http://ml.scribd.

com/doc/36952039/JURNAL-SARAF

BELL PALSY

Oleh: Michael Lambert, MD.
Fellowship Director of Emergency Ultrasound, ClinicalAssistant Proffesor, Department of
Emergency Medicine, Resurrection Medical center


PENDAHULUAN
Bel l pal s y mer upakan s al ah s at u gangguan neur ol ogi k yang pal i ng
s er i ngmempengaruhi nervus cranialis
Gangguan ini berupa paresis atau paralisis fasial perifer yang terjadi tiba-tiba,
bersifat unilateral tanpa penyebab yang jelas. Sindroma paralisis fasial idiopatik ini pertama kali
dijelaskan lebih dari satu abad yang lalu oleh S i r Ch a r l e s Be l l , mes ki pun mas i h
banyak kont r over s i mengenai et i ol ogi dan penatalaksanaannya,
Bell palsy merupakan penyebab paralisis fasial yang paling sering di
dunia.I ngat l ah bahwa kemungki nan mer upakan s uat u gangguan Bell palsy
harus di s i ngki r kan t er l ebi h dahul u. Penyaki t l ai n yang t ampak at au
kondi s i nya ber upa paralisis parsial sering salah didiagnosa sebagai gangguan idiopatik.
Pasien-pasien dengan Bell palsy sering dibawa ke bagian gawat darurat sebelum berobat ke
dokter ahli yang lain. Perubahan bentuk wajah dan kerusakan fungsional yang
t er j adi t i ba - t i ba menyebabkan or ang ber f i ki r s ebaga i keadaan yang
gawat darurat. Pasien sering merasa takut menderita stroke atau tumor dan bila
perubahan bentuk wajah mereka akan menetap. Peran dokter ahli kegawatdaruratan terdiri dari:
Menyingkirkan penyebab lain dari paralisis parsial
Memberikan pengobatan yang tepat
Melindungi mata
Mengatur perawatan medis lanjutan.

Patofisiologi
Patofisiologi pasti gangguan ini tidak diketahui; hal ini masih diperdebatkan.
Sebuah teori yang paling sering dipakai adalah inflamasi yang terjadi pada
nervus facialis. Selama proses ini, diameter nervus bertambah dan menjadi terdesak
oleh tulang temporal.
Nervus facialis berjalan melalui bagian tulang temporal yang disebut
canalis facialis. Bagian pertama canalis fasialis (segmen labirintus) merupakan yang paling
sempit. Lubang kecil (diameter sekitar 0.66 mm) pada segmen ini disebut foramen
meatal.
Nervus facialis ditinjau dari perjalanannya yang melalui canalis facialis yang
sempit. Maka secara logis dapat terjadi berbagai proses inflamasi,
demielinisasi,iskemia, atau penekanan yang kemudian dapat merusak kondisi neuron
pada jalur anatomis ini.

Anatomi
Nervus facialis (nervus cranialis ke tujuh) memiliki dua komponen. Bagian
yang l ebi h bes ar t er di r i dar i s er abut s ar af ef er en yang mer angs ang
eks pr es i ot ot wajah. Bagian yang kecil terdiri dari serabut saraf perasa di sepertiga anterior
lidah,serabut sekretomotor ke glandula lacrimalis dan salivarius, dan beber apa s er abut
saraf nyeri.

Jalur saraf
Jalur n e r v u s f a c i a l i s a d a l a h s a n g a t k o mp l e k s , a k i b a t n y a s a r a f
i n i r e n t a n me n g a l a mi l u k a / j e j a s . Ke d u a b a g i a n nervus facialis
meni nggal kan ot ak di cerebellopontine , mel al ui fossa cranialis posterior, m a s u k
k e meatus acusticus internus, me l a l u canalis facialis di t ul ang t empor al ,
s el anj ut nya ber bel ok ke belakang melewati belakang tulang tengah dan keluar
dari cranium pada foramen stylomastoideus. Dari sini,nervus facialis menembus glandula
parotis dan cabang terminalnya keluar dari pleksus parotis untuk merangsang terjadinya
ekspresi wajah.

Frekuensi
Di Amerika Serikat : insiden Bell palsy di Amerika Serikat adalahsekitar 23 kasus per
100.000 orang. Kondisi ini mempengaruhi sekitar 1 orang pada 65 kehidupan.
Di dunia: insiden penyakit sama dengan Amerika Serikat.
Mortalitas/Morbiditas
Bell palsy dapat menyebabkan gangguan estetik, fungsional dan psikologis pasien-
pasien yang mengalami disfungsi nervus residual selama fase penyembuhan atau pada
pasien-pasien dengan penyembuhan yang tidak sempurna.
Paralisis parsial
Si nki nes i s mot or i k ( ger akan i nvol unt er yang menyer t ai ger akanvolunter)
Sinkinesis otonom (lakrimasi involunter setelah gerakan otot volunter)

Ras
Insiden Bell palsy tampak cukup tinggi pada orang-orang keturunan Jepang.
Jenis kelamin
Tidak ada perbedaan distribusi jenis kelamin pada pasien-pasien dengan Bell palsy
Usia
Usia mempengaruhi probabilitas kontraksi Bell palsy. Insiden paling tinggi pada orang dengan
usia antara 15-45 tahun. Bell palsy lebih jarang pada orang-orang yang berusia di bawah 15
tahun dan yang berusia di atas 60 tahun.

GEJALA KLINIS
Riwayat yang diserang. Perhatikan gerakan volunter bagian atas wajah pada sisi
yangdiserang.
Pada lesi supranuklear seperti stroke kortikal (neuron motorik atas; diatas nucleus facialis
d i p o n s ) , d i ma n a s e p e r t i g a a t a s wa j a h me n g a l a mi kelemahan dan dua
per tiga bagian bawahnya mengalami paralisis. Musculus orbicularis, frontalis dan
corrugator diinervasi secara bilateral, sehingga dapat dimengerti mengenai pola paralisis
wajah.
Lakukan pemer i ks aan ner vus cr ani al i s l ai n: has i l pemer i ks aan biasanya
normal.
Membr an t i mpani t i dak bol eh mengal ami i nf l amas i ; i nf eks i yangt ampak
meni ngkat kan kemungki nan adanya ot i t i s medi a yang
mengal ami komplikasi.

Penyebab
semua yang berkilau bukan berarti emas (William Shakespeare)
Etiologi Bel l pal s y hi ngga s aat i ni mas i h t i dak j el as , mes ki pun
penyebabvaskuler, infeksi, genetik dan imunologis telah dicari. Pasien-pasien dengan
penyakitatau kondisi lain kadang-kadang juga mengalami palsy nervus facialis perifer, tetapi
gangguan ini tidak digolongkan sebagai Bell palsy.
I nf eks i vi r us : Dat a kl i ni s dan epi demi ol ogi s menunj ukkan adanya s uat u
i nf eks i pada awal gangguan, yang mencet us k an r es pon
i munol ogi s , s ehi ngga t er j adi ker us akan ner vus f aci al i s . Ku ma n - k u ma n
p a t o g e n y a n g mungkin adalah virus herpes simpleks tipe I (HSV-1); herpes
simpleks virustipe II (HSV-2); Human her pes vi r us ( HHV) ; virus varicella
zoster (VZV);Mycopl as ma pneumoni a; Bor r el i a bur gdor f er i ; i nf l uenz a B;
adenovi r us ; coxsackie virus; virus Eibsein-Barr ; hepat i t i s A, B, dan C;
c yt omegal ovi r us (CMV); dan virus rubella.

Kehamilan: Bell palsy jarang terjadi pada kehamilan; tetapi, prognosis adalah lebih
buruk pada wanita hamil dengan Bell palsy dari pada wanita tidak hamil yang men
derita penyakit ini.
Genet i k: Ti ngkat r ekur ens i ( 4. 5 - 15%) dan i ns i den f ami l i al ( 4. 1%)
telah dinyatakan dalam berbagai penelitian. Faktor genetik mungkin
berperan pada Bell palsy, tetapi mengenai faktor mana yang diwariskan masih
belum jelas.





DIAGNOSA BANDING
Diabetes mellitus, tipe 1-A
Diabetes mellitus tipe 2-A
Fraktur, mandibula
Herpes zoster
Sklerosis multipel
Penyakit Tick-Borne, Lyme

Gangguan lain yang harus diperhatikan :
Herpes zoster
Kehamilan (terutama pada trimester ke tiga)
Polyneuritis
Otitis akut
Otitis kronis
Fraktur tulang temporal
Mononucleosis infeksius

Human immunodeficiency virus (HIV)
Analisa cairan serebrospinal
T i t e r I mmu n o g l o b u l i n M ( I g M) , i mmu n o g l o b u l i n G ( I g G) ,
d a n immunoglobulin A (IgA) untuk CMV, rubella, HSV, hepatitis A, hepatitisB,
hepatitis C, VZV, M pneumonia,dan B burgdorferi.

Pemeriksaan pencitraan
Bell palsy masih menjadi suatu diagnosis klinis. Pemeriksaan pencitraan tidak
diindikasikan di bagian gawat darurat. Untuk menyingkirkan penyebab palsy
facial harus dilakukan pemeriksaan pencitraan berikut sesuai dengan gambaran
klinis yang dijumpai.
CT scan wajah atau foto polos: Untuk menyingkirkanfraktur atau metastase tulang
C T s c a n d i i n d i k a s i k a n b i l a
s t r o k e , Acquired immunodeficiency syndrome (AIDS)-keterlibatan SSP
digunakan sebagai diagnosa banding.
MRI : Bi l a di cur i gai adanya neopl as ma pada t ul angt empor al , ot ak,
kel enj ar par ot i s , at au s t r ukt ur t ubuh l ai n, at au unt uk mengevaluasi
sklerosis multipel, MRI merupakan pencitraan yang lebih tinggi. Perjalanan nervus
facialis regio intratemporal dan ekstratemporal dari otak ke otot -otot dan kelenjar di
wajah dapat dilihat dengan MRI. MRI juga diindikasikan selain CT scan.

