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1. Application of immunotherapy for neurological manifestations in hypermobile Ehlers–Danlos syndrome

Author

Manabu Araki, Youwei Lin, Hirohiko Ono, Wakiro Sato, and Takashi Yamamura

Subjects
Neurology. Diseases of the nervous system, RC346-429
Abstract

Ehlers–Danlos syndrome (EDS) is a heterogeneous heritable connective tissue disorder with various neurological manifestations, including chronic pain. The neurological manifestations in EDS are often regarded as being caused by the associated musculoskeletal disorders or polyneuropathy. Here, we present two patients with hypermobile EDS (hEDS), presenting with relapsing central nervous system (CNS) manifestations. Although the two patients showed relapsing signs of CNS manifestations like multiple sclerosis (MS) or neuromyelitis optica spectrum disorder (NMOSD), they were unique in that they had widespread opioid-dependent chronic pain, which is not consistent with the symptoms of MS/NMOSD. Unexpectedly, the serious pain of unknown origin was remarkably mitigated by plasmapheresis, and magnetic resonance imaging (MRI) examinations conducted for one of the patients were negative. Collectively, we speculate that hEDS may be more susceptible to ‘normal-appearing imaging, neuroimmunologically justified, autoimmune-mediated encephalomyelitis (NINJA).’ Analysis of the presented cases and an additional three patients with EDS with chronic pain indicates that treatable immune-mediated mechanisms deserve considerations for neurological symptoms observed in hEDS.

Published
2018
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3. Safety and efficacy of rozanolixizumab in patients with generalised myasthenia gravis (MycarinG): a randomised, double-blind, placebo-controlled, adaptive phase 3 study

Author

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

Subjects
Neurology (clinical)
Published
2023

4. Skewing of the B cell receptor repertoire in myalgic encephalomyelitis/chronic fatigue syndrome

Author

Ryuji Suzuki, Masakazu Nakamura, Keiko Amano, Takaji Matsutani, Isu Shin, Hirohiko Ono, Wakiro Sato, and Takashi Yamamura

Subjects
musculoskeletal diseases, 0301 basic medicine, Encephalomyelitis, Immunology, B-cell receptor, Clone (cell biology), Receptors, Antigen, B-Cell, Priming (immunology), 03 medical and health sciences, Behavioral Neuroscience, 0302 clinical medicine, medicine, Chronic fatigue syndrome, Humans, B cell, Fatigue Syndrome, Chronic, Endocrine and Autonomic Systems, business.industry, medicine.disease, 030104 developmental biology, medicine.anatomical_structure, IGHD, IGHV@, business, 030217 neurology & neurosurgery
Abstract

Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a debilitating condition characterized by fatigue and post-exertional malaise, accompanied by various signs of neurological and autonomic dysfunction. ME/CFS is often triggered by an infectious episode and associated with an aberrant immune system. Here we report that ME/CFS is a disorder characterized by skewed B cell receptor gene usage. By applying a next-generation sequencing to determine the clone-based IGHV/IGHD/IGHJ repertoires, we revealed a biased usage of several IGHV genes in peripheral blood B cells from ME/CFS patients. Results of receiver operating characteristic (ROC) analysis further indicated a possibility of distinguishing patients from healthy controls, based on the skewed B cell repertoire. Meanwhile, B cell clones using IGHV3-30 and IGHV3-30-3 genes were more frequent in patients with an obvious infection-related episode at onset, and correlated to expression levels of interferon response genes in plasmablasts. Collectively, these results imply that B cell responses in ME/CFS are directed against an infectious agents or priming antigens induced before disease onset.

Published
2021

5. Staging of astrocytopathy and complement activation in neuromyelitis optica spectrum disorders

Author

Kazuo Fujihara, Tatsuro Misu, Yoshiki Takai, Masashi Aoki, Shuhei Nishiyama, Hans Lassmann, Y. Matsumoto, Yasuto Itoyama, Ichiro Nakashima, Mika Watanabe, Hiroyoshi Suzuki, Shinya Tanaka, Hirohiko Ono, Toshiyuki Takahashi, Kenji Okita, Chihiro Namatame, Hiroshi Kuroda, Shunichi Sasou, Hiromi Okada, and Kimihiko Kaneko

Subjects
Male, 0301 basic medicine, Pathology, medicine.medical_specialty, 03 medical and health sciences, 0302 clinical medicine, medicine, Humans, Complement Activation, Aged, Autoantibodies, Aquaporin 4, Neuromyelitis optica, Glial fibrillary acidic protein, biology, business.industry, Multiple sclerosis, Neuromyelitis Optica, Brain, Middle Aged, medicine.disease, Complement system, 030104 developmental biology, medicine.anatomical_structure, Gliosis, Astrocytes, biology.protein, Female, Neurology (clinical), medicine.symptom, Complement membrane attack complex, business, 030217 neurology & neurosurgery, Astrocyte
Abstract

