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4. Autoimmune encephalitis: what the radiologist needs to know

Author

Sanvito, Francesco, Pichiecchio, Anna, Paoletti, Matteo, Rebella, Giacomo, Resaz, Martina, Benedetti, Luana, Massa, Federico, Morbelli, Silvia, Caverzasi, Eduardo, Asteggiano, Carlo, Businaro, Pietro, Masciocchi, Stefano, Castellan, Lucio, Franciotta, Diego, Gastaldi, Matteo, and Roccatagliata, Luca

Published
2024
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12. Safety and efficacy of rozanolixizumab in patients with generalised myasthenia gravis (MycarinG): a randomised, double-blind, placebo-controlled, adaptive phase 3 study

Author

Genge, Angela, Massie, Rami, Berube, Maxime, Bril, Vera, Daniyal, Lubna, Mannan, Shabber, Ng, Eduardo, Raman, Ritesh Rohan Raghu, Sarpong, Evelyn, Alcantara, Monica, Dionne, Annie, Siddiqi, Zaeem, Blackmore, Derrick, Hussain, Faraz, Matte, Genevieve, Botez, Stephan, Tyblova, Michaela, Jakubikova, Michala, Junkerova, Jana, Vissing, John, Witting, Nanna, Holm-Yildiz, Sonja, Stemmerik, Mads, Andersen, Henning, Obál, Izabella, Solé, Guilhem, Mathis, Stéphane, Violleau, Marie-Hélène, Tranchant, Christine, Messai, Sihame, Chanson, Jean-Baptiste, Nadaj-Pakleza, Aleksandra, Verloes, Arnaud, Zaidi, Leila, Sacconi, Sabrina, Gambella, Manuela, Cavalli, Michele, Stojkovic, Tanya, Demeret, Sophie, Le Guennec, Loic, Querin, Giorgia, Weiss, Nicolas, Masingue, Marion, Magy, Laurent, Ghorab, Karima, Rukhadze, Ia, Tsiskaridze, Alexander, Janelidze, Marina, Margania, Temur, Then Bergh, Florian, Hänsel, Eike, Kalb, Andrea, Meilick, Bianca, Reuschel, Mandy, Teußer, Lars-Malte, Unterlauft, Astrid, Goedel, Clemens, Hagenacker, Tim, Totzeck, Andreas, Stolte, Benjamin, Blaes, Franz, Bindler, Christine, Tsoutsikas, Vasilios, Roediger, Annekathrin, Geis, Christian, Schmidt, Jens, Zschüntzsch, Jana, Schwarz, Margret, Meyer, Stefanie, Kummer, Karsten, Glaubitz, Stefanie, Zeng, Rachel, Wiendl, Heinz, Klotz, Luisa, Lammerskitten, Anna, Lünemann, Jan, Diószeghy, Péter, Mantegazza, Renato, Maggi, Lorenzo, Rinaldi, Elena, Gastaldi, Matteo, Mazzacane, Federico, Businaro, Pietro, Iorio, Raffaele, Antonini, Giovanni, Fionda, Laura, Rinaldi, Rita, Rossi, Simone, Habetswallner, Francesco, Tuccillo, Francesco, Umehara, Haruna, Uenaka, Eiko, Takahashi, Masanori, Higashi, Keiko, Kinoshita, Makoto, Yoneda, Emika, Nakamura, Noriko, Fujita, Saeka, Kubota, Tomoya, Ono, Masami, Yamamoto, Sana, Hatano, Taku, Oikoshi, Kazuki, Yokoyama, Kazumasa, Oji, Yutaka, Tomizawa, Yuji, Uzawa, Akiyuki, Yasuda, Manato, Akita, Sachiko, Ozawa, Yukiko, Onishi, Yosuke, Takaki, Miki, Yamada, Hiromi, Minemoto, Kanako, Sanko, Miki, Izawa, Nanae, Nakayama, Mayumi, Masuda, Masayuki, Tsuji, Rune, Ido, Nobuhiro, Hyodo, Yumi, Okubo, Yoshihiko, Minohara, Akiko, Haraguchi, Nana, Naito, Makiko, Yoshida, Seiko, Fukushige, Yuri, Tsujino, Akira, Nagaoka, Atsushi, Miyazaki, Teiichiro, Yoshimura, Shunsuke, Hirayama, Takuro, Shima, Tomoaki, Okamoto, Naoko, Matsumoto, Riki, Sekiguchi, Kenji, Ueda, Takehiro, Chihara, Norio, Kirimura, Mari, Sunagawa, Emi, Suzuki, Ayaka, Suzuki, Shigeaki, Wada, Aozora, Ishizuchi, Kei, Suzuki, Yasushi, Yata, Mitsuo, Komatsu, Yuka, Tsukita, Kenichi, Watanabe, Genya, Sato, Kazuki, Kawasaki, Emiko, Yamamoto, Naoki, Ono, Hirohiko, Tsuda, Tomoko, Ohashi, Shigeki, Utsugisawa, Kimiaki, Fujisawa, Yuka, Yokota, Yumiko, Nagane, Yuriko, Ayumi, Kameda, Takematsu, Yuka, Naito, Hiroyuki, Sugimoto, Takamichi, Kuwada, Kumiko, Rejdak, Konrad, Szklener, Sebastian, Kitowska, Monika, Derkacz, Kandyda, Druzdz, Artur, Berkowicz, Tomasz, Budzinska, Paulina, Halas, Marek, Zaslavskiy, Leonid, Skornyakova, Evgeniya, Kotov, Sergey, Novikova, Ekaterina, Sidorova, Olga, Goldobin, Vitalii, Alekseeva, Tatiana, Isabekova, Patimat, Malkova, Nadezhda, Korobko, Denis, Djordjevic, Gordana, Stojanov, Aleksandar, Peric, Stojan, Lavrnic, Dragana, Bozovic, Ivo, Palibrk, Aleksa, Casasnovas, Carlos, Nedkova-Hristova, Velina, Vidal Fernández, Nuria, Cortés Vicente, Elena, Querol Gutiérrez, Luis, Salvadó Figueras, Maria, Canovas Segura, Anna, Juntas Morales, Raúl, Sanchez Tejerina, Daniel, Saiz, Albert, Blanco Morgado, Yolanda, Llufriú Durán, Sara, Sepúlveda Gázquez, María, Martínez Hernández, Eugenia María, Gutiérrez Gutiérrez, Gerardo, Iniesta, Paqui, Meca Lallana, José, Guo, Yuh-Cherng, Chiu, Hou-Chang, Yeh, Jiann-Horng, Chen, Ya Hui, Lee, Mei Fen, Lee, Yi-Chung, Lai, Kuan Lin, Beydoun, Said, Akhter, Salma, Vu, Tuan, Lam, Lucy, Thomas, Alisha, Rivner, Michael, Quarles, Brandy, Lange, Dale, Holzberg, Shara, Pavlakis, Pantelis, Goutham, Ashwathy, Kaminski, Henry, Aly, Radwa, Ashworth, Lisa, Bender, Kathryn, Bond, Karie, Buckner, Joanne, Byerly, Sara, Caress, James, Clemons, Jessyca, Farmer, Asha, Franklin, Catherine, Harris, Summer, Hiatt, Meredith, Gandhi Mehta, Rachana, Miller, Gina, Smith, Lynn, Smith, Rose, Strittmatter, Brian, Mozaffar, Tahseen, Habib, Ali A, Hernandez, Isela, Moulton, Kelsey, Karam, Chafic, Ravikumar, Pranali, Lomen-Hoerth, Catherine, Rosow, Laura, George, Hannah, Irodenko, Viktoriya, Kang, Min, Denny, Carol, Hanson, Bart, Klein, Sara, Martinez-Thompson, Jennifer, Naddaf, Elie, Padgett, Denny, Sorenson, Eric, L Sultze, Jane, Weis, Delena, Rezania, Kourosh, Thonhoff, Jason, Shroff, Sheetal, Pascuzzi, Robert, Micheels, Angela, Bodkin, Cynthia, Comer, Adam, Baras, Gelasio, Wagner, Renee, Mahuwala, Zabeen, Ryan, Stephen, Su, Kai, Sharma, Khema, Brown, Andrew, Liow, Kore, Drużdż, Artur, Grosskreutz, Julian, Boehnlein, Marion, Bozorg, Ali, Gayfieva, Maryam, Greve, Bernhard, Woltering, Franz, and Kaminski, Henry J

