1. health and fitness
2. disease

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International Journal of Pediatric Otorhinolaryngology (2005) 69, 1521—1528
www.elsevier.com/locate/ijporl
Pediatric facial nerve paralysis: Patients,
management and outcomes
Adele Karen Evans a, Gregory Licameli a,b, Scott Brietzke c,
Kenneth Whittemore d, Margaret Kenna a,b,*
a
Department of Otology and Laryngology, Harvard Medical School, 243 Charles Street,
Boston, MA 02214, USA
b
Department of Otolaryngology and Communication Disorders, Children’s Hospital Boston,
Fegan 9, 300 Longwood Avenue, Boston, MA 02215, USA
c
Walter Reed Army Medical Center, 6900 Georgia Avenue, NW, Washington, DC 20307-5001, USA
d
Department of Otolaryngology, University of Rochester School of Medicine,
2365 S. Clinton Street, Rochester, NY 14618, USA
Received 19 January 2005; accepted 18 April 2005
KEYWORDS
Facial nerve paralysis;
Bell’s palsy;
Otitis media;
Temporal bone;
Pediatric
Summary
Objective: To characterize the causes and treatment of facial nerve paresis (FNP) in
pediatric patients.
Method: Retrospective study in a tertiary care pediatric hospital. Thirty-four
patients identified with partial or complete FNP evaluated between 1997 and
2003. A review of the medical records including sex, age, laterality, etiology, therapy,
severity of paralysis according to House—Brackman (HB) six-point grading scale,
duration, and degree of recovery.
Results: Thirty-five cases of FNP. Causes of FNP were infectious (13), traumatic (7),
iatrogenic (5), congenital (4), Bell’s/Idiopathic (3), relapsing (2) and neoplastic (1).
Peak age distributions for both infectious and traumatic etiologies were bimodal:
1—3 and 8—12 years.
Of the 13 infectious cases, 11 were associated with acute otitis media with effusion
(AOME). Four (4/11) were bacterial-culture negative. Seven (7/11) were bacterialculture positive, four (4/7) of which required prolonged, broth-medium culture.
Bacteria cultured predominantly included Staphylococcus non-aureus species (5/7)
and Propionobacterium acnes (3/7). One (1/13) was viral culture positive (Herpes
Simplex Virus).
* Corresponding author. Tel.: +1 617 355 4534; fax: +1 617 730 0337.
E-mail addresses: adeleyarrington@rcn.com (A.K. Evans), greg.licameli@childrens.harvard.edu (G. Licameli),
Kenneth_Whittemore@umc.rochester.edu (S. Brietzke), SBrietzke@aol.com (K. Whittemore),
margaret.kenna@childrens.harvard.edu (M. Kenna).
0165-5876/$ — see front matter # 2005 Elsevier Ireland Ltd. All rights reserved.
doi:10.1016/j.ijporl.2005.04.025
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1522
A.K. Evans et al.
All six patients who received intravenous steroids for OME-associated FNP received
the doses within the first week of presentation and had complete recovery (HB I/VI);
three of five patients who did not receive steroids had complete recovery.
There were five iatrogenic cases; two (2/5) were planned surgical sacrifices and
three (3/5) were complications of middle ear/mastoid surgery.
Facial nerve function associated with infection returned in 0.5—2 months while,
when associated with trauma, returned in 0.25—30 months.
Conclusions: In infectious or traumatic FNP, children aged 1—3 and 8—12 years are the
primary groups involved. In AOME FNP, culture-identified organisms may not be representative of traditional pathogens. Infectious FNP averaged 1 month for recovery while
traumatic FNP averaged 9 months. Intravenous steroid therapy may improve the
outcome. Recovery was complete (HB I/VI) in 8/10 infectious and 4/6 traumatic cases.
# 2005 Elsevier Ireland Ltd. All rights reserved.
1. Introduction
Paralysis of the seventh cranial nerve, the facial
nerve, is usually immediately obvious. Whether it
develops in a child or an adult, it results in weakness
of the musculature of the face, impacting verbal
communication, social interaction with respect to
facial expression, oral competence, taste and, most
importantly, protection of the cornea, ocular globe
and vision. Such a paralysis can seem devastating
when it occurs in a child and parents present with
not unreasonable concerns for the well-being of
their child. Questions arise regarding the reason
that their child has been affected, the utility of
treatment modalities, the anticipated outcome,
and the duration of time until recovery is complete.
Whereas several studies began to address these
issues, the largest of these studies are now years to
decades old [1—3]. With several recent patients
presenting to the emergency ward at Children’s
Hospital Boston, our group began to ask the following questions: Is FNP occurring more frequently?
What is the distribution of patients in our population, regarding age, year of onset, and etiology of
onset? What is the anticipated duration of symptoms? What have been our management techniques?
What are our outcomes?
2. Methods
A literature search for the years 1977 to October
2003 using the NLM PubMed using the keyword
groups ‘‘facial nerve paralysis pediatrics’’ and
‘‘facial nerve paralysis otitis media’’ was performed. Pertinent articles identified were published
in 2003, 2000, 1990, 1981, 1974 and 1972.
The Children’s Hospital Boston Otolaryngology
Foundation records were searched from 1997 to
2003 for the following diagnostic codes and their
associated representative diagnoses: 767.5 (facial
nerve injury with facial paralysis–—birth trauma),
951.4 (injury to facial nerve–—trauma), 998.2 (accidental iatrogenic injury), 351.0 (Bell’s Paralysis–—
unilateral facial nerve paralysis due to lesion on
nerve), 351.8 (other facial nerve disorders), 351.9
(other facial nerve disorder, NOS). The Children’s
Hospital Boston IRB approved the retrospective
chart review proposal.
The electronic charts, hospital records and foundation records were then reviewed for detailed information, which included sex, age at presentation, the
results of middle ear cultures, the results of temporal
bone imaging studies obtained, the details of pertinent operative reports and the outcomes, including
degree of and time to recovery. The House—Brackman
grade scale for facial nerve paralysis recovery was
used to classify the degree of paralysis at the nadir
and after recovery. This information was compiled
into a database using Microsoft Excel_XP#, removing
all unique identifiers in compliance with HIPAA regulations. Analysis was then performed using the database, with more extensive evaluation performed for
the patients whose facial nerve diagnosis was of
infectious or traumatic etiology. Medical records
were available with sufficient data for 34 patients.
3. Results
There were 35 cases of FNP identified. There were 14
(40%) males and 21 (60%) females affected. The left
facial nerve was affected in 15 (43%) cases; the right
facial nerve was affected in 19 (54%) cases, and one
case was not recorded (2.9%). Thirteen cases of facial
nerve paralysis were of infectious etiology (37%); this
was followed by traumatic (7 cases, 20%), iatrogenic
(5 cases, 14%), congenital (4 cases, 11%), Bell’s/
idiopathic (3 cases, 9%), relapsing (2 cases, 6%),
and neoplastic (1 case, 3%). Basic patient demographics are detailed in Table 1, and the mechanism
of paralysis and the outcome is listed in Table 2.
The overall average age at presentation was 7.32
years (range: 2.4 months—20 years). However for
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Pediatric facial nerve paralysis: Patients, management and outcomes
1523
Table 1 FNP patient demographics
Case #
Age (years)
Gender
Side
Etiology
Mechanism
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
0.7
1.1
12
1.8
12
12
10
9
3
14
2.5
2
13
10
8
2
9
10
1.75
6
5
3.8
0.5
0.2
1.6
14
15
M
M
F
F
F
M
F
M
F
F
M
F
F
M
F
F
F
M
F
F
F
M
M
F
F
F
M
F
M
M
F
F
M
F
M
L
R
R
L
R
R
L
R
R
L
R
R
?