Aquaporin 4 (AQP4)-IgG-positive neuromyelitis optica spectrum disorder (AQP4-IgG+NMOSD) is an autoimmune astrocytopathic disease pathologically characterized by the massive destruction and regeneration of astrocytes with diverse types of tissue injury with or without complement deposition. However, it is unknown whether this diversity is derived from differences in pathological processes or temporal changes. Furthermore, unlike for the demyelinating lesions in multiple sclerosis, there has been no staging of astrocytopathy in AQP4-IgG+NMOSD based on astrocyte morphology. Therefore, we classified astrocytopathy of the disease by comparing the characteristic features, such as AQP4 loss, inflammatory cell infiltration, complement deposition and demyelination activity, with the clinical phase. We performed histopathological analyses in eight autopsied cases of AQP4-IgG+NMOSD. Cases comprised six females and two males, with a median age of 56.5 years (range, 46–71 years) and a median disease duration of 62.5 months (range, 0.6–252 months). Astrocytopathy in AQP4-IgG+NMOSD was classified into the following four stages defined by the astrocyte morphology and immunoreactivity for GFAP: (i) astrocyte lysis: extensive loss of astrocytes with fragmented and/or dust-like particles; (ii) progenitor recruitment: loss of astrocytes except small nucleated cells with GFAP-positive fibre-forming foot processes; (iii) protoplasmic gliosis: presence of star-shaped astrocytes with abundant GFAP-reactive cytoplasm; and (iv) fibrous gliosis: lesions composed of densely packed mature astrocytes. The astrocyte lysis and progenitor recruitment stages dominated in clinically acute cases (within 2 months after the last recurrence). Findings common to both stages were the loss of AQP4, a decreased number of oligodendrocytes, the selective loss of myelin-associated glycoprotein and active demyelination with phagocytic macrophages. The infiltration of polymorphonuclear cells and T cells (CD4-dominant) and the deposition of activated complement (C9neo), which reflects the membrane attack complex, a hallmark of acute NMOSD lesions, were selectively observed in the astrocyte lysis stage (98.4% in astrocyte lysis, 1.6% in progenitor recruitment, and 0% in protoplasmic gliosis and fibrous gliosis). Although most of the protoplasmic gliosis and fibrous gliosis lesions were accompanied by inactive demyelinated lesions with a low amount of inflammatory cell infiltration, the deposition of complement degradation product (C3d) was observed in all four stages, even in fibrous gliosis lesions, suggesting the past or chronic occurrence of complement activation, which is a useful finding to distinguish chronic lesions in NMOSD from those in multiple sclerosis. Our staging of astrocytopathy is expected to be useful for understanding the unique temporal pathology of AQP4-IgG+NMOSD.

Published
2021

6. Myelin oligodendrocyte glycoprotein antibody-associated disease: an immunopathological study

Author

Mari Yoshida, Teppei Komatsu, Monika Bradl, Kiyotaka Nakamagoe, Tatsuro Misu, Ichiro Nakashima, Masashi Aoki, Hiroshi Kuroda, Kazuo Fujihara, Koichi Narikawa, Hiroyoshi Suzuki, Toshimasa Ikeda, Hans Lassmann, Hiroya Nishida, Kimihiko Kaneko, Takashi Komori, Morinobu Seki, Yoshiki Takai, Shuhei Nishiyama, Hirohiko Ono, Norio Chihara, Satoko Tsuchida, and Toshiyuki Takahashi

Subjects
Adult, Male, 0301 basic medicine, Pathology, medicine.medical_specialty, Adolescent, Myelitis, Demyelinating Autoimmune Diseases, CNS, Autoantigens, Myelin oligodendrocyte glycoprotein, Young Adult, 03 medical and health sciences, Myelin, 0302 clinical medicine, medicine, Demyelinating disease, Humans, Optic neuritis, Child, Autoantibodies, Neuromyelitis optica, biology, business.industry, Multiple sclerosis, Brain, Middle Aged, medicine.disease, 030104 developmental biology, medicine.anatomical_structure, Acute disseminated encephalomyelitis, biology.protein, Female, Myelin-Oligodendrocyte Glycoprotein, Neurology (clinical), business, 030217 neurology & neurosurgery
Abstract

Conformation-sensitive antibodies against myelin oligodendrocyte glycoprotein (MOG) are detectable in patients with optic neuritis, myelitis, opticomyelitis, acute or multiphasic disseminated encephalomyelitis (ADEM/MDEM) and brainstem/cerebral cortical encephalitis, but are rarely detected in patients with prototypic multiple sclerosis. So far, there has been no systematic study on the pathological relationship between demyelinating lesions and cellular/humoral immunity in MOG antibody-associated disease. Furthermore, it is unclear whether the pathomechanisms of MOG antibody-mediated demyelination are similar to the demyelination patterns of multiple sclerosis, neuromyelitis optica spectrum disorders (NMOSD) with AQP4 antibody, or ADEM. In this study, we immunohistochemically analysed biopsied brain tissues from 11 patients with MOG antibody-associated disease and other inflammatory demyelinating diseases. Patient median onset age was 29 years (range 9–64), and the median interval from attack to biopsy was 1 month (range 0.5–96). The clinical diagnoses were ADEM (n = 2), MDEM (n = 1), multiple brain lesions without encephalopathy (n = 3), leukoencephalopathy (n = 3) and cortical encephalitis (n = 2). All these cases had multiple/extensive lesions on MRI and were oligoclonal IgG band-negative. Most demyelinating lesions in 10 of 11 cases showed a perivenous demyelinating pattern previously reported in ADEM (153/167 lesions) and a fusion pattern (11/167 lesions) mainly in the cortico-medullary junctions and white matter, and only three lesions in two cases showed confluent demyelinated plaques. In addition, 60 of 167 demyelinating lesions (mainly in the early phase) showed MOG-dominant myelin loss, but relatively preserved oligodendrocytes, which were distinct from those of AQP4 antibody-positive NMOSD exhibiting myelin-associated glycoprotein-dominant oligodendrogliopathy. In MOG antibody-associated diseases, MOG-laden macrophages were found in the perivascular spaces and demyelinating lesions, and infiltrated cells were abundant surrounding multiple blood vessels in and around the demyelinating lesions, mainly consisting of macrophages (CD68; 1814 ± 1188 cells/mm2), B cells (CD20; 468 ± 817 cells/mm2), and T cells (CD3; 2286 ± 1951 cells/mm2), with CD4-dominance (CD4+ versus CD8+; 1281 ± 1196 cells/mm2 versus 851 ± 762 cells/mm2, P

Published
2020

7. Brain abnormalities in myalgic encephalomyelitis/chronic fatigue syndrome: Evaluation by diffusional kurtosis imaging and neurite orientation dispersion and density imaging

Author

Keiko Amano, Yoko Shigemoto, Isu Shin, Takashi Yamamura, Hirohiko Ono, Mikako Enokizono, Hiroshi Matsuda, Emiko Morimoto, Yukio Kimura, Wakiro Sato, Noriko Sato, and Miho Ota

Subjects
education.field_of_study, Genu of the corpus callosum, Internal capsule, business.industry, Population, Superior longitudinal fasciculus, medicine.disease, 030218 nuclear medicine & medical imaging, 03 medical and health sciences, 0302 clinical medicine, medicine.anatomical_structure, Fractional anisotropy, Chronic fatigue syndrome, Medicine, Radiology, Nuclear Medicine and imaging, business, Nuclear medicine, education, Pathological, Diffusion MRI
Abstract

