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Prednisolone in Bell's palsy

Bandolier is more and more frequently being asked by GPs about particular problems. Not all can be answered, but we thought we could try for the question "Should steroids be used to treat ell!s palsy"", and whether it is important that treatment should be started within the first #$ hours for it to be effective. %ittle did we realise& 'he te(tbook answer is straightforward. )ecil *+,th edition, +-./0 states1 "2ost authorities recommend treatment with prednisone" and "it is claimed that prednisone treatment should be instituted as soon as possible". 'he 3(ford 'e(tbook of 2edicine *+--4, 5rd edition0 says "'here is some evidence that corticosteroids may be advantageous by reducing oedema in the nerve", and "it is 6ustifiable to treat all cases with corticosteroids if seen within a few days of onset, providing no contraindications to such treatment e(ists." Not much equivocation here. ut neither source uses references in support of their statements 7 and, indeed, why should they" 'e(tbooks are not original articles, but condensates of knowledge, or general maps of a sub6ect. 8f we want to know more, then we should consult maps with more miles to the inch 7 and do some searching of our own, even though here is a problem which is not rare *one case per GP per year0 and for which there are clear te(tbook statements. 'he searching strategy to find relevant studies used the free7te(t terms " ell!s" and "palsy" between the years +-44 and +--/. 9e found three reports since +--:, only one of which was relevant. 'his is reported in detail below, and is followed by a commentary about the quality of the study and the level of evidence that it represents. 'he study ;+< was relatively recent, being published in November +--$ from the =niversity of >le(andria in ?gypt. 8t was not randomised because it was considered unethical to withhold steroids from patients with no contraindications. 8t was an open study, and blinding of treatments was not used.

Patients
3ne hundred and si(ty patients with acute non recurrent unilateral ell!s palsy of no more than si( days duration were studied. >ll had complete or nearly complete facial paralysis. None had severe hypertension, glaucoma, peptic ulcer, cardiac disease, diabetes or were pregnant.

'he study group of -, patients received prednisolone tablets at a dose of + mg@kg body weight *ma(imum ,: mg0 in divided doses with meals for si( days, and the dose was then reduced gradually over the ne(t four days. 'he control group of 4, patients were not given prednisolone or any other treatment other than oral paracetamol for pain. 'his group comprised patients who had refused prednisolone because of fears of complications or who had a relative contraindication like heartburn or moderate hypertension. >ll patients received superficial muscle heating, massage and electrical muscle stimulation for all the paralysed facial muscles, three sessions a week until complete recovery or up to si( months.

Evaluations
8nitial clinical gradings and later evaluations were made by a doctor who was blind to the patients! grouping. ?lectrophysiological measurements were also made of nerve function. Aour categories of clinical recovery were defined17 ?(cellent recovery 7 patients with no evidence of facial muscle denervation and no residual facial asymmetry within si( months without complication. Good recovery 7 patients with minimal or no facial muscle denervation, but had negligible residual facial asymmetry only on close inspection during ma(imum effort on smiling and within si( months of onset. Aair recovery 7 patients with partial facial muscle denervation and mild residual facial muscle weakness on ma(imal effort within one year of disease onset. Poor recovery 7 patients with facial nerve denervation and incomplete clinical recovery *obvious facial weakness0 in spite of physical therapy for one year after disease onset. > satisfactory recovery was defined as e(cellent or good, and an unsatisfactory recovery was defined as fair or poor.

Results
'he results are shown in the table and figure. 9ithout steroid treatment there was a high rate of satisfactory recovery *by $4 of 4, patients, 4-B0.

