The Laryngoscope
C 2013 The American Laryngological,
V
Rhinological and Otological Society, Inc.
The Prevalence and Clinical Course of Facial Nerve Paresis
Following Cochlear Implant Surgery
Joshua J. Thom, MD; Matthew L. Carlson, MD; Michael D. Olson, MPAS, PA-C; Brian A. Neff, MD;
Charles W. Beatty, MD; George W. Facer, MD; Colin L. W. Driscoll, MD
Objectives/Hypothesis: To describe the prevalence, clinical course, and outcomes of facial nerve paresis following cochlear implantation and to identify variables associated with poor definitive facial nerve function.
Study Design: Retrospective cohort study with systematic literature review.
Methods: All patients who underwent cochlear implantation between January 1990 and December 2010 at a single tertiary academic referral center were reviewed. Data including clinical presentation, intraoperative findings, onset, severity,
management, and outcomes of all patients who experienced facial nerve paresis following cochlear implantation were
recorded.
Results: Eight hundred eighty-eight cochlear implants (282 pediatric, 606 adult) were performed in 768 patients. Eleven
patients with postoperative facial nerve paresis were identified. Ten patients (1.1%) developed delayed-onset paresis and had
complete recovery within 6 months of surgery, whereas a single patient (0.1%) demonstrated immediate onset paresis and
experienced incomplete return of facial nerve function. Seventeen additional cases were identified in the literature and were
summarized.
Conclusions: Facial nerve paresis following cochlear implantation is rare. Most cases demonstrate a delayed onset and
have complete recovery within months of surgery. Delayed onset facial nerve paresis following cochlear implantation heralds
an excellent prognosis, whereas immediate onset facial paresis prognosticates a poorer outcome. In the absence of medical
contraindications, corticosteroid therapy should be considered in facial paresis following cochlear implant surgery.
Key Words: Cochlear implant, facial nerve, surgical complications.
Level of Evidence: 2b.
Laryngoscope, 123:1000–1004, 2013
INTRODUCTION
Cochlear implantation (CI) has emerged as the
treatment of choice for hearing rehabilitation in pediatric and adult patients with severe to profound
sensorineural hearing loss (SNHL). The widespread popularity of the procedure has made contemporary CI safe
and effective, with relatively low complication rates.1–6
Although uncommon, major complications do exist and
can be distressing to both the patient and surgeon.1–20
Although facial nerve (FN) injury following tympanomastoidectomy21 and vestibular schwannoma surgery22
has been well studied, FN paresis following CI has
received little attention.
CI is most commonly performed through a transmastoid posterior tympanotomy (facial recess) approach.
Electrode insertion into the scala tympani can be
From the Department of Otorhinolaryngology–Head and Neck
Surgery, Mayo Clinic School of Medicine, Rochester, Minnesota, U.S.A.
Editor’s Note: This Manuscript was accepted for publication February 29, 2012.
Colin L. W. Driscoll, MD, is a consultant for Cochlear Corporation,
Advanced Bionics Corporation, and Med-El GmbH. The authors have no
other funding, financial relationships, or conflicts of interest to disclose.
Send correspondence to Colin L. W. Driscoll, MD, Department of
Otorhinolaryngology–Head and Neck Surgery, Mayo Clinic School of
Medicine, 200 First Street SW, Rochester, MN 55905.
E-mail: [email protected]
DOI: 10.1002/lary.23316
Laryngoscope 123: April 2013
1000
achieved either through the round window or through a
cochleostomy created immediately anterior-inferior to
the round window. Despite the close proximity of the
FN, direct mechanical injury is exceedingly rare. However, FN paresis can occur even when the FN is not
obviously exposed or directly injured.3–5,7–17,20,23 The literature suggests that etiologies other than direct
mechanical injury play a prominent role in postoperative
FN paresis. The various mechanisms of injury likely
influence patient presentations and outcomes. The current study examines the prevalence, clinical courses,
and outcomes of FN paresis following CI at a tertiary
academic referral center. These data are further supplemented by a systematic review of the world literature.
MATERIALS AND METHODS
After institutional review board approval (IRB No.
11-001316), a retrospective chart review of all patients who
underwent CI at a single tertiary academic referral center from
January 1990 through December 2010 was performed. Patients
with incomplete data and those receiving surgery at an outside
institution were excluded. CI through a transmastoid facial
recess approach was performed, and intraoperative electromyographic FN monitoring (Nerve Integrity Monitor; Medtronic
Xomed, Jacksonville, FL) was routinely used after 1999. Subjects with postoperative FN paresis were identified, and data
including patient demographics, clinical history, intraoperative
findings, onset and severity of FN paresis, treatment, and
Thom et al.: FN Paresis Following CI Surgery
TABLE I.
Summary of Patients With Facial Nerve Paresis Following Cochlear Implantation.
