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Books on the topic 'Polyneuropaty'

Author: Grafiati
Published: 4 June 2021
Last updated: 2 February 2022

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1

Lawson, Erin, and Miroslav "Misha" Backonja, eds. Painful Diabetic Polyneuropathy. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6299-6.

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2

Evers, Eileen. CIDP (Chronic Inflamatory Demyelinating Polyneuropathy): A guide for patients, relatives and friends. 2nd ed. Leaford: GBS Support Group, 1998.

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3

International, Symposium on Familial Amyloidotic Polyneuropathy and Other TTR Related Disorders (3rd 1995 Lisbon Portugal). Abstracts from the third International Symposium on Familial Amyloidotic Polyneuropathy and Other TTR Related Disorders: 2nd International Workshop on Liver Transplantation in FAP ; held in Lisbon, 27-29 October 1995. London: Pergamon, 1996.

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4

Donaghy, Michael. Polyneuropathy. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569381.003.0453.

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Typically polyneuropathy will cause the combination of distal limb muscle weakness, loss of tendon reflexes, and reduced distal limb sensation. There is variable involvement of the autonomic innervation, damage to which causes a dry, vasodilated foot or hand. Loss of tendon reflexes is a cardinal sign of polyneuropathy, often restricted to the ankle jerks in axonal degeneration, but involving more proximal reflexes in acquired demyelinating neuropathies which may involve more proximal segments or the nerve roots. Clinical features suggestive of demyelinating or conduction block polyneuropathy include: a relative lack of muscle wasting in relation to the degree of weakness because no denervation has occurred; weakness of proximal muscles as well as distal, because of nerve root involvement; and disproportionate loss of joint position and vibration sensations compared to relative preservation of pain and temperature sensations which are carried by unmyelinated fibres.
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5

Miller, Aaron E., and Teresa M. DeAngelis. Chronic Inflammatory Demyelinating Polyneuropathy. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199732920.003.0025.

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The diagnostic approach to a patient with chronic peripheral neuropathy can be daunting, with several candidate etiologies. In this chapter, we review the typical symptomatology, temporal course, examination, and laboratory findings, which raise suspicion for chronic inflammatory demyelinating polyneuropathy, and discuss the available therapeutic modalities.
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6

Reilly, Mary M. Genetic studies of familial amyloid polyneuropathy. 1996.

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7

Familial Amyloid Polyneuropathy Therapeutics Market Analysis. https://www.fortunebusinessinsights.com/familial-amyloid-polyneuropathy-therapeutics-market-102086, 2020.

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8

Miller, Aaron E., and Teresa M. DeAngelis. Acute Inflammatory Demyelinating Polyneuropathy (Guillain-Barré Syndrome). Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199732920.003.0024.

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Acute inflammatory demyelinating polyneuropathy (AIDP), also known as Guillain-Barré syndrome (GBS), is a common acute neurological presentation encountered in both the outpatient setting and hospital wards. The hallmark of the disorder is the development of ascending motor paralysis with loss of deep tendon reflexes. In this chapter, we outline the classical clinical and laboratory findings in GBS as well as critical therapeutic and supportive measures along with prognosis.
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9

Bozzetto Ambrosi, Patricia, ed. Demystifying Polyneuropathy - Recent Advances and New Directions. IntechOpen, 2019. http://dx.doi.org/10.5772/intechopen.73946.

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10

Lawson, Erin, and Miroslav "Misha" Backonja. Painful Diabetic Polyneuropathy: A Comprehensive Guide for Clinicians. Springer, 2016.

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11

Lawson, Erin, and Miroslav "Misha" Backonja. Painful Diabetic Polyneuropathy: A Comprehensive Guide for Clinicians. Springer, 2015.

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12

Painful Diabetic Polyneuropathy A Comprehensive Guide For Clinicians. Springer-Verlag New York Inc., 2013.

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13

Lawson, Erin, and Miroslav Backonja. Painful Diabetic Polyneuropathy: A Comprehensive Guide for Clinicians. Springer, 2013.