BACKGROUND Diffusional kurtosis imaging (DKI) and neurite orientation dispersion and density imaging (NODDI) metrics provide more specific information regarding pathological changes than diffusion tensor imaging (DTI). PURPOSE To detect microstructural abnormalities in myalgic encephalomyelitis (ME) / chronic fatigue syndrome (CFS) patients by using DKI and NODDI metrics. STUDY TYPE Prospective. POPULATION Twenty ME/CFS patients and 23 healthy controls were recruited. FIELD STRENGTH/SEQUENCE Three-b value DWI (b-values = 0, 1000, and 2000 sec/mm2 ) and 3D T1 -weighted images were at 3.0T. ASSESSMENT Mean kurtosis (MK), neurite density index (NDI), orientation dispersion index (ODI), fractional anisotropy (FA), and mean diffusivity (MD) were calculated. STATISTICAL TESTING The two-sample t-test analysis in SPM12 software was used to compare the differences between ME/CFS and control groups. RESULTS In the ME/CFS patients, we observed significant FA decreases in the genu of the corpus callosum and the anterior limb of the right internal capsule (P

Published
2018

8. Benefits of eculizumab in AQP4+ neuromyelitis optica spectrum disorder: Subgroup analyses of the randomized controlled phase 3 PREVENT trial

