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We need greater vigilance, with more rigid or standard criteria for atypical CIDP
Chronic inflammatory demyelinating polyneuropathy (CIDP) is an immune-mediated neuropathy progressive for more than 2 months, including several clinical subtypes.1 2 In 1975, Dyck et al 3 described the classical prototype of CIDP, and emphasised that a prominent clinical feature is weakness of the proximal and distal muscles about equally which is very rarely seen in other nerve length-dependent polyneuropathies. They proposed that such non-length-dependent pattern was caused by lesions in the nerve roots, presumably affecting the long and short nerves equally. From a current viewpoint, the assumption is partly correct; in classical CIDP, the distal nerve terminals and nerve roots, where the blood–nerve barrier is anatomically deficient, are predominantly affected, evidenced by electrodiagnostic and neuroimaging findings.4
However, later in 1991 the …
Contributors SK wrote the draft, and SM and MM made revisions.
Funding This work was supported in part by the Health and Labour Sciences Research Grant on Intractable Diseases (Neuroimmunological Diseases) from the Ministry of Health, Labour and Welfare of Japan.
Competing interests None declared.
Patient consent Not required.
Provenance and peer review Commissioned; internally peer reviewed.
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