Application of a Clinical-electrophysiologic Model for Distinguishing Chronic Inflammatory Demyelinating Neuropathy (CIDP) in an Australian Cohort
Grace Swart1, Nidhi Garg1, Michael Skolka2, Con Yiannikas1, Ostoja (Steve) Vucic1, John Pollard1, Antonia Carroll1, Judith Spies3, Matthew Kiernan4, Christopher Klein2, Susanna Park1
1University of Sydney, 2Mayo Clinic, 3Royal Prince Alfred Hospital, 4Neuroscience Research Australia
Objective:

To investigate performance of a clinical-electrophysiological model for distinguishing chronic inflammatory demyelinating neuropathy (CIDP) in an Australian cohort.

Background:

A probability calculator for CIDP, based on statistical modelling of clinical-electrophysiologic variables, was developed from a US center1. This clinical decision support tool uses four clinical (progression over 8 weeks, absent autonomic involvement, absent muscle atrophy, proximal limb weakness) and two electrodiagnostic variables (ulnar motor conduction velocity slowing <35.7 m/s and ulnar motor conduction block).

 

Design/Methods:
We applied the model retrospectively on a consecutive Australian cohort of patients fulfilling definite or probable criteria for CIDP2, between April 2015 and January 2017. Standardized neurophysiological assessments were performed using Synergy software (Version 20.0) (Middleton, WI, USA). All patients gave written informed consent for use of their information.
Results:

Twenty-nine patients were identified; mean age 43.4 ± 15.2 years, 69% male, mean disease duration 12.5 ±  11.3 years. CIDP phenotypes included typical (34%), multifocal/focal (24%), distal (17%), sensory/sensory-predominant (14%), and motor-predominant (7%). Mean number of nerve conductions assessed were motor n=5 (range 4-7) and sensory n=5 (range 1-7). At least one supportive diagnostic criteria was present in 86% of patients, including CSF protein elevation, imaging (ultrasound/MRI), nerve biopsy, and/or objective treatment response. Using 92% probability cut-off, 27/29 (93%) of patients were correctly identified. One multifocal and one distal CIDP patient were not identified, due to the presence of muscle atrophy and lack of proximal weakness. At 98% probability cut-off, sensitivity was 86% (25/29).

Conclusions:

Findings in an Australian CIDP cohort support 92% probability cut-off in the model to minimize Type II error and indicates good sensitivity for CIDP, maximal in typical phenotypes. False negatives were likely contributed to by model application in a stable cohort with longer disease duration. Prospective validation studies in patients at initial evaluation for CIDP are required.

10.1212/WNL.0000000000212523
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