Case
Sex
Age
Onset of
Paresis
HB
Grade
Treatment
HB
Recovery
Time to
Recovery
Notable Case Details
FN
Monitoring
1
M
80 yr
0d
5/6
Observation
2/6
1 yr
Chorda tympani sacrificed
2
F
24 mo
3d
4/6
Observation
1/6
2 mo
Mondini malformation
Yes
No
3
4
F
M
76 yr
27 yr
11 d
8d
4/6
6/6
Observation
Steroids and valacyclovir
1/6
1/6
3 wk
6 mo
None
Chorda tympani sacrificed, FN exposed
Yes
Yes
5
M
70 yr
16 d
3/6
Steroids
1/6
2 mo
Fallopian bridge, FN exposed
Yes
6
7
F
M
23 mo
58 yr
7d
13 d
3/6
5/6
Observation
Steroids
1/6
1/6
1 mo
2.5 mo
Mondini malformation, aberrant FN course
Postoperative wound infection
Yes
Yes
8
M
37 yr
5d
3/6
Steroids
1/6
1 mo
Chorda tympani sacrificed
No
9
10
F
M
44 yr
64 yr
4d
12 d
4/6
4/6
Steroids
Steroids
1/6
1/6
3 mo
1 mo
None
Chorda tympani sacrificed
Yes
No
11
M
86 yr
9d
3/6
Steroids
1/6
1 mo
None
No
HB ¼ House-Brackmann; FN ¼ facial nerve; M ¼ male; F ¼ female.
definitive FN outcomes were recorded. The timing of onset was
classified according to the following scheme: 1) immediate onset
paresis, occurring within 1 hour of surgery; 2) early-onset
delayed paresis, occurring between 1 and 48 hours; and 3) lateonset delayed paresis occurring beyond 48 hours.7,20,24 FN function was reported according to the House-Brackmann (HB)
grading system.25 Study data were supplemented with a systematic review of the international literature.
RESULTS
Eight hundred eighty-eight CI surgeries (282 pediatric, 606 adult; 851 primary, 37 revision) among 768
patients were reviewed. Of these, 11 patients (two pediatric, nine adult) developed postoperative FN paresis
within 3 weeks of surgery and were included (Table I).
Ten patients (1.1%) demonstrated delayed onset paresis
and had complete recovery (HB grade 1) within 6 months
of surgery, whereas a single patient (0.1%) developed immediate onset paresis and experienced incomplete
recovery (HB grade 2) at 1 year from surgery.
The mean onset of delayed paresis was 8.8 days
(range, 3–16 days) following surgery, and the average
time to complete FN recovery (HB grade 1) of the 10
patients with delayed onset FN paresis was 2 months
(range, 3 weeks–6 months.). The two pediatric patients
(Table I, cases 2 and 6) who experienced delayed paresis
had Mondini malformations, one with a normal FN position and the other with an aberrant FN course. One
adult patient (Table I, case 5) with delayed paresis
underwent concurrent tympanomastoidectomy with fallopian bridge for cholesteatoma that was discovered
intraoperatively. One adult patient (Table I, case 7)
acquired a postoperative wound infection during the second week following surgery. Two days after the onset of
infection the patient developed facial weakness that
responded to antibiotic therapy. The FN was uncovered
or found dehiscent in two cases, and the chorda tympani
nerve was divided in four cases. The remaining 3
patients did not have any notable medical history, inner
ear or FN anomalies, or extraordinary operative findings. There was a 4.5-times increased risk of delayed
postoperative FN paresis in cases where intraoperative
Laryngoscope 123: April 2013
FN monitoring was not used (P ¼ .027). However, in the
seven cases where neural integrity testing was
employed, the monitor never alarmed.
A comprehensive literature search was conducted,
and 17 additional patients with FN paresis following CI,
who had sufficient data for analysis, were aggregated,
providing a cumulative total of 28 patients for
study.7,10,20,23,26 There were seven patients with immediate onset, three with early-onset delayed, and 18 with
late-onset delayed FN paresis (Fig. 1). There was a statistically significant difference between the mean peak
FN paresis HB grade, mean recovered HB grade, and
mean time to recovery when comparing patients
with immediate-onset and late-onset delayed FN paresis
Fig. 1. Clinical course and outcome of facial nerve (FN) paresis
following cochlear implantation among 28 reported cases where
sufficient data were available for review.7,10,20,23,26 The timing of
onset following surgery was classified according to the following
scheme: 1) immediate onset paresis, occurring within 1 hour of
surgery; 2) early-onset delayed paresis, occurring between 1 and
48 hours; and 3) late-onset delayed paresis, occurring beyond 48
hours. Peak FN paresis as House-Brackmann (HB) grade, recovered FN function (HB grade), and time to recovery, in months
(mo), are presented as means with standard deviation bars. The
means of peak FN paresis, FN recovery, and recovery time in immediate-onset and late-onset delayed patients demonstrate a
statistically significant difference (P < .01).