Published
2023
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17. Characterization and management of neurological adverse events during immune-checkpoint inhibitors treatment: an Italian multicentric experience

Author

Diamanti, Luca, Picca, Alberto, Bini, Paola, Gastaldi, Matteo, Alfonsi, Enrico, Pichiecchio, Anna, Rota, Eugenia, Rudà, Roberta, Bruno, Francesco, Villani, Veronica, Galiè, Edvina, Vogrig, Alberto, Valente, Mariarosaria, Zoccarato, Marco, Poretto, Valentina, Giometto, Bruno, Cimminiello, Carolina, Del Vecchio, Michele, and Marchioni, Enrico

Published
2022
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19. Diagnostic accuracy of voluntary and stimulated neuromuscular jitter studies in ocular myasthenia gravis.

Author

Cosentino, Giuseppe, Prunetti, Paolo, Tammam, Giulia, Zaffina, Chiara, Gastaldi, Matteo, Tassorelli, Cristina, Alfonsi, Enrico, and Todisco, Massimiliano

Abstract

Introduction/Aims: There is a lack of studies comparing the accuracy of neuromuscular jitter analysis during voluntary activation (v‐jitter study) versus axonal stimulation (s‐jitter study). The study aimed to compare these two techniques in the same population of patients with suspected ocular myasthenia gravis (OMG). Methods: Fourteen control subjects (mean age: 55.5 ± 15.2 years) and 34 patients with suspected OMG (mean age: 59 ± 13.9 years) were prospectively evaluated. Twenty spike pairs and 30 individual spikes were analyzed during v‐jitter and s‐jitter study, respectively. Two different criteria for abnormal individual jitter values were evaluated: ≥ or > than 10% values exceeding the upper normal limit. Results: OMG was diagnosed in 19 patients based on clinical and laboratory findings, without considering jitter measurements. In most patients, v‐jitter and s‐jitter analyses provided comparable results. The maximum sensitivity (89%) was achieved with s‐jitter study using the ≥10% criterion, while the maximum specificity (93%) was found with v‐jitter study using the >10% criterion. Discussion: Both v‐jitter and s‐jitter studies showed good to very good accuracy for the diagnosis of OMG, in the absence of any statistically significant difference. Therefore, the patient's cooperation level and examiner's experience should guide the choice of performing v‐jitter or s‐jitter analysis in patients with suspected OMG. [ABSTRACT FROM AUTHOR]

Published
2024
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23. Early Immunotherapy and Longer Corticosteroid Treatment Are Associated With Lower Risk of Relapsing Disease Course in Pediatric MOGAD

Author

Nosadini, Margherita, Eyre, Michael, Giacomini, Thea, Valeriani, Massimiliano, Della Corte, Marida, Praticò, Andrea D., Annovazzi, Pietro, Cordani, Ramona, Cordelli, Duccio Maria, Crichiutti, Giovanni, Di Rosa, Gabriella, Dolcemascolo, Valentina, Fetta, Anna, Freri, Elena, Gallo, Paolo, Gastaldi, Matteo, Granata, Tiziana, Grazian, Luisa, Iorio, Raffaele, Lombardini, Martina, Margoni, Monica, Mariotto, Sara, Matricardi, Sara, Melani, Federico, Nardocci, Nardo, Papetti, Laura, Passarini, Alice, Pisani, Francesco, Poʼ, Chiara, Puthenparampil, Marco, Ragona, Francesca, Savasta, Salvatore, Siliquini, Sabrina, Toldo, Irene, Tozzo, Alessandra, Turco, Emanuela Claudia, Varone, Antonio, Vogrig, Alberto, Zuliani, Luigi, Bugin, Samuela, Rossato, Sara, Orsini, Alessandro, Cantalupo, Gaetano, Mancardi, Maria Margherita, Ferilli, Michela Ada Noris, Foiadelli, Thomas, and Sartori, Stefano

Published
2023
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28. Unravelling the Acute, Chronic and Steroid-Refractory Management of High-Grade Neurological Immune-Related Adverse Events: A Call to Action.

