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Frequent detection of anti-GQ1b IgG antibodies shapes the disease concept ‘anti-GQ1b antibody syndrome,’ which has either peripheral nervous system (PNS) or central nervous system (CNS) origins.1 Various phenotypes are known in the PNS origin, which predominantly shows ophthalmoplegia (Miller Fisher syndrome (MFS)), limb weakness (Guillain-Barré syndrome (GBS) with ophthalmoplegia), or sensory ataxia (acute sensory ataxic neuropathy). In contrast, only one phenotype is known in the CNS origin, Bickerstaff brainstem encephalitis (BBE), which accounts for a major proportion of brainstem encephalitis with the clinical triad of ophthalmoparesis, ataxia and impaired consciousness.2 The relatively uniform clinical presentation in the CNS origin …
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