Thom et al.: FN Paresis Following CI Surgery
1001
(P < .01). No statistically significant differences were
found when comparing means in the early-onset delayed
group with the immediate-onset or late-onset delayed
groups (P > .05). This may in part be due to the low
number and high variability of the early-onset delayed
patients.
On postoperative day 11, the patient experienced
incomplete right-sided FN paresis (HB grade 4). Similar
to the first patient, she did not receive steroid therapy
given her history of poorly controlled diabetes. Improvements were noted as early as 10 days after onset, and by
3 weeks the patient had regained full motor function
(HB grade 1).
Illustrative Cases
Immediate-onset FN paresis. An 80-year-old type
2 diabetic male (Table I, case 1) presented to our institution for consideration of CI. He had a history of
progressive bilateral mixed hearing loss secondary to
otosclerosis. High-resolution computed tomography (CT)
of the temporal bones revealed bilateral osteolytic
changes of the otic capsule, further confirming retrofenestral disease. The patient was implanted on the left
with a Nucleus 24RE (Cochlear Ltd., Lane Cove, Australia) device using a transmastoid facial recess
approach. FN monitoring was used throughout the procedure without stimulation. The facial recess was
narrow, and the chorda tympani nerve was sacrificed to
assist with access. The FN was identified but not uncovered during the procedure.
Upon awakening from general anesthesia, the
patient was found to have a left-sided HB grade 4 FN
paresis. Steroids were withheld given his history of
poorly controlled diabetes. The FN paresis peaked (HB
grade 5) by postoperative day 18, and he underwent a
left tarsal strip with tarsorrhaphy to prevent exposure
keratitis. At 12 months, the patient recovered to HB
grade 2 FN function and the tarsorrhaphy was reversed.
Pediatric delayed-onset FN paresis. A 2-year-old
female (Table I, case 2) presented to our department
with congenital bilateral profound SNHL. CT imaging
revealed bilateral inner ear dysplasia with incomplete
partitions of the cochlea, enlarged vestibules, and hypoplastic semicircular canals consistent with Mondini
malformations. The patient underwent a right-sided CI
with the Nucleus 24M device. Intraoperatively, the
descending portion of the FN was identified in the
expected position and was not dehiscent. The facial
recess was opened and a cochleostomy was performed
anteroinferior to the round window niche.
On postoperative day 3, the patient developed right
incomplete (HB grade 4) FN weakness. Her FN paresis
improved without steroid use or antiviral therapy, and by
2 months she regained normal FN function (HB grade 1).
Adult delayed-onset FN paresis. A 76-year-old
female (Table I, case 3) with severe peripheral vascular
disease and type 2 diabetes presented for CI candidacy
evaluation. She had a history of sudden bilateral SNHL
3 years prior, and her hearing continued to deteriorate
over the ensuing years. The patient underwent rightsided CI with a Nucleus CI24RCS device through a
transmastoid facial recess approach. FN monitoring was
used, and no stimulation was detected during the procedure. Both the facial and chorda tympani nerves were
identified and not exposed. A cochleostomy was created
anteroinferior to the round window niche, and a full
electrode insertion was achieved.
Laryngoscope 123: April 2013
1002
DISCUSSION
The current study demonstrates that FN paresis
following CI is rare. Although approximately 1.1% of
patients may experience temporary weakness with
delayed onset, only approximately 0.1% develop incomplete recovery. Late-onset delayed weakness presages a
favorable course, whereas patients with immediate onset
paresis generally acquire more severe weakness, require
longer intervals for improvement, and more frequently
develop incomplete recovery.
The disparity in timing and clinical course between
these groups suggests that the underlying mechanisms
of injury may be different.7,23,24 Intraoperative factors,
including mechanical trauma and thermal injury, can
cause progressive inflammation, neural edema, and ischemia resulting in immediate or early-onset delayed
FN paresis. Specific to CI surgery, thermal insult may
occur when drilling the facial recess using inadequate
irrigation or applying overly aggressive drill pressure.
Additionally, direct mechanical or thermal injury may
result when the shaft of the drill is inadvertently placed
against the FN when drilling the cochleostomy. We suspect the single case of immediate onset FN paresis
(Table I, case 1) was due to heat transfer from the burr
or drill shaft while opening the facial recess or cochleostomy; there was no obvious direct mechanical injury to
the FN, and the FN monitor never alarmed during the
operation. This was the only patient in our series with
immediate onset FN paresis and was also the only individual without complete recovery (HB grade 2). A
similar case of FN paresis has been reported in which
thermal injury from the drill shaft was implicated.26
The phenomenon of late-onset delayed FN paresis
following otologic surgery is less well understood.
