In the 1950s, Bickerstaff and Fisher independently described cases with a unique 
presentation of ophthalmoplegia and ataxia. The neurological features were 
typically preceded by an antecedent infection and the majority of patients made 
a spontaneous recovery. In the cases with Bickerstaff brainstem encephalitis, 
there was associated altered consciousness and in some, hyperreflexia, in 
support of a central pathology whereas in Fisher syndrome, patients were 
areflexic in keeping with a peripheral aetiology. However, both authors 
recognised certain similarities to Guillain-Barré syndrome such as the presence 
of peripheral neuropathy and cerebrospinal fluid albuminocytological 
dissociation. The discovery of immunoglobulin G anti-GQ1b antibodies in patients 
with Fisher syndrome and later in Bickerstaff brainstem encephalitis was crucial 
in providing the necessary evidence to conclude that both conditions were in 
fact part of the same spectrum of disease by virtue of their common clinical and 
immunological profiles. Following this, other neurological presentations that 
share anti-GQ1b antibodies emerged in the literature. These include acute 
ophthalmoparesis and acute ataxic neuropathy, which represent the less extensive 
spectrum of the disease whereas pharyngeal-cervical-brachial weakness and Fisher 
syndrome overlap with Guillain-Barré syndrome represent the more extensive end 
of the spectrum. The conditions can be referred to as the 'anti-GQ1b antibody 
syndrome'. In this review, we look back at the historical descriptions and 
describe how our understanding of Fisher syndrome and Bickerstaff brainstem 
encephalitis has evolved from their initial descriptions more than half a 
century ago.