Author

Malvaso, Antonio, Giglio, Pierpaolo, Diamanti, Luca, Gastaldi, Matteo, Vegezzi, Elisa, Pace, Andrea, Bini, Paola, and Marchioni, Enrico

Subjects
DRUG side effects, PERIPHERAL nervous system, IMMUNE checkpoint inhibitors, CENTRAL nervous system, PATHOLOGY
Abstract

Rare side effects of immune-checkpoint inhibitors (ICIs) are known as neurological immune-related adverse events (n-irAEs). Typically, n-irAEs affect the peripheral nervous system, primarily presenting as myositis, polyradiculoneuropathy, or cranial neuropathy. Less commonly, they impact the central nervous system, resulting in encephalitis, meningitis, or myelitis. High-grade n-irAEs managing and recognizing remains challenging, considering the risk of mortality and long-term disability. To date, strong scientific data are lacking to support the management of high-grade clinical forms. We performed a systematic literature search, selecting all articles describing high-grade steroid-resistance n-irAEs. and we reported them in a practical review. Specifically, current recommendations advise stopping ICI use and beginning corticosteroid treatment. Our findings highlighted that in steroid-resistant n-irAEs, it should be recommended to quickly escalate to plasma exchange (PLEX) and/or intravenously immunoglobulins (IVIg), usually in association with other immunosuppressants. Furthermore, newer evidence supports the use of drugs that may specifically block inflammation without reducing the anti-tumour effect of ICIs. In this practical review, we provide new evidence regarding the therapeutic approach of high-grade n-irAEs, particularly in steroid-resistant cases. We would also stress the importance of informing the scientific community of the discrepancy between current guidelines and clinical evidence in these rare forms of pathology. [ABSTRACT FROM AUTHOR]

Published
2024
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29. Overcoming therapeutic challenges: Successful management of a supposedly triple seronegative, refractory generalized myasthenia gravis patient with efgartigimod.

Author

Sorrenti, Benedetta, Laurini, Christian, Bosco, Luca, Strano, Camilla Mirella Maria, Scarlato, Marina, Gastaldi, Matteo, Filippi, Massimo, Previtali, Stefano Carlo, and Falzone, Yuri Matteo

Subjects
MYASTHENIA gravis, FC receptors, CHOLINERGIC receptors, REFRACTORY materials, THERAPEUTICS, TREATMENT effectiveness
Abstract

Background and purpose: This study was undertaken to highlight neonatal Fc receptor inhibition (efgartigimod) as a valuable therapeutic option for patients with refractory seronegative myasthenia gravis (MG) and to emphasize the concept that seronegative MG is greatly constrained by the limitations of currently available diagnostic methods and therapeutic measures. Methods: We describe the first refractory, generalized MG (gMG) patient successfully treated with efgartigimod after testing negative on standard autoantibody detection tests. Results: Our patient presented with severe fluctuating bulbar and generalized weakness, resulting in multiple myasthenic crises requiring intubation. After a 28‐year medical history of multiple failed lines of treatment, our patient was started on efgartigimod. Over five treatment cycles, a definite improvement in her clinical condition was observed (Myasthenia Gravis Foundation of America class: IIIb to IIb; MG‐Activities of Daily Living score: 11 to 0; MG‐Quality of Life 15 score: 30 to 0; Quantitative MG score: 28 to 6). Standard autoantibody detection tests failed to detect known pathogenic autoantibodies, but cell‐based assay (CBA) identified autoantibodies against clustered adult acetylcholine receptor (AChR). Conclusions: In light of recent approvals of efgartigimod by the European Medicines Agency and US Food and Drug Administration exclusively for AChR‐positive gMG forms, our case highlights evidence suggesting that such an approach might be shortsighted and could limit therapeutic options for patients with refractory seronegative gMG. Additionally, introducing more sensitive analytical techniques, exemplified by CBA, may help bridge the gap between seronegative and seropositive patients. This represents an urgent unmet need for gMG patients, as the antibody profile dramatically influences the therapeutic approach. [ABSTRACT FROM AUTHOR]