'he rate of satisfactory recovery in all steroid treated patients was higher *,- of -5 patients, ./B0. 'his produced an NN' of 4C that is, for every si( patients treated with prednisolone within si( days of onset of the paralysis, one e(tra patient had a satisfactory recovery compared with no treatment. 9hen sub groups were e(amined, the e(tra benefits conferred by steroid treatment were seen only with treatment within the first #$ hours, where satisfactory recovery was +::B. Dere the odds ratio lower confidence interval was +.- *well above +0, and the NN' was 5.#. 'hat is, for every three patients treated with prednisolone within #$ hours of onset of the paralysis, one e(tra patient had a satisfactory recovery compared with no treatment. 'reatment after #$ hours failed to show a statistically significant difference from the recovery rate in the control group. 'here was a higher recovery rate in all treatment subgroups than in the control group, the lowest rate of satisfactory recovery being ,4B.

Comment
'here are very serious problems with this paper. Aoremost is the fact that the study was not random *perhaps for good reasons0, and, while the evaluations were said to be blind, it is very difficult to limit leakage of blinding in a study which must have taken at least two years. >bsence of randomisation and blinding will lead to overestimation of treatment effects. Neither is the design of the study a classical case7control design.

'he numbers in the subgroups were not large. 9ith larger numbers of patients *or more patients included in a meta7analysis0, beneficial effects which may be present with corticosteroid administration later than #$ hours after the onset of the facial paralysis. > case perhaps of absence of evidence not being the same as evidence of absence ;#<. Dowever, it is also the case that there are at least two randomised controlled trials ;5,$<, published over #: years ago, one of which ;5< e(amined large numbers of patients treated with steroid and placebo. 'hey both came to a negative conclusion, that treatment with corticosteroid did not increase overall cure rates. Neither, however, looked specifically at the effects of early treatment, and the preponderance of patients in these studies began steroid treatment more than #$ hours after the onset of facial paralysis. > number of non7randomised studies, also in the +-,:s, showed significant benefit with steroid. 8n andolier +,, the way in which inadequate randomisation and blinding led to over7estimation of treatment effects was e(amined, and steroid treatment of ell!s palsy seems to be an e(ample of that. 3nly one report in our search mentioned the effects of early treatment. 'his study in an 8ndian 6ournal is still awaited, but there was no indication that it was randomised.

What should GPs do?

2ake up their own minds based on local guidelines and their e(perience, 6ust as now. 'he evidence that corticosteroid treatment of ell!s palsy is effective more than #$ hours after the onset of facial paralysis, and the *weak0 evidence that early treatment may have some beneficial effects, come from non7randomised trials. 9e know that these are likely to e(aggerate the effects of treatmentC two randomised trials were negative. 'his is a classic problem, where te(tbooks appear to be regurgitating the advice from non7randomised studies and ignoring the randomised. 9hat is needed for ell!s palsy is a thorough systematic review of the literature, and we hope that friends of andolier will undertake it. ?ven then, this may not be enough. 'o answer the original questions, especially that of the benefits of early administration of steroids, a new randomised controlled trial may yet be needed.

References:
+. 'S Shafshak, >E ?ssa, A> akey. 'he possible contributing factors for the success of steroid therapy in ell!s palsy1 a clinical and electrophysiological study. Fournal of %aryngology and 3tology +--$ +:.1 -$:75. #. GG >ltman, F 2 land. >bsence of evidence is not evidence of absence. ritish 2edical Fournal +--/ 5++1 $./. 5. S2 9olf, FD 9agner, S Gavidson, > Aorsythe. 'reatment of ell palsy with prednisone1 a prospective randomiHed study. Neurology +-,. #.1 +/.74+. $. 2 2ay, I 9ette, 9 Dardin, 'he use of steroids in ell!s palsy1 a prospective

controlled study. %aryngoscope +-,4 .41++++7#.

Bell's Palsy: A Case Study

Serafina Domanico, RN, CEN, CCRN, MA, MS, ANP-CS/FNP Citation:
Serafina Gomanico1 ell!s Palsy1 > )ase Study. The Internet Journal of Advanced Nursing Practice. +--.. Jolume # Number +.