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14

Hinder, Lucy M., Kelli A. Sullivan, Stacey A. Sakowski, and Eva L. Feldman. Mechanisms Contributing to the Development and Progression of Diabetic Polyneuropathy. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0114.

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Advances in our understanding of diabetes in human patients and experimental models indicate that a number of mechanisms may contribute to sensory nerve damage in diabetic polyneuropathy (DPN). In addition to oxidative stress, hyperglycemia and hyperlipidemia, recent research in pain, advanced glycation endproduct (AGE), and proteomics specify a contributory role for altered neuronal calcium homeostasis in DPN. Technology advances indicate neuronal energy balance and mitochondrial biogenesis, fission, and fusion are additional potential mechanisms. The effects of dysregulation or loss of insulin signaling and the effects of glucagon-like peptide-1 (GLP-1) and its receptor (GLP-1R) are also implicated.
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15

Cohen, Jeffrey A., Justin J. Mowchun, Victoria H. Lawson, and Nathaniel M. Robbins. A 41-Year-Old Male with Foot Drop and Malaise. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190491901.003.0018.

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Distal, symmetric polyneuropathy can occur in a number of conditions including in association with HIV infection. The most common neurologic complication of HIV infection is a painful, distal sensory polyneuropathy (HIV-DSP). Other neuromuscular manifestations of HIV are myriad especially in the setting of fluctuating immunocompetence and the potential impact of neurotoxic medications. In the patient described in the case, peroneal neuropathy as the cause for foot drop is suggested by ankle dorsiflexion and eversion weakness with preservation of inversion and knee flexion strength. Mononeuropathy in the setting of HIV should prompt consideration of vasculitic, lymphomatous, and infectious causes, some of which can manifest with systemic findings. A rare neuromuscular complication of HIV-infected patients with sicca symptoms suggestive of Sjogren’s syndrome is diffuse infiltrative lymphocytosis syndrome. This syndrome can manifest as an acute or subacute painful sensory polyneuropathy but also as a mononeuropathy multiplex. This is discussed in the chapter.
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16

Katirji, Bashar. Case 26. Edited by Bashar Katirji. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190603434.003.0030.

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Peripheral polyneuropathy is a common clinical presentation, and most cases seen in clinical practice are axonal, dying-back, sensorimotor polyneuropathies. Axonal polyneuropathies should be distinguished from the acquired demyelinating peripheral polyneuropathies which are often immune-mediated and amenable to treatment. This case presents a typical patient with a dying-back sensorimotor axonal peripheral polyneuropathy and presents a practical approach to the etiologic diagnoses of peripheral neuropathy. It then highlights its distinguishing features on nerve conduction studies. A comparison between axonal and demyelinating polyneuropathies is revealed. An algorithmic approach to the workup of a patient presenting with a peripheral neuropathy is recommended.
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17

Katirji, Bashar. Case 7. Edited by Bashar Katirji. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190603434.003.0011.

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Diabetic amyotrophy is a relatively uncommon neurological complication of diabetes mellitus. However, the disorder is often not recognized by internists and neurologists and misdiagnosed as myopathy, radiculopathy, or peripheral polyneuropathy. The discussion starts by outlining the classification of the diabetic neuropathies. This case highlights the classical clinical presentation of diabetic amyotrophy, also referred to as diabetic polyradiculoplexopathy or subacute diabetic neuropathy, in a man with pain in the anterior thigh and knee followed by thigh and hip weakness. It also emphasizes the electrodiagnostic findings including the subacute needle electromyography changes and stresses the frequent coexistence of diabetic amyotrophy with the more common distal peripheral polyneuropathy in the majority of patients.
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18

Publications, ICON Health. The Official Patient's Sourcebook on Chronic Inflammatory Demyelinating Polyneuropathy: A Revised and Updated Directory for the Internet Age. Icon Health Publications, 2002.

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19

Leung, Doris G. Neuropathies Associated with Infection or Toxic Exposure. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0113.

