The Application of Clinical, Electrophysiological and Nerve Ultrasound Parameters in Distinguishing Acute-onset Chronic from Acute Inflammatory Demyelinating Polyneuropathy

2015 ◽  
Vol 10 (01) ◽  
pp. 85 ◽  
Author(s):  
Antonios Kerasnoudis ◽  
Kallia Pitarokoili ◽  
Ralf Gold ◽  
Min-Suk Yoon ◽  
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...  

History-taking and nerve conduction studies are fundamental for the diagnosis and assessment of the severity of acute (AIDP) or chronic inflammatory demyelinating polyneuropathy (CIDP). The diagnostic challenge of distinguishing these two immune-mediated subacute polyradiculoneuropathies remains high, as intravenous immunoglobulin and steroids exert short-term clinical improvement in the majority of the CIDP cases, whereas steroids have no effect on AIDP patients. Accordingly, the precise classification of subacute polyradiculoneuropathies significantly affects the early application of steroids in CIDP. This review aims to give a timely update on the application of clinical, electrophysiological and nerve ultrasound parameters in distinguishing subacute CIDP from AIDP.

2021 ◽  
pp. 72-76
Author(s):  
Anna P. Patnaik ◽  
Joseph Mininni ◽  
Neil C. Porter ◽  
Nicholas A. Morris

Acute-onset chronic inflammatory demyelinating polyneuropathy (A-CIDP) is an immune mediated neuropathy characterized by progressive weakness and sensory impairment lasting over 2 months. Guillain-Barré-Strohl syndrome (GBS) is an immune mediated polyneuropathy with a similar presentation often over less than 4 weeks. While some have argued for the existence of recurrent GBS, most classify the syndrome as a form of relapsing-remitting CIDP. However, there are cases of GBS with treatment-related fluctuations that must be distinguished from A-CIDP as patients with A-CIDP require long-term immunotherapy. In this case report, we discuss a patient with multiple relapses over 3 years, who is more likely to have A-CIDP. His ganglioside profile, which has rarely been reported in A-CIDP, included high concentrations of anti-GM1, anti-GD1a, and anti-GD1b antibodies, which may account for his severe disease course.


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