Abstract
'his paper discusses ell!s palsy in a five year old child who was evaluated at a pediatric emergency department. She awakened with the symptoms of left sided facial paralysis. 'he mother denied any further symptoms. Past medical history was noncontributory, although family history revealed that a sibling had previously e(perienced an episode of ell!s palsy . Gifferential diagnosis is discussed as are treatment modalities for idiopathic ell!s palsy, infectious causes of facial paralysis and central nervous system causes *)NS0. 'he following information was obtained at a pediatric emergency department situated in a medical center. 'he patient is a five year old hispanic female who was brought in by her mother with complaint of Ktwisted faceL.

H S!"R# A$% PH#S CA& E'A( $A! "$

Distory of Present 8llness1 > five year old hispanic female is accompanied by her mother with complaint of twisted face upon awakening this morning. 2other states that food tends to dribble from the left side of her mouth and she has difficulty with left eye closure. She denies e(cessive eye tearing, fever, cough, vomiting, diarrhea, cold or recent travel. No gait disturbances, weakness, numbness, hyperacusis, tingling and taste disturbances noted. Past 2edical Distory1 =nremarkable e(cept for one episode of right otitis media 4 months prior. No history of varicella or parotitis. 8mmuniHations are up to date, and a PPG done #@-, is negative. irth history is non7contributory and growth and development are consistent with anticipated standards. Aamily 2edical Distory1 2other is age $: is well. Aather is age $$ and well. 'he patient has two female siblings 7 a $ year old with resolved case of ellMs palsy and a healthy + year old. Grandparents are living with history significant for angina in maternal grandmother. Personal@Social Distory1 Patient lives in an apartment. 'he neighborhood is noisy, dirty and unsafe in some areas. She shares a room with her two siblings. She en6oys

drawing, playing with other children, chores and trying on new outfits, and demonstrates interest in kindergarten and attends church. Ieview of Systems1 General1 9ell nourished child of appropriate height and weight for stated age. Skin@Dair1 No lesions, or masses. Nails1 9ithout changes . Dead and Aace1 Genies diHHiness and frequent headaches. ?yes1 Genies use of corrective or prosthetic devices, diplopia, pain, or photophobia. %ast eye e(am .@-4 was normal. ?ars1 Genies prosthetic devices, infections, and tinnitus. Nose and Sinuses1 Genies olfactory deficits. 2outh and 'hroat1 Genies hoarseness or lesions. %ast dental e(am /@-,, without caries. Neck1 No masses@node enlargement or pain with movement or palpation. reasts1 'anner Stage + . Iespiratory1 Genies cough, shortness of breath, or wheeHing. Deart1 Genies murmur, chest pain or swollen e(tremities. Deme1 Genies anemia, bruising, bleeding. G81 Genies abdominal pain, nausea and vomiting. G=1 Genies urgency, frequency or bloody urine. Genitalia1 'anner Stage +. 2usculoskeletal1 Status post fractured radius # years ago. 9ithout current problems. Neuro1 Genies seiHures, lack of coordination, tingling, difficult speech, tremors, tics or weakened grips. 2ental Dealth1 Genies irritability, troubled speech, learning disabilities. ?ndocrine1 Genies weight gain or loss, heat or cold intolerances, thirst or polyuria. Gevelopmental1 Genies retardation. Skips@hops@broad 6umps@copies shapes. Gresses and undresses with minimal supervision. Gisplays normal se(ual curiosity and identifies coins and four out of five colors. Physical ?(amination1 Slim, cheerful five year old hispanic female in no apparent distress. General1 >lert and oriented times 5, P -:@/:C p +::C II #:C ' --poC ht $/ inC wt $. lbs *-/th percentile0. Skin1 9arm to touch, pink. risk capillary refill. D??N'1 =nremarkable e(cept for left facial asymmetry. '2Ms pearly bilaterally. Pharyn( without erythema or e(udate. Neck supple without adenopathy. 'hyroid borders within normal limits. 9ithout carotid bruits. )hest1 %ungs clear, bilateral breath sounds, equal and resonant. Jocal and tactile fremitus equal. )ardiovascular1 S+S# without murmur, rate and rhythm regular. No clicks, rubs or e(tra heart sounds. >bdomen1 Soft and non7tender. Normoactive bowel sounds. Palpation reveals no masses or organomegly. ?(tremities1 Aull range of motion of all e(tremities. Iadial, femoral dorsalis pedis and posterior tibial pulses equal bilaterally. Strength /N@/N in all e(tremities. Neurologic1 Pupils equal and reactive to light. )ranial nerves 887O88 grossly intact e(cept for ,th left peripheral cranial nerve palsy. No atrophy, fasciculations, tremors noted. Gait, heel 7 to 7 toe, heel and toe walking, knee bends, and hopping all within normal limits. Iomberg negative. Grips and arms strong and equal bilaterally. Sensory e(am reveals pain, vibration, light touch and stereognosis intact. Iefle(es #N@#N bilaterally. Gifferential Giagnosis1 ased on the sub6ective and ob6ective data a list of differential diagnosis can be developed. 'he differential diagnosis appropriate for this clinical presentation may include1 +. ellMs palsy #. 8nfectious disease, including herpes simple(, %ymeMs disease and ?pstein7 arr.

