Comparison of antibody reactivity in the first and second episodes of recurrent Miller Fisher syndrome
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LETTER TO THE EDITOR
Comparison of antibody reactivity in the first and second episodes of recurrent Miller Fisher syndrome Hirokazu Uchigami 1
&
Yoshito Saito 1 & Takeyuki Tsuchida 1 & Ayumi Uchibori 2 & Atsuro Chiba 2 & Masaaki Saito 1
Received: 7 July 2020 / Accepted: 19 October 2020 # Fondazione Società Italiana di Neurologia 2020
Dear Editor, Miller Fisher syndrome (MFS) is a postinfectious autoimmune disease characterized by a monophasic disease course, whose recurrence is rare [1]. Although recurrent episodes of MFS are usually similar to the first, some signs/symptoms during relapse may be worse than the initial signs/symptoms for some patients [2]. The immunological mechanism of recurrent MFS is not yet fully understood. Evaluating signs/ symptoms and antiganglioside antibodies during different episodes of MFS could be elucidating, but there is a limited number of studies that show detailed comparisons of antibodies against gangliosides including antibody titers and ganglioside complexes (GSCs). We report a woman with recurrent MFS whose signs/symptoms were more severe during relapse as compared to her first episode; we compared her signs/ symptoms and antibodies against gangliosides, including GSCs, during each episode. A 71-year-old woman developed double vision and gait instability after a week of sore throat and fever. Neurological examination revealed limited upward, downward, and inward extraocular movements; right-sided blepharoptosis; diminished deep tendon reflexes; and truncal ataxia. She had difficulty walking but could keep seated. Cerebrospinal fluid (CSF) examination showed albuminocytologic dissociation (cell count, 1/mm3; protein level, 48 mg/dL). IgG anti-GQ1b and anti-GT1a antibodies were found in blood serum collected 8 days after the neurological signs/symptoms appeared (GQ1b titer, 0.863; GT1a titer, 0.504; normal range for both, < 0.1), as were anti-GSC antibodies (GQ1b/GA1, GQ1b/GM1,
* Hirokazu Uchigami [email protected] 1
Department of Neurology, Tokyo Kyosai Hospital, 2-3-8 Naka-Meguro, Meguro-ku, Tokyo, Japan
2
Department of Neurology, Faculty of Medicine, Kyorin University, Tokyo, Japan
GT1a/GA1, and GT1a/GM1), which confirmed MFS (Fig. 1a). Her signs/symptoms were not aggravated during her hospitalization, and she underwent physical therapy. She was discharged to home on day 32. Five years later, she was admitted to our hospital with the complaints of dizziness, double vision, and difficulty walking after a week of cough and sore throat. On hospitalization day 4, she had bilateral blepharoptosis, total external ophthalmoplegia, total areflexia, and difficulties in staying in a seated position due to truncal ataxia. CSF examination showed albuminocytologic dissociation (cell count, 1/mm 3 ; protein level, 61 mg/dL). Her signs/ symptoms progressed rapidly; under suspicion of recurrent MFS, she was treated with intravenous immunoglobulin (17.5 g/day for 5 days) starting on hospitalization day 5. Compared with the first episode, anti-GQ1b and anti-GT1a antibody
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