Pemeriksaan lain
Elektrodiagnosis nervus facialis: pemeriksaan ini dilakukan untuk menilai fungsi
dari nervus facialis. Pemeriksaan berikut jarang dilakukan pada keadaan gawat darurat.
Elektromiografi (EMG) dan kecepatan konduksi saraf menghasilkan gambaran grafik
listrik akibat perangsangan pada nervus facialis dan dapat merekam eksitabilitas otot-otot
wajah yang d i l a l u i o l e h s a r a f i n i . Ba n d i n g k a n d e n g a n s i s i
k o n t r a l a t e r a l u n t u k menentukan luas jejas pada nervus dan pemeriksaan ini dapat
menentukan prognosis. Pemeriksaan ini tidak dilakukan pada masa akut.
Pada pemer i ks aan eks i t abi l i t as s ar af , dapat di t ent ukan ambang r angs ang
l i s t r i k aki bat kont r aks i ot ot yang terjadi.
E l e k t r o n e u r o g r a f i ( E N o G ) membandingkan
evoked potential p a d a s i s i y a n g me n g a l a mi p a r e s i s dengan sisi yang sehat.

PENGOBATAN
Di bagian gawat darurat: pengobatan awal bagi pasien dengan Bell palsy di ruang gawat
dar ur at adal ah penanganan f ar makol ogi s . Per awat an s el anj ut nya
adal ahedukasi pasien, anjuran perawatan mata, dan perawatan lanjutan yang sesuai.
Steroid
Pengobatan Bell palsy dengan menggunakan steroid masih merpakan suatu
k o n t r o v e r s i . Be r b a g a i a r t i k e l p e n e l i t i a n t e l a h d i t e r b i t k a n
me n g e n a i keuntungan dan kerugian pemberian steroid pada Bell palsy.
P a r a p e n e l i t i l e b i h c e n d e r u n g me mi l i h me n g g u n a k a n s t e r o i d
u n t u k m e m p e r o l e h h a s i l y a n g l e b i h b a i k . B i l a t e l a h
d i p u t u s k a n u n t u k menggunakan steroid, maka harus segera dilakukan
konsensus.
Zat ant i vi r al : mes ki pun pa da penel i t i an yang pernah dilakukan masih
kurang menunjukkan efektifitas obat -obat antivirus pada Bell palsy, hampir
semua ahli percaya pada etiologi virus. Oleh karena itu,zat antiviral merupakan pilihan
yang logis sebagai penatalaksaan farmakologis dan sering dianjurkan pemberiannya.
Perawatan mata: mata sering tidak terlindungi pada pasien-psien denganBell
palsy.Sehingga pada mata beresiko terjadinya kekeringan kornea dan terpapar
benda asing. Atasi dengan pemberian air mata pengganti, lubrikan, dan pelindung
mata.
Air mata pengganti: digunakan selama pasien terbangun untuk mengganti air
mata yang kurang atau tidak ada.
Lubrikan digunakan saat sedang tidur. Dapat juga digunakan saat terbangun j i k a a i r
m a t a p e n g g a n t i t i d a k c u k u p m e l i n d u n g i m a t a . S a l a h
s a t u kerugiannya adalah pandangan kabur selama pasien terbangun.
Kaca mat a at au pel i ndung yang dapat mel i ndungi mat a dar i j ej as
danmengurangi kekeringan dengan menurunkan jumlah udara yang mengalamikontak
langsung dengan kornea.
Konsultasi: d o k t e r y a n g me n a n g a n i p a s i e n i n i h a r u s me l a k u k a n
p e me r i k s a a n l a n j u t a n y a n g k e t a t . Do k u me n t a s i y a n g d i l a k u k a n
h a r u s me n c a k u p k e ma j u a n penyembuhan pasien. Berbagai pendapat
muncul mengenai perlunya rujukan ke dokter spesialis. Indikasi untuk merujuk
adalah sebagai berikut:
A h l i n e u r o l o g i : b i l a d i j u m p a i t a n d a - t a n d a n e u r o l o g i k
p a d a pemeriksaan fisik dan tanda-tanda yang tidak khas dari Bell palsy, maka
segeradirujuk.
Ahl i penyaki t mat a: bi l a t er j adi nye r i okul er yang t i dak j el as
at augambaran yang abnormal pada pemeriksaan f isik, pasien harus
dirujuk untuk pemeriksaan lanjutan.
Ahli otolaryngologi: pada pasien-pasien dengan paralisis
persisten,kel emahan ot ot waj ah yang l ama, at au kel emahan yang
r ekur en, s ebai knya dirujuk.
Ahli bedah: pembedahan untuk membebaskan nervus facialis kadang
dianjurkan untuk pasien dengan Bell palsy .Pasien dengan prognosis yang
buruk setelah pemeriksaan nervus facialis atau paralisis persisten cukup baik
untuk dilakukan pembedahan.

OBAT-OBATAN
Hampi r s emua pas i en dapat s embuh t anpa pengobat an, maka dokt er dapat
menangani pasien tanpa pemberian pengobatan. Pilihannya adalah menunggu; tetapi beberapa
individu dengan Bell palsy tidak sembuh sempurna. Dua jenis obat di bawah ini menurut
penelitian cukup efektif mengobati penyakit ini.
Kat egor i obat :
kortikosteroid
m e m i l i k i e f e k a n t i i n f l a m a s i d a n d a p a t me n y e b a b k a n
b e r b a g a i e f e k me t a b o l i k . Me n g u b a h r e s p o n i mu n t u b u h
u n t u k menghasilkan rangsang.
Nama obat
P r e d n i s o n e ( D e l t a s o n e , O r a s o n e , S t e r a p r e d )
e f e k f ar makol ogi s yang ber guna adal ah ef ek ant i i nf l amas i nya, yang
menurunkan kompresi nervus facialis dicanalis facialis
.Dosis dewasa
1 mg/kg/hari peroral selama 7 hari
Dosis pediatrik
Pemberian sama dengan dosis dewasa
Kontraindikasi
Per nah di l apor kan adanya hi per s ens i t i vi t as ; i nf eks i vi r us , jamur, jaringan
konektif, dan infeksi kulit tuberkuler; penyakit tukak lambung; disfungsi hepatik; penyakit
gastrointestinal

Interaksi obat
Pember i an ber s amaan dengan es t r ogen dapat menur unkan k l i r e n s
p r e d n i s o n e ; p e n g g u n a a n d e n g a n d i g o k s i n d a p a t m e n y e b a b k a n
t o k s i s i t a s d i g i t a l i s a k i b a t h i p o k a l e m i a ; f enobar bi t al , f eni t oi n,
dan r i f ampi n dapat meni ngkat kan metabolisme glukokortikoid (tingkatkan dosis
pemeliharaan); moni t or hi pokal emi a bi l a pember i an ber s ama dengan
obat diuretik.
Kehamilan
B b i a s a n y a a m a n t e t a p i k e u n t u n g a n o b a t i n i
d a p a t memperberat resiko
Perhatian
Penghentian pemberian glukokortikoid secara tiba-tiba dapatm e n y e b a b k a n
k r i s i s a d r e n a l ; h i p e r g l i k e m i a , e d e m a , osteonekrosis, miopati, penyakit
tukak lambung, hipokalemia,osteoporosis, euforia, psikosis, myasthenia gravis, penurunan
pertumbuhan, dan infeksi dapat muncul dengan penggunaan bersama glukokortikoid

Kategori obat:
antivirus
infeksi herpes simpleks merupakan penyebab palingsering dari Bell palsy
. Acyclovir merupakan yang paling sering digunakan, tetapi antiviral lain mungkin lebih
sesuai.
Nama obat
Ac y c l o v i r ( Zo v i r a x ) me n u n j u k k a n a k t i v i t a s h a mb a t a n langsung
melawan HSV-1 dan HSV-2, dan sel yang terinfeksisecara selektif.
Dosis dewasa
4000 mg/24 jam peroral selama 7-10 hari
Dosis pediatrik
< 2 tahun : tidak dianjurkan> 2 tahun : 1000 mg peroral dibagi 4 dosis selama 10 hari
Kontraindikasi
Pernah dilaporkan adanya hipersensitivitas
Interaksi obat
Penggunaan ber s ama dengan pr obeneci d at au zi dovudi ne d a p a t
m e m p e r p a n j a n g w a k t u p a r u h d a n m e n i n g k a t k a n toksisitas acyclovir
terhadap SSP
Kehamilan
C keamanan penggunaan selama kehamilan belum pernahdilaporkan
Perhatian
Hati-hati pada gagal ginjal atau bila menggunakan obat yang bersifat nefrotoksik

PERAWATAN LANJUTAN
Pasien rawat inap/jalan
Pertimbangkan pemberian prednisone dengan dosis awal 1 mg/kg/hari.
Prednisone merupakan obat yang poten dengan resiko mengalami efek samping yang
tinggi. Bukti efektivitas obat masih belum dapat dipastikandalam berbagai literatur.
Sebelum efektivitas obat ini jelas, sebaiknyatidak digunakan sebagai standar
pengobatan.
Tanpa kontraindikasi, dan jika dokter memilih untuk menggunakan steroid,
pilihan yang tepat adalah prednisone dengan dosis tinggi, mulai pemberian
seawal mungkin pada pengobatan. (pertimbangkan penurunandosis bertahap
pada hari ke lima hingga 5 mg, 2 x sehari selama 5 hari).

