The Miller Fisher syndrome (MFS), characterized by ataxia, areflexia, and ophthalmoplegia, was first recognized as a distinct clinical entity in 1956. MFS is mostly an acute, self-limiting condition, but there is anecdotal evidence of benefit with immunotherapy. Pathological data remain scarce. MFS can be associated with infectious, autoimmune, and neoplastic disorders. Radiological findings have suggested both central and peripheral involvement. The anti-GQ1b IgG antibody titer is most commonly elevated in MFS, but may also be increased in Guillain-Barré syndrome (GBS) and Bickerstaff's brainstem encephalitis (BBE). Molecular mimicry, particularly in relation to antecedent Campylobacter jejuni and Hemophilus influenzae infections, is likely the predominant pathogenic mechanism, but the roles of other biological factors remain to be established. Recent studies have demonstrated the presence of neuromuscular transmission defects in association with anti-GQ1b IgG antibody, both in vitro and in vivo. Collective findings from clinical, radiological, immunological, and electrophysiological techniques have helped to define MFS, GBS, and BBE as major disorders within the proposed spectrum of anti-GQ1b IgG antibody syndrome.

Postoperative radiculopathy has previously been reported as a common complication of transforaminal lumbar interbody fusion (TLIF). However, no data has been published on lumbar plexopathy following TLIF. We present a rare case of lumbar plexopathy occurring following TLIF (L5-S1) in a patient with spondylolisthesis. Although initially a diagnostic challenge, sinister causes of neuropathy such as bleeding or neoplastic growths were excluded by imaging. A diagnosis of acute lumbar plexopathy of left L2 to L4 was eventually made after electromyographic studies was performed in consultation with a senior neurologist. The patient was treated supportively with good functional recovery.