence suggests additional factors such as supersensitivity and possibly increased numbers of spinal alpha adrenoreceptors and peripheral microvascular adrenoreceptors as well as accumulation of substance P below the lesion. It has been suggested that substance P acts as a modulator, initiating the sympathetic event to produce a strong, slow and prolonged excitatory action. Autonomic dysreflexia is further accentuated by the absence of gamma amino benzoic acid (GABA), norepinephrine (NE) and 5-hydroxytryptamine (5-HT) below the lesion. GABA is an inhibitory neurotransmitter. It has been suggested that either NE or 5-HT may also act as an inhibitory neurotransmitter. Resetting of the baroreceptors at a lower level also plays an important role. The anatomical transection at or above T-6 then helps in maintaining and accentuating the biochemical changes that develop in patients with high spinal cord lesions. The current article reviews the pathophysiology and management of this potentially life threatening, yet easily treatable, phenomenon.

Autonomic Nervous System Diseases↗

Autonomic dysreflexia presenting as a severe headache.

Hypertension, bradycardia, and severe headache have been associated with autonomic dysreflexia. Autonomic dysreflexia affects those with spinal transection above the level of T6 after plastic changes of the afferent pathways. This restructuring in the presence of noxious stimuli below the level of the lesion leads to autonomic dysreflexia. The onset of the first episode of autonomic dysreflexia has been documented as soon as 30 days and as late as 13 years after the injury. This report presents a case study of a paraplegic man 8 years after injury with autonomic dysreflexia associated with a urinary tract infection.

Adult↗

Autonomic dysreflexia in traumatic myelopathy.

Autonomic dysreflexia is a syndrome which occurs in patients with lesions of the spinal cord above T6, and it is characterized by exaggerated autonomic responses to stimuli which are innocuous in normal individuals. Clinical features of 68 patients with autonomic dysreflexia in traumatic myelopathy are presented and special attention is drawn to ocular manifestations of autonomic dysreflexia. The symptoms, signs, laboratory findings, differential diagnosis, pathophysiology and management have been critical analysed and pertinent literature has been extensively reviewed. A plea is made for those involved in the management of spinal cord injury patients (irrespective of specialty) to be aware that autonomic dysreflexia can be a life-threatening problem if not promptly recognized and appropriately treated.

Adolescent↗

Autonomic dysreflexia.

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Autonomic Nervous System Diseases↗