Pemberian acyclovir (zovirax) 800 mg peroral, 5 x sehari selama 10hari; 20
mg/kg pada pasien yang berusia < 2 tahun. Bukti menunjukkan bahwa70%
kasus Bell palsy disebabkan oleh HSV.
Komplikasi
Ha mp i r s e mu a p a s i e n d e n g a n Be l l p a l s y d a p a t s e mb u h
t a n p a mengalami deformitas kosmetik, tetapi sekitar 5% mengalami gejala sisa
cukup berat yang tidak dapat diterima oleh pasien.
Regenerasi motorik yang tidak sempurna.
Bagian terbesar dari nervus facialis terdiri dari serabut saraf eferenyang
merangsang otot-otot ekspresi wajah. Bila bagian motorik mengalamir egener as i
yang t i dak opt i mal , maka dapat t er j adi par es i s s emua at au beberapa otot
wajah tersebut.
Gangguan tampak sebagai (1) inkompetensi oral, (2) epifora (produksi air mata
berlebihan), dan (3) obstruksi nasal.
Regenerasi sensoris yang tidak sempurna.
Dysgeusia (gangguan rasa).
Ageusia (hilang rasa).
Dysesthesia g a n g g u a n s e n s a s i a t a u s e n s a s i y a n g t i d a k s e s u a i
d e n g a n stimulus normal).
Reinervasi aberan dari nervus facialis
Setelah gangguan konduksi neuron pada nervus facialis dimulai
denganregenerasi dan proses perbaikan, beberapa serabut saraf akan
mengambil j a l a n l a i n d a n d a p a t b e r h u b u n g a n d e n g a n s e r a b u t
s a r a f d i d e k a t n y a . Rekoneks i aber an i ni dapat menye babkan j al ur
neur ol ogi k yang t i dak normal.
Bi l a t er j adi ger akan vol unt er , bi as anya akan di s er t ai dengan
ger akaninvolunter (seperti gerakan menutup mata yang satu diikuti dengan gerakan
menutup mata disebelahnya). Gerakan involunter yang menyertai
gerakanvolunter ini disebut synkinesis.

Prognosis
Perjalanan Bell palsy bervariasi mulai dari penyembuhan awal yang komplit pada jejas
nervus disertai dengan gejala sisa yang permanen. Secara prognostik, pasien terbagi
dalam tiga kelompok dengan sejumlah gejala sisa pada masih-masing kelompok.
Kel ompok 1 mengal ami per bai kan f ungs i mot or i k waj ah secara sempurna
tanpa disertai gejala sisa.
Kel ompok 2 mengal ami per bai kan f ungs i mot or i k waj ahyang t i dak
s empur na, t et api t i dak mengal ami def ek kos met i k pada mat a yang tidak
dilatih.
Kel ompok 3 mengal ami gej al a s i s a neur ol ogi k yang ber at yang tampak
secara kosmetik dan klinis.
Hampir semua pasien mengalami paralisis facial inkomplit selamafase akut.
Kelompok pasien ini memiliki prognosis yang baik untuk sembuhsempurna.
Pasien yang mengalami paralisis komplit lebih beresiko mengalamigejala sisa yang berat.
Dari semua pasien dengan Bell palsy, 85% sembuh sempurna. 10% s edi ki t
t er ganggu dengan ot ot waj ah ya ng as i met r i s , s ement ar a 5%
s i s anyamengalami gejala sisa yang berat.

Edukasi pasien
Perawatan mata:
oLindungi mata dari paparan benda asing dan cahaya matahari.
oBerikan lubrikasi yang cukup.
oEdukasi psaien untuk segera berobat jika terjadi gangguan okuler yang baru seperti nyeri, sulit
digerakkan, atau perubahan visual.

2. http://www.jfponline.com/Pages.asp?AID=1797
3. http://lib.atmajaya.ac.id/default.aspx?tabID=61&src=a&id=122953











4. http://emedicine.medscape.com/article/1146903-overview#aw2aab6b2b2aa
Background
Facial paralysis is a disfiguring disorder that has a great impact on the patient. Facial nerve
paralysis may be congenital or neoplastic or may result from infection, trauma, toxic exposures,
or iatrogenic causes. The most common cause of unilateral facial paralysis is Bell palsy, more
appropriately termed idiopathic facial paralysis (IFP). Bell palsy is an acute, unilateral,
peripheral, lower-motor-neuron facial-nerve paralysis that gradually resolves over time in 80-
90% of cases. (See Etiology.)
Controversy surrounds the etiology and treatment of Bell palsy. The cause of Bell palsy remains
unknown, though it appears to be a polyneuritis with possible viral, inflammatory, autoimmune,
and ischemic etiologies. Increasing evidence implicates herpes simplex type I and herpes zoster
virus reactivation from cranial-nerve ganglia.
[1]
(See Etiology.)
Bell palsy is one of the most common neurologic disorders affecting the cranial nerves, and it is
the most common cause of facial paralysis worldwide. Bell palsy is thought to account for
approximately 60-75% of cases of acute unilateral facial paralysis. Bell palsy is more common in
adults, in people with diabetes, and in pregnant women. (See Epidemiology.)
Determining whether facial-nerve paralysis is peripheral or central is a key step in the diagnosis.
A lesion involving the central motor neurons above the level of the facial nucleus in the pons
causes weakness of the lower face alone. Thorough history taking and examination, including the
ears, nose, throat, and cranial nerves, must be performed. (See Clinical Presentation.)
The minimum diagnostic criteria include paralysis or paresis of all muscle groups on one side of
the face, sudden onset, and absence of central nervous system disease. Note that the diagnosis of
IFP is made only after other causes of acute peripheral palsy have been excluded. (See
Diagnosis.)
If the clinical findings are doubtful or if paralysis lasts longer than 6-8 weeks, further
investigations, including gadolinium-enhanced magnetic resonance imaging of the temporal
bones and pons, should be considered.
[2]
Electrodiagnostic tests (eg, stapedius reflex test, evoked
facial-nerve electromyography [EMG], audiography) may help improve the accuracy of
prognosis in difficult cases. (See Workup.)
Treatment of Bell palsy should be conservative and guided by the severity and probable
prognosis in each particular case. Studies have shown the benefit of high-dose corticosteroids for
acute Bell palsy.
[3, 4]
Although antiviral treatment has been used in recent years, evidence is now
available indicating that it may not be useful.
[3]
(See Medication.)
Topical ocular therapy is useful in most cases, with the exception of those in which the condition
is severe or prolonged. In these cases, surgical management is best. Several procedures are aimed
at protecting the cornea from exposure and achieving facial symmetry. These procedures reduce
the need for constant use of lubrication drops or ointments, may improve cosmesis, and may be
needed to preserve vision on the affected side. (See Treatment and Management.)
Anatomy
In 1550, Fallopius noted the narrow lumen in the temporal bone through which a part of the
seventh cranial nerve passes. In 1828, Charles Bell made the distinction between the fifth and
seventh cranial nerves; he noted that the seventh nerve was involved mainly in the motor
function of the face and that the fifth nerve primarily conducted sensation from he face. The
seventh cranial nerve is commonly referred to as the facial nerve.
The fac ial nerve contains parasympathetic fibers to the nose, palate, and lacrimal glands. Its
course is tortuous, both centrally and peripherally. The facial nerve travels a 30-mm interosseous
course through the internal auditory canal (with the eighth cranial nerve) and through the internal
fallopian canal in the petrous temporal bone. This bony confinement limits the amount that the
nerve can swell and thereby cause acute paralysis.
The nucleus of the facial nerve lies within the reticular formation of the pons, adjacent to the
fourth ventricle. The facial nerve roots include fibers from the motor, solitary, and salivatory
nuclei. The preganglionic parasympathetic fibers that originate in the salivatory nucleus join the
fibers from nucleus solitarius to form the nervus intermedius.
The nervus intermedius comprises sensory fibers from the tongue, mucosa, and postauricular
skin as well as parasympathetic fibers to the salivary and lacrimal glands. These fibers then
synapse with the submandibular ganglion, which has fibers that supply the sublingual and
submandibular glands. The fibers from the nervus intermedius also supply the pterygopalatine
ganglion, which has parasympathetic fibers that supply the nose, palate, and lacrimal glands.
The fibers of the facial nerve then course around the sixth cranial nerve nucleus and exit the pons
at the cerebellopontine angle. The fibers go through the internal auditory canal along with the
vestibular portion of the eighth cranial nerve.
The facial nerve passes through the stylomastoid foramen in the skull and terminates into the
zygomatic, buccal, mandibular, and cervical branches. These nerves serve the muscles of facial
expression, which include frontalis, orbicularis oculi, orbicularis oris, buccinator, and platysma.
Other muscles innervated by the facial nerve include stapedius, stylohyoid, posterior belly of the
digastric, occipitalis, and anterior and posterior auricular muscles. All muscles of the facial nerve
are derived from the second brachial arch.



Bell Palsy Slideshow
Click the image below to see a slideshow of images for Bell Palsy.
The facial nerve.

