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Books on the topic 'Autonomic neuropathy'

Author: Grafiati

Published: 4 June 2021

Last updated: 20 February 2023

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1

Gilbey, Stephen George. Studies in diabetic autonomic neuropathy. Birmingham: University of Birmingham, 1988.

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2

Javorka, Michal. Cardiovascular signals in diabetes mellitus: A new tool to detect autonomic neuropathy. Hauppauge, N.Y: Nova Science, 2009.

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3

Low, Phillip A. Autonomic Neuropathies. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0118.

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Autonomic neuropathy is a peripheral neuropathy with selective or disproportionate involvement of autonomic fibers. Because autonomic nerves innervate all organ systems, the manifestations of dysautonomia are protean. There are many causes of the autonomic neuropathies (Table 118.1). Some of the disorders in Table 118.1 are described in detail in other chapters. This chapter provides a brief description of the autonomic neuropathies, going from the acute/subacute to the more slowly evolving categories and finishing with some entities with less generalized dysautonomia.

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4

Publications, ICON Health. Autonomic Neuropathy - A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References. ICON Health Publications, 2004.

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5

Keltner, John R., Cherine Akkari, and Ronald J. Ellis. Neurological Complications of HIV in The Peripheral Nervous System. Edited by Mary Ann Cohen, Jack M. Gorman, Jeffrey M. Jacobson, Paul Volberding, and Scott Letendre. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199392742.003.0027.

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HIV sensory neuropathy affects approximately 50% of persons diagnosed with HIV and, in 40%, results in disabling symptoms including paresthesia and/or pain. This chapter focuses on providing guidance to psychiatrists in the clinical management of pain in persons with HIV and sensory neuropathy. The differential diagnostic evaluation of HIV sensory neuropathy, other peripheral neuropathies, and spinal cord mimics and management of HIV sensory neuropathy are reviewed, as well as management of HIV distal neuropathic pain. The differential diagnostic evaluation of peripheral neuropathies is simplified using a graphical decision tree. The chapter also reviews the pathophysiology of HIV sensory neuropathy and warning signs of advanced disease. Procedures to diagnose HIV sensory neuropathy, including nerve conduction studies and electromyography, quantitative sensory testing, skin biopsy, and the autonomic sweat test are discussed, as are clinical aspects of HIV distal neuropathic pain. The chapter addresses the impact of HIV distal neuropathic pain on quality of life and depression and concludes with a discussion of treatments for HIV distal neuropathic pain.

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6

Cohen, Jeffrey A., Justin J. Mowchun, Victoria H. Lawson, and Nathaniel M. Robbins. A 50-Year-Old Woman with Burning Feet. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190491901.003.0020.

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Small-fiber neuropathy typically presents with burning pain or with widespread brief stabbing pains, by atypical presentations including asymmetric sensory symptoms are common. Nerve conduction studies are usually normal, as this disorder test only interrogates large fiber function; in small-fiber neuropathy the pathology is restricted to smaller unmyelinated fibers. Autonomic neuropathy can accompany the painful peripheral neuropathy but can be difficult to recognize since the symptoms can be protean. In this chapter, clinical characteristics of small-fiber and autonomic neuropathy are discussed. Various diagnostic modalities are described, including the benefits and pitfalls of available options. The most common conditions causing small-fiber and autonomic neuropathy are reviewed. The controversy surrounding impaired glucose tolerance as an etiological factor is dicusssed. We discuss the available medications and outline a rational approach to treatment.

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7

Hartwig, Mary Steen. THE RELATIONSHIP OF DIABETIC AUTONOMIC NEUROPATHY TO IMPAIRED FUNCTIONAL ABILITY IN PERSONS WITH INSULIN-DEPENDENT DIABETES MELLITUS. 1993.

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8

Cohen, Jeffrey A., Justin J. Mowchun, Victoria H. Lawson, and Nathaniel M. Robbins. A 44-Year-Old Male with Subacute Onset of Syncope. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190491901.003.0032.

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Syncope in a patient with orthostatic hypotension (OH) may indicate autonomic dysfunction. The definition of OH is presented. Clinical features of parasympathetic and sympathetic function are discussed. The differential of acute autonomic dysfunction includes a number of conditions. An autoimmune etiology may occur autoimmune autonomic ganglionopathy. Serologic testing can assist in this diagnosis. If autoimmune immune modulating therapies may be indicated. Autonomic neuropathy may be a paraneoplastuc syndrome. Autonomic testing can also help with documenting autonomic neuropathy as well as the whether the defects are predominately parasympathetic or sympathetic. Amyloid should be considered as should diabetes but both have a more chronic course. An appropriate tissue biopsy with Congo Red staining can help to confirm the diagnosis of amyloid.

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9

Pitt, Matthew. Pathophysiological correlations in neuropathies. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198754596.003.0004.

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This chapter begins with an explanation of the pathophysiological correlations between the recorded changes and the underlying diagnosis which allow classification into demyelinating and axonal neuropathy. Demyelinating neuropathies are discussed first. The extensive and ever expanding literature in hereditary neuropathies is highlighted. The different variants of the acute inflammatory demyelinating polyneuropathy encountered in children are discussed along with the electrodiagnostic criteria for the diagnosis. Chronic inflammatory demyelinating polyneuropathy is then covered, both in its clinical presentation and electrodiagnosis. Other causes such as MNGIE and Lyme disease are highlighted. In the section on axonal neuropathy, division into hereditary and acquired is made. The diagnosis of sensorimotor hereditary neuropathies is discussed along with primarily sensory neuropathies including ataxia telangiectasia, Friedreich’s ataxia, and abetalipoproteinaemia, finishing with discussion of the hereditary sensory and autonomic neuropathies. The many different causes of acquired axonal neuropathy are listed and discussed including neoplasia, endocrine disturbances, metabolic conditions, infective agents, autoimmune conditions, mitochondrial disease, drugs, and vitamin deficiency, finishing with critical illness neuromyopathy.

