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 …
No takes yet. Share an insight, caveat, or question.
Kuwabara et al. (2018) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: