Viral Titers and Delayed Facial Palsy after Acoustic Neuroma Surgery

2002 ◽  
Vol 127 (5) ◽  
pp. 427-431 ◽  
Author(s):  
Gerard J. Gianoli
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Facial Nerve ◽  
Acoustic Neuroma ◽  
Facial Palsy ◽  
Nerve Function ◽  
Facial Nerve Function ◽  
Acoustic Neuroma Surgery ◽  
Simplex Virus ◽  
Viral Titers

OBJECTIVE: Delayed facial palsy (DFP) after acoustic neuroma surgery has been reported to occur in up to one third of cases. Reactivation of latent virus has been proposed as an etiology for DFP. However, only retrospective case reports and case series have offered data to support this theory. The objective of this study was to correlate DFP with change in viral titers. PATIENTS AND METHODS: Twenty consecutive patients who underwent acoustic neuroma surgery were prospectively evaluated for viral titers immediately preoperatively and at 3 weeks postoperatively. Viral titers measured included herpes simplex virus 1 (HSV-1), herpes simplex virus 2 (HSV-2), and varicella zoster virus (VZV) and included both IgG and IgM titers. The status of facial nerve function was documented preoperatively and throughout the postoperative period. Patients were categorized according to the presence or absence of DFP. RESULTS: Seven patients developed DFP after acoustic neuroma surgery, while the remaining 13 patients did not. There was no difference in preoperative and 3-week postoperative IgG titers for any of the 3 viruses tested. However, IgM titers were much higher postoperatively in DFP patients for all 3 viruses tested. The average HSV-1 IgM titer rose 92% in DFP patients compared with only 4.5% in the patients who did not develop DFP. Average HSV-2 IgM titers rose 70% compared with a decline of 8.5% in non-DFP patients. Most strikingly, VZV IgM titers rose an average 495% postoperatively among DFP patients compared with a decline of 14% in the non-DFP patients. CONCLUSION: Elevation of the IgM titers of the viruses measured in this study implies that recrudescence of the virus has occurred. The absence of this rise among patients who did not develop DFP implies that viral recrudescence plays a role in the etiology of DFP. These findings support treatment or prophylaxis of DFP with antiviral therapy. Although the finding of normal facial nerve function immediately after acoustic neuroma surgery is an excellent prognostic indicator for the ultimate outcome of facial nerve function, it is not uncommon for the patient to exhibit deterioration of facial nerve function in the first few days to weeks after surgery. When facial palsy is not complete, the prognosis remains excellent. However, when there is total loss of facial nerve function, the final outcome is more variable. Delayed facial palsy (DFP) after acoustic neuroma surgery has been defined as initially normal facial nerve function noted immediately postoperative with subsequent deterioration of facial nerve function. 1 This phenomenon has been noted to occur in up to one third of cases. Numerous causes for this entity have been proposed, including neural devascularization, vasospasm, edema, immune reactions, and viral reactivation. Varicella zoster virus (VZV) and herpes simplex virus (HSV) are ubiquitous, with more than 90% of the adult population demonstrating evidence of prior infection. 2 Reactivation of latent VZV has been implicated as the cause of Ramsay Hunt syndrome. 3 There is mounting evidence that HSV reactivation is the cause of Bell's palsy. 4 In the present study, viral titers for VZV and HSV were assessed before and after acoustic neuroma surgery. DFP and non-DFP patients were compared in an attempt to determine whether there was any correlation between viral recrudescence and DFP.

Facial Nerve Dissection by use of Acoustic (Loudspeaker) Facial EMG Monitoring

1986 ◽  
Vol 95 (4) ◽  
pp. 458-463 ◽  
Author(s):  
Sam E. Kinney ◽  
Richard Prass
Keyword(s):  
Facial Nerve ◽  
Acoustic Neuroma ◽  
Internal Auditory Canal ◽  
Subsequent Development ◽  
Lateral Approach ◽  
Nerve Function ◽  
Facial Nerve Function ◽  
Facial Emg ◽  
Acoustic Neuroma Surgery ◽  
Total Tumor Removal

The development of the surgical microscope in 1953, and the subsequent development of microsurgical instrumentation, signaled the beginning of modern-day acoustic neuroma surgery. Preservation of facial nerve function and total tumor removal is the goal of all acoustic neuroma surgery. The refinement of the translabyrinthine removal of acoustic neuromas by Dr. William House’ significantly improved preservation of facial nerve function. This is made possible by the anatomic identification of the facial nerve at the lateral end of the internal auditory canal. When the surgery is accomplished from a suboccipital or retrosigmoid approach, the facial nerve may be identified at the brain stem or within the internal auditory canal. Identifying the facial nerve from the posterior approach is not as anatomically precise as from the lateral approach through the labyrinth. The use of a facial nerve stimulator can greatly facilitate Identification of the facial nerve in these procedures.

