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Books on the topic 'Chronic Inflammatory Demyelinating Polyneuropathy (CIDP)'

Author: Grafiati

Published: 4 June 2021

Last updated: 12 February 2022

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1

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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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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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11

Thaisetthawatkul, Pariwat, and Eric Logigian. Guillain-Barré Syndrome and Chronic Inflammatory Demyelinating Polyradiculoneuropathy in Pregnancy. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190667351.003.0026.

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Guillain-Barré syndrome (GBS) and chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) are both immune-mediated diseases of the peripheral nervous system that typically present with symmetric, progressive muscle weakness, areflexia, and sensory symptoms or signs. GBS evolves rapidly with a nadir at 2–4 weeks usually with an antecedent viral illness, while CIDP progresses more slowly over months to years. GBS is sometimes complicated by life-threatening respiratory failure or dysautonomia. Onset of GBS and relapse of CIDP can occur during pregnancy or postpartum. But with appropriate supportive care and immunotherapy, maternal and fetal outcome in both conditions is typically excellent. The exception is fetal outcome in GBS triggered by maternal CMV or Zika infection transmitted to the fetus. Full-term vaginal delivery and regional anesthesia are preferred in maternal GBS and CIDP, but if C-section and general anesthesia are indicated, non-depolarizing agents such as succinylcholine should be avoided.

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12

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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13

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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14

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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15

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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16

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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17

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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