A case of Guillain–Barré syndrome with meningeal irritation

Ashikari, Yuka; Kobayashi, Satoru; Tago, Akari; Yoneyama, Mizuki; Ito, Midori; Fukuda, Keiko; Mizuno, Yoshifumi; Tsunoda, Yuko; Shimizu, Seiki; Yokoi, Kyoko; Kamioka, Naomi; Hamajima, Naoki; Suzuki, Satoshi

doi:10.1016/j.braindev.2015.06.001

Cited by 6 publications

(1 citation statement)

References 9 publications

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“…MRI with gadolinium enhancement is a standard tool for MS diagnosis and disease monitoring (102, 134) and is a sensitive diagnostic tool for GBS. Based on our studies on the animal model for S. pyogenes -induced BGE, we argue that MRI with gadolinium enhancement may reveal latent BBB damage in AE patients or foci of BBB damage (135–137). Our working hypothesis that barrier breakdown is a crucial step during AE pathogenesis would, therefore, be strengthened by evidence from patient MRI with gadolinium enhancement or careful analysis of BBB integrity using intravenous fluorescently labeled low- or high-molecular-weight tracers in animal models for other types of AE (55).…”

Section: Treatment Of Ae Syndromesmentioning

confidence: 97%

Hello from the Other Side: How Autoantibodies Circumvent the Blood–Brain Barrier in Autoimmune Encephalitis

2017

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Antibodies against neuronal receptors and synaptic proteins are associated with autoimmune encephalitides (AE) that produce movement and psychiatric disorders. In order to exert their pathological effects on neural circuits, autoantibodies against central nervous system (CNS) targets must gain access to the brain and spinal cord by crossing the blood–brain barrier (BBB), a tightly regulated gateway formed by endothelial cells lining CNS blood vessels. To date, the pathogenic mechanisms that underlie autoantibody-triggered encephalitic syndromes are poorly understood, and how autoantibodies breach the barrier remains obscure for almost all AE syndromes. The relative importance of cellular versus humoral immune mechanisms for disease pathogenesis also remains largely unexplored. Here, we review the proposed triggers for various autoimmune encephalopathies and their animal models, as well as basic structural features of the BBB and how they differ among various CNS regions, a feature that likely underlies some regional aspects of autoimmune encephalitis pathogenesis. We then discuss the routes that antibodies and immune cells employ to enter the CNS and their implications for AE. Finally, we explore future therapeutic strategies that may either preserve or restore barrier function and thereby limit immune cell and autoantibody infiltration into the CNS. Recent mechanistic insights into CNS autoantibody entry indicate promising future directions for therapeutic intervention beyond current, short-lived therapies that eliminate circulating autoantibodies.

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