Author

Jacqueline Palace, Dean M. Wingerchuk, Kazuo Fujihara, Achim Berthele, Celia Oreja-Guevara, Ho Jin Kim, Ichiro Nakashima, Michael Levy, Murat Terzi, Natalia Totolyan, Shanthi Viswanathan, Kai-Chen Wang, Amy Pace, Marcus Yountz, Larisa Miller, Róisín Armstrong, Sean Pittock, Daniel Julio Muñoz, Jorge David Amor, Carolina Bocchiardo, Julieta Iourno Danielle, Alfredo Laffue, Carolina Daniela Diaz Obregon, Maria Fernanda Paez, Roberto Martin Perez, Viviana Ana Maria Rocchi, Loreley Deborah Teijeiro, Jesica Gómez, Andres Maria Villa, Florencia Aguirre, Victoria Carla Fernández, Ramon F. Goicoechea, Luciana Melamud, Ana Stillman, Mariana de Virgiliis, Fatima Pagani Cassara, Marta Cordoba, Maria Teresa Gutierrez, Mariana Ingolotti, Natalia Larripa, Anahi Lupinacci, Josefina Arroyo, Alejandra Romano, Mariana Foa Torres, Carlos Héctor Ballario, Ana Elisa Chiesa, Hernán Gustavo Gómez, Hernán Gabriel Lattini, Carolina Natalia Mainella, Gisel Edith Bolner, María Soledad Eschoyez, Simon Andrew Broadley, Saman Heshmat, Arman Sabet, Andrew Swayne, Susan Freeman, Sofia Jimenez Sanchez, Neil Shuey, Linda Dalic, Ann French, Guru Kuma, Joshua Laing, Lai Yin Law, Jennifer MacIntyre, Andrew Neal, Christopher Plummer, Prashanth Ramachandran, Leslie Sedal, Ian Wilson, Antony Winkel, Wenwen Zhang, Tina Chen, Rani Watts, Michael Barnett, Joshua Barton, Heidi Beadnall, Justin Garber, Todd Andrew Hardy, Benjamin Trewin, Marinda Taha, Deleni Walters, Federico Arturo Silva Sieger, Nhora Patricia Ruiz Alfonso, Anna Maria Pinzon Camacho, Alexander Pabón Moreno, Jorge Armando Castellanos Prad, Adriana Paola Duarte Rueda, Tatiana Castillo, Karol Melissa Castillo Gonzalez, Martha Yolanda Moreno Pico, Judith Castill, Mario Habek, Ivan Adamec, Barbara Barun, Luka Crnosija, Tereza Gabelic, Petra Nytrova, Eva Krasulova, Jana Pavlickova, Michaela Tyblova, Jana Zubkova, Thor Petersen, Gro Helen Dale, Peter Vestergaard Rasmussen, Morten Stilund, Kristina Bacher Svendsen, Vivi Brandt, Nicolas Collongues, Marie-Celine Fleury, Laurent Kremer, Sandrine Bendele, Valérie Neff, Ricarda Diem, Michael Platten, Anne Berberich, Jonabelle Jansen, Hannah Jaschoneck, Brigitte Wildemann, Ursula Aures, Tanja Brandenburger, Tanja Haut, Maria-Lourdes Treceno Fernández, Lilian Aly, Kirsten Brinkhoff, Dorothea Buck, Daniel Golkowski, Mirjam Hermisson, Muna-Miriam Hoshi, Miriam Kaminski, Markus Christian Kowarik, Helena Kronsbein, Klaus Lehmann-Horn, Viola Maria Pongratz, Andreas Schweiker, Lisa-Ann Leddy, Silvia Mueller, Kim Obergfell, Marion Wanka, Uwe Klaus Zettl, Jan Klinke, Micha Loebermann, Stefanie Meister, Florian Rimmele, Alexander Winkelmann, Ina Schroeder, Alexander Yuk-Lun Lau, Lisa Wing-Chi Au, Florence Sin-Ying Fan, Vincent Hing-Lung Ip, Karen Ka-Yan Ma, Sze-Ho Ma, Vincent Chung-Tong Mok, Cheryl Chung-Kwan Au, Pauline Wing-Lam Kwan, Francesco Patti, Andrea Salvatore Caramma, Clara Grazia Chisari, Salvatore Lo Fermo, Silvia Messina, Maria Projetto, Cinzia Caserta, Alessandro Filla, Teresa Costabile, Chiara Pane, Francesco Sacca, Angela Marsili, Giorgia Puorro, Roberto Bergamaschi, Eliana Berra, Giulia Mallucci, Cinzia Fattore, Claudio Gasperini, Simonetta Galgani, Shalom Haggiag, Serena Ruggieri, Claudio Vento, Esmeralda Maria Quartuccio, Carlo Pozzilli, Valeria Teresa Barletta, Giovanna Borriello, Laura De Giglio, Fabiana Marinelli, Miriam Tasillo, Alessandra Amadori, Mariano Fischetti, Flavia Gurreri, Masahiro Mori, Hiroki Masuda, Ryohei Ohtani, Yukari Sekiguchi, Tomohiko Uchida, Akiyuki Uzawa, Hiromi Ito, Emi Kabasawa, Yoko Kaneko, Takuya Matsushita, Dai Matsuse, Hiroyuki Murai, Shintaro Hayashi, Katsuhisa Masak, Hidenori Ogata, Koji Shinoda, Taira Uehara, Mitsuru Watanabe, Hiroo Yamaguchi, Ryo Yamasaki, Tomomi Yonekawa, Maki Jingu, Makiko Nagano, Yumiko Nakamura, Yoshiko Sano, Manabu Araki, Youwei Lin, Madoka Mori, Yohei Mukai, Terunori Sano, Wakiro Sato, Naoya Gogun, Yuriko Maeda, Asami Nishimoto, Sachiko Tsukamoto, Ritsuko Yanagi, Takahiko Saida, Shinichi Nakamura, Tetsuya Nasu, Kyoko Saida, Yuko Shikata, Yoshimi Kodani, Megumi Saeki, Yukako Sawada, Hiroo Yoshikawa, Takashi Kimura, Masamitsu Nishi, Shun Sakamoto, Shinichiro Ukon, Shohei Watanabe, Saori Ebisuya, Nami Kimura, Manami Matsuura, Yukie Morisaki, Yoshiko Muroi, Kuniko Onishi, Ikuko Oshima, Yuki Washino, Tomomi Yamashita, Tatsuro Misu, Kimihiko Kaneko, Masaaki Kato, Hiroshi Kuroda, Kazuhiro Kurosawa, Shuhei Nishiyama, Hirohiko Ono, Yoshiki Takai, Keiko Abe, Hitomi Hoshi, Mari Jinushi, Azusa Oyama, Motonari Sakuma, Yuko Sawada, Satoru Ishibashi, Takanori Yokota, Yoichiro Nishida, Kokoro Ozaki, Nobuo Sanjo, Nozomu Sato, Fuki Denno, Haruko Hiraki, Yumi Matsubara, Takashi Kanda, Masaaki Abe, Masaya Honda, Motoharu Kawai, Michiaki Koga, Toshihiko Maeda, Junichi Ogasawara, Masatoshi Omoto, Yasuteru Sano, Ryota Sato, Fumitaka Shimizu, Hideki Arima, Sachie Fukui, Yoshiko Ishikawa, Tomoko Koyama, Shigemi Shimose, Hirokazu Shinozaki, Masanori Watanabe, Sachi Yasuda, Chieko Yoshiwaka, Suffian Adenan, Mohd Azman M Aris, Ahmad Shahir bin Mawardi, Muhammad Al Hafiz Adnan, Nanthini Munusamy, Siti Nur Omaira Razali, Punitha Somasundram, Jae Won Hyun, In Hye Jeong, Su-Hyun Kim, Hyun-June Shin, Ji Sung Yoo, HyunMin Jang, AeRan Joung, Byung-Jo Kim, Seol-Hee Baek, Jung Bin Kim, Yoo Hwan Kim, Yong Seo Koo, Chan Nyoung Lee, Hung Youl Seok, Jinhee Hwang, Sung Min Kim, So Hyun Ahn, Kyomin Choi, Seok-Jin Choi, Jun-Soon Kim, Young Nam Kwon, Je-Young Shin, Hyeonju Kwon, Byoung Joon Kim, Eun Bin Cho, Hye-Jin Cho, Misong Choi, DongSun Kim, Ju Hyeon Kim, SeungJu Ki, Hye Lim Lee, Kwang-Ho Lee, Ju-Hong Min, Ji-Hyung Park, Jinmyoung Seok, Eunhwa Choi, Sang Ae Park, Seung Min Kim, Ha-Neul Jeong, Bong Jeongbin, Jin Woo Jung, Seung Woo Kim, Yool-hee Kim, Hyung Seok Lee, Ha Young Shin, Yeon Jung, Min Jung Kim, Nou Ri Lee, MiJu Shin, Farit A Khabirov, Lyudmila Averyanova, Natalya Babicheva, Eugenii Granatov, Sergey Kazarov, Timur Khaybullin, Alexander