MOG antibody disease manifesting as progressive cognitive deterioration and behavioral changes with primary central nervous system vasculitis

Toshikazu Baba, Koji Shinoda, mitsuru watanabe, Shoko Sadashima, Dai Matsuse, Noriko Isobe, Ryo Yamasaki, Kimihiko Kaneko, Toshiyuki Takahashi, Toru Iwaki, Jun-Ichi Kira

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

We report a 60-year-old male with anti-myelin oligodendrocyte glycoprotein (MOG) antibody who developed progressive cognitive deterioration and behavioral changes, with no other focal signs, over 9 months. MRI showed numerous T2-hyperintense lesions with partial contrast enhancement in white and grey matter of cerebrum, cerebellum and spinal cord. A brain biopsy revealed perivascular inflammatory cell infiltration, disturbed vascular continuity and no demyelination, indicative of a lymphocytic pattern of primary CNS vasculitis (PCNSV). Contrast enhancement disappeared after immunotherapy; however, cognitive impairment was not improved. Neurologists should note that MOG antibody disease can present as immunotherapy-resistant progressive cognitive impairment with PCNSV-like histopathology.

Original languageEnglish
Pages (from-to)48-50
Number of pages3
JournalMultiple Sclerosis and Related Disorders
Volume30
DOIs
Publication statusPublished - May 1 2019

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Myelin-Oligodendrocyte Glycoprotein
Central Nervous System Vasculitis
Immunotherapy
Antibodies
Cerebrum
Demyelinating Diseases
Cerebellum
Blood Vessels
Spinal Cord
Biopsy
Brain
Cognitive Dysfunction
Neurologists
White Matter
Gray Matter

All Science Journal Classification (ASJC) codes

  • Neurology
  • Clinical Neurology

Cite this

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abstract = "We report a 60-year-old male with anti-myelin oligodendrocyte glycoprotein (MOG) antibody who developed progressive cognitive deterioration and behavioral changes, with no other focal signs, over 9 months. MRI showed numerous T2-hyperintense lesions with partial contrast enhancement in white and grey matter of cerebrum, cerebellum and spinal cord. A brain biopsy revealed perivascular inflammatory cell infiltration, disturbed vascular continuity and no demyelination, indicative of a lymphocytic pattern of primary CNS vasculitis (PCNSV). Contrast enhancement disappeared after immunotherapy; however, cognitive impairment was not improved. Neurologists should note that MOG antibody disease can present as immunotherapy-resistant progressive cognitive impairment with PCNSV-like histopathology.",
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T1 - MOG antibody disease manifesting as progressive cognitive deterioration and behavioral changes with primary central nervous system vasculitis

AU - Baba, Toshikazu

AU - Shinoda, Koji

AU - watanabe, mitsuru

AU - Sadashima, Shoko

AU - Matsuse, Dai

AU - Isobe, Noriko

AU - Yamasaki, Ryo

AU - Kaneko, Kimihiko

AU - Takahashi, Toshiyuki

AU - Iwaki, Toru

AU - Kira, Jun-Ichi

PY - 2019/5/1

Y1 - 2019/5/1

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AB - We report a 60-year-old male with anti-myelin oligodendrocyte glycoprotein (MOG) antibody who developed progressive cognitive deterioration and behavioral changes, with no other focal signs, over 9 months. MRI showed numerous T2-hyperintense lesions with partial contrast enhancement in white and grey matter of cerebrum, cerebellum and spinal cord. A brain biopsy revealed perivascular inflammatory cell infiltration, disturbed vascular continuity and no demyelination, indicative of a lymphocytic pattern of primary CNS vasculitis (PCNSV). Contrast enhancement disappeared after immunotherapy; however, cognitive impairment was not improved. Neurologists should note that MOG antibody disease can present as immunotherapy-resistant progressive cognitive impairment with PCNSV-like histopathology.

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