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Among the many causes of peripheral neuropathy are those mediated by environmental exposure to infectious and toxic agents. The most common neuropathy associated with HIV is HIV-associated distal sensory polyneuropathy (HIV-DSP). The clinical presentation of HIV-DSP is one of a distal, symmetric, often painful, small-fiber sensory axonal polyneuropathy. Other infectious causes of neuropathy include hepatitis C, leprosy, Lyme disease, rabies, and diphtheria, and antibiotic drugs such as isoniazid can also cause neuropathy. Heavy metals and a variety of other toxins including chemotherapeutic agents such as platinum, vincristine, and thalidomide disrupt peripheral nerve function. High doses of pyridoxine can cause damage to the dorsal root ganglia and foodbourne toxins such as saxitoxins found in shellfish.
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20

Kaplan, Tamara, and Tracey Milligan. Demyelinating Diseases 2: NMO, ADEM, GBS, CIDP (DRAFT). Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190650261.003.0014.

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The video in this chapter explores demyelinating diseases, and focuses on neuromyelitis optica (NMO), acute disseminated encephalomyelitis (ADEM), Guillain-Barré syndrome (GBS) and chronic inflammatory demyelinating polyneuropathy (CIDP), including their symptoms, causes, and diagnostic tests.
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21

Katirji, Bashar. Case 18. Edited by Bashar Katirji. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190603434.003.0022.

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Immune-mediated polyneuropathies are important to recognize since the majority of them are treatable. Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is the prototype of the acquired chronic demyelinating polyneuropathies. It should be distinguished from other acquired demyelinating polyneuropathy such as those associated with monoclonal gammopathy, myeloproliferative disorder, and myelin-associated glycoprotein. This case presents a patient with a chronic demyelinating polyneuropathy associated with monoclonal gammopathy of unknown significance. The discussion includes the clinical and electrodiagnostic criteria for CIDP and distinguishing features from axonal polyneuropathies, other acquired demyelinating polyneuropathies, and inherited demyelinating polyneuropathies such as Charcot-Marie-Tooth disease type I. The case also highlights the diagnostic criteria for conduction block and temporal dispersion based on analysis of compound muscle action potential amplitude, area, and duration.
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22

Nageshwaran, Sathiji, Heather C. Wilson, Anthony Dickenson, and David Ledingham. Neuropathic pain. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199664368.003.0005.

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This chapter on neuropathic pain discusses the classification, clinical features, and evidence-based management of major neuropathic pain syndromes (painful polyneuropathy, diabetic neuropathy, post-herpetic neuralgia, HIV neuropathy, cancer neuropathic pain, phantom pain, traumatic neuropathic pain, chronic radiculopathy, central neuropathic pain, and trigeminal neuralgia).
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23

Kaplan, Tamara, and Tracey Milligan. Peripheral Nervous System 1: Neuropathy (DRAFT). Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190650261.003.0019.

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The video in this chapter explores the peripheral nervous system (PNS) and focuses on neuropathy. It outlines classifications of PNS injury (by process, etiology, distribution, affected fibers), examples of polyneuropathy, common mononeuropathies (carpal tunnel syndrome, ulnar neuropathy, radial neuropathy), and plexopathies (Erb Duchenne palsy, Klumpke’s palsy).
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24

Nageshwaran, Sathiji, Heather C. Wilson, Anthony Dickenson, and David Ledingham. Disorders of peripheral nerves and motor neuron disease. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199664368.003.0007.

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This chapter discusses the clinical features and evidence-based drug treatment regimens of polyneuropathies (Guillain–Barré syndrome (GBS), chronic inflammatory demyelinating polyneuropathy (CIDP), multifocal motor neuropathy, paraproteinaemic neuropathies, and vasculitic neuropathies), mononeuropathies (Bell’s palsy), systemic conditions with peripheral nerve involvement (Sjögren’s and sarcoidosis), and motor neuron disease (MND).
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25

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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26

Rosenbaum, Richard B. Systemic Lupus Erythematosus. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0192.