Pathophysiology
The precise pathophysiology of Bell palsy remains an area of debate. The facial nerve courses
through a portion of the temporal bone commonly referred to as the facial canal. A popular
theory proposes that edema and ischemia results in compression of the facial nerve within this
bony canal. The cause of the edema and ischemia has not yet been established. This compression
has been seen in magnetic resonance imaging (MRI) scans with facial nerve enhancement.
[5]

The first portion of the facial canal, the labyrinthine segment, is narrowest; the meatal foramen in
this segment has a diameter of only about 0.66 mm. This is the location that is thought to be the
most common site of compression of the facial nerve in Bell palsy. Given the tight confines of
the facial canal, it seems logical that inflammatory, demyelinating, ischemic, or compressive
processes may impair neural conduction at this site.
The location of injury of the facial nerve in Bell palsy is peripheral to the nerves nucleus. The
injury is thought to occur near, or at, the geniculate ganglion. If the lesion is proximal to the
geniculate ganglion, the motor paralysis is accompanied by gustatory and autonomic
abnormalities. Lesions between the geniculate ganglion and the origin of the chorda tympani
produce the same effect, except that they spare lacrimation. If the lesion is at the stylomastoid
foramen, it may result in facial paralysis only.
Etiology
In the past, situations that produced cold exposure (eg, chilly wind, cold air conditioning, or
driving with the car window down) were considered the only triggers to Bell palsy. Currently,
several authors believe that the herpes simplex virus (HSV) is a common cause of Bell palsy.
However, a definitive causal relationship of HSV to Bell palsy may be difficult to prove because
of the ubiquitous nature of HSV.
In 1972, McCormick first suggested that HSV is responsible for idiopathic facial paralysis.
[6]
This was based on the analogy that HSV was found in cold sores, and he hypothesized that HSV
may remain latent in the geniculate ganglion. Since then, autopsy studies have shown HSV in the
geniculate ganglion of patients with Bell palsy. Murakami et al, who performed polymerase
chain reaction (PCR) testing for HSV in the endoneural fluid of the facial nerve in 14 patients
who underwent surgery for Bell palsy, found that 11 of the 14 had HSV in the endoneural
fluid.
[7]

Assuming that HSV is the etiologic agent in Bell palsy is a plausible argument. If this is true,
then the virus is most likely to travel up the axons of the sensory nerves and reside in the
ganglion cells. At times of stress, the virus will reactivate, causing local damage to the myelin.
Additional support for a viral etiology was seen when intranasal inactivated influenza vaccine
was strongly linked to the development of Bell palsy, although whether another component of
the vaccine caused the paresis, which was then accompanied by a reactivation of herpes simplex
virus, is not clear.
[8, 9]

Besides HSV infection, possible etiologies for Bell palsy include other infections (eg, herpes
zoster, Lyme disease, syphilis, Epstein-Barr viral infection, cytomegalovirus, HIV, and
mycoplasma); inflammation alone; and microvascular disease (diabetes mellitus and
hypertension).
[10, 11, 12, 13, 14, 15, 16]
Bell palsy may be secondary to viral and/or autoimmune
reactions causing the facial nerve to demyelinate, resulting in unilateral facial paralysis
A family history of Bell palsy has been reported in approximately 4% of cases. Inheritance in
such cases may be autosomal dominant with low penetration; however, which predisposing
factors are inherited is unclear.
[17]

Epidemiology
Bell palsy is thought to account for approximately 60-75% of cases of acute unilateral facial
paralysis. It can also be recurrent, with a reported recurrence range of 4-14%.
[11]

Rarely, bilateral simultaneous Bell palsy can occur at a rate of less than 1% of unilateral facial
nerve palsy.
[18, 19]
Bell palsy accounts for only 23% of bilateral facial paralysis. The majority of
patients with bilateral facial palsy have Guillain-Barr syndrome (GBS), sarcoidosis, Lyme
disease, meningitis (neoplastic or infectious), or bilateral neurofibromas (in patients with
neurofibromatosis type 2).
In general, Bell palsy occurs more commonly in adults, in people with diabetes, and in pregnant
women. It is also more common in people who are immunocompromised or in women with
preeclampsia.
[20]

Persons with diabetes have a 29% higher risk of being affected by Bell palsy than persons
without diabetes. Thus, measuring blood glucose levels at the time of diagnosis of Bell palsy
may detect undiagnosed diabetes. Diabetic patients are 30% more likely than nondiabetic
patients to have only partial recovery; recurrence of Bell palsy is also more common among
diabetic patients.
[21]

United States Statistics
The annual incidence of Bell palsy is approximately 23 cases per 100,000 persons.
[22]
The right
side is affected 63% of the time. Very few cases are observed during the summer months.
International Statistics
The highest incidence was found in a study in Seckori, Japan, in 1986, and the lowest incidence
was found in Sweden in 1971. Most population studies generally show an annual incidence of
15-30 cases per 100,000 population.
Sex distribution for Bell palsy
Bell palsy appears to affect the sexes equally. However, young women aged 10-19 years are
more likely to be affected than men in the same age group. Pregnant women have a 3.3 times
higher risk of being affected by Bell palsy than nonpregnant women; Bell palsy occurs most
frequently in the third trimester.
Age distribution for Bell palsy
Slightly higher predominance is observed in patients older than 65 years (59 cases per 100,000
people). A lower rate of incidence is observed in children younger than 13 years (13 cases per
100,000 people). The lowest incidence is found in persons younger than 10 years, and the highest
incidence is in persons aged 60 years or older. Peak ages are 20-40 years. The disease also
occurs in elderly persons aged 70-80 years.
[23]

Prognosis
The natural course of Bell palsy varies from early complete recovery to substantial nerve injury
with permanent sequelae (eg, persistent paralysis and synkinesis). Prognostically, patients fall
into 3 groups:
Group 1 - Complete recovery of facial motor function without sequelae
Group 2 - Incomplete recovery of facial motor function, but no cosmetic defects are apparent to
the untrained eye
Group 3 - Permanent neurologic sequelae that are cosmetically and clinically apparent
Patients generally have a good prognosis; approximately 80-90% recover without noticeable
disfigurement within 6 weeks to 3 months. Most patients who suffer from Bell palsy have
neurapraxia or local nerve conduction block. These patients are likely to have a prompt and
complete recovery of the nerve. Patients with axonotmesis, with disruption of the axons, have a
fairly good recovery but it is usually not complete.
The risk factors thought to be associated with a poor outcome in patients with Bell palsy include
(1) age greater than 60 years, (2) complete paralysis, and (3) decreased taste or salivary flow on
the side of paralysis (usually 10-25% compared to the patients normal side). Other factors
thought to be associated with poor outcome include pain in the posterior auricular area and
decreased lacrimation.
Patients aged 60 years or older have an approximately 40% chance of complete recovery and
have a higher rate of sequelae. Patients younger than 30 years have only a 10-15% chance of less
than complete recovery and/or long-term sequelae.
The sooner the recovery, the less likely are the chances that sequelae will develop, as
summarized below:
If some restoration of function is noted within 3 weeks, then the recovery is most likely to be
complete.
If the recovery begins between 3 weeks and 2 months, then the ultimate outcome is usually
satisfactory.
If the recovery does not begin until 2-4 months from the onset, likelihood of permanent
sequelae, including residual paresis and synkinesis, is higher.
If no recovery occurs by 4 months, then the patient is more likely to have sequelae from the
disease, which include synkinesis, crocodile tears, and rarely hemifacial spasm.
Bell palsy recurs in 4-14% of patients, with one source suggesting a recurrence rate of 7%. It
may recur on the ipsilateral or contralateral side of the initial palsy. Recurrence usually is
associated with a family history of recurrent Bell palsy. Higher recurrence rates were reported in
the past; however, many of these patients have been found to have an underlying etiology for the
recurrence, which eliminates the diagnosis of Bell palsy.
[24]

Patients with recurrent ipsilateral facial palsy should undergo MRI or high-resolution computed
tomography (CT) to rule out a neoplastic or inflammatory (eg, multiple sclerosis, sarcoidosis)
cause of recurrence. Recurrent or bilateral disease should suggest myasthenia gravis.
Most patients with Bell palsy recover without any cosmetically obvious deformities.
Approximately 30% of patients with Bell palsy experience sequelae of the paralysis, which
include incomplete motor regeneration, incomplete sensory regeneration, and aberrant
reinnervation of the facial nerve. Approximately 5% are left with an unacceptably high degree of
sequelae.
The Sunnybrook grading scale, a numeric score used occasionally to help direct decisions
regarding further treatment needs, may provide additional information about possible
outcomes.
[25]