5. )NS causation, including invasive tumor or vascular lesion.

P&A$
Giagnostics1 ) ) with differential, sedimentation rate, ? J@%ymes titer1 follow7up on ? J@%yme titers taken. 8nfectious diseases such as viral illnesses, ? J@%yme can be eliminated by evaluation of the diagnostic tests listed above. 'herapeutics1 >rtificial tears to left eye # drops tid in order to offset corneal abrasions secondary to impaired tearing. ?ye patch during night time if eye is not closing properly. ?ducative1 ?ducate patient and family about disease process, therapeutic interventions and anticipated course of the disease. Dealth maintenance education should include information regarding annual PPG, dental care, routine physical at 4 year old, height@weight@hearing@vision@vital signs@=>@lead level@GP', polio and 22I to be provided by primary care provider. >nticipatory Guidance1 8n6ury prevention, good parenting practices, se( education, nutrition, discipline as well as information regarding the course of the acute illness. Aollow7up1 I') in + week for reevaluation with pediatric neurology or sooner if any other problems occur.

BE&&)S PA&S#
'he diagnosis is predominantly one of e(clusion and based on clinical findings *$0. Negative history should include trauma, local infection, or disease of the central nervous system. 'he facial nerve originates in the pons. 8ts brachial motor fibers e(it the brainstem at the level of cerebellopontine angle to enter the internal auditory meatus on the opposite side. 'hese fibers travel through the geniculate ganglion, where they enter the facial canal, eventually leaving the skull through the stylomastoid foramen. Gistal to this foramen, the large nerve fibers branch into small fibers that supply the muscles of facial movement. %esions in the vicinity of the stylomastoid foramen have been identified during surgical e(ploration */0. )omplete paralysis of the nerve results in loss of motor, sensory, and parasympathetic function ipsilateral to the lesion. 2otor paralysis is characteriHed by complete loss of voluntary and automatic e(pression over the affected hemiface. 'he involved side of the face is immobile during attempts at e(pression. 'here is flattening of the nasolabial fold, sagging at the corner of the mouth, and displacement of the lips towards the unaffected side. 'he forehead flattens and the eyebrows lose their symmetry. 'he palpebral fissure widens. 3n attempts at eye closure, ellMs phenomenon is seen. 'his phenomenon is characteriHed by rotation of the affected eyeball in an upward position with inability to close the lid. %oss of blinking results in collection of tears in the lower lid. 'he ipsilateral corneal blink refle( is absent */0.

