1、Chronic acquired demyelinating multiple neuropathy1. Curr Neurol Neurosci Rep. 2014 Oct;14(10):487. doi: 10.1007/s11910-014-0487-z.Neurologic manifestations of gastrointestinal and liver diseases.Ferro JM(1), Oliveira S.Author information: (1)Department of Neurosciences, Service of Neurology, Hospit
2、al de Santa Maria,University of Lisbon, Av. Prof. Egas Moniz, 1649-035, Lisboa, Portugal,jmferrofm.ul.pt.Hepatic and gastrointestinal disorders can produce a wide spectrum of neurologic complications both affecting the central nervous system (CNS) and the peripheral nervous system. These manifestati
3、ons range in severity from coma in acute liverfailure and acute pancreatitis, to minor cognitive changes in chronicportosystemic encephalopathy and hepatitis C. Cerebrovascular diseases cancomplicate hepatitis C infection and inflammatory bowel disease. Demyelinatingdisorders may co-exist with infla
4、mmatory bowel disease. Anti-tumor necrosisfactor alpha drugs may induce demyelination. Ataxia may occur in malabsorptionsyndromes and in gluten related disorders. Characteristic movement disorders are key features of acquired hepatocerebral degeneration and of Whipple disease.Multiple types of neuro
5、pathy can be found in association with hepatitis,inflammatory bowel disease and gluten related disorders.PMID: 25171900 PubMed - indexed for MEDLINE2. Neuroimaging Clin N Am. 2013 May;23(2):321-36. doi: 10.1016/j.nic.2012.12.010.Epub 2013 Jan 23.Mimics and rare presentations of pediatric demyelinati
6、on.OMahony J(1), Shroff M, Banwell B.Author information: (1)Divison of Neurology, Department of Pediatrics, Research Institute, TheHospital for Sick Children, Toronto, Ontario, Canada.This article reviews the features that should prompt consideration of diseasesthat mimic acquired demyelinating synd
7、romes and multiple sclerosis usingvignettes to highlight unusual clinical and radiologic features. Cases oftransverse myelitis, spinal infarction, acute disseminated encephalomyelitis,fever-induced refractory epileptic encephalopathy in school-aged children,small-vessel vasculitis, Griscelli syndrom
8、e type 2, cysticercosis, vitamin B12deficiency, and chronic relapsing inflammatory optic neuropathy are presented.Crown Copyright 2013. Published by Elsevier Inc. All rights reserved.PMID: 23608693 PubMed - indexed for MEDLINE3. Muscle Nerve. 2013 Feb;47(2):292-6. doi: 10.1002/mus.23629. Epub 2012 N
9、ov 21.Distal acquired demyelinating symmetric polyneuropathy progressing to classicchronic inflammatory demyelinating polyneuropathy and response to fludarabine andcyclophosphamide.Leitch MM(1), Sherman WH, Brannagan TH 3rd.Author information: (1)Department of Neurology, Neurological Institute, Colu
10、mbia University, 710 W168th Street, Box 163, New York, New York 10032 USA.INTRODUCTION: Distal acquired demyelinating symmetric polyneuropathy (DADS) isproposed as a distinct entity from classic chronic inflammatory demyelinatingpolyneuropathy (CIDP).METHODS: We report a 58-year-old woman with DADS
11、that progressed to a severe caseof classic CIDP.RESULTS: She had distal numbness and paresthesias, minimal distal weakness andimpaired vibratory sensation. She had anti-MAG antibodies, negative Western blot,and lacked a monoclonal gammopathy. There were prolonged distal motor latencies. She remained
12、 stable for 6 years until developing proximal and distal weakness.Nerve conduction studies showed multiple conduction blocks. She developedquadriparesis despite first-line treatment for CIDP. She was started oncyclophosphamide and fludarabine. Twenty-five months after receivingchemotherapy, she had
13、only mild signs of neuropathy off all immunotherapy.CONCLUSIONS: DADS may progress to classic CIDP and is unlikely to be a separatedisorder. Fludarabine and cyclophosphamide may be effective for refractory CIDP.Copyright 2012 Wiley Periodicals, Inc.PMID: 23168526 PubMed - indexed for MEDLINE4. Semin
14、 Neurol. 2012 Jul;32(3):187-95. doi: 10.1055/s-0032-1329194. Epub 2012 Nov1.Chronic inflammatory demyelinating polyradiculoneuropathy: from bench to bedside.Peltier AC(1), Donofrio PD.Author information: (1)Department of Neurology, Vanderbilt Medical Center, Medical Center North,Nashville, Tennessee
15、 37232-2551, USA. amanda_c_peltiervanderbilt.eduChronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is the mostcommon treatable chronic autoimmune neuropathy. Multiple diagnostic criteria havebeen established, with the primary goal of identifying neurophysiologic hallmarksof acquired de
16、myelination. Treatment modalities have expanded to include numerousimmunomodulatory therapies, although the best evidence continues to be forcorticosteroids, plasma exchange, and intravenous immunoglobulin (IVIg). Thisreview describes the pathology, epidemiology, pathogenesis, diagnosis, andtreatmen
17、t of CIDP.Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.PMID: 23117943 PubMed - indexed for MEDLINE5. Ann Indian Acad Neurol. 2011 Apr;14(2):81-92. doi: 10.4103/0972-2327.82789.Chronic dysimmune neuropathies: Beyond chronic demyelinatingpolyradiculoneuropathy.Khadilkar SV(1),