Incomplete motor regeneration
The largest portion of the facial nerve comprises efferent fibers that stimulate muscles of facial
expression. Suboptimal regeneration of this portion results in paresis of all or some of these
facial muscles. This manifests as (1) oral incompetence, (2) epiphora (excessive tearing), and (3)
nasal obstruction.
Incomplete sensory regeneration
Dysgeusia (impairment of taste) or ageusia (loss of taste) may result, as well as dysesthesia
(impairment of sensation or disagreeable sensation to normal stimuli).
Aberrant reinnervation of the facial nerve
During regeneration and repair of the facial nerve, some neural fibers may take an unusual
course and connect to neighboring muscle fibers. This aberrant reconnection produces unusual
neurologic pathways. When voluntary movements are initiated, they are accompanied by
involuntary movements (eg, eye closure associated with lip pursing or mouth grimacing that
occurs during blinking of the eye). These involuntary movements accompanying voluntary
movement are termed synkinesis.
Patient Education
To prevent corneal abrasions, patients should be educated concerning eye care. They also should
be encouraged to do facial muscle exercises using passive range of motion as well as actively
closing their eyes and smiling.
For excellent patient education resources, visit eMedicines Brain and Nervous System Center.
Also, see eMedicines patient education article Bell Palsy.
History
The diagnosis of Bell palsy must be made on the basis of a thorough history and physical
examination and use of diagnostic testing when necessary. Bell palsy is a diagnosis of exclusion.
Clinical features of Bell palsy that may help distinguish it from other causes of facial paralysis
include sudden onset of unilateral facial paralysis, absence of signs and symptoms of central
nervous system (CNS) disease, and absence of signs and symptoms of ear or posterior fossa
disease.
The onset of Bell palsy is typically sudden, and symptoms tend to peak in less than 48 hours.
This sudden onset can be frightening for patients, who often fear they have had a stroke or have a
tumor and that the distortion of their facial appearance will be permanent (see the image below).
Left-sided Bell palsy.
Because the condition appears so rapidly, patients with Bell palsy frequently present to the
emergency department (ED) before seeing any other health care professional. More people first
notice paresis in the morning. Because the symptoms require several hours to become evident,
most cases of paresis likely begin during sleep.
No evidence of CNS disease is noted in patients with Bell palsy. In addition, no evidence of ear
or cerebellopontine angle disease is noted. Bell palsy may follow recent upper respiratory
infection (URI).
Symptoms of Bell palsy include the following:
Acute onset of unilateral upper and lower facial paralysis (over a 48-h period)
Posterior auricular pain
Decreased tearing
Hyperacusis
Taste disturbances
Otalgia
Early symptoms include the following:
Weakness of the facial muscles
Poor eyelid closure
Aching of the ear or mastoid (60%)
Alteration of taste (57%)
Hyperacusis (30%)
Tingling or numbness of the cheek/mouth
Epiphora
Ocular pain
Blurred vision
Facial paralysis
The paralysis must include the forehead and lower aspect of the face. The patient may report
inability to close the eye or to smile on the affected side. He or she also may report increased
saliva on the side of the paralysis. If the paralysis involves only the lower portion of the face, a
central cause should be suspected (ie, supranuclear). If the patient complains of contralateral
weakness or diplopia in conjunction with the supranuclear facial palsy, a stroke or intracerebral
lesion should be strongly suspected.
If a patient has gradual onset of facial paralysis, weakness of the contralateral side, or history of
trauma or infection, other causes of facial paralysis must be strongly considered. Progression of
the paresis is possible, but it usually does not progress beyond 7-10 days. A progression beyond
this point suggests a different diagnosis. Patients who have bilateral facial palsy must be
evaluated for Guillain-Barr syndrome (GBS), Lyme disease, and meningitis.
Many patients report numbness on the side of the paralysis. Some authors believe that this is
secondary to involvement of the trigeminal nerve, whereas other authors argue that this symptom
is probably due to lack of mobility of the facial muscles and not lack of sensation.
Ocular manifestations
Early ocular complications include the following:
Lagophthalmos (inability to close the eye completely)
Paralytic ectropion of the lower lid
Corneal exposure
Brow droop
Upper eyelid retraction
Decreased tear output/poor tear distribution
Loss of nasolabial fold
Corneal erosion, infection, and ulceration (rare but may occur)
Late ocular manifestations include the following:
Mild, generalized mass contracture of the facial muscles, rendering the affected palpebral
fissure narrower than the opposite one (after several months)
Aberrant regeneration of the facial nerve with motor synkinesis
Reversed jaw winking (ie, contracture of the facial muscles with twitching of the corner of the
mouth or dimpling of the chin occurring simultaneously with each blink)
Autonomic synkinesis (ie, crocodile tears-tearing with chewing)
Rare, permanent, disfiguring facial paralysis
Two thirds of patients complain about tear flow.
[1]
This is due to the reduced function of the
orbicularis oculi in transporting the tears. Fewer tears arrive at the lacrimal sac, and overflow
occurs. The production of tears is not accelerated.
Posterior auricular pain
Half of the patients affected with Bell palsy may complain of posterior auricular pain.
[1]
The pain
frequently occurs simultaneously with the paresis, but pain precedes the paresis by 2-3 days in
about 25% of patients. Ask the patient if he or she has experienced trauma, which may account
for the pain and facial paralysis. One third of patients may experience hyperacusis in the ear
ipsilateral to the paralysis, which is secondary to weakness of the stapedius muscle.
Taste disorders
While only one third of patients report taste disorders,
[1]
80% of patients show a reduced sense of
taste. Patients may fail to note reduced taste because of normal sensation in the uninvolved side
of the tongue.
Facial spasm
Facial spasm is a very rare complication of Bell palsy. It occurs as tonic contraction of one side
of the face. Spasms are more likely to occur during times of stress or fatigue and may be present
during sleep. This condition may occur secondary to compression of the root of the seventh
nerve by an aberrant blood vessel, tumor, or demyelination of the nerve root. It occurs most
commonly in the fifth and sixth decades of life, and sometimes the etiology is not found. The
presence of progressive facial hemispasm with other cranial nerve findings indicates a possibility
of a brainstem lesion.
Synkinesis is an abnormal contracture of the facial muscles while smiling or closing the eyes. It
may be mild and result in slight movement of the mouth or chin when the patient blinks or in eye
closure with smiling. Crocodile tears can be observed; patients shed tears while they eat.
Cranial neuropathies
Some believe that other cranial neuropathies may also be present; however, this is not uniformly
accepted. The symptoms in question include the following:
Hyperesthesia or dysesthesia of the glossopharyngeal or trigeminal nerves
Dysfunction of the vestibular nerve
Hyperesthesia of the cervical sensory nerves
Vagal or trigeminal motor weakness

Physical Examination
Weakness and/or paralysis from involvement of the facial nerve affects the entire face (upper and
lower) on the affected side. A careful examination of the head, ears, eyes, nose, and throat
(HEENT) must be carried out in all patients with facial paralysis.
Focus attention on the voluntary movement of the upper part of the face on the affected side: in
supranuclear lesions such as a cortical stroke (upper motor neuron; above the facial nucleus in
the pons), the upper third of the face is spared while the lower two thirds are paralyzed. The
orbicularis, frontalis, and corrugator muscles are innervated bilaterally at the level of the
brainstem, which explains the pattern of facial paralysis in these cases.
[19]

Initial inspection
Initial inspection of the patient demonstrates flattening of the forehead and nasolabial fold on the
side affected with the palsy. When the patient is asked to raise the eyebrows, the side of the
forehead with the palsy will remain flat. When the patient is asked to smile, the face becomes
distorted and lateralizes to the side opposite the palsy.
Otologic examination
An otologic examination includes pneumatic otoscopy and tuning fork examination. An otologic
cause should be considered if the history or physical examination demonstrates evidence of acute
or chronic otitis media, including a tympanic membrane perforation, otorrhea, cholesteatoma, or
granulation tissue, or if a history of previous ear surgery is noted. Concurrent rash or vesicles
along the ear canal, pinna, and mouth should raise the suspicion for Ramsay Hunt syndrome
(herpes zoster oticus).
The external auditory canal must be inspected for vesicles, injection, infection, or trauma. The
patient may have decreased sensation to pinprick in the posterior auricular area. The patient who
has paralysis of the stapedius muscle will report hyperacusis. Tympanic membranes should be
normal; the presence of inflammation, vesicles, or other signs of infection raises the possibility
of complicated otitis media.
Ocular examination
With weakness/paralysis of the orbicularis oculi muscle (facial nerve innervation) and normal
function of the levator muscle (oculomotor nerve innervation) and Mueller muscle (sympathetic
innervation), the patient frequently is not able to close the eye completely on the affected side.
On attempted eye closure, the eye rolls upward and inward on the affected side. This is known as
Bell phenomenon and is considered a normal response to eye closure.
The tear reflex may also be absent in many cases of Bell palsy. For these reasons, the patient
may have decreased tearing and susceptibility to corneal abrasion and dryness of the eye. The
patient may appear to have loss of corneal reflex on the affected side; however, the contralateral
eye blinks when testing the corneal reflex on the affected side.
Oral examination
A careful oral examination must be performed. Taste and salivation are affected in many patients
with Bell palsy. Taste may be assessed by holding the tongue with gauze and testing each side of
the tongue independently with salt, sugar, and vinegar. The mouth must be washed after testing
with different substances. The affected side has decreased taste as compared to the normal side.
Neurologic examination
Careful neurologic examination is necessary in patients with facial paralysis. Neurologic
examination includes complete examination of all the cranial nerves, sensory and motor testing,
and cerebellar testing. A neurologic abnormality warrants neurologic referral and further testing,
such as MRI of the brain, lumbar puncture, and electromyography (EMG) where appropriate.
Skin examination
Time must also be taken to examine the patients skin for signs of squamous cell carcinoma,
which can invade the facial nerve, and parotid gland disease.
Grading
The grading system developed by House and Brackmann categorizes Bell palsy on a scale of I to
VI, as follows
[26, 27]
:
Grade I - Normal facial function.
Grade II - Mild dysfunction. Slight weakness is noted on close inspection. The patients may have
a slight synkinesis. Normal symmetry and tone is noted at rest. Forehead motion is moderate to
good; complete eye closure is achieved with minimal effort; and slight mouth asymmetry is
noted.
Grade III - Moderate dysfunction. An obvious but not disfiguring difference is noted between the
2 sides. A noticeable but not severe synkinesis, contracture, or hemifacial spasm is present.
Normal symmetry and tone is noted at rest. Forehead movement is slight to moderate;
complete eye closure is achieved with effort; and a slightly weak mouth movement is noted with
maximum effort.
Grade IV - Moderately severe dysfunction. An obvious weakness and/or disfiguring asymmetry is
noted. Symmetry and tone are normal at rest. No forehead motion is observed. Eye closure is
incomplete, and an asymmetric mouth is noted with maximal effort.
Grade V - Severe dysfunction. Only a barely perceptible motion is noted. Asymmetry is noted at
rest. No forehead motion is observed. Eye closure is incomplete, and mouth movement is only
slight.
Grade VI - Total paralysis. Gross asymmetry is noted. No movement is noted.
In this system, grades I and II are considered good outcomes, grades III and IV represent
moderate dysfunction, and grades V and VI describe poor results. Grade VI is defined as
complete facial paralysis; all the other grades are defined as incomplete. An incomplete facial
paralysis denotes an anatomically and, to some degree, functionally intact nerve. The degree of
facial nerve function should be noted in the chart at the initial visit of the patient.
Diagnostic Considerations
In most cases, the diagnosis of Bell palsy is straightforward as long as the patient has undergone
a thorough history and physical examination. Failure to recognize structural, infectious, or
vascular lesions leading to seventh cranial nerve (facial nerve) damage may result in further
deterioration of the patients condition. For example, if other cranial nerve, motor, or sensory
symptoms were present, then treatable or preventable nervous system diseases should be sought
(eg, stroke, Guillain-Barr syndrome [GBS], basilar meningitis, or cerebellar pontine angle
tumor).
Symptoms associated with seventh nerve neoplasm include slowly progressive paralysis, facial
hyperkinesis, severe pain, recurrent palsy, and other cranial nerve involvement. Cerebellopontine
tumors may affect the seventh, eighth, and fifth cranial nerves simultaneously. Patients with a
progressive paralysis of the facial nerve lasting longer than 3 weeks should be evaluated for
neoplasm.
Recurrent ipsilateral facial paralysis must raise the suspicion of a tumor of the facial nerve or
parotid gland. Tumors in the temporal bone such as facial nerve neuromas, meningiomas,
hemangiomas, and malignant primary and metastatic lesions should be considered as well.
If a patient is from the Northeast, Lyme disease should be considered as a cause of facial
paralysis, and serologic testing should be performed. Approximately 5-10% of untreated Lyme
patients may have a peripheral facial nerve palsy.
If the patient reports sudden onset of hearing loss and severe pain with the onset of facial
paralysis, Ramsay Hunt syndrome must be considered.
Other problems to be considered include the following:
Acoustic neuroma and other cerebellopontine angle lesions
Acute or chronic otitis media
Amyloidosis
Aneurysm of vertebral, basilar artery, or carotid arteries
Autoimmune syndromes
Botulism
Carcinomatosis
Carotid disease and stroke, including embolic phenomenon
Cholesteatoma of the middle ear
Congenital malformation
Diabetes mellitus
Facial nerve schwannoma
Geniculate ganglion infection
Glomus tumors
Guillain-Barr syndrome
Herpes zoster
HIV
Leukemia/lymphoma
Leukemic meningitis
Lyme disease
Malignant otitis externa
Melkersson-Rosenthal syndrome
Meningitis
Mycoplasma pneumonia
Nasopharyngeal carcinoma
Osteomyelitis of the skull base
Otitis media
Parotid gland disease or tumor
Pontine lesions
Pregnancy (especially third trimester)
Ramsay Hunt syndrome
Sarcoma
Skull base tumor
Teratoma
Tuberculosis
Viral syndromes
Wegener granulomatosis
Wegener vasculitis
In the setting of an appropriate history, additional considerations include the following:
Alcoholic neuropathy
Anesthesia nerve blocks
Basal skull fractures
Barotrauma
Benign intracranial hypertension
Birth trauma
Carbon monoxide exposure
Diphtheria
Facial injuries
Facial trauma (blunt, penetrating, iatrogenic)
Forceps delivery
Iatrogenic (as in otologic, neurotologic, skull base, or parotid surgery)
Infectious mononucleosis
Kawasaki disease
Leprosy
Metastatic disease
Mumps
Polyneuritis
Temporal bone fracture
Tetanus
Thalidomide exposure
Toxic
Differential Diagnoses
Anterior Circulation Stroke
Benign Skull Tumors
Brainstem Gliomas
Cerebral Aneurysms
Intracranial Hemorrhage
Meningioma
Meningococcal Meningitis
Neurosyphilis
Sarcoidosis
Tick-Borne Diseases, Lyme
Tuberculous Meningitis
Bell Palsy Workup
Approach Considerations
In many cases, the history and physical examination lead to the diagnosis of Bell palsy. If the
clinical findings are doubtful or if paralysis lasts longer than 6-8 weeks, further investigations
should be considered.
[2]