Rogozhin, Dmitry V Pokhabov, Vladislav Abramov, Anastasia Amelina, Yulia Nesteroca, Tatyana Bozhenkina, Aleksey N Boyko, Elena G Demyan, Inessa Khoroshilova, Mikhail Melnikov, Ekaterina V Popova, Svetlana N Sharanova, Sergey G Shchur, Denis V Sazonov, Larisa Babenko, Elena Bayandina, Asya Yarmoschuk, Victor A Baliazin, Elena Baliazina, Elena Budaeva, Irina Chernikova, Zoya Goncharova, Vladimir Krasnov, Marina Myatleva, Olga V. Rodionova, Iuliana Samulyzhko, Alla A. Timofeeva, Sabas Boyero Duran, Maria Mar Mendibe Bilbao, Irene Diaz Cuervo, Jose Maria Losada Domingo, Amaia Gonzalez Eizaguirre, Jose Eulalio Barcena Llona, Roberto Valverde Moyano, Carmen Bahamonde, Fernando Sanchez Lopez, Raquel Pinar Morales, Eduardo Agüera Morales, Carmen Bahamonde Roman, Juan Jose Ochoa Sepulveda, Maria del Carmen Blanco Valero, Nazaret Pelaez Viña, Cristina Conde Gavilan, Ana Maria Jover Sanchez, Sara Vila Bedmar, Nuria Gonzalez Garcia, Aida Orviz Garcia, Ines Gonzalez-Suarez, Elena Miñano Guillamon, Miguel Kawiorski, Elena Guerra Schulz, Alba Garcia Alonso, Francisco Jesus Lopez Perez, Marta Palacios Sarmiento, Guillermo Izquierdo Ayuso, Guillermo Navarro Mascarell, Cristina Paramo Camino, Asuncion Varas Garcia, Yaiza Montserrat Mendoza, Veronica Ines Vargas Muñoz, Patricia Torres Tonda, Ching-Piao Tsai, Jiu-Haw Yin, Mei-Jung Chen, Shan-Ni Li, Fei-Ti Wang, Suwat Srisuwannanukorn, Thanatat Boonmongkol, Duangporn Borisutbuathip, Duangkamol Singwicha, Krittika Siritanan, Chidchanoke Thearapati, Kwanmuang Sornda, Metha Apiwattanakul, Saharat Aungsumart, Narupat Suanprasert, Kaona Suksuchano, Nittaya Parkinsee, Kongkiat Kulkantrakorn, Praween Lolekha, Artit Potigumjon, Puchit Sukphulloprat, Dararat Suksasunee, Chankawee Komaratat, Sunattana Luangtong, Arkhom Arayawichanont, Phanpaphon Konpan, Nathapol Riablershirun, Thaddao Wiroteurairuang, Panadda Jantaweesirirat, Aslı Kurne, Irem Erkent, Ebru Bekircan Kurt, Ezgi Saylam, Yagmur Caliskan, Gulsah Orsel, Yahya Celik, Canan Celebi, Aslan Tekatas, Tugce Banbal, Gulsen Akman Demir, Burcu Altunrende, Zeliha Matur, Baris Topcular, Tules Elmas, Aysenur Gulo, Selin Ozdemir, Cansu Ozkoklesen, Mahinur Ozturk, Mertkan Yanik, Elif Yildirim, Melih Tutuncu, Ayse Altintas, Abdulsamet Cam, Ayse Deniz Elmali, Sabahattin Saip, Aksel Siva, Uygur Tanrıverdi, Ugur Uygunoglu, Sinem Caliskan, Pinar Gulo, Esra Kozig, Sakine Sakiz, Ihsan Sukru Sengun, Egemen Idiman, Rahmi Tumay Ala, Duygu Arslan, Utku Bulut, Yasemin Karakaptan, Derya Kaya, Zaur Mehdiyev, Bengu Balkan, Berfu Kuku, Mujgan Ozhun, Celal Tuga, Muzeyyen Ugur, Husnu Efendi, Sena Destan Bunul, Hakan Cavus, Yunus Emre Gorke, Ayse Kutlu, Seda Ozturk, Cansu Egilmez Sarikaya, Gulsah Becerikli, Cansu Semiz, Ozlem Tun, Sehriban Ayer, Musa Kazim Onar, Mehlika Berra Ozberk, Sedat Sen, Tugce Kirbas Cavdar, Adife Veske, Cavit Boz, Didem Altiparmak, Cigdem Ozen Aydin, Sibel Gazioglu, Duygu Bekircan, Anu Jacob, Heike Arndt, Liene Elsone, Shahd Hassan Mahmoud Hamid, Daniel Hugh Whittam, Martin Wilson, Imelda O'Brien, Maria Isabel da Silva Leite, Pedro Maria Rodriguez Cruz, Damian Robert Jenkins, George Tackley, Ana Cavey, Rosie Everett, Joy Hodder, Abigail Koelewyn, Ellen Mowry, Walter Royal, Robert Shin, Christopher Bever, Daniel Harrison, Horea Rus, Wei Zheng, Karen Callison, Kerry Naunton, Benjamin M Frishberg, Andrew M Blumenfeld, Andrew Inocelda, Kalyani Korabathina, Michael Lobatz, Melissa M Mortin, Irene J Oh, Jay H Rosenberg, Mark Sadoff, Gregory A Sahagian, Anchi Wang, Yasmin Camberos, Guadalupe Sanchez, Estela Soto, Jacqueline A Nicholas, Aaron Boster, Geoffrey Eubank, Katy Groezinger, Meghan Lauf, Annette F Okai, Rashedul Hasan, Chaouki Khoury, Victoria Stokes, Stacey Clardy, Melissa Cortez, John Greenlee, John Rose, Mateo Paz Soldan, Amanda Emett, Lawanda Esquibel, Lilly Fagatele, Ka-Ho Wong, James C Stevens, Thomas M Banas, Marlene C Bultemeyer, Andrea Haller, Natalie Manalo, Keri Aeschliman, Debi Kocks, Michael Racke, Aaron Lee Boster, Michelle Bowman, Jaime Imitola, Yasushi Kisanuki, Misty Green, Stephanie Scarberry, Sharon G Lynch, Heather S Anderson, Gary S Gronseth, Nancy E Hammond, Yasir N Jassam, Manoj K Mittal, Muhammed M Nashatizadeh, Nicholas Levine, Lisa Schmidt, Jill Sibley, Vonda Whitley, James Winkley, Timothy Coleman, Gregory Cooper, Stephanie Sheffield, Keri Turner, Dana Galloway, Robert S Tillett, Geeta A Ganesh, Brian M Plato, Tad D Seifert, Diana Godwin, Deborah Lockridge, Kottil W Rammohan, William A Sheremata, Silvia Delgado, Jose Gonzalez, Alexis Lizarraga, Janice Maldonado, Melissa Ortega, Leticia Tornes, Yanet Babcock, Osmara Cailam, Yesica Campos, Irlisse Couvertier, Bettina Daneri, Jeremy Deni, Jeffrey Hernandez, Tatiana Jaramillo, Tenita Morris, Daniel Nobel, Anjelis Oliveira, Reshma Richardson, Gloria Rodriguez, Ana Romero, Carlos Sandova, Ruta Sawant, Lissett Tueros, Eric S Zetka, Chao Zheng, Daniel H Jacobs, Constance Easterling, Jennifer Fairbank, Revathi Iyengar, Mark Klafter, Justin Lindquist, Ahmed H Sadek, Elizabeth Carmona Toro, Navin Verma, Brigith Patino Castro, Nadia Sukhraj-Singh, Joseph Berger, Eric Williamson, Salim Chahin, Dina Jacobs, Clyde Markowitz, Jessica Dobbins, Lauren Mace, Maria Martin, Ashley Pinckney, Amber Roberts, Islam Zaydan, Galen W Mitchell, Rock A Heyman, Ryan L Orie, Valerie R Suski, Kerry Oddis, Darlene Punjack, Eoin Flanagan, Avi Gadoth, Andrew McKeon, W Oliver Tobin, Anastasia Zekeridou, Katie Dunlay, Jessica Sagen, Jonathan L Carter, Bachir Estephan, Brent P Goodman, Charlene R Hoffman Snyder, Andrea Francone, Irene Galasky, Martha Thomas, Pavle Repovic, James Bowen, Angeli Mayadev, Peiqing Qian, Yuriko Courtney, Lauren Lennox, Robert Thomas Naismith, Anne Haney Cross, Emily Evans, Erin E Longbrake, Megan E Orchard, Gregory F Wu, Linda Heinrich, Susan Sommers, Faria Amjad, Erika Mitchell, Carlos Mora, Bethany Schreiber, Carlo Tornatore, Alexis Carlson, Sacha McCarthy, and Alexandria Oliver

