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dc.contributor.author | Graus Ribas, Francesc |
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dc.contributor.author | Saiz Hinajeros, Albert |
dc.contributor.author | Lai, Marina |
dc.contributor.author | Bruna, Jordi |
dc.contributor.author | López, Francisca |
dc.contributor.author | Sabater, Lidia |
dc.contributor.author | Blanco, Yolanda |
dc.contributor.author | Rey, María Jesús |
dc.contributor.author | Ribalta Farrés, Teresa María |
dc.contributor.author | Dalmau Obrador, Josep |
dc.date | 2019-01-23T10:53:58Z |
dc.date | 2019-01-23T10:53:58Z |
dc.date | 2008-09-16 |
dc.date | 2019-01-23T10:53:58Z |
dc.identifier | 0028-3878 |
dc.identifier | 612250 |
dc.identifier | 18794496 |
dc.identifier.uri | http://hdl.handle.net/2445/127545 |
dc.description | Objective: To report the frequency and type of antibodies against neuronal surface antigens (NSA-ab) in limbic encephalitis (LE). Methods: Analysis of clinical features, neuropathologic findings, and detection of NSA-ab using immunochemistry on rat tissue and neuronal cultures in a series of 45 patients with paraneoplastic (23) or idiopathic (22) LE. Results: NSA-ab were identified in 29 patients (64%; 12 paraneoplastic, 17 idiopathic). Thirteen patients had voltage-gated potassium channels (VGKC)-ab, 11 novel NSA (nNSA)-ab, and 5 NMDA receptor (NMDAR)-ab. nNSA-ab did not identify a common antigen and were more frequent in paraneoplastic than idiopathic LE (39% vs 9%; p = 0.03). When compared with VGKC-ab or NMDAR-ab, the nNSA associated more frequently with intraneuronal antibodies (11% vs 73%; p = 0.001). Of 12 patients (9 nNSA-ab, 2 VGKC-ab, 1 NMDAR-ab) with paraneoplastic LE and NSA-ab, concomitant intraneuronal antibodies occurred in 9 (75%). None of these 12 patients improved with immunotherapy. The autopsy of three of them showed neuronal loss, microgliosis, and cytotoxic T cell infiltrates in the hippocampus and amygdala. These findings were compatible with a T-cell mediated neuronal damage. In contrast, 13 of 17 (76%) patients with idiopathic LE and NSA-ab (8 VGKC-ab, 4 NMDAR-ab, 1 nNSA-ab) and 1 of 5 (20%) without antibodies had clinical improvement (p = 0.04). Conclusions: In paraneoplastic limbic encephalitis (LE), novel antibodies against neuronal surface antigens (nNSA-ab) occur frequently, coexist with antibodies against intracellular antigens, and these cases are refractory to immunotherapy. In idiopathic LE, the likelihood of improvement is significantly higher in patients with NSA-ab than in those without antibodies. |
dc.format | 7 p. |
dc.format | application/pdf |
dc.language | eng |
dc.publisher | Lippincott, Williams & Wilkins. Wolters Kluwer Health |
dc.relation | Reproducció del document publicat a: https://doi.org/10.1212/01.wnl.0000325917.48466.55 |
dc.relation | Neurology, 2008, vol. 71, num. 12, p. 930-936 |
dc.relation | https://doi.org/10.1212/01.wnl.0000325917.48466.55 |
dc.rights | (c) American Academy of Neurology, 2008 |
dc.rights | info:eu-repo/semantics/openAccess |
dc.subject | Encefalitis |
dc.subject | Immunoglobulines |
dc.subject | Immunoteràpia |
dc.subject | Encephalitis |
dc.subject | Immunoglobulins |
dc.subject | Immunotheraphy |
dc.title | Neuronal surface antigen antibodies in limbic encephalitis: clinical-immunologic associations |
dc.type | info:eu-repo/semantics/article |
dc.type | info:eu-repo/semantics/publishedVersion |