18、 Deshmukh SS, Dhonde PD.Author information: (1)Department of Neurology, Grant Medical College and Sir JJ Group of Hospitals, Mumbai, India.The spectrum of chronic dysimmune neuropathies has widened well beyond chronicdemyelinating polyradiculoneuropathy (CIDP). Pure motor (multifocal motorneuropathy
19、), sensorimotor with asymmetrical involvement (multifocal acquireddemylinating sensory and motor neuropathy), exclusively distal sensory (distalacquired demyelinating sensory neuropathy) and very proximal sensory (chronicimmune sensory polyradiculopathy) constitute the variants of CIDP. Correctdiagn
20、osis of these entities is of importance in terms of initiation ofappropriate therapy as well as prognostication of these patients. The rates ofdetection of immune-mediated neuropathies with monoclonal cell proliferation(monoclonal gammopathy of unknown significance, multiple myeloma, etc.) have been
21、facilitated as better diagnostic tools such as serum immunofixationelectrophoresis are being used more often. Immune neuropathies associated withmalignancies and systemic vasculitic disorders are being defined further andtreated early with better understanding of the disease processes. As this field
22、of dysimmune neuropathies will evolve in the future, some of the curious aspects of the clinical presentations and response patterns to differentimmunosuppressants or immunomodulators will be further elucidated. This reviewalso discusses representative case studies.PMCID: PMC3141494PMID: 21808468 Pu
23、bMed6. Eur Biophys J. 2008 Feb;37(2):183-95. Epub 2007 Sep 5.Membrane property abnormalities in simulated cases of mild systematic and severe focal demyelinating neuropathies.Stephanova D(1), Daskalova M.Author information: (1)Institute of Biophysics, Bulgarian Academy of Sciences, Acad. G. Bontchev
24、Str., Bl. 21, Sofia, 1113, Bulgaria. dstephshiva.bio.bas.bgThe investigation of multiple nerve membrane properties by mathematical modelshas become a new tool to study peripheral neuropathies. In demyelinatingneuropathies, the membrane properties such as potentials (intracellular,extracellular, elec
25、trotonic) and indices of axonal excitability(strength-duration time constants, rheobases and recovery cycles) can now bemeasured at the peripheral nerves. This study provides numerical simulations ofthe membrane properties of human motor nerve fibre in cases of internodal,paranodal and simultaneousl
26、y of paranodal internodal demyelinations, each of themmild systematic or severe focal. The computations use our previous multi-layered model of the fibre. The results show that the abnormally greater increase of the hyperpolarizing electrotonus, shorter strength-duration time constants andgreater ax
27、onal superexcitability in the recovery cycles are the characteristicfeatures of the mildly systematically demyelinated cases. The small decrease ofthe polarizing electrotonic responses in the demyelinated zone in turn leads to acompensatory small increase of these responses outside the demyelinated
28、zone ofall severely focally demyelinated cases. The paper summarizes the insights gainedfrom these modeling studies on the membrane property abnormalities underlying thevariation in clinical symptoms of demyelination in Charcot-Marie-Tooth diseasetype 1A, chronic inflammatory demyelinating polyneuro
29、pathy, Guillain-Barrsyndrome and multifocal motor neuropathy. The model used provides an objectivestudy of the mechanisms of these diseases which up till now have not beensufficiently well understood, because quite different assumptions have been givenin the literature for the interpretation of the
30、membrane property abnormalitiesobtained in hereditary, chronic and acquired demyelinating neuropathies.PMID: 17786424 PubMed - indexed for MEDLINE7. J Neurol Sci. 2006 May 15;244(1-2):77-87. Epub 2006 Mar 9.The natural history and long-term outcome of 57 limb sarcoidosis neuropathycases.Burns TM(1),
31、 Dyck PJ, Aksamit AJ, Dyck PJ.Author information: (1)Department of Neurology, Mayo Clinic College of Medicine, Rochester, MN 55905,USA.Fifty-seven patients with biopsy-proven sarcoidosis causing limb neuropathy were reviewed in order to delineate the characteristic symptoms, impairments,disability,
32、course, outcome and response to corticosteroid treatment of limbsarcoid neuropathy. Typically the neuropathy had a definite date of symptomaticonset. Prominent were positive neuropathic sensory symptoms (P-NSS), especiallypain, overshadowing weakness and sensory loss. P-NSS were the main cause ofdis
33、ability. Almost always the pattern was asymmetric and not length-dependent(unlike distal polyneuropathy). We inferred (from kind and distribution ofsymptoms, signs and electrophysiologic and other test results) that thepathologic process was focal or multifocal, involving most classes of nervefibers
