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Pathophysiology and management of chronic inflammatory demyelinating polyneuropathy

Published on July 30, 2026   26 min

A selection of talks on Immunology

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Hello. Today, I'm going to talk about the pathophysiology and management of CIDP. My name is Urvi Desai. I am Director of Carolina's MDA Care Center for both adult and pediatric patient population. I'm also Director for Levine Children's Neuromuscular Program at Atrium Health and a Professor of Neurology at Wake Forest University School of Medicine in North Carolina, United States. As mentioned, we'll be talking about the pathophysiology and management of CIDP today.
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Let us go back to the history of CIDP, and how did we come about this diagnostic category of peripheral neuropathy? Austin in almost 1958 described a condition, but he noticed that there was fluctuating motor predominant weakness, which was responsive to steroids. He noticed that there was weakness but no significant atrophy. He hypothesized that focal areas of segmental demyelination rather than axonal degeneration was the cause of this presentation. He labeled this as CIPN or chronic inflammatory polyradiculoneuropathy, which Dr. Dyck in 1975 refined as CITP when seminating word was added afterwards. What he described was the motor predominant polyradiculoneuropathy with proximal and distal weakness, ataxic gait, and variable sensory symptoms. They also noticed that the patient had elevated CSF protein, and there was a non-uniform slowing of conduction in proximal nerve segments with conduction block. Pathologically, there were areas of segmental demyelination, onion bulb formation, perivascular mononuclear infiltrates in endonurium, and perineurium.

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Pathophysiology and management of chronic inflammatory demyelinating polyneuropathy

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