Objective:

We aim to highlight a case of recurrent facial palsy and chronic inflammatory demyelinating polyneuropathy (CIDP) associated with anti-GQ1b positivity. 

Background:

A 77-year-old man with a medical history of atrial fibrillation, coronary artery disease, gastroesophageal reflux disease, hyperlipidemia, benign prostatic hyperplasia, severe canal stenosis, and recurrent unilateral facial palsy presented with progressive proximal weakness and tingling in the feet. Initially, the symptoms were stable for a year, manifesting as tingling in the feet. However, the patient later developed proximal muscle weakness, difficulty standing, and recurrent falls. He also reported three previous episodes of left-sided facial palsy. Electromyography revealed demyelinating peripheral neuropathy, and serological tests showed positive antiganglioside antibodies, particularly anti-GQ1b. These findings led to a diagnosis of CIDP. The patient was treated with a five-day course of intravenous immunoglobulin (IVIG). The positive anti-GQ1b antibodies provided a unifying diagnosis for his recurrent facial nerve palsy and demyelinating neuropathy. 

Design/Methods:

Records of patient was reviewed to collect information. Case was written based on collected information with review by GPT 4o.

Results:

This case emphasizes the relationship between cranial neuropathies and CIDP in the context of antiganglioside antibody positivity. The inflammatory process, involving complement deposition on peripheral and cranial nerves, is a potential mechanism. Literature reports multiple cases of relapsing cranial neuropathy with antiganglioside positivity, which may be explained by antigenic mimicry involving ganglioside composition. Autoimmune ganglionopathies should be considered a cause of idiopathic cranial neuropathies, particularly recurrent facial palsy, especially in the absence of other explanations like viral infections. 

Conclusions:

This case highlights the need for increased clinical awareness of autoimmune causes in patients with recurrent facial palsy, particularly those with atypical presentations. Future studies are necessary to elucidate the pathophysiologic mechanisms underlying these manifestations and to explore more targeted treatment approaches for patients with antiganglioside-associated neuropathies if deemed potentially causative.