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CANOMAD (chronic ataxic neuropathy, ophthalmoplegia, IgM paraprotein, cold agglutinins, disialosyl antibodies) is a rare monoclonal gammopathy where IgM antibodies act against disialosyl epitopes on gangliosides leading to chronic demyelinating neuropathy.¹ The median age of onset is 58 and CANOMAD affects men more than women with a 4:1 ratio.² Symptoms include sensory ataxia, areflexia, and bulbar and oculomotor weakness with relative preservation of limb motor function.^1,2

Guillain-Barre syndrome and Miller Fisher syndrome are important differentials.² Diagnosis is based on neurologic examination findings, presence of IgM antibodies, and elevated serum IgM paraprotein.^1,2 Nerve conduction studies typically show a pattern of demyelination, with axonal loss in rare cases.² Therapeutic options include IVIg, rituximab, and B-cell targeted therapies.² Prognosis is good with treatment.¹

References:

1. Le Cann M, Bouhour F, Viala K, et al. CANOMAD: A neurological monoclonal gammopathy of clinical significance that benefits from B-cell–targeted therapies. Blood 2020;136(21):2428-2436; doi:10.1182/blood.2020007092
2. Rickli, JM, Pomaleski G, Magno Gonçalves MV. CANOMAD: A multi-faceted disease. International Journal of Neurology and Neurotherapy 2020;7(2):104; doi:10.23937/2378-3001/1410104

Submitted by: Sahariar Siddik, MD, Bangabandhu Sheikh Mujib Medical University (BSMMU), Dhaka, Bangladesh.

Dr. Sahariar Siddik reports no disclosures.