Subjects
Adult, medicine.medical_specialty, Population, Placebo, Antibodies, Monoclonal, Humanized, 03 medical and health sciences, Complement inhibitor, 0302 clinical medicine, Internal medicine, medicine, Humans, 030212 general & internal medicine, education, Aquaporin 4, education.field_of_study, Neuromyelitis optica, business.industry, Neuromyelitis Optica, General Medicine, Eculizumab, medicine.disease, Comorbidity, ddc, Neurology, Concomitant, Rituximab, Neurology (clinical), business, 030217 neurology & neurosurgery, medicine.drug
Abstract

Background Antibodies to the aquaporin-4 (AQP4) water channel in neuromyelitis optica spectrum disorder (NMOSD) are reported to trigger the complement cascade, which is implicated in astrocyte damage and subsequent neuronal injury. The PREVENT study demonstrated that the terminal complement inhibitor eculizumab reduces adjudicated relapse risk in patients with anti-AQP4 immunoglobulin G-positive (AQP4+) NMOSD. The objective of this analysis was to evaluate the efficacy of eculizumab in reducing relapse risk and its safety in AQP4+ NMOSD across clinically relevant subgroups in PREVENT. Methods In the randomized, double-blind, time-to-event, phase 3 PREVENT trial, 143 adults received eculizumab (maintenance dose, 1200 mg/2 weeks) or placebo (2:1), with stable-dose concomitant immunosuppressive therapy (IST) permitted (except rituximab and mitoxantrone). Post hoc analyses of relapses and adverse events were performed for prespecified and post hoc subgroups based on concomitant IST and prior rituximab use, demographic and disease characteristics, and autoimmune comorbidity. Results The significant reduction in relapse risk observed for eculizumab versus placebo in the overall PREVENT population was consistently maintained across subgroups based on concomitant IST and previous rituximab use, age, sex, region, race, time since clinical onset of NMOSD, historical annualized relapse rate, baseline Expanded Disability Status Scale score, and history of another autoimmune disorder. The serious infection rate was lower with eculizumab than placebo regardless of rituximab use in the previous year, concomitant IST use, or history of another autoimmune disorder. Conclusion Across a wide range of clinically relevant AQP4+ NMOSD patient subgroups in PREVENT, eculizumab therapy was consistently effective versus placebo in reducing relapse risk, with no apparent increase in serious infection rate. Trial registration NCT01892345 (ClinicalTrials.gov).

Published
2020

9. Application of immunotherapy for neurological manifestations in hypermobile Ehlers–Danlos syndrome

Author

Wakiro Sato, Youwei Lin, Takashi Yamamura, Manabu Araki, and Hirohiko Ono

Subjects
0301 basic medicine, medicine.medical_specialty, lcsh:RC346-429, 03 medical and health sciences, 0302 clinical medicine, Medicine, Case Series, Spectrum disorder, lcsh:Neurology. Diseases of the nervous system, neuropathic pain, Pharmacology, Neuromyelitis optica, medicine.diagnostic_test, business.industry, Multiple sclerosis, Chronic pain, Magnetic resonance imaging, hypermobile Ehlers–Danlos syndrome, medicine.disease, Dermatology, 030104 developmental biology, plasmapheresis, Neurology, neurological manifestations, Ehlers–Danlos syndrome, Neuropathic pain, immunotherapy, Neurology (clinical), business, Polyneuropathy, 030217 neurology & neurosurgery
Abstract

Ehlers–Danlos syndrome (EDS) is a heterogeneous heritable connective tissue disorder with various neurological manifestations, including chronic pain. The neurological manifestations in EDS are often regarded as being caused by the associated musculoskeletal disorders or polyneuropathy. Here, we present two patients with hypermobile EDS (hEDS), presenting with relapsing central nervous system (CNS) manifestations. Although the two patients showed relapsing signs of CNS manifestations like multiple sclerosis (MS) or neuromyelitis optica spectrum disorder (NMOSD), they were unique in that they had widespread opioid-dependent chronic pain, which is not consistent with the symptoms of MS/NMOSD. Unexpectedly, the serious pain of unknown origin was remarkably mitigated by plasmapheresis, and magnetic resonance imaging (MRI) examinations conducted for one of the patients were negative. Collectively, we speculate that hEDS may be more susceptible to ‘normal-appearing imaging, neuroimmunologically justified, autoimmune-mediated encephalomyelitis (NINJA).’ Analysis of the presented cases and an additional three patients with EDS with chronic pain indicates that treatable immune-mediated mechanisms deserve considerations for neurological symptoms observed in hEDS.

