FACIAL PARALYSIS IN CHRONIC OTITIS MEDIA

Dragoslava Djeric

Clinic for Otorhinolaryngology and Maxillofacial Surgery, Medical Faculty, University of Belgrade, Serbia

Introduction

Chronic suppurative otitis media is a destructive process that can involve the facial nerve and may result in an impairment of its function. In the pre-antibiotic era, facial paralysis occurred in 2.3% of patients with chronic otitis media. The frequency of otogenic facial palsy has decreased since the introduction of antibiotics, but it still occurs in about 1% of the patients with chronic middle-ear infection.

Mechanisms of the effects of chronic otitis media on the facial nerve are complex but can be summarized as follows: direct extension of the inflammatory process to the facial nerve, pressure from the pathological process (cholesteatoma, granulation), and toxic action upon the nerve itself. Although numerous studies have dealt with otogenic facial paralysis, this still is a controversial issue.13

Subjects and methods

The study was performed on 136 patients with otogenic facial paralysis who were surgically treated at our clinic. Ages of the patients ranged between 15 to 82 years. The medical records of the patients were analyzed in order to determine the factors of importance for facial paralysis. Attention was paid to the types of chronic infection, location of bone destruction of the facial canal, pre-operative and post-operative nerve function and follow up. Computed tomography was performed in most of the cases and magnetic resonance imaging was obtained in some patients. Evaluation of degree of recovery of facial function depended on the methods used in the follow-up period.

Results

Surgical intervention was performed as early as possible in all cases of chronic otitis media with a pre-operative facial paralysis. The period of time from onset of paralysis to surgery ranged from five days to two years. Surgery (canal-wall-up or canal-wall-down) and facial-nerve decompression was performed in the majority of cases. Cholesteatoma was found in 52 (80%) of the patients while in the remaining 12 (20%) chronic inflammation manifested as granulation or fibrocystic tissue. Decompression was done from geniculate ganglion to the stylomastoid foramen with or without epineural incision in 75% cases. In some patients, aggressive cholesteatoma and granulation fibrous tissue were involved which interrupted the facial nerve. Because of that, the patients underwent direct end to end neural anastomosis or neural graft with auricular nerve, after the resection of the involved segment of the facial nerve.

Otogenic facial paralysis was more common as an isolated complication than associated with other complications (68.8% : 31.2%). A fistula of the lateral semicircular canal was the most common complication (18.7%). Other complications, such as destruction on the promontory and intracranial complications, occurred less frequently (6.3% : 6.2%).

The site of bone destruction of the facial canal was confirmed at surgery in 48 (75%) of the cases, while such a site was not discovered in 16 (25%) cases. The tympanic segment of he facial canal was the most common site of involvement (77.2%). In the majority of these the bone destruction was adjacent to the oval window. In some cases, the facial nerve was protruding in the tympanic cavity, and in some cases the nerve partly covered the oval widow itself. Destruction of the mastoid part of the facial canal was found in six (12.7%) of the cases. All these cases showed an opening in the lateral bone canal with exposed nerve in the facial recess. In five cases (10.1%), the facial canal was extensively destroyed and the nerve almost totally exposed from its proximal part to the stylomastoid foramen.

There may be a number of reasons why in 25% of our patients evidence of bone destruction of the facial canal was not present. In some cases, a pathological process can destroy the facial canal at a place which is not possible to see at surgery, such as the bony recess adjacent to the facial canal and the medial wall of the facial canal. Also, the presence of communications between the blood vessels of the facial canal and surrounded structures allowed spread of the inflammatory process into the facial nerve. In some cases, an osteitic process can involve the facial canal as localized focus of infection. The bony facial nerve canal was open and the nerve decompressed depending on the place of pathological involvement.

Follow up and evaluation of the degree of recovery of the facial function depends upon the method used and possibility.

In our study we recognized three conditions: 1) Complete recovery is characterized by a full restoration of the facial function without synkinesis (70%); 2) Partial recovery is characterized by slight asymmetry at rest and weakness of voluntary movements (24%); 3) Failure to recover was found in 6% of the cases. It manifested with asymmetry at rest, slight return of muscle function, contractures, hemi-facial spasms and synkinesis.

Discussion

Chronic otitis media causing facial paralysis is frequently associated with cholesteatoma. But, acute exacerbation of the inflammatory process plays an important role in the pathogenesis of facial palsy. Our previous human-temporal-bone studies have described that chronic otitis media is associated with degenerative changes in the facial nerve without clinical alteration of its function. Nonetheless, these changes may predispose to the development of facial paralysis in chronic otitis. The findings suggest that facial paralysis occurs in chronic supportive obits when the inflammatory process specifically involves the facial-nerve trunk.4,5

Infection may involve the facial canal at any point but most often occurred in the tympanic segment. The main reason for this occurrence is that this part of the facial canal is most frequently dehiscent and the wall of the facial canal at this site is extremely thin. A pathological process such as cholesteatoma or granulation tissue is very often localized around the tympanic part of the facial canal.

Concerning the management and prognosis of facial paralysis due to chronic middle-ear infection, some questions are still open. Firstly, the type of the pathological process, cholesteatoma or other (granulation, fibrosis). In cases with facial palsy, cholesteatoma is most commonly present. Also, at surgery, it is important to remove its matrix, not only for better recovery of facial-nerve function, but also to prevent potential recurrence and additional ear surgery. Secondly, the occurrence of facial paralysis does not depend on the extent of destruction of the facial canal. In some cases, destruction of the canal was very small, but in some cases it was very massive, indicating that the facial nerve may have been uncovered and exposed to the pathological process for a long period of time prior to the facial paralysis. Thirdly, it is important to make the incision on the epineurium and always leave the perineurim intact to form a protective barrier to infection. We believe that in some cases, after removal of pathological process, it is useful to open the epineurium in a limited area, which has a relieving effect in cases with severe edema and inflammation.The results of surgical intervention were better in cases with shorter duration of paralysis prior to the surgery. We believe that early surgical intervention is crucial for recovery of the facial function. However, eradication of cholesteatoma and possible occurrence of its residual/recurrence types, can be a concern for the treatment of chronic otitis and its complications.

Conclusion

Otogenic facial paralysis most commonly occurs due to chronic otitis media with cholesteatoma. We believe that early surgical intervention is crucial for better recovery of the facial-nerve function. Also, it is important to perform a successful surgical procedure with the aim to remove the pathological process from the middle-ear spaces and to prevent recurrence or serious complications.

References

1.Kim J, Jung G, Park S. Facial nerve paralysis due to chronic otitis media. Yonsei Med J 1(53):642–648, 2012

2.Savic D, Djeric D. Facial paralysis in chonic suppurative otitis media. Clin Otolaryngol, 14:515–517, 1989

3.Harker A, Pignatari S. Facial nerve paralysis secondary to the otitis media. Am J Oto 13:372–374, 1992

4.Djeric D. Neuropathy of the facial nerve in chronic otitis media without associated facial paralysis. Eur Arch Otorhinolaryngol 247:232–236, 1990

5.Djeric D, Savic D. Otogenic facial paralysis. Eur Arch Otorhinolaryngol 247:143–146, 1990


Address for correspondence: Dragoslava Djeric, dragadj@beotel.rs

Cholesteatoma and Ear Surgery – An Update, pp. 125–127

Edited by Haruo Takahashi

2013 © Kugler Publications, Amsterdam, The Netherlands