No specific diagnostic tests are available for Bell palsy, though the following may be useful:
Rapid plasma reagin (RPR) and/or venereal disease research laboratory (VDRL) test or
fluorescent treponemal antibody absorption (FTA-ABS) test
Human immunodeficiency virus (HIV) screening by means of enzyme-linked immunosorbent
assay (ELISA) and/or Western blot
Complete blood cell count
Determination of the erythrocyte sedimentation rate
Thyroid function studies
Serum glucose level
Cerebrospinal fluid analysis
If the history and physical examination lead to a diagnosis of Bell palsy, then immediate imaging
is not necessary. Imaging is not required because most patients with Bell palsy improve within 8-
10 weeks. If the paralysis does not improve or worsens, imaging may be useful. If the patient has
a palpable parotid mass, imaging may be necessary.
Blood glucose or hemoglobin A
1c
levels may be obtained to determine if the patient has
undiagnosed diabetes.
Serum titers for herpes simplex virus may be obtained, but this is usually not helpful owing to
the ubiquitous nature of this virus.
Antineutrophil cytoplasmic antibody (cANCA) levels are indicated if applicable to exclude
Wegener granulomatosis.
Measurement of Serum Immunoglobulin Titers
In areas where Lyme disease is endemic, serum titers (IgM and IgG) for Borrelia burgdorferi
should be obtained.
Serum titers (IgM and IgA) for Mycoplasma pneumoniae may be obtained. A study in Germany
measured titers in patients with Bell palsy and found that several patients had elevated titers to M
pneumoniae, and only 2 of those who tested positive had respiratory symptoms.
[28]

Computed Tomography
Radiological evaluation by computed tomographic (CT) scanning and other methods is indicated
if there are other associated physical findings or if the paresis is progressive and unremitting. CT
scanning demonstrates the architecture of the temporal bone and may be used if some other
pathology is suspected.
Magnetic Resonance Imaging
Magnetic resonance imaging (MRI) of patients with Bell palsy may show enhancement of the
seventh cranial nerve (facial nerve) at, or near, the geniculate ganglion. However, if the paralysis
progresses over weeks, the possibility is high of a neoplasm compressing the facial nerve.
Tumors that compress or involve the facial nerve include schwannoma (most common),
hemangioma, meningioma, and sclerosing hemangioma. Perform gadolinium-enhanced MRI
when findings are atypical or when the facial nerve paralysis appears central to rule out a tumor
or vascular compression.
[29]

Little correlation between the enhancement of the facial nerve and the clinical outcome has been
noted. However, a recent analysis of early MRIs with gadolinium of the intratemporal facial
nerve demonstrated the ability to predict the long-term outcome of the facial paralysis; these
findings (increased signal intensity in the internal auditory canal after administration of
gadolinium) correlated favorably with those of electrodiagnostic testing. Thus, MRI is useful as a
means of excluding other pathologies as the cause of paralysis. MRI is preferred for imaging the
cerebellopontine angle.
Stethoscope Loudness Test
The stethoscope loudness test may be used to assess the functioning of the stapedius muscle. The
patient wears the stethoscope, and the activated tuning fork is placed at the bell of the
stethoscope. The loud sound will lateralize to the side of the paralyzed stapedius muscle.
Conduction Testing and Electromyography
Useful tests for evaluation of the function of the facial nerve include nerve conduction testing
and electromyography (EMG). These tests may aid in assessing the outcome of a patient who has
persistent and severe Bell palsy. They are most useful when performed 3-10 days after the onset
of paralysis. Do note that most electromyographic studies/nerve conduction studies do not show
an abnormality for 3 weeks following a peripheral nerve injury. EMG and nerve conduction
velocities produce a graphic readout of the electrical currents displayed by stimulating the facial
nerve and recording the excitability of the facial muscles it supplies.
Comparison to the contralateral side helps determine the extent of nerve injury and has
prognostic implications. This is not part of the acute workup. Nerve conduction responses are
abnormal if a difference of 50% in amplitude between the paralyzed and normal side is detected;
a difference of 90% between the 2 sides suggests a poorer prognosis. May et al demonstrated that
prognosis may be favorable if the motor amplitude of the affected side was greater than 25% of
that of the normal side. An incomplete recovery was observed in patients whose results
demonstrated less than 25% amplitude on the paralyzed side.
[30]
Blink reflexes can be used to
measure conduction across the involved segment, but they are commonly absent in Bell palsy.
Electroneurography
Electroneurography is a physiological test that uses EMG to objectively measure the difference
between potentials generated by the facial musculature on both sides of the face in response to a
supramaximal electrical stimulation of the facial nerve. Because all electrodiagnostic testing is
performed on the nerve distal to the proposed site of injury, sufficient time is needed for
wallerian degeneration to occur, usually 48-72 hours. Testing should begin 3 days from the onset
of complete paralysis.
Electrodiagnostic testing measures the facial nerve degeneration indirectly. If a patient does not
reach 90% degeneration within the first 3 weeks of onset of paralysis, some studies suggest the
prognosis is excellent, with over 80-100% of the patients recovering with excellent function. The
patients who reach over 90% degeneration within the first 3 weeks of onset of paralysis have a
much more guarded prognosis, with only 50% having good recovery of facial motion. The rate
of degeneration also predicts the prognosis. Those who have 90% degeneration by 5 days have a
worse prognosis than those with 90% degeneration at 14 days.
Brainstem Auditory Evoked Response
Brainstem auditory evoked response (BAER) may be obtained in patients with peripheral facial
nerve lesions and other neurologic involvement. This test measures the transmission of response
through the brainstem and is effective in detecting, notably, retrocochlear lesions. Hendrix and
Melnick evaluated BAER of 17 patients with Bell palsy. They found no evidence of
retrocochlear lesions of the auditory system in any of their patients with Bell palsy.
[31]
In another
study by Shannon et al, BAER was recorded in 27 patients with Bell palsy; only 6 patients had
prolonged brainstem transmission but normal auditory function.
[32]
These studies were small and
do not support routine use of BAER in patients with Bell palsy. However, when a patient
presents with multiple cranial neuropathies (eg, of the seventh and eighth cranial nerves), BAER
may be useful.
Audiometry
If hearing loss is suspected, audiography and auditory evoked potentials (AEPs) should be
pursued once an underlying structural lesion has been excluded. Typically, the hearing threshold
is not affected by Bell palsy. Impedance testing may reveal an absent or diminished stapedial
reflex because of paresis of the stapedial branch of the facial nerve.
Blepharokymographic Analysis
Blepharokymographic analysis, a high-speed eyelid motion-analysis system, has been recently
used to evaluate movement of the eyelids. Computerized-based analysis may prove helpful in
diagnosing Bell palsy, predicting prognosis, and evaluating response to therapeutic measures
such as a gold weight placement (used in cases in which spontaneous recovery has been limited).
Other Tests
Salivary flow also may be tested. The physician places a small catheter into both the paralyzed
and normal submandibular glands. The patient is then asked to suck on a lemon, and the salivary
flow is compared between the 2 sides. The normal side is the control.
The nerve excitability test determines the threshold of the electrical stimulus needed to produce
visible muscle twitching.
The Schirmer blotting test may be used to assess tearing function. The use of benzene will
stimulate the nasolacrimal reflex, and the degree of tearing can be compared between the
paralyzed and normal sides.
Histologic Findings
A review of 12 autopsy cases of patients with Bell palsy was summarized in Peter Dycks
Peripheral Neuropathy
[33]
. This review stated that most cases showed inflammatory changes
around the mastoid cells and walls of the arteries. The most common site of involvement was the
geniculate ganglion. Surgical findings described constriction of the nerve at the stylomastoid
foramen with swelling of the nerve itself. Microscopic findings showed an inflammatory reaction
with infiltration of macrophages on the nerve.