Symptoms generally present over a #$7$. hour time period with 4:B of patients e(periencing a viral prodrome, characteriHed by stuffy nose, sore throat, and generaliHed achiness *40. ellMs palsy often follows an upper respiratory infection, most often viral, and is believed to be due to postinfectious demyelination of the facial nerve *,0. Aifty7percent of patients will also e(perience sensory loss of the face, neck or tongue, and -:B will e(perience hyperacusis which is painful sensitivity to sound *$0. Grinking and eating may be affected secondary to paresis, and lacrimation may be decreased *,0.

% AG$"S S
>s stated previously, the diagnosis of ellMs palsy is predominantly one based on clinical findings and the e(clusion of other possible causes of facial paralysis. 'he practitioner bases her diagnosis on a thorough neurologic e(amination, history, and physical, history of prodromal viral infection, as well as negative ? J titers@ %yme titer. 3nly when all other causes are ruled out can a diagnosis of ellMs palsy be made. Giagnostic assessment should include an audiogram in order to evaluate function of the auditory nerve. '+ magnetic resonance imaging *2I80 with contrast may also be ordered, especially in instances of unresolved paresis or aberrant presentation. ellMs palsy is often associated with segmental enhancement not e(tending into the auditory canal on 2I8 *$0. 3ther testing may include the Schirmer test, stapedial refle(, and evaluation of taste and salivation. 'he Schirmer test measures the amount of tears secreted in / minutes in response to irritation. 8t is measured by a filter paper strip. > normal response is +/ mm of strip moistened. 'he stapedial refle( is the refle( of the stapes of the inner ear *$0. ?lectroneurography, electromyography, and blink refle( have also been used in evaluation *.0.

!REA!(E$!
2anagement is predominantly supportive. ?ye care is essential. 'he affected eye should be taped shut during the night if the patient is unable to fully close it. >rtificial tears may also be administered # drops '8G. 8t is the responsibility of the nurse practitioner to ensure that the patient and family understands the importance of in6ury prevention and the course of the disease. 8n this case, because the patient is a child, it is important that annual PPG, dental care and well child visits be scheduled on a regular basis. >nticipatory guidance by the nurse practitioner should include in6ury prevention education, good parenting practices, se( education, nutrition and appropriate discipline techniques. 'he administration of steroids is controversial. ?ighty7four percent of patients recover without any intervention whatsoever *$0. Prognosis, of course, is dependent on age, severity of symptoms, and concomitant disease processes. Iecovery occurs within #7$ weeks following presentation with complete recovery by 47+# months following paresis *,0. 8n severe cases, oral steroids such as prednisone are often administered in doses of $:74: mg@day on a tapered dose over , to +: days in order to facilitate resolution of symptoms */0. 'his intervention is based on the belief that ellMs palsy results from inflammation and edema of the nerve secondary to a viral causation *,0.

)omplications include incomplete recovery of facial nerve function, *+:7#/B0 faulty reinnervation, and reoccurrence *,B0 */0. )ontractures of facial muscles and facial spasms have also been known to occur. Surgery should only be considered when facial paralysis is complete and e(tensive. 8n these instances decompression of the facial nerve has been recommended *$0. 8n e(treme cases, physical therapy may also be indicated.

$*EC! "+S CA+SES

)ommon infectious causes of sudden onset facial paralysis include such conditions as Lymes disease, Epstein Barre, erpes simple! and I" disease, among others. Ta#le$% &acial 'ea(ness in )hildhood
Congenital-structural Chiari malformation Depressor anguli oris muscle absence (cardiofacial syndrome) Inner ear and/or facial nerve malformations Mobius syndrome Syringobulbia 'rauma-nerve compression orceps pressure during delivery Cleidocranial dysostosis (istiocytosis ) (yperostosis cranialis interna Increased intracranial pressure *etrous bone fracture *ressure from maternal sacrum Genetic acio-scapulo-humeral dystrophy amilial cranial neuropathy (recurrent) a!io-"onde disease Myasthenia gravis (nonimmune mediated) Myotonic dystrophy #emaline myopathy Metabolic conditions (yperparathyroidism (ypothyroidism Idiopathic infantile hypercalcemia +steopetrosis

