To present a rare case of CANDA syndrome with acute deterioration in the context of influenza A infection, displaying a more typical CANOMAD phenotype, followed by spontaneous improvement to baseline.

CANOMAD (chronic ataxic neuropathy, ophthalmoplegia, immunoglobulin M paraprotein, cold agglutinins and disialosyl antibodies) is a clinical syndrome characterised by chronic neuropathy, ataxia and ophthalmoplegia with IgM paraprotein reacting against gangliosides. The term CANDA (chronic ataxic neuropathy with disialosyl antibodies) has been proposed to encompass a wider clinical cohort who may not display all features of CANOMAD. 

A 55-year-old woman presented with a 1-day history of rapidly progressive ataxia and diplopia. She also reported a 5-year history of distal sensory neuropathy of unknown aetiology for which she was attending a neurologist. On examination there was marked gait ataxia with positive Romberg’s sign, absent vibration sense to ankles bilaterally, and diffuse areflexia.

Influenza A was positive. SPEP showed IgM paraprotein band. MRI brain and angiogram were normal. Miller Fisher syndrome was suspected however GQ1B Abs were negative. On neurophysiological testing sensory nerve action potentials were diffusely absent. The patient spontaneously improved to her baseline within 2 weeks without any specific treatment. The patient was referred to haematology and diagnosed with Waldenstrom Macroglobulinemia. Anti-ganglioside antibodies of IgM isotype including anti GM2, anti GM3, anti GM4, anti GD1b and anti GD2 were positive. The patient was diagnosed with CANDA/CANOMAD syndrome.