Bell Palsy Treatment & Management
Approach Considerations
Because persons with true Bell palsy generally have an excellent prognosis, and because
spontaneous recovery is fairly common, treatment of Bell palsy is still controversial. The goals
of treatment are to improve facial nerve (seventh cranial nerve) function and reduce neuronal
damage.
Many issues must be addressed in treating patients with Bell palsy. The most important
consideration is the onset of symptoms. Treatment may be considered for patients who have the
onset of paralysis within 1-4 days of the initial office visit.
Patients with Bell palsy frequently present to the ED. The role of the ED clinician consists of the
following:
Initiate appropriate treatment.
Protect the eye.
Arrange appropriate medical follow-up care.
The American Academy of Neurology (AAN) published a practice parameter in 2001 stating that
steroids are probably effective and acyclovir (with prednisone) is possibly effective for treatment
of Bell palsy. Any recommendation on facial decompression surgery had insufficient evidence.
A variety of nonpharmacologic measures have been used to treat Bell palsy, including physical
therapy (eg, facial exercises
[34]
and neuromuscular retraining
[35]
) and acupuncture.
[36]
No adverse
effects of these treatments have been reported. Reviews suggest that physical therapy may result
in faster recovery and reduced sequelae, but further randomized controlled trials are needed to
confirm any benefit.
Pharmacologic Therapy
The most widely accepted treatment for Bell palsy is corticosteroids. However, the use of
steroids is still controversial because most patients recover without treatment. Antiviral agents
have also been studied in this setting, as have combinations of the 2 types of drugs.
Corticosteroids
Many trials have been carried out to study the efficacy of prednisone in Bell palsy. In 1972, for
example, Adour et al conducted a large, controlled clinical trial that found that 89% of patients
treated with prednisone had full recovery compared with 64% of patients treated with placebo.
[37]

This study and other early studies have shown conflicting results using steroids in treating Bell
palsy,
[38]
and they have been limited in their size. However, 3 recent randomized, controlled trials
showed significant improvement in outcomes when prednisolone was started within 72 hours of
symptom onset.
[3, 4, 39]
Based on these 3 studies, steroids should be strongly considered to
optimize outcomes. Once the decision to use steroids is made, the consensus is to start
immediately.
One of these 3 recent studies, a double-blind, randomized trial from Scotland involving 551
patients with Bell palsy recruited within 72 hours of the onset of symptoms, demonstrated that
early treatment with prednisolone significantly improved the chances of complete recovery at 3
and 9 months.
[3]
In contrast, acyclovir given alone did not show any significant difference in the
rate of facial recovery compared to placebo, and there was no additional benefit from combining
acyclovir and prednisolone compared to prednisolone alone.
A larger double-blind, controlled trial showed that prednisolone significantly shortened the time
to complete recovery, whereas valacyclovir did not affect facial recovery compared to placebo.
[4]

The recommended dose of prednisone for the treatment of Bell palsy is 1 mg/kg or 60 mg/d for 6
days, followed by a taper, for a total of 10 days. Caution should be used in patients with
tuberculosis, immunocompromise, pregnancy, an active infection, sarcoidosis, sepsis, peptic
ulcer disease, diabetes mellitus, renal or hepatic dysfunction, or malignant hypertension.
High-dose steroids (>120 mg/d of prednisone) have been safely used to treat Bell palsy in
patients with diabetes
[40, 41]
; however, optimal dosing has not been established. Caution should
be given in these cases due to the risk of hyperglycemia.
Antiviral agents
Evidence evaluating the efficacy of antiviral medicines in Bell palsy has shown limited
benefit,
[42, 29]
with 3 recent randomized controlled trials showing no benefit.
[3, 4, 39]
However, there
is evidence to suggest a large percentage of Bell palsy cases may result from a viral infection.
[16,
43]
Therefore, antiviral agents may be reasonable in certain situations.
The AAN guidelines suggest that the use of acyclovir for the treatment of Bell palsy is only
possibly effective and that this agent alone is not effective in facial recovery. The Scottish study
cited earlier suggested that prednisolone, and not acyclovir, is useful for facial recovery in Bell
palsy.
[3]

A Cochrane review analyzed 7 studies (1987 patients) from 1966-2008 looking at the efficacy of
antivirals in the complete recovery from Bell palsy. In their review, antivirals showed no
significant benefit over placebo in the rate of incomplete recovery (relative risk [RR], 0.88; 95%
confidence interval [CI], 0.65-1.18).
[44]

Acyclovir (Zovirax) is administered at a dosage of 400 mg orally 5 times a day for 10 days.
Evidence supports herpes simplex virus (HSV) as a major cause of Bell palsy; if varicella zoster
virus (VZV) is suspected, higher doses may be needed (800 mg orally 5 times a day).
Valacyclovir (Valtrex), 500 mg orally twice a day for 5 days, may be used instead of acyclovir.
Although it is more expensive, it may be associated with better compliance. If VZV is the cause
of Bell palsy, higher doses may be needed (1000 mg orally 3 times a day). Because of increased
cost and increased risk of side effects with higher doses, valacyclovir cannot be routinely
recommended at this time.
Corticosteroid-antiviral combinations
A prospective randomized trial with 101 patients comparing prednisone and acyclovir
demonstrated that the prednisone group had a better clinical recovery.
[45]
In another prospective,
randomized trial with 99 patients, prednisone monotherapy was compared with the combination
of prednisone and acyclovir. This study demonstrated that combination therapy was more
effective in preventing nerve degeneration as measured by electrodiagnostic tests.
[46]

A Japanese randomized, prospective study of 221 patients with Bell palsy showed significant
improvement in facial function using both prednisone and valacyclovir therapy as compared with
those who used prednisone alone. This improvement was noted in those who had severe to
complete facial palsy.
[12]

Quant et al conducted a meta-analysis of published studies from 1984 to January 2009 that
showed no improved benefit (with respect to degree of facial muscle recovery in patients with
Bell palsy) with corticosteroids plus antivirals as compared to corticosteroids alone (odds ratio
1.50; 95% confidence interval, 0.83-2.69).
[47]
Six trials (representing pooled data of 1145
patients) were examined and included 574 patients who received corticosteroids alone and 571
patients who received corticosteroids and antiviral agents.
Quant et al suggest that the routine use of antivirals is not warranted; however, future studies
should improve diagnostic efforts to identify herpes virus as a potential etiology. Additionally,
newer antiviral agents may prove more beneficial than older antiviral agents used in the studies
analyzed to date.
[47]