Published
2024
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31. Cell-based assays for the detection of MOG antibodies: a comparative study

Author

Gastaldi, Matteo, Scaranzin, Silvia, Jarius, Sven, Wildeman, Brigitte, Zardini, Elisabetta, Mallucci, Giulia, Rigoni, Eleonora, Vegezzi, Elisa, Foiadelli, Thomas, Savasta, Salvatore, Banfi, Paola, Versino, Maurizio, Benedetti, Luana, Novi, Giovanni, Mancardi, Margherita Maria, Giacomini, Thea, Annovazzi, Pietro, Baroncini, Damiano, Ferraro, Diana, Lampasona, Vito, Reindl, Markus, Waters, Patrick, and Franciotta, Diego

Published
2020
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33. Neurological complications due to copper deficiency in the context of Wilson disease treatment: a case report with long-term follow-up and review of the literature.

Author

Tornabene, Danilo, Bini, Paola, Gastaldi, Matteo, Vegezzi, Elisa, Asteggiano, Carlo, Marchioni, Enrico, and Diamanti, Luca

Subjects
COPPER, LITERATURE reviews, BLOOD cell count, PERIPHERAL neuropathy, IODINE deficiency
Abstract

The objective is to investigate the presentation, complications, management, and outcomes of copper deficiency-induced neurological pathologies due to Wilson disease (WD) overtreatment. We examined the case of a WD patient who developed a low thoracic dorsal myelopathy due to chronic hypocupremia from excessive zinc therapy. A comprehensive literature review was conducted to identify similar cases. Ten additional cases of neurological pathology resulting from copper deficiency in the context of WD over-treatment were identified, all occurring during therapy with zinc salts. Myelopathy and peripheral neuropathy were the most common complications, while two additional groups reported leukoencephalopathy. Early cytopenia was often associated with copper deficiency-related neurological pathology appearing early in the context of copper deficiency. WD patients undergoing treatment, especially with zinc salts, should be closely monitored to prevent over-treatment and the consequent copper deficiency. Regular complete blood counts could provide early detection of copper deficiency, avoiding irreversible neurological damage. Swift recognition of new neurological signs not consistent with WD and timely discontinuation of the decoppering therapy are critical for improving outcomes. The optimal management, including the potential benefit of copper supplementation in patients with WD and subsequent therapy adjustments, remains unclear and necessitates further investigation. Despite the general poor functional neurological outcomes, there were some exceptions that warrant further exploration. [ABSTRACT FROM AUTHOR]

Published
2024
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35. A single T cell epitope drives the neutralizing anti-drug antibody response to natalizumab in multiple sclerosis patients

Author

Cassotta, Antonino, Mikol, Vincent, Bertrand, Thomas, Pouzieux, Stéphanie, Le Parc, Josiane, Ferrari, Paul, Dumas, Jacques, Auer, Michael, Deisenhammer, Florian, Gastaldi, Matteo, Franciotta, Diego, Silacci-Fregni, Chiara, Fernandez Rodriguez, Blanca, Giacchetto-Sasselli, Isabella, Foglierini, Mathilde, Jarrossay, David, Geiger, Roger, Sallusto, Federica, Lanzavecchia, Antonio, and Piccoli, Luca

Published
2019
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39. Central nervous system immune-related disorders after SARS-CoV-2 vaccination: a multicenter study.