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The neurological manifestations of systemic lupus erythematosus are protean: headache, affective disorders, cognitive dysfunction, seizures, strokes, psychosis, acute confusional states, myelopathies, chorea, mimics of demyelinating disease, meningitis, polyneuropathy, mononeuropathy or mononeuritis multiplex, cranial neuropathies, autonomic dysfunction, Guillain-Barre syndrome, or myasthenia gravis make an incomplete list. Each neurological manifestation needs to be analyzed separately to understand pathogenesis, possible relation to primary lupus-related inflammation and vasculopathy, and optimal treatment.
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27

Jenkins, Liberty. Neuropathy. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0234.

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Neuropathy is disease of the peripheral nerves. The pathological process may affect the nerve at the root (radiculopathy), the dorsal root ganglion (ganglionopathy), the plexus (plexopathy), or anywhere along the terminal pathway, typically at sites of entrapment or in a length-dependent pattern. The cranial nerves may also be affected. The process may affect a single nerve (a mononeuropathy) or multiple discrete nerves (mononeuritis multiplex) or form a confluent, typically distal, and symmetrical pattern (polyneuropathy).
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28

Shaibani, Aziz. Dyspnea. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199898152.003.0009.

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The most common causes of dyspnea are not neuromuscular but rather are cardiac and pulmonary. However, dyspnea is an important and serious manifestation of many neuromuscular disorders, and it may compound an underlying pulmonary or cardiac problem. The diaphragm is a skeletal muscle under the control ofperipheral nerves(phrenic nerves) and may be targeted by inflammatory neuropathies such as Guillain-Barrésyndrome(GBS), chronic inflammatory demyelinating polyneuropathy(CIDP), and brachial plexitis, myopathies such as acid maltase deficiency and muscular dystrophies, and neuromuscular disorders such as myasthenia gravis. Periodic measurement of pulmonary function isrecommended in neuromuscular clinics.
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29

Franssen, Hessel. Generalized peripheral neuropathies. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199688395.003.0020.

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The chapter on generalized peripheral neuropathies describes how to perform and interpret electrophysiological studies aimed at diagnosing polyneuropathy. It first reviews methodological issues, such as stimulation and recording, and takes into account temperature. Next, the relevant pathophysiology of single myelinated axons, as found in animal experiments, is discussed and related to findings on nerve conduction studies performed in patients. This is followed by a discussion of criteria for axon loss and demyelination. Finally, typical findings in specific neuropathies are described and examples of typical findings are shown in the figures.
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30

Cohen, Jeffrey A., Justin J. Mowchun, Victoria H. Lawson, and Nathaniel M. Robbins. A 68-Year-Old Male with Progressive Numbness and Gait Difficulties. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190491901.003.0015.

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Paraproteinemic demyelinating peripheral neuropathies require specific diagnostic and management approaches. The clinical features as well as the type of monoclonal protein and possible associated antibodies are all important considerations in evaluation and management of these complex presentations. It is important to recognize anti-myelin associated glycoproteins positive peripheral neuropathy, which is associated with IgM gammopathy, and typically presents with a sensory ataxia. Hematologic disease may mimic chronic inflammatory demyelinating polyneuropathy. This chapter also describes the role of hematological evaluation for patients with peripheral neuropathy and a monoclonal gammopathy.
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31

Cohen, Jeffrey A., Justin J. Mowchun, Victoria H. Lawson, and Nathaniel M. Robbins. A 55-Year-Old Female with Slowly Progressive Weakness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190491901.003.0010.

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Chronic inflammatory demyelinating polyneuropathy (CIPD) typically presents with both proximal and distal weakness, areflexia, and distal sensory findings. Two-thirds of patients have a progressive course over many months to years, however one-third of patients have a relapsing course with partial or complete recovery. It is important to be aware of several systemic disorders which may be associated with CIDP. Immunoglobulin M antibody–producing neuropathies have a monoclonal protein that is usually detected with serum protein electrophoresis, which may mimic CIDP. This chapter emphasizes the importance of differential diagnosis and workup. Treatment options are also described.
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32

Shaibani, Aziz. Dyspnea. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190661304.003.0009.

