Since the initial descriptions of Miller Fisher Syndrome (MFS) and Bickerstaff Brainstem Encephalitis (BBE), substantial advancements have refined our understanding of these disorders, highlighting shared features such as anti-GQ1b IgG antibodies, preceding infectious triggers, and overlapping neurophysiological findings. These commonalities support the hypothesis that MFS and BBE are not distinct entities but rather components of a unified autoimmune condition, often referred to as "Fisher-Bickerstaff syndrome."

The subsequent identification of anti-GQ1b-positive atypical variants, incomplete forms with shared serological profiles that fail to meet the full clinical criteria for MFS or BBE and overlap syndromes with features of Guillain-Barré Syndrome (GBS), has broadened this classification. This evolving understanding has led to the conceptualization of a broader entity termed "Anti-GQ1b Antibody Syndrome."

This syndrome encompasses a spectrum of disorders characterized by a consistent serological hallmark and a variable degree of involvement of the peripheral (PNS) and central nervous systems (CNS). Within this spectrum, MFS and BBE represent opposite ends, with intermediate and atypical phenotypes bridging these extremes.

This review aims to provide a comprehensive analysis of Anti-GQ1b Antibody Syndrome, emphasizing its phenotypic continuum and the atypical variants that contribute to its expanding classification. By integrating recent advances in diagnostic approaches and clinical understanding, we propose a unified framework for conceptualizing this syndrome as a dynamic spectrum of anti-ganglioside antibody-associated diseases.

Miller Fisher syndrome, Bickerstaff brainstem encephalitis, Anti-GQ1b antibody syndrome, Anti-ganglioside antibody syndrome, Atypical forms, Formes frustes