Published
2018

10. Brain abnormalities in myalgic encephalomyelitis/chronic fatigue syndrome: Evaluation by diffusional kurtosis imaging and neurite orientation dispersion and density imaging

Author

Yukio, Kimura, Noriko, Sato, Miho, Ota, Yoko, Shigemoto, Emiko, Morimoto, Mikako, Enokizono, Hiroshi, Matsuda, Isu, Shin, Keiko, Amano, Hirohiko, Ono, Wakiro, Sato, and Takashi, Yamamura

Subjects
Adult, Male, Brain Mapping, Fatigue Syndrome, Chronic, Brain, Middle Aged, Diffusion Magnetic Resonance Imaging, Diffusion Tensor Imaging, Case-Control Studies, Image Processing, Computer-Assisted, Neurites, Anisotropy, Humans, Female, Prospective Studies, Encephalomyelitis
Abstract

Diffusional kurtosis imaging (DKI) and neurite orientation dispersion and density imaging (NODDI) metrics provide more specific information regarding pathological changes than diffusion tensor imaging (DTI).To detect microstructural abnormalities in myalgic encephalomyelitis (ME) / chronic fatigue syndrome (CFS) patients by using DKI and NODDI metrics.Prospective.Twenty ME/CFS patients and 23 healthy controls were recruited.Three-b value DWI (b-values = 0, 1000, and 2000 sec/mmMean kurtosis (MK), neurite density index (NDI), orientation dispersion index (ODI), fractional anisotropy (FA), and mean diffusivity (MD) were calculated.The two-sample t-test analysis in SPM12 software was used to compare the differences between ME/CFS and control groups.In the ME/CFS patients, we observed significant FA decreases in the genu of the corpus callosum and the anterior limb of the right internal capsule (P 0.05), but no significant difference in MD (P = 0.164); there were also significant MK decreases in the right frontal area, anterior cingulate gyrus, superior longitudinal fasciculus (SLF), and left parietal area (P 0.05). Significant NDI decreases were observed in the right posterior cingulate gyrus, SLF, and left frontal area of the ME/CFS patients (P 0.05). Significant ODI decreases were seen in the bilateral occipital areas, right superior temporal gyrus, the anterior limb of internal capsule, and the posterior cingulate gyrus (P 0.05), and significant ODI increases were revealed in the bilateral occipital and right temporal areas (P 0.05).Right SLF abnormalities may be a diagnostic marker for ME/CFS.1 Technical Efficacy: Stage 2 J. Magn. Reson. Imaging 2019;49:818-824.

Published
2018

11. [Immunopathogenesis of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS)]

Author

Takashi, Yamamura, Hirohiko, Ono, and Wakiro, Sato

Subjects
Adult, Aged, 80 and over, Male, Fatigue Syndrome, Chronic, Adolescent, Middle Aged, Gastrointestinal Microbiome, Killer Cells, Natural, Young Adult, Cytokines, Humans, Female, Aged, Autoantibodies
Abstract

A recent study on the pathogenesis of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) has revealed an elevation of inflammatory and anti-inflammatory cytokines in the sera and cerebrospinal fluids of the patients and presence of autoantibodies in subgroups of ME/CFS patients. Furthermore, investigator-initiated clinical trials have proved the efficacy of anti-CD20 antibody (rituximab), that eliminate B cells, in the treatment of ME/CFS. Based on these findings, we hypothesize that immune abnormalities, such as enhanced autoimmune responses, may play an essential role in the neuroinflammatory pathogenesis of ME/CFS.

Published
2018

12. Hypoxia-like tissue injury and glial response contribute to Balo concentric lesion development

Author

Kazuo Fujihara, Ichiro Nakashima, Tatsuro Misu, Mika Watanabe, Shunji Mugikura, Shuhei Nishiyama, Ryuta Saito, Yukihiko Sonoda, Yoshiki Takai, Hirohiko Ono, Masayuki Kanamori, Hiroshi Kuroda, Toshihiro Kumabe, and Masashi Aoki

Subjects
0301 basic medicine, Male, Chemokine, Pathology, medicine.medical_specialty, Concentric, Article, Proinflammatory cytokine, Lesion, 03 medical and health sciences, 0302 clinical medicine, Downregulation and upregulation, Glial Fibrillary Acidic Protein, medicine, Humans, Myelin Sheath, biology, business.industry, Macrophage infiltration, Diffuse Cerebral Sclerosis of Schilder, Myelin Basic Protein, Hypoxia (medical), Middle Aged, Hypoxia-Inducible Factor 1, alpha Subunit, 030104 developmental biology, Diffusion Magnetic Resonance Imaging, biology.protein, T2 lesions, Cytokines, Neurology (clinical), medicine.symptom, business, Neuroglia, 030217 neurology & neurosurgery
Abstract

Objective: To clarify the pathogenic factors and mechanisms underlying the development of concentric demyelinating lesions in Balo disease. Methods: We conducted serial clinical, MRI, and histopathologic assessments of concentric lesion formation in a case of relapsing Balo disease. Results: The patient experienced 2 attacks caused by left parietal and left frontal lesions in 5 years. In MRI findings from both episodes of expanding lesions, there were diffusion-restricted rings that antedated the appearance of gadolinium enhancement; subsequently, typical concentric T2 lesions appeared concurrently with the disappearance of this enhancement. Histopathologic examinations of biopsied brain tissues revealed definite concentric demyelinating layers typical of Balo disease with massive macrophage infiltration but preserved axons. Numerous hypertrophic astrocytes were observed beyond the edges of and within the demyelinating layers. The expression of hypoxia-inducible factor-1α, a protein related to hypoxia-induced tissue preconditioning that contributes to survival and protection against further hypoxia-like injury, was upregulated primarily in glial cells located beyond the edge of the demyelinating layers but was also elevated in hypertrophic astrocytes on the inner sides of resected lesions and in oligodendrocytes in nondemyelinating layers. In addition, these astrocytes expressed CC motif chemokine 2 and/or interleukin-1β, which are inducible by hypoxia-inducible factor-1α and potentially promote demyelination. Conclusions: Our study suggests that a unique interplay between hypoxia-induced tissue preconditioning and proinflammatory cytokines derived from glial cells may contribute to the development of concentric demyelinating lesions in Balo disease.