Causes of Facial Nerve Paresis after Translabyrinthine Surgery for Acoustic Neuroma

1992 ◽  
Vol 101 (10) ◽  
pp. 821-826 ◽  
Author(s):  
Mirko Tos ◽  
Jens Thomsen ◽  
Mahmoud Youssef ◽  
Suat Turgut
Keyword(s):  
Facial Nerve ◽  
Brain Stem ◽  
Acoustic Neuroma ◽  
Facial Palsy ◽  
Cerebellopontine Angle ◽  
Patient Records ◽  
Nerve Function ◽  
Facial Nerve Function ◽  
Common Site ◽  
Nerve Paresis

Forty-six consecutive video-recorded translabyrinthine operations at Gentofte Hospital, for tumors of 5 to 25 mm, were investigated for possible damage to the facial nerve from cauterization, suction, stretching, pushing, and other instrumental trauma at the following regions: fundus, internal meatus, porus, cerebellopontine angle, and brain stem. House-Brackmann grading of the postoperative facial nerve function was determined from the patient records for the 1st, 3rd, and 10th days and 3 months and 6 months postoperatively, as well as the final status. Suction on the nerve seems to be the most important factor for perioperative facial nerve damage. The most common site of damage was the porus region. This investigation shows thermic drilling lesions to be very relevant. There was no correlation between the degree and character of damage and the postoperative facial nerve function. In eight patients we cannot explain the postoperative facial palsy.

Observer variations in the evaluation of facial nerve function after acoustic neuroma surgery

1993 ◽  
Vol 107 (12) ◽  
pp. 1119-1121 ◽  
Author(s):  
Christian Buchwald ◽  
Mirko Tos ◽  
Jens Thomsen ◽  
Henrik MØller ◽  
Agnete Parving
Keyword(s):  
Facial Nerve ◽  
Acoustic Neuroma ◽  
Nerve Function ◽  
Surgical Team ◽  
Facial Nerve Function ◽  
Face To Face ◽  
Translabyrinthine Approach ◽  
Acoustic Neuroma Surgery ◽  
Grading Scale

This investigation was performed in order to evaluate the observer variations in facial nerve function after surgery for an acoustic neuroma. From 1976–90, 507 patients were operated on by the same surgical team (M.T. and J.T.) using a translabyrinthine approach. One hundred and forty-four patients living in Copenhagen City and County were invited for interview and objective examination. Only 128 patients attended the interview and examination which were carried out by the same ENT physician. Data concerning observation of the facial nerve function only is presented. Its function was clinically evaluated (using the House and Brackmann (1985) grading scale) by two different observers i.e the ENT physician and one of the surgeons. The patients were asked face-to-face with the ENT physician to estimate the degree of facial nerve function according to a 0–100 per cent scale. Comparing normal and abolished facial nerve function the judgments of the ENT physician and the surgeon agreed with the patient‘s own evaluation.

Facial nerve injury in acoustic neuroma (vestibular schwannoma) surgery: etiology and prevention

1997 ◽  
Vol 87 (1) ◽  
pp. 60-66 ◽  
Author(s):  
Prakash Sampath ◽  
Michael J. Holliday ◽  
Henry Brem ◽  
John K. Niparko ◽  
Donlin M. Long
Keyword(s):  
Facial Nerve ◽  
Nerve Injury ◽  
Acoustic Neuroma ◽  
Facial Nerve Palsy ◽  
Nerve Function ◽  
Facial Nerve Function ◽  
Content Type ◽  
Facial Nerve Injury ◽  
Acoustic Neuroma Surgery ◽  
Fine Print

✓ Facial nerve injury associated with acoustic neuroma surgery has declined in incidence but remains a clinical concern. A retrospective analysis of 611 patients surgically treated for acoustic neuroma between 1973 and 1994 was undertaken to understand patterns of facial nerve injury more clearly and to identify factors that influence facial nerve outcome. Anatomical preservation of the facial nerve was achieved in 596 patients (97.5%). In the immediate postoperative period, 62.1% of patients displayed normal or near-normal facial nerve function (House—Brackmann Grade 1 or 2). This number rose to 85.3% of patients at 6 months after surgery and by 1 year, 89.7% of patients who had undergone acoustic neuroma surgery demonstrated normal or near-normal facial nerve function. The surgical approach appeared to have no effect on the incidence of facial nerve injury. Poor facial nerve outcome (House—Brackmann Grade 5 or 6) was seen in 1.58% of patients treated via the suboccipital approach and in 2.6% of patients treated via the translabyrinthine approach. When facial nerve outcome was examined with respect to tumor size, there clearly was an increased incidence of facial nerve palsy seen in the immediate postoperative period in cases of larger tumors: 60.8% of patients with tumors smaller than 2.5 cm had normal facial nerve function, whereas only 37.5% of patients with tumors larger than 4 cm had normal function. This difference was less pronounced, however, 6 months after surgery, when 92.1% of patients with tumors smaller than 2.5 cm had normal or near normal facial function, versus 75% of patients with tumors larger than 4 cm. The etiology of facial nerve injury is discussed with emphasis on the pathophysiology of facial nerve palsy. In addition, on the basis of the authors' experience with these complex tumors, techniques of preventing facial nerve injury are discussed.

Facial nerve injury in acoustic neuroma (vestibular schwannoma) surgery: etiology and prevention

1998 ◽  
Vol 5 (3) ◽  
pp. E8 ◽  
Author(s):  
Prakash Sampath ◽  
Michael J. Holliday ◽  
Henry Brem ◽  
John K. Niparko ◽  
Donlin M. Long
Keyword(s):  
Facial Nerve ◽  
Nerve Injury ◽  
Acoustic Neuroma ◽  
Postoperative Period ◽  
Nerve Palsy ◽  
Facial Nerve Palsy ◽  
Nerve Function ◽  
Facial Nerve Function ◽  
Facial Nerve Injury ◽  
Acoustic Neuroma Surgery

Facial nerve injury associated with acoustic neuroma surgery has declined in incidence but remains a clinical concern. A retrospective analysis of 611 patients surgically treated for acoustic neuroma between 1973 and 1994 was undertaken to understand patterns of facial nerve injury more clearly and to identify factors that influence facial nerve outcome. Anatomical preservation of the facial nerve was achieved in 596 patients (97.5%). In the immediate postoperative period, 62.1% of patients displayed normal or near-normal facial nerve function (House-Brackmann Grade 1 or 2). This number rose to 85.3% of patients at 6 months after surgery and by 1 year, 89.7% of patients who had undergone acoustic neuroma surgery demonstrated normal or near-normal facial nerve function. The surgical approach appeared to have no effect on the incidence of facial nerve injury. Poor facial nerve outcome (House-Brackmann Grade 5 or 6) was seen in 1.58% of patients treated via the suboccipital approach and in 2.6% of patients treated via the translabyrinthine approach. When facial nerve outcome was examined with respect to tumor size, there clearly was an increased incidence of facial nerve palsy seen in the immediate postoperative period in cases of larger tumors: 60.8% of patients with tumors smaller than 2.5 cm had normal facial nerve function, whereas only 37.5% of patients with tumors larger than 4 cm had normal function. This difference was less pronounced, however, 6 months after surgery, when 92.1% of patients with tumors smaller than 2.5 cm had normal or near normal facial function, versus 75% of patients with tumors larger than 4 cm. The etiology of facial nerve injury is discussed with emphasis on the pathophysiology of facial nerve palsy. In addition, on the basis of the authors' experience with these complex tumors, techniques of preventing facial nerve injury are discussed.

Prediction of postoperative facial nerve function in acoustic neuroma surgery

1999 ◽  
Vol 24 (6) ◽  
pp. 483-486 ◽  
Author(s):  
J. E. Fenton ◽  
R. Y. K. Chin ◽  
A. Shirazi ◽  
P. A. Fagan
Keyword(s):  
Facial Nerve ◽  
Acoustic Neuroma ◽  
Nerve Function ◽  
Facial Nerve Function ◽  
Acoustic Neuroma Surgery

Traintime as a Quantitative EMG Parameter for Facial Nerve Function during Acoustic Neuroma Surgery

Skull Base ◽  
2005 ◽  
Vol 15 (S 2) ◽  
Author(s):  
Julian Prell ◽  
S. Ramp ◽  
J. Romstöck ◽  
R. Fahlbusch ◽  
C. Strauss
Keyword(s):  
Facial Nerve ◽  
Acoustic Neuroma ◽  
Nerve Function ◽  
Facial Nerve Function ◽  
Acoustic Neuroma Surgery ◽  
Quantitative Emg
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