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The most common causes of dyspnea are not neuromuscular, but rather cardiac and pulmonary. However, dyspnea is an important and serious manifestation of many neuromuscular disorders, and it may compound an underlying pulmonary or cardiac problem. The diaphragm is a skeletal muscle under the control of a peripheral nerve and may be targeted by inflammatory neuropathies such as Guillain-Barré syndrome (GBS), chronic inflammatory demyelinating polyneuropathy (CIDP), and brachial plexitis or myopathies such as acid maltase deficiency, muscular dystrophy (MD), and neuromuscular disorders such as myasthenia gravis (MG). Periodic measurement of pulmonary function is a recommended measure in neuromuscular clinics.
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33

Katirji, Bashar. Case 27. Edited by Bashar Katirji. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190603434.003.0031.

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Mononeuropathy multiplex is a disorder which distinguishes itself from peripheral polyneuropathy by involvement of specific individual peripheral nerves. Mononeuropathy multiplex is often asymmetrical and is classified, based on electrophysiologic and pathologic findings, into axonal and demyelinating types. Mononeuritis multiplex is a term that is used exclusively for cases of axonal multiple mononeuropathies due to peripheral nerve vasculitis. This may be associated with connective tissue disease or hepatitis B and C infection. This case outlines the clinical and electrophysiological findings in mononeuritis multiplex and discusses the differential diagnosis of systemic and nonsystemic vasculitic neuropathy. The causes and pathological findings that characterize vasculitic neuropathy are highlighted.
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34

Popadich, Miriana, and Thomas J. Wilson. Peripheral Nerve Biopsy. Edited by Meghan E. Lark, Nasa Fujihara, and Kevin C. Chung. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190617127.003.0013.

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Nerve biopsy is an important part of the diagnostic armamentarium in the evaluation of a number of diseases, including vasculitis, some hereditary neuropathies, toxic and metabolic neuropathies, inflammatory demyelinating conditions (such as chronic inflammatory demyelinating polyneuropathy), and neoplastic and nonneoplastic infiltrative diseases, such as sarcoidosis, amyloidosis, neurolymphomatosis, and other metastatic tumor infiltration. Options for nerve biopsy include whole-nerve biopsy (e.g., biopsy of the sural nerve, superficial peroneal nerve, or superficial sensory radial nerve) or targeted fascicular biopsy. This chapter identifies indications for nerve biopsy, discusses important considerations for choosing the biopsy target, and explains in detail the surgical procedure for common nerve biopsies.
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35

Shaibani, Aziz. Proximal Arm Weakness. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190661304.003.0012.

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Proximal arm muscles include supra and infra spinatii, pectoralis major and minor, teres major and minor, rhomboids, serratus anterior, deltoids, biceps, and triceps. The main function of these muscles is to abduct the arms. The first sign of proximal weakness is difficulty raising arms above the horizontal level. Shoulder conditions like supraspinatus tendonitis are often confused as proximal weakness. In myopathies, usually proximal arm weakness is associated with proximal leg weakness. Motor neuron diseases (MNDs) like amyotrophic lateral sclerosis (ALS) and spinal muscular atrophy (SMA) and neuropathies like chronic inflammatory demyelinating polyneuropathy (CIDP) may present with symmetrical proximal weakness. For differentiation, electromyography/nerve conduction study (EMG/NCS) is crucial.
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36

Shaibani, Aziz. Proximal Leg Weakness. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190661304.003.0013.

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Proximal leg weakness is a common presentation to neuromuscular clinics. Hip flexion, abduction, adduction, and rotation is mainly achieved by the iliopsoas, glutei, and obturator muscles. Hip pathology, especially when painless, may lead to diagnostic confusion that needs a good electromyogram (EMG) of these muscles to be cleared. Most myopathies present with painless proximal leg weakness (difficulty climbing stairs and arising out of a deep chair). chronic inflammatory demyelinating polyneuropathy (CIDP), diabetic amyotrophy, motor neuron diseases (MNDs), and lumbar plexitis may all present similarly. Pain is more typical of these conditions that myopathies. Students should be taught to avoid the assumption that proximal weakness is caused only by myopathies.
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37

Hough, Catherine L. The Impact of Critical Illness on Skeletal Muscle Structure. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199653461.003.0034.