Infectious-inflammatory $asiliar meningitis $ell%s palsy &pstein-$arr infection (infectious mononucleosis) Guillain-$arre syndrome

#eoplasms $rainstem glioma *arotid gland tumors

,ascular

.rterial hypertension Miller- isher syndrome Mycoplasma pneumoniae infection "yme disease ($orreliosis) +titis media and mastoiditis *arotitis *oliomyelitis -amsay (unt syndrome (herpes !oster) Sarcoidosis 'richinosis 'uberculosis ,ascular syndromes of the cranial nerves

+ther Idiopathic cranial neuropathy Mel/ersson--osenthal syndrome Multiple sclerosis Myasthenia gravis (immune mediated) Myasthenia gravis (transient neonatal)

Source1 >dapted with permission from Smith S.>. *+--$0. Pediatric Neuropathies in )hildren. 8n P. A. Swaiman, Pediatric Neurology1 Principles and practice *#nd ?d., pp. +$#-7+$/#0C 2osby7Eear book, 8nc. St. %ouis, 2issouri *,0. Giagnostic evaluation should includes a complete blood count *) )0 and sedimentation rate to evaluate infectious etiology. )erebral spinal fluid *)SA0 studies add additional information if borrelia *%yme0 infection is considered. 'esting for ?pstein arre and D8J should also be considered. Distory and physical e(amination findings provide direction as to possible causation. Aor instance, a history of previous tic bites or recent history of travel in a %yme endemic area may lead the practitioner to look for %yme disease. 'he presence of a macular rash may be indicative of %ymeMs varicella or herpes *+0. GeneraliHed adenopathy may direct the practitioner towards infectious mononucleosis *+0. Positive risk factors as well as other systemic immunodeficient symptoms may lead the practitioner towards evaluation of cranial nerve neuropathy in a D8J patient * # 0. ecause of the wide variety of possible infectious agents, treatments may vary. %ymeMs disease is generally treated with systemic antibiotics such as do(ycycline, while mononucleosis is of viral origin and does not require treatment. %ikewise herpes simple( causation may necessitate treatment with acyclovir and steroids, while D8J infection has its own specific treatment protocols.

CE$!RA& $ER,"+S S#S!E(

%esions in the deep frontal cerebrum or pons can produce an ipsilateral facial paralysis *40. 3f times, this can be volitional, as seen with deep frontal lesions, or

associated with paralysis of the abducens in pontine lesions. > cerebellopontine angle lesion can also cause facial paralysis associated with tinnitus and deafness *40. Generally symptoms associated with )NS lesions do not develop spontaneously, but rather evolve over time. 'here is no associated prodromal syndrome which can be described, as there is in ellMs palsy or occasionally in infectious causation. >ssociated symptoms in the pediatric population may include headaches, lethargy, personality changes, and episodes of vomiting associated with increased intracranial pressure. Particular care should be taken when evaluating patients under two years of age, as facial palsies are seen more commonly in this age group, secondary to )NS lesions, than in adults * 5 0. Giagnostic criteria involve evaluation via )' scan or 2I8. 'reatment is dependent on grading, location, and metastasis associated with the lesion, and may involve surgery, radiation, or chemotherapy.

S+((AR#
'he case study reviews the clinical presentation of a pediatric patient with ellMs palsy. 9hile this is a relatively rare event in the pediatric population, ellMs palsy does occur and behooves the practitioner to become familiar with the diagnostic criteria and appropriate interventions for this disease process.

