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Published on: February 23, 2015
Immunologic abnormalities and surgical experiences in recurrent facial nerve paralysis
Sertac Yetiser1, Bulent Satar, Mustafa Kazkayasi
1Department of Otorhinolaryngology-Head and Neck Surgery, Gulhane Medical School, Etik-Ankara, Turkey. syetiser@yahoo.com
Insights
Recurrent facial paralysis (RFP) may involve immune system dysfunction. Surgical decompression prevented recurrence in a small study, while medical treatment did not fully resolve symptoms.
Area of Science:
- Neurology
- Immunology
Background:
- Recurrent facial paralysis (RFP) presents a diagnostic challenge, with potential links to immune system dysregulation.
- Melkersson-Rosenthal syndrome and idiopathic RFP share immunologic findings, complicating differential diagnosis.
Observation:
- Immunoglobulin G (IgG) elevation in serum (77%) and cerebrospinal fluid (CSF) (44%) was noted in RFP patients.
- Elevated albumin fraction in CSF (66%) suggests a compromised blood-brain barrier.
- No oligoclonal bands were detected in CSF, indicating peripheral antibody origin.
Findings:
- Surgical decompression via transmastoid and transattic routes in four patients resulted in no recurrences over a mean follow-up of 5.2 years.
- Medical treatment (steroids, vitamin B) in five patients led to initial recovery, but three experienced recurrence within 3 years.
- Immunologic testing showed immune system involvement in both idiopathic RFP and Melkersson-Rosenthal syndrome.
Implications:
- Findings support an immune-mediated pathogenesis for recurrent facial paralysis.
- Surgical intervention may offer a promising strategy for preventing recurrent facial paralysis.
- Further research is warranted to elucidate the precise role of immune factors in RFP.
Objective:
To document immunologic findings in patients with recurrent facial paralysis (RFP) and to compare the results of the surgery with the results of medical treatment.
Study Design:
Retrospective case review.
Setting:
Tertiary care referral center.
Patients:
Nine patients with RFP were reviewed.
Intervention:
Patients underwent nonspecific antibody detection, protein electrophoresis (in blood and cerebrospinal fluid [CSF]) and oligoclonal band determination for immunoglobulin G, A, and M (in CSF). The extended subtotal facial nerve decompression via the transmastoid and transattic route was performed in four patients. Five patients received medical treatment only (steroids, vitamin B).
Results:
Two patients had the complete and four patients had the oligosymptomatic form of Melkersson-Rosenthal syndrome. The other three patients were diagnosed with idiopathic RFP. Serum immunoglobulin G was high in seven of nine patients (77%). CSF protein electrophoresis demonstrated an elevated albumin fraction in six of nine patients (66%). CSF immunoglobulin G was high in four of nine patients (44%). The oligoclonal band in CSF was negative in all patients. Mean follow-up time was 5.2 +/- 2.6 years and 3 +/- 1.5 years for surgically treated patients and medically treated patients, respectively. None of the patients who underwent the surgery demonstrated recurrence. Although marked recovery was observed in patients who had received medical treatment, three of them had recurrence during the follow-up period.
Conclusion:
Serologic test results have demonstrated immune system involvement in cases of idiopathic RFP and in cases of Melkersson-Rosenthal syndrome, providing no distinction between the two. There was no sign substantiating local antibody production in CSF, which implies that the elevated antibodies in CSF were peripheral in origin. Although the serologic test results were not conclusive for a specific diagnosis, they support an immune-mediated pathogenesis. Despite the small number of patients who underwent the extended transmastoid facial nerve decompression, our follow-up data were suggestive for the prevention of recurrences.
