I’ve been interested in the diseases and disorders that can be mis-diagnosed as CMT (or vice versa) for a while. One that has come up a lot is Chronic Inflammatory Demyelinating Polyradiculoneuropathy (CIDP). CIDP can look like CMT cases where demyelination is prominent, usually the CMT variants that have been classified as Type 1/1A. In one international study of more than 1,100 people diagnosed with CIDP, 3.2% actually had CMT.
Update, October 2026: The Hauw et al. (2021) study also estimated that treating the 35 misdiagnosed patients for CIDP cost €4.6 million, while CMT genetic testing for all 1,104 patients would have cost about €2.7 million. The authors conclude that CMT genetic testing should be used more widely before diagnosing CIDP. In November 2025, Health Canada authorized efgartigimod alfa (Vyvgart SC) for adults with active CIDP, the first neonatal Fc receptor (FcRn) blocker authorized in Canada for the condition.
People with CIDP showed a higher Compound Muscle Action Potential (CMAP, the size of the electrical response recorded from a muscle when its nerve is stimulated) than people with CMT in one recent study with a small test pool of 58 people in Japan. The researchers also noted some potential diagnostic value in using nerve ultrasounds to measure the width of nerves in patients, which tend to be wider in people with CMT.
Additionally, people with CMT1A tend to have nerve conduction velocities of 21.10±10.60m/s as compared with 31.52±12.46m/s in CIDP, according to a Chinese study. The potential overlap between the two groups makes this less useful as a key diagnostic, but the same research also showed the CMT1A group was about 30 percentage points more likely than the CIDP group (43.3% vs. 13.3%) not to elicit an F wave in nerve conduction tests.
These are useful diagnostic tools that should be added to neurologists’ toolkits. The signature foot deformities associated with CMT are probably overly associated, and clinicians should be more aware of how many different conditions can cause them.
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