Brain & Development 33 (2011) 644650 www.elsevier.

com/locate/braindev

Review article

Facial nerve palsy in childhood

Evangelos Pavlou , Anastasia Gkampeta, Maria Arampatzi
2nd Department of Pediatrics, Aristotle University of Thessaloniki, AHEPA General Hospital, Thessaloniki, Greece Received 2 September 2010; received in revised form 9 November 2010; accepted 10 November 2010

Abstract Facial nerve palsy in children is usually idiopathic but can also result from many conditions such as neoplasias, systemic diseases, or congenital anomalies with poor prognosis. Children with idiopathic facial palsy (Bells palsy) have a very good prognosis, while treatment with prednisone does not certainly improve the outcome. The causes of facial nerve palsy in childhood dier from those in adults. A detailed investigation and dierential diagnosis are recommended for facial palsy in children. 2010 The Japanese Society of Child Neurology. Published by Elsevier B.V. All rights reserved.
Keywords: Facial palsy; Idiopathic; Children

1. Introduction epidemiological data Facial nerve palsy is a common malady with severe consequences in patients quality of life. An estimated 1540 per 100,000 people per year are aected by facial nerve palsy [1]. The most common cause of unilateral facial palsy is Bells palsy, also known as idiopathic facial palsy. The lowest incidence of Bells palsy is found in persons younger than 20 years old, while the highest incidence in persons aged 60 years or older. There seems to be a correlation between the age and incidence of Bells palsy. The incidence in patients older than 10 years is 2.7/100,000, while in patients between 10 and 20 years old is approximately 10.1/100,000 [2,3]. There are insucient studies concerning young children and infants with Bells palsy, so the data about causes, treatment and prognosis are poor, in contrast to them concerning adults with Bells palsy. 2. Neuroanatomy The facial nerve (7th of 12 paired cranial nerves) emerges from the brainstem between the pons and the
Corresponding author. Address: Elaiones Pilaias, Thessaloniki 55535, Greece. Tel.: +30 2310994815; fax: +30 2310993514. E-mail address: eepav@yahoo.gr (E. Pavlou).

medulla, and enters the petrous portion of the temporal bone via the internal auditory canal. On its course, facial nerve approaches tympanic cavity and stylomastoid foramen, providing parasympathetic bers to the submandibular gland and sublingual glands via chorda tympani. It also supplies parasympathetic innervations to the nasal mucosa and the lacrimal gland and also receives taste sensation from the anterior two-thirds of the tongue. The facial nerve exits the skull through the stylomastoid foramen and terminates into the zygomatic, buccal, mandibular and cervical branches. The examination of patients with Bells palsy demonstrates attening of the forehead and nasolabial fold on the side aected with the palsy, eyebrow sagging, inability to close the eye and the mouth drawn to the non-aected side. Diculties in feeding and speech, hyperacusis, lack of taste, lacrimation, and sialorrhea are also present. So, it is a complicated condition aecting basic functions with psychological and cosmetic complications. 3. Dierential diagnosis Idiopathic facial nerve palsy (or Bells palsy) is less common in younger children and infants than it is in teenagers and adults. Other conditions such as infections, inammatory conditions, injuries, neoplasias,

0387-7604/$ - see front matter 2010 The Japanese Society of Child Neurology. Published by Elsevier B.V. All rights reserved. doi:10.1016/j.braindev.2010.11.001

E. Pavlou et al. / Brain & Development 33 (2011) 644650

645

metabolic diseases, congenital anomalies should be excluded from diagnosis in children after a detailed examination (Table 1). Manning et al. studying the causes of facial nerve palsy in 61 children concluded that 50% of cases had Bells palsy, 14.8% had an infection, 11.5% had injuries and 3.3% congenital problems [7]. Likewise, May et al. during a retrospective study in 1981 found 170 cases of facial nerve palsy in a period of 17 years, from which 42% had Bells palsy, 21% injuries, 13% infection, 8% congenital anomalies and 2% neoplasias [8]. In 1990, Grundfast et al. concluded that 84% of children had facial nerve palsy due to a specic etiology and only 16% had Bells palsy as a diagnosis of exclusion [9]. Specic causes of facial palsy included injuries (24%), otitis media (16%), infections (12%), neoplasias (12%) and congenital anomalies (8%). Similar conclusions conducted by Evans et al. in a recent study in 2005 [10]. In this study, from 34 children with facial nerve palsy only 8.6% had Bells palsy, 37.1% infection and 34.3% injuries (Table 2). This dierential proportion of each category between the old and recent studies can be explained by the more detailed investigation of children present with facial nerve palsy in recent years. 4. Idiopathic facial nerve palsy (Bells palsy) Bells palsy is an acute unilateral idiopathic paralysis of the facial nerve. The pathophysiology is unknown, but many authors believe that the autoimmune system is involved by causing local damage to the myelin after a viral infection [4]. It has been suggested the possibility that reactivation of herpes virus may be responsible for demyTable 1 Causes of facial nerve palsy in childhood. Idiopathic Bells palsy.

elination. Herpes simplex virus, has been implicated as a cause in several studies. Infection with this virus is thought to cause inammation of the facial nerve [5]. Herpes simplex virus (HSV) genes have been isolated from the geniculate ganglia, endoneurial uids, and posterior auricular muscles of patients with facial nerve palsy, suggesting that its pathogenetic mechanism involves HSV reactivation within the geniculate ganglion, followed by inammation and entrapment of the nerve at the meatal foramen [5]. In several studies, the enzyme-linked-immunosorbent assay (ELISA) in patients with Bells palsy indicated an acute viral infection (herpes simplex, varicella zoster, cytomegalovirus) [6]. All these infections were due to viruses belonging to the herpesvirus group. These results indicate that either initial infection or reactivation of HSV can be the cause of idiopathic facial nerve palsy. The trademark of Bells palsy is rapid onset of partial or complete palsy, usually in a single day. Bells palsy is characterized by facial drooping of the aected half, due to malfunction of the facial nerve, which controls the muscles of the face. All functions controlled by facial nerve are aected, such as blinking and closing the eyes, smiling, frowning, lacrimation and salivation. Physical examination reveals attening of the forehead and nasolabial fold on the side aected with the palsy, eyebrow sagging, inability to close the eye and the mouth drawn to the non-aected side. On attempted eye closure, the eye rolls upward and inward on the aected side. This is known as Bell phenomenon and is considered a normal response to eye closure. The rest neurological examination is normal. A neurologic abnormality should lead the diagnostic approach to other similar conditions. Usually, the symptoms remain for 24 weeks and Bells

Infectious-inammatory Otitis media and mastoiditis, meningitis, Epstein Barr infection (infectious mononucleosis), Mycoplasma pneumoniae infection, Lyme disease, syndrome, MillerFisher syndrome, vasculitis (Kawasaki disease, HenochScho parotits, Ramsay-Hunt syndrome, tuberculosis, GuillainBarre nlein purpura), sarcoidosis. Trauma-nerve compression Perinatal trauma, temporal bone fracture, increased intracranial pressure, iatrogenic trauma, cleidocranial dysostosis, histiocytosis {. Neoplasms Brainstem glioma, parotid gland tumors, leukemias. Congenital ArnoldChari syndrome, absence of depressor anguli oris muscle (cardiofacial syndrome), inner ear and/or facial nerve malformations, Moebius syndrome, syringobulbia. Genetic Facioscapulohumeral dystrophy, myotonic dystrophy, myasthenic syndromes. Metabolic conditions Diabetes, hyperparathyroidism, hypothyroidism. Other Arterial hypertension, haemophilia, Melkersson-Rosenthal syndrome, etc.

646

E. Pavlou et al. / Brain & Development 33 (2011) 644650

Table 2 Literature concerning causes of facial nerve palsy in childhood. Study Manning et al. [7] May et al. [8] Grundfast et al. [9] Evans et al. [10] Idiopathic (%) 60.7 42 16 8.6 Trauma (%) 11.5 21 24 34.3 Neoplasm (%) 2 12 2.8 Congenital (%) 3.3 8 8 11.4 Infection (%) 14.8 13 28 37.1 Other (%) 9.7 13 12 5.8 Total 61 170 25 34

palsy is considered to be a self-limited condition. Early treatment (within 3 days after the onset) with steroids per os seems to be eective in adults, though its eectiveness in children has not been proved yet. 5. Infectious/inammatory causes Nowadays, inadequate treatment of acute otitis media can cause severe complications such as facial nerve palsy, mastoiditis, cholesteatoma, labyrinthitis, meningitis and abscess [11]. Ramsay-Hunt syndrome is caused by reactivation of varicella zoster virus (VZV), which lies dormant in the sensory ganglion after primary infection. The syndrome is characterized by facial palsy associated with a painful vesicular eruption within the external auditory canal and vestibulocochlear dysfunction (sensorineural hearing loss, vertigo, nystagmus, ataxia) [12]. Less frequent causes of facial nerve palsy are infection with Epstein-Barr virus (EBV) (infectious mononucleosis) (40% of cases present with bilateral facial palsy), Lyme dis syndrome ease, tuberculosis, pernio lupus, GuillainBarre and recurrent central nervous system leukemia [1316]. In all these conditions mentioned above patients present with bilateral facial nerve palsy. Lyme disease has become the most common cause of acute facial palsy among children in areas endemic for this infection [17,18]. syndrome facial nerve is usually In GuillainBarre aected in combination with muscle weakness and paralysis. There is a reference in literature concerning a case of syndrome presenting only a patient with GuillainBarre with facial nerve palsy without any other symptom [19]. Dysfunctions of central or peripheral nervous system with or without hypertension are sometimes documented in Henoch-Scho nlein vasculitis. These dysfunctions include cranial nerve neuropathies such as facial nerve palsy [20]. Facial nerve palsy is a rare but well established complication of Kawasaki disease. Facial palsy can present at any stage of the disease and has been correlated with higher risk of coronary vasculitis, which means poorer prognosis [21]. 6. Injuries Perinatal injuries are the most frequent causes of traumatic facial nerve palsy. Birth weight greater than 3,500 g, forceps-assisted delivery and prematurity are

all risk factors associated with traumatic facial nerve paralysis. This is a self-limited condition and neonates recover within rst 4 months of life, with no abnormalities remained [22]. Physical trauma, especially fractures of the temporal bone, may also cause acute facial nerve palsy. The likelihood of facial palsy after trauma depends on the location of the trauma and the type of fracture [23,24]. Temporal bones fractures can cause from transient neuroapraxia to complete dissection of facial nerve which leads to permanent dysfunction of the nerve. There are also many references to traumatic injury of exocranial part of facial nerve resulting from head injuries without any fracture of the skull bones and with excellent prognosis [25,26]. Iatrogenic causes of facial nerve palsy include surgical procedures of mainly parotid gland and also middle ear and mastoid cavern [27]. 7. Neoplasias Rare primary tumors of facial nerve include neurinoma and hemangioma [28,29]. More frequently, facial nerve palsy present as a symptom in patients with central nervous system tumors, head and neck tumors, rhabdomyosarcoma, Burkitt lymphoma, middle ear primary lymphoma and more [3032]. In patients with recurrent leukemia, facial nerve palsy is a common complication due to invasion of leukemic cells to the central nervous system. In this case facial palsy is bilateral. Rarely, is the rst clinical symptom in children with leukemia [33]. In this case treatment should be very aggressive even if the neuroimaging and cytological tests of cerebrospinal uid (CSF) are normal [34,35].

Table 3 Indications for further investigation by a specialist. Hearing loss Any abnormality on otoscopic examination Associated neurologic abnormality Single branch of facial nerve involved Progression of paralysis beyond 3 weeks Recurrent facial nerve palsy Antecedent trauma Lymphadenopathy, bleeding manifestations Hypertension Parotid mass

E. Pavlou et al. / Brain & Development 33 (2011) 644650

647

A number of clinical features should alert the clinician to the possibility of a neoplastic etiology. These are: slow progression beyond three weeks, no return to function after six months, bilateral or recurrent unilateral facial palsy, other cranial nerve involvement, facial hyperkinesia or spasm, single branch paralysis and pain [36,37]. 8. Congenital causes Congenital facial nerve palsy may be the result of many conditions. Congenital underdevelopment of cranial nerves nucleus or hypoxic-ischemic encephalopathy can be the cause of Moebius syndrome. The Moebius syndrome is a rare congenital disorder of varying severity, involves multiple cranial nerves and is characterized predominantly by bilateral or unilateral paralysis of the facial and abducens nerves [38]. Congenital pseudobulbar paralysis (syringobulbia) is a dysfunction of brain cortex, clinically expressed with facial palsy, dysphagia and diculty in speech [39]. Another phenomenon that should be considered during dierential diagnosis of congenital facial palsy is congenital facial asymmetry during cry. This condition is due to a congenital absence or weakness of depressor anguli oris muscle (cardiofacial syndrome), so when the child is crying the corner of the mouth does not lowers, which leads to facial asymmetry [40]. In conditions mentioned above the facial palsy is not reversible and is considered to be the result of a developmental or genetic anomaly or even an event during pregnancy [41]. 9. Genetic causes This category includes primary hereditary muscle diseases such as myotonic dystrophy, myasthenic syndromes, congenital myopathies characterized by facial nerve weakness, diculty in lactation and swallowing, or even severe respiratory problems [42]. Facioscapulohumeral dystrophy with mental retardation often remains undiagnosed before emergence of generalized muscular symptoms during school-age, but facial muscle involvement often appears since infancy [43].

10. Other causes Hypertension is a rare cause of facial nerve palsy in children. The ignorance of this etiological correlation can lead to delayed diagnosis or even worsening of hypertension due to administration of steroids for the idiopathic facial nerve palsy. Many authors recommend the measure of blood pressure in all patients with facial palsy [4446]. It is important to mention that the younger patient with facial palsy as the rst symptom of hypertension was an infant (11 weeks of age) with severe stenosis of the aorta [47]. 11. Investigation A full clinical history and a detailed clinical examination are recommended [48]. Children with atypical signs and symptoms should be estimated by a specialist (Table 3). Otoscopy, audiogram, blood pressure check and full blood count are mandatory in all children presenting with facial nerve palsy. The utility of further investigation, in the absence of additional symptoms or specic ndings on physical examination, is debatable. CSF tests are only recommended if meningitis or Guillain syndrome is suspected. In these cases there is a Barre characteristic increase in CSFs protein without any increase in cells count (leukocytal bifurcation). Radiological imaging is essential if additional neurological abnormalities are identied or if malignancy is suspected [49]. Magnetic resonance imaging is especially helpful in identifying brainstem pathology. High resolution computed tomography scanning is better in the evaluation of the intratemporal portion of the nerve. Contrast enhanced magnetic resonance imaging can identify sections of aected nerve in idiopathic facial palsy, but this test is not indicated in the majority of children [50]. More recent techniques such as CISS (constructive interference in steady state) and 3D MPRAGE (magnetization prepared rapid gradient echo) can also be used in the evaluation of anatomical details of the inner ear and facial nerve [51]. Concerning prognosis, the most valuable examination is the assessment of palsy (partial or total). The

Table 4 HouseBrackman facial paralysis scale. Grade I II III IV V VI Impairment Normal Mild dysfunction (slight weakness, normal symmetry at rest) Moderate dysfunction (obvious but not disguring weakness with synkinesis, normal symmetry at rest) complete eye closure w/maximal eort, good forehead movement Moderately severe dysfunction (obvious and disguring asymmetry, signicant synkinesis) incomplete eye closure, moderate forehead movement Severe dysfunction (barely perceptible motion) Total paralysis (no movement)

648

E. Pavlou et al. / Brain & Development 33 (2011) 644650

severity of paralysis is usually estimated with the HouseBrackman (HB) six-point grading scale ( Table 4). Patients with partial paralysis of facial nerve have favorable prognosis. Extensive investigation is recommended when the paralysis is total or when there is no return to function after 3 weeks from onset. Neurophysiological studies include the measurement of brillation potentials (as part of electromyography) and recording of the blink reex. The presence of brillation potentials implies signicant axonal degeneration, while blink reex tests the path trigeminal nerve-brainstem-facial nerve [52]. Some authors suggest that idiopathic facial palsy (Bells palsy) is a polyneuritis, where the frequent association with hyperacusis represents a cochlear involvement. In order to detect the acoustic pathway and/or brain-stem involvement in Bells palsy, BAEPs (Acoustic brain-stem evoked potentials), otoacustic emissions and electrocochleography can be used in order to estimate facial nerve impairment [53]. 12. Treatment The treatment of idiopathic facial nerve palsy is controversial. The use of steroids early at onset of palsy signicantly improves the chances of complete recovery. This theory has been conducted through extensive studies in adults. In children the benet from the administration of steroids has not been proved yet [54,55]. This is in part because majority of children present with complete recovery, with or without the use of steroids [56]. Many studies concerning the correlation between age of patients with facial palsy and prognosis demonstrate that children have generally better outcome [57]. In patient unable to close the eye, appropriate eye care is required to help avoid corneal abrasions. This care generally entails the administration of articial tears, sun protection and rarely tarsorrhaphy [58]. Acyclovir, combined or not with steroids, has also been studied for treatment of Bells palsy because reactivation of HSV has been implicated as the cause in many patients. Some studies suggest that early diagnosis and treatment within 3 days of the onset of paralysis are necessary for maximal ecacy of combined acyclovir and prednisolone therapy for Bells palsy [59]. Patient with Ramsay-Hunt syndrome should be aggressively treated with intravenous administration of acyclovir plus steroids. Surgical middle cranial fossa decompression of the labyrinthine segment of the facial nerve is not recommended in patients with Bells palsy. Patients with traumatic facial nerve palsy should be treated either with steroids or with surgical procedures, depending on the severity of their condition. Generally, the prognosis of facial nerve palsy depends on the cause. Congenital facial nerve palsy, when caused by perinatal injury has a very good prognosis without treatment, while when caused by congenital dysplastic

structural causes is permanent. In this case the paralysis can be partly improved with plastic surgery procedures [60,61]. Patients with traumatic facial nerve palsy recover within 30 months, with better results when the paralysis is partial or treated with steroids, physiotherapy or surgical procedures. Patients with facial palsy caused by infections recover within 0.52 months with the intravenous administration of antibiotics [62]. Even without treatment, Bells palsy tends to carry a favorable prognosis in children. In neoplasmatic facial palsy the prognosis depends on type and stage of neoplasm and also the therapeutic protocol applied in each case. 13. Conclusions Facial nerve palsy is a rare condition in children with causes dierent from those concerning adults [63]. Facial palsy may be congenital, infectious, traumatic, neoplastic or idiopathic (Bells palsy) and sometimes may be the rst and only symptom of a severe condition [64]. So, when a child presents with facial palsy, a full clinical history and a detailed clinical examination are recommended. The diagnosis of Bells palsy in children should be a diagnosis of exclusion and the administration of steroids is not recommended, as the benet has not been proved yet and it could mislead the diagnosis of an infection or even neoplasia. Further studies concerning children with Bells palsy should be conducted to improve the knowledge about causes, dierential diagnosis and treatment. References
[1] May M, Klein SR. Dierential diagnosis of facial nerve palsy. Otolaryngol Clin North Am 1991;24:61341. [2] Falco NA, Eriksson E. Facial nerve palsy in the newborn: incidence and outcome. Plast Reconstr Surg 1990;85:14. [3] Peitersen E. Bells palsy: the spontaneous course of 2500 peripheral facial nerve palsies of dierent etiologies. Acta Otolaryngol Suppl 2002;549:430. [4] Murakami S, Mizobuchi M, Nakashiro Y, Doi T, Hato N, Yanagihara N. Bells palsy and herpes simplex virus: identication of viral DNA in endoneurial uid and muscle. Ann Intern Med 1996;124:2730. [5] Furuta Y, Fukuda S, Chida E, Takasu T, Ohtani F, Inuyama Y, et al. Reactivation of herpes simplex virus type 1 in patients with Bells palsy. J Med Virol 1998;54:1626. [6] Mang WL, Bonkowsky VM. Acute viral infections in association with idiopathic peripheral facial paralysis. HNO 1987;35:3103. [7] Manning JJ, Adour KK. Facial paralysis in children. Pediatrics 1972;49:1029. [8] May M, Fria TJ, Blumenthal F, Curtin H. Facial paralysis in children: dierential diagnosis. Otolaryngol Head Neck Surg 1981;89:8418. [9] Grundfast KM, Guarisco JL, Thomsen JR, Koch B. Diverse etiologies of facial paralysis in children. Int J Pediatr Otolaryngol 1990;19:22339. [10] Evans AK, Licameli G, Brieztzke S, Whittemore K, Kenna M. Pediatric facial nerve paralysis: patients, management and outcome. Int J Pediatr Otolaryngol 2005;69:15218.

E. Pavlou et al. / Brain & Development 33 (2011) 644650 [11] Goldstein NA, Casselbrant ML, Bluestone CD, Kurs-Lasky M. Intratemporal complications of acute otitis media in infants and children. Otolaryngol Head Neck Surg 1998;119:44454. [12] Sweeney CJ, Gilden DH. Ramsay Hunt syndrome. J Neurol Neurosurg Psychiatry 2001;71:14954. [13] Terada K, Niizuma T, Kozaka Y, Inoue M, Ogita S, Kataoka N. Bilateral facial nerve palsy associated with Epstein-Barr virus infection with a review of the literature. Scand J Infect Dis 2004;36:757. [14] Pitcher R, Thandar MA. Bilateral tuberculous mastoiditis and facial palsy. S Afr Med J 2004;94:8934. [15] Hadeld PJ, Shah BK, Glover GW. Facial palsy due to tuberculosis: the value of CT. Laryngol Otol 1995;109:10102. [16] Sharma OP. Neurosarcoidosis: a personal perspective based on the study of 37 patients. Chest 1997;112:2208. [17] Vanzieleghem B, Lemmerling M, Carton D, Achten E, Vanlangenhove P, Matthys E, et al. Lyme disease in a child presenting with bilateral facial nerve palsy: MRI ndings and review of the literature. Neuroradiology 1998;40:73942. [18] Henningsson AJ, Malmvall BE, Ernerudh J, Matussek A, Forsberg P. Neuroborreliosis an epidemiological, clinical and health economical study from an endemic area in the south-east of Sweden. Clin Microbiol Infect 2010;16:124551. [19] Atsumi M, Kitaguchi M, Nishikawa S, Susuki K. A variant of syndrome with prominent bilateral peripheral GuillainBarre facial nerve palsyfacial diplegia and paresthesia. Rinsho Shinkeigaku 2004;44:54952. [20] Garzoni L, Vanoni F, Rizzi M, Simonetti GD, Goeggel Simonetti B, Ramelli GP, et al. Nervous system dysfunction in HenochScho nlein syndrome: systematic review of the literature. Rheumatology (Oxford) 2009;48:15249. [21] Wright H, Waddington C, Geddes J, Newburger JW, Burgner D. Facial nerve palsy complicating Kawasaki disease. Pediatrics 2008;122:7835. [22] Laing JH, Harrison DH, Jones BM, Laing GJ. Is permanent congenital facial palsy caused by birth trauma? Arch Dis Child 1996;74:568. [23] Guerissi JO. Facial nerve paralysis after intratemporal and extratemporal blunt trauma. J Craniofac Surg 1997;8:4317. [24] Hsu KC, Wang AC, Chen SJ. Mastoid bone fracture presenting as unusual delayed onset of facial nerve palsy. Am J Emerg Med 2008;26:386.e12. [25] Simo R, Jones NS. Extratemporal facial nerve paralysis after blunt trauma. J Trauma 1996;40:3067. [26] Christian W. Car seat palsy. Emerg Med J 2006;23:43. [27] Ferreira PC, Amarante JM, Rodrigues JM, Pinho CJ, Cardoso MA, Reis JC. Parotid surgery: review of 107 tumors (19902002). Int Surg 2005;90:1606. [28] Thompson AL, Aviv RI, Chen JM, Nedzelski JM, Yuen HW, Fox AJ, et al. Magnetic resonance imaging of facial nerve schwannoma. Laryngoscope 2009;119:242836. [29] Shelton C, Brackmann DE, Lo WW, Carberry JN. Intratemporal facial nerve hemangiomas. Otolaryngol Head Neck Surg 1991;104:11621. [30] Proops DW, Mann JR. The presentation of rhabdomyosarcomas of the head and neck in children. J Laryngol Otol 1984;98:38190. [31] Katz J, Polliack A, Harushouski I, Ben Oliel R, Marmary Y. Bells palsy as a sign of Burkitts lymphoma in children. Blood 1995;86:2052. [32] Lang EE, Walsh RM, Leader M. Primary middle-ear lymphoma in a child. J Laryngol Otol. 2003;117:2057. [33] Bilavsky E, Scheuerman O, Marcus N, Hoer V, Garty BZ. Facial paralysis as a presenting symptom of leukemia. Pediatr Neurol 2006;34:5024. [34] Krishnamurthy Shedthikere N, Weinstock Arie L, Smith Sharon H, Duner Patricia K. Facial palsy, an unusual presenting feature of childhood leukemia. Pediatr Neurol 2002;27:6870.

649

[35] Buyukavci M, Tan H, Akdaq R. An alarming sign of serious diseases in children: bilateral facial paralysis. Pediatr Neurol 2002;27:3123. [36] Jackson CG, Glasscock 3rd ME, Hughes G, Sismanis A. Facial paralysis of neoplastic origin: diagnosis and management. Laryngoscope 1980;90:158195. [37] Fenton CJ, Coddington R, Ramsay AD, Garth RJ. Primary neuroblastoma of the facial nerve presenting as a recurrent facial paralysis. J Laryngol Otol 1996;110:1513. [38] Jemec B, Grobbelaar AO, Harrison DH. The abnormal nucleus as a cause of congenital facial palsy. Arch Dis Child 2000;83:2568. [39] Kuzniecky R, Andermann F, Tampieri D, Melanson D, Olivier A, Leppik I. Bilateral central macrogyria: epilepsy, pseudobulbar palsy, and mental retardation a recognizable neuronal migration disorder. Ann Neurol 1989;25:54754. lar B. Neonatal asymmetric crying face. [40] Seyhan T, Borman H, Cag J Plast Reconstr Aesthet Surg 2008;61:14034. [41] Westin LM, Zuker R. A new classication system for facial paralysis in the clinical setting. J Craniofac Surg 2003;14:6729. [42] Kiliaridis S, Katsaros C. The eects of myotonic dystrophy and Duchenne muscular dystrophy on the orofacial muscles and dentofacial morphology. Acta Odontol Scand 1998;56:36974. [43] Tawil R, Van Der Maarel SM. Facioscapulohumeral muscular dystrophy. Muscle Nerve 2006;34:115. [44] Siegler RL, Brewer ED, Corneli HM, Thompson JA. Hypertension rst seen as facial paralysis: case reports and review of the literature. Pediatrics 1991;87:3879. [45] Harms MM, Rotteveel JJ, Kar NC, Gabree ls FL. Recurrent alternating facial paralysis and malignant hypertension. Neuropediatrics 2000;31:31820. [46] Aynaci FM, Sen Y. Peripheral facial paralysis as initial manifestation of hypertension in a child. Turk J Pediatr 2002;44:735. [47] Margabanthu G, Brooks J, Barron D, Miller P. Facial palsy as a presenting feature of coarctation of aorta. Interact Cardiovasc Thorac Surg 2003;2:913. [48] Riordan M. Investigation and treatment of facial paralysis. Arch Dis Child 2001;84:2867. [49] Veillona F, Ramos-Taboada L, Abu-Eid M, Charpiot A, Riehm S. Imaging of the facial nerve. Eur J Radiol 2010;74:3418. [50] Phillips CD, Bubash LA. The facial nerve: anatomy and common pathology. Semin Ultrasound CT MR 2002;23:20217. [51] Held P, Fellner C, Fellner F, Seitz J, Strutz J. MRI of inner ear anatomy using 3 DMP-RAGE and 3D CISS sequences. Br J Radiol 1997;70:46572. [52] Sittel C, Stennert E. Prognostic Value of Electromyography in Acute Peripheral Facial Nerve Palsy. Otol Neurotol 2001;22:1004. [53] Assimakopoulos D. Clinical investigation on spontaneous otoacoustic emission (SOAE). Auris Nasus Larynx 2008;35:5978. [54] Worster A, Keim SM, Sahsi R. Pancioli AM; Best Evidence in Emergency Medicine (BEEM) Group. Do either corticosteroids or antiviral agents reduce the risk of long-term facial paresis in patients with new-onset Bells palsy? J Emerg Med 2010;38:51823. [55] Danielidis V, Skevas A, Van Cauwenberge P, Vinck B. A comparative study of age and degree of facial nerve recovery in patients with Bells palsy. Eur Arch Otolaryngol 1999;256:5202. [56] Unuvar E, Oguz F, Sidal M, Kilic A. Corticosteroid treatment of childhood Bells palsy. Pediatr Neurol 1999;21:8146. [57] Chen WX, Wong V. Prognosis of Bells palsy in children analysis of 29 cases. Brain Dev 2005;27:5048. [58] Rahman I, Sadiq SA. Ophthalmic management of facial nerve palsy: a review. Surv Ophthalmol 2007;52:12144. [59] Hato N, Matsumoto S, Kisaki H, Takahashi H, Wakisaka H, Honda N, et al. Ecacy of early treatment of Bells palsy with oral acyclovir and prednisolone. Otol Neurotol 2003;24:94851. [60] Udagawa A, Arikawa K, Shimizu S, Suzuki H, Matsumoto H, Yoshimoto S, et al. A simple reconstruction for congenital unilateral lower lip palsy. Plast Reconstr Surg 2007;120:23844.

650

E. Pavlou et al. / Brain & Development 33 (2011) 644650 [63] Shargorodsky J, Lin HW, Gopen Q. Facial nerve palsy in the pediatric population. Clin Pediatr (Phila) 2010;49: 4117. [64] Shih WH, Tseng FY, Yeh TH, Hsu CJ, Chen YS. Outcomes of facial palsy in children. Acta Otolaryngol 2008;15:16.

[61] Terzis JK, Noah ME. Analysis of 100 cases of free-muscle transplantation for facial paralysis. Plast Reconstr Sur. 1997;99:190521. [62] Popovtzer A, Raveh E, Bahar G, Oestreicher-Kedem Y, Feinmesser R, Nageris BI. Facial palsy associated with acute otitis media. Otolaryngol Head Neck Surg 2005;132:3279.