34、 and variable levels of proximal to distal levels of roots and peripheralnerves. Additional features aiding in diagnosis were: systemic symptoms such asfatigue, malaise, arthralgia, fever and weight loss; involvement of multipletissues (i.e. skin, lymph nodes and eye); the patterns of neuropathy; MR
35、Ifeatures; and ultimately tissue diagnosis. Axonal degeneration predominated,although an acquired demyelinating process was observed in 3 patients. For mostcases, the disease had a chronic, monophasic course. MRI studies done in lateryears of affected neural structures were helpful in identifying le
36、ptomeningealthickening, hilar adenopathy; and enlargement and T2 enhancement of nerve roots, plexuses, and limb nerves. Corticosteroid treatment appeared to amelioratesymptoms more than impairments. Several variables were associated withneuropathic improvement: CSF pleocytosis, short duration betwee
37、n symptom onsetand treatment, and a higher grade of disability at first evaluation-a possiblerationale for future earlier diagnosis and treatment.PMID: 16524595 PubMed - indexed for MEDLINE8. Rev Neurol (Paris). 2004 Mar;160(3):363-70.The diagnosis of acquired sensory neuropathies.Article in FrenchC
38、range A(1).Author information: (1)Service de Neurologie, INSERM E0011, Facult de Mdecine, Crteil, France.creangeuniv-paris12.frINTRODUCTION: Peripheral neuropathies usually include a sensory component ofvarious causes. The diagnosis approach requires careful a clinical assessment anda precise electr
39、ophysiological exploration.STATE OF ART: Axonal sensory polyneuropathies are classified according to thetype of fibers involved (large or small fibers). While there is a large number ofcauses, current emphasis is placed on glucose intolerance as a source ofsmall-fiber sensory neuropathies. Demyelina
40、ting polyneuropathies are oftenassociated with a monoclonal IgM gammapathy with anti-MAG activity. Multiplesensory mononeuropathies are exceptional and suggest possible early-phasevasculities, sensorymotor neuropathy with conduction blocks or leprosy. Sensoryneuronopathies can also suggest Sjgrens s
41、yndrome or a paraneoplastic syndrome. Finally chronic sensory polyradiculoneuritis constitute a rare subgroup clearlydefined as demyelinating inflammatory neuropathy.CONCLUSION: The diagnostic approach to sensory neuropathies requires carefulnosological electroclinical classification to reduce the n
42、umber of explorationsperformed for etiological diagnosis.PMID: 15037854 PubMed - indexed for MEDLINE9. Rev Neurol. 2003 Sep 1-15;37(5):481-5.Diseases of the peripheral and visual nervous system during infection with humanimmunodeficiency virus.Article in SpanishCasanova-Sotolongo P(1), Casanova-Carr
43、illo P, Casanova-Carrillo C.Author information: (1)Neurologa, Policlnico Docente, La Habana, Cuba. pcasanovinfomed.sld.cuINTRODUCTION: Infection with human immunodeficiency virus (HIV) is oftenaccompanied by neurological complications. One of these includes disordersaffecting the peripheral and visu
44、al nervous system, especially during theacquired immunodeficiency syndrome (AIDS) stage.DEVELOPMENT: The peripheral neuropathies associated with infection by HIV are an assorted group of disorders, which include acute or chronic inflammatorydemyelinating polyneuropathy, multiple mononeuropathy and n
45、europathies related tothe herpes zoster virus or cytomegalovirus. The most common and clinicallyimportant of the neuropathies is painful distal sensory polyneuropathy (DSP). Themost severely affected cranial nerves are V and VII. The isolation of HIV fromthe affected nerves suggests a direct role, b
46、ut an immune mechanism is alsopossible. Although cytomegalovirus may be associated with a variety of peripheralnerve syndromes, its clinical presentation as a primary demyelinatingpolyneuropathy is unusual.CONCLUSIONS: DSP and antiretroviral toxic neuropathy are the most commonHIV-associated neuropa
47、thies. Both HIV infection, by itself, and the neurotoxicityof certain drugs in tritherapy contribute to the development of painfulperipheral sensory neuropathy. In researching into the cause of HIV-associatedneuropathy further studies are needed to determine the relative roles played bythe viral inf
48、ection and the activation of the immunological factors thatcontribute to the pathogenesis of the damage done in axons, the dorsal rootganglion and in the sensory pathways in the spinal cord.PMID: 14533099 PubMed - indexed for MEDLINE10. Rev Neurol. 2003 Jun 16-30;36(12):1145-9.Electrophysiological e
49、valuation of a case of sensory-motor multifocal acquireddemyelinating neuropathy. The effects of immunoglobulin therapy.Article in SpanishPolitei JM(1), Pagano MA, Amores M, Yorio AA.Author information: (1)Servicio de Neurologa, Hospital General de Agudos Juan A. Fernndez, BuenosAires, Argentina. INTRODUCTION: Sensory motor multifocal acquired demyelinating neuropathy (SMMADN)is a variant of the chronic multifocal neuropathies. Several reports have beenpublished about the clinical and electrophysiological progression in mot