L
L
R
L
L
L
L
R
R
R
L
R
R
R
R
L
L
L
R
R
L>R
R
Infectious
Infectious
Infectious
Infectious
Infectious
Infectious
Infectious
Infectious
Infectious
Infectious
Infectious
Infectious
Infectious
Trauma
Trauma
Trauma
Trauma
Trauma
Trauma
Trauma
Neoplasm
Congenital
Congenital
Congenital
Congenital
Idiopathic
Idiopathic
Idiopathic
Iatrogenic
Iatrogenic
Iatrogenic
Iatrogenic
Iatrogenic
Relapsing
Relapsing
AOM w/o mastoiditis
AOM w/o mastoiditis
AOM w/o mastoiditis
AOM w/o mastoiditis
AOM w/o mastoiditis
AOM w/mastoiditis
AOM w/o mastoiditis
AOM w/o mastoiditis
AOM w/o mastoiditis
AMO w/mastoiditis
AOM w/o mastoiditis
MAI
HSV
Blunt trauma to cheek
Blunt trauma to cheek
T-bone frx (ped v MV)
T-bone frx (seizure/fall)
T-bone frx (sledding)
bil T-bone frx (ped v MV)
Snowball to cheek
Embryonal rhabdomyosarcoma R cheek
COM AD; ? ME mass on CT
Goldenhar syndrome; small CN7 by CT
CN 12 palsy
CHARGE
14
19
17
1.6
20
3.5
0.75
both traumatic and infectious causes there was a
bimodal distribution of ages, with average peaks at
approximately 2 years (1.85—2.38 years) and 11.5
years (8.6—11.71 years) of age (see Fig. 1).
3.1. Infectious
There were 13 patients diagnosed with facial nerve
paralysis of infectious etiology. Of these thirteen
Fig. 1
Age distribution of facial nerve palsy patients.
Resxn of nasal angiofibroma w/MCF extension
Transparotid Infratemporal Fossa Approach
AS tympanomastoidectomy
s/p cochlear implant
Tympanoplasty
dx hemiplegic migraine
patients, one was diagnosed with disseminated
Herpes simplex virus and one with Mycobacterium
avium-intracellulare complex parotitis.
There were 11 cases of facial nerve paralysis due
to acute otitis media. Seven cases (64%) involved the
right and 4 cases (36%) involved the left. Although
the overall average age at presentation for the
infectious group was 7.1 years, there was a clear
bimodal distribution with peaks at 1.85 and 11.7
years. Two patients were clearly diagnosed with
acute coalescent mastoiditis based on physical
exam and CT scan findings involving the temporal
bone. One patient had a strong history of chronic
otitis media; one patient had a remote childhood
history of Eustachian tube dysfunction.
The House—Brackman (HB) grading scale was
used to characterize all patients with an infectious
etiology at the nadir of function [4]. The findings are
detailed in Fig. 2.
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1524
A.K. Evans et al.
Table 2 FNP outcomes
Case #
Etiology
Initial H-B grade
Outcome H-B grade
Duration (month)
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
Infectious
Infectious
Infectious
Infectious
Infectious
Infectious
Infectious
Infectious
Infectious
Infectious
Infectious
Infectious
Infectious
Trauma
Trauma
Trauma
Trauma
Trauma
Trauma
Trauma
Neoplasm
Congenital
Congenital
Congenital
Congenital
Idiopathic
Idiopathic
Idiopathic
Iatrogenic
Iatrogenic
Iatrogenic
Iatrogenic
Iatrogenic
Relapsing
Relapsing
6/6
6/6
6/6
6/6
5/6
4/6
5/6
6/6
2/6
2/6—3/6
6/6
5/6
6/6
2/6—3/6
6/6
6/6
6/6
6/6
6/6
6/6
NA
NA
3/6
4/6—5/6
6/6
6/6
NA
3/6
NA
NA
6/6
6/6
3/6
NA
NA
1/6
1/6
1/6
1/6
1/6
NA
1/6
1/6
2/6
2/6
Deceased
NA
1/6
1/6
2/6
3/6
1/6
1/6
NA
1/6
1/6 a
NA
NA
NA
6/6
1/6
1/6
1/6
NA
NA
1/6
1/6
1/6
1/6
1/6
1
1
0.5
0.75
1.25
NA
2
0.5
0.5
NA
Deceased
NA
0.38
<0.25
6
30
1
2
NA
2
60
NA
NA
NA
72
<1
8
1
NA
NA
4
2.5
2
NA
NA
a
Eye only, after free flap reconstruction with heavy scarring in the buccal and marginal branch distributions.
In patients with otitis media, myringotomy and
ventilation tube placement was performed in all 11
patients (100%). Mastoidectomy was performed in
one patient (9.5%). Intravenous antibiotics were
administered to all 11 patients (100%). Intravenous
antibiotics were used while the child was an inpatient and switched to oral antibiotics for outpatient care. Topical antibiotic drops containing
topical steroids, most often neomycin/polymixin
B/hydrocortisone otic suspension or solution or
ciprofloxacin/hydrocortisone solution, were used
in all 11 patients (100%). Intravenous steroids,
usually dexamethasone, were administered to five
patients.
In the 11 cases associated with acute otitis media
with effusion, a sample of middle ear fluid was
obtained and sent to the Microbiology Lab for Gram
stain and culture. Data was not available for one
patient. Of the seven bacterial-culture positive
results, three specimens grew immediately on
plates. Four specimens resulted in no growth on
plates, but demonstrated growth in broth with prolonged culture. Four specimens had a final report of
no growth. Viral culture was obtained for one
patient, revealing Herpes Simplex Virus (HSV).
Overall, culture results demonstrated Staphylococcus non-aureus species in five (5/7) cases, Pro-
Fig. 2
Degree of loss of facial nerve function.
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Pediatric facial nerve paralysis: Patients, management and outcomes
Fig. 3
Degree of recovery of facial nerve function.
1525
Four patients (57%) were treated with steroids.
One had a nadir HB grade of VI/VI and had complete
recovery. One had a nadir HB grade of VI/VI and had
a near-complete recovery to HB grade II/VI. One had
a nadir HB grade of III/VI and complete recovery.
The degree of recovery was not available for one
patient who had a nadir HB grade of VI/VI. Results of
recovery are detailed in Fig. 3.
The average length of duration of the paralysis
for the six trauma patients with complete follow-up
was 6.875 months.
pionobacterium acnes in three (3/7) cases, Streptococcus viridans in two (2/7) cases, Staphylococcus
aureus in one (1/7) case, and Corynebacterium
afermentans in one (1/7) case. Four (4/7) cultures
had polymicrobial growth.
The results of recovery are detailed in Fig. 3.
There were three cases without available outcome
measures: one patient died of his underlying leukemia before recovery of his FNP and two patients had
no documented follow-up visits. The average length
of paralysis for these 10 patients until resolution was
0.875 months.
3.3. Congenital
3.2. Trauma
Two (2/5) of our iatrogenic etiologies were the
anticipated result of a surgical procedure performed
to access the parapharyngeal space and the skull
base for resection of a tumor. In these cases, the
facial nerve branches were identified, labeled,
transected, and then neurorrhaphy was performed
for each branch. Outcome data was not available for
these patients.
The other three (3/5) iatrogenic cases occurred
with cases of middle ear surgery, two delayed and
one immediate in onset. In no case was there
direct evidence of damage to the facial nerve
either at the time of the original surgery or upon
re-exploration. In the first case a mastoidectomy
and tympanoplasty was performed for chronic
otitis media with cholesteatoma in a patient with
Smith-Lemli-Opitz Syndrome and pre-operative
facial asymmetry. One week after surgery, she
developed a facial nerve paralysis. She was not
explored, but she was treated with systemic steroids. She recovered function over the course of 5
months.
The second patient was a healthy teenage male
who underwent an uncomplicated Type-I tympanoplasty. On post-operative day 4, he noted onset and
progression over a few hours of an ipsilateral facial
nerve paralysis. He was treated with steroids and
antivirals, and he underwent surgical exploration
with removal of middle-ear Gelfoam1 packing. He
completely recovered facial nerve function within 2
months.
There were seven cases of facial nerve paralysis due
to traumatic injury. Two occurred in males, five
occurred in females. One case involved the right
side, six cases involved the left. Although the overall
average age at presentation for the group was 5.8
years, there was a clear bimodal distribution with
peaks at 2.38 and 8.6 years. The predominant traumatic mechanisms included blunt trauma to the
cheek (n = 3) (a direct hit from a flying snowball,
running into a pole while trying to look over the
shoulder, and ‘‘blunt trauma to the cheek’’) and
temporal bone fracture (n = 4) (sledding, fall during
seizure and in two direct strikes by motor vehicles).
The HB grading scale was used to characterize all
seven of these patients at the nadir of function. The
findings are detailed in Fig. 2.
Six (6/7) of the patients underwent CTscan of the
temporal bone. Of these patients, three (3/6) had
significant, associated CT findings (congenital
absence of the parotid gland, temporal bone fracture, skull base fracture, extraparotid facial nerve
edema). The seventh patient (1/7) underwent MRI
evaluation with resultant significant MRI findings.
One patient (14%) underwent operative management of the injury with middle ear exploration and
decompression of the facial nerve. This patient had
a nadir HB grade of VI/VI and recovered to HB III/VI
(normal resting tone, eye closure with effort, moderate weakness).
Of our five patients with congenital facial nerve paralysis, two (2/5) had craniofacial syndromes and a
third (1/5) patient had multiple cranial nerve neuropathies. One (1/5) patient had a suggestion of a
middle ear mass by CT scan and underwent surgical
exploration that was unrevealing of an etiology.
Outcomes data were not available for this group
of patients.
3.4. Iatrogenic
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1526
A.K. Evans et al.
The third patient had a history of profound sensorineural hearing loss and underwent simple mastoidectomy with facial recess approach to the round
window for cochlear implantation. Complete
paralysis on the operated side was noted upon
awakening. She was treated with systemic steroids
and explored with facial nerve decompression 48 h
later. She recovered completely.
3.5. Bell’s/idiopathic
Three (3/3) patients with Bell’s palsy or idiopathic
facial nerve paralysis were treated with steroids,
and two (2/3) were treated with antiviral agents and
antibiotics. Two (2/3) of them had evidence on MRI
of contrast-enhancement of a segment of the facial
nerve. All three patients completely recovered
nerve function.
3.6. Relapsing
There were two patients with diagnoses of relapsing
facial nerve paralysis. One patient presented at 3.5
years of age with bilateral involvement, the left side
more frequently than the right. The paralysis consisted of 45—60 s of facial droop followed by complete resolution. The patient had no significant
findings on MRI. This patient’s ultimate diagnosis
was hemiplegic migraine. The second patient presented at the age of 9 months with a right-sided
relapsing facial nerve paralysis that lasted anywhere from 1 week to 1 month at a time. Events
were followed by complete resolution of the paralysis. There were no significant findings on CT scan of
the temporal bone or on MRI. No further diagnosis
was given.
3.7. Neoplastic
Our single case of neoplasm-associated facial nerve
paralysis was due to an embryonal cell rhabdomyosarcoma of the cheek in a 5-year-old patient. Management included resection of the lesion and
reconstruction of the defect with a myoadipofascial
free flap. She had excellent eye closure 5 years postoperatively, but heavy scarring in the buccal and
marginal branch distributions made isolated assessment of VII function difficult.
4. Discussion
In 1972, a large study of pediatric facial nerve
paralysis was conducted at the Kaiser-Permanente
Facial Paralysis Clinic in Oakland, California. In this
study, 61 children under the age of 14 were diag-
nosed with facial nerve paralysis. This study determined demographics of facial nerve paralysis in a
primary care establishment whose patient population closely reflected the demographics of the
entire region of Northern California. More than
50% were diagnosed with Bell’s Paralysis; other
palsies were secondary to otitis media (9.8%), birth
trauma (7.1%), other infections (6.5%), neoplasia
(Histiocytosis-X) (3.2%), other trauma (3.2%), congenital (3.2%) and unknown (3.2%) [5].
Similarly, May et al. in Pittsburgh published a
comprehensive article in 1981 reviewing 170 cases
of pediatric facial nerve paralysis over 17 years and
discussing differential diagnosis of pediatric facial
nerve paralysis. In this study, Bell’s Paralysis represented the ultimate diagnosis in 42% of the patients.
Other causes included trauma (15%), otitis media
(12%), congenital (7.6%), birth trauma (5%) and
neoplasia (4%) [1].
In contrast to those results are the results published by Dr. Grundfast et al. in 1990 from the
Children’s National Medical Center in Washington,
DC. Twenty-five patients were diagnosed with a
facial nerve paralysis; 84% were due to specific
etiology or were associated with a recognizable
syndrome and only 16% were ultimately diagnosed
as Bell’s Palsy. Specific causes were trauma (24%),
otitis media (16%), other infectious agents (12%),
neoplastic origin (12%), and congenital (8%). One
patient (4%) presented with paralysis secondary to
osteopetrosa tarda [2].
In our study, infectious causes were the most
common etiologies of the facial nerve paralysis,
representing 36% of the cases. This was followed
by trauma (19%), iatrogenic (14%), congenital (14%),
Bell’s/idiopathic (8%), relapsing (6%) and neoplastic
(3%). Our data is similar to the Grundfast et al. data.
Both data sets underscore the importance of searching for the specific etiology of a facial nerve paralysis (i.e., otitis media, trauma, neoplasm) in order to
provide the appropriate treatment for the paralysis
(i.e., antibacterials, antivirals, steroids, surgical
decompression) as well as to identify any occult
disorder (i.e., CNS or temporal bone neoplasm).
The largest single cause of FNP in our series was
acute otitis media. The age distribution was bimodal, with peaks at 1.85 and 11.7 years. In 10/11
cases, true coalescent mastoiditis was not present.
The one patient who underwent mastoidectomy had
an acute episode of otitis media superimposed on a
chronic otitis media.
In 1998, Drs. Joseph and Sperling published a
small series of case reports in which adult patients
with acute otitis media presented with acute facial
nerve paralysis. Despite the fact that the patients
were all treated for the acute otitis media with
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Pediatric facial nerve paralysis: Patients, management and outcomes
antibiotics, they developed a facial nerve paralysis. Of the three patients, two patients had a dry
ear on myringotomy and one patient had serous
effusion [6]. All three patients recovered facial
nerve function within a few weeks of myringotomy.
Similarly, most of our patients had already started
antibiotic therapy for otitis media prior to presentation. All patients went to the OR for myringotomy and tympanostomy tube placement. They all
received intravenous antibiotics. Half of the
patients received intravenous steroids. Although
few ears contained frankly purulent effusions at
myringotomy, effusion was present in all patients.
Often, organisms were not readily isolated from
the intraoperative cultures. Broth inoculation
grew Staphylococcus non-aureus species (5/7),
Propionobacterium acnes (4/7), Streptococcus viridans (2/7), Staphylococcus aureus (1/7) and Corynebacterium afermentans (1/7). Controversy will
exist as to whether these were etiologic organisms
or contaminants.
Drs. Elliot, Zalzal and Gottlieb published an
outcomes study in 1996 in which they reviewed
the etiology, management and outcomes of 10
pediatric patients who presented with facial nerve
paralysis due to otitis media. Their ultimate findings were that incomplete paralysis recovered
more quickly than did complete paralysis [3].
Given the overall small population in our study
and even smaller population with only partial
paralysis, it is difficult to refute or support this
statement with our data.
4.1. Trauma
Our second greatest etiologic contribution came
from trauma, representing 19% of the patient population. Interestingly, more commonly girls were
affected. Again, there was a bimodal age distribution, with peaks at 2.38 and 8.6 years of age. The
majority of patients had a complete paralysis (VI/
VI). This group did contain blunt facial trauma and
temporal bone fractures. Our patient group did not
contain any patients with birth-associated facial
nerve paralysis.
A 1990 study of congenital facial nerve paralysis
conducted at Brigham & Women’s Hospital yielded
results that may well be considered applicable to
blunt facial nerve trauma. In this study, 81
acquired cases were identified in 92 documented
congenital facial nerve pareses. They found the
acquired pareses to be associated with forceps
delivery, delivery weight of 3500 g or more and
primaparity. Of those patients for whom follow-up
was adequate, there was an 89% complete recov-
1527
ery rate and a mean recovery time of nearly 3
years [7].
A large French study published in 2001 compared
medical and surgical management and outcomes of
temporal bone fractures. They found that 98% of
medically managed fractures associated with facial
nerve paralysis resulted in recovery of function to
normal or near-normal (House—Brackman grade I—
II/VI). Surgical management identified a nerve gap
in only 14% of cases. It resulted in a 94% recovery to
normal or near-normal (House—Brackman grade I—
III/VI) at 2 years post-operatively [8].
Half of our trauma patients underwent imaging
studies of the temporal bone with identification of a
lesion (i.e., congenital absence of the parotid gland,
temporal bone fracture, skull base fracture, extraparotid facial nerve edema). Four of the seven of
the patients were treated with steroids independent of the CT or MRI findings. Only one patient
underwent surgical management. Four patients
experienced complete recovery (HB grade I/VI)
and one experienced near-complete recovery (HB
grade II/VI) with an average duration of approximately 10 months. As a group, these good outcomes
reflect the results obtained by Falco and Eriksson,
and Darrouzet et al. In contrast to both studies, less
than a year was adequate time for recovery of
function rather than 2 years.
4.2. Iatrogenic
At our hospital, a total of 919 surgeries involving the
temporal bone were performed throughout the
duration of this study. Of those surgeries, 467
involved myringoplasty and/or tympanotomy without mastoidectomy; 178 involved mastoidotomy or
simple mastoidectomy with or without ossiculoplasty; 51 involved radical or modified radical mastoidectomy; and 223 involved middle cranial fossa
approach, posterior cranial fossa approach or the
implantation of cochlear devices. There were only
three unanticipated iatrogenic complications that
resulted in facial nerve paralysis, a rate of 0.3%. All
three patients experienced complete recovery to
baseline function with a mean time to recovery of
2.8 months. It would be safe to say that this complication is very rare and expected to be fully
reversible if no direct damage to the facial nerve
occurred intraoperatively.
5. Conclusions
Facial nerve paresis or paralysis has a tremendous
impact on the patient as well as the family, particularly when a pediatric patient is involved. Tod-
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1528
A.K. Evans et al.
dlers (children between ages 1 and 3 years) and preteenagers (between ages 8 and 12 years) may be at
higher risk for facial nerve paralysis due to infectious and traumatic causes. These complications of
infection and facial or temporal bone trauma are
still rare. Other broad categories of differential
diagnoses include congenital defects, neoplasms,
idiopathic/Bell’s palsy, and iatrogenic injury during
facial or middle ear surgery.
Recovery of facial nerve paralysis usually takes 1
month or less in cases of infectious etiology but 8
months in cases of traumatic etiology. In these
cases, recovery is nearly always substantial (II/VI)
to complete (I/VI), except in cases of laceration and
reconstruction.
The date concerning infectious etiologies for
facial nerve paralysis provides new information
for the pediatric population and supports similar
data in the adult population.
This article exemplifies the need for prospective
study of treatment algorithms to answer clinical
questions regarding management in contrast to
the available retrospective review which helps us
to define the questions.
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