Decoding the Diverse Colours of Guillain-Barré Syndrome (GBS): A Case Report and Narrative Review of Atypical Miller Fisher-GBS Overlap Syndrome

The classic presentation of Guillain-Barré syndrome (GBS), as described in older medical textbooks, is that of a patient with a preceding history of diarrhoea who develops rapidly progressive, symmetrical quadriparesis with areflexia. These clinical features have often been deeply entrenched in the minds of physicians, such that deviation from this pattern frequently casts doubt on the diagnosis of GBS. In contrast, it is widely recognised that GBS presents across a diverse spectrum of variants sharing a similar pathophysiology. The heterogeneity of GBS is driven by the different neural targets in different parts of the neural axis. This explains the diverse manifestations of GBS and alerts clinicians to focus on the hard and invariable signs of GBS rather than the other soft and variable features of GBS chameleon to ensure early diagnosis and prompt initiation of immunomodulatory treatment. GBS presentation can range from the classic acute inflammatory demyelinating polyradiculoneuropathy (AIDP) to rarer variants such as Miller Fisher syndrome (MFS), acute pan-dysautonomia, Bickerstaff encephalitis, and even triple overlap syndromes involving Miller Fisher syndrome, GBS, and Bickerstaff encephalitis, among others, documented in the literature. This case report and narrative review follows a 69-year-old Caucasian man who presented atypically and was diagnosed with Miller Fisher-GBS overlap syndrome. This article highlights an atypical presentation of a Miller Fisher-GBS overlap syndrome with right-sided weakness and severe back pain, ophthalmoparesis, and proximal limb weakness, before progressing to classical GBS with quadriparesis. Despite initial misdiagnoses of vasculitis and myasthenic crisis, a definitive diagnosis of GBS was eventually made, and the patient received prompt immunomodulatory treatment with a favourable outcome. It underscores the importance of thorough neurological localisation, emphasising the need to build diagnostic frameworks on hard neurological signs rather than variable and inconsistent soft signs. Most importantly, it highlights the varied presentations of GBS and reviews the underlying immunopathogenesis and management of GBS variants.