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10

Waldmann, Carl, Neil Soni, and Andrew Rhodes. Physical disorders. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199229581.003.0029.

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Hypothermia 498Drowning and near-drowning 500Rhabdomyolysis 502Pressure sores 504Defined as core temperature <35°CMild 32–35°C; moderate 26–32°C; severe <26°CIncreasing age, abnormal mental state, immobility (orthopaedic, Parkinsonism), drugs (alcohol, barbiturate, major tranquillizers, antidepressants), endocrine (hypothyroidism, hyperglycaemia, adrenal insufficiency, hypopituitarism), autonomic neuropathy (diabetes mellitus, Parkinsonism), malnutrition, renal failure, sepsis (excessive heat loss from vasodilatation), exposure (inadequate clothing/eating, near drowning)....

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11

Mittal, Sajjan. Amyloidosis. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0181.

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Amyloidosis is a multisystem disease caused by the extracellular deposition of insoluble abnormal fibrils that injure tissues and organs. The fibrils are formed by the aggregation of misfolded, normally soluble proteins. Systemic amyloid light-chain (AL) amyloidosis (primary amyloidosis) is the commonest type of amyloidosis in the developed world, accounting for 80% of cases. The remainder are due to AA amyloidosis (secondary or reactive amyloidosis), familial amyloidosis, or other rare types of amyloidosis. The most common clinical features at diagnosis are nephrotic syndrome, heart failure (typically with predominant right heart failure), sensorimotor and/or autonomic peripheral neuropathy, and hepatosplenomegaly.

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12

Strian, Friedrich, and Andrea J. S. Hin. Autonome Neuropathie bei Diabetes mellitus. Springer, 2012.

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13

Ploog, D., Friedrich Strian, Manfred Haslbeck, and H. Mehnert. Autonome Neuropathie Bei Diabetes Mellitus. Springer London, Limited, 2013.

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14

Cuocolo, Alberto, and Emilia Zampella. Role of Imaging in Diabetes Mellitus. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199392094.003.0018.

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Although there has been a marked decline in mortality due to coronary artery disease (CAD) in the overall population in the past three decades, reducing CAD mortality in patients with diabetes mellitus (DM) has proven exceptionally difficult. Several epidemiological studies have shown that DM is associated with a marked increase in the risk of CAD. The symptoms are not a reliable means of identifying patients at higher risk considering that angina is threefold less common in DM than in non-DM. Noninvasive cardiac imaging, such as echocardiography, nuclear cardiology, computed tomography, and magnetic resonance imaging, can provide insight into different aspects of the disease process, from imaging at the cellular level to microvascular and endothelial dysfunction, autonomic neuropathy, coronary atherosclerosis, and interstitial fibrosis with scar formation. In particular, stress myocardial perfusion imaging has taken a central role in the diagnosis, evaluation, and management of CAD in DM patients.

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15

Flower, Oliver, and Raymond Raper. Ongoing management of the tetraplegic patient in the ICU. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0345.

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This chapter focuses on the intensive care management of patients who have suffered cervical spinal cord injury (CSCI). This includes new CSCI, following initial resuscitation and stabilization, and the common issues faced when managing longstanding tetraplegic patients who require critical care. For patients with a new diagnosis of CSCI, a comprehensive systems-based approach is suggested covering topics including terminology, the standardized neurological examination, muscle spasticity, neuropathic pain, venous thromboembolism prophylaxis, as well as renal, gastrointestinal, and pressure care considerations. Particular attention should be paid to respiratory care, including ventilation strategies, tracheostomy, and the management of respiratory complications. The importance of early rehabilitation and appropriate psychosocial support is discussed. Common critical care issues affecting patients with chronic tetraplegia include autonomic dysreflexia, respiratory failure, peri-operative care, sepsis and complications of indwelling intrathecal devices.

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16

Levy, David. Management of microvascular and associated complications. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198766452.003.0007.

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While end-stage microvascular complications are now relatively uncommon, the burden of microvascular disease is still heavy. National diabetic retinopathy screening programmes have contributed to reducing advanced retinal disease, as has improved laser technology and vitreoretinal surgery. More recently intravitreal anti-VEGF agents (bevacizumab, ranibizumab, and aflibercept) have been effective in reducing visual loss from macular oedema. Diabetic nephropathy has a variable phenotype, and high rates of natural regression from microalbuminuria to normoalbuminuria mandate careful and regular review with regular urinary albumin-creatinine ratio (ACR) measurements. Up to one-quarter of patients with renal impairment have never had microalbuminuria. Long-term glycaemic control is the most important treatment for early diabetic nephropathy; angiotensin blockade treatment (ACE-inhibitors, angiotensin receptor blockers) are less important. In established diabetic nephropathy, intensive multimodal treatment is needed. Neuropathic complications are usually plantar ulceration, Charcot neuroarthropathy, and autonomic, especially gastroparesis and erectile dysfunction.

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