Distinguishing Chronic Inflammatory Demyelinating Polyneuropathy From Mimic Disorders: The Role of Statistical Modeling.

Background And Aims: Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is difficult to distinguish from mimicking disorders, with misdiagnosis resulting in IVIG overutilization. We evaluate a clinical-electrophysiological model to facilitate CIDP versus mimic neuropathy prediction.

Methods: Using the European Academy of Neurology/Peripheral Nerve Society (EAN/PNS) 2021 CIDP guidelines we derived 26 clinical and 144 nerve conduction variables.

IgLON5 autoimmunity secondary to immune checkpoint inhibitor.

IgLON5 autoimmunity is characterized by a diverse range of clinical presentations, including neuropsychiatric symptoms, sleep disturbances, gait instability, and bulbar symptoms, that are usually insidiously progressive. While some individuals with specific HLA haplotypes may be more susceptible to developing anti-IgLON5 disease, this antibody is typically not associated with a paraneoplastic etiology nor known to be induced by immune checkpoint inhibitors (ICI). We present a clinical and serological workup of a patient who developed symptoms of IgLON5 autoimmunity following treatment with pembrolizumab.

Optimizing Anti-Myelin-Associated Glycoprotein and IgM-Gammopathy Testing for Neuropathy Treatment Evaluation.

Background And Objectives: Patients with typical anti-myelin-associated glycoprotein (anti-MAG) neuropathy have IgM-gammopathy, mimic distal chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), and are treatment resistant. Anti-MAG patients go unrecognized when IgM-gammopathy is undetected or with atypical phenotypes. We investigated an optimal anti-MAG titration cutoff for excluding CIDP and the impact of IgM-gammopathy detection on neuropathy treatment evaluation without anti-MAG antibodies.