References
+. unch , >vner F. Neurologic ?mergencies. 8n ? )rain, F Gershel. )linical 2anual of ?mergency Pediatrics. 5rd ed. New Eork1 2cGraw DillC +--,C$5,7,$. #. Geraint F. >ll that palsies is not ell!s. 8n Fournal of the Ioyal Society and 2edicine. +--4C.-,+.$7.,. 5. 8namura D, >oyagi 2, 'o6ima D, Pohsyu D, Poike E. Aacial nerve palsy in children1 )linical aspects of diagnosis and treatment. 8n >cta 3tolaryngology, suppl, /++. +--$C+/:7/#. $. Fabor 2>, Gianoli G. 2anagement of ell!s palsy. 8n Fournal %ouisiana State 2edical Society. +--4C+$., #,-7.5. /. %ynch P. Aacial nerve disorders. 8n ?. arker, editors. Neuroscience Nursing. St. %ouis, 2issouri1 Eear ook 8nc.C +--$C$//7/.. 4. Iengachary SS. )ranial nerve e(amination. 8n ID 9ilkins, SS Iengachary, editors. Neurosurgery. #nd ed. New Eork1 2cGraw DillC +--4C4,7.4. ,. Smith S>. Peripheral neuropathies in children. 8n PA Swaiman. Pediatric Neurology1 Principles and Practice. #nd ed. St. %ouis, 2issouri1 2osby7Eear book, 8nc.C +--$C+$#-7/#.

.. 9ong J. 3utcome of facial nerve palsy in #$ children. rain and Gevelopment. +--/C+,, #-$7-4.

$&""0S *."S1
$ell%s palsy is a neurological disorder caused by damage to the seventh cranial nerve2 also /no3n as the facial nerve2 3hich results in 3ea/ness or paralysis on one side of the face4 'he paralysis causes distortion of facial features and interferes 3ith normal functions2 such as closing the eye and eating4 'he onset of $ell%s palsy is usually sudden4 Many people 3a/e up in the morning and find that one side of their face is paraly!ed4 *atients often fear that they have suffered a stro/e2 but $ell%s palsy is not related to stro/e4 Milder symptoms include tingling around the lips or a dry eye2 and usually progress 5uic/ly2 reaching ma6imum severity in 78 hours or less4 Anatomy 'he facial nerve controls the muscles that move the eyebro3s2 close the eyes2 and move the mouth and lips4 It also controls the tear glands2 one of the salivary glands2 and the taste buds in the front of the tongue4 &lectrochemical signals are relayed bet3een the brain and many facial muscles by 9::: nerve fibers that comprise the facial nerve4 ;hen the facial nerve is damaged2 as in $ell%s palsy2 the action of each nerve fiber is disrupted4 $ecause the facial nerve controls several functions2 several symptoms occur4 Incidence and Prevalence $ell%s palsy affects about 7:2::: people in the <nited States every year4 It affects appro6imately = person in >? during a lifetime4 It is more commonly seen in young adults2 and persons of @apanese descent have a slightly higher incidence of the condition4 $ell%s palsy is the most common cause of facial paralysis 3orld3ide and one of the most common neurological disorders involving a cranial nerve4 Causes ,iral infections such as herpes2 mumps2 or (I,2 and bacterial infections such as "yme disease or tuberculosis can cause inflammation and s3elling of the facial nerve that causes $ell%s palsy4 . tumor2 s/ull fracture2 or neurological condition caused by chronic disease (e4g42 diabetes2 Guillain-$arre syndrome) can also lead to $ell%s palsy4 Risk Factors Conditions that compromise the immune system2 such as (I,2 increase the ris/ for $ell%s palsy4 Stress2 pregnancy2 and diabetes are also ris/ factors4 Diabetics are more than 7 times as li/ely to develop the disorder compared to the general population4 +ther ris/ factors include the follo3ingA $acterial infections such as "yme disease or typhoid fever #eurological disorders such as Guillain-$arre syndrome2 multiple sclerosis2 and myasthenia gravis

'raumatic inBury to the head or face 'umor causing nerve compression ,iruses such as influen!a2 the common cold2 or infectious mononucleosis