Author

Vogrig, Alberto, Tartaglia, Sara, Dentoni, Marta, Fabris, Martina, Bax, Francesco, Belluzzo, Marco, Verriello, Lorenzo, Bagatto, Daniele, Gastaldi, Matteo, Tocco, Pierluigi, Zoccarato, Marco, Zuliani, Luigi, Pilotto, Andrea, Padovani, Alessandro, Villagrán-García, Macarena, Davy, Vincent, Gigli, Gian Luigi, Honnorat, Jérôme, and Valente, Mariarosaria

Subjects
NEUROMYELITIS optica, CENTRAL nervous system, POSTVACCINAL encephalitis, VACCINATION, SARS-CoV-2, NEUROLOGIC manifestations of general diseases
Abstract

Background: COVID-19 vaccines have been approved due to their excellent safety and efficacy data and their use has also permitted to reduce neurological complications of SARS-CoV-2. However, clinical trials were underpowered to detect rare adverse events. Herein, the aim was to characterize the clinical spectrum and immunological features of central nervous system (CNS) immunerelated events following SARS-CoV-2 vaccination. Methods: Multicenter, retrospective, cohort study (December 1, 2020-April 30, 2022). Inclusion criteria were (1) de novo CNS disorders developing after SARSCoV-2 vaccination (probable causal relationship as per 2021 Butler criteria) (2); evidence for an immune-mediated etiology, as per (i) 2016 Graus criteria for autoimmune encephalitis (AE); (ii) 2015 Wingerchuk criteria for neuromyelitis optica spectrum disorders; (iii) criteria for myelitis. Results: Nineteen patients were included from 7 tertiary referral hospitals across Italy and France (one of them being a national referral center for AE), over almost 1 year and half of vaccination campaign. Vaccines administered were mRNA based (63%) and adenovirus-vectored (37%). The median time between vaccination and symptoms onset was 14 days (range: 2-41 days). CSF was inflammatory in 74%; autoantibodies were detected in 5%. CSF cytokine analysis (n=3) revealed increased CXCL-10 (IP-10), suggesting robust T-cell activation. The patients had AE (58%), myelitis (21%), acute disseminated encephalomyelitis (ADEM) (16%), and brainstem encephalitis (5%). All patients but 2 received immunomodulatory treatment. At last follow-up (median 130 days; range: 32-540), only one patient (5%) had a mRS>2. Conclusion: CNS adverse events of COVID-19 vaccination appear to be very rare even at reference centers and consist mostly of antibody-negative AE, myelitis, and ADEM developing approximately 2 weeks after vaccination. Most patients improve following immunomodulatory treatment. [ABSTRACT FROM AUTHOR]

Published
2024
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40. General features, pathogenesis, and laboratory diagnostics of autoimmune encephalitis.

Author

Masciocchi, Stefano, Businaro, Pietro, Scaranzin, Silvia, Morandi, Chiara, Franciotta, Diego, and Gastaldi, Matteo

Subjects
ENCEPHALITIS diagnosis, TREATMENT of encephalitis, ENCEPHALITIS, AUTOIMMUNE diseases, DISEASE management, EARLY medical intervention, DISEASE complications
Abstract

Autoimmune encephalitis (AE) is a group of inflammatory conditions that can associate with the presence of antibodies directed to neuronal intracellular, or cell surface antigens. These disorders are increasingly recognized as an important differential diagnosis of infectious encephalitis and of other common neuropsychiatric conditions. Autoantibody diagnostics plays a pivotal role for accurate diagnosis of AE, which is of utmost importance for the prompt recognition and early treatment. Several AE subgroups can be identified, either according to the prominent clinical phenotype, presence of a concomitant tumor, or type of neuronal autoantibody, and recent diagnostic criteria have provided important insights into AE classification. Antibodies to neuronal intracellular antigens typically associate with paraneoplastic neurological syndromes and poor prognosis, whereas antibodies to synaptic/neuronal cell surface antigens characterize many AE subtypes that associate with tumors less frequently, and that are often immunotherapy-responsive. In addition to the general features of AE, we review current knowledge on the pathogenic mechanisms underlying these disorders, focusing mainly on the potential role of neuronal antibodies in the most frequent conditions, and highlight current theories and controversies. Then, we dissect the crucial aspects of the laboratory diagnostics of neuronal antibodies, which represents an actual challenge for both pathologists and neurologists. Indeed, this diagnostics entails technical difficulties, along with particularly interesting novel features and pitfalls. The novelties especially apply to the wide range of assays used, including specific tissue-based and cell-based assays. These assays can be developed in-house, usually in specialized laboratories, or are commercially available. They are widely used in clinical immunology and in clinical chemistry laboratories, with relevant differences in analytic performance. Indeed, several data indicate that in-house assays could perform better than commercial kits, notwithstanding that the former are based on non-standardized protocols. Moreover, they need expertise and laboratory facilities usually unavailable in clinical chemistry laboratories. Together with the data of the literature, we critically evaluate the analytical performance of the in-house vs commercial kit-based approach. Finally, we propose an algorithm aimed at integrating the present strategies of the laboratory diagnostics in AE for the best clinical management of patients with these disorders. [ABSTRACT FROM AUTHOR]