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Patients with critical illness are at risk of profound weakness and skeletal muscle loss, and recovery is marked by prolonged physical functional impairment in many survivors. Muscle and nerve abnormalities found in critically ill patients include loss of muscle mass, muscle membrane inexcitability, polyneuropathy, mitochondrial dysfunction with bioenergetic failure, as well as changes in skeletal muscle structure. The most common histological abnormalities are atrophy of both type I and II fibres and thick filament loss; muscle necrosis is less common. While recent studies have illuminated the pathogenesis of critical illness myopathy, additional high-quality translational research is needed to identify targets for therapeutic intervention.
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38

Cornblath, David R., and Richard A. C. Hughes. Peripheral neuropathy. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199658602.003.0013.

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Disorders of peripheral nerves are one of the most common neurological problems today and include the increasing number of people with diabetes worldwide and those with inherited neuropathy, toxic neuropathy, carpal tunnel syndrome, inflammatory neuropathy, radiculopathies, and, increasingly, traumatic nerve injuries. Neuropathic pain is a growing problem without solution. In this chapter, ten landmark papers in peripheral nerve disorders have been selected, covering Bell’s palsy, Charcot-Marie-Tooth disease, carpal tunnel syndrome, paraneoplastic neuropathy, neurophysiology, familial amyloid polyneuropathy, chronic inflammatory demyelinating polyradiculoneuropathy, toxic neuropathy, diabetic neuropathy, and Guillain–Barré syndrome. These important papers set the stage for many subsequent advances in the field but may be forgotten now, so they are brought to the reader’s attention.
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39

Katirji, Bashar. Case 6. Edited by Bashar Katirji. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190603434.003.0010.

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Tarsal tunnel syndrome is relatively rare entrapment syndrome, and should be considered in patients with foot pain or numbness. It is the result of compression or entrapment of the tibial nerve or any of its three terminal branches under the flexor retinaculum. This case discusses a patient with typical manifestations of tarsal tunnel syndrome and highlights its causes, differential diagnosis and electrodiagnostic findings. It also covers the challenges in making an accurate diagnosis in view of the technical difficulties encountered with foot and sole nerve conduction studies. Tarsal tunnel syndrome is often overdiagnosed, since it may be confused with other more common causes of foot pain and numbness including plantar fasciitis, peripheral polyneuropathy, and S1 radiculopathy.
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40

Katirji, Bashar. Case 23. Edited by Bashar Katirji. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190603434.003.0027.

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Guillain-Barré syndrome is the prototype of acute immune-mediated neuropathies. Guillain-Barré syndrome has several subtypes including acute inflammatory demyelinating polyneuropathy, acute motor axonal neuropathy, and acute motor sensory axonal neuropathy. Guillain-Barré syndrome has also several variants including Miller Fisher syndrome, ataxic form, and pharyngeal–cervical–brachial form. This case highlights the clinical findings in Guillain-Barré syndrome and discusses in details the diagnostic criteria that are essential in confirming the diagnosis and excluding mimickers of the disorder. This is followed by a detailed discussion on the electrodiagnostic findings in Guillain-Barré syndrome during the acute presentation and recovery phase. The diagnostic sensitivity and specificity of the various findings seen on nerve conduction studies are included.
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41

Cohen, Jeffrey A., Justin J. Mowchun, Victoria H. Lawson, and Nathaniel M. Robbins. A 45-Year-Old Male with Toxin Exposure. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190491901.003.0004.

