Original Article

Journal of Child Neurology

2014, Vol. 29(11) 1473-1478
Peripheral Facial Palsy in Children ª The Author(s) 2013
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DOI: 10.1177/0883073813503990
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Ünsal Yılmaz, MD1, Duygu Çubukçu, MD1, Tuba Sevim Yılmaz, MD2,
Gülçin Akıncı, MD1, Muazzez Özcan, MD1, and Orkide Güzel, MD1

Abstract
The aim of this study is to evaluate the types and clinical characteristics of peripheral facial palsy in children. The hospital charts of
children diagnosed with peripheral facial palsy were reviewed retrospectively. A total of 81 children (42 female and 39 male) with a
mean age of 9.2 + 4.3 years were included in the study. Causes of facial palsy were 65 (80.2%) idiopathic (Bell palsy) facial palsy,
9 (11.1%) otitis media/mastoiditis, and tumor, trauma, congenital facial palsy, chickenpox, Melkersson-Rosenthal syndrome,
enlarged lymph nodes, and familial Mediterranean fever (each 1; 1.2%). Five (6.1%) patients had recurrent attacks. In patients with
Bell palsy, female/male and right/left ratios were 36/29 and 35/30, respectively. Of them, 31 (47.7%) had a history of preceding
infection. The overall rate of complete recovery was 98.4%. A wide variety of disorders can present with peripheral facial palsy
in children. Therefore, careful investigation and differential diagnosis is essential.

Keywords
peripheral facial palsy, Bell palsy, children, etiology

Received June 15, 2013. Received revised August 14, 2013. Accepted for publication August 14, 2013.

Peripheral facial palsy is a relatively common, usually idiopathic
and generally self-limited, nonprogressive and spontaneously
remitting disorder in children.1 However, it could be a sign of
a serious underlying disease such as a neoplasm, systemic dis-
ease, trauma or congenital anomaly, and recovery might not
always be complete in all cases.2
The most common type of peripheral facial palsy in chil-
dren is Bell palsy, which is defined as an acute, idiopathic,
unilateral paralysis of the facial nerve without any associated
disorders.1 It is a diagnosis of exclusion, and congenital
causes, genetic disorders such as Melkersson-Rosenthal syn-
drome, and acquired causes such as neoplasms, autoinflam-
matory disorders, infections, and trauma need to be ruled
out before the diagnosis is made.1,3 Etiology of Bell palsy
remains unclear although genetic, vascular, infectious, and
immunologic causes have all been postulated.1 It has an inci-
dence rate of 19 to 21 cases per 100 000 in children younger
than 18 years.4,5 Males and females are affected equally, as
are both sides of the face.2,3,6 The evidence for a familial ten-
dency is weak.4 Recurrence rates range from 6%7 to 10%.6
Corticosteroids and antiviral agents are widely used to treat
the peripheral facial palsy, but their effectiveness is uncertain.
In adults, significant benefit has been shown from treatment
with corticosteroids, particularly if used early in the course of
the illness.8-10 A Cochrane review of antiviral treatment did not
show a significant benefit from antiviral use when compared
with placebo in producing complete recovery.11 A single
randomized controlled study of steroid use did not demonstrate
a significant difference in improvement between treated and
untreated children.12 In many cases, complete resolution occurs
within 2 months of the onset of the facial palsy and by 6 months
in most cases.2
In contrast to adults, the natural course of peripheral facial
palsy in children is not well documented, and there are still
many unresolved issues regarding etiology, treatment, and
prognosis. The aim of this study was to report our experience
of clinical characteristics, etiology, association with nonspeci-
fic viral infections, and prognosis of facial palsy in children.
Method
Hospital records of children under 18 years of age attending the pedia-
tric neurology outpatient clinic at Dr. Behçet Uz Children’s hospital
between July 2011 and May 2013 were retrospectively reviewed, and
children diagnosed with peripheral facial palsy were identified.
Criteria for inclusion were acute isolated unilateral peripheral facial
nerve palsy and a follow-up period until satisfactory recovery or at
least 1 year. Children with central facial palsy were excluded. The
Hospital Ethical Committee approved the study.
All patients were referred to pediatric neurology outpatient clinic
by pediatricians. Each child was evaluated by the same child
1
Dr. Behçet Uz Children’s Hospital, Izmir, Turkey
2
Department of Public Health, Dokuz Eylul University Hospital, Izmir, Turkey
Corresponding Author:
Ünsal Yılmaz, MD, Department of Pediatric Neurology, Dr. Behçet Uz
Children’s Hospital, 35210, Konak, Izmir, Turkey.
Email: drunsalyilmaz@yahoo.com

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1474 Journal of Child Neurology 29(11)

neurologist with a standardized workup and follow-up, and the same Table 1. Types of Peripheral Facial Palsy by Diagnosis and Age at
physician recorded all the demographic, clinical, laboratory, and radi- Onset for Each Disorder.
ologic results into a standardized file. Following a thorough history, a
detailed physical and neurologic examination was performed, and Mean age at
selected laboratory investigations were obtained based on the sus- onset + SD
pected diagnosis. All children were also examined by an otolaryngol- Disorders n (%) (y range)
ogist, an ophthalmologist, and a physiatrist during the initial Bell palsy 65 (80.2) 9.87 + 3.76 (1-16)
evaluation. The severity of facial nerve dysfunction was graded Otitis media/mastoiditis 9 (11.1) 6.22 + 5.82 (1-15)
according to House Brackman Facial Nerve Grading scale, and the Varicella 1 (1.2) 6
facial palsy was defined as severe when it was grade 3 or more and Remote trauma related meningitis 1 (1.2) 13
mild when it was less than grade 3. Detailed information was collected Enlarged lymph nodes in the parotid 1 (1.2) 1
on child’s age, gender, the type of facial palsy by etiology, side of gland
involvement, medical history, family history of facial palsy, severity Tumor 1 (1.2) 2
of facial palsy, diagnostic investigations, treatment received and Congenital 1 (1.2) 0
recovery. The diagnosis of Bell palsy was made when other causes Familial Mediterranean fever 1 (1.2) 14
of peripheral facial palsy such as central nervous system disorders, oti- Melkersson-Rosenthal syndrome 1 (1.2) 13
tis media, trauma, or Ramsay Hunt syndrome were excluded by his- Total 81 (100) 9.22 + 4.39 (0-16)
tory, physical examination, and diagnostic investigations. Recurrence 5 (6.2)
In patients with Bell palsy, when the grade was 3 or more, oral pre-
Abbreviation: SD, standard deviation.
dnisolone therapy was initiated with a dose of 2 mg/kg up to 60 mg
daily for 5 days followed by 5 days’ taper. When a viral infection is
suspected, antiviral medication was initiated. In addition, a physical
therapy consisting of training of the facial muscles following a stan- male, with an average age of 9.87 + 3.76 years ranging from 1
dardized protocol were initiated in all patients at the time of the diag- to 16 years. Most patients were distributed in the age groups
nosis. In patients who did not show at least partial recovery after 15 from 9 to 13 years (Figure 1), with a peak incidence at 11 years
days or residual symptoms at 3 months and electroneuromyography and 13 years (each 8 patients, 12.9%). There were 35 (53.8%)
for facial nerve involvement and magnetic resonance imaging (MRI) right and 30 (46.2%) left peripheral facial palsies. Forty-two
of the brain and/or temporal bone were performed. Recovery was (64.6%) patients had severe and 23 (35.4%) patients had mild
assessed with follow-up visits once a week during the first month and peripheral facial palsy. Thirty-one (47.7%) patients had a his-
subsequently every 1 or 2 months until satisfactory recovery, which
tory of nonspecific upper airway infections 1 to 4 weeks before
was defined as the achievement of grade 1.
The outcome measures of the study were frequency of the types of
the onset of facial palsy. A family history of Bell palsy was
facial palsy, frequency of preceding infection, proportion of patients noted in 7 (10.8%) patients. Of the 65 patients with Bell palsy,
who received corticosteroids, imaging results, and outcome. 42 (64.6%) patients with severe involvement received treat-
ment with oral prednisolone 2 mg/kg/d for 5 days followed
by taper for another 5 days. Twenty-six (40%) patients received
Statistics oral acyclovir treatment. Remaining 23 (35.4) patients with
All data were descriptively analysed with SPSS 15. For data interpre- mild Bell palsy did not receive any medication. All patients
tation, frequencies and cross-tables were used. received a physical therapy consisting of training of the facial
muscles. Of the 65 patients with Bell palsy, 12 (18.5%) showed
complete recovery at 1 month, another 46 (70.8%) patients
Results recovered fully at 3 months, and all except 1 patient completely
A total of 81 children diagnosed with peripheral facial palsy recovered at 12 months. Only 1 patient had residual symptoms
from July 2011 to May 2013 were identified. Of them, 42 at 12 months.
(51.9%) were female and 39 (48.1%) were male. The overall The causes of peripheral facial nerve palsy were acute otitis
average age at presentation was 9.22 + 4.39 years ranging media in 8 (9.8%) patients and mastoiditis in 1 (1.2%) patient.
from 2 months to 16 years. Diagnosis of otitis media and mastoiditis was based on physical
As regards the etiology, of the 81 children, 65 (80.2%) were examination and/or MRI scanning of the temporal bone. One of
diagnosed with Bell palsy, 9 (11.1%) patients with otitis media the patients with otitis media had a history of hepatitis B vac-
or mastoiditis, and 1 (1.2%) patient each with tumor, remote cination 9 days before the clinical presentation. Patients with
trauma-related meningitis, enlarged lymph nodes in the parotid otitis media or mastoiditis were treated with antibiotics, acyclo-
gland, Melkersson-Rosenthal syndrome, vasculitis related with vir, and prednisolone. Myringotomy and ventilation tube place-
familial Mediterranean fever, congenital facial palsy, and var- ment were performed in 2 patients. All patients with otitis
icella infection. Distribution of the types of facial paralysis by media and mastoiditis were recovered completely at 3 months.
etiology are presented in Table 1. Five (6.2%) patients had One child had a varicella infection 2 weeks before the onset of
recurrent peripheral facial palsy. facial palsy, and facial palsy in this patient was regarded as a
Demographic characteristics and clinical features of the neurologic manifestation of chickenpox.
patients with Bell palsy are shown in Table 2. Of the 65 patients A 2-year-old boy presented with an acute-onset right-sided
with Bell palsy, 36 (55.4%) were female and 29 (44.6%) were peripheral facial palsy as the sole symptom. Cerebral MRI

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Yılmaz et al 1475

Table 2. Demographic Characteristics of Patients With Bell Palsy. chemotherapy was initiated at the pediatric oncology
department.
Parameter n (%)
One patient had multiple enlarged lymph nodes in the left
Number 65 parotid gland. MRI scanning of the parotid gland was compa-
Mean age (+ SD) at diagnosis, y 9.87 + 3.76 tible with enlarged lymph nodes. He received antibiotic treat-
Sex ment and recovered completely within a month.
Female 36 (55.4) In one patient, bacterial meningitis was diagnosed 15 days
Male 29 (44.6)
before the onset of facial paralysis. He had a history of fracture
Sides
Right 35 (53.8) of temporal bone 3 years ago. Temporal bone MRI revealed a
Left 30 (46.2) cholesteatoma. He received prednisolone for 14 days in addi-
Recurrence 3 (4.6) tion to intravenous antibiotic therapy for meningitis and recov-
History of preceding infection within 30 days prior to 31 (47.7) ered completely at 9 months.
diagnosis One patient with a suspected neurometabolic disorder of
Family history of Bell palsy 7 (10.8) unknown etiology had congenital peripheral facial palsy. She
Severity of facial palsy
had diffuse cerebral atrophy and bilateral cystic degeneration
Mild 23 (35.4)
Severe 42 (64.6) in temporal lobes. Severity of facial palsy decreased over time,
Complete recovery 64 (98.4) but she had residual symptoms at 12 months.
At month 1 12 (18.5) Five (6.2%) patients had recurrent episodes of peripheral
At month 3 46 (70.8) facial palsy. Three of them were diagnosed with Bell palsy
At month 6 5 (7.7) after exclusion of tumor, stroke, demyelinating syndromes,
At month 12 1 (1.5) vasculopathies, and infectious and inflammatory causes by
Residual symptoms 1 (1.5)
clinical, serologic investigations, and neuroimaging studies.
Treatment
None 17 (26.2) During the study period, one child presented with a left then
Prednisolone 42 (64.6) a right-sided facial palsy 3 months apart. Another child with
Acyclovir 26 (40.0) left-sided facial palsy had ipsilateral peripheral facial palsy
Both 19 (29.2) 7 years ago, and another child with right-sided facial palsy
Patients underwent neuroimaging, MRI (n ¼ 11), had ipsilateral facial palsy 5 years ago. One patient had
CT (n ¼ 1) 2 facial palsy attacks with an interval of 6 years. He had
Normal 9 (13.8)
fissured tongue on examination, and he was diagnosed with
Abnormal findings irrelevant to diagnosisa 3 (4.6)
Abnormal findings relevant to diagnosis 0 Melkersson-Rosenthal syndrome. The last patient with recur-
rent peripheral facial palsy had 3 right-sided facial palsy
Abbreviations: MRI, magnetic resonance imaging; SD, standard deviation. episodes during a 9-month period. She had been following
a
Mega cisterna magna, fluid in mastoid cells, ventricle asymmetry.
up at the immunology department with a diagnosis of familial
Mediterranean fever homozygous with m694 V mutation for
8 years, and she was on colchicine therapy. Recurrent periph-
eral facial palsy is regarded as a neurologic manifestation of
vasculitis in familial Mediterranean fever, after exclusion of
tumor, stroke, demyelinating syndromes, vasculopathies, and
infectious and inflammatory causes through clinical, serolo-
gic, cerebrospinal fluid investigations, and neuroimaging
studies.
An MRI scan of brain and/or temporal bone was carried out
in 12 (18.4%) patients with Bell palsy; 2 times for 3 children
with recurrent facial palsy and once for 9 children with unsatis-
factory recovery in 2 weeks. Three of 12 patients with Bell
palsy showed MRI abnormalities, which were mega cisterna
magna, fluid in the mastoid cells, and lateral ventricle asymme-
try in 1 patient each, and all were regarded as abnormalities
unrelated with facial palsy. Electroneuromyography was per-
formed in 12 (14.8%) of patients and varying degrees of
abnormalities of facial nerve were found in all studies.
Figure 1. Age distribution of patients with Bell palsy.

scanning revealed a space-occupying lesion within pons Discussion

extending into the spinal cord. The patient was submitted to Facial nerves are prone to injuries caused by middle-ear or tem-
a brain biopsy that was reported as ependymoblastoma, and poral bone infections, trauma, surgery, and compression by

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1476
tumors within the vicinity of nerves, because they have a long
intracranial course and pass through the narrow bony canal
within the intratemporal bone. Systemic diseases and congeni-
tal anomalies can also cause facial nerve palsy. However, idio-
pathic facial palsy accounts for the majority of cases,1 and the
exact mechanism that leads to facial nerve injury in most cases
is still unknown.
In this observational study, the most common type of facial
palsy was Bell palsy, making up 80.2% of the causes, followed
by infections of middle ear or mastoids in 11.1% of patients.
A malignant tumor, Melkersson-Rosenthal syndrome, enlarged
lymph nodes in the parotid gland, remote traumatic injury to the
temporal bones, congenital facial palsy and familial Mediterra-
nean fever accounted for the remaining causes of the peripheral
facial palsy. These results were in accordance with previous stud-
ies which have reported that Bell palsy accounted for 66% to 78%
of children with facial palsy.2,3 In these reports, facial palsy was
associated with infection in 4% to 23%, tumor in 1% to 5%, con-
genital anomalies in 5%, and trauma in 3% to 7% of patients.2,3,13
Bell palsy is an acute unilateral idiopathic paralysis of the
facial nerve. The pathophysiology is unknown, but it is pro-
posed that the autoimmune system is involved by causing local
damage to the myelin after activation by a viral infection.14
Because attention has recently focused on infection as a possi-
ble cause of Bell palsy,15-17 we have searched for if there was a
relation between nonspecific viral infections and attacks of
facial palsy. About half of the patients with Bell palsy in our
series had a history of preceding nonspecific upper airway
infections, suggesting an association between viral infections
and Bell palsy. Although a study has reported a female predo-
minance,4 other studies showed no clear gender predilec-
tion.2,3,6 There is also no predominance of the side affected.6
In line with these reports, there was no predominance in gender
or side involved in our series. The evidence for a familial ten-
dency of Bell palsy is weak. Seven (11.3%) children in our
series had a familial history of Bell palsy, similar with the rates
of 8.5% to 10.3% reported previously.4,6
The facial nerve, as it transverses the middle ear and mastoid
bone, can be affected by adjacent infection. The incidence of
peripheral facial palsy caused by acute otitis media in children
has been reported in a wide range of 4% to 37% of all periph-
eral facial palsies.1,16 Consistent with previous reports, acute
otitis media with or without complicated mastoiditis accounted
for 11% of patients in our series. These data underscore the
importance of searching for otitis media and mastoiditis as an
etiology of a facial nerve palsy, in order to provide the appro-
priate treatment. One of the patients with otitis media also had a
history of vaccination with hepatitis B 9 days before the onset
of symptoms. Although a single patient who developed Bell
palsy following hepatitis B vaccination has been reported
before,18 this association has not been confirmed in other stud-
ies.19 It is not easy to demonstrate an exact etiopathogenic rela-
tionship between this vaccination and peripheral facial palsy.
Thus, there remains a need to explore if there is an etiopatho-
genic relationship between hepatitis B vaccination and periph-
eral facial paralysis.
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Journal of Child Neurology 29(11)
An association between peripheral facial palsy and chicken-
pox has been reported previously, and this is thought to be a
complication rather than reactivation.20,21 One of the patients
in our series had a varicella infection 2 weeks before the onset
of facial palsy, supporting the hypothesis that there is an asso-
ciation between chickenpox and peripheral facial palsy.
Physical trauma, such as birth trauma, temporal bone frac-
ture, middle-ear surgery, or cochlear implantation, can cause
acute facial nerve injury. Trauma involving temporal bones
accounted for 7%13 to 43%1 of patients with facial paralysis.
In our series, trauma was not a direct cause in any of the
patients. In 1 patient, however, facial palsy occurred following
an attack of recurrent meningitis, which likely developed
because of a temporal bone fracture that occurred 3 years ago.
The patient had a finding of cholesteatoma in temporal bone on
MRI scanning.
The incidence of neoplasms causing facial palsy in children
was reported between 2% and 12% of patients.2,16,22 In our
series, the single case of neoplasm-associated facial nerve
palsy was due to a pontine ependymoblastoma. Although typ-
ical presentation of tumor-related facial palsy is gradual
progression of paralysis that lasts greater than 3 weeks associ-
ated with other cranial neuropathies, in our case, the onset was
acute and there was no other associated cranial nerve paralysis.
Thus, we can propose that peripheral facial palsy in a young
child can be a sole presenting symptom of an intracranial
malignancy. In another patient, the facial palsy was due to com-
pression of the facial nerve by multiple enlarged lymph nodes,
which were shown on MRI scanning. The specific infectious
agent could not be identified in this patient; however, symp-
toms disappeared as lymph nodes regressed with antibiotic
treatments in 2 months.
Recurrent facial palsy is uncommon in children. It has been
reported in 6% of children with facial palsy.2,7 Similarly, 5
(6.5%) children had recurrent facial palsy in our series. Three
of them were diagnosed with recurrent Bell palsy after exclu-
sion of tumor, stroke, demyelinating syndromes, vasculopa-
thies, and infectious and inflammatory causes by clinical and
serologic investigations and neuroimaging studies. One of the
patients with recurrent Bell palsy presented with facial palsy
on opposite sides 3 months apart, and the remaining 2 children
had recurrent ipsilateral facial palsy attacks outside the study
period, 5 and 7 years ago, respectively. In consistent with pre-
vious reports, all children with recurrent facial palsy showed
complete recovery.2 Recurrent facial palsy can be due to a vari-
ety of infectious, neoplastic, traumatic, or inflammatory disor-
ders. There was no serologic evidence of a viral infection such
as herpes simplex virus, Epstein-Barr virus, cytomegalovirus,
enterovirus, rubella, varicella, human immunodeficiency virus,
or a bacterial infection such as Borrelia, brucella, or myco-
plasma. Although we did not identify a specific cause, 3 of 5
patients with recurrent facial palsy had a history of preceding
viral infections, which suggests a causative or triggering role
of infections in the etiology. One of 5 patients with recurrent
facial palsy was diagnosed with Melkersson-Rosenthal syn-
drome, which is an inherited disorder characterized by a triad
Yılmaz et al
of recurrent attacks of intermittent facial nerve palsy, facial
swelling, and the presence of a fissured tongue. The last patient
with recurrent facial palsy had been following at the immunol-
ogy department with the diagnosis of familial Mediterranean
fever, homozygous with the M694 V mutation for 8 years.
Recurrent peripheral facial palsy in this patient is regarded as
a neurologic manifestation of vasculitis in familial Mediterra-
nean fever, after exclusion of tumor, stroke, demyelinating syn-
dromes, vasculopathies, and infectious and inflammatory
causes through clinical, serologic, cerebrospinal fluid investi-
gations, and neuroimaging studies. Recurrent peripheral facial
palsy has been reported in association with autoimmune disor-
ders such as multiple sclerosis, Behçet disease, or celiac dis-
ease.23,24 These reports along with the present case with
familial Mediterranean fever support the hypothesis that acti-
vated immunologic system against self neural antigens is
involved in the pathogenesis of facial palsy.
The treatment of peripheral facial nerve palsy in children
remains controversial and variable depending on etiology.
Recovery rates have been shown to depend on the cause of facial
nerve palsy. Similar with a reported recovery rate of 97.6%,5
overall complete recovery was found in 97.5% of patients in
our series. In another study, complete recovery has been
reported in 93% of patients with Bell palsy, 90% in patients
with infection, and 43% in patients with trauma.3 In adult
patients with Bell palsy, the use of steroids early in the course
of the disease significantly improves the chances of complete
recovery, however acyclovir given alone or in combination
with steroids has no such a significant benefit.8-11 In contrast,
another study has shown a higher recovery rate in patients
treated with a combination of steroids and acyclovir, when
compared to those treated with steroids alone,25 which sup-
ported the hypothesis of viral etiology in the pathogenesis
of Bell palsy.17 Limited data are available on the benefit of
steroids in the pediatric population. Bell palsy seems to
recover earlier in children than adults when matched for
severity.26 Since the Bell palsy has up to 97% spontaneous
recovery rate,2,5,6 it is difficult to prove the benefit from the
administration of steroids in children as compared to adults
where complete recovery has been reported for about 80%
of patients.1,12,27 Consistently, the majority of patients
showed complete recovery at 3 months regardless of whether
they received corticosteroid treatment. As more severely
affected patients have received corticosteroids, we could not
compare the effectiveness of corticosteroid between treated
and untreated patients. Only one patient with Bell palsy had
residual symptoms at 12 months. In contrast, it has been
reported that approximately 16% of patients with Bell palsy
did not achieve even satisfactory recovery.28 Surgical meth-
ods have been used for those patients. None of the patients
with Bell palsy in our series needed decompression surgery.
Facial nerve palsy occurring as a complication of acute otitis
media usually resolves more rapidly in comparison with facial
palsy because of other causes.13 Similarly, all patients with
otitis media and mastoiditis showed complete recovery at 3
months in our series.
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1477
In addition to drug treatments, physical therapy remains an
important treatment method for patients with facial palsy.
Because significant benefit has been shown previously from
facial muscle exercises in Bell palsy,29 all the patients in our
series were referred to the department of rehabilitation medi-
cine early in their disease course for physical therapy, which
likely increased the recovery rate and recovery time in our
series.
Imaging studies for acquired facial nerve palsy, excluding
trauma, has been recommended only for atypical facial palsy
lasting more than 2 months, or for recurrent or progressive pal-
sies.30 Although all radiologic investigations performed in 12
(18.4%) patients with Bell palsy were uninformative in regard
to cranial or facial nerve pathology, MRI studies revealed mas-
toiditis, tumor, cystic degeneration in temporal lobe, and
enlarged lymph nodes in the parotid gland as the cause of facial
palsy in one patient each. Therefore, when assessing a child
with peripheral facial palsy, although it is suggested to obtain
neuroimaging only if systemic disorders, such as trauma, infec-
tions, or inflammatory disorders, are suspected by a detailed
history and clinical examination, it should be kept in mind that
in young children, peripheral facial palsy could constitute the
sole initial clinical manifestation of a brain tumor.
Conclusion
Although the most common cause of peripheral facial palsy in
children is Bell palsy, a wide variety of congenital or acquired
pathologies can present with peripheral facial palsy. Therefore,
careful investigation and differential diagnosis are essential in
children presented with peripheral facial palsy. Nonspecific
viral infections can be a causative or triggering factor for Bell
palsy. The majority of children with peripheral facial palsy
follow a favorable course in children, and patients usually
recover within 3 months.
Acknowledgments
This work was completed at the Department of Pediatric Neurology,
_
Dr. Behçet Uz Children’s Hospital (Izmir, Turkey). The authors thank
all colleagues for their help in follow-up of the patients.
Author Contributions
ÜY was involved in the diagnosis and follow-up of the patients, col-
lected data, and wrote the whole article. DÇ was involved in the phys-
ical therapy of all patients. TSY was involved in developing the
project, writing the article, and analyzing the data. GA was involved
in the diagnosis and follow-up of the patients. MÖ has made the
otolaryngologic examinations of the patients. OG performed the
electrophysiologic studies of the patients.
Declaration of Conflicting Interests
The authors declared no potential conflicts of interest with respect to
the research, authorship, and/or publication of this article.
Funding
The authors received no financial support for the research, authorship,
and/or publication of this article.
1478
Ethical Approval
The study was approved by the Hospital Ethical Committee of Health
IRB# 28.3.2013 / 13.
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