Contrary to the Quant et al and Cochrane meta-analyses, de Almeida et al found that antiviral
agents, when combined with corticosteroids, were associated with greater risk reduction of
borderline significance than were corticosteroids alone (relative risk, 0.75; 95% CI, 0.56-
1.00).
[48]
Their meta-analysis examined 18 trials including 2786 patients. If antivirals are to be
initiated, they should be done so in conjunction with corticosteroids. Future studies will be
needed to determine which population will most benefit from antiviral therapy.
Whether to use prednisone alone or combination therapy is left to the discretion of the treating
physician.
Local Treatment
It is universally accepted that eye care is imperative in Bell palsy. The patients eye is at risk for
drying, corneal abrasion, and corneal ulcers.
In most cases, topical ocular lubrication (with artificial tears during the day and lubricating
ophthalmic ointment at night, or occasionally ointment day and night) is sufficient to prevent the
complications of corneal exposure.
[49]
Punctal plugs may be helpful if dryness of the cornea is a
persistent problem.
Occluding the eyelids by using tape or by applying a patch for 1 or 2 days may help to heal
corneal erosions. Care must be taken to prevent worsening the abrasion with the tape or a patch
by ensuring that the eyelid is securely closed. Clear plastic wrap, cut to 8 X 10 cm and applied
with generous amounts of ointment as a nighttime occlusive bandage, may be required.
External eyelid weights are available to improve mechanical blink. The weights are attached to
the upper lid with an adhesive and are available in different skin tones.
Lower-lid ectropion or droop can temporarily be helped by applying tape below the lid margin in
the center of the lower lid; pull the lid laterally and upward to anchor on the orbital rim.
Botulinum toxin can be injected transcutaneously or subconjunctivally at the upper border of the
tarsus and aimed at the levator muscle to produce complete ptosis and to protect the cornea.
[26]
Botulinum toxin may help in relaxing the facial muscles after they have developed mass
contraction, though the results are not as satisfying in patients with Bell palsy as in patients with
idiopathic hemifacial spasm.
Surgical Options
Surgical options include facial nerve decompression, subocularis oculi fat (SOOF) lift,
implantable devices placed into the eyelid, tarsorrhaphy, transposition of the temporalis muscle,
facial nerve grafting, and direct brow lift.
In the authors experience, surgical repair by using a combination of procedures tailored to the
patients clinical findings works well for improving symptoms and exposure. Most patients who
have had severe corneal exposure due to lagophthalmos with or without paralytic ectropion
received a combination of lateral tarsal strip placement, SOOF lift, and gold-weight
implantation. Patients without severe exposure have received a single procedure or combinations
of procedures.
Decompression of facial nerve
Surgery to decompress the facial nerve is controversial when performed in patients with
complete Bell palsy that has not responded to medical therapy and with greater than 90% axonal
degeneration, as shown on facial nerve electromyography (EMG) within 3 weeks of the onset of
paralysis.
[50, 19]
The problem must be localized with magnetic resonance imaging (MRI); then, the
surgeon can decide if the maxillary segment should be decompressed externally or if the
labyrinthine segment and geniculate ganglion should be decompressed with a middle-fossa
craniotomy.
Patients with a poor prognosis, identified by facial nerve testing or persistent paralysis, appear to
benefit the most from surgical intervention. However, studies have been mixed as far as benefit
from surgery.
[51]

A study compared a cohort of patients with degeneration greater than 90% who underwent
middle-fossa decompression with a cohort of similar patients who chose not to pursue surgical
decompression. The surgical group exhibited a House-Brackmann grade I or II in 91% of the
cases. The nonsurgical group had a poor result in 58% of the patients, with a House-Brackmann
grade III or IV at 7 months. This study also demonstrated that best results were obtained if the
decompression was attempted within 14 days after the onset of paralysis.
[52]

Subocularis oculi fat lift with lateral tarsal strip procedure
The SOOF lift is designed to lift and suspend the midfacial musculature. The SOOF is deep to
the orbicularis oculi muscle and superficial to the periosteum below the inferior orbital rim.
Lifting the SOOF may also elevate the upper lip and the angle of the mouth to improve facial
symmetry. A SOOF lift is commonly done in conjunction with a lateral tarsal strip procedure to
tighten the eyelid.
[53]

A lateral tarsal strip procedure is performed to correct horizontal lower-lid laxity and to improve
apposition of the lid to the globe. First, lateral canthotomy and cantholysis is performed. Then,
the anterior lamella is removed, and the lateral tarsal strip is shortened and attached to the
periosteum at the lateral orbital rim.
Implants in eyelid
Implantable devices have been used to restore dynamic lid closure in cases of severe,
symptomatic lagophthalmos. These procedures are best for patients with poor Bell phenomenon
and decreased corneal sensation. Gold or platinum weights, a weight-adjustable magnet, or
palpebral springs can be inserted into the eyelids. Pretarsal gold-weight implantation is most
commonly performed. The weight allows the upper eyelid to close with gravity when the levator
palpebrae are relaxed. Therefore, patients must sleep with their head slightly elevated.
The implants are inert and composed of 99.99% pure gold or platinum. Sizes range from 0.6-1.8
g. They are easily removed if nerve function returns. Complications include migration of the
implant, inflammation, allergic reaction, or extrusion.
Tarsorrhaphy
Tarsorrhaphy decreases horizontal lid opening by fusing the eyelid margins together to improve
support of the precorneal lake of tears and to improve coverage of the eye during sleep. The
procedure can be done in the office and is particularly suitable for patients who are unable or
unwilling to undergo other surgery. It can be completed as either a temporary or a permanent
measure. Permanent tarsorrhaphy is done if nerve recovery is not expected.
Tarsorrhaphy can be performed laterally, centrally, or medially. The lateral procedure is most
common; however, it can restrict the monocular temporal visual field. Central tarsorrhaphy
offers good corneal protection, but it occludes vision and can be cosmetically unacceptable.
Medial or paracentral tarsorrhaphy is performed lateral to the lacrimal puncta and can offer good
lid closure without substantially affecting the visual field.
Transposition of temporalis
Transposition of the temporalis muscle can be used to reanimate the face and to provide lid
closure by using the fifth cranial nerve. Strips from the muscle and fascia are placed in the upper
and lower lids as an encircling sling. Patients initiate movement by chewing or clenching their
teeth.
Facial nerve grafting or hypoglossal-facial nerve anastomosis
Reinnervation of the facial nerve by means of facial nerve grafting or hypoglossal-facial nerve
anastomosis can be used in cases of clinically significant permanent paralysis to help restore
relatively normal function to the orbicularis oculi muscle or eyelids.
Direct brow lift
Brow ptosis is repaired with a direct brow lift. Care should be taken in the presence of corneal
decompensation because lifting the brow can cause worsening of lagophthalmos, especially if lid
closure is poor. A gold-weight implant can be placed or lower-lid resuspension can be performed
simultaneously to prevent this complication.
Consultations
If the initial impression based on the history and physical examination is not Bell palsy, then
consultation with a neurologist or otolaryngologist is needed. For example, consultation with an
otolaryngologist should be made for the patient who has facial palsy and pain and in whom the
ear, nose, and throat examination does not show auricular vesicles (as in Ramsay Hunt
syndrome). These patients should be evaluated for malignancy or other structural lesion of the
facial nerve.
If the paralysis persists for several months, consultation with a neurologist or otolaryngologist
should be sought. An evaluation with an otolaryngologist may be indicated for patients with a
prolonged course, for the consideration of surgical decompression of the facial nerve.
Patients who report persistent dry eye or painful eye should be referred to an ophthalmologist.
An evaluation by a specialist in infectious disease may be indicated if results of laboratory
studies are positive for Lyme disease, syphilis, or HIV infection.
Long-Term Monitoring
If the paralysis is not resolved or is progressing to complete paralysis, a thorough neurologic and
head, eyes, ears, nose, and throat (HEENT) examination should be performed to rule out
neoplastic causes of facial nerve palsy.
The patient should be monitored if the initial EMG shows the involved facial muscles to have
less than 25% of the function of the normal side.
If the residual paralysis is severe, the patient should be referred for counseling.
Bell Palsy Medication
Medication Summary
The goals of pharmacotherapy are to reduce morbidity and prevent complications. Agents used
in cases of Bell palsy include corticosteroids and antivirals.
Corticosteroids
Class Summary
Prednisone can be used but has many adverse effects, including fluid retention, hypokalemia,
myopathy, peptic ulcer, headache (pseudotumor), menstrual irregularities, cataracts, glaucoma,
and manifestation of latent diabetes mellitus. Signs of infection may also be masked in patients
taking prednisone. Physicians should use caution when using prednisone in patients with the
aforementioned conditions.
View full drug information
Prednisone (Deltasone, Orasone, Sterapred)
Prednisone is a glucocorticoid that is absorbed readily from the gastrointestinal tract. It has anti-
inflammatory and immune-modulating effects, as well as profound and varied metabolic effects.
Antiviral Agents
Class Summary
These have been used in the treatment of Bell palsy in combination with prednisone or used
alone in patients who cannot take prednisone.
View full drug information
Acyclovir (Zovirax)

Acyclovir is a prodrug activated by phosphorylation by virus-specific thymidine kinase that
inhibits viral replication. Herpes virus thymidine kinase (TK), but not host cells TK, uses
acyclovir as a purine nucleoside, converting it into acyclovir monophosphate, a nucleotide
analogue. Guanylate kinase converts the monophosphate form into diphosphate and triphosphate
analogues that inhibit viral DNA replication.
Acyclovir has affinity for viral thymidine kinase and, once phosphorylated, causes DNA chain
termination when acted on by DNA polymerase. It inhibits activity of both herpes simplex virus
(HSV)-1 and HSV-2. Patients experience less pain and faster resolution of cutaneous lesions
when used within 48 hours from rash onset. Acyclovir may prevent recurrent outbreaks. Early
initiation of therapy is imperative.
View full drug information
Valacyclovir (Valtrex)

Valacyclovir is a prodrug that is rapidly converted to the active drug acyclovir. It is more
expensive but has a more convenient dosing regimen than acyclovir.
5. http://www.nlm.nih.gov/medlineplus/bellspalsy.htm
If you have Bell's palsy, the muscles in your face become temporarily paralyzed. It usually
affects just one side of the face. Symptoms appear suddenly - you can't shut your eye and your
mouth droops. Symptoms are usually worst about 48 hours after they start.
Scientists think that a viral infection makes the facial nerve swell or become inflamed. You are
most likely to get Bell's palsy if you are pregnant, diabetic or sick with a cold or flu.
Three in four patients improve without treatment. With or without treatment, most people begin
to get better within 2 weeks and most recover completely within 3 to 6 months.
NIH: National Institute of Neurological Disorders and Stroke
6.http://www.fkumyecase.net/wiki/index.php?page=GEJALA+DAN+TANDA+KLINIS+BELL
%E2%80%99S+PALSY+PADA+LAKI-
LAKI+58+TAHUN+DENGAN+FAKTOR+RISIKO+DIABETES+MELITUS
7. http://www.ilmukesehatan.com/198/kenali-tanda-dan-gejala-bells-palsy.html