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A patient presents with a sensorimotor neuropathy and believes he has been poisoned. The approach to the differential diagnosis of arsenic toxicity is presented. Comparisons with mimics of this entity are made, and clinical clues to its early detection are provided. There are typical skin and nail changes with can occur with arsenic poisoning. Arsenic poisoning can appear similar to Guillain-Barre syndrome with gastrointestinal symptoms and later an ascending paralysis. Urine arsenic levels are more reliable than blood levels. Hair and nail samples are very useful in confirming the diagnosis. Electrodiagnostic testing confirmed an axonal polyneuropathy. Treatment of arsenic poisoning is discussed. The recent lead contamination in Flint Michigan points out that heavy metal poisoning still occurs despite public health awareness.
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42

Katirji, Bashar. Case 14. Edited by Bashar Katirji. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190603434.003.0018.

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Carpal tunnel syndrome is the most common entrapment neuropathy encountered in clinical practice. It is also the most common reason for referral to the electromyography laboratory. The anatomy of the median nerve and the carpal tunnel are outlined in details in this case presentation. The recommended nerve conduction studies needed to make a diagnosis are outlined. This includes internal comparison nerve conduction studies in which the median nerve is compared to a neighboring nerve such as ulnar or radial nerves, as well as the inching studies across the carpal tunnel. Finally, special situations are emphasized including severe carpal tunnel syndrome, carpal tunnel syndrome associated with peripheral polyneuropathy, carpal tunnel syndrome in the presence of Martin–Gruber anastomosis, and carpal tunnel syndrome during pregnancy.
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43

Roze, Emmanuel, and Frédéric Sedel. Gangliosidoses (GM1 and GM2). Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0050.

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GM1 gangliosidosis is due to beta-galactosidase deficiency. The adult-onset form is characterized by progressive generalized dystonia, often associated with akineto-rigid Parkinsonism. Mild skeletal dysplasia and short stature are good diagnostic clues. GM2 gangliosidosis is due to beta-hexosaminidase deficiency. The adult-onset form is characterized by complex neurological disorders, in which features resulting from cerebellar and motor neuron dysfunction are the most frequent. Movement disorders, psychotic symptoms, mild pyramidal signs, axonal polyneuropathy, autonomic dysfunction, and vertical supranuclear palsy can also be observed. Clinical severity and the rate of progression both vary widely from one patient to another. Diagnosis is based on measurements of enzyme activity and molecular analysis. Physiotherapy, speech therapy and management of swallowing are crucial for these patients’ quality of life and prognosis.
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44

Park, Susanna B., Cindy S.-Y. Lin, and Matthew C. Kiernan. Axonal excitability: molecular basis and assessment in the clinic. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199688395.003.0009.

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Axonal excitability techniques were developed to assess axonal resting membrane potential and ion channel function in vivo, and thereby provide greater molecular understanding of the activity of voltage gated ion channels and ion pumps underlying nerve and membrane function. Axonal excitability studies provide complimentary information to conventional nerve conduction studies, using submaximal stimuli to examine the properties underlying the excitability of the axon. Such techniques have been developed both as a research technique to examine disease pathophysiology and as a clinical investigation technique. This chapter provides an overview of axonal excitability techniques, addressing the role of key ion channels and pumps in membrane function and highlighting examples of clinical case studies, where such techniques have been utilized, including motor neuronopathies, tracking progression of chemotherapy-induced peripheral neuropathy, and assessing treatment response in chronic inflammatory demyelinating polyneuropathy.
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45

de Koning, Tom J. Serine Deficiency. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0023.

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Serine deficiency is a rare cause of intractable seizures and severe psychomotor retardation in infants and young children. However, in recent years it has become clear that serine deficiency in adolescents and adults can give rise to milder forms of seizure disorders and mild mental retardation or to a phenotype with severe progressive polyneuropathy. Serine deficiency can be diagnosed on the basis of low values of serine in plasma and CSF using routine amino acid analysis. However, with the introduction of next generation sequencing in clinical diagnostics the majority of patients are diagnosed through molecular testing of the three genes of the synthesis pathway. L-serine therapy is highly effective in the treatment of seizures and improvement of wellbeing and daily activities. Early diagnosis and timely treatment are important to prevent irreversible damage to the central or peripheral nervous system.
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Donaghy, Michael. Focal peripheral neuropathy. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569381.003.0487.