Published
2015

13. Normal brain imaging accompanies neuroimmunologically justified, autoimmune encephalomyelitis

Author

Masakazu Nakamura, Hirohiko Ono, Yuji Takahashi, Wakiro Sato, Daiki Takewaki, Youwei Lin, Takashi Yamamura, Miho Ota, Tomoko Okamoto, Noriko Sato, Yukio Kimura, and Manabu Araki

Subjects
0301 basic medicine, medicine.medical_specialty, medicine.medical_treatment, Gastroenterology, Article, 03 medical and health sciences, 0302 clinical medicine, Neuroimaging, Internal medicine, Fractional anisotropy, medicine, Expanded Disability Status Scale, Neuromyelitis optica, business.industry, medicine.disease, 030104 developmental biology, Neurology, Methylprednisolone, Plasmapheresis, Neurology (clinical), Differential diagnosis, business, 030217 neurology & neurosurgery, Diffusion MRI, medicine.drug
Abstract

ObjectiveTo examine cases with a clinical course, signs, and symptoms mimicking MS, but without abnormalities on conventional MRI.MethodsAmong 550 people with a tentative diagnosis of MS or neuromyelitis optica spectrum disorder (NMOSD), we selected patients, who met the 2010 McDonald diagnosis criteria for MS, but did not show abnormal findings on conventional brain and spinal cord MRI. After evaluating their clinical data, we analyzed fractional anisotropy (FA) values in the brain white matter on diffusion tensor MRIs and the frequencies of B-cell subsets in the peripheral blood in the corresponding cases as compared to healthy controls.ResultsEleven patients (age: 41.1 ± 8.0 years, 9 women and 2 men) met the selection criteria. They were functionally disabled, with a median expanded disability status scale score of 6.0 (2.0–8.0). CSF oligoclonal bands were negative in all cases. IV methylprednisolone and plasmapheresis (PP) were found to be efficacious. Diffusion tensor MRI analysis revealed extensive white matter abnormalities characterized by significantly decreased FA values. The frequency of plasmablasts in the peripheral blood was significantly increased in these patients similar to NMOSD.ConclusionsThe neurologic disabilities in these patients could be ascribed to brain white matter damage, as revealed by MRI analysis, whereas the efficacy of PP and B-cell abnormalities in the patients suggested an autoimmune-mediated pathogenesis. In the differential diagnosis of MS, we propose that this condition be referred to as, “Normal-appearing Imaging-associated, Neuroimmunologically Justified, Autoimmune encephalomyelitis.”

Published
2018

15. Laparoscopic surgery in a patient with foramen of Winslow hernia due to large uterine fibroids: a case report and literature review

Author

Shusaku Honma, Takenori Itohara, Seigo Sha, and Hirohiko Onoyama

Subjects
Foramen of Winslow hernia, Internal hernia, Laparoscopy, Uterine fibroid, Surgery, RD1-811
Abstract

Abstract Background Foramen of Winslow hernia (FWH) is a rare but emergent condition caused by an increase in the foramen diameter, visceral mobility, and intra-abdominal pressure. To the best of our knowledge, this is the first study to report a case of FWH secondary to large uterine fibroids that was successfully treated with laparoscopic surgery. Case presentation A 52-year-old woman with large uterine fibroids was diagnosed with FWH. Because of the absence of signs of bowel ischemia and peritonitis, we performed an elective laparoscopic surgery through a 5-port system after bowel decompression using a long intestinal tube. Although foramen of Winslow closure was not performed, her postoperative course was uneventful. Conclusions Laparoscopic surgery for FWH is considered an extremely effective surgical treatment option because of its safety and efficacy in performing delicate procedures (such as adhesiolysis) with a good magnified field of view.

Published
2021
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16. Elevated serum aldolase activity in a patient of non-eosinophilic myofasciitis and synovitis with perifascicular atrophy

Author

Yasuto Itoyama, Hideki Mizuno, Maki Tateyama, Masashi Aoki, Hirohiko Ono, and Naoki Suzuki

Subjects
Adult, Male, myalgia, Pathology, medicine.medical_specialty, Synovitis, Muscle biopsy, Myositis, medicine.diagnostic_test, business.industry, medicine.disease, Mononuclear cell infiltration, Atrophy, Fructose-Bisphosphate Aldolase, Eosinophilic, Biopsy, Humans, Medicine, Eosinophilia, Neurology (clinical), Fasciitis, medicine.symptom, business
Abstract

A 35-year-old man suffered from myalgia and joint pain on walking for 5 months. Physical and neurological examinations revealed dermal sclerosis, skin swelling, redness of forearms, Raynaud's phenomenon, joint pain, myalgia and muscle weakness. Eosinophilia was not found and serum creatine kinase activity was normal, while aldolase was markedly elevated. Abnormal signals suggesting synovitis and myofasciitis were found on MRI images. Biopsy of the fascia of quadriceps femoris showed perivascular mononuclear cell infiltration. A muscle biopsy showed mononuclear cell infiltration mainly in the perimysium extending to the endmysium. Eosinophilic cells were not found, Perifascicular atrophy was observed. Corticosteroid therapy improved clinical symptoms and serum aldolase level. We diagnosed him as non-eosinophilic myofasciitis and synovitis with perifascicular atrophy. The serum aldolase activity is usuful for diagnosis and for monitoring the disease activity.

17. Effect of a Selective Inhibitor of Secretory Phospholipase A2, S-5920/LY315920Na, on Experimental Acute Pancreatitis in Rats

Author

Yasuhiko Tomita, Kenji Kuwabara, Shingo Furue, Kazushige Tanaka, Katsutoshi Yamada, Masahiko Ueno, Takashi Ono, Toshiyuki Maruyama, Tetsuo Ajiki, Hirohiko Onoyama, Masahiro Yamamoto, and Yozo Hori

Subjects
Therapeutics. Pharmacology, RM1-950
Abstract

We investigated the efficacy of a potent inhibitor of secretory phospholipase A2 (sPLA2), S-5920/LY315920Na, in an experimental model of acute pancreatitis in rats. Combined intraductal injection of sodium taurocholate (5 mg/rat) and porcine pancreatic sPLA2-IB (300 μg/rat) caused severe hemorrhagic necrotizing pancreatitis resulting in high mortality, along with rapid increases of catalytic PLA2 and lipase activities in plasma and ascites and with gradual increases of plasma amylase and aspartate aminotransferase levels over 9 h after the pancreatitis. Prophylactic intravenous treatment with S-5920/LY315920Na significantly reduced mortality at 7 days, and strongly abrogated PLA2 activities in both plasma and ascites along with significant reduction of lipase activity, amylase, aspartate aminotransferase, and hemorrhage at 6 h. It also significantly reduced histological damage such as edema and parenchymal and fat necroses of the pancreatic tissue. This sPLA2 inhibitor could become an effective agent for the treatment of severe acute pancreatitis. Keywords:: phospholipase A2, pancreatitis, parenchymal necrosis, S-5920/LY315920Na

Published
2004
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