Published
2024
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41. Antibodies to neurofascin, contactin-1, and contactin-associated protein 1 in CIDP: Clinical relevance of IgG isotype

Author

Cortese, Andrea, Lombardi, Raffaella, Briani, Chiara, Callegari, Ilaria, Benedetti, Luana, Manganelli, Fiore, Luigetti, Marco, Ferrari, Sergio, Clerici, Angelo M., Marfia, Girolama Alessandra, Rigamonti, Andrea, Carpo, Marinella, Fazio, Raffaella, Corbo, Massimo, Mazzeo, Anna, Giannini, Fabio, Cosentino, Giuseppe, Zardini, Elisabetta, Currò, Riccardo, Gastaldi, Matteo, Vegezzi, Elisa, Alfonsi, Enrico, Berardinelli, Angela, Kouton, Ludivine, Manso, Constance, Giannotta, Claudia, Doneddu, Pietro, Dacci, Patrizia, Piccolo, Laura, Ruiz, Marta, Salvalaggio, Alessandro, De Michelis, Chiara, Spina, Emanuele, Topa, Antonietta, Bisogni, Giulia, Romano, Angela, Mariotto, Sara, Mataluni, Giorgia, Cerri, Federica, Stancanelli, Claudia, Sabatelli, Mario, Schenone, Angelo, Marchioni, Enrico, Lauria, Giuseppe, Nobile-Orazio, Eduardo, Devaux, Jérôme, and Franciotta, Diego

Published
2020
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43. Beyond Myelin Oligodendrocyte Glycoprotein and Aquaporin-4 Antibodies: Alternative Causes of Optic Neuritis.

Author

Greco, Giacomo, Colombo, Elena, Gastaldi, Matteo, Ahmad, Lara, Tavazzi, Eleonora, Bergamaschi, Roberto, and Rigoni, Eleonora

Subjects
MYELIN oligodendrocyte glycoprotein, OPTIC neuritis, OPTIC disc edema, AQUAPORINS, OPTIC disc, IMMUNOGLOBULINS, EYE movements, AUTOANTIBODIES
Abstract

Optic neuritis (ON) is the most common cause of vision loss in young adults. It manifests as acute or subacute vision loss, often accompanied by retrobulbar discomfort or pain during eye movements. Typical ON is associated with Multiple Sclerosis (MS) and is generally mild and steroid-responsive. Atypical forms are characterized by unusual features, such as prominent optic disc edema, poor treatment response, and bilateral involvement, and they are often associated with autoantibodies against aquaporin-4 (AQP4) or Myelin Oligodendrocyte Glycoprotein (MOG). However, in some cases, AQP4 and MOG antibodies will return as negative, plunging the clinician into a diagnostic conundrum. AQP4- and MOG-seronegative ON warrants a broad differential diagnosis, including autoantibody-associated, granulomatous, and systemic disorders. These rare forms need to be identified promptly, as their management and prognosis are greatly different. The aim of this review is to describe the possible rarer etiologies of non-MS-related and AQP4- and MOG-IgG-seronegative inflammatory ON and discuss their diagnoses and treatments. [ABSTRACT FROM AUTHOR]

Published
2023
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44. Granulocyte activation markers in cerebrospinal fluid differentiate acute neuromyelitis spectrum disorder from multiple sclerosis.

Author

Leppert, David, Mitsuru Watanabe, Schaedelin, Sabine, Piehl, Fredrik, Furlan, Roberto, Gastaldi, Matteo, Lambert, Jeremy, Evertsson, Björn, Fink, Katharina, Takuya Matsushita, Katsuhisa Masaki, Noriko Isobe, Jun-ichi Kira, Benkert, Pascal, Maceski, Aleksandra, Willemse, Eline, Oechtering, Johanna, Orleth, Annette, Meier, Stephanie, and Kuhle, Jens

Subjects
NEUROMYELITIS optica, GLIAL fibrillary acidic protein, CEREBROSPINAL fluid, MULTIPLE sclerosis, VASCULAR cell adhesion molecule-1, CELL adhesion molecules
Published
2023
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45. Caspr1 antibodies autoimmune paranodopathy with severe tetraparesis: Potential relevance of antibody titers in monitoring treatment response.

Author

Bresciani, Lorenzo, Salvalaggio, Alessandro, Vegezzi, Elisa, Visentin, Andrea, Fortuna, Andrea, Anglani, Mariagiulia, Cacciavillani, Mario, Masciocchi, Stefano, Scaranzin, Silvia, Carecchio, Miryam, Martinuzzi, Andrea, Gastaldi, Matteo, and Briani, Chiara

Subjects
RITUXIMAB, IMMUNOGLOBULINS, MAGNETIC resonance imaging, SEVERITY of illness index, TREATMENT effectiveness, GUILLAIN-Barre syndrome, GLYCOPROTEINS, QUADRIPLEGIA, CEREBROSPINAL fluid
Abstract

Aim: Nodopathies and paranodopathies are autoimmune neuropathies associated with antibodies to nodal–paranodal antigens (neurofascin 140/186 and 155, contactin‐1, contactin‐associated protein 1 [Caspr1]) characterized by peculiar clinical features, poor response to standard immunotherapies (e.g., intravenous immunoglobulins, IVIg). Improvement after anti‐CD20 monoclonal antibody therapy has been reported. Data on Caspr1 antibodies pathogenicity are still preliminary, and longitudinal titers have been poorly described. Methods: We report on a young woman who developed a disabling neuropathy with antibodies to the Caspr1/contactin‐1 complex showing a dramatic improvement after rituximab therapy, mirrored by the decrease of antibody titers. Results: A 26‐year‐old woman presented with ataxic‐stepping gait, severe motor weakness at four limbs, and low frequency postural tremor. For neurophysiological evidence of demyelinating neuropathy, she was diagnosed with chronic inflammatory demyelinating polyradiculoneuropathy and treated with IVIg without benefit. MRI showed symmetrical hypertrophy and marked signal hyperintensity of brachial and lumbosacral plexi. Cerebrospinal fluid showed 710 mg/dL protein. Despite intravenous methylprednisolone, the patient progressively worsened, and became wheelchair‐bound. Antibodies to nodal–paranodal antigens were searched for by ELISA and cell‐based assay. Anticontactin/Caspr1 IgG4 antibodies resulted positive. The patient underwent rituximab therapy with slow progressive improvement that mirrored the antibodies titer, measured throughout the disease course. Conclusions: Our patient had a severe progressive course with early disability and axonal damage, and slow recovery starting only a few months after antibody‐depleting therapy. The close correlation between titer, disability, and treatment, supports the pathogenicity of Caspr1 antibodies, and suggest that their longitudinal evaluation might provide a potential biomarker to evaluate treatment response. [ABSTRACT FROM AUTHOR]

Published
2023
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48. Caspr1 antibodies autoimmune paranodopathy with severe tetraparesis: potential relevance of antibody titers in monitoring treatment response

Author

Bresciani Lorenzo, Salvalaggio Alessandro, Vegezzi Elisa, Visentin Andrea, Fortuna Andrea, Anglani Mariagiulia, Cacciavillani Mario, Stefano Masciocchi, Silvia Scaranzin, Carecchio Miryam, Martinuzzi Andrea, Gastaldi Matteo, and Briani Chiara

Subjects
rituximab, Caspr1/contactin-1 complex, autoimmune neuropathy, nodo-paranodopathy, General Neuroscience, Neurology (clinical)
Published
2023

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