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Some causes of focal peripheral nerve damage are self-evident, such as involvement at sites of trauma, tissue necrosis, infiltration by tumour, or damage by radiotherapy. Focal compressive and entrapment neuropathies are particularly valuable to identify in civilian practice, since recovery may follow relief of the compression. Leprosy is a common global cause of focal neuropathy, which involves prominent loss of pain sensation with secondary acromutilation, and requires early antibiotic treatment. Mononeuritis multiplex due to vasculitis requires prompt diagnosis and immunosuppressive treatment to limit the severity and extent of peripheral nerve damage. Various other medical conditions, both inherited and acquired, can present with focal neuropathy rather than polyneuropathy, the most common of which are diabetes mellitus and hereditary liability to pressure palsies. A purely motor focal presentation should raise the question of multifocal motor neuropathy with conduction block, which usually responds well to high-dose intravenous immunoglobulin infusions.
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Rich, Mark M. Critical Illness Neuropathy, Myopathy, and Sodium Channelopathy. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199653461.003.0033.

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Skeletal muscle weakness is a common problem that complicates recovery from critical illness. The primary causes of weakness include neuropathic disorders, myopathic disorders, and mixed disorders. Recent studies have demonstrated that reduced excitability of the nerve and muscle cell membranes might contribute to weakness during the acute stages of the polyneuropathy and myopathy encountered in critically ill patients. In both tissues, an acquired sodium channelopathy can lead to increased inactivation of channels, leading to inexcitability an paralysis. Experimental sepsis models have demonstrated a similar reduction in excitability in myocardial cells as well as in motor neurons within the spinal cord. The presence of a channelopathy in multiple tissues raises the possibility that reduced excitability of neurons within the CNS might contribute to septic encephalopathy. If this is the case, a single therapy to improve excitability might treat failure of a number of electrically active tissues.
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48

Fuglsang-Frederiksen, Anders, Kirsten Pugdahl, and Hatice Tankisi. Quantitative electromyography. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199688395.003.0008.

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Several quantitative electromyography (QEMG) methods are used for diagnosing and monitoring in patients with neuromuscular disorders. At weak effort of the muscle, motor unit potential (MUP) analyses as individual MUP, multi-MUP, and macro-EMG are diagnostically sensitive and well tested. At higher effort of the muscle, interference pattern analyses such as the turns amplitude analysis are also diagnostically sensitive. Other potential diagnostic methods are power spectrum analysis, muscle fibre conduction velocity analysis, and some surface EMG methods. In patients with myopathy, QEMG has an important role in the diagnosis as a supplement to blood tests, muscle biopsy, and genetic testing. In patients with neurogenic disorders such as anterior horn cell disorders, peripheral nerve lesions, or polyneuropathy, QEMG has important roles in characterizing the lesion and differential diagnosis. Furthermore, QEMG may be useful in the examination of patients with neuromuscular transmission failure, critical illness disorders, and in treatment of dystonic muscle with botulinum toxin.
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Latronico, Nicola, Simone Piva, and Victoria McCredie. Long-Term Implications of ICU-Acquired Muscle Weakness. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199653461.003.0024.

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Intensive care unit-acquired weakness (ICUAW) is a significant and common complication with major implications for survivors of critical illness. ICUAW is a clinical diagnosis made in the presence of generalized muscle weakness that occurs in the setting of critical illness when other causes of muscle weakness have been excluded. Critical illness polyneuropathy and myopathy are the most common causes of ICUAW. Short-term implications of ICUAW include alveolar hypoventilation and an increased risk of pulmonary aspiration, atelectasis, and pneumonia—factors which may contribute to acute respiratory failure and ICU re-admission. In the long term, ICUAW has been associated with physical disturbances, including unsteady gait, sensory loss, foot drop, and, in more severe cases, persistent quadriparesis and ventilator dependency. ICUAW appears to heavily influence the failure of ICU patients to return to baseline health status post-discharge. There is a paucity of evidenced-based therapeutic strategies to reduce the incidence of ICUAW; however, early rehabilitative therapy might represent an effective measure in improving functional status.
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