Although several mechanisms have been proposed, reactivation of latent virus, including herpes simplex (HSV)
and varicella zoster (VZV), residing in the geniculate
ganglion seems most probable.7,20,21,23,24,27–30 Reactivation may occur following manipulation, heat transfer, or
injury to the chorda tympani nerve or other sensory
branches of the FN.7,20,21,23,24,27–30 In our practice,
chorda tympani nerve sacrifice is rarely performed; disproportionally, four of the 11 cases of FN paresis
occurred with chorda tympani nerve division, and two
patients had exposed FN epineurium. The diagnosis of
herpes virus reactivation following otologic surgery has
been traditionally clinical; however, diagnostic testing
including immunologic assays and polymerase chain
reaction of oral saliva and serum are available.23,30–34
Recent studies have shown large increases in immunoglobulin (Ig)M and/or IgG titers of HSV-1, HSV-2, and
VZV in patients with delayed-onset FN palsy following
Thom et al.: FN Paresis Following CI Surgery
stapedectomy and acoustic neuroma surgery.28,29,34 Further affirming the theory, magnetic resonance imaging
may demonstrate labyrinthine enhancement.35 None of
the patients in this series underwent viral diagnostic
testing.
Herpes virus reactivation in other sensory nerves following surgery has been well documented.36–38 Neurons
of sensory ganglia contain a high number of the capsaicin
receptors known as vanilloid receptor-1 (VR-1).31 In vitro
studies by Hunsperger and Wilcox demonstrated that
when agonists of the VR-1 receptor, capsaicin, and heat
are applied to sensory ganglia neurons, they induce reactivation of HSV-1.31 Similar stimuli, including heat from
drilling and inflammatory molecules, occur with surgery
that may initiate viral reactivation. Herpes virus reactivation requires an incubation period, consistent with the
delay in onset of FN paresis following surgery. The mean
onset of delayed FN paresis in the current study was 8.8
days following surgery, long after one would expect direct
mechanical or thermal injury to manifest.
Although prognostic testing in idiopathic (Bell’s
palsy) and traumatic FN paralysis has been well studied, the role of testing in delayed-onset FN paresis
following otologic surgery is less well defined. Within the
surgical literature, delayed-onset FN paresis following
vestibular schwannoma resection has received the most
attention due to a more frequent occurrence. Given the
very high probability of full recovery, electromyography
and electroneurography are not routinely employed.39
The data from the current study report similar convalescence, making such testing seem unwarranted in this
group as well.
Treatment of delayed-onset FN paresis following
otologic surgery includes observation, corticosteroids,
antiviral therapy, and surgical decompression. Brackmann et al. showed a significant decrease in delayed FN
paresis in patients undergoing acoustic neuroma resection when treated with prophylactic famciclovir.40
Because the risk of FN paresis is far less following CI, it
would seem unnecessary to prophylactically treat
patients with antivirals. Borrowing from the Bell’s palsy
literature, corticosteroids have been shown to significantly improve FN outcomes compared to placebo.41–43
The benefit of concurrent corticosteroid and antiviral
therapy remains controversial, with most randomized,
controlled trials41,42 and meta-analyses44,45 failing to
demonstrate an advantage over steroids alone. In the
current series, four patients were observed, six were
given oral steroids alone, and one received oral steroids
and valacyclovir. There were no differences seen
between the treated and untreated groups with respect
to final outcome or time to recovery. All patients with
delayed-onset paresis regained normal FN function
regardless of management, including one patient with
transient HB grade 6 weakness (Table I, case 4).
Our data suggest that steroid therapy is of uncertain benefit in patients with delayed-onset FN paresis.
That is, the expected outcome is excellent regardless of
treatment. However, immediate onset FN weakness indicates more severe neural injury with an increased risk
for incomplete recovery. Given the small sample size
Laryngoscope 123: April 2013
resulting from the rare prevalence of facial nerve weakness following CI, we are limited in our ability to draw
definitive conclusions regarding optimal medical management. However, borrowing from the vestibular
schwannoma and Bell’s palsy literature,22,41–43 it seems
prudent to treat patients who experience FN paresis following CI with corticosteroids unless there are medical
contraindications to use.
CONCLUSION
FN paresis following CI surgery is rare. Approximately 1% of patients may experience temporary
delayed weakness, whereas the prevalence of permanent
paresis is 0.1%. Delayed-onset portends a favorable
course; patients achieved full motor recovery within
months of onset regardless of medical treatment. Immediate onset weakness implies more severe neural injury;
the time to recovery and definitive FN outcome is less
favorable. In the absence of medical contraindications,
steroid therapy should be strongly considered in patients
with facial weakness following CI. These findings may
be useful in preoperative risk disclosure. Additionally,
they may guide clinicians in postoperative counseling
and treatment to provide reassurance for patients that
experience this rare but distressing complication.
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