Address for correspondence : Jin Kim, MD, PhD, Department of Otorhinolaryngology, Yonsei University College of Medicine, 250 Seongsan-ro, Seodaemun-gu Seoul 120-752, Korea
Tel : +82-2-2228-3602, Fax : +82-2-393-0580, E-mail : jinsound@gmail.com
Introduction
Many intratemporal diseases can cause extrinsic or intrinsic chronic compressive neural injuries on the facial nerve because it is confined to the rigid fallopian canal in the infratemporal area. The most common diseases causing slow, progressive facial paralysis are cholesteatoma, vestibular schwannoma and facial nerve schwannoma.1,2,3) In the field of carpel tunnel syndrome, chronic compression injury is known to an important factor for nerve paralysis, tingling sensation, muscular atrophy and weakness. Like as carpel tunnel syndrome, mass located in intratemporal area can induce chronic compression injury on facial nerve. But, there is no report on the chronic nerve change and facial function.
With the advent of the surgical microscope in 1960,4) cure rates for the surgical excision of intratemporal diseases have increased, making facial function a greater concern rather than morbidity rate in the surgical excision of these diseases.5)
Due to the gradual nature of chronic neural injury, it has previously been characterized as a mild form of Wallerian degeneration. Yet the patients who have facial paralysis due to chronic compressive injuries frequently present clinically in a way that cannot be explained by mild Wallerian degeneration. The poor understanding of their underlying pathogenesis makes the path to postoperative facial restoration unclear and the surgical prognosis yields unpredictable courses of facial function.
In this study, we analyzed the characteristics of facial paralysis and recovery after surgical intervention for cholesteatoma, vestibular schwannoma and facial nerve schwannoma in order to understand chronic compressive neural injuries and their surgical outcome.
Subjects and Methods
Thirty six patients with facial paralysis due to intratemporal diseases were treated in our department between 1990 and 2008.
Twenty-three patients had facial paralysis caused by cholesteatoma, 6 patients by vestibular schwannoma, and 7 patients by facial nerve schwannoma. Through retrospective chart review, data were collected on the age of presentation, sex, clinical presentation, tumor location, preoperative and postoperative facial nerve function and follow-up data. Computed tomography (CT) or magnetic resonance imaging (MRI) was obtained in all cases. The severity of facial paralysis was evaluated by the House-Brackmann (HB) grading system.6)
Tumor size, duration of preoperative facial paralysis, surgical outcome, and preoperative facial function were compared according to intratemporal diseases using either an unpaired or independent sample t-test, as appropriate. The size of the tumor was determined based on linear planimetric measurements according to international criteria,7) and only the largest extra-meatal diameter was used. The portion of tumor located inside the internal auditory canal (IAC) was not included in the measurement. The threshold for significance was
p<0.05. Although HB scale is an ordinate rather than interval measure, some facial function was represented using the mean value for the HB scale in order to investigate detailed changes in facial function. Mean surgical gain was calculated by subtracting the final HB grading score from the initial HB grading score. Except where noted, results are expressed as mean±standard deviation (SD).
The patients with complete facial paralysis were not included in this study because of the presence of facial nerve interruption or the replacement of the nerve by fibrous tissue discovered in the operative field and followed interpositional graft according to the size.
All patients were informed of possible surgical complications and the unpredictable prognosis of facial paralysis beyond limited reversibility of good facial nerve function. Recovery of facial function was assessed no earlier than one year after surgical intervention.
Results
Of all the 36 patients, the mean age was 45.9±14.8 years (range 21-78), and there were 16 men and 20 women. The left side was involved in 22 cases and the right in 14. The sizes of tumors range from 8 mm to 35 mm, with a mean size of 20.4±7.19 mm by the largest diameter based on linear planimetric measurements.
The 23 patients with facial paralysis due to cholesteatoma had an average age of 47.3±15.5 years. The male to female ratio was 14:9. Preoperative and postoperative facial function as represented by the average HB grade was 3.6±0.45 and 1.9±0.36, respectively
(p<0.05). Mean surgical gain was the difference in HB score of 1.74.
Mean duration from onset to surgery was 1.66±1.58 months. Average tumor size on CT scanning was 19.9±6.82 mm. The tympanic segment was the most common site of involvement (n=15 patients; 65%), and the mastoid segments were involved in 8 patients (35%). Among them, two patients had geniculate ganglion exposure, and two had labyrinthine segment exposure. There was a large exposure of the mastoid segment in two patients.
Six patients had facial paralysis due to vestibular schwannoma with an average age of 48.7±14.7 years. The male to female ratio was 4:2. Preoperative and postoperative facial function represented by the average HB grade was 2.6±0.50 and 2.6±0.30, respectively. Mean surgical gain was the difference in HB score of 0.33.
Mean duration from onset to surgery was 6.33±8.9 months. Average tumor size on gadolinium-enhanced MRI scan was 27.0±5.66 mm. The IAC was the most common site of involvement in all 6 patients (100%), 2 of these patients had involvement on the labyrinthine segment. There was a large indentation on the cerebellum in two patients.
Seven patients had facial paralysis due to facial nerve schwannoma, with an average age of 39.0±12.4 years. The male to female ratio was 5:2. Preoperative and postoperative facial function represented by the average HB grade was 2.3±0.48 and 2.1±0.89 respectively. Mean surgical gain was a difference in HB score of 0.14.
Mean duration from onset to surgery was 12.9±8.0 months. Average tumor size on gadolinium-enhanced MRI scan was 16.1±6.25 mm. The geniculate ganglion was the most common site of involvement (n=4; 59%), and of these patients, one had involvement on the labyrinthine segment, two had involvement on the tympanic segment, and one had IAC involvement. There was an involvement of the mastoid segment in three patients.
Statistical analysis of facial paralysis and surgical outcome
The involved segments of the facial nerve had statistical significance between cholesteatoma and schwannoma
(p<0.05). In case of cholesteatoma, the most common involved segment of the facial nerve was the tympanic segment, followed by the mastoid segment (Fig. 1).
Although preoperative facial function was worse in cholesteatoma than in the other diseases, surgical intervention brought the most effective improvement in facial function, with the gain in HB score of 1.9
(p<0.05)(Fig. 2). In cases of schwannoma, surgical intervention did not change postoperative facial function.
Surgical intervention in intratemporal chronic diseases was effective when the duration of preoperative facial paralysis was shorter (less than 1 month;
p<0.05)(Fig. 3). Improvement of facial function was greater when the preoperative facial function showed a high HB grade
(p<0.05)(Fig. 4).
Discussion
Many authors have reported animal, electrophysiologic or histologic studies related to compression neuropathies usually occur near joints, where the nerve passes through a fibrous tunnel as it courses, like carpal tunnel syndrome or cubital tunnel syndrome.7) In the neurotologic field, however, much less attention has been given to the various compression neuropathies that occur in the rigid bony fallopian canal and many re-searches have concentrated on acute facial nerve injuries and surgical decompression, which has been supported by electrophysiologic tests.8,9,10)
Most physicians have been less concerned with secondary chronic facial nerve compression injuries, because they concentrate on treating the severe underlying disease itself. Moreover, the lack of correlation between electrophysiological tests and clinical features of chronic facial nerve compression injuries makes it difficult to predict surgical outcome and overcome facial paralysis.11)
Usually, the complete reversal of facial weakness is limited in chronic facial nerve compression injuries. The mechanism of chronic compression injuries and their effective management needs to be better understood, because the pathogenesis of chronic nerve compression injuries appears to be quite different from acute nerve injuries.12)
Based on our analysis, we identified several notable details about chronic nerve compression injuries from intratemporal diseases. First, there can be clinical differences in facial paralysis and recovery between chronic infectious and non-infectious compressive injuries. Our patients with facial paralysis due to cholesteatoma were managed with concurrent surgical decompression of the facial nerve and eradication of the infectious source. The surgical interventions had a much greater impact on facial recovery in cases of cholesteatoma than in schwannoma, indicating that inflammation of the facial nerve or fallopian canal influences on neural deterioration, adding to the compressive injuries.
Second, the segment of the facial nerve with tumor involvement may be an important factor in the prognosis of postoperative facial function. With the absence of the epineurium and perineurium, especially proximal to the IAC,13) the facial nerve is vulnerable to injury. In the tympanic and mastoid segments of the facial nerve, there are sufficient epineurium and perineurium to protect from external pressure and infection. In contrast, the geniculate ganglion, labyrinthine segment and cysternal segment have a sparse epineurium and perineurium with few blood vessels.14,15)
Third, some patients with facial paralysis due to chronic compression injuries can regain considerable facial function after early surgical intervention even if poor facial function is indicated. Late intervention after facial paralysis did not result in positive outcomes. Other authors report, however, that even late facial nerve exploration may help the final outcome in facial function.16,17,18)
In summary, the characteristics of facial paralysis and facial recovery in chronic intratemporal compressive diseases vary considerably according to preoperative duration, preoperative facial function and tumoral nature.
Conclusion
Surgical intervention in intratemporal chronic diseases was effective when the duration of preoperative facial paralysis was shorter, and was greater when the preoperative facial function showed a high HB grade. Also it had a much greater impact on facial recovery in cases of cholesteatoma than schwannoma, indicating that inflammation of the facial nerve or fallopian canal can influence reversible neural deterioration.
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