Inflammatory Demyelinating Polyradiculitis in a Patient With Multiple Sclerosis

Lassmann, Hans; Budka, Herbert; Schnaberth, G

doi:10.1001/archneur.1981.00510020057008

Cited by 83 publications

(30 citation statements)

References 23 publications

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“…Although this combination is rare, it has occasionally been mentioned for acute demyelinating disease [10,23,38,43] as well as for chronic demyelinating disease [8,21,29]. In our patient, involvement of the CNS (multifocal neurological deficits, severely abnormal EEG) and the PNS (conduction block on neurography) was obvious.…”

Section: Discussionmentioning

confidence: 53%

Acute disseminated encephalomyelitis in adults: a reappraisal of clinical, CSF, EEG, and MRI findings

Höllinger¹,

Sturzenegger²,

Mathis³

et al. 2000

J Neurol

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The EEG as an investigation of brain function can be crucial in establishing the organic nature of disease. MRI is important to exclude other diffuse or multifocal encephalopathies. However, in contrast to previous reports in the literature abnormal MRI should not be considered mandatory in adult ADEM. Difficulties in the diagnosis of ADEM are discussed and the importance of clinical and paraclinical findings for establishing the diagnosis is outlined.

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Section: Discussionmentioning

confidence: 53%

Acute disseminated encephalomyelitis in adults: a reappraisal of clinical, CSF, EEG, and MRI findings

Höllinger¹,

Sturzenegger²,

Mathis³

et al. 2000

J Neurol

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“…This proposal is supported by the tissue distribution of MOG which is restricted to the CNS, as is the pathological response after the transfer of the MOG peptide-reactiveT cell 1ine.This is an essential difference to EAE induced by MBP-specificT cells, where, in addition to those seen in the CNS, histological and electrophysiological abnormalities are also seen in the PNS [41]. MS is also generally a CNS-specific disease, although exceptional cases of acute disease do present with inflammatory demyelinating lesions in both the CNS and PNS [42,43].…”

Section: Discussionmentioning

confidence: 99%

T cells specific for the myelin oligodendrocyte glycoprotein mediate an unusual autoimmune inflammatory response in the central nervous system

et al. 1993

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Myelin oligodendrocyte glycoprotein (MOG)-specific T cells mediate an autoimmune inflammatory response in the central nervous system (CNS) that differs radically from conventional models of T cell-mediated experimental allergic encephalomyelitis (EAE). Using synthetic peptides an encephalitogenic T cell epitope of MOG for the Lewis rat was identified within the extracellular IgG V-like domain of the protein, amino acids 44-53 (FSRVVHLYRN). The adoptive transfer of CD4+ T cells specific for this epitope induce an intense, dose-dependent inflammatory response in the CNS of naive syngeneic recipients. However, unlike the inflammatory response induced by myelin basic protein (MBP)-specific T cell lines, inflammation mediated by the MOG peptide-specific T cells failed to induce a gross neurological deficit. This unexpected observation was not due to a reduction in the overall inflammatory response in the CNS, but was specifically associated with a decrease in the extent of parenchymal (as opposed to perivascular) inflammation, a selective decrease in the number of ED1+ macrophages infiltrating the CNS, and a total lack of peripheral nerve inflammation. The decreased recruitment of macrophages into the CNS could not be ascribed to deficiencies in the synthesis of interferon-gamma, tumor necrosis factor-alpha, interleukin (IL)-6 or IL-2 by the T cell line. Moreover, this sub-clinical inflammatory response induced severe blood-brain barrier dysfunction as demonstrated by the induction of severe clinical disease following intravenous injection of a demyelinating MOG-specific monoclonal antibody. The neurological deficit in EAE thus exhibits an unexpected dependence on the identity of the target autoantigen, which determines the extent and nature of the local inflammatory response and ultimately the extent of the neurological deficit.

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“…In our series, Schwann cell hyperplasia due to axonal degeneration is unlikely to occur since AChE staining showed mostly normal nerve densities. Some authors, however, de scribed demyelination or axonal degeneration in periph eral nerves associated with CNS involvement by MS [19,20,[37][38][39][40][41], but no primary morphological changes were reported in the PNS. Our results make it tempting to state that demyelination in MS is not restricted to the CNS but also involves the autonomic PNS and that this is the main factor leading to increased immunoreactivity [18].…”

Section: Discussionmentioning

confidence: 99%

Neuropathological Examination of the Alterations of the Intrinsic Innervation in Multiple Sclerosis Cystopathy (With 1 color plate)

Poppel¹,

Stessens

Lazarides

et al. 1989

Urol Int

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Morphometric analysis of the innervation pattern of the stromal layer of the urinary bladder was done on biopsies from 88 patients with definite multiple sclerosis (MS). The biopsies were stained for acetylcholinesterase and for S100 protein, and a semiquantitative score was assigned. Nearly 30% of the samples showed increased immunoreactivity for S100, indicating Schwann cell hyperplasia. In 16% a decreased S100 immunoreactivity was found, the significance of which is unclear. More than 90% had normal acetylcholinesterase activity. No correlation could be demonstrated for age, sex, severity and duration of the disease, the presence of cystitis and the type of detrusor dysfunction. The finding of altered S100 immunoreactivity in MS bladders could indicate that MS also affects the peripheral nervous system and is not limited to the central nervous system as classically described. This finding warrants further investigation.

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Inflammatory Demyelinating Polyradiculitis in a Patient With Multiple Sclerosis

Cited by 83 publications

References 23 publications

Acute disseminated encephalomyelitis in adults: a reappraisal of clinical, CSF, EEG, and MRI findings

Acute disseminated encephalomyelitis in adults: a reappraisal of clinical, CSF, EEG, and MRI findings

T cells specific for the myelin oligodendrocyte glycoprotein mediate an unusual autoimmune inflammatory response in the central nervous system

Neuropathological Examination of the Alterations of the Intrinsic Innervation in Multiple